IHMA Kerala Model Homeopathy MD Entrance Exam 2011 Paper.1

Time Allowed: 1 Hour and 30 minutes
Maximum Marks: 600

  2. Please verify that your test booklet contains 16 pages, including answer sheet.
  3. This Test Booklet contains 150 items (questions). Each item comprises four responses (answers). You will select the response which you want to mark on the Answer Sheet. In case you feel that there is more than one correct response, mark the response which you consider the best. In any case, choose ONLY ONE response for each item.
  4. You have to mark all your responses by shading the bubbles on the separate Answer Sheet provided. DO NOT write anything on the Answer sheet.
  5. Negative Marking: In order to discourage wild guessing, the score will be subject to penalization formula based on the number of right answers actually marked and the number of wrong answers marked. Each correct answer will be awarded 4 mark. 1 mark will be deducted for each incorrect answer. More than one answer marked against a question will be deemed as an incorrect response and will be negatively marked. No negative marks for un attended questions
  6. The Answer key along with the results of this exam will be published in our website www.ihma.in
  7. Please note the matching ROLL NUMBERS given in your question booklet and answer sheet

1) Empty, faint feeling in stomach with loathing of food and obstinate constipation with no desire for stool is a combination that must generally have

  • a) Alumina     b) Opium
  • c) Hydrastis   d) Anacardium

2) The extreme restlessness of the limbs is like Ars and it is a deep acting medicine like Ars., and it sometimes has cured where Ars. has failed although it seemed well selected

  • a) Ars iod                    b) Tarentula
  • c) Anthracinum       d) Calcarea Ars

3) Potatoes and starchy foods disagree with the patient like Alumina., according to Dr. Kent

  • a) Bryonia                   b) Colocynth
  • c) Natrum Sulph      d) Natrum Mur

4) In its chronic manifestations is overburdened with heat, but in an acute trouble is chilly

  • a) PuIsatiIIa           b)SiIicea
  • c) Merc sol              d) Natrum Mur

5) Which patient is “sensitive to cold and there is a marked lack of vital heat” but at the same time “sensitiveness to a warm atmosphere when there are head and spine symptoms”

  • a) Sepia           b)Lycopodium
  • c) Merc sol    d) Ledum pal

6) “In acute complaints there is violent thirst, in chronic complaints thirstIessness.” The remedy is

  • a) PuIsatiIIa & Apis    b) Ars Alb & Apis
  • c) Camphor & Apis     d) Camphor & Ars Alb

7) He goes into a rage when he sees the doctor, saying: “Go home, I am not sick, I did not send for you.” The remedy is

  • a) Arnica only                  b) Arnica & Apis
  • c) Arnica & Bryonia      d) Arnica & Stram

8) Children are late in learning to talk and walk, thus combining the features of two remedies, Natrum muriaticum, which has the symptom “Iate learning to walk” and Calcarea carb, which has the symptom “Iate learning to talk”. Remedy is

  • a) Borax                    b) Agaricus
  • c) Natrum carb     d) Causticum

9) Remedy “is the very opposite of all things fastidious. Arsenicum is the typical fastidious patient, and these two remedies are the extremes of each other”. Kent speaks about Arsenic and

  • a) SuIphur       b)Capsicum
  • c) Merc sol      d)Psorinum

10) “The rattling in the chest is as marked as in Antimonium tartaricum; the tenacious mucus is as copious, as gluey and stringy as in Kali bichromicum” in

  • a) KaIi suIph        b) Senega
  • c) KaIi iod             d) Causticum

11) In which remedy do you find rectal symptoms with “we find the haste of Sulphur, the flatulence of Oleander. and Aloe, and difficulty of expelling a soft stool like Alumina, China and Nux moschata” ?

  • a) Psorinum                 b) Podophyllum
  • c) Lycopodium          d) Veratrum Alb

12) “HystericaI subjects may not have chorea constantly, but as soon as she retires at night the whole of the side Iain on will commence to jerk and prevent her from going to sleep”.Remedy is

  • a) Ignatia                               b) Agaricus
  • c) Tarentula Hispanica   d) Actea Racemosa

13) Nausea from Mental Exertion, thinking etc. is found in

  • a) Borax                          b) Natrum Mur
  • c) Natrum Carb           d) Natrum Phos

14) “CompIaints develop slowly, i.e. , slowly for acute conditions.” in

  • a) Bryonia             b) Rhus Tox
  • c) Ferrum Phos d) Kali Mur

15) Pains are increased by noise in

  • a ) Coffea only                      b) Coffea and Nux vomica
  • c) Nux vomica only        d) None of the above

Download the full question paper (150 questions) : www.similim.com/pdf/ihma-mdentrance-2011-1.pdf

Download revised answer key : www.similima.com/pdf/ihma-answerkey2011.pdf

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Rajiv Gandhi University Homoeopathy MD Entrance Test 2011

Maximum Marks : 100                                                             Maximum Time : 90 Minutes

1. Carrying any electronic gadgets like Pager, Cell Phone, Cordless Phone, Bluetooth, Calculator etc. to the Examination Hall amounts to malpractice may lead to debarring the candidate from writing exam.

2. Do not write/mark anything on the question paper booklet except Register Number. Any other markings made on the Question Booklet would be considered as Mal-practice may lead to debarring the candidate from writing exam.

3. Do not open the booklet during the first ten minutes after the 2nd  bell at 9.50, a.m. You should not look inside the Questions Booklet or start answering on the answer sheet during initial 10 minutes. Remove the seal on the side to open this booklet only after the 3rd  bell at 10.00 a.m. and start answering.

4. The initial 10 minutes are meant to enter your Name, Roll No., Question Booklet No., on the Optical Mark Reader (OMR) answer sheet. As the OMR sheet is designed for the Optical Mark Reader (OMR) system, special care should be taken to fill items accurately.

5. The question paper and OMR answer sheet are issued separately at the start of the examination.

6. This Question Booklet contains 100 questions and 90 minutes given for answering. Any variation should be brought to the notice of the invigilator immediately.

7. During the 90 minutes:

(i) Read each question carefully.
(ii) Choose the most appropriate single answer from out of the four available alternatives under each question.
(iii) Completely darken the relevant oval with a blue or black ball-point pen against the question number on the answer sheet.
(iv) Any inadvertent drop/mark of pen/ink on the other oval marks makes the answer invalid.

For Example :

Q. No. 14: In which of the following, air borne transmission occurs ?
(a) French fever            (b) Kyasanur Forest disease
(c)   Q fever                  (d)  Relapsing fever

As the most appropriate single answer is option “c” you should darken the oval corresponding to the option “c” completely with a blue or black ball-point pen, on the OMR sheet once marked, any corrections using eraser, whitener or any sharp object is treated as malpractice.

8. For each correct answer, one mark will be awarded.
(a) There shall be no deduction of marks for wrong answer.
(b) If more than one alternative is marked, it will be considered as a wrong answer.
(c) Wrong answers carry no marks.

9. Rough work should be done only on the blank page at the end of the Question Booklet. Rough work should not be done on the OMR sheet.

10. Please stop writing when the last bell at 11.30 a.m. Hand over the OMR sheet set to the invigilator who will separate the top sheet and will retain the same with him and return the duplicate copy to you to carry it home.

11. If you want to leave the Examination Hall earlier, you should hand over the question paper and the OMR answer sheet to the invigilator and collect the question paper and the duplicate copy of the OMR sheet at the end of the scheduled dosing time 11.30 a.m.

1. HIV virus attacks

  • a) Helper T cells             b) Suppressor T cells
  • c) Cytotoxic T cells         d) Memory cells

2. Auerbach’s plexus of GIT are concerned with

  • a) Secretion of GIT
  • b) Motor functions of GIT
  • c) Above all
  • d) None

3. The respiratory centers are situated in

  • a) Pons and medulla       b) Cerebellum
  • c) Hypothalamus            d) Thalamus .

4. Athletes show resting bradycardia due to

  • a) increase vagal tone
  • b) decrease vagal tone
  • c) increased sympathetic stimulation
  • d) none

5. Renin – Angiotensin mechanism associated with

  • a) Fall in BP       b) Rise in BP
  • c) Hypertension d) None

6. Misanthropic wants to fly away from his own family, mistrustful are the symptom of

  • a) Hepar sulph   b) Fluoric acid
  • c) Bryonia         d) Lycopodium

7. Atrophic rhinitis is the main symptom in

  • a) Lemna Minor  b) Ledum
  • c) Mer. sol.        d) Kali Carb

8. Milk in the breast instead of menses is the symptom of

  • a) Silicea           b) Pulsatilla
  • c) Phytolacca     d) Mercurius sol

9. The characteristic tongue of Ipecac is

  • a) clean             b) thickly coated
  • c) mapped         d) red tipped

10. Calcarea carb is adapted to constitution of

  • a) Leucophlegmatic        b) Scrofulous
  • c) Phlegmatic                 d) None of these

11. Systematic Alphabetic Repertory of Homoeopathic Remedy Doctrine

  • a) Woss             b) Rucket
  • c) Jahr              d) Hempel

12. The methods of cross repertorisation are

  • a) Rearranging totality    b) Integrated approach
  • c) All of the above          d) None of the above

13. Stimulare is a

  • a) New Repertory
  • b) New Software Programme
  • c) New Drug
  • d) New method of prescription

14. ‘Dolphin’ is related to

  • a) Repertory
  • b) Software programme
  • c) Text book in repertory
  • d) None of the above

15. Miasmatic Repertory by R.P Patel was published on

  • a) 1995    b) 1996
  • c) 2006    d) 2000

16. Chronic asthma in summer is a feature of

  • a) Psorinurn       b) Medorrhinum
  • c) Bovista          d) Syphillinum

17. Fear of being assassinated is in

  • a) Lac Can         b) Aurum Met
  • c) Zincurn          d) Plumbum Met

18. 1st  Edition of Organon book published in 1810 by

  • a) Gillbert          b) Lord Bacon
  • c) Sarkar           d) Arnold Dresden

19. Hyoscyamus cough is characterized by

  • a) Nervous cough
  • b) Aggravated by lying down when head touches the pillow
  • c) Caused by elongated uvula
  • d) All of these

20. In Cuprum met convulsion, the aura begins in

  • a) Lower extremities
  • b) Upper extremities
  • c) Abdomen
  • d) Face

21 . BTPB is published in

  • a) 1896
  • b) 1897
  • c) 1846
  • d) 1833

22. Headquarters of WHO situated in

  • a) USA
  • b) Geneva
  • c) Tokyo
  • d) New Delhi

23. Incubation period of measles

  • a) 2 weeks
  • b) 3 weeks
  • c) 4 weeks
  • d) 5 weeks

24. Vector of Chikungunya

  • a) Housefly
  • b) Mosquito
  • c) Tick
  • d) Cockroach

25. The optimum level of total cholesterol should be less than

  • a) 100 mg/dl
  • b) 200 mg/dl
  • c) 250 mg/dl
  • d) 350 mg/dl

26. Guernsey’s Card Repertory was based on

  • a) BBCR        b) Lippe’s Repertory
  • c) BTPB         d) Kent’s Repertory

27. ‘Quis’ means

  • a) Diseases    b) Location
  • c) Modality     d) Personality

28. “Quando’ means

  • a) Location
  • b) Personality
  • c) Modality
  • d) Time

29. The abbreviation CoCl

  • a) Coccus cacti
  • b) Cocculus
  • c) Coccainuem
  • d) Coca

30. ‘Fragmenta Deviribus; Medicarnentorus Postious’ was published in

  • a) 1806
  • b) 1810
  • c) 1805
  • d) 1811

31. Treatment of Indisposition

  • a) Slight alteration of diet and regimen
  • b) Constitutional remedy
  • c) Acute remedy
  • d) Anti Miasmatic

32. Test to find out true mental disease and mental disease of doubtful origin is given in

  • a) 93                 b) 210
  • c) 224               d) 230

33. Reason for Homeopathic aggravation

  • a) Massive dose             b) Drug abuse
  • c) Small dose                 d) Dose is riot sufficiently small enough

34. § no. 4 of Organon of Medicine deals with

  • a) Preserver of health     b) Unprejudice observer
  • c) Science of hygiene     d) Preventive medicine

35. Glycated Hemoglobin is a. combination of

  • a) Carbon dioxide + HbA             b) Ferric iron + HbA
  • c) Glucose + HbA                       d) Glycine + HbA

36. Homoeopathy and Child Care was published by

  • a) Dr. S.K. Tiwari           b) R.P.Patil
  • c) Sivaraman                 d) None of the above

37. The word ‘rubric’ originated from

  • a) Latin             b) German
  • c) Greek            d) English

38. Gentry Repertory consists of f6flowing volumes

  • a) 4      b) 3
  • c) 5       d) 6

39. Knerr’s Repertory was published in

  • a) 1898             b) 1896
  • C) 1996             d) 1847

40. The Repertory which is related to clinical repertories

  • a) Bell’s Diarrhoea
  • b) Kent’s Repertory
  • c) Murphy’s Repertory
  • d) Synthesis

41. All are features of Vitamin A deficiency EXCEPT

  • a) Xerophthalmia
  • b) Osteomalacia
  • c) Follicular hyperkeratosis
  • d) Keratomalacia

42. Chest pain due to pericarditis is

  • a) Precipitated by exertion
  • b) Radiated to left arm
  • c) Relieved by sitting up and leaning forward
  • d) Associated with sweating

43.) The ‘a’ wave in the Jugular venous tracing is due to

  • a) Ventricular Diastole    b) Ventricular Systole
  • c) Atrial Diastole                        d) Atrial Systole

44. Continuous murmur is heard in

  • a) Atnal Septal Defect     b) Ventricular Septal Defect
  • c) Pallet’s Tetroiogy        d) Patent-Ductus Arteriosus

45. The part of Electro cardiogram that corresponds with Ventricular depolarisation is

  • a) P wave          b) QRS complex
  • c) PR interval     d) ST-segment

46. P wave of ECG is due to

  • a) Atrial repolarization                b) Atria depolarization
  • c) Ventricular depolarization        d) Ventricular repolarization

47. Concise Repertory of Homoeopathic  Medicine was published by

  • a) Phatak          b) Carke
  • c) Murphy          d) Schroyens

48. Phatak’s Repertory was published on

  • a) 1963             b) 1964
  • c) 1974             d) 1984

49. Roger von Zandoort is associated with

  • a) Complete repertory
  • b) Repertorium Universale
  • c) All the above
  • d) None of the above

50. Phoenix Repertory is published by

  • a) J.P.S. Bakshi              b) S.P.S. Bakshi
  • c) D. Bakshi                   d) None of the above

51. Calcutta Homoeopathic Medical College was established by Dr. D.N.Roy and

  • a) Rajendralal Dutt         b) Diwan Jai Chand
  • c) Father Muller              d) Dr. Pratapchandra Majumdar

52. Father of Indian Homoeopathy

  • a) Dr. Pradeep C. Majumdar        b) B. C, Roy
  • c) Rajendralal Dutt                          d) D.     Roy

53. “Medicine of Experience” by Samuel Hahnemann in

  • a) 1810             b) 1847
  • c) 1828             d) 1805

54. 6th  edition of Organon of Medicine published in

  • a) 1809             b) 1804
  • c) 1790             d) 1921

55. Title of 1st  edition of Organon book

  • a) Medicine of Experience
  • b) My Experiments With Truth
  • c) Fragmenta de Virubus
  • d) Organon of Rational Art of Healing

56. Thyrotoxicosis is characterised by the following features, EXCEPT

  • a) Tachycardia               b) Constipation
  • c) Tremor                      d) Weightless

57. Hypertension is a feature of all the following EXCEPT

  • a) Renal Artery stenosis              b) Pheochromo cytoma
  • c) Addison’s disease                     d) Cushing’s syndrome

58. Trousseau’s sign is characteristic of

  • a) Hyper thyroidism        b) Hypo thyroidism
  • c) Tetanus                            d) Tetany

59. Ptosis is caused by paralysis of

  • a) III Cranial Nerve
  • b) IV Cranial Nerve
  • c) V Cranial Nerve
  • d) V1 Cranial Nerve

60. First heart sound occurs due to

  • a) opening of the AV valve
  • b) closure of the semilunar valve
  • c) closure of the AV valve
  • d) opening of the semilunar valve

61. Kreosoturn is inimical to

  • a) Carbo veg                 b) Kali carb
  • c) Nux vomica.           d) Phosphorous

62. Dreams that she is drinking

  • a) Arsenic,         b) Medorrhinum
  • c) Phosphorus    d)  All the above

63. Fear of financial ruin

  • a) Kali phos       b) Calc fluor
  • c) Calc phos       d) Natrurn phos

64. Nodular swellings in joints is the symptom of

  • a) Bryonia              b) Conium
  • c) Lithium Carb  d) Allium Cepa

5. Diarrhoea of green watery frothy like scum on frogs pond is a symptom of

  • a) Mag Mur        b) Mag Carb
  • c) Arnica           d) Aconite

66. Birth year of J.T. Kent

  • a) 2nd  July 1843             b) 10th April 1847
  • c) 31st March 1849          d) 1st  1847

67. “Chronic Diseases” by Samuel Hahnemann  published in the year

  • a) 1804             b) 1828
  • c) 1905             d) 1811

68. Author of ‘Repertory of the Antipsoric Medicines

  • a) C.H. Allen
  • b) AllenT.F.
  • c) Dr. C.M.F. Von Boenninghausen
  • d) Jahr

69 “Encyclopedia of Pure Materia Medica” belongs to

  • a) H.C. Allen       b) Lippe
  • c) 114 TF. Allen  d) Hahnemann

70. Who proved Lachesis

  • a) Hahnemann
  • b) Dr. C. Hering
  • c) Clarke J.H.
  • d) Boger

7 1. In tonsillitis purple colour of throat beginning on left side is a symptom of

  •  a) Ruta                b) Conium
  • C) Lachesis        d) Hepar Sulph

72. Complaints of Fluoric acid are better by

  • a) Warmth                           b) Open air
  • c) Cold application          d) All of these

73. Toothache aggravation by drawing cold air into mouth or cold drinks; teeth turn black, crumble and decay on edges. Drug is

  • a) Mercurius      b) Mezerium
  • c) Staphysagria  d) None of these

74. Headache or neuralgia begin lightly, increase gradually to the highest point and then gradually decline seen in

  • a) Kali bichromicum        b) Pulsatilla
  • c) Stannum met             d) None of these

75. Malignant Hypertension occurs in

  • a) Diabetes Mellitus        b) Heart Disease
  • c) Renal Disease            d) None of above

76. Number of § in the 6t’ edition of Organon of Medicine

  • a) 219               b) 258
  • c) 291               d) 286

77. Treatment of Mental diseases comes under

  • a) 269-271                    b) 210 – 230
  • c) 252-256                     d) 245-251

78. Importance of PQRS symptoms explained in the § number

  • a) 2 6                b)153
  • c) 270               d) 5

79.Samuel Hahnemann has mentioned about obvious cause in the § number

  • a) 93                 b)39
  • c)36                 d)63

80. Idiosyncrasies has been explained in the § number

  • a) 117               b)07
  • c)143                d)153

81. Lead I + Lead III = Lead II

  • a) Einthoven’s law
  • b) Marey’s law
  • c) Starling’s law
  • d) Landsteiner’s law

82. Keratomalacia – a feature of

  • a) Vitamin A deficiency
  • b) Vitamin K deficiency
  • c) Vitamin C deficiency
  • d) Vitamin D deficiency

83. ADH – a secretion of

  • a) Adrenal cortex               b) Anterior pituitary
  • c) Posterior pituitary       d) Pancreas

84. Semicircular canal and otolithic organs of ear are concerned with

  • a) Hearing         b) Equilibrium
  • c) Olfaction        d) None

85. Devil’s Dung is the common name of’

  • a) Baptisia tinctoria        b) Asafoetida
  • C)Melilotus                    d) Helleborus niger

86. Title page of 1st  edition of Organon has the words from a Poe m by

  • a) Arnold           b) Christian Gellert
  • C)Stapf,            d) Dudgeon

87. Number of § in 2nd  edition of Organon

  • a) 292               b) 315
  • c) 271               d) 319

88. The 3rd edition of Organon had number of §

  • a) 317         b) 320
  • c) 315       d) 292

89. Number of § in 5th edition of Organon

  • a) 292            b) 294
  • c) 320         d) 271

90. ‘Novum Organum’ was written by

  • a) Lord Dalhousie           b) Lord Bacon
  • c) Lord Mountbatton        d) R. E. Dudgeon

91. Specific enzyme detected in blood in Acute MI is

  • a) CKMB            b) SGOT
  • c) SGPT             d) Aldosterone

92. Koilonychia is seen in

  • a) Vit. C deficiency         b) Malignancy
  • c) Folic acid deficiency    d) Iron deficiency anemia

93. Faecal-oral route of spread of infection is found in

  • a) Hepatitis-B     b) Hepatitis-C
  • c) Hepatitis-D     d) Hepatitis-E

94. Clinical finding NOT associated with Typhoid fever

  • a) Splenomegaly                              b) Rose-spots
  • c) Erythema marginatum            d) Abdominal distention

95. Bradycardia is seen in the following situations EXCEPT

  • a) Hyper thyroidism
  • b) Obstructive Jaundice
  • c ) Hypothyroidism
  • d) Complete Heart Block

96. Which of the following is NOT a feature of systemic Lupus Erythematosis ?

  • a) Malar Rash    b) Leucoc_ytosis
  • c) Serositis        d) Anti-DNA antibodies

97. HBsAG is found to be associated with

  • a) Poly Myositis                   b) Rheumatoid Arthritis
  • c) Polyarteritis Nodosa    d) SLE

98. Hyperpigmentation is NOT a  feature of

  • a) Pheochromo cytoma
  • b) Haemochronatosis
  • c) Addison’s diseases
  • d) Nelson’s syndrome

99. Flag sign is characteristic of

  • a) Psoriasis                        b) Leprosy
  • c) Kwashiorkor               d) Malnutrition

100. `Kent’s Repertorium Genrale was published by

  • a) P. Schmidt
  • b) Jost Kunzili
  • c) P. Sivaraman
  • d) R.P.Patel

This is a question paper of  Post Graduate Homoeopathy Entrance Test (AHPNP) 2011 conducted by Rajiv Gandhi University of Health Sciences. Karnataka

  We are thankful to Dr.Ram Jyothis & Vivek Sakthidharan for this question booklet

Download answer Key : www.similima.com/pdf/rguhs-md-2011-key.pdf  

All rights reserved @ similima

Kerala PSC Homeopathy Medical Officer Examinations 2007

 A  Series
Time: 75 Minutes      Maximum: 100 Marks


  1. The question paper will be given in the form of a Question Booklet. There will be four versions of question booklets with question booklet alpha code viz. A, B, C & D.
  2. The Question Booklet Alpha Code will be printed on the top left margin of the facing sheet of the question booklet.
  3. The Question Booklet Alpha Code allotted to you will be noted in the address list intended for obtaining your signature and also in the seat allotted to you in the Examination Hall.
  4. If you get a question booklet where the alpha code does not match to the allotted alpha code in the address list/seating position, pl~ase draw the attention ofthe Invigilator IMMEDIATELY.
  5. The Question Booklet Serial Number is printed on the top right margin of the facing sheet. If your question booklet is unnumbered, please get it replaced by new question booklet with same alpha code ..
  6. Write the question booklet alpha code in the space provided in Part B of the answer sheet and darken the appropriate bubble.
  7. The question booklet will be sealed at the middle of the right margin. Candidate should not open the question booklet, until the indication is given to start answering.
  8. Immediately after the commencement of the examination, the candidate should check that the question booklet supplied to him contains all the 100 questions in serial order. The question liooklet does not have unprinted or torn or missing pages and if so he/she should bring it to the notice of the Invigilator and get it replaced by a complete booklet with same alpha code. This is most important.
  9. A blank sheet of paper is attached to the question booklet. This may be used for rough work.
  10. Please read carefully all the instructions on the reverse of the Answer Sheet before marking your answers.
  11. Each question is provided with four choices (A), (B), (C) and (D) having one correct answer. Choose the correct answer and darken the bubble corresponding to the question number using Blue or Black Ball-Point Pen in the OMR answer sheet.
  12. Each correct answer carries 1 mark and for each wrong answer 1/3 mark will be deducted. No negative mark for unattended questions.
  13. No candidate will be allowed to leave the examination hall till the end of the session and without handing over his/her Answer Sheet to the Invigilator. Candidates should ensure that the Invigilator has verified all the entries in the Register Number Coding Sheet and that the Invigilator has affixed his/her signature in the space provided.
  14. Strict compliance of instructions is essential. Any malpractice or attempt to commit any kind of malpractice in the Examination will result in the summary disqualification of the candidate.

1. Enzyme deficiency in Diabetes Mellitus is :
(A) Glycokinase     (B) Hexokinase
(C) Phosphorylase (D) Phosphate dehydrogenase

2. Herberden nodes are seen in :
(A) Rheumatoid Arthritis (B) Rheumatic Arthritis
(C) S.L.E.                    (D) Osteoarthritis

3. Japanese Encephalitis is caused by:
(A) Human retrovirus (B) Enterovirus
(C) Arbovirus           (D) Cytomegalovirus

C. Normal human requirement of Potassium per day is:
(A) 100meq.    (B) 120 meq.
(C) 130 meq.   (D) 150 meq.

5. Most common opportunistic infection in AIDS is :
(A) Aspergillosis (B) Cryptococcosis
(C) Candidiasis  (B) Tuberculosis

6. Cavernous breathing is seen in:
(A) Calung            (B) Consolidation
(C) Pleural effusion (D) Cavity lung

7. Diagnosis of typhoid fever in the first week is by :
(A) Widal test     (B) Stool culture
(C) Urine culture  (D) Blood culture

8. pH of gastric acid is :
(A) 1.5 to 2.0   (B) 0.5 to 2.5 .
(C) 2.3 to 3     (D) 3 to 3.5

9.Daily requirement of Vitamin K in adult is :
(A) 10-20 microgram    (B)20-50 microgram .
(C) 70-140 microgram   (D)More than 150 microgram

10. Diagnostic characteristic in Carcinoma prostrate with metastasis is raise in :
(A) ESR                   (B) Alakline phosphatase
(C) Acid phosphatase (D)Bilirubin

11. Commonest degenerative joint disease is :
(A) Gout                      (B) Osteoporosis
(C) Rheumatoid Arthritis (D) Osteoarthritis

12. Most common bone fracture in body is :
(A) Clavicle   (B) Femur
(C) Radius    (D) Vertebra

13. Herpes ‘Zoster is commonly seen in :
(A) Cervical region   (B) Geniculate ganglia
(C) Lumbar region    (D) Thoracic region

14. Causative organism of Molluscum Contagiosum is :
(A) Papova virus       (B) Pox virus
(C) Orthomyxo virus  (D) Parvo virus

15.Which of the following infection has the most neurological complications :
(A) Measles        (B) Rubella
(C) Scarlet fever (D) Small pox

16.Normal heart rate per minute at birth is :
(A) 60-80     (B) 80-110
(C) 70-120   (D) 110-150

17 . Kwashiorkor is due to:
(A) Protein deficiency           (C)Energy deficiency
(B) Malabsorption of Vitamins (D) Protein and energy deficiency

18. Iron is absorbed actively in the:
(A) Stomach         (B) Duodenum
(C) Lower jejunum (D) Proximal ileum

19. Liver does not produce:
(A) Albumin     (B) Gama globulin
(C) Fibrinogen  (D) Prothrombin

20. Main function of Mitochondria is :
(A)Protein synthesis (B)Oxidation
©Electron transfer   (D) Fat synthesis

21. Ketone body formation takes place in :
(A) Liver    (B) Kidney
(C) Spleen  (D) Blood

22.Sensation of coldness about the heart is the symptom of:
(A) Petroleum (B) Cactus G
(C) Digitalis (D) Naja

23. Palpitation before and during menses is present in :
(A) Ammonium carb (B) Natrum mur
(C) Spongia.          (D) Sepia

24. Toothache from tobacco sqlOking is the symptom of:
(A) Tabacum (B) Nuxvom
(C) Coffea    (D) Spigelia

25. Cannot walk on uneven ground is present in :
(A) Lachesis (B) Lobelia
(C) Lyssin    (D) Lil. tig

26. The medicine for acute affection of prostrate after maltreated stricture is :
(A) Merc bin-iodide     (B) Merc cynide
(C) Merc proto-iodide  (D) Merc dulcis…

27. Pain from naval to uterus is the symptom in:
(A) Cimicifuga   (B) Colocynthis
(C) Ipecac       (D) Magphos

28. Constipation on going to sea is treated with:
(A)D Bryonia alb   (B) Platina
(C) Plumb met      (D) Sepia

29. Pain as if bones were torn into pieces is present in :
(A) Eup per    (C) Theridion
(B) Ipecac     (D) Thuja

30. Convulsions during teething with fever is the symptom in :
(A) Acon nap   (B) Belladonna
(C) Cicuta       (D) Mag Phos

31. Convulsion during teething without fever is characteristic of:
(A) Acon nap   (C) Cup met
(B) Belladonna (D) Mag phos

32. Cough with expectoration of green mucus is a symptom of:
(A) Bryonia (B) Kali carb
(C) Benzoic acid (D) Rhus tox

33. Pain and numbness in right ovary, running down the thigh of that side is present in :
(A) Coniummac    (B) Medorrhinum
(C) Podophyllum. (D) Psorinum

34. Nosebleed when menses should appear is symptom in:
(A) Bryonia     (B) China
(C) Millifolium  (D) Sanguinaria

35. Cough relieved by drinking cold water is one of the symptom of :
(A) Cuprum met (B) Drosera
(C) Kali carb     (D) Spongia

36. Vertigo on seeing the flowing water is present in :
(A) Belladonna   (B) Conium mac
(C) Cocculus     (D) Fer. Met

37 . Convulsion of children after fright in mother is in :
(A) Opium       (B) Coffea
(C) Chamoinilla (D) Aconite

38. Vomiting in any position except lying on right side is in:
(A) Antim tart   (B) Aethusa
(C) Ipecac       (D) Verat alb

39. Sweat in axilla, smells like onions is a symptom in :
(A) Bovista       (B) Thuja
(C) Phosphorus  (D) Silicea

40. Dryness of eyes; too dry to close the lids is the symptom in :
(A) Bryonia     (B) Cyclamen
(C) Nuxmosch (D) Thuja

41. Pain in distant parts on coughing is a symptom in:
(A) Causticum   (B) Capsicum
(C) China         (D) Plumb met

42. Body large and fat, but legs too thin is type of :
(A) Silicea            (B) Cal- phos
(C) Ammonium mur (D) Ammonium carb

43. Children; impudent, teasing, laugh at reprimands is found in:
(A) Anacardium  (B) Graphites
(C) Ignatia        (D) Nitic acid

44. Can only void urine while sitting bent backwards is characteristic of:
(A) Conium        (B) Hep-sulph
(C) Medorrhinum (D) Zincum met.

45. Feels unusually well day before an acute attack of disease:
(A) Opium         (B) Psorinum
(C) Stramonium (D) Verat vir

46. Dyspnoea aggravated while sitting, after sleep, in room; relieved by walking rapidly is found in:
(A) Can. sat       (B) Kali carb
(C) Natrum sulph (D) Sepia

47. Cough returns every winter:
(A) Hep. sulph (B) Psorinum
(C) Sepia       (D) Silicea

48. Always feels better by walking slowly about, although weakness obliges the patient to lie down:
(A) Causticum((B) Diascorea
(C) Ferr met (D) (D) Sepia

49. Sailors suffer from asthma at “onshore”
(A) Spongia       (B) Natrum sulph
(C) Medorrhinum (D) Bromium

50. Palpitation: violent when lying on left side, goes off when turning to the right:
(A) Calc ars     (B) Lac defloratum
(C) Tabacum    (D) Lachesis

51. First edition of Organon was published in the year of:
(A) 1796 (B) 1810
(C) 1798 (D) 1800

52. Theory of Chronic disease was introduced for the first time in which edition of Organon:
(A) 2nd edition (B) 3rd edition
(C) 4th edition (D) 5th edition

53. Aude Sapere has originated from:
(A) Latin     (B) Greek
(C) German (D) Hibru

54. Hahnemann died in the city of:
(A) Kothen (B) Leipzig
(C) London (D) Paris

55. Essays on a new principle for ascertaining the curative power of drugs was published by Hahnemann in :
(A) 1790    (B) 1795
(C) 1796    (D) 1798

56. Homoeopathy is based on :
(A) Deductive logic (B) Inductive logic
(C) Both.              (D) None

57. “Fragmenta de Viribus ….. Human observatis” was published in the year:
(A) 1796     (B) 1800
(C) 1805     (D) 1779

58.Homoeopathic concept says mental diseases are:
(A) Psoric origin     (B) Pseudo-psoric in origin
(C) Acute diseases   (D) Pseudo-chronic diseases-

59. Most appropriate time for administering the medicines in epidemic or sporadic intermittent fever is:
(A) Immediately before the paroxysm                   (B) Any time before paroxysm
(C) Immediately after the termination of paroxysm  (D) Any time after the paroxysm

60. The name “50 Millesimal potency” was given by:
(A) Dr. C. Hering       (B) Dr. Hahnemann
(C) Dr. W. Boericke    (D) Dr. P. Schmidt

61. The word “Miasam” originated from:
(A) Greek (B) German
(C) Latin  (D) French

62. Hahnemann was not averse to external applications for the treatment of:
(A) Chancre (B) Veneral miasam
(C) Figwarts (D) N one of the above

63. The term Pseudo-Psora was first used by:
(A) Dr. J. T. Kent (B) Dr. J. H. Allen
(C) Dr. H.C. Allen (D) Dr. T. F. Allen

64. A prolonged aggravation and final decline of the patient interprets that:
(A) The medicine is not correct (B) The disease is an incurable one.
(C) The medicine is too deep    (D) The patient is idiosyncratic

65. No aggravation, with recovery of the patient means:
(A) The remedy is shallow and short acting (B) The potency is suitable
(C) Slight organic change                         (D) The disease is organic and incurable

66. Which observation of Kent does not cover the disease state:
(A) 3rd Observation     (B) 12th Observation
(C) 9th Observation     (D) All the above

67. Number of drugs proved by Dr. Hahnemann:
(A) 97 (B) 98
(C) 99 (D) 100

68. Mesmerism was introduced in which edition of Organon:
(A) 2nd (B) 3rd
(C) 5th (D) 6th

69. Accessory symptoms are found in :
(A) Acute diseases (B) Chronic diseases
(C) In drug proving (D) After 1st Prescription

70. In Kent’s Repertory rubric “Dream” is found in :
(A) Sleep (B) Generalities
(C) Mind  (D) Head

71. In Kent’s repertory, “Shaving aggravates” is found in the chapter:
(A) Face          (B) Skin
(C) Generalities (D) Conditions

72. In Kent’s Repertory, number of sections is :
(A) 37    (B) 38
(C) 31   (D) 33

73. First edition of Kent’s Repertory was published in the year:
(A) 1894 (B) 1897
(C) 1899 (D) 1900

74. Sixth edition of Kent’s Repertory was published in the year:
(A) 1840   (B) 1900
(C) 1925   (D) 1961

75. In Kent’s Repertory, rubric “Convulsion” is to be looked in :
(A) Head          (B) Mind
(C) Generalities (D) Dreams

76. The plan of Repertory part of Therapeutic Pocket Book by Boenningauessen is divided into:
(A) Four parts   (B) Eight parts
(C) Five parts   (D) Seven parts

77. The first edition of Therapeutic Pocket Book by Boenningauessen was published in the year:
(A) 1837 (B) 1931
(C) 1935 (D) 1938

78. The Concordance Repertory is :
(A) Gentry’s (B) Kent’s
(C) Boger’s  (D) Pathak’s

79. “The doctrine of Analogy” concept is given by :
(A) Boericke (B) Boenningauessen
(C) Knerr     (D) Kent

80. Boenningauessen’s Repertory was translated to English by:
(A) Boericke       (B) Boger
(C) William Oscar (D) Knerr

81. Largest chapter in Kent’s Repertory is :
(A) Mind          (B) Extremities
(C) Generalities (D) Genitalia

82. Smallest chapter in Kent’s Repertory is :
(A) Vision (B) Hearing’
(C) Dream (D) External throat

83. Gradation of medicines is first done by :
(A) Dr. Hering               (B) Dr. Boger
(C) Dr. Boenningauessen (D) Dr. Hahnemann

84. “Therapeutic Pocket Book” by Boenningauessen was originally written in:
(A) English (B) Latin
(C) German (D) Greek

85. “Therapeutic Pocket Book” by Boenningauessen had originally:
(A) 124 remedies (B) 126 remedies
(C) 136 remedies (D) 156 remedies

86. Kent started his works on repertory from:
(A) Lee’s Repertory                   (B) Lippe’s Repertory
(C) Boenningauessen’s Repertory (D) Jhar’s Repertory

87. Eliminating Rubric was first introduced in Homoeopathy by:
(A) Margret Tyler        (B) Sir John Weir
(C) None of the above (D) Both the above

88. The word Rubric originated from the word:
(A) Rubra    (B) Rubus
(C) Rubrera (D) Rubrika

89. In Kent’s Repertory, the complaint “Ailments from bad news” can be located in the Rubric:
(A) Ailments (B) Bad
(C) News    (D) Complaints

90. In Kent’s Repertory, “Tabes Messenterica” is found in the chapter:
(A) Abdomen  (B) Generalities
(C) Rectum    (D) Stomach

91. Repertory of the intermittent Fever is written by :
(A) W. A. Allen (B) H. C. Allen
(D) Boger        (C) Gurnessy

92. Globule No. 10 having weight 1 grain is equivalent to:
(A) 1 globule     (B) 10 globules
(C) 100 globules (D) 200 globules

93. Science that deals with different aspects of the drug is called:
(A) Pharmacy         (B) Pharmacology
(C) Pharmocognesy (D) Pharmocodynamics

94. British Homoeopathic Pharmacopoeia by the Homoeopathic Society was published in:
(A) 1850 (B) 1860
(C) 1870 (D) 1890

95. The first volume of the HPI was published by Government of India in the year:
(A) 1962 (B) 1971
(C) 1976 (D) 1978

96. The Eighth Volume of HPI published by Government of India was in the year:
(A) 1998 (B) 2000
(C) 2002 (D) 2004

97. By the method of sucussion Hahneman made potencies up to:
(A) 30X (B) 60X
(C) 30C (D) 60C

98. The process of passing a liquid through some porous medium is :
(A) Straining (B) Decantation
(C) Desiccation (D) Filtration

99. The drug Causticum belongs to :
(A) Sodium Group (B) Calcium Group
(C) Carbon Group (D) Potassium Group

100. One dessertspoonful is equivalent to:.
(A) 4ml  (B) 8ml
(C) 15ml (D) 20 ml 

This is a question paper of Kerala Public Service Commission Homeopathy Medical Officer  Examinations 2007

All rights reserved@similima

Rajasthan PSC Homoeopathy Medical Officer Exam June 2011

Rajasthan Public Service Commission Homoeopathy Medical Officer Question Paper 2011

1.Commonest cause of  low vision India-is
(1) Uncorrected refractive error
(2) Cataract
(3) Glaucoma
(4) Squint

2. Treatment of so called mental or emotional disease is mentioned  in aphorism

  • (1) 105 — 145         (2) 180- 200
  • (3) 210-230           (4) 150-170

3. Hering’s law of cure is depicted in Kent’s philosophy under

  • (1) 8th observation
  • (2) 9th obsvation
  • (3) 10th observation
  • (4) 11th  observation

4.  Modus operandi of homeopathic medicines is explained in Organon of medicine in aphorism

  • (1)  26        (2) 25
  • (3) 40          (4) 29

5.  Which one of following causes pseudo chronic diseases ?

  • (1) Maintaining cause
  • (2) Fundamental cause
  • (3) Sycosis
  • (4) Syphilis

6. Who gave the idea of complete symptom

  • (1) Dr. S. Hahnemann
  • (2) Dr. J.T. Kent
  • (3) Dr. Stuart Close
  • (4) Dr. Boenninghausen

7.The action of medicine upon prover is …………observation  of  Kent

  • (1) Tenth               (2) Ninth
  • (3) Seventh           (4) Sixth

8. The  first original book of  Hahnemann  was published  at………in………

  • (1) Vienna, 1783
  • (2) Gommern, 1784
  • (3) Leipsic, 1784
  • (4) Erlanga, 1785

9. The sixth edition of Organon was first published in

  • (1) English      (2) Greek
  • (3) German      (4) French

10. In case of intermittent fever the guidelines for prescription are given in which aphorism?

  • (1)236          (2) 36
  • (3) 136         (4) 266

11. Diet in acute disease

  • (1) 259-261           (2) 267-268
  • (3) 142 – 143        (4) 262 – 263

12. Therapeutic law of nature consist of …..aspects

  • (1) Five                  (2) Four
  • (3) Three                (4) Two

13.Inapropriately called chronic disease given in

  • (1) 69-70               (2) 40-42
  • (3) 74-75               (4) 77

14. In which aphorism  Hahnemann had said that he opened the path of great truth homoeopathy fr blessing of humanity

  • (1) 109                   (2) 110
  • (3) 111                   (4) 112

15. Of the below which constitute intermittent disease

  • (1) Sporadically appear
  • (2) Epidemically appear
  • (3) Complicated with sycosis
  • (4) Psoric complicated syphilis

16. Homoeopathic drugs are derived from ……..different sources

  • (1) Eight                 (2) Seven
  • (3) Six                    (4) Nine

17. The drug Kreosote belongs to

  • (1) Nosode
  • (2) Sarcode
  • (3) Animal Kingdom
  • (4) Mineral Kingdom

18.Gutta Purcha Bottles are used for storing acids

  • (1) Hydrochloric    (2) Sulphur
  • (3) Nitric              (4) Fluoric

19. Pellet is the

  • (1) Solid vehicle
  • (2) Liquid vehicle
  • (3) Other name of placebo
  • (4)  Synonym of globule

20. There are…….. types of alcohol.

  • (1) 5        (2) 15
  • (3) 10     (4) 8

21.Glycerol is mildly

  • (1)) Antipyretic                     (2) Bactericidal
  • (3) Germicidal                      (4) Antiseptic

22. The iodine value of olive oil is

  • (1) 90 to 92           (2) 79 to 88
  • (3) 60 to 85           (4) 50 to 70

23. In fifty millesimal scale the un substance is reduced to…….. level by trituration.

  • (1) 5 C                    (2)10 C
  • (3) 6 C                    (4) 3 C

24. Total number of chapters in Knerr’s repertory is

  • (1) 38                     (2) 48
  • (3) 47                     (4) 37

25. Author of repertory of urinary organ is

  • (1) W C. Allen       (2) Possart
  • (3) A.R. Morgan  (4) Lippe

26.Analytical repertory of  Hering published in

  • (1) 1881                 (2) 1825
  • (3 ) 1790                (4) 1921

27. Repertory of Anti-psoric was published by

  • (1) Dr. Samuel Habnmann
  • (2) Dr. JT. Kent
  • (3) Dr. Constantine Hering
  • (4) Dr. Boeninghausen

28. In Boenning Hausen’s repertory  “Dislocations” is in Chapter

  • (1) Extremities      (2) Joints
  • (3) Complaints     (4) Sensations

29. Rubric ‘Cyanosis’ Boenning Hausen’s repertory

  •  (1) Skin                 (2) Generalities
  • (3) Sensations      (4) Complaints

30. In which chapter of Kent’s repertory is the sensation of  formication, in anus found?

  • (1) Stool                  (2) Rectum
  •  (3) Stomach          (4) Generalities

31.What does word ‘Quando’ means ?

  • (1) Personality                     (2) Cause
  • (3) Seat of disease               (4) Time

32. ‘Anthrax’ belongs to Chapter in Kent’s Repertory.

  • (1) Perspiration                     (2) Skin
  • (3)Abdomen                          (4) Extremities

33. Whooping cough belongs to……. Chapter in ‘Kent’s Repertory.

  • (1) Generalities                     (2) Expectoration
  • (3) Chest                                  (4) Cough

34.Remedy for benevolence is….in  Kent’s repertory.

  • (1) Nux. Moschata
  • (2) Puls  nig
  • (3) Coffica Cruda
  • (4) Bryonia.

35.Head reeling belongs to chapter in Kent’s repertory –

  • (1)Head                 (2) Mind
  • (3) Vertigo          (4) Generalities

36. Biting belongs to sub-chapter in Boenninghausen’s repertory

  • (1) Mouth              (2) Skin
  • (3) Sensations     (4) Complaints

37. Which of patient “feels unusually well day before attack”

  • (1) Cuprum-met                   (2) Tuberculinum
  •  (3) Psorinurn                        (4) Medorrhinum

38. “Vomiting as soon as he raises head  from pillow’comes under

  • (1 ) Phosphorus                    (2)Bismuth
  • (3) Stramornurn                   (4) Hyoscyamus

39.”Children cannot bear to be washed or bathed  is characteristic of

  • (1) Aethusa  Cynapium      (2)Sulphur
  • (3) Rheum                             (4) Charnomila

40. “Chronic sick headache, ascending from nape of neck to the vertex” is characteristic of

  • (1) Glonine            (2) Belladonna
  • (3) Sambucus       (4) Silicea

41.. In diarrhoea “stools are green frothy like scum on a frog pond” is found in

  •  (1) Podophyllum                 (2) Mag. Carb
  •  (3) Thuja                              (4) Baryta Carb

42. Constipation with in effectual urging ameliorated by drinking cold milk found in

  • (1) lodum                              (2) Bromium
  • (3) Colchicurn                      (4) Capsicum

43. “Cough has gurgling sound as was being poured in bottle’ comes under

  • (1) Spongia                           (2) Drossera
  • (3) Cuprum-met                    (4) Rumex

44. ……….has cured umbilical hernia  with obstinate constipation after Nux failed.

  • (1) Opiurn                              (2) Cocculus
  • (3) Lycopodiurn                   (4) Alumina

45. Eczema, intolerable itching < in bed and from  touch; copious, serous exudation is characteristic of

  • (1) Heparsulph                     (2) Mezerium
  • (3) Psorinum                          (4) Sulphur

46. Vertigo when moving slowly, but not when taking violent exercise is  characteristic of

  • (1) Bryonia                           (2) Millefolium
  • (3) Stnumonium                  (4) Helleborus

47. Tongue, white or yellow  down with red streaks in the middle is characteristic

  • (1) Stannum-met                 (2) Veratrurn-viride
  • (3) Aurum-Triphyllum     (4) Aurum-Met

48. Backache relieved by lying on back is characteristic of

  • (1)Kali Carb                          (2) Zincum met
  • (3) Ruta.Grav                       (4) Gelsemium.

49. Rhododendron belongs to family.

  • (1) Ericaceae        (2) Loganiaceae
  • (3) Curbitaceae    (4) Solanaceae

50. Delirium or during sleep, imagines that one leg is double, that there are two babies in the bed is characteristic of

  • (1) Petroleum                        (2) Stramonium
  • (3) Colchicum                      (4) Hyoscyamus

51. Pain as if bones were all torn to pieces –   is particular of

  • (1) Cimicifuga                      (2) Rhus. Tox
  • (3) Ipecac                              (4) Mag. Phos.

52. Perspiration smelling like honey is characteristic of

  • (1) Apis Mel                          (2) Thuja
  • (3) AntmCrude                     (4) Alliumcepa

53.’Which of following  medicine is fastidious ?

  • (1) Lycopodiurn                   (2) Aconite Napalleus
  • (3) Carcinosin                       (4) Tubeculinum

54. Toothache during pregnancy at night is torn of

  • (1) Nag. Carb                        (2)Thyroidinum
  • (3) Plantago                          (4) Mag. Phos

55. “Profuse sweat over entire body during waking hours” is a symptom of

  • (1) Thuja
  • (2) Sambulus Nigra
  • (3) China Officinalis
  • (4) ConiUrn Mac

56. Retraction of nipples, nipples are small withered unexcitable” is characteristic of

  • (1) Pu1satilla                        (2) Sarsaparilla
  • (3) Berberis Vulgaris       (4) Podophyllum

 57. Permanent dilatation and distortion of bronchi is called as

  • (1) Emphysema                   (2) Bronchitis
  • (3) Fibrous of lung            (4) Bronchiectasis

 58. Aschoff giant cells are found in

  • (1) Rheumatoid Arthritis                    (2) Rheumatic Fever
  • (3) Hodgkin’s disease                          (4) Sarcoidosis

59. Causes of ‘Viral Hepatitis are following except

  • (1) Cytomegalo Virus
  • (2)Epstin-Barr Virus
  • (3) RNA Virus
  • (4) Yellow Fever

60. Earliest sensation lost in Diabetic Neuropathy is

  • (1) Weakness of muscles of hand   (2) Pain
  • (3) Temperature                                   (4) Vibration

61. In case of Mitral Stenosis  investigations will show follow except

  • (1) Right Ventricular Hypertrophy
  • (2) Atrial Fibrillation
  • (3) Left Ventricular Hypertrophy
  • (4) Signs of Pulmonary Congestion

62. The commonest cause of intra cranial  haemorrhage is

  • (1) Rupture of Aneurysm   (2) Diabetes Mellitus
  • (3) Hypertension                  (4) Trauma

63. Complications of pneumonia following except

  • (1) Empyema       (2) Hepatitis
  • (3) Renal failure  (4) Asthma

64. Risk factors for leukemia are the following except

  • (1) Down’s syndrome         (2) Industrial exposure to Benzene
  • (3) Japanese Encephalitis   (4) Radiotherapy of Spondylitis

65. Systemic lupus erethmatosus presents following features except

  • (1) Leucocytosis                  (2)Malar Rash
  • (3) Serositis                           (4) Anti DNA antibodies

66. Kussamaul’s respiration occurs in

  • (1) Respiratory failure        (2)Metabolic acidosis
  • (3) Cardiac failure               (4) Head injury

67. Hypertension is a feature of all the following except

  • (1) Renal Artery Stenosis
  • (2) Pneochromohtorna
  • (3) Addison’s disease
  • (4) Cushing’s Syndrome

68. Cause of Aortic Regurgitation are following except

  • (1) Rheumatic disease
  • (2) Trauma
  • (3) Diabetes Mellitus
  • (4) Infective Endocarditis

69. Increased level of serum amylase is of great importance in

  • (1) Acute pancreatitis
  • (2) Chronic hepatitis
  • (3) Toxemia of pregnancy
  • (4) Parotitis

70. The uterus is developed from

  • (1) Pronephric ducts
  • (2) Mesonephric ducts
  • (3) Mullerian ducts
  • (4) Urogenital ducts

71. Commonest congenital anomaly uterus is

  • (1) Uterus Bicornous Unicolis
  • (2) Uterus Unicornous
  • (3) Uterus Biconious Bicolis
  • (4) Uterus Dideiphus

72. Fetal component of placenta is

  • (1) Chorion leave
  • (2) Chorion frondusum
  • (3) Decidua capsularis
  • (4) Decidua Basalis

73. True statement regarding adenomyosis is

  • (1) More common in nullipara
  • (2) Surgery only treatment
  • (3) Presents with menorrhagia, dysmenorrhea & enlarged uterus
  • (4) More common in young women

74. Commonest cause vulvo vaginitis children/s

  • (1) Gonococcus                    (2) Trichomoniasis
  • (3) Axyuriasis                       (4) Candida

75. The most common cause of secondary amenorrhoea in India is

  • (1) Endometrial Tuberculosis
  • (2) Premature ovarian failure
  • (3) Polycystic ovarian syndrome
  • (4) Sheehan’s syndrome

76.Where are intramural fibroids present

  • (1) Within walls of uterus
  • (2) In cervix
  • (3) Outward of uterine surface
  • (4) In interior of  uterine cavity

77. In a case of dysgerminoma of ovary one of the follow likely to be raised

  • (1) Serurn HCG
  • (2) Scrurn Alpha-fetoprotein
  • (3) Serum Lactic Debydrogenase
  • (4) Serum Inhibin

78. The karyotype of a patient with androgen insensitivity syndrome is

  • (1) 46XX                               (2) 46XY
  • (3) 47 XXY                           (4) 45 XO

79. Risk of pre-term delivery is increased in cervical length is

  • (1) 25 mm             (2)           30 mm
  • (3)3 5 mm             (4)           40 mm

80. All of the following pelvic structures support vagina except

  • (1) Perneal body
  • (2) Pelvic diaphragm
  • (3) Levator ani muscle
  • (4) Infundibulo pelvic ligament

81. From which of following, layers, the regeneration of endometriurn takes

  • (1) Zona Basalis
  • (2) Zona Pellucidum
  • (3) Zona Compacta
  • (4) Zona Spongiosa

82. The most common site of intestinal obstruction in  gall stone ileus is

  • (1) Jejunum
  • (2) Ileum
  • (3) Transverse colon
  • (4) Sigmoid colon

83. Which of the following is an absolute indication for surgery in benign prostatic hyperplasia ?

  • (1) Bilateral hydrourcteronephrosis
  • (2) Nocturnal frequency
  • (3) Recurrent urinary tract infection
  • (4) Voiding bladder pressures > 50 cms of water

84. Thoracic extension of cervico goitre is usually approached through

  • (1) Neck
  • (2) Chest
  • (3) Combined cervico thoracic route
  • (4) Thoracoscopic

85.Superior oblique muscle is supplied by

  • (1) 3rdcranial nerve
  • (2) 4th  cranial nerve
  • (3) 5th  cranial nertc
  • (4) 6th  cranial nerve

86.Bilatemi ptosis is not seen in

  •  (1) Marfani’s Syndrome                    (2) Myaesthenia Gravis
  •  (3) Myotonic Dystrophy                 (4)Kearns-Sayre Syndrortie

87. Carpel Tunnel Syndroine is due to compression of

  • (1) Radial nerve
  • (2) Ulnar nerve P
  • (3) Palmar branch of ulnur nerve
  • (4) Median nerve

88. All of  following  are risk  factors for carcinoma  gall bladder except

  • (1) Typhoid carriers
  • (2) Adenomatous gall bladder polyp
  • (3) Choledochal cysts
  • (4) Oral contraceptives

89. Virchow’s triad includes all of following except

  • (1 ) Venous stasis
  • (2) Injury to vein
  • (3) Blood hypercoagulability
  • (4) Venous thrombosis

90. The commonest site of carcinoma esophagus in India is

  • (1) Upper 1/3        (2) Middle 1/3
  • (3) Lower 1/3        (4) GE junction

91. The incubation period for diphtheria is

  • (1) 2 to 6 days
  • (2) 7 to 14 days
  • (3) 10 to 21 days
  • (4) 12 to 24 hours

92. 2. The most common site of benign (Peptic) Gastric Ucer

  • (1) Upper third of lesser curvature
  • (2) Greater curvature
  • (3) Pyloric antrum
  • (4) Lesser curvature near incisura angularis

93.Common features of dengue syndrome are following except

  • (1) Shock
  • (2) Circulatory failure
  • (3) Convulsions
  • (4) Haernorrhage

94. Incubation period of yaws is

  • (1) 7 to 14 days
  • (2) 3 to 5 weeks
  • (3) I week
  • (4) more than 5 weeks

95. Mantoux Test will be considered doubtful  if size   of induration is

  • (1) 3 to 6 mm                       (2) 6 to 9 mm
  • (3) 9 to 12 mm                     (4) 12 to I5 mm

96. The analytical study where population is  the unit of study is

  • (1) Cross Sectional
  • (2) Ecological
  • (3) Case control
  • (4) Cohort

97. Which one of’ following arbovirus diseases has not been reported in India ‘?

  • (1) Japanese  Encephaltis
  • (2) Yellow Fever
  • (3) Chikungunya fever
  • (4) Kyasanur Forest Disease

98. Niacin deficiency in a maize eating population is due to

  • (1) High tryptophan
  • (2)  High isoleucine
  • (3) High Ieucine
  • (4) High phenylalamine

99. Hoghiest. biological value of protein is seen in

  • (1) Egg
  • (2) Fish
  • (3) Soyabean
  • (4) Gram

100. The parameters of sensitivity and specificity are used for assessing

  • (1) Criterion validity
  • (2) Construct validity
  • (3) Discriminant validity
  • (4) Content validity

We are thankful to Dr Anil K of B R Sur Homoeopathic Medical College New Delhi for this question paper.

This is a Question Paper of Rajasthan PSC Homoeopathy Medical Officer Examination June 2011

All rights reserved @ similima                   

Homeopathy University – Rajasthan MD Entrance Paper 2011

1. Superior mediastinum contains
A.  Heart
B.  Lungs
C.  Blood vessels coming to and going away from heart, Trachea, Oesophagus etc.
D.  None of them

2. Which cerebral artery is called artery of  haemorrhage

  • A. Anterior cerebral
  • B. Middle cerebral
  • C. Posterior cerebral artery
  • D. None of them

3. The integrity of arches of the foot are maintained by

  • A. Shape of the bones
  • B. Planter side ligaments of foot joints
  • C. Planter aponeurosis
  • D. Muscles of the soles
  • E. All of them

4. Axillary lymph nodes are divided into following groups

  • A. Lateral
  • B. Pectoral
  • C. Subscapular
  • D. Apical
  • E. Central
  • F. All of them
  • G None of them

5. The primary curvatures of the vertebral column are present since birth while secondary curvatures develop after birth due to certain activities of the child. which are the secondary curvatures

  • A. Cervical
  • B. Thoracic
  • C. Lumbar
  • D. Sacrococcygeal
  • E. A and C above
  • F. B and D above

6. Anterior Pituitary gland secrets

  • A. Growth harmone  (GH)
  • B. Adrenocorticotrphic harmone (ACTH)
  • C. Thyroid stimulating harmone (TSH)
  • D. Follicular stimulating harmone(FSH)
  • E. Luteinising harmone (LH)
  • F. Vasopressin or (ADH)
  • G. All except one
  • H. None of them 

7. The cardiac output is the product of

  • A.Heart rate and stroke volume
  • B. Sympathetic and parasympathetic   stimulation
  • C. Filling of the ventricles and contraction of the cardiac muscle
  • D. None of them
  • E. All of them

8. The kidneys are concerned with

  • A. Removal of nitrogenous substances
  • B. Maintenance of electrolyte and water balance
  • C. Regulation of acid base equilibrium
  • D. Secretion of rennin and erythropoietin
  • E. All of them
  • F. All except one

9. When flexors are contracted the extensor muscles relax. This phenomenon is called

  • A. Reciprocal innervations
  • B. Act of inter-neurone system
  • C. None of them
  • D. Both of them

10. Liver is associated with

  • A. Protein metabolism,
  • B. Fat metabolism
  • C. Carbohydrate metabolism
  • D. Alcohol metabolism
  • E. Inactivation of hormones
  • F. Inactivation of drugs and pharmacological agents
  • G. all of them
  • H. None of them

11.  Koch’s postulates in relating a micro Organism causally to a given infection is

  • A. The organism must be observed in every Case of disease;
  • B. The organism can be isolated in pure Culture;
  • C. The disease can be reproduced in  suitable experimental animal by introducing pure culture;
  • D. The organism can be recovered in pure culture from the diseased experimental  animal;
  • E. All of the above
  • F. Some of the above 

12.  The development of a specific infection depends upon the following

  • A. The nature and the number of infective organisms
  • B. The route or avenue of infection
  • C. The state of host’s defense mechanismsand reaction
  • A. Some of them
  • D.All of them 

13. Immunity produced in an animal byaction of micro-organisms is called as

  • A. passive immunity
  • B. active immunity 

14.  What is common in acute Rheumatic fever, Myasthenia gravis, Rheumatoid      arthritis and Systemic lupus  erythematosus

  • A. Musculoskeletal disorders
  • B. Systemic disorders
  • C. Autoimmune diseases
  • D. Immunodeficiency diseases 

15. There are two mechanisms of spread of malignant tumors- infiltration and metastasis. The statement is-

  • A. True
  • B. False 

16. Odor of Phosphorus poisoning is

  • A. Foul
  • B. Garlicky
  • C. Aromatic
  • D. Sweetish 

17. Is not present in Arsenic poisoning

  • A. Constipation
  • B. Diarrhoea
  • C. Burning
  • D. Throat pain
  • E. Vomiting

18. X-Ray of wrist is useful for determination of-

  • A. Sex of a person
  • B. Age of an adult
  • C. Age of a child
  • D. Race of a person

19. Both mother and father have AB blood group. Blood group in their children will be

  • A.  A only
  • B.  A and AB
  • C.  B and AB
  • D.  A, B, and AB only

20. Ballistic expert is an

  • A. Forensic expert
  • B. Finger print expert
  • C. Chemical analyzer
  • D. Firearm expert 

21.  Cellulitis is spreading infection of

  • A. Hair follicle
  • B. Nail bed
  • C. Subcutaneous spaces
  • D. None of the above

22. Multiple cold nodules in thyroid scan is a   feature of

  • A. Multinodular goiter
  • B. Graves disease
  • C. Hashimoto’s disease
  • D. All of the above

23. Paroxysmal vertigo, tinnitus and deafness is characteristics of

  • A. Meniere’s disease
  • B. Acoustic neuroma
  • C. Serous Otitis media
  • D. Otosclerosis

24. Dead bone seen in chronic Osteomyelitis is called as

  • A. Sequestrum
  • B. Sinus debris
  • C. Involucrum
  • D. Cloasae

25. Retinoscopy  is used to study

  • A. Refractive error
  • B. Lesion of the macula
  • C. Lesions of retina
  • D. All of them

26. Following are the clinical features of  PCOD

  • A. Irregularities of menstruation
  • B. Hirsutism
  • C. Hyper insulinism
  • D. All of the above

27. Commonest cause of secondary amenorrhoea is

  • A. Pregnancy
  • B. Turner’s syndrome
  • C. Fibroid
  • D. PCOD

28. A patient of uterine fibroid will not have  amenorrhoea unless she is

  • A. Pregnant
  • B. Menopausal
  • C Both of the above
  • D. None of the above

29. Ideal test for the tubal pregnancy is

  • A. HSG
  • B. USG
  • C. Chromotubation
  • D. Shirodkar’s test

30. Following is a method of early detection of Ca cervix

  • A.Vaginal cytology
  • B. Endocervical aspiration
  • C. Cervical cytology
  • D. FNAC

31. High output cardiac failure in which of  the below mentioned conditions

  • A. Severe anaemia
  • B. Beri –Beri
  • C. Thyrotoxicosis
  • D. All these conditions

32. Which condition of the following  Conditions is contra indicated for CSF Examination

  • A. Meningitis
  • B. Venous thrombosis
  • C. Raised intra cranial pressure
  • D. Encephalitis

33. Koilonychias is a sign of the following type of anaemia

  • A. Iron deficiency
  • B. Folic acid deficiency
  • C. Haemolytic
  • D. Aplastic

34. Clubbing is seen in which of the condition

  • A. Myocarditis
  • B. Pericarditis
  • C. Infective endocarditis
  • D. None of the above

35. Bell’s palsy is

  • A. Upper motor neuron facial nerve palsy
  • B. Lower motor neuron facial nerve palsy
  • C. Pseudo bulbar palsy
  • D. All of the above

36. Xerosis occurs because of deficiency of

  • A. Zinc
  • B. Vitamin A
  • C. Iron
  • D. Vitamin K

37. Vitamin D deficiency in adults is called as

  • A. Rickets
  • B. Osteomyelitis
  • C. Osteomalacia
  • D. Osteoporosis

38. Role of the Public Health Authorities in  prevention and control of epidemics is

  • A. Declaring it a National Eradication  Programme
  • B. Legislation for elimination and effective  enforcement
  • C. Community awareness and their  cooperation
  • D. Minimizing Vector Population
  • E. All of them
  • F. None of them 

39. Aedes aegypti mosquito is responsible for transmission of which of the following

  • A. Chikungunya
  • B. Dengue
  • C. Both of them
  • D. None of them 

40. In epidemics occurrence of the case in the community needs to be communicated     immediately to the nearest public health official for identification of clusters by     person, place and time and for expansion     of the control measures in the community. The above statement is-

  • A. True
  • B. False 

41. Which of the following is NOT a plant  Nosode

  • A. Secale cor
  • B. Ustilago
  • C. Psorinum
  • D. Nectrianium 

42. Garden marigold is the common name of

  • A. Aconite
  • B. Arnica
  • C. Calendula
  • D. Pulsatilla 

43. Coffea cruda and Nux vomica tinctures  are prepared from

  • A. Bark
  • B. Roots
  • C. Seeds
  • D. leaves

44. Application for grant of License to   manufacture homoeopathic medicines is made under

  • A. Form 26 C
  • B. Form 24 C
  • C. Form 20 C
  • D. Form 19 B

45. In proving of narcotics drugs, symptoms recorded are of

  • A. Alternating action
  • B. Secondary action
  • C. Primary action
  • D. Pharmacological action

46. The unofficial pharmacopoeia in India was first written by

  • A. East India Company
  • B. Willmar Schwabe
  • C. M. Bhattacharya & Co.
  • D. B K Sarkar

47. 1M potency is same as

  • A. 1000 CH
  • B. 1000 X
  • C. 0/1
  • D. LM1

48. Decimal scale was introduced by

  • A. Hahnemann
  • B. Hering
  • C. Hartmann
  • D. Huffeland

49. Continuous fluxion potencies were prepared by

  • A. Fincke
  • B. Korsakoff
  • C. Hahnemann
  • D. Burt

50. Trituration of liquid substances is done   as per

  • A. Class V
  • B. Class VI
  • C. Class VII
  • D. Class VIII

51. 100 strokes are given in

  • A. Decimal scale
  • B. Centesimal scale
  • C. L M Potencies
  • D. Jumping scale 

52. Process involved in purification of sugar  of milk is

  • A. Sublimation
  • B. Crystallization
  • C. Distillation
  • D. Condensation

53. Thin   Layer   Chromatographic   study of drug helps to identify

  • A. Drug constituents
  • B. pH value
  • C. Refractive index of drug
  • D. Melting point

54. Venoms are prepared in

  • A. Water
  • B. Oils
  • C. Alcohol
  • D. Glycerin

55. Aphorisms 264 -285 in the Organon of  Medicine deal with pharmacy

  • A. True
  • B. False

56. Meaning of ‘Quibis Auxilus’ is

  • A. Accompanying Symptom
  • B. Cause of disease
  • C. Seat of disease
  • D. Personality &the individualization

57. Totality of symptoms according to  Boenninghausen is

  • A. Doctrine of Analogy
  • B. Doctrine of Concomitants
  • C. Grand Generalization
  • D. Grand Symptom

58. The concomitant symptom is to the  totality what the —- is to the single  symptom.

  • A. Sensation
  • B. Location
  • C. Modality
  • D. None of the Above 

59. In maze of symptoms, there are —– symptoms

  • A. Too many
  • B. Too many common
  • C. Too many characteristics
  • D. Too many basic

60. Following physician translated and edited Therapeutic Pocket Book

  • A. Dr. Charles Hempel
  • B. Dr. Horward  Okie
  • C. Dr T. F. Allen
  • D. All of above

61. Mental  aggravations  are  given  in  Therapeutic   Pocket   Book   under

  • A. Mind
  • B. Aggravations and amelioration
  • C. Both of them
  • D. None of them

62. Itching  of  the  lobule of ear immediately after wearing a metal ring is given in T.P.B under chapter

  • A. Ear
  • B. Aggravations
  • C. Sensations
  • D. Skin

63. Tearing pain in right side of chest during Cough is given in T.P.B. under chapter

  • A. Chest
  • B. Cough
  • C. Sensations
  • D. Aggravation 

64. Who   wrote   this,“  To   learn   the   materia  medica,  one  must  master  of Hahnemann’s      Organon, after which the symptomatology and the Organon go hand in hand. The Organon, the symptomatology and a full Repertory must be the constant reference books, if careful homoeopathic prescription is to be attained and maintained. ”

  • A. C.M. Boger
  • B. Hahnemann
  • C. J.T. Kent
  • D. Boenninghausen

65. Who   wrote   this, “Materia   Medica   study  is    a    constant,   diligent,    comprehensiveand  in  leisure  hours,  where  as  Repertory   study  is, in practice, at bed-side to aid   his memory, and abridged easy consultation without a too  great loss of time.”

  • A. J.T. Kent
  • B. C.M. Boger
  • C. Constantine Hering
  • D. Boenninghausen

66. Concept of ‘Remedy Relationship’ is elaborated in the repertory by

  • A. Boenninghausen
  • B. C. M. Boger
  • C. Both of them
  • D. None of them

67. First edition of Kent’s Repertory was   published

  • A. In 1897
  • B. It came in parts
  • C. Has undergone six editions
  • D. All are true
  • E. Some are true
  • F. None is true 

68. Dr. C. M. Boger’s  Boenninghausen’s Characteristics and Repertory

A. Was published in India posthumously
B. Has seven sections like that of  Therapeutic Pocket Book of Boenninghausen, namely Locations-(1)Mind, (2) Intellect, (3)Parts of the Body, (4) Sensations & Complaints, (5) Fever, (6) Modalities, and (7)Relationships
C. Is a bridge between Boenninghausen and Kent’s repertory

  1. Some are true
  2. None is true
  3. All are true

69.  Sixth edition of Organon of Medicine was translated in English by

  • A. Hahnemann
  • B. Hering
  • C. William Boericke
  • D. Bradford
  • E.  Dudgeon

70. Hahnemann’s First edition of Organon of Medicine was published in 1810, second   in 1819, third in 1824, fourth in 1829, fifth in 1833 and sixth posthumously

  • A. True
  • B. False

71. Introduction in the sixth edition of   Organon of Medicine is written by

  • A. Hahnemann
  • B. William Boericke
  • C. James Krauss

72. Organon of Medicine revolves around  three business of a physician which are  these

  • A. Knowledge of Disease
  • B. Knowledge of drugs
  • C. Knowledge of how to apply knowledge of drug to the knowledge of disease
  • D. All of the above
  • E. None of the above
  • F. Some of the above

73. The year of birth of Homoeopathy is

  • A. 1810
  • B. 1796
  • C. 1755
  • D. None of the above

74. Hahnemann’s  three earlier publications namely ‘Essay on New Principle for Ascertaining  the Curative Power of  Drugs’, ‘The Medicine of Experience’,  and ‘Spirit of the Homoeopathic Doctrine of Medicine’ are considered to be precursor   to the first edition of Organon

  • A. False
  • B. True

75. Concept of vital force and dynamisation were added by Hahnemann in third and  Sixth editions respectively

  • A. True
  • B. False 

76. What did Hahnemann exactly write  about the physician’s high and only  mission is to

  • A. Restore the sick to original health
  • B. To cure as it is termed
  • C. Annihilate disease in its entire extents
  • D. Restore sick to health, to cure, as it is   termed
  • E. To restore sick to health

77. Aphorisms dealing with Case-taking in the sixth edition of Organon of Medicines  are

  • A.83-104
  • B.  1-70
  • C. 105-145
  • D. 264-272
  • E.None of them 

78. Mental diseases are

  • A. One sided diseases
  • B. Chronic diseases
  • C. Have Psora at the base
  • D. All of them are characteristics of them
  • E. None of them
  • F. Some of them 

79. Aphorism 72 to 104 in the sixth edition of  Organon deal with

  • A. Investigation of the disease
  • B. Acquiring knowledge of drugs
  • C. Mode of employment of drugs to the  Diseases
  • D.None of the above 

80. Following have violent palpitation;  anxiety, with congestion of blood to head and chest after exertion; pulse small, feeble, rapid, irregular, visible beating of carotid and temporal arteries

  • A. Belladonna
  • B. Glonoine
  • C. Aurum met
  • D. Some of them
  • E. All of them
  • F. None of them

81. Child is sulky, does not wish to speak  or be spoken to is characteristic of  following-

  • A. Antimonium crudum
  • B.Silicea
  • C.Iodum
  • D.All of them
  • E.Some of them
  • F.None of them 

82. Following remedies are indicated when the vis medicatrix naturae is too weak to develop exanthemata

  • A. Sulphur
  • B.Cuperum
  • C.Tuberculinum
  • D. Zincum metallicum
  • E. All of them
  • F. None of them

83. Constipation where stools are like round, black balls is characteristic of

  • A. Veratrum album
  • B.Chelidonium
  • C.Opium
  • D. Plumbum
  • E.All of them
  • F.None of them

84. Rapid and pronounced emaciation is seen in following:

  • A. Tuberculinum
  • B. Natrum mur
  • C. Iodum
  • D. Calcarea
  • E Some of them
  • F. All of them

85. Stool recedes after being partly expelled  is characteristic of

  • A. Thuja
  • B. Sanicula
  • C. Silicea
  • D. All of them
  • E. Some of them

86.  Vertigo on closing the eyes is characteristic of

  • A. Lachesis
  • B. Thuja
  • C. Theridion
  • D. None of them
  • E. All of them

87. Mapped tongue is characteristic of

  • A. Merc  sol
  • B. Natrum mur
  • C. Lachesis
  • D.Taraxacum
  • E. All of them
  • F.None of them

88. Pains that begin with twilight and end with day light are characteristic of

  • A. Syphilinum
  • B. Phytolacca
  • C. Merc sol
  • D. Some of them
  • E. All of them

89. Child has a sour odor despite careful washing is characteristic of

  • A. Sulphuric acid
  • B. Mag Carb
  • C. Heper Sulph
  • D. Rheum
  • E. All of them
  • F. Some of them

90. Diarrhoea driving out of bed early in the morning is characteristic of

  • A. Sulphur
  • B. Psorinum
  • C. Aloes
  • D. Some of them
  • E. All of them

91. Styes on eyelids one after another leaving hard nodosities in their wake is characteristic of

  • A. Thuja
  • B. Colnium
  • C. Staphysdagaria
  • D. All of them
  • E. None of them

92. Following are indicated in rheumatic Heart condition

  • A. Kali Carb
  • B. Naja
  • C. Ledum
  • D. Spigelia
  • E. True
  • F. False

93. Sepia and Lycopodium patients could be  Very miserly and greedy

  • A. True
  • B. False

94. Secale corundum is a Nosode, its common  name is spurred rye or ergot and has a  haemorrhagic diathesis

  • A. All the above are true
  • B.  Some are true
  • C. None of above is correct

95. Psorinum is a Nosode, it is Antipsoric and all its excretions – stools, menses, leucorrhoea, perspiration have carrion like odor and is a chilly remedy

  • A.  All above are true
  • B.  Some of the above are true
  • C.  None of the above statements are  true.

96. Magnesia carbonica is carbonate of  Magnesium, its chemical formula is  (MgCO3)4 Mg(OH)2+5H2O and  like Ammonium Mur, and Kreosotum has  menstrual flow only at night or when   lying it ceases when walking just reverse  of Lilium Tigrinum

  • A. Some of the above are facts
  • B. None is a fact
  • C. Everything stated above is true

97. Slightest injury causes suppuration in

  • A. Merc sol
  • B. Graphites
  • C. Heper Sulph
  • D. In all of them
  • E. Some of them
  • F. None of them

98. Headache as if a nail was driven out through the side, relieved by lying on the side is characteristic of

  • A. Ignatia
  • B. Coffea
  • C. Nux vomica
  • D. Thuja
  • E. All of the
  • F. None of them

99. Aethusa  cynapium is known as Fool’s parsley, belongs to umbelliferae family  and  has great intolerance of milk in any form and is a good remedy in convulsions

  • A.  All above statements are true
  • B. Some of the statements are true
  • C. None of the statement is true

100. Laughing excites cough and produce profuse mucus in larynx in

  • A. Drosera
  • B. Phosphorus
  • C. Stannum
  • D. Argentum Metallicum
  • E. All of them
  • F. Some of them
  • G. None of them

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Post graduate Entrance Examination at Homeopathy University – Rajasthan MD Entrance Question Paper 2011

Homoeopathy’s growth in India is stunning: George Vithoulkas

homeopathy- IndiaNothing seems to excite him more than the thought of his days in India. George Vithoulkas, widely regarded as ‘the maestro of classical homoeopathy’, says it is heartening to see homoeopathy growing in India at a fast clip. For the record, the homoeopathic market is expected to double in the country to Rs 5,873 crore in five years. He offers a reason for this growth, “Morality and spirituality in its essential sense are stronger in India than other countries.”

He admits that his explanation sounds strange. “But it is true,” he insists. “I know India from my experience of living there for a long period.” Vithoulkas, now 79, studied homoeopathy in South Africa and in Kolkata. He passed out from the Indian Institute of Homoeopathy, Calcutta, in 1966, and returned to Greece to practise and teach the world’s youngest system of medicine. 

The Greek physician says tragedy is yet to engulf India and other developing countries in a big way. The tragedy he is referring to is the one caused by the overuse of allopathic drugs. “Countries such as India, Pakistan and those in South America are lucky that they cannot supply chemical drugs for all their people.” According to him, shortage of medical supplies is in a way a blessing in disguise for these non-developed countries: they haven’t yet suffered the damage that chemical drugs inflict upon people in rich countries.

But Vithoulkas knows it only too well that homoeopathy needs to grow much more to emerge as a ‘real alternative’ to the ‘chemicals-infested’ modern medicine, which has already made inroads into emerging markets.

“At this moment, homoeopathy is not ready to take over the bulk of medical care in any country,” he notes. But, he says, poor countries can afford to invest in promoting homoeopathy. “The conventional system of medicine has reached a dead end, and the new medicine will be the energy medicine that homoeopathy offers,” he claims. But then, what was that about homoeopathy lacking in scientific evidence?

He counters the argument raised famously in a 2005 Lancet article that compared the effect of homoeopathicmedicines to that of the placebo effect. “This is not an argument against homoeopathy. 

Link : http://articles.economictimes.indiatimes.com/2011-10-22/news/30309898_1_homoeopathy-countries-medicine

How to prepare for competitive examinations

exam11Dr K R Mansoor Ali
Govt. Homoeopathic Medical College, Calicut.Kerala

In order to succeed you must know what you are doing, like what you are doing, and believe in what you are doing- Will Rogers .

This work is meant for the serious candidates of competitive examinations in Homoeopathy. The work has been made with the purpose of helping the students   who my wish to make themselves familiar with competitive examinations like MD entrance, PSC,UPSC,MOH(UAE) etc. I make no pretence that this work is either complete or final. My aim is to stimulate the students to make their own ideas and observations.

There are no shortcuts. Competition is quite fierce these days and a casual approach to exam is not going to help. But if you plan properly and keep your cool during exam, there is no reason that you cant make it.

Multiple Choice Questions
Multiple choice questions are widely used for examination purposes and are reliable and accurate in evaluation also comparing to descriptive mode. Lack of familiarity with MCQ may result in unexpected failure but at the same time adequate reading, understanding and systemic study of subject is highly essential.

Students preparing for competitive examinations are recommended to read the appropriate chapters from the text books  and then to asses themselves using the MCQs.  Try to record your reasoning before checking the correct answer.

Many of the MCQs at any entrance examinations   have been repeated (about 35%) in same or altered form, so a candidate who revised the previous year’s questions had a definite advantage over a candidate who had not.

Text books
Reading previous years MCQ’s will help to a certain extent, but this is not the sole method of preparation advisable. If the question paper setter is an expert he will never take questions from guide but from standard text book. Read Textbooks thoroughly. This is a must for every aspirant. One can get the basic concept only through the textbooks. Select the book which provides genuine materials picked up from the standard text books.

Time management
Self assessment is an important part in the preparation. Practice as many Mock Tests as possible in close to examination environment as possible. Because time management is very important. Don’t try to read the entire question paper first. Try to answer easy questions first with care.

You have to answer for a large number of questions with in a short time. For example as per Kerala PSC exam pattern you will get only less than one minute for answering one question (100 questions to be answered with in one hour and fifteen minutes). The experiences of the author as well as many selected candidates show that you should have 90 or above correct answer out of  100 questions to get a call for interview.

  • Spend more time on the subjects in which you are weak. This is the key to success.
  • You have to identify which subjects made you suffer during your profs or during your previous attempt(s). Its always a good idea to finish them first.
  • You can follow any order in doing subjects as you like.

Time to spend on each subject: It depends upon how strong(or weak) you are in a particular subject. You have to spend less time on subjects from which less questions area asked.
Its very important not to get stuck at one subject for too long.

Questions can be asked from every nook and corner of the subject and therefore it is not at all advisable to omit any chapter or area. Because even a single wrong answer could miss  you a prestigious medical officer seat. We are living in an era of tough competition. Unless & until you have a well planned strategy you will miss the target.

Previous question papers show that plenty of questions are asked from Allen’s Key notes. Candidates Should have a thorough knowledge of all medicines in Key note. Generally many questions are asked from Relationship part of the book. Candidates should recollect comparison that is given in the book. A detailed understanding of Boericke`s materia medica is also expected. Questions regarding Common name of drugs are also asked. Family wise study of medicine should be done. Candidates should know the source and family of common medicines (Clinical materia medica by Farrington, last part of Clinical repertory by J.H.Clarke  & Articles regarding Family wise study given in materia medica portion of www.similima.com  can be referred).

Questions regarding History of Repertory, different repertories their philosophical background, year of publications, word  meaning, grading of rubrics, Computer repertories, Card repertories are asked usually. Some rubrics with their chapters,  rubrics in Kent’s repertory in which only one medicine is given are also asked

Questions regarding drug preparation, Pharmacopoea, source of drugs, rules& regulations are asked usually.

You have to study Social & preventive medicine including scope of homeopathy in epidemics with latest census parameters such as literacy rate, life expectancy, population  etc…  

You can guess if you are able to narrow down the answers to two, otherwise not.

Beware of negative marks. Each correct answer carries 1 mark and for each wrong answer 1/3 mark will be deducted in Kerala PSC, no negative marks in UPSC, 1 minus mark in Kerala PG Entrance exam (4 marks for correct entry). No negative mark for unattended questions.

During preparation

  • Avoid heavy oily food just before exam – your brain will concentrate on digestion not on your question paper.
  • Take more vegetables & fresh water – like green leaves, carrots etc. which will decrease your eyestrain and sharpen your memory. 
  • Avoid smoking, excess tea & drinks- Many of us have a belief that smoking, black tea etc. will stimulate our brain so that we can able to study for a long time – but these will definitely decrease your energy, and you will become tired with in short time. 
  • Sleep deprivation will result in decreased mental alertness – Many of the students will prepare thoroughly before the exam, but in the night before the exam, they avoid sleep and try to revise the whole topic. This will definitely decrease their mental alertness and they are unable to grasp the questions. So go to bed early in the night before exam.

Recommended books
There are many books available in the market, but the following books are more comprehensive   with essential and quality materials and their authors adopted a novel way in presenting the matter. This will help the students to remember the facts and conceptualize the topic. Moreover   important information about some topics is given in the form of charts and boxes for ready reference.

A comprehensive and up-to-date knowledge on all the 12 subjects of BHMS syllabus are essential.   In addition to the standard text books (which are of top priority) – these books provide a comprehensive outline to the essential content of the subject with summaries and tables.

In addition to the text books we advise the following books- these are highly useful

  1. Post graduate Medical entrance review –Salgunan (Which contains MCQs from major competitive examinations in India)
  2. SARP or PARAS series of condensed books on PG medical admission- in Medicine, OBG, Physiology, Anatomy, FMT etc-(These books  provide a comprehensive outline to the essential content of the subject with summaries and tables) Published by Scientific Book Company. Ashok Rajpath Patna. 800004

Try to purchase the latest edition of books on competitive examinatins, since medicine is an ever changing science and confirm any doubts with standard text books since few mistakes are there in majority of the books.

Analysis of previous question papers show that questions are asked from all the subjects of B.H.M.S course. A concise idea  about all the 12 subjects of BHMS syllabus in required- with more importance to clinical subjects. Normal biochemical values, Death Certificate, Medical certificates etc. Common disease with their aetiology, clinical features, diagnosis with Homoeopathic medicines.

Online support
Now days many of the question paper setters are taking questions from websites. You can download these questions with answers on various subjects free of cost.

Study materials (MCQ) available in http://www.fleshandbones.com – A website based on Davidson’s practice of medicine. MCQs and descriptive questions based on all the chapters of Davidson’s practice of medicine are available in this site.

Study materials (MCQ)  available in http://www.homeobook.com- This is the largest portal on homoeopathic education & research developed by postgraduate homeopaths which provide online coaching for PSC,UPSC,MOH(UAE) and MD(Hom) entrance examinations.

Study materials (MCQ) available in http://www.surgical-tutor.org.uk

Studymaterials(MCQ)available at http://www.webhealthcentre.com/mcq/postreg.aspThousands of MCQs, Online Tests, Study Material etc.

Study materials available at http://www.aippg.com – the premier Postgraduate Entrance / PLAB / USMLE / MRCP /IELTS resource online.

Plan your studies at least 2 months prior to exam – this is the most important aspect towards securing a good rank. The plan should ideally be drafted up to 2 months prior to the date of examination; thereafter a revised schedule might be put into operation. Prepare a simple timetable with sufficient time for each subject.

Make notes in a separate paper in abbreviated form (a must). It will considerably shorten the revision time & improve your memory. This proves very useful while revising the textbook also. Use different colored pencil or pen for marking tricky confusing questions.

Take a small notebook and start taking notes of difficult to remember points, some important flow charts and tables – not an elaborate note but small and precise.

Group discussion is also an important factor in preparation. One among you asks questions in haphazard/ rapid manner and others try to answer. This will quicken or sharpen your memory and reflexes. But not conceal any points for fear of others knowing it.  It is always said to be good to do group study. But it depends upon your nature. I have always studied alone.

Our memory

  • We may forget 75% of topics with in first 48 hours
  • So try to read the same topic 2-3 times with in 2 days – other wise you will not be able to remember majority of the points.

Last moment revision
It pertains to the last three days before the examination. Relax the schedule’s bit, try recapitulating the information, and revise the matter which you couldn’t recollect. Revise the easily forgettable information like Biochemical values, aphorisms, observations etc.

Read the notes you prepared in abbreviated form. 

Remember that there is no magic formula for success in an interview. Good preparation, judicious application of common sense and self-confidence are the key factors that will help us in an interview.

Regular assignments
Regular assignments and home works are unavoidable for getting a higher score

Pattern of questions

  • 50% can be answered by an average student
  • 30% can be answered by above average
  • 20% very difficult to answer (You should very careful while answering it) 

Avoid anxiety & jealousy

  1. It is very difficult to comprehend and concentrate if you are over anxious.
  2. If you are jealous towards your friend and classmates on competitive exams- it will create turmoil in your brain – so you are unable to concentrate.
  3. Make preparation – a thrilling experience

Remember the famous words of swami Chinmayananda : “ You cannot get into the ocean without getting wet, you cannot get into the fire without getting hot”.

    “Success is not the result of spontaneous combustion you must set yourself on fire”

With best wishes
Dr.K.R.Mansoor Ali

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How to study Materia Medica for MCQ Examinations

exam2Dr  Jitesh T K  MD(Hom) Materia medica Medical officer (Homoeopathy) Directorate of Indian System of Medicine & Homoeopathy, Govt of N.C.T of Delhi Email:  drjitheshtk@yahoo.co.in

There are different methods to study the Materia medica. It is the individual’s choice to choose the best way for the particular drug, without compromising with the essence of the drug. The method of study to increase your knowledge and the method of study to appear for the examinations is different. For that matter it is different for different types of examinations (subjective & objective) too. After going through the previous year’s U.P.S.C/P.S.C question papers, it has been observed that the majority of questions are asked from the following portions.

1. Allen’s Keynotes One should be thorough with each and every line in Allen’s Keynotes. Due importance should be given to the drugs given in the brackets and also the “Relations” section given under each drug.

2. Boericke’s Materia medica One must be familiar with all the medicines mentioned in the syllabus of concerned examinations. Due importance should be given to following portions (1) Introductory part of each drug (2) Symptoms in italics (3) Modalities & Relationship section

3. Relationship of remedies with duration of action – by Gibson Miller At least 1-2 questions regarding relationship of drugs are asked in each and every UPSC/PSC question paper. The orders of importance are as follows (1) Inimical & complementary (2) Cognates (3) Analogues

4. Family-wise study Study the drugs coming under important families. E.A.Farrington’s “Lectures on clinical matria medica”, J.H.Clarke’s “A clinical repertory to the Dictionary of Homoeopathic Materia medica”, Otto lesser’s “Text-book of Homoeopathic Materia medica”, Farokh. J. Master’s “The fascinating fungi”, “Agitated Argentums”,”Web spinners”, “Snakes in homoeopathic grass” etc are useful reference books for family wise study.

(1) Vegetable kingdom– important families are • Anacardiaceae • Compositae • Coniferae • Cucurbitaceae • Ericaceae • Euphorbiaceae • Fungi, Algae & Lichens • Labiatae • Liliaceae • Leguminosae • Loganiaceae • Myrtaceae, Myristicaceae & Myricaceae • Polygonaceae • Papaveraceae • Polygonaceae & Polygalaceae • Ranunculaceae • Rubiaceae • Rutaceae • Solanaceae • Umbelliferae • Urticaceae

(2) Animal kingdom • Insecta • Ophidia • Spiders • Milk and milk products

(3) Mineral kingdom • Acids • Noble metals • Halogen group • Carbon group • Ferrum group • Kali group • Magnesia group • Mercury group • Natrum group • Mineral – spring water

(3) Nosodes • Diseased products of human beings • Diseased products of other animals • Diseased plant products • Bowel nosodes

(Note: Materia medica of Nosodes by H.C.Allen, Materia medica of nosodes with repertory by O.A.Julian & Bowel nosodes by Paterson J are useful for studying Nosodes)

(4) Sarcodes • Sarcodes from healthy endocrine glands (e.g. Thyroidinum) • Sarcodes from healthy secretions [Hormones & Enzymes] (e.g. Adrenalin) • Sarcodes from extracts (e.g. Oophorinum) • Other Sarcodes (e.g.: Cholesterinum, Fel tauri, Vulpis fel)

(5) Impoderabilia • Natural • Human made (Artificial)

5. Provers of the drugs (1) Medicines proved by Dr.Hering & Dr.Hahnemann are very important (2) One should be well aware of the provings of Dr.Burnett, Swan, Burt, Stapf, Lux etc (3) Knowledge of provers of common drugs like Tuberculinum, Carcinocin etc (4) Provers of Indian drugs

6. Source books in Materia medica One should have a basic idea about the source books in Materia medica and their year of publication.

(1) “The Encyclopedia of pure Materia medica” by T.F.Allen • Year of publication • Number of volumes • Number of drugs

(2) “Materia medica pura” by S.Hahnemann • Year of publication • Volumes • Contributors • Translations • Schema • Number of medicines

(3) “Chronic diseases” by S.Hahnemann • Year of publication • Volumes • Number of drugs

(4) “ The Guiding symptoms of our Materia medica” by C.Hering • Year of publication • Number of volumes & drugs • Evaluation of symptoms • Grading • Construction • Arrangement • The introduction given by Dr.Jugal kishore is very useful

(5)“Dictionary of Practical Materia medica by J.H.Clarke • Year of publication & Number of drugs • Introductory part of polychrest medicines • Schema

(6)“ A Manual of Pharmacodynamics by Richard Hughes” • Year of publication & Number of drugs • The introductory chapters are important, Hughes gives a good picture of the sources of Materia medica

(7)“A Cyclopaedia of drug pathogenesy by Richard Hughes” • Year of publication • Number of drugs & number of volumes

7. Desires, Aversions & Complaints from One should be thorough with the desires, aversions and complaints from of at least the polychrest remedies. One of the standard repertories can be referred to for easy study.

8. Miasmatic background, Thermal reaction, Constitution & Side affinity of Common remedies • Study the important medicines comes under each miasm • Go through Dr.Gibson Miller’s Hot & Cold remedies given in the introductory chapters of Kent’s Repertory • Basic knowledge of constitution & diathesis is important. • Side affinity of medicines & those symptoms, which are contradictory to the general side affinity of a particular drug. e.g. Lachesis is given for right-sided sciatica even though it is a left-sided drug

9. Modalities The modalities given in italics/bold in Boericke’s Materia medica & Allen’s Keynotes are very important.

10. Authors and their important books in Materia medica Names of Materia medica of following authors are important • S. Hahnemann • H.C.Allen • T.F.Allen • E.A.Farrington • M.L.Tyler • J. T. Kent • J.H.Clarke • C.Hering • R.Hughes • E.B.Nash • C.Dunham

11. Basic idea about Tissue remedies Read the introductory lectures of Schussler’s Tissue remedies

12. Common names (Vernacular names) Common names of important drugs are frequently asked. Study the common names mentioned against each drug in Allen’s keynotes and Boericke’s Materia medica

13. Indian drugs Common names, prover etc are important e.g. (1) Blatta orientalis (2) Azadiracta indica

14. Other useful Materia medicas • “The prescriber” by J.H.Clarke • “Expanded works of E.B.Nash” • “A Study of remedies by comparison” by H.A.Roberts • “Special pathology and diagnostic with Homoeopathic Therapeutic hints” by C.G.Raue • “A Synoptic key of the Materia medica” by C.M.Boger • “A Study of Materia medica” by N.M.Choudhury • “Essentials of Materia medica & Pharmacy” by W.A.Dewey • “Regionals of Boericke Materia medica” by Satya paul • “Materia medica of homoeopathic Medicines” by S.R.Phatak • “Prescriber to Allen’s Keynotes & Characteristics” by R.P.Sangar • “Text book of Materia medica” by S.K.Dubey • “Select your remedy” by Bishamber Das

15. Latest Materia medicas It will be a waste of time and energy if undue importance is given to the study of the latest Materia medicas, because symptoms are quoted and questions asked only from the authentic Materia medica textbooks

Different authors explain relationships of remedies in different ways. Important points mentioned by them can be studied as follows.

1. Dr.Hahnemann: 1. Antidote – In the aphorism 249 he suggests “If the aggravation be considerable (after a medicine) be first partially neutralized as soon as possible by an antidote before giving the next remedy chosen more accurately according to similarity of action”

2. Dr.E.A.Farrington

  1. Family relation – From the similarity in their origin
  2. Concordant – Similar drugs with dissimilar origin
  3. Complement – The drug that completes the cure which the other begins, but unable to effect
  4. Antidote – The medicine which modify the effects of a wrongly selected potency or an apt potency
  5. Inimical – They also will be similar, but the resemblance will be so great, in fact the drugs are so nearly “idem” that it is not well to follow one with the other.

3. Dr.Clarke

  1. Complementary remedies
  2. Remedies that follows well (after)
  3. Remedies followed well by
  4. Compatible remedies
  5. Incompatible remedies
  6. Remedy antidotes
  7. Remedy is antidoted by

4. Dr.Boenninghausen

  1. Remedies related to mind and localities
  2. Other remedies (Represents a general relationship of the remedies in the unclassified symptom groups, to the remedy under consideration)
  3. Antidotes
  4. Injurious

5. Dr.Boger

  1. Remedies related to mind and localities
  2. Related remedies
  3. Antidote
  4. Inimical – Two very similar remedies do not follow each other well

6. Dr.J.T.Kent

  1. Chronic remedy – In managing a chronic sickness the remedy that conforms with an acute experience of the illness is worth knowing, as very often its chronic may be just the one that conforms to its symptoms. (e.g.: 1. Calcarea is the natural chronic of Belladonna and Rhus tox, 2. Natrum mur is the chronic of Apis & Ignatia)
  2. Complementary – Medicine that completes the action of the first one when it is no longer acting.
  3. Inimical – They do not like to work after each other (e.g.: Causticum & Phos, Apis & Rhus tox)
  4. Antidote – when there appears new symptoms, the new symptoms combining with the old ones must be again studied and the second remedy must correspond more particularly to the new than to the old.

7. Dr.C.Hering

  1. Complementary to
  2. Follows well after
  3. Followed well by
  4. Antidotes (Lyco antidotes Cinchona)
  5. Antidotes to (Antidotes to Lyco: Acorn,Camphor)
  6. Inimical
  7. Collateral relation (Belonging to the same family)
  8. Concordances
  9. Conjunctive relation (Bryonia & Colocynth)

8. Dr.Elizabeth Wright

  1. Complementary – (a) Acute complements of chronic remedies (b) Chronic complements of acute remedies (c) Remedies in series
  2. Incompatible
  3. Vegetable analogues & Chemical analogues

9. Dr.Gibson Miller

  1. Complements
  2. Remedies that follow well
  3. Inimicals
  4. Antidotes 

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Approach to Competitive Exams in Materia Medica

exam9Dr Arun Prasad K P MD (Hom)
Govt.Homeopathic Medical College. Calicut

A thorough preparation is essential, as you would before a final BHMS exam. The complexity and depth of the questions ensures that one cannot succeed with a hit and miss approach. Questions are asked on all aspects of remedy – Name / common name, family / source, alkaloid, prover, action /affinity, temperament / constitution, symptomatology, relationship, caution / warnings on use etc. Expect questions also from general topics like source books / materia medicae, observations / quotes of authors and even rare topics like bowel nosodes, tissue remedies etc.

Read standard books on materia medica. MCQ books though very important, should be used mainly for exercise / revision purposes and not as the primary source of information. Of the text books the most important are Allen’s “Key Notes” and Boericke’s Materia Medica Nash’s “Leaders”, Farrington’s Clinical Materia Medica, and Kent’s “Lectures” should also be referred. Questions can be asked directly from these books (eg. According to boericke / Nash, which remedy has this symptom etc)

Allen’s “Keynotes” should be known inside out to answer some questions.
Example :-
Which of the following is not correct in respect of bad effects of tobacco ?
Phos – tobacco heart b) Ign – hiccough c) Nux-v – occipital headache and vertigo d) Sepia – right sided facial neuralgia
Comment – Question asked from the relationship section of Tabacum

While reading “key notes”, make special attempt to collect all the remedies known for a particular symptom. Questions invariably require knowledge of more than one remedy.
Example :-
Which of the following symptoms are common to kali-bi, Apis and Lac-c ?
a) shifting pains b)thirstlesness with dry tongue c) offensiveness with forgetfulness d) delayed painful, scanty menses with increased sexual desire and weeping
Comment – Apis is not given in brackets after the symptom under Kali-bi

Candidates should not forget to make adequate repertory reference (Kent’s repertory). Peculiar / Single medicine rubrics should be gone through, especially mind and generals chapters. Sometimes questions are asked directly quoting repertory.
A) Choose the correct remedy for the rubric “Perspiration profuse, sitting quietly, while”
(a) Sambucus Nigra (b) Psorinum (c) Kali bichromicum (d) Calc. C

B)Match List-I (Symptoms) with List-II (Medicines) and select the correct answer using the codes given below the lists (UPSC)
List-I List II
(Symptoms)        (Medicines)
A. Ardent             1. Merc.
B. Hypocrisy         2. Ign.
C. Inconsistency   3. Phos.
D. Precocity         4.Nux v.
(a) A B C D
2 3 4 1
(b) A B C D
4 1 2 3
(c) A B C D
2 1 4 3
(d) A B C D
4 3 2 1
Comment –Phos and Merc are the only medicines in their respective rubrics – but both are hardly highlighted in the materia medica.

Though as mentioned above all aspects of remedies are important, special attention should be paid to, food desires /aversion < & >, relationship of remedies synonyms, families etc
Example :-
Which one of the following is the correct order of remedies that matches with > coffee, < coffee and desire coffee ?
a) Ign-Ang-Cham b) Ang-Ign-Cham c) Ign-Cham-Ang d) Cham-Ign-Ang

While going through Boerick’s materia medica pay special attention to introductory paragraph, italicised symptoms and relationship of remedies

The Pattern of questions for UPSC is different from that followed by the Kerala PSC and come in various level of complexities. Examples of some of the more common types of questions asked are given below. MD Hom candidates can focus on these as well, as there is a tendency for paper setters in Kerala to follow UPSC questions.

A. Find symptom / s for remedy
Consider the following symptoms
1) stool partly expelled, recedes 2) Much urging, but inability to expel
3) Stool lies in rectum without urging until there is a large accumulation
4) stool hard as stone

Which if the above form the indication for Sanicula ?
a) 2 & 3 b) 1 & 3 c) 1,2,3,4 d) 1 only
Comment – Answer requires more than a superficial knowledge of the symptom

B. Match symptoms & remedy
See example given earlier under repertory reference

C. Find remedy for a case
I) A 7-years old child with convulsions, screams and has violent jerking of hands and feet. He, has pinching colic in abdomen before passing stool with mucus like white pieces of popped corn; also grinds teeth at night. Choose the correct remedy from the following :
(a) Bell .
(b) Chamomilla
(c) Cicuta
(d) Cina

II) A nine-year old child is brought to you. with complaints of moderate fever and sore throat for 2 days. There is sore aching, bruised feeling all over the body. On examination, head is hot and limbs are cold. Tonsils are red with white patches. He also feels as if a hot coal were present in his throat. Which one of the following will you choose for him ?
(a) Bell
(b) Arnica
(c) Merc-.Cya.
(d) Phytolacca

D Logic & reasoning
The following items consist of two statements; one labelled as the ‘Assertion (A)’ and the other as ‘Reason(R)’. You are to examine these two statements carefully and select the answers to these items using the codes given below:
(a) Both A and R are individually true and R is the correct explanation of A.
(b) Both A and R are individually true but R is not the correct explanation of A.
(c) A is true but R is false.
(d) A is false but R is true.

Eg. Code (b)
1) Assertion (A): Sulphur is a great antipsoric remedy.
Reason (R) : Sulphur often has a great use in beginning the treatment of the psoric cases.

Eg. Code (c)
2) Assertion (A): Thuja is the king of antisycotic remedies.
Reason (R) : Thuja can cure each and every type of warts at each and every locations.

Eg. Code (d)
3) Assertion (A): Hamamelis and Millefolium belong to same family.
Reason (R):Hamamelis and Millefolium are antihaemorrhagic medicines.

Comment – First see whether both assertions are individually correct – if yes choose code a or b, if no choose code c or d

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Laboratory investigations and indications

lab2Dr  Sunila


HAEMOGLOBIN: Male- 13-18 gm/ dl; Female- 12-16gm/dl (Normal values)

HAEMATOCRIT: Male-45-62%; Female- 37-48%

MEAN CORPUSCULAR VOLUME (MCV): 83-103 fl (femtolitres) or cum m/red cell (Normal); increased in liver disease, alcoholism, sprue, deficiency of folate or B12; decreased in iron deficiency anaemia, pernicious anaemia, thalassemia & chlorosis.

MEAN CORPUSCULAR HAEMOGLOBIN CONCENTRATION (MCHC): 32-36% (Normal); increased in spherocytosis; decreased in iron deficiency, macrocytic anaemia, pyridoxine responsive anaemia & thalassemia.


PLATLET COUNT: 150000-350000 per cmm (Normal); increase in cancer, chronic leukemia, polycythemia vera, splenectomy, heart disease & rheumatoid arthritis.

WBC COUNT: 4,300-10,800 cells/ µL/ cu mm (Norma)

Leukocytosis: increase of WBC above 10000/ cu mm; increased in any infection, haemorrhage, trauma/ tissue injury, serum sickness, malignancy, leukemia & tissue necrosis; decreased in viral infection, hypersplenism, & bone marrow depression due to drugs. 

Neutrophils: 40-70% 

Eosinophilia: increase more than 5%; increased in allergies, parasitic diseases, lung & bone cancer, chronic skin affections & Hodgkin’s disease; decreased in infectious mononucleosis, hypersplenism, congestive cardiac failure, cushing’s syndrome, aplastic anaemia & use of ACTH. 

Basophils: < 1% 

Lymphocytes: 20-40% (Normal); increased in upper respiratory tract infections, viral diseases like mumps, bacterial infections like TB, hypothyroidism & lymphocytic leukemia; decreased in hodgkin’s disease, L.E, after ACTH, after burns & trauma & chronic uraemia. 

2. RBC: 4. 2- 6. 9 million/ µL/ cu mm (Normal value) 

3. ESR : Male: 1-13 mm/hr; Female: 1-20mm/ hr 

ESR is raised in
Slow rising ESR: pregnancy (after 4th month), anaemia, acute myocardial infarction, rheumatoid arthritis, carcinomatosis, pulmonary TB, acute gout, burns, acute infections & after fracture & operations.

Rapid rise in ESR: kala azar & multiple myeloma.



  • Normal total                      0.3-1.1 mg/100 ml
  • Direct                                 0.1- 0.4 mg/100ml
  • Indirect                              0.2- 0.7 mg/100ml
  • Rise of indirect serum bilurubin In haemolytic diseases, Gilbert’s disease&Acute or chronic hepatitis
  • Rise of total bilurubin: Biliary tract obstruction, Cancer of head of pancreas& inGall stones



  1. Normal    3.5-5.5gm/100ml.
  2. Increased in Haemoconcentration shock & Dehydration
  3. Decreased in Malnutrition, Starvation, Glomerulonephritis, Hepatic insufficiency, Leukemia & in Other malignancies


  • Normal       : 1. 5-3 gm/100 ml.
  • Elevated  in Hepatic disease, Multiple myeloma, Bacterial & viral infection, Typhus & malaria
  • Decreased in Starvation with malnutrition, Lymphatic leukemia& Agammaglobulinemia 


  • Normal     : 5-13 KA or 2-5 Bodansky units/100 ml
  • Elevated in Severe osteomalacia, Osteogenic sarcoma, Metastasis to bone, Paget’s disease, Myeloid leukemia, Hyperthyroidism & in Pregnancy
  • Decreased in Hypothyroidism & Growth retardation 


  • Normal      : 5-35 sigma frankel/ml, 4-24 IU/litre
  • Increased in Hepatocellular diseases, Active cirrhosis, Metastatic liver tumour & obstructive liver tumour, Obstructive jaundice, Liver congestion, Pancreatitis& inHepatic injury in myocardial infection 


  • Normal       : 5-40 sigma frankel/ml, 0-36 IU/litre
  • Increased in MI, Liver diseases, Acute pancreatitis, Acute haemolytic anaemia, Severe burns, Recent brain trauma
  • Decreased  in Beriberi & Uncontrolled diabetes 

PROTHROMBIN TIME: normal- 11-16 seconds; increased in prothrombin deficiency, Vit. K deficiency, haemorrhagic disease, liver disease, biliary obstruction & hypervitaminosis A. 


  • Normal     : < 165 mg/100 ml
  • Elevated in Hyperthyroidism, Diabetes mellitus, Biliary obstruction & Primary hyperproteinemias.
  • Decreased in Malabsorption, Malnutrition & Primary hypolipoproteinemias.


  • Normal      150-250 mg/ 100ml
  • Increased in Xanthomatosis, Pregnancy, Alcohol & fatty diet, Myxoedema, Diabetes mellitus, Obesity & Nephritic syndrome.
  • Decreased in Hyperthyroidism, Acute infections & Anaemia with malnutrition.


  • Normal       44mg/ 100ml in men & 55 mg/dl in women.
  • Increased in Chronic liver disorder, increased physical activity & Moderate intake of alcohol.
  • Decreased in Smokers & High risk patients of MI.


VLDL: 25-50%.


  • Normal        10-15 mg/100ml.
  • Increased in Impaired renal function, Shock/ dehydration, Diabetes, Acute myocardial infarction, Gout & Excessive protein intake.
  • Decreased in Liver failure, Malnutrition, Impaired absorption, In celiac disease,Nephritic syndrome&Over hydration. 

7. UREA NITROGEN (BUN): 7-18 mg/dl (Normal value)

8. CREATININE: 0. 6- 1. 2 mg/ dl;        BUN/CREATININE RATIO: 5-35


     Normal                                      : 20-200 IU/ LITRE.


  • MM fraction                            : 94-95%
  • MB fraction                             : 0-5%
  • BB fraction                              : 0-2%

      Heart: 80% MM, 20% MB      Brain: 100% BB       Skeletal muscles: 95% MM, 2% MB.


  • Normal      2.2-8 mg%
  • Increased in Gout, Metastatic cancer, Starvation/shock, Alcoholism, Multiple myeloma, Diabetic ketosis & leukemia
  • Decreased in Aspirin  & Sulfinpyrazone 


  • Normal        9.6- 10.9 mg/ 100ml
  • Elevated in Hyperparathyroidism (20 mg), Hypervitaminosis D (17 mg), Multiple myeloma & Cushing’s syndrome.
  • Decreased in Hyperparathyroidism, Osteomalacia/ rickets & Malabsorption syndrome.


  • Normal     : 0. 5- 2 Bodansky units
  • Elevated in Acute pancreatitis, Carcinoma of pancreas, perforated peptic ulcer, acute cholecystitis, Cirrhosis liver, Mumps & Renal failure.
  • Decreased in Necrotising hepatitis, Severe burns, Toxaemia of pregnancy.


  • Normal       : 75 mcg/100 ml.
  • Elevated  in Haemochromatosis, Aplastic anaemia, Haemosiderosis, Haemolytic anaemias, Pernicious anaemia
  • Decreased in Iron deficiency anaemia, Nephrosis, Chronic renal insuffiency, Paroxysmal nocturnal haematuria. 


  • Normal        : 63-155 units
  • Increased in Acute MI, Acute leukemia, Hepatic disease, Extensive cancer, Shock & anoxia
  • Decreased in: Good response to cancer 


  • Normal    : 5-12. 5 µg/ dl
  • Increased in Hyperthyroidism , Acute thyroiditis, Sub acute thyroiditis, Hepatitis
  • Decreased in Cretinism, Myxoedema, Simmond’s disease, Hypothyroidism, Nephrosis. 


  • Normal: 110-230ng/ 100 ml.
  • Increased in hyperthyroidism, T3 thyrotoxicosis, acute thyroiditis, idiopathic TBG elevation.
  • Decreased in hypothyroidism, starvation, acute illness, idiopathic TBG decrease.

Fasting blood sugar: normal value- 60-100 mg %. Increased in diabetes, cushing’s disease, acute stress, pheochromocytoma, hyperthyroidism, pancreatitis, chronic liver disease &chronic malnutrition.

Decreased in over dose of insulin, addison’s disease, bacterial sepsis, islet cell carcinoma, hepatic necrosis, hypothyroidism & psychogenic causes.


  • Normal: Below 2oo units.
  • Increased: recent infection with streptococci or an exaggerated immune response to an earlier exposure in a hypersensitive person. 

Specific gravity: 1. 003- 1. 030; specific gravity increases if excretion of urine decreases.

It is increased in diabetes mellitus or nephrosis & in excessive water loss.

Low specific gravity: diabetes insipidus, glomerulonephritis, pyelonephritis & in severe renal damage. 

  • Protein: 2-8 mg/ dl (normal value)
  • Protienuria due to kidney causes: TB &cancer of kidney, nephritis, polycystic kidney, ascitis & nephrosis.
  • Protienuria due to non- renal causes: fever, toxaemia, trauma, severe anaemias & aspirin.
  • PH: 4. 6- 8. 0

 Colour of urine: 

  1. Colourless urine: large fluid intake, untreated diabetes mellitus, diuretic therapy, alcohol ingestion, nervousness.
  2. Orange coloured urine: concentrated urine, excessive sweating, restricted fluid intake & fever.
  3. Red or reddish dark brown: haemoglobinuria, myoglobin & porphyries.
  4. Slack urine: alkaptonuria
  5. Brown black: Lysol poisoining, melanin. 
  • Turbidity: fresh urine is clear. Urine becomes turbid due to UTI.
  • Sugar normal values: 100 mg/ 24 hours. Increased in diabetes mellitus, brain injury & MI.
  • Red cell cast: acute glomerulonephritis, collagen disease, renal infarction & endocarditis.
  • Increased red cells: pyelonephritis, renal stone, trauma to kidney, haemophilia, lupus vulgaris, cystitis, TB & malignancy.
  1. White blood cells: large number of WBC’S indicates bacterial infection in urinary tract; if infection is in kidney, there may be associated cellular or granular casts, bacteria, epithelial cells & few RBC’S. 
  2. White blood cells & casts: pyelonephritis, acute glomerulonephritis & interstitial inflammation of kidney. 
  3. Epithelial cells & casts: renal epithelial cell casts are formed by cast of tubular cells, hence occasional renal epithelial cells are found. Increased in amyloidosis & poisoining from heavy metals. 

Diarrhoea mixed with mucus & blood: typhus, typhoid, cholera, amoebiasis & large bowel cancer. 

Diarrhoea mixed with mucus & pus: ulcerative colitis, shigellosis, regional enteritis, salmonellosis, obstruction of common bile duct (putty like appearance), sprue & celiac disease (stool resembles like aluminium) & in cystic fibrosis (greasy butter stool).

Alteration in shape & size: narrow ribbon like stool: spastic bowel, rectal narrowing, decreased elasticity or partial obstruction; excessive hard stool: increased absorption of fluids, constipation; very large caliber stool: dilatation of viscus; small, round, hard stool: habitual moderate constipation. 

Colour of feces: yellow to yellow green: during breast fed; green colour: chlorophyll rich vegetables; black colour: iron, charcoal & bismuth; light coloured stool: diets high in milk & low in meat; clay coloured: due to excessive fat; red colour: due to beets. 

CSF/ normal values
Bilurubin: 0                    Cells: 0-5 / mm3; all lymphocytes            Chloride: 110-129 meq/ litre.

Glucose: 48- 86 mg/dl or 60% serum glucose.                                 PH: 7. 34- 7. 43.

Pressure: 7-20 cm water                                                        Protein, lumbar CSF: 15- 45 mg/ dl

Albumin:  58%      alpha 1: 9%       alpha 2: 8%       beta: 10%    gamma: 10%

Protein, cisternal CSF:  15-25 mg/dl                                Protein, ventricular CSF: 5-12 mg/ dl. 

Volume:  2- 6. 6 ml.             Count: >50 million/ ml.                    Motility: > 75 %

PH: 7. 2- 8                                         Morphology of sperms: > 60 % normal forms.        Liquefaction: complete in 15 minutes.                              Spermatocrit: 10%

BLOOD SMEAR:        Burr cells: Uraemia            Spur cells: Cirrhosis

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Triads and Pentads in Medicine

shoppingCompiled by Dr Nupur

Triad of Alports Syndrome
Sensorineural deafness
Progressive renal failure
Ocular anomalies

Triad of Behcet’s Syndrome
Recurrent oral ulcers
Genital ulcers

Beck’s Triad
Muffled heart sound
Distended neck veins

Charcot’s Triad

Pain + fever + jaundice

Gradenigos Triad

Sixth cranial n. Palsy
Persistent ear discharge
Deep seated retro orbital pain

Triad of Hypernephroma
Pain + hematuria + renal mass

Hutchinson’s Triad
Hutchison’s teeth
Interstitial keratitis
Nerve deafness

Triad of Kwashiorkar
Growth retardation
Mental changes

Saint’s Triad
Gall stones
Hiatus hernia

Trotter’s Triad
Conductive deafness
Immobility of homolateral soft palate
Trigeminal neuralgia

Virchow’s Triad
Vessel injury

Whipple’s Triad
Hypoglycaemia during attacks
S.glucose 10%
Lytic bone lesions

Hemolytic Uremic Syndrome Triad
Renal failure

Fanconi Syndrome Triad

Tetany in Children – Triad
Carpopedal spasm

Alkaptonuria Triad
Ochronotic arthritis
Ochronotic pigmentation
Urine darkens on standing

Anderson Triad
Cystic fibrosis
Vitamin A deficiency

Triad of Albinism
Black locks
Occulo-cutaneous Albinism
Deafness of sensorineural type

Pentad of TTP
Microangiopathic haemolytic anaemia
Disturbed neurological function
Renal failure

Triad of Causes of Biotin Deficiency

Reynolds Pentad

Abdominal pain,
Shock, and
Depression of central nervous system function (usually indicative of acute suppurative cholangitis)

Pentalogy of Fallot

Fallot’s tetralogy with, in addition, a patent foramen ovale or
Atrial septal defect.

Triple Test
Estimation of hcg,
and AFP
(for diagnosis of downs syndrome)

O’ Donoghue Triad
Twisting force in a weight bearing knee joint

O’ Donoghue Triad
Twisting force in a weight bearing knee joint causes injury to
1. Medial collateral ligament
2. Anterior cruciate ligament
3. Medial meniscus

Congestive Heart Failure Triad
Tender hepatomegaly

Cushing Triad of Increased Intracranial Pressure

Hemobilia – Triad
(Triad of Sandblom)
Obstructive jaundice
Biliary colic

Kartagener’s Syndrome Triad
Triad of bronchiectasis
Recurrent sinusitis, and
Situs inversus

NB : E&O expected

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Infection – Last Moment Revision for exams

diseases1Dr  Sunila MD(Hom)
Medical Officer, Department of Homeopathy, Govt of Kerala.

  • Infection: Lodging & multiplication of the organisms in or on the tissues of host.
  • Primary infection: Initial infection of a host by a parasite.
  • Re-infection: Subsequent infections by the same parasite in the same host.
  • Secondary infection: Infection by another organism in a person suffering from an infectious disease.
  • Nosocomial infection: Cross infections occurring in hospitals.
  • Super infections: Infections caused by a commensal bacterium in patients who receive intensive chemotherapy.
  • Opportunistic infections: Organisms that ordinarily do not cause disease in healthy persons may affect individuals with diminished resistance.
  • Latent infections: When a pathogen remains in a tissue without producing any disease, but leads to disease when the host resistance is lowered.
  • Commonest infective disease: common cold.


When the temperature is raised above 38.3°C for more than 2 weeks without the cause being detected by physical examination or laboratory tests is PUO (FUO) 


a) Occult tuberculosis

b) Chronic suppurative lesions of the liver, pelvic organs, urinary tract, peritoneum, gall bladder, brain, lungs, bones & joints & dental sepsis (occasionally).

c)  Viral infections:

  • Viral hepatitis
  • Infectious mononucleosis
  • Cytomegalovirus infection
  • Aids

d) Connective tissue disorders:

  • Giant cell arteritis.
  • RA
  • Rheumatic fever
  • SLE
  • PAN (polyarteritis nodosa)

e)   Chronic infections:

  • Syphilis
  • Hepatic amoebiasis
  • Cirrhosis liver
  • Malaria
  • Filariasis
  • Leprosy
  • Brucellosis
  • Sarcoidosis

f)  Haematological malignancies

  • Leukemia
  • Lymphoma
  • Multiple myeloma

g)   Other malignant lesions: Tumours of lungs, kidney etc.

h)   Allergic conditions

i)    Miscellaneous conditions: Hemolytic anaemia, dehydration in infants etc.

j)    Factitious fever: Self induced fever in patients with psychological abnormalities..


Endotoxines of gram negative bacilli are responsible for most of the cases.

More frequent in men.

Toxic shock syndrome in women: caused by toxigenic strains of staphylococci (gram positive) contaminating vaginal tampons.

Clinical features:

  •  Features of shock: Hypotension, Weak thready pulse, Cold clammy skin, Tachycardia & Peripheral cyanosis.
  •  Death is caused by: pulmonary oedema, tissue anoxia, cardiac arrythmias & Disseminated intravascular coagulation 




  • Hypersensitivity reaction to group A streptococci.
  • Rheumatic fever follows 2-3 weeks after an attack of streptococcal pharyngitis.

Age group: 5-15 years (mean age- 6 years)

Pathology: 2 stages: 

  • Exudative stage: acute phase.
  • Proliferative stage: prolonged process. Hallmark of proliferative phase is Aschoff bodies.

Heart: Endocarditis, myocarditis & pericarditis (pancarditis). MacCallum’s patch is seen in posterior wall of left atrium due to scarring of mural endocarditis.

Pericardium: bread & butter appearance (fibrinous inflammation in pericardium). 

Joints: Acute synovitis. 


  • Throat swab culture.
  • Serodiagnosis
  • Anti-streptolysin O titer (ASO)
  • Anti-streptokinase (ASK)
  • AntiDNAse B
  • Anti- nicotinamide- adenine dinucleotidase (anti- NADase)
  • Anti- hyaluronidase (AH)
  • Anti- streptozyme test (ASTZ)
  • Acute phase reactants → lab tests helpful in acute phase.
  • ESR & C – reactive protein – increased.
  • ECG:
  •       Sinus tachycardia, ectopic beats & 1st & 2nd degree heart blocks.
  •       ST elevation in pericarditis.


  1. This may follow either cutaneous or pharyngeal lesion by group A streptococcus.
  2. 10- 15% of children getting recurrent skin infections may develop glomerulonephritis.
  3. Serotypes 12, 44, 2, 52, 55, 57 & 4 are more often nephritogenic.
  4. Latent period for the development of acute GN is 10 days after pharyngitis & 3weeks after pyoderma. 


Pneumococcal Pneumonia (Syn: Lobar pneumonia)

Most common pneumococcal lesion in adults is pneumonia.

Pathology: Formation of inflammatory exudate in alveoli.

Stages: Red hepatisation (alveoli are filled with red cells & fibrin), Grey hepatisation (neutrophil leucocytes predominate) & Resolution. 

Clinical features

  1. Fever, chills & herpes simplex.
  2. Pleuritic pain & Cough with pinkish or rusty sputum
  3. Signs of consolidation over the affected lobe.

Laboratory findings

  1. Rusty sputum
  2. Pneumococci can be demonstrated by gram staining, Blood culture is positive in 20-25% cases in early stage of the disease. Leucocytosis
  3. Skiagram of the chest shows a homogenous opacity corresponding to the lobe involved.


  • Local: atelectasis, lung abscess, delayed resolution
  • Due to spread of inflammation to adjacent structures: pleural effusion, empyema, pericarditis & peritonitis
  • Haematogenous spread: septicaemia, meningitis etc.


Agent: Salmonella paratyphi A, B, C.

Illness resembles typhoid, though the toxemia & complications are milder. 


Shigellae: 4 species

  1. Shigella dysentriae type 1 & 2(S. shigae & S. schimitzii)
  2. S. flexneri.
  3. S. sonnei.
  4. S. boydii.

Source: contaminated food or water.


  • The entire colon may be affected.
  • Toxins are responsible for secretory diarrhea.
  • Necrosed mucosa→ intestinal casts. 


  1. Dehydration
  2. Electrolyte imbalance
  3. Circulatory failure
  4. Renal failure
  5. Intestinal perforation & rectal bleeding
  6. Paralytic ileus.

ANTHRAX (Wool Sorter’s disease)

Agent: Bacillus anthracis (gram +ve)

Source: infected animals, contaminated wool, hair etc.

Clinical features

  1. Cutaneous form (malignant pustule)
  2. Pulmonary form: anthrax pneumonia (wool sorter’s disease)
  3. Gastrointestinal form
  4. Meningitic form


  1. Blood Culture: polymorph leucocytosis
  2. CSF: haemorrhagic in anthrax meningitis
  3. Agar gel precipitation inhibition test: a four fold rise in serum antibody titer confirms the diagnosis. 

Klebsiella pneumoniae: Freidlander’s bacillus 

Pseudomonas aeruginosa: produces a greenish pigment pycocyanin 

Proteus: 4 species: P. mirabilis, P. vulgaris, P. morganii, and P. rettgeri. 

They cause super infection in areas of tissue damage (eg. umbilical stump in newborn – bacteremia & septic meningitis) 


  • Group: Enterobacteriaceae.
  • Gram negative


  • Somatic (O)
  • Flagellar (H)
  • Capsular(K)

Clinical presentation

  1. UTI
  2. Peritonitis
  3. Septicemia
  4. Neonatal infection
  5. Biliary tract disease
  6. Gastroenteritis:

 Enterotoxigenic strains of E. coli (ETEC) cause gastroenteritis in children’s nurseries.
Traveller’s diarrhea 


  •  Coli serotypes O15, K7, and H7 cause haemorrhagic colitis.
  •  Watery diarrhoea→ bloody.
  •  Verocytotoxines are responsible for haemolytic uraemic syndrome 


  • Zoonosis.
  • Causative agent: Yersinia pestis (previously known as Pasteurella pestis); gram negative.
  • Vector:  Xenopsylla cheopis; infected rat flea.
  • Reservoir of infection: infected domestic rodents such as Rattus norwegius, Rattus rattus & Mus musculus. 

Pathogenesis: The organisms enter through the skin. The bacilli reach the local lymph nodes which enlarge & suppurate: Bubo. Bacilli proliferate and enter the blood stream to produce metastatic lesions. Spleen may be enlarged twice or thrice its normal size. In primary pneumonic plague, the organisms reach the lungs through the respiratory tract. 

Clinical manifestations:

Bubonic plague: 

  • a.  I. P: 2-6 Days.
  • b. Fever & lymphadenopathy
  • c. Buboes: in inguinal & axillary region.
  • d. Pestis minor: milder cases seen during epidemics. These present only with buboes.

Septicemic Plague:

  • a. Chills, fever, tachycardia, headache, vomiting and delirium
  • b. Death may occur with in a few days before localizing lesions are evident.
  • c.  Haemorrhagic manifestations may develop.

Pneumonic Plague:  Primary and Secondary

  • a.  Primary: More fulminant and rapidly fatal. Organisms reach the lungs by inhalation.
  • b.  Secondary: Organisms reach the lungs through the blood stream


  1. Diagnosis is confirmed by demonstrating the organisms by smear, culture or animal inoculation studies.
  2. Bubo-fluid can be aspirated and stained for the organisms.
  3. Sputum can be stained for the organisms and cultured.
  4. In septicemic plague blood culture yields the organism. There is neutrophil leukocytosis. Specific antibodies develop in patients who recover from the disease. 

Prevention: A heat killed vaccine (Haffkine) is available for immunizing the population at risk. 

BRUCELLOSIS (Undulent fever, Malta fever, Abortus fever) 

It is an infectious disease of animals which is transmitted to man by handling infective material.

Causative organism: gram negative coccobacilli.

  • Brucella abortus: causes abortion in cattle.
  • Brucella melitensis: infection spreads through goat’s milk
  • Brucella suis: obtained from pigs.

Pathogenesis: Organisms enter through GIT, RT, and conjunctiva or through the skin. They pass through the local lymph nodes into the blood stream to localize in the reticuloendothelial system. They multiply in RE tissues to produce granulomas.

Clinical features: 

  1. I.P: 2-3 weeks
  2. Fever, malaise, sweating, chills, arthralgia & backache.
  3. Spinal tenderness, arthritis & orchitis are common.
  4. Chronic brucellosis may present as PUO. 


  1. Endocarditis
  2. CNS: meningoencephalitis, myelitis & polyradiculoneuropathy.
  3. Nephritis
  4. Hepatic & splenic suppuration
  5. Calcification in the liver & spleen & cholecystitis
  6. Uveitis


  • Clinical features: typhoid like illness especially if associated with spondylitis or arthritis.
  • Diagnosis is confirmed by isolation of the organism from blood, bone marrow etc.
  • Special lab techniques are necessary to grow brucella.
  • Standard tube agglutination tests, Coomb’s antiglobulin tests, complement fixation test & ELISA test are used for detecting agglutinating antibodies. Coomb’s test & ELISA are more reliable. If the initial test is negative, test is repeated after 3-4 weeks. 



Causative organism:  Vibrio cholerae; gram negative. 92 serogroups are identified based on O (somatic) antigen. The strain producing epidemic cholera possesses O1 antigen; hence this vibrio is designated as vibrio cholerae O1.

  • Inaba, Ogawa & Hikojima are the most important pathogenic subtypes.
  • Others are collectively designated non- O1 V. cholerae.
  • Eltor biotype is a variant of V. cholerae O1; it is characterized by hemolytic activity & resistance to polymyxin. Differentiation between Eltor & V. cholerae is by phage typing.
  • Classic disease is caused by Vibrio cholerae, but the majority of outbreaks occurring in India are due to Eltor biotype.
  • Main vehicles of infection are water, cooked food kept unhygenically exposed to flies, sea foods, fruits & vegetables.

Pathogenesis: Vibrio cholerae multiply in the jejunum & small intestine & produce an enterotoxin. By the influence of this toxin the enterocytes (intestinal mucosal cells) secrete large amount of isotonic fluid. The result is watery diarrhea which leads to loss of isotonic fluid. Excessive loss of fluid & electrolyte gives rise to hypovoluemic shock & metabolic acidosis.

Cholera enterotoxin:

  • It is a protein of Mol. Wt: 84000.
  • 2 immunologically distinct regions: A (active) & B (binding).
  • Binding enables A region to penetrate the mucosal cells
  • This toxin leads to formation of adenylate cyclase which induces excessive production of cyclic –AMP (cAMP), which in turn is responsible for over secretion of electrolytes & water by the enterocytes. 

Clinical features:

  • Eltor cholera: usually mild & asymptomatic.
  • Moderate & severe cases: last for 3-5 days.
  1. Painless watery diarrhea & effortless vomiting (clear, watery fluid).
  2. Excreta: rice- water appearance due to the presence of flakes of mucus & large number of vibrios.
  3. Dehydration (when severe: sunken eyes, shriveled skin, collapsed neck veins), acidosis & shock. Thirst with dryness of mouth & tongue (earliest indication of fluid deficit); Oliguria & renal shutdown. Mental state is clear.
  4. Painful muscular cramps due to hyponatremia.
  5. Cold extremities.
  6. Abdomen: scaphoid.
  7. Cholera sicca: rarely large amount of fluid may collect in the intestinal lumen & a severe dehydration, shock & death may result even before evacuation occurs. 


  • Isolating he organism from stool sample.
  • Suitable medium for transporting specimen is: Venkataraman & Ramakrishnan fluid or Carry & Blair medium.


  1. Dehydration & severe shock leads to renal cortical necrosis & renal failure.
  2. Hypokalemia leads to fatal cardiac arrythmias, abdominal distension & muscle paralysis.
  3. Injudicious administration of electrolyte solutions intravenously without correcting metabolic acidosis may result in pulmonary oedema.
  4. Convulsions in children due to cerebral venous thrombosis.
  5. Severe hypoglycemia.
  6. Prolapse of rectum in children.
  7. Florid malnutrition.

Cholera is a notifiable disease.


  1. Rotavirus affects mainly infants & young children aged 6 months to 2 years.
  2. I. P: 1 to 7 days; usually less than 48 hours.
  3. Vomiting occurs early & it precedes diarrhea.
  4. Diarrhea extends over 5-7 days but virus is shred up for 10 days.
  5. Breast milk may have a protective role due to the presence of maternal Ig A antibodies.
  6. Rotavirus group A: major cause of endemic diarrhea in infants & young children worldwide. 

Norwalk & Norwalk like agents: Cause mild gastroenteritis in school, community & family settings.

Calcivirus:  Cause Rotavirus like illness in children & Norwalk like in adults.

Astrovirus:  Pediatric diarrhea reported in nursing homes.

Campylobacter jejuni (vibrio fetus):

Complications of campylobacter jejuni dysentery:

  • Reactive arthritis
  • Guillain-Barre syndrome(GBS) 

Pseudomembranous colitis: syn: antibiotic associated diarrhea. 

BARTONELLOSIS (Syn: carrion’ s disease, Oroya fever, Verruga Peruana) 

Bartonella consists of 3 main pathogens.

  1. Bartonella bacilliformis: Carrion’s disease. Disease is transmitted by sandfly phlebotomous verrucarum.
  2. Bartonella henselae: cat- scratch disease & bacillary angiomatosis in patients with AIDS.
  3. Bartonella Quintana: trench fever.

Clinical picture

2 distinct clinical syndromes:

A)    Oroya fever:

i.      Fever, rigor, headache etc. lasts for 3-4 weeks.

ii.     Organism can be demonstrated in blood smears stained by Giemsa’s or Wright’s strain.

iii.    Death may occur due to severe anaemia or super infection salmonella.

B)    Verruga Peruana:

i.      Hemangiomatous tumours of skin and mucous membranes

ii.     Mortality is very low


  • Causative agent: Legionellaceae; gram negative; natural habitat: water
  • Over 36 species; among them L. pneumophila is the most common human pathogen.

Clinical features:

Two main clinical syndromes

a)    Legionnaire’s disease

  • Infection is by inhalation of aerosols
  • I.P: 2-10 days
  • Pneumonia is the commonest presentation followed by GIT symptoms such as watery diarrhoea

b)    Pontiac fever

  • Brief febrile illness resembling influenza caused by other species of legionella


  • Culture of the organism from the sputum & direct fluorescent antibody staining: quick and ready method but less sensitive


TETANUS (Syn: Lockjaw) 

Exotoxin produced by Clostridium tetani.

Exotoxin: neurotoxin; tetanospasmin & hemolysin; tetanolysin.

I. P: generally less than 2 weeks; it may range from 2-60 days.

Clinical features:

  1. Diagnosis becomes evident when lockjaw sets in.
  2. Opisthotonous: hyperextension of the spine & neck due to rigidity and spam of back muscles.
  3. Risus sardonicus: grinning expression due to sustained contraction of facial muscles.
  4. Interval between first symptom & the first convulsion is called the onset period.
  5. Deep tendon reflexes are exaggerated but the plantar response is flexor.
  6. Local tetanus: symptoms confined to a part near the site of injury.
  7. Cephalic tetanus: local tetanus involves the facial muscles.
  8. Tetanus neonatorum: tetanus occurs within 10 days of birth; inability to suck the nipple, irritability & excessive crying associated with grimacing movements of the face. Muscles of the back, neck & abdomen become spastic.


  1. Respiratory obstruction &aspiration pneumonia.
  2. Hyperpyrexia
  3. Myocarditis leads to cardiac failure & hypotension.
  4. Decubitus ulcers &UTI due to prolonged immobility. 
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Toxicology – A comprehensive study

lab12Dr  Sanil Kumar BHMS MD(Hom)
Department of Forensic Medicine & Toxicology
Govt Homeopathic Medical College. Calicut

General considerations
Toxicology: is the branch of medicine that deals with properties, actions, lethal dose, toxicity, detection or estimation of, and treatment poisons.
Forensic toxicology:
Forensic toxicology deals medical and legal aspects of the harmful effects of chemicals on human body.
Poison is a substance, which may be liquid, solid or gas, which when administered in small quantity into the living body or brought into contact with any part of it, leads to injury or ill-health by its constitutional or local effects or both.
Clinical toxicology deals with human diseases, caused by, or associated with abnormal exposure to chemical substances.

Characteristics of Ideal suicidal and Homicidal poisons
Characteristics Suicidal Homicidal
1. Signs and symptoms nil/few Resemble diseases
2. Death Painless Definite
3. Physical quality Tasteless or of pleasant taste
Colourless, Odourless, Tasteless Highly toxic
4. Examples Opium, Barbiturates, Organo-phosphorus compounds, Endrin Organic fluorine compound, Thallium, Arsenic, Aconite

Section under Cr.P.C / IPC relevant to poisoning
1. Section under Cr PC — section 39, 40, 175
2. Section under IPC — section 176, 193, 202, 284, 299, 300, 304A, 324, 326, 328.

The law on poisons:
1. Poison’s act, 1919: It was passed to regulate the importation, possession and sale o poisons.
2. The drug and cosmetics act, 1940: It regulates the import, manufacture, distribution, and sale of all kinds of drugs. One of its main features is the control of the quality, purity and strength of drugs.
3. The drugs and cosmetic rules, 1945: They are framed under the Drugs Act, 1940, to regulate the importation of drugs, the functions and procedures of the Central Drugs Laboratory, the appointment of licensing authorities, and the manufacture, distribution and sale of drugs.
4. The pharmacy act, 1948: It was passed in order to regulate the profession of pharmacy and to constitute Central Council of Pharmacy and State Councils of Pharmacy. The object of this act is to allow only registered pharmacists to compound, prepare, mix or dispense any medicine on the prescription of a medical practitioner.
5. The drugs control act, 1950: It provides for the control of sale, supply and distribution of drugs, the issue of cash memo for sale, marking of prices, and exhibiting list of prices and stocks.
6. The drugs and magic remedies (objectionable advertisement) act, 1954: The object of this act is to ban advertisements which offend decency or morality, and to prevent self-medication and treatment which cause harmful effects.
7. Narcotic drugs and Psychotropic substances act, 1985: It repeals 3 acts; (1) The opium act, 1957 (2) The opium act, 1978 (3) The dangerous drugs act, 1930.
8. Prevention of illicit traffic in narcotic drugs and psychotropic substances act, 1988.

A love philter is a drug, which is supposed to increase the love between the giver and taker. Examples are all aphrodisiacs, such as Arsenic, Cantharides, Alcohol, Opium, Cocaine and Cannabis.

Classifications: Poisons may be classified according to the chief symptoms they produce:
I. Corrosives:
1. Strong acids
(a) Inorganic acids—Sulphuric, nitric, hydrochloric.
(b) Organic acids—Carbolic, oxalic, acetic, salicylic.
2. Strong alkalies— Hydrates & carbonates of sodium, pota¬ssium & ammonia.
3. Metallic salts—Zinc chloride, ferric chloride, potassium cyanide, chromates.

II. Irritants:
1. Inorganic
(a) Non-metallic—Phosphorus, chlorine, bromine, iodine.
(b) Metallic—Arsenic, antimony, mercury, copper, lead, zinc, silver etc.
2. Organic
(a) Vegetables—Abrus precatorius, castor, croton, calotro-pis, aloes.
(b) Animal— Snake & insect bites, cantharides, ptomaines.
3. Mechanical—Powdered glass, diamond dust, hair etc.

III. Systemic
1. Cerebral—
(a) Somniferous—Opium, barbiturates.
(b) Inebriant—Acoho, ether, chloroform.
(c) Deliriant— Dhatura, belladona, hyocyamus, cannabis etc.
2. Spinal—Nux vomica, gelsemium.
3. Peripheral—Conium, curare.
4. Cardiovascular—Aconite, digitalis, quinine, oleander, tobacco, hydrocyanic acid.
5. Asphyxiants—CO, CO2, hydrogen sulphide.

IV. Miscellaneous

Food poisoning, Botulism.

Fate of Poisons in the body

Some inorganic poisons like arsenic and antimony are retained in nails, hair, bones etc. for a considerable time. Certain poisons like chloroform, phosphorus, nitrates, aconite and acetic acid are destroyed in the body and no trace of them can be detected in the viscera or tissues if post-mortem is delayed.

Action of poisons:

1. Local
— By direct contact.
— Chemical destruction – > by corrosives.
— Congestion & inflammation by irritants.
— Tingling of skin and tongue by aconite.
— Dilatation of pupils by belladonna or dhatura.
2. Remote
— By shock caused by corrosives.
— Cantharides acting on kidneys produce nephritis.
— Nux vomica on spinal cord produces convulsions.
3. Combined
— Both local & remote, e.g. oxalic acid, phosphorus etc.

Toxicity of poisons:
(1) Extremely toxic = 1 mg/kg or less
(2) Highly toxic = 1 to 50 mg/kg
(3) Moderately toxic = 50 to 500 mg/kg
(4) Slightly toxic = 0.5 to 5 gm/kg
(5) Practically non-toxic = 5 to 11 gm/kg
(6) Relatively harmless = > 15 gm/kg

Acute poisoning: Is caused by an excessively single dose, or several smaller doses of a poison taken over a short interval of time.
Chronic poisoning :It is caused by smaller doses over a period of time resulting in gradual worsening e.g. arsenic, phosphorus, antimony and opium.

Self poisoning (attempted suicide, parasuicide, or pseudocide)
It is a conscious, often impulsive, manipulative act, undertaker to rectify an intolerable situation.

1. Stomach wash (entire quantity).
2. 10 ml. blood.
3. Urine, as much as possible.
10 mg of sodium fluoride for 10 ml of blood acts bo¬as a preservative and as an anticoagulant.

Diagnosis of Poison in the Dead

I. Post-mortem appearances
(a) External
1. The colour changes in the corroded skin and mucous membrane: Sulphuric and Hydrochloric acid: grey, becoming black; nitric acid: brown; hydrofluoric acid: reddish-brown; carbolic acid: greyish-white; oxalic acid: grey, blackened by blood; cresols: brown, leathery; caustic alkalies: greyish-white; mercuric chloride: bluish-white; zinc chloride: whitish; chromic acid and potassium chromate: orange, leathery.
2. Colour of post-mortem staining—the skin may be dark-brown or yellow in phosphorus and acute copper poisoning. Cherry red in carbon-monoxide. Chocolate coloured in cases of death from poison¬ing by nitrites, aniline, nitrobenzene, acetanilide and chlorate of potash owing to the formation of methaemoglobin.
3. Smell about the mouth and nose — Substances which may be recognised by their odour are cyanides, phenol, cresol, opium, alcohol, ether, chloroform, camphor, paraldehyde etc.

(b) Internal
1. Smell—The skull should be opened first to detect unusual odours in the brain tissues. This is useful in cyanide, alcohol, phenol, cresol, ether, chloroform and camphor poisoning.
2. Oesophagus—Corrosive alkalies produce marked softening and desquamation of the mucous membrane. In acute cantharidin poisoning —>mucous membrane is swollen, congested and may show patches of ulceration.
3. Upper respiratory tract—Corrosive alkali or acid poi¬soning —> oedema of glottis, congestion & desquama¬tion of the mucous membrane of the trachea & bronchi.
4. Stomach:
(i) Hyperemia—Irritant poison.
(ii) Softening—Corrosive & irritant poisons,
(iii) Ulcers—Corrosive & irritant poisons,
(iv) Perforation—Seen in strong mineral acid, espe¬cially sulphuric acid.
5. Duodenum and Intestines—In intestine, characteristic change seen is mercury poisoning. It is a colitis, which may resemble enteritis of acute bacillary dysentery.
6. Liver:
Liver necrosis—Substances such as arsphenamine, chloroform, trinitrotoluene, carbon tetrachloride and senecio.
Fatty liver— Arsenic, carbon tetrachloride, amanita phylloides, yellow phosphorus, iodine, rarely ferrous sulphate.
7. Kidney—Parenchymatous degenerative changes found in irritant metal poisoning and in cantharidine poisoning. Extensive necrosis of proximal convoluted tubules may be found in deaths from poisoning by mercuric chlorides, phenol, lysol and carbon tetrachloride.
8. Heart—Subendocardial hemorrhage in left ventricle-acute arsenical poisoning.


Duties of Medical practitioner in a case of suspected poisoning
I. Medical
Care and treatment of the patient.

II. Legal
Assist the police to determine manner of death.
1. In case of suspected homicidal poisoning—Doctor has to confirm his suspicion before opinion. For this he must:-
(a) Collect vomit and urine and submit for analysis.
(b) Observe and record the symptoms in relation to food; other persons affected at the same time.
(c) Consult senior practitioner.
(d) Remove the patient to hospital or appoint nurses of his confidence.
(e) If suspicion of homicide is confirmed, shift the patient to hospital.
2. Suspected articles preserved.
3. If a private practitioner is convinced of homicidal poisoning, he is bound to inform the police officer or magistrate.
4. In suicidal poisoning—not bound to inform police.
5. If practitioner is summoned by investigating police officer, he is bound to give all information (Sec. 175 I.P.C.)
6. Govt. Medical officer has to report the police all cases of suspected poisoning.
7. If the condition of patient is serious, arrange to record dying declaration.
8. If the patient dies he should not issue death certificate, but inform police.

Differential diagnosis of Poisoning based on Vital signs and CNS activity
1. Sympathomimetic syndromes:
(a) Amphetamines (b) Caffeine (c) Cocaine (d) Ergot alkaloid (e) MAO inhibitors (f) Theophylline.
2. Anticholinergic syndromes:
(a) Antidepressants (tricyclic) (b) Antihistamines (c) Belladonna alkaloids (d) Mydriatics (topical) (e) Plant / mushrooms.
3. Hallucinogenic syndromes.
(a) LSD & synthetic analogue (b) Marijhuana (c) Mescaline (d) Phencyclidine.
4. Withdrawal syndromes.
(a) Alcohol (b) Antidepressants (c) Beta-blockers (d) Clonidine (e) Narcotics (f) Sedative hypnotics.

1. Sympatholytic syndromes:
(a) Adrenergic blockers (b) Calcium channel blockers (c) Digoxin.
2. Cholinergic syndromes:
(a) Bethanecol (b) Carbamate insecticides (c) Organophosphate insecticides (d) Myasthenia gravis drugs (e.g. Pyridostigmine) (e) Physostigmine.
3. Narcotic syndromes:
(a) Analgesics (b) Antispasmodics (Gl).
4. Sedative-hypnotic syndromes:
(a) Alcohol (b) Anti epileptics (c) Barbiturates (d) Benzodiazepines (e) Hydrocarbons.

An anion metabolic acidosis is characteristic of methanol, ethylene glycol and salicylate intoxication. An increased anion gap metabolic acidosis with respiratory alkalosis, ketosis and tinnitus suggests salicylate poisoning. An increased osmolal gap accompanied by visual symptoms suggests methanol poisoning. Pulmonary edema (ARDS) can occur with carbon monoxide, cyanide, narcotic, paraquat, phencyclidine, sedative-hypnotics, salicylate poisoning, irritant gas. Aspiration pneumonia is common in patients with coma, seizures and petroleum distillate poisoning. Radio-opaque densities may be visible in abdominal X-rays, followed by ingestion of calcium salts, chloral hydrate, enteric coated tablets, heavy metals, lithium, phenothiazine, salicylates etc. Bradycardia and AV block may occur in patients poisoned by anti-arrhythmic agents, beta blockers, cholinergic agents (carbamate and organophosphorus insecticides), digitalis, lithium.

Treatment of Poisoning
The treatment of patient consists of
I. Removal of unabsorbed poison from the body.
II. Administration of antidotes.
III. Elimination of poison by elimination.
IV. Symptomatic treatment.

1. Inhaled poison— Patient must be removed into fresh air; artificial respiration and oxygen (6 to 8 litres per minute) should be given. Air-passages should be kept free from mucus by postural drainage or by aspiration.
2. Injected poisons—If the poison has been injected subcutaneously by a bite or injection, a tight ligature is applied immediately above wound; wound should be excised & poison sucked out.
3. Contact poisons—Removed by washing with water or should be neutralised by specific chemical.
4. Ingested poisons—

Gastric lavage is useful within three hours after ingestion of a poison.
(i) The only absolute contraindication is corrosive poisoning (except carbolic acid)
due to danger of perforation,
(ii) Stomach wash is done with proper precautions in
(a) Convulsant poisons, as it may lead to convulsions.
(b) Comatose patients, because of the risk of aspiration of fluid into the air-passages.
(c) Volatile poison, which may be inhaled.
(d) Upper alimentary disease e.g. oesophageal varices
(e) In patient with marked hypothermia.

Emetics: When difficulty in obtaining or using stomach tube.
Household emetics:
(i) Large amount of warm water.
(ii) Mustard powder in warm water.
(iii) Common salt in warm water.
(iv) Vomiting can also be produced by tickling the back of the throat with a
finger, leaf twig or, wooden tongue depressor. It is the best method.
(i) Same as stomach wash
(ii) Severe heart & lung diseases
(iii) Advanced pregnancy.

Antidotes are substances which counteract or neutralise the effect of poison.

1. Mechanical or Physical antidotes:
They neutralise poisons by mechanical action or prevent their absorption.
(a) Animal charcoal.
(b) Demulcents are substances which form a protective coating on the gastric mucous membrane and thus do not permit the poisons to cause any damage e.g. milk, starch, egg white, mineral oil, milk of magnesia, aluminium-hydroxide gel etc. Fats and oils should not be used for oil soluble poisons as kerosene, phosphorus, organo-phosphorus com¬pound, DDT, phenol, carbon tetra- chloride etc.
(c) Bulky food acts as a mechanical antidote to glass powder.

2. Chemical antidotes
They counteract the action of poison by forming harmless or insoluble compound or by oxidising poison.
(i) Common salt decomposes silver nitrate.
(ii) Albumen precipitates mercuric chloride.
(iii) Dialysed iron is used to neutralise arsenic.
(iv) Copper sulphate is used to precipitate phosphorus.
(v) Alkalies neutralise acids by direct chemical action. It is safer to give a little weak solution of an alkaline hydroxide, magnesia or ammonia. Bicarbonates should not be given because of the possible risk of rupturing the stomach due to liberated CO2
(vi) Acids neutralise alkalies by direct chemical action: Only harmless substances should be given e.g. vinegar, lemon juice, canned fruit juice.
(vii) Potassium permanganate has oxidising property. 1: 5000 solution is used in poisoning for opium, stry¬chnine, phosphorus, cyanide, barbiturate, atropine and other alkalies.
(viii) A solution of tincture iodine or Lugol’s iodine precipi¬tates most alkaloids, lead, mercury, silver, quinine, strychnine etc.
(ix) Tannic acid tends to precipitate apomorphine, cinchona, strychnine, nicotine, cocaine, aconite, pilocarpine, lead, silver, aluminium, cobalt, copper, mercury, nickel and zinc.

Universal antidote:

When the exact poison is not known, or when a combination of two or more poisons had been taken, universal antidote is given. It consists of powdered animal charcoal 2 parts; magnesium oxide 1 part; tannic acid (strong tea) 1 part. Charcoal absorbs alkaloids; tannic acid precipitates alkaloids, glucosides and many of the metals. Magnesia neutralises acids without gas formations. It is combination of physical and chemical antidotes.

3. Physiological antidotes
They act on the tissues of the body and proc exactly opposite to those caused by the poison. Atropine and physostigmine are two real physiological antidotes. Other examples are barbiturate & picrotoxin or amphetamine; strychnine and barbiturates; cyanides and amyl nitrite.

Chelating agents:
(a) B.A.L (British anti-lewisite; dimercaprol) — It is used as physiological antidote in arsenic, bismuth, mercury, copper, gold and other heavy metals. Dimercaprol has two unsaturated sulphydryl group and thus prevents union of Arsenic with the – SH group of the respiratory enzyme system.
(b) E.D.T.A. (Ethylenediaminetetra-acetic acid; calcium disodium versenate): It is a chelating agent and is effective in lead, mercury, copper, cobalt, cadmium, iron and nickel poisoning.
(c) Penicillamine (cuprimine)—It is a hydrolysis product of penicillin, having stable – SH group. It is the chelating agent of maximum efficiency for the heavy metals. Penicillamine is commonly used for the management of heavy metal poisoning of copper, lead, mercury.
(d) Desferroxamine: Useful in acute iron poisoning.


1. Renal excretion:
Salicylates and phenobarbitone can be easily excreted in alkaline urine. Alkalinisation is usually carried out with sodium bicarbonate. Amphetamine, quinine and quinidine can be excreted in acid urine. Acidification can be achieved with ammonium chloride, arginine or lysine.
2. Purging:
30 gm of sodium sulphate with large amount of water hastens the elimination of poison in the stool. Magnesium sulphate should be avoided as it may produce CNS depression in cases of renal failure.
3. Diaphoretics:
Agent increases perspiration. Agents are pilocarpine nitrate, alcohol, salicylates, and antipyretics.
4. Peritoneal dialysis
Alcohols, long acting barbiturates, chloral hydrate, lithium, salicyiate & sodium chlorate are effectively removed by peritoneal dialysis.
5. Hemodialysis or Hemoperfusion
Hemoperfusion -» Many substances that cannot be removed effectively by aquous dialysis can be removed by hemoperfusion through specially designed coated charcoal columns. It has same indications as for dialysis.
Hemodialysis may be used for following poisons: BLAST
B—Barbiturates, L—Lithium, A—Alcohol-Methanol, S—Salicylates, T—Theophylline.


1. Phosphorus —» Demulcents because, they increase absorption.
2. Sulphuric acid —» Sodium bicarbonate reacts with acid and liberates CO2 gas, which may cause per¬foration.
3. Carbaryl poisoning —» Pralidoxime.
4. Oxalic acid —» Large amounts of water.
5. In Liver damage —» BAL is contraindicated. –

Preservation of Organs
1. Rectified spirit is used as preservative for many poisons except alcohol, kerosene, phosphorus, paraldehyde, carbolic .acid, acetic acid because the organic acids and paraldehyde are soluble in alcohol and the phosphorescence of phosphorus is diminished by alcohol.
2. Saturated Sodium chloride is used for preservation of organs in poisoning with—(a) Alcohol, (b) Acetic acid, (c) Carbolic acid, (d) Paraldehyde, (e) Phosphorus poisoning, (f) Corrosive poisoning, (g) Organophosphorus poisoning, (h) Lead poisoning.
3. In alcoholic poisoning—Store blood in sodium flouride + oxalate. Store urine in phenyl mercuric nitrite.
4. Never use formalin as a preservative for chemical analysis because extraction of poison, especially non-volatile organic compounds becomes difficult.
5. Minimum quantity of blood required to be preserved for chemical analysis is 10 ml.
6. Brain is preserved in Normal saline, Rectified spirit.
7. Uterus, Brain, Heart are preserved in Rectified spirit.

Organs to be preserved
1) Nails & Hairs—In chronic arsenic poisoning.
2) Skin—In gun shot injuries and when injectable poison is used
3) Heart—In strychnine poisoning, cardiac poisons, arsenic.
4) Brain—In Barbiturate, anaesthetic gas, strychnine, organophosphorus & volatile organic acid poisoning.
5) Lung—In gas poisoning (CO-poisoning), HCN, alcohol. chloroform poisoning.
6) Bone—In Arsenic, Thallium, Antimony, Lead and Radium poisoning.
7) Hair about 20 gms—In Aconite and Arsenic poisoning.
8) CSF—Alcohol poisoning & Sodium fluoride.
9) No preservatives are required—In Lungs, Long bones, Hairs & Nails.
10) Urine should be preserved in—Opium, Barbiturate, Alcohol poisoning.

Peculiar odour (smell) emitted on opening the abdomen at autopsy:
1. Fruity Ethyl alcohol
2. Kerosene like odour Kerosene, organophosphorus compounds
3. Phenolic odour Carbolic acid, lysol
4. Rotten eggs Hydrogen sulphide
5. Garlic odour Arsenic, phosphorus, thallium
6. Fishy (mushy) Zinc phosphide
7. Bitter almonds odour Cyanide
8. Burnt rope Cannabis (marijuana)

Colour changes observed with post mortem lividity (post mortem stains)
1. Purple —> In Hypoxia (due to reduced hemoglobin).
2. Chocolate colour -> In Sodium nitrite, Quinine, Potassium chlorate.
3. Cherry red —> In CO, Hydrocyanic acid poisoning.
4. Bluish green —> Hydrogen sulphide.
5. Blue —> Copper sulphate.
6. Yellow / brownish —> Phosphorus.

A corrosive poison fixes, destroys and erodes the surface with which it comes in contact. They act by extracting water from the tissues, and coagulate cellular proteins and convert haemoglobin into haemin.


They produce coagulation necrosis. They have no remote action. Nitric acid produces a yellowish stain. Sulphuric acid and caustic alkalis reddish-brown stains; hydrochloric acid and carbolic acid whitish or greyish-yellow stains on the skin and mucous membranes.


Sulphuric acid is the strongest corrosive poison. Pure sulphuric acid (H2SO4) is a heavy, odourless, colourless, non-fuming, hygroscopic, oily liquid and has tendency to carbonise organic substances.

Signs and symptoms:
Burns of the mouth result in excess salivation, pain, dysphonia and dysphagia. Oesophageal symptoms and signs include drooling, painful swallowing, retrostemal pain and neck-tenderness. Vomiting of blood & mucous may occur. In sulphuric acid poisoning, stomach mucosa is stained black. It is like blotting paper. The vomit is brown or black, mucoid, strongly acid, and may contain shreds of charred wall of the stomach. Teeth are chalky-white. Constipation is severe and there is tenesmus. Edema, erythema and ulceration of the oesophagus may be followed by fibrosis with stricture formation and obstruction of the gastric outlet.
Fatal dose—5 to 10 ml.
Fatal period—24 hours.

Causes of death:
(i) Circulatory collapse, (ii) Spasm or oedema of glottis, (iii) Collapse due to perforation of stomach, (iv) Toxaemia (v) Delayed death may occur due to hypostatic, pneumonia, secondary infection, renal failure or starvation due to stricture of oesophagus.

Gastric lavage or emetics are contraindicated. The acid should be immediately diluted and neutralised by giving 250 ml of water or milk mixed with 4 tsf. of calcium or magnesium oxide (antidote), aluminium hydroxide gel or calcined magnesia or soap water may be used. Alkaline carbonates and bicarbonates which liberate carbon dioxide should not be used as they cause gastric dilatation and sometimes rupture. Prednisolone may be given to prevent oesophageal stricture and for shock.

Post-mortem appearances:
Corrosion of the mucous membranes of lips, mouth and throat and of the skin over the chin, angles of mouth and hands is seen. The necrotic areas are at first greyish-white but soon become brown or black and leathery.
The greater part of stomach may be converted into a soft spongy black mass which disintegrates when touched. The stomach wall has a brown or black colour. Perforation may occur in sulphuric acid poisoning with the escape of the gastric contents into the peritoneal cavity. Chemical peritonitis & corrosion of organs is seen.

VITRIOLAGE (Vitriol throwing)
Throwing of sulphuric acid on another individual is known as vitriolage. Most common agent used as vitriolage is sulphuric acid. Jealous or disgruntled persons may throw a corrosive to disfigure and harm their enemies. Blindness may occur. Death may result from shock or toxaemia. The burns are painless, penetrating and the acid devitalises the tissues and predispose to infection. Sometimes, corrosive alkali or juice of marking nut or calotropis is used to disfigure the face.
The affected part is washed with plenty of water and soap or sodium or potassium carbonate. Later, a thick paste of magnesium oxide or carbonate is applied.


Nitric acid (aqua fortis) is a clear, colourless, fuming, heavy liquid and has a peculiar and choking odour. In concentrated form, it combines with organic matter and produces an yellow discolouration of tissue due to the production of picric acid (xanthoproteic reaction).

Signs & Symptoms:
They are those of poisoning by sulphuric acid. It causes yellow discolouration of the tissues including the crowns of the teeth and yellow stains on the clothing. Inhalation of fumes causes lacrimation, photophobia, irritation of air passages and lungs producing sneezing, coughing, dyspnoea & asphyxia. Brown colour of urine is seen in Nitric acid poisoning.
Fatal dose — 10 to 15 ml.
Fatal period — 12 to 24 hours.
Post-mortem appearance:
They are those of sulphuric acid but the tissues are stained yellow, except stomach. The stomach is soft, friable and ulcerated & greenish in colour.
Treatment : Same as for Sulphuric acid.


It is a pungent, colourless, fuming liquid. It is a natural constituent of the fluid of the stomach and bowels.
Signs and Symptoms:
The mucous membrane is at first grey or grey white, and later becomes brown or black, due to production of acid haematin.
Fatal dose—15 to 20 ml. Fatal period—18 to 24 hours.

It occurs in the form of colourless, transparent, prismatic crystals, and resembles in appearance the crystals of magne¬sium sulfate & zinc sulphate. It is used as ink-remover solution in forgeries.
(i) Local— Corrosive poison. Corrodes mucous membrane of the digestive tract.
(ii) Systemic—(a) Shock, (b) Hypocalcemia, (c) Renal damage: oxalates produce tubular nephrosis or necrosis and cause death from uremia in 2 to 14 days.
Fatal dose—15 to 20 gms. Fatal period—One to two hours.
Signs and Symptoms
(a) Fulminant poisoning: There is a burning, sour, bitter taste in the mouth with a sense of constriction around the throat and burning pain from the mouth to stomach. Vomit usually contains altered blood and mucus and has a ‘coffee ground’ appearance. Thirst may be present. In oxalic acid poisoning, pulse is feeble and rapid. If life is prolonged, diarrhoea will occur.
(b) Acute poisoning: If the patient survives for a few hours, hypocalcaemia and digestive upset occurs. There is muscle irritability and tenderness, tetany usually convulsions, numbness & tingling of the fin tips & legs. Cardiovascular collapse, stupor or coma.
(c) Delayed poisoning: Symptoms of uraemia are seen. The urine may be scanty or suppressed and may contain traces of blood, albumin and calcium oxalate crystals
The stomach is washed out carefully using calcium lactate or gluconate. The antidote for oxalate poisoning is calcium gluconate 10%, 10 ml i.v. at frequent intervals.
Post-mortem appearances:
Mucous membrane of the tongue, mouth, pharynx a oesophagus will be whitened, as if bleached. Stomach is reddened or, eroded or, almost black. The stomach contents are gelatinous and brownish due acid haematin formation. The kidneys are swollen by oedema, congested and the tubules are filled with oxalate crystals.

When pure, the acid consists of short, colourless, prismatic needle-like crystals, which have a burning sweetish taste, which turn pink and liquefy when exposed to air. It has a characteristic carbolic or phenolic smell. Commercial carbolic acid is dark brown liquid. It is readily absorbed from the alimentary tract, respiratory tract, rectum, vagina, serous cavities, wounds and through the skin. Phenol is converted into hydroquinone and pyrocatechoi in the body before being excreted in the urine.
Fatal dose—One to two gm.
Fatal period—3 to 4 hours.

Signs & Symptoms: —Poisoning by carbolic acid is known as carbolism.
1. Local
(a) Skin: It causes burning and numbness. It precipitates protein and coagulates cell contents. Produces white opaque eschar.
(b) Digestive tract: Hot burning pain extends from the mouth to the stomach followed by tingling and later anaesthesia.
(c) Respiratory tract: Pulmonary & laryngeal oedema develop due to irritation.
2. Systemic effects
Depressant of nervous system, especially the respi¬ratory centre. Headache, giddiness, tinnitus, muscular spasm and later collapse, unconsciousness and coma occur. The temperature is subnormal. In phenol poisoning, pupils are contracted. Breathing is stertorous. Pulse is rapid, feeble and irregular in carbolic acid poisoning. Face is covered with cold sweat, dusky cyanosis. There is strong odour of phenol in breath.
Urine is scanty and contains albumin & free hemoglobin; suppression may follow. In carboluria, the urine may be colourless or slightly green at first, but turns green or even black on exposure to air.
In the body, phenol is partly oxidised to hydroquinone and pyrocatechol, which with unchanged phenol are excreted in the urine. The further oxidation of hydroquinone and pyrocatechol in the urine is the cause of green colouration. This is known as Carboluria. The hydroquinone and pyrocatechol may cause pigmen¬tation in the cornea and various cartilages—a condition called ochronosis.

The stomach should be washed with plenty of lukewarm water containing animal charcoal, olive oil, castor oil, magnesium or sodium sulphate or, saccharated lime with which phenol combines and forms harmless products. Magnesium sulphate or medicinal liquid paraffins should be left in the stomach.
Post-mortem appearances
Corrosion of the skin, especially in tracks from the angles of the mouth on to chin, has a greyish or brown colour. The tongue is usually white and swollen and there is smell of phenol about the mouth. The stomach mucosal folds are swollen and covered by opaque, coagulated, grey or brown thickening and looks leathery. Kidneys show hemorrhagic nephritis.


There are two varieties: (1) White or crystalline, (2) Red or amorphous.
It is a protoplasmic poison, which affects cellular oxidation.

Difference between White and Red phosphorus

Trait White Phosphorus Red Phosphorus
1 Colour White or yellow Reddish-brown.
2. Appearance Translucent, waxy cylinders Amorphous, solid mass
3 Smell Garlic like Odourless.
4 Taste Garlic like Tasteless.
5. Luminosity Luminous in dark Non-luminous.
6. Exposure to air Oxidises   &    emits   white fumes; ignites at 34°C and as such is kept under water Non-oxidised, Non-fuming, Non-inflammable.
   7. Toxicity Highly toxic Non-toxic

Signs and Symptoms:
1. Fulminating poisoning
This is seen when more than 1 gm. is taken. Death usually occurs within 12 hours due to shock.

2. Acute poisoning
(A): First stage: Symptoms occur within a few minutes to a few hours & lasts 8 hours to 3 days. Ingestion produces burning pain in the throat and abdomen with intense thirst, nausea, vomiting, diarrhoea & severe abdominal pain. Breath & excreta have garlic like odour. Luminescent vomit and faeces are diagnostic. Skin contact produces painful penetrating second & third degree burns.
(B) Second stage: This is a symptom-free period lasting for 2 to 3 days.
(C) Third stage: Symptoms of systemic toxicity. There is nausea, vomiting, diarrhoea, haema-temesis. Liver tenderness and enlargement. Jaundice and pruritis. Hemorrhages occur into skin, mucous membrane & viscera, due to injury of blood vessels and inhibition of blood clotting. Renal damage results in oliguria, haematuria, casts, albuminuria. Convulsions, delirium and coma occurs. Death may result from shock, hepatic failure, central nervous system damage, hematemesis or, renal insufficiency.
Fatal dose — 60 to 120 mg.
Fatal period — 2 to 8 days.

1. Gastric lavage using 1: 5000 solution of potassium permanganate oxidises phosphorus into phosphoric acid and phosphates, which are harmless.
2. Antidote—copper sulphate: It coats the particles of phosphorus with a_ film of copper phosphide which is relatively harmless.
3. Vitamin K.
4. Peritoneal or hemodialysis.

Post-mortem appearances:
In acute poisoning jaundice is produced. The gastric and intestinal contents may smell of garlic and may be luminous. The mucous membranes of the stomach and intestine are yellowish or greyish white in colour. The liver becomes swollen, yellow, soft, fatty and is es ruptured. After a week, acute yellow atrophy appears.

Chronic Poisoning:
The frequent inhalation of fumes over a period of ye causes necrosis of the lower jaw in the region of a decay tooth. This condition is known as ‘Phossy Jaw’, in osteomyelitis and necrosis of the jaw occurs, with mull sinuses discharging foul smelling pus.
Phosphorus is known as Diwali poison. Accidental poisoning in children may occur due to chewing of fireworks or by eating rat poison.

It occurs as bluish-black, soft, scaly crystals and has a metallic lustre and an unpleasant taste.
Action: It is a protoplasmic poison fixing protein and causes necrosis.
Signs & Symptoms:
It acts as acid corrosive poison. There is intense thirst, vomiting and lips are stained brown. Vomiting matter -> dark yellow or blue in colour wifi peculiar odour of Iodine. Urine -» scanty, red-brown in colour.
Fatal dose: 2 to 4 gm (30 to 60 ml of tincture). Fatal period: Several days.
Chronic poisoning (lodism):
The symptoms are pain over the frontal sinus, running of nose, conjunctivitis, bronchial catarrh, salivating nausea vomiting, purging, emaciation, wasting of breasts, testes etc. and acne & erythematous patch on the skin.


Insecticide poisoning is most common form of suicide.

It reacts with acid in the stomach and liberates phosphine. The symptoms are vomiting, diarrhoea, cyanosis, respiratory distress, fever and death.
Fatal dose: 5 gm. Fatal period: 24 hours.
It has a garlic odour in stomach contents. Blood is cherry red.


They are derived from phosphoric acid and form two series of compounds
(1) Alkyl phosphates—
(i)HETP (hexaethyltetraphosphate) (ii) TEPP (tetraethyl-pyrophosphate) (iii) OMPA (octamethylpyrophosphoramide) (iv) Malathion (kill bug).
(2) Aryl phosphates—
(i) Parathion (follidol) (ii) Diazinon (tik-20).

Organophosphorus insecticides irreversibly inhibit acetyl cholinesterase and cause accumulation of acetyl choline at muscarinic and nicotinic synapses.

They have three distinct toxic effects :
1. A muscarinic-like effect—Nausea, vomiting, abdominal cramps, urinary and fecal incontinence, increased bronchial secretions, sweating, salivation, urinary frequency and incontinence. Porphyrinaemia, resulting in chromolachyorrhoea (shedding of red tears) due to accumulation of prophyrin in the lacrymal gland. Contracted pin point pupils (miosis), blurring of vision may occur. In severe poisoning, bradycardia, hypotension, pulmonary edema.
2. Nicotinic sign include—twitching, fasciculations, weaness, hypertension, respiratory rate decreased with respira¬tory failure.
3. CNS effects—anxiety, restlessness, tremor, convulsic confusion, weakness and coma.
Fatal dose:
TEPP, HETP, OMPA, Parathion—80 mg i.m. or, 175 orally.
Malathion and diazinon one gram orally.
Fatal period — Usually within 24 hours.

Cause of Death:
Death is caused by paralysis of respiratory muscles, respiratory arrest due to failure of respiratory centre or intense broncho constriction.
Diagnosis is by giving atropine. Symptoms are relieved without atropinizing.

1. Atropine, a muscarinic receptor antagonist, should be administered for muscarinic effect upto drying of bronchial and mucous membrane secretions.
2. Pralidoxime (2-PAM), an oxime that reactivates cholineterase, is indicated for nicotinic symptoms in organophosphorus poisoning.
3. Gastric lavage and contaminated skin is washed with 2g and water.
Post-mortem appearances:
Blood stained froth is seen at the mouth and nose. The stomach content may smell of kerosene. Suicide is very common.

Carbamate insecticides include carbaryl, aldicarb, baygon, ficam and propoxur. Carbamates reversibly inhibits acetyl cholinesterase enzyme. Atropine is the antidote.

It is a polycyclic, polychlorinated hydrocarbon. It is also called plant penicillin.


Arsenic poisoning causes premalignant condition. Metallic arsenic is not poisonous, as it is not absorbed from the alimentary canal. When volatilised by heat, arsenic unites and forms poisonous vapour of arsenic trioxide.

Poisonous compounds:
1. Arsenious oxide or, Arsenic trioxide (sankhya or, somal-khar)—It is known as white arsenic or arsenic. A pinch of Arsenic trioxide can kill as many as 5 persons.
2. Copper acetoarsenate (paris green)—It combines with sulphydryl enzymes and interferes with cell metabolism.
Signs and Symptoms:
1. The Fulminant type—Large doses of arsenic can cause death in one to 3 hours from shock.
2. The Gastroenteric type —This is acute poisoning, resem¬bling bacterial food poisoning or, cholera. The stools are expelled frequently and involuntarily, are dark coloured, stinking and bloody, but later becomes colourless, odourless and water resembling rice-water stools of cholera. Dehydration with muscular cramps, cyanosis, feeble pulses, syncope, coma, exhaustion, convulsion, general paralysis and death, skin eruptions.
3. Narcotic form—Tenderness of the muscle, delirium, coma and death.
Fatal dose: 0.1 to 0.2 gm or, 100 to 200 mg. Fatal period: One to two days.

Difference between Arsenic poisoning and Cholera:

Trait Arsenic poisoning Cholera
1. Pain in throat Before vomiting After vomiting
2. Purging Follows vomiting Precedes vomiting
3. Stools Like    rice-water    in   early stage, later bloody Rice-watery and pass in continuous involuntary jet
4. Tenesmus Present Absent
5. Vomited matter Contains mucous, bile and blood Watery    without   mucous, bile and blood

Freshly prepared precipitated hydrated ferric oxide (arsenic antidote) is given. In arsenic poisoning BAL is an antidote. Calcium disodium versenate. Penicillamine.
Post-mortem appearance:
Red-Velvety appearance of the stomach mucosa.
Chronic poisoning:
1. CNS—Polyneuritic, optic neuritis.
2. Skin—finely mottled brown change mostly on the temples eyelids and neck (rain drop type).
Chronic arsenic poisoning causes (i) Basal cell carcinoma. (ii) Cirrhosis of liver.
here may be a rash resembling fading measles rashes. Hyperkeratosis & Hyperpigmentation of the part and soles with irregular thickening of the nails is seen. Development of bands of opacity in the finger nails are called Aldrich-Mess lines. Arsenophagists are people who take arsenic daily as tonic or as an aphrodisiac and they acquire a tolerance of ia 0.3 gm or more in one dose.
Poisoning : Homicidal
Arsenic is the most popular homicidal poison. It delays putrefaction. It can be detected in completely decomposed body. It can be found in bones, hair and nails for a long time. It can be detected in charred bone and ashes. It is sometimes used in abortion sticks.
Tests for detection: Marsh’s test and Reinsch’s test.

Most poisonous salt of Hg is mercuric chloride (corrosive sublimate), occurs as colourless masses of prismatic crystals.
Symptoms — Acrid metallic taste, hoarse voice, greyish white coating of tongue, blood-stained stool, circulatory collapse, necrosis of jaw, membranous colitis, proximal renal tubular necrosis.
Fatal dose: 1 to 4 gm. Fatal period: 3 to 5 days.
Gastric lavage with sodium formaldehyde sulphoxylate. BAL (BALMIER) is chelator of choice. Penicillamine. 10 gm of sulphoxylate in 100 – 200 cc of distilled water by slow i.v. injection is repeated after 4 – 6 hours acts as an antidote.
Chronic Poisoning:
The symptoms are salivation, a blue line on gum, sore mouth & throat, fine tremors of the tongue, hands, arms, anaemia. Shaking palsy is associated c Hg poisoning. Mercurial tremors are also called hatter’s shakes or glass blower’s shake. Mercurial erethism is seen in persons working with mercury in mirror manufacturing firms. Erethism is characterised by shyness, timidity, irritability, loss of confidence, mental depression, loss of memory & insomnia. Mercurialentis is a peculiar eye change due to brownish deposit of mercury through the cornea on the anterior lens capsule. It is bilateral and has no effect on visual acuity.

Acute poisoning —The symptoms are metallic taste, dry throat, peripheral circulatory collapse, paraesthesias, depression, coma and death.
Fatal dose—Lead acetate 20 gm; lead carbonate 4 gm. Fatal period—One to two days.
The combination of BAL and calcium disodium versenate is effective.
Chronic poisoning (plumbism)—causes:
Inhalation of lead dust and fumes by makers of white lead, smelters, plumbers, glass-polishers. Chronic poisoning results from a daily intake of one to two mg. of lead.

Signs and Symptoms:
LAPEC : L -» Lead line; A -» Anemia; P -» Palsy, Pallor, Punctate basophilia, E -» Encephalopathy; C —> Colic, consti¬pation.
Facial pallor—The facial pallor about the mouth is one of the earliest and most consistent sign. Anemia—In early stage polycythemia but later there is anaemia which is associated with punctuate basophilia, polychromasia, nucleated RBC, and an increase in mononuclear cells of microcytic hypochromic anaemia. Punctate basophilia or basophilic stippling means the presence of many dark-blue coloured pinhead sized spots in the cytoplasm of red blood cells due to toxic action of lead on porphyrin metabolism. Lead line—A stippled blue line, called Burtonian line, is seen on the gums in 50 to 70% of cases. A similar blue line is seen in cases of poisoning by mercury, copper, bismuth, iron and silver. Abdominal colic and constipation—later symptoms. Lead palsy—wrist drop, peripheral neuropathy, foot drop. Encephalopathy—Lead encephalopathy is most common in children. The symptoms are vomiting, headache, insomnia, visual disturbances, delirium, hallucinations, convulsions, coma and death. In adult, encephalopathy is rare. Menstrual irregularity—amenorrhoea, dysmenofrhoea. Renal dysfunction. Sterility.
In poisoning, the concentration of lead in blood is usually between 0.1 to 0.6 mg. per 100 ml. X-ray evidence of increased radio-opaque bands of lines at the metaphyses of long bones is seen in children.
Most effective treatment of plumbism is calcium-disodium versenate. BAL Penicillamine.

Copper as a metal is not poisonous. Copper compounds are powerful inhibitors of enzymes. Ptysalism is seen in copper poisoning.
Fatal dose—15 gm. Fatal period—1 to 3 days.
Treatment: (i) Stomach wash c solution of potassium ferrocyanide. (ii) N-penicillamine.
(iii) EDTA. (iv) BAL.


The castor plant (arandi) grows all over India. Seeds are smooth, flattened-oval, mottled, light and dark brown. Entire plant is poisonous, containing toxalbumen RICIN, a water-soluble glycoprotein and a powerful allergen (CBA). A toxalbumen or phytotoxin is a toxic protein, which resembles a bacterial toxin in action and causes agglutination of red cells with some hemolysis and is antigenic.
Signs and Symptoms—Symptoms include salivation, bloody diarrhoea, impaired sight, delirium, convulsions, uremia and jaundice. The powder of seeds when applied to the eye causes conjunctivitis.
Fatal dose—Ten seeds; ricin 6 mg.
Fatal period—Two to several days.
P.M. appearances—Ricin produces haemorrhagic inflamma¬tion of the G.I. tract.

Croton tiglium (Jamalgota or naepala) seeds contain toxalbumen CROTIN and CROTONOSIDE, a glycoside, which is not expressed with the oil. Seeds are oval, dark-brown with longitudinal lines.
Signs and Symptoms —There is hot burning pain from mouth to stomach, salivation, vomiting, purging, vertigo, prostration, collapse and death.
Fatal dose — 4 seeds; 1.5 cc. of oil.
Fatal period — 6 hours to 3 days.
Treatment: Stomach wash, demulcent drink and symptomatic treatment.

It is also known as Jequirity or Indian liquorice (gunchi or, rati). The seeds are egg-shaped, bright scarlet colour with a large black spot at one end. The seeds contain an active principle abrin, a toxalbumen, which is similar to viperine snake venom.
In seeds also present is abrine, an amino acid, haemoglutinin in the cotyledons, a lipolytic enzyme, and abralin, a glycoside.
Signs and Symptoms:
After ingestion, symptoms include abdominal pain, diarrhoea, weakness, cold perspiration, trembling of the hands, weak rapid pulse and rectal bleeding. When an extract of seeds is injected under the skin of the animal, inflammation, oedema, oozing of hemorrhagic fluid from the site of puncture, necrosis. The animal drops down after 3 to 4 days. Tetanic convulsions occur.
Fatal dose — 90 to 120 mg. by injection, 10 gm. orally. Fatal period — 3 to 5 days.
Poisoning — The seeds are used for killing cattle, small sharp-pointed spikes on needles or ‘suis’ are prepared which are then dried in the sun.
Treatment: Injection with antiabrin.

Ergot is the dried sclerotinum of the fungus Calviceps purpurea, which grows on cereals like rye, barley, wheat, oats etc. It contains alkaloids, ergotoxin, erqotamine. and ergometrine.
Signs and Symptoms:
In acute cases, there is nausea, vomiting, diarrhoea, giddiness, tightness in the chest, difficulty, in breathing, marked muscular weakness and exhaustion. There may be tingling and numbness in the hands and feet, paraesthesias, followed by twitchings or cramps in the muscles Bleeding from nose and other mucous surface is common.
Chronic poisoning:
There is tingling and numbness of the skin, vasomotor disturbances leading to dry gangrene of the fingers. There is a sensation of insects creeping under the skin (tactile hallucination).
Fatal dose—One to two gm. Fatal period—One to several days.
Poisoning: The consumption of bread made with contaminated rye is the chief cause of ergotism. Ergot is commonly used as an abortifacient.

Marking nuts (bhilawa) are black, heart-shaped with rough projections at the base. Their pericarp contains an irritant juice which is brownish, oily and acrid but turns black on exposure to air.
The active principles are semecarpol and bhilawanol.
Signs and Symptoms:
The lesion resembles a bruise. The juice, when applied externally causes irritation and a painful blister, which contains acrid serum.
Fatal dose — 5 to 10 gm.
Fatal period — 12 to 24 hours.

The juice is taken by mouth or introduced into uterus on an abortion stick for criminal abortion and as a cattle poison. Also used as arrow poison. To produce artificial bruise. The juice produces an acrid bitter taste, salivation, dilated pupils, tetanic convulsions, collapse and death.
Treatment: Stomach wash, demulcents and symptomatic.

The Poisonous snakes may be divided into five families—
1. Cortalidae — Pit viper, Rattle snake, Bush master.
2. Viperidae (true viper) — Russel’s viper, Saw-scaled viper.
3. Elapldae — Cobra and Krait
4. Hydrophidae — Sea snakes
5. Colubridae — Boom slangs, Bird snakes.
In India, out of 200 species of poisonous snakes, five are dangerously poisonous to man. — King cobra, cobra, common krait, Russell’s viper and saw-scaled viper.
The most common poisonous snake is Common krait. Rat-snake is a non-poisonous snake.

Difference between Poisonous and Non-poisonous snakes



  1 Belly scales Large and cover entire breadth.Middle scale hexagonal. Small and do not cover entirebreadth.
   2. Head scales 1. Small (vipers)2. Large and(a) If there is a opening betweeneye and nostril (pit-viper)

(b) Third labial touches the eye

and nasal shields (cobra)

(c) Central row of scales on back

enlarged; under surface of the

mouth has only 4 infralabials, the

fourth being the largest (kraits)

Head scales large with theexceptions    as    mentionedunder the poisonous snakes.
  3. Fangs Hollow like hypodermic needles Short and solid.
 4. Tail Compressed Not much compressed.
 5. Habits Usually nocturnal          , Not so.
 6. Teeth Two long fangs Several small teeth.

Snake venom:
1) The venom of the Indian cobra (Naja-Naja) contains a neurotoxin, a hemolysin, a cardiotoxin, a cholinesterase, phosphatidase.
2) Venom of pit viper contains hyaluronidase and proteolytic enzyme.
3) Venom of elapids {cobra, krait) are neurotoxic. Death occurs from respiratory paralysis.
4) The viperine venom is mainly hemolytic, causes intra-vascular hemolysis and depression of coagulation mechanism.
5) The sea snake venom is myotoxic.

Clinical manifestations—The most common manifestation following snake bite (poisonous or non-poisonous) is fright.
Local symptoms start within 6 to 8 minutes. The bitten area is tender with slight burning pain. The patient feels sleepy, slightly intoxicated, weakness of legs and is unable to stand or move. There may be extra-ocular muscle weakness, ptosis and strabismus. Coma sets in and finally the respiration stops with or without convulsions and the heart stops.

There is no swelling and burning pain at the site of the bite.
True viper (Russel viper):
When venom is injected, the spot develops severe pain, the swelling starts within 15 minutes. Tingling and numbness over the tongue and mouth or scalp and paraesthesia around the wound occur. The main feature is persisting shock. A hemorrhagic syndrome with blood stained sputum, hemorrhages from gums, rectum, the site of bite etc. occur due to increased coagulation time. Intravascular hemolysis may lead to hemoglobinuria and renal failure.

After half to one hour, the patient develops pain, stiffness, and weakness of the skeletal muscles.
Fatal dose: — Cobra 12 mg; Russell’s viper 15 mg; Echis 8 mg; Krait 6 mg, of dried venom.
Fatal period: — Cobra half to six hours; viper one to two days.
Treatment: Polyvalent antisnake venom serum should be given to neutralise the poison.

The powder of dried body of Spanish fly (blister beetle) is used externally as an irritant.



Opium (afim) is also known as Kasoomba or, Madak or, Chandu. Opium is the dried juice of the poppy (papaver somniferum).
Opium contains two chemically different groups of alkaloids—
(a) The phenanthrenes—morphine 10%, codeine 0.5% and thebaine 0.3%, which are narcotic.
(b) The isoquinolines—papaverine 10% and narcotine 6%, no narcotic property.
The artificial derivatives are heroin, dihydromorphine.
Opiates exert their effects because of their chemical similarity to natural substances called endorphins. Opioid drugs are capable of producing physical addiction, and also psychological and euphoria.
Fatal dose — opium 2 gm.; morphine 0.2 gm. Fatal period — 6 to 12 hours.

Signs and Symptoms:
The contact of morphine with the skin of sensitive persons may cause erythema, urticaria and itching dermatitis. It first stimulates, then depresses and finally paralyses the nerve centres.
I. Stage of excitement—There is a sense of well being, increased mental activity, freedom from anxiety, talka¬tiveness, restlessness, hallucinations, flushing of face, maniacal condition.
II. Stage of stupor—The symptoms are headache, incapacity for exertion, a sense of weight in the limbs, giddiness, drowsiness and stupor.
III. Stage of coma—The patient passes into deep coma from which he cannot be aroused. The pupils are contracted to pinpoint size and do not-react to light, but in late stage they may be found to be dilated. — An overdose of narcotics cause hypotension, depressed reflexes and coma (except — dilated pupils).
Differential diagnosis of Opiate poisoning:
1) Opium poisoning—The odour of breath, bradycardia, pinpoint immobile pupils, stertorous respiration, slow pulse, moist perspiring skin are prominent features.
2) Acute alcoholic poisoning—Pupils are dilated and reacting.
3) Barbiturate poisoning—Shallow respiration, deep coma, no response to painful stimuli, deep reflexes are depressed, low blood pressure, dilated pupils.
4) CO poisoning—Intermittent convulsions, cherry red colour of skin and carboxy-hemoglobin in blood.
5) Uraemic coma—Cheyne-Stokes respirations, ammoniacal odour.
6) Diabetic coma—Deep respirations with air, hunger, odour of acetone in heart, sugar and acetone in the urine.

Naloxone hydrochloride is a specific opioid antagonist. Atropine is not recommended. N-allyl normorphine (lethidrone or nalorphine) is a specific antidote for morphine codeine, pethidine and methadone. Naltrexone is 17 times more potent than naloxone. When coma is deep -» artificial respiration and oxygen. Substitution with oral methadone, followed by gradual withdrawal of methadone.
Post-mortem appearances:
Signs of asphyxia are prominent. Froth is seen at the mouth and nostrils. The brain, meninges and abdominal organs are congested.
Chronic poisoning (morphinism; morphinomania):
The patient becomes restless, irritable, disturbed by dreams or insomnia. Loss of memory, mental fatigue, gradual intellectual, and moral deterioration occur. Constipation, contracted pupils, impotence are frequent.
Withdrawal symptoms of opioids tend to be opposite to the acute effects of the drug and include nausea and diarrhoea, coughing, lacrimation, rhinnorrhea, profuse sweating, twitching muscles, and piloerection or, goose bumps (except—miosis).
In addition, sensations of diffuse body pain, insomnia and yawning occur with intense drug craving.
Test for detection: Marquis test.


Absolute alcohol contains 99.95% alcohol; rectified spirit contains 90% alcohol.
The approximate percentage of alcohol in beverages is— Rum and liquors—50 to 60%; Whisky, gin, brandy 40 to 45%; Port, Sherry 20%; Wine 10 to 15%; Beers 4 to 8%.
Arrack—It is a liquor distilled from palm, rice, sugar or jaggery etc. and has a strength of 40 to 50%. It may be mixed with chloral hydrates and potassium bromide for getting a greater kick.
Absorption—About 20% of alcohol is absorbed from the stomach and 80% through small intestines.
Alcohol is a well known stimulant, but is a selective depressant, especially of the higher nervous centres which it inhibits. It is a hypnotic and diaphoretic.
1. Stage of excitement—There is increased confidence and a lack of self control. When jerking movement is in the direction of the gaze and independent of the position of the head, it is known as alcohol gaze nystagmus and appears at blood levels of 40 to 100 mg/100 ml. Mental concentration is poor and judgement impaired. These effects are usual between 50 to 150 mg/100 ml of blood alcohol.
2. Stage of incoordination—When alcohol content of the blood attains a level of 150-250 mg/100 ml.
3.Stage of coma—The person passes into a state of coma with stertorous breathing. The pupils are contracted, but stimulation of the person e.g., by pinching or slapping, causes them to dilate with slow return (Mc Evan sign).

Death occurs from asphyxia due to respiratory paralysis, but it may occur from shock.
‘Legal intoxication’ requires a blood alcohol concentra¬tion of atleast 80-100 mg/dl.
Fatal dose — 150 to 200 ml of absolute alcohol consumed in 1 hour.
Fatal period — 12 to 24 hours.
Treatment — Hemodialysis and peritoneal dialysis is performed.

Chronic poisoning:
Alcohol addicts are people, who cannot stop drinking for long, or who experience withdrawal symptoms. Chronic alcoholics are those who have reached a state of irreversible somatic or brain changes caused by alcohol.
Antabuse (disulfiram) is given in a single daily dose. Antabuse inhibits the enzyme aldehyde dehydroqenase. Antabuse leads to accumulation of acetaldehyde (aldshyde syndrome) in the blood and tissues and causes unpleasant symptoms, such as flushing, palpitation, anxiety, sweating, headache, abdominal cramps, nausea and vomiting due to which the patient dislikes alcohol.

A person is held responsible for crime committed in the voluntary drunkenness condition.
Widmark’s formula‘ is used to calculate the quantity of ethyl alcohol in the body. The widmark formula is a = prc, where (a) is the weight of alcohol in gm in the body (p) is the body weight in kg (c) is the concentration of alcohol in blood in mg/kg and (r) is a constant (0.6) for men and (0.5) for women.
Widmark’s formula for urine analysis, is a = ¾ prq, where (q) is the alcohol concentration in mg/kg.
Delirium tremens occur in chronic alcoholics due to (1) temporary excess (2) sudden withdrawal of alcohol (3) shock after receiving an injury, such as fracture of a bone, or (4) from acute infection, such as pneumonia, influenza, erysipelas etc.

All individuals with a blood alcohol level of 140 mg % are intoxicated to the point where they cannot deal with unusual, emergency or non-customary problems. Law in some countries have made it an offence to driye a motor vehicle above a specified blood alcohol level; e.g. England — 80 mq %, and USA — 150. mg %

Below 10 mg% = Sober, 20 – 70mg% = Drinking, 80 – 100 mg% = Under the influence, 150 – 300 mg% = Drunk, 400 mg% and above = Coma and death.
Saturday night paralysis occurs in the stage of coma and due to pressure on the radial nerve.
Breath analysis machines operate on the principle that alcohol absorbs radiation in the infra-red region of the spectrum and that the amount of infra-red light absorbed by a vapour is proportional to the concentration of alcohol in that vapour. 60 to 100 ml of breath received into a dry baloon and analysed by drunkotester, intoximeter, alcometer, alcotest or breathalyser.

The person is asked to blow into a plastic balloon through a glass tube, containing a crystalline bichromate-sulphuric acid mixture. If blood alcohol is 80 mg% or more, the crystals will become green to a predetermined distance. The test may be false positive because alcohol may remain in the mouth even after a small drink. The residual alcohol in the mouth disappears in 20 minutes. As such, the test should be repeated after 20 minutes.

Mineralised methylated spirit consists of 90% of ethyl alcohol, 9.5% of wood naphtha and 0.5% of crude pyridine.
Signs and Symptoms:
There may be delirium and coma. Urine is strongly acid and may contain acetone and a trace of albumin. Acidosis is caused. The pupils are dilated and fixed. Visual disturbances like photophobia and blurred vision, concentric diminution of visual fields for colour and form, followed by sudden loss of vision or complete blindness occur due to optic neuritis and atrophy..
Fatal dose — 60 to 240 ml. Fatal period — 24 to 36 hours.
(i) Gastric lavage with 5% bicarbonate solution. (ii) Ethyl alcohol. (iii) Hemodialysis is the treatment of choice in severe poisoning.
The most effective treatment of withdrawal of ethyl alcohol including delirium tremens is Benzodiazepines.

Barbiturate administration is contraindicated in Porphyria, Anaphylaxis and Asthma. They have a depressant action on the central nervous system. Large doses directly depress the medullary respiratory centre. Involuntary suicide is accidental barbiturate poisoning.

Signs and Symptoms:
The first symptom is usually drowsiness. A short period of confusion, excitement, delirium and hallucination is common. Hypothermia, cyanosis, hypotension, weak rapid pulse and cold clammy skin occurs. The pupils are usually slightly contracted but react to light; they may dilate during terminal asphyxia. Respiration becomes irregular, sometimes Cheyne-Stokes in character and finally stop (respiratory depression). The finding of blisters on the skin, often at the area of erythema, strongly suggests barbiturate poisoning. Death may occur from respiratory failure or ventricular fibrillation in early stage and bronchopneumonia and irreversible anoxia in later stage (flaccid coma).

The combination of alcohol and barbiturate causes rapid death.
Fatal dose: Short acting—1 to 2 gm. Medium acting— 2 to 3 gm. Long acting—3 to 5 gm.
Fatal period: 1 to 2 days.
— No specific antidote.
1. Gastric lavage, with warm water mixed with potassium permanganate and a suspension of animal charcoal or tannic acid.
2. Supportive measures (i.e. ABC) (i.e. Airway, Breathing, Circulation).
3. Forced alkaline diuresis – it is helpful only in long acting barbiturates which are eliminated primarily by renal excretion.
4. Hemodialysis & Hemoperfusion (through a column of activated charcoal) – is highly effective in removing long acting as well as short acting agents. Therefore it is better than forced alkaline diuresis.
Scandinavian method uses anti-shock measures, maintenance of airway and adequate respiratory support.
Chronic poisoning:
Dependence is both psychic and physical.

It is colourless, crystalline substance having peculiar pungent odour and a pungent bitter taste. It depresses CNS.
Fatal dose — 5 to 10 gm.
Fatal period — 8 to 12 hours.
Accidental poisoning results by taking large doses as hypnotic. It is given in food or drink to render a person suddenly helpless for the purpose of robbery or rape. Its action is so rapid that it has been given the name ‘knockout drops’.
A combination of alcohol and chloral hydrate is commonly known as ‘Mickey Finn’


Signs and Symptoms:
If the fumes are inhaled, there is feeling of dizziness, headache, nausea and vomiting. There may be pneumonitis, intense excitement, hallucina¬tions and convulsions, the person becomes unconscious & passes into coma. After ingestion, there is usually burning pain in throat nausea, vomiting, colicky pain and diarrhoea. There is giddiness, heaviness in the head, dyspnoea, cyanosis, drowsiness and coma.
Fatal dose — 15 to 30 c.c. of kerosene. Fatal period — Within 24 hours.


There are two varieties:
(i) Datura alba—white flowered plant.
(ii) Datura niger—a deep purple flowered plant.
The fruits are spherical and have sharp spines (thorn-apple). Datura stramonium is known as thorn apple. They contain 0.2 to 1.4% of hyoscine (scopolamine), hyoscyamine, and atropine.
Signs and Symptoms:
A bitter taste, dryness of mouth and throat, dysphagia, voice hoarse, Fever. The face becomes flushed, conjunctivae congested, widely non-reacting dilated pupils, temporary blindness, photophobia and diplopia. Restlessness, agitation. Delirium is restless and purposeless; in earlier stage indicated by excitement, talkativeness and unintelligent speech. Hallucinations of sight and hearing and delusion occurs.
Fatal dose — 1 gm (100 to 125 seeds).
Fatal period —. 24 hours.
Physostigmine is specific in Datura poisoning. Pilocarpine nitrate.
Poisoning: —Crushed or powdered seeds or an extract is used by criminals for stupefying a victim prior to robbery, rape or kidnapping.
Mydriatic test—The pupil dilates within half an hour, if datura is present.


It is also known as Indian hemp, hashish or marihuana. The principal constituent of resin of marijuana is tetrahydro cannabinol. It is a CNS stimulant.
It is used in the following forms:
1. Bhang—It is prepared from the dried leaves and fruit shoots.
2. Majoon—It is a sweet prepared with bhang. It increases appetite and sexual desire.
3. Ganja—It is prepared from the flower tops of female plant.
4. Charas or hashish—It is the resin exuding from the leaves and stems of the plant.
Signs and Symptoms
Large doses cause –
1. Inebriation—The person becomes dreamy or semi¬conscious and he has realistic vision, usually of sexual nature e.g. he sees nude beautiful women dancing before him, playing music, singing sexual love song. It causes psychological high, raises heart rate, delays psychomotor skills.
2. Narcosis—There is giddiness and ataxia, tingling and numbness of the skin, general anaesthesia.
Fatal dose—Charas 2 gm; ganja 8 gm; bhang 10 gm/kilo body weight.
Fatal period—Several days.
Chronic poisoning:
Used in excess, it causes degeneration of CNS. There is loss of appetite, weakness, wasting, tremors, vacant look, red eyes, impotence, mental deterioration. Rarely, they become insane, and may suffer from hallucinations and delusions of persecution. There may be an impulse to kill. The person may run amok i.e. he develops a psychiatric disturbance marked by a-period of depression followed by violent attempt to kill people. He first kills a person against whom he may have real or imaginary enemitv. and then kills anyone that comes in his way until homicidal tendency lasts. Then he may commit suicide or surrender himself.
Poisoning—Majoon and charas are sometimes used by road poisoners to stupefy person to facilitate robbery.

It is obtained from leaves of Erythroxylum coca. It is colourless, odourless, crystalline substance with bitter taste. It is used as a local anaesthetic, acts as a vaso constrictor. The usual route of intake is snorting and skin popping.
Signs and Symptoms:
(i) Stage of excitement—There is bitter taste, dryness of mouth, fatigue, black teeth and tongue & visual hallucination (ii) Stage of depression—Within an hour, respirations become feeble, collapse, convulsions and death occurs. Death is due to respiratory failure or vascular collapse.
Fatal dose — 1 to 1.5 gm orally.
Fatal period — Few hours.
Treatment — Amyl nitrite is antidote and given by inhalation.
Cocaine habit—The patient may surfer from hallucinations, convulsions, delirium and insanity.
Magnan’s symptoms or cocaine bug is characteristic, in which there is feeling as if grains of sand are lying under the skin or some small insects are creeping on the skin (tactile hallucinations).

Drug addiction—The most important drugs of addiction are alcohol, opium, pethidine, heroin, barbiturates, cannabis and amphetamine.
Drug habituation (habits) -There is psychological or emotional dependence on the drug.
Drug dependence—It includes both the term addiction and habituation.
Addiction consists of physical and psychological dependence.

Withdrawal symptoms:
May begin within 6 to 8 hours following stoppage of drug. It includes chilliness, yawning and rhinorrhoea, goose skin, lacrimation. gross tremors, and dilatation of pupils are seen. Narcotic addicts may be killed by a hot shot i.e. a dose of narcotic with a poison as strychnine in it.
Psychoactive Drug classification:
1. Sedatives—Barbiturates, minor tranguilisers, alcohol.
2. Stimulants—Amphetamines, cocaine.
3. Opiates—Heroin, methadone, morphine.
4. Marihuana.
5. Major tranquilisers—Chlorpromazine.
6. Anti depressants—Tricyclics, MAO Inhibitors. (Mono Amino Oxidases)
MAO – A inhibitors — Clorgiline Moclobemide
MAO – B inhibitor — Selegeline (Depremyl).

Cocaine and LSD do not produce physical dependence. Street heroin is known as smack, junk or dope. Amphetamines cause paranoid, psychosis and psychic dependence. Hallucinogenic drugs—LSD, phencyclidine (angel dust).

In the infection type, organisms belong mainly to salmonella, proteus, coli, streptococcus, shigella. In the toxic type, is due to ingestion of preformed toxin in prepared food.
—Exotoxins e.g. enterotoxin of staphylococci and the botulinum toxin, produce intoxication.
Incubation period of staphylococcal food poisoning is 1-6 hours.

There are no symptoms of gastroenteritis (i.e. no diarrhoea) It is caused by neurotoxjn, an exotoxin of clostridium botulinum multiplied in the food e.g. tinned meat| fish, fruits etc.
The fatal dose, for an adult is 0.01 mg, The toxin paralyses the nerve ending.
Signs and Symptoms:
The incubation period is 12 to 30 hours. There is nausea, vomiting, constipation, ocular pharyngeal paralysis, salivation, sometimes aphonia. Excessive fatigue, diplopia. marked muscular weakness. The patient is conscious till death, which is preceded by coma or-delirium. Bulbar palsy and descending paralysis is seen.
Differential diagnosis of botulism includes Tetanus, Epilepsy and Acute gastroenteritis.

Consumptjon exceeding 30% of the total diet for more than 6 months; produces lathyrism. The active neurotoxic principle is B(N)-oxalyl aminoalanine -> BOAA.
The continuous use of L. sativus produces neurolathvrism, characterised by progressive spastic paraplegia, sphincters, sensation and mental faculties are preserved.

The Argemone oil contains two alkaloids -> sanguinarine and dihydro sanguinarine. Causes epidemic dropsy.
Hypersecretory glaucoma, Diarrhoea, CCF are seen iq —> Epidemic dropsy (But no convulsions). Sanguinarine interferes with the oxidation of pyruvic acid, which accumulates in blood.
The symptoms of epidemic dropsy consists of sudden non¬-inflammatory, bilateral swelling of legs.
Tests for detection of Argemone oil are
(i) Nitric acid test: The colour becomes brown to orange-red shows presence of Argemone oil, positive when concentration is 0.25 percent.
(ii) Paper chromatography test: This is the most sensitive test. It can detect argemone oil up to 0.0001 percent in all edible oils and fats.-

Mechanism of action of strychnine poisoning is post synaptic block. Strychnine (kuchila) is a powerful alkaloid obtained from the seeds of the strychnos nux vomica. The seeds contain two principal alkaloids -> strychnine 1.5% and brucine 1 55%. Strychnine poisoning resembles tetanus poisoning. The action is particularly noted in anterior horn cells. In strychnine poisoning convulsions affect all muscles at a time. The mouth is covered with froth, frequently blood stained. The convulsions are most marked in antigravity muscles, so that the body typically arches in hyperextension opisthotonus. Sometimes spasm of abdominal muscle may bend the body forward (emprosthotonus), or to the side (pleurosthotonus). Consciousness is not lost.
Fatal dose — 30 to 100 mg; one crushed seed.
Fatal period — One to two hours.
(i) Short acting barbiturates, (ii) Diazepam, (iii) Stomach wash with potassium permanganate.
Post-mortem appearance — In strychnine poisoning, brain is required to be preserved.
Post-mortem caloricity is seen in strychnine poisoning.

Cardiac poisons are
(i) Nicotiana tabacum (ii) Digitalis purpurea (iii) Nerium odurum (iv) Yellow oleander (v) Cerbera odallam (vi) Quinine
(vii) Aconite — Fatal period : 1 – 8 hours, antidote : atropine. (viii)Hydrocyanic acid.

DIGITALIS (D. purpurea, D.lanata, Strophathus gratus)
Entire plant is toxic, containing over 30 cardiac and steroidal toxins. The roots, leaves and seeds of digitalis contain digitoxin, digitonin and digitalin.
Action: By inhibiting the Na+K+ATPase. Digitalis prolongs the diastolic period of the heart. In therapeutic doses, it depresses both excitability and conductivity. But in toxc dose, excitability is increased with extrasystole.
Signs and symptoms:
Nausea, vomiting, abdominal pain, nervous irritability, tingling and coldness in extremities, increased heart rate, varying degrees of AV block, ectopic beats, coupled rhythm, Atrial Fibrillation and Ventricular Fibrillation. Patient becomes drowsy, coma sets in and death occurs.
Fatal dose: 15 to 30 mg of digitalin, 4 mg of digitoxin,
Fatal period: 1 to 24 hours.

(1) Stomach wash with tannic acid
(2) Bowels should be evacuated
(3) Specific antidotes (i) 100 mg lignocaine i.v / dilantin / propranalol
(4) Trisodium EDTA to lower serum Ca level.
(5) Potassium salts to reduce extrasystoles and arrythmias.
(6) Bradycardia is treated with atropine sulphate 0.6 mg i.v repeated for 4 days.
(7) Symptomatic.

NERIUM ODORUM (White oleander)
Grow wild in India.
All parts of plant are poisonous, containing several cardiac glycosides, primarily oleandroside (oleandrin), and nerioside (nerin), which resembles digitalis in action.
Signs and symptoms:
It produces contact dermatitis. Ingestion causes difficulty in swallowing and articulation, abdominal pain, vomiting, profuse frothy salivation, and diarrhoea. Pulse is at first slow, then later rapid and weak, BP falls, respiratory rate increased, pupils dilated, muscular twitchings, tetanic spasm, lock-jaw, drowsiness, coma, respiratory paralysis and death occurs.
Fatal dose: 15 gm of root.
Fatal period: 24 to 36 hours.

CERBERA THEVETIA (Yellow oleander)
All parts are poisonous. Seeds contain 3.5 to 4% of the cardiac glycoside thevetin. which is similar to digitalis in action, others are thevetoxin, nerifoliun, peruvoside and ruvoside and cerebrin.
Signs and symptoms:
Pulse is rapid, weak and irregular, BP low. Heart block, collapse and death from peripheral circulatory failure.
(1) Stomach wash
(2) Sodium molar lactate transfusion with glucose and 1 mg. atropine, 2 cc adrenaline and 2 mg noradrenaline.
(3) Symptomatic.

Active principles: Cerberin, cerebroside, odollin, odolotoxin, thevetin and cerapain.
Signs and symptoms:
Initial symptoms are gastro-intestinal. Cardiac toxicity within 3 hours of ingestion. There is bitter taste, nausea, severe retching, vomiting, abdominal pain and in few cases diarrhoea, general weakness, blurring of vision, sinus bradycardia, irregular respiration, collapse and death from heart failure.
Chief bio-chemical changes are Hyperkalemia, and depression of transaminase activity.
Fatal dose: Kernel of one fruit.
Fatal period: 1 or 2 days or more.
(1) Stomach wash
(2) Atropine 0.5 mg i.v and repeated every 15 to 30 min to keep heart rate above 50 per minute
(3) Correct hyperkalemia.

It is a strong protoplasmic poison with anaesthetic and sclerosing action. It stimulates and then depresses central nervous system.
Signs and symptoms:
Headache, giddiness, ringing in the ears, partial deafness, disorders of vision, pupils are fixed and dilated. Mental confusion, pain in the abdomen, nausea and vomiting, confusion of thought, muscular weakness, itching, erythematous or urticarial rash on the skin, methaemoglobinemia, tachycardia, hypotension, cyanosis, delirium and coma.
Fatal dose: 8 to 10 gm.
Fatal period: Few minutes to 2 days.
(1) Gastric lavage
(2) i.v. fluids to promote diuresis
(3) Bilateral stellate ganglion blocks causes return of vision.
(4) Symptomatic.

It is also called prussic acid or cyanogen. The pure acid is a colourless, transparent volatile liquid with an odour like bitter.almonds. Cyanides are white powders. More than 5% carboxyhemoglobin is seen in cyanide poisoning. Cyanide inhibits the action of cytochrome oxidase and carbonic anhydrase. It kills by creating histotoxic or cvtotoxic anoxia. Cyanide acts by reducing the oxygen carrying capacity of the blood, and by combining with the ferric iron atom of intra-cellular cytochrome oxidase, prevents the uptake of oxygen for cellular respiration.
Signs and Symptoms:
Massive doses may produce sudden loss of consciousness and prompt death from respiratory arrest. People suffering from achlorhydria may not suffer from toxic effect of oral ingestion of potassium cyanide. The mouth is covered with foam which is sometimes blood-stained. Death occurs from respiratory failure.
Fatal Dose -50 to 60 mg of pure acid; 200 to 300 mg of potassium cyanide.
Fatal period—2 to 10 minutes.
(i) Amyl nitrite is used by inhalation. (ii) Sodium nitrite is given i.v. (iii) Sodium thiosulphate in 50% solution i.v. converts cyanide to non-toxic thiocyanates.
(iv) Methylene blue i.v. (v) Cobalt EDTA. (vi) Para amino prophenone (PAPP) acts by forming meth.Hb. (vii) Qxygen.
P. M. appearance:
The blood is bright cherry red due to formation of cyan-met-haemoglobin. The post mortem staining may be cherry-red or brick red.


It is a colourless, tasteless, non-irritant gas which is produced due to incomplete combustion of carbon. It is insoluble in water. It burns with a blue flame.
Upper limit of safety of carbon monoxide in air is 0.01%.
50% COHb produces symptoms like alcoholic intoxication. 50%-60% produces syncope or coma with intermittent convulsions. Exposure of atmosphere containing 0.2% of gas will cause death in about 4 hours, 0.4% in one hour, and 10% in 20 to 30 minutes.
Symptoms of CO poisoning:




0 to 10%

10 to 20%

20 to 30%

30 to 40%

40 to 50%

50 to 60%

60 to 70%

70 to 80%

Above 80%

= No appreciable symptoms= Breathlessness on moderate exertion, mild headache= Throbbing headache, irritability, emotional instability, disturbed judgment, defective memory and rapid fatigue= Severe headache, nausea, vomiting, dizziness, dimness of vision, confusion.

= Increased confusion, sometimes hallucinations, severe ataxia, rapid respirations and collapse with attempts at exertion

= Syncope or coma with intermittent convulsions, rapid respirations, tachycardia with a weak pulse and pink or red discoloration of the skin.

= Increasing depth of coma with incontinence of urine and faeces.

= Profound coma with depressed or absent reflexes, a weak thready pulse, shallow and irregular perspiration.

= Rapid death from respiratory arrest

P. M appearance: Death by CO poisoning is called Conflagration.
A cherry – red colouration of the skin, mucous membranes, areas of hypostasis. Fine froth may be seen at mouth and nose. Bilateral symmetrical necrosis of the lenticular nuclei and punctiform hemorrhages in the white matter of brain.

It is found in large quantity in sewer –> sewer gas. It has a smell of rotten eggs.

(i) Vesicant—Mustard gas, lewisites.–
(ii) Asphyxiant—Chlorine, phosgene.
(iii) Tear gases—Chlor acetophenone (CAP), ethyloidoaretate (K.S.K), bromobenzyl cyanide (B.B.C.).
(iv) Nerve gases—They are compounds related to phosphate easters in action and toxicity.

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Forensic Medicine & Toxicology – A comprehensive study-II

doctors15Dr  Sanil Kumar BHMS MD(Hom)
Department of Forensic Medicine & Toxicology
Govt Homeopathic Medical College. Calicut
Email : drsakumkumar@yahoo.co.in

Abnormal Sexual Perversions
1. Necrophagia—Necros = corpse; phagia = to eat.
2. Masochism—Opposite to sadism. Derived from the name of Leopold von Sacher-masoch, an Austrian novelist. Being whipped by his wife used to be a stimulant for his literary work.
3. Necrophilia—Sexual intercourse with dead body.
4. Fetichism—Sexual satisfaction by contact with articles of opposite sex.
5. Voyeurism (Scoptophilia)—Peeping Tom. It is sexual enjoy¬ment from watching.
6. Frotteurism—Contact with other persons to obtain sexual gratification.
7. Undinism—Sexual pleasure by witnessing the act of Urination.
8. Transvestism—Trans = opposite, Vesta = clothing or Eonism. The term is derived from the name of Chevelier d’ Eon Beamont, a Frenchman. It is usually found in the males who derive sexual pleasure by wearing female dress.
9. Satyriasis—Incessant sexual desire.
10. Priapism—Painful penile erection in absence of sexual desire.
11. The combining of Sadism and Masochism is called bondage.
12. Pyromania — Sexual stimulation while seeing flames or, destruction of buildings.

Classification of Sexual Offences
I. Natural offences (1) Rape (2) Incest
II. Unnatural offences (1) Sodomy (2) Tribadism (3) Bestiality (4) Buccal coitus.
III. Sexual perversions: (1) Sadism (2) Masochism (3) Necrophilia (4) Fetichism (5) Transvestism (6) Exhibitionism (7) Masturbation (8) Voyeurism (9) Frotteurism (10) Undinism, etc.

Rape (S. 375, IPC)
A man is said to commit rape, if he has sexual intercourse with a woman:

  1. against her will,
  2. without her consent,
  3. with her consent, when her consent has been obtained by putting her or any person whorn she is interested in fear of death, or of hurt,
  4. with her consent, when the man knows that he is not her husband and that she has given consent because she believes that he is another man to whom she is lawfully married.
  5. with her consent, when at the time of giving such consent, by reason of unsoundness of mind or intoxication or the administration of any stupefying substance, she is unable to understand the nature and consequences of that to which she gives consent,
  6. with or without her consent when she is under 16 years of age;

Exception:— sexual intercourse by a man with his own wife is not rape, if she is above 15 years of age (Sec 375 IPC).

Rape offence is punishable under Sec- 376 IPC.
(1) Whoever commits rape shall be punished with imprisonment for a term of not less than 7 years, but which may be for life or ten years and also fine. If the woman raped is his own wife and is not under 12 years, the imprisonment may extend to 2 years or fine or with both.
(2) Whoever, (a) being a police officer commits rape, within the limits of his jurisdiction, in the premises of any station house, or on a woman in his custody, (b) being a public servant takes advantage of his official position and commits rape on a woman in his custody, (c) being on the management or the staff of a jail, remand home, etc., commits rape on any inmate, (d) being on the management of a staff of a hospital commits rape on a woman of that hospital, (e) commits rape on a woman knowing her to be pregnant, (f) commits rape on a woman below 12 years, or (g) commits gang rape, shall be punished with rigorous imprisonment of not less than 10 years or life imprisonment and also fine.

A woman of 16 years and above can give valid consent for sexual intercourse. The slightest penetration of the penis within the vulva, with or, without emission of semen or rupture of hymen constitutes rape. Rape can be committed even when there is inability to produce erection of penis. Under the law, rape can only be committed by a man and a woman cannot rape a man, although she may be guilty of an indecent assault upon him. In India, there is no age limit under which a boy is considered physically incapable of committing rape. Medical proof of intercourse is not legal proof of rape. Rape is a cognizable offence.
False rape is called simulated rape.

Incest: Incest is a sexual intercourse by a man with a woman, who is closely related to him by blood e.g. a daughter, grand daughter, sister, stepsister, aunt and mother. In India, incest as such is not an offence.

Paraphilias: Abnormal and unorthodox sex play by using unusual objects or parts of the body are known as paraphilia.

Unnatural Offences
Voluntary sexual intercourse against the order of nature with any man or woman or animal is an unnatural sex offence (S. 377, IPC). These offences are punishable with imprisonment for life or up to 10 years and also with fine.

Homosexuality means persistent emotional and physical attraction to members of same sex.

Sodomy is anal intercourse between two males or, between a male and female. It is also called buggery. It is called gerontophilia when the active agent is an adult and paederasty, when the passive agent is a young boy, who is known as catamite.

A paedophile is an adult who repeatedly engages in sexual activities with children below the age of puberty. The consent of sodomy is of no value, as both partners are punishable.

Buccal coitus (coitus per os or sin of Gommorrah): The male organ is introduced into mouth, usually of a young child.
1. Male prostitutes are called—Eunuchs.
2. Castrated Eunuchs—Hijrahs.
3. Eunuchs with intact genitalia—Zenana.

Female homosexuality is known tribadism or lesbianism. Sexual gratification of a woman is obtained by another woman by simple lip kissing, generalised body contact, deep kissing, manual manipulation of breast and genitalia, genital apposition, friction of external genital organs etc. In some cases, enlarged clitoris is used as an organ of passion or some artificial penis or phallus may be used. Many lesbians are masculine in type, possibly because of endocrine disturbances. The practice is usually indulged in by women who are mental degenerates or who suffer from nymphomania (excessive sexual desire). Lesbians who are jealous of one another, when rejected may commit homicide, suicide or both.

Bestiality: Bestiality is sexual intercourse by a human being with a lower animal. Dogs and cats are common animals for female. Usually the animal manipulates the genitalia with its mouth and the actual coitus is very rare.

Sexual Perversions: Sexual perversions are persistently indulged sexual acts in which complete satisfaction is sought and obtained without sexual intercourse.
1. Uranism—Perversion of sexual instinct.
2. Sadism—In sadism, sexual gratification is obtained or increased from acts of physical cruelty or causing of pain upon one’s partner. The term is derived from the name of a French nobleman, the Marquis de Sade, infamous for his crimes and writings. Many of his stories were about sexuality, cruelty, and torture.
3. Lust murder—In extreme cases of sadism, murder serves as a stimulus for sexual act and becomes equal to coitus.
4. Sexual oralism—It is the obtaining of sexual pleasure from the application of the mouth to the sexual organs.
—Sin of Gommorrah —>Buccal coitus, coitus per os.
—Felatio —> is the oral stimulation or manipulation of the penis either by the female or male.
— Cunnilingus is the oral stimulation of the female genitalia.

5. Masturbation (Onanism, ipsation)—Masturbation is the deliberate self stimulation, which effects sexual arousal. In females, a finger is gently and rhythmically moved over clitoris or labia minora or steady pressure is applied over these parts with several fingers or whole hand. Masturbation is an offence when practiced openly e.g. in telephone booth, lavatories etc.

6. Exhibitionism: It is a willful and intentional exposure of the genitalia in a public place while in the presence of others, to obtain sexual pleasure. This is punishable under Sec 294 IPC with imprison¬ment up to 3 months or fine.

7. Indecent Assault: Indecent assault is an offence committed on a female, with the intention or knowledge to outrage her modesty.
— This includes: Kissing of any part of female body, Pressing the breasts or private parts, Touching private parts or- thereabout including thighs, Exposing her genital parts or breasts,
 A medical practitioner can be accused of indecent assault if he examines a female patient by stripping her clothes without her consent and even with her consent in the absence of a female attendant (viz. nurse).
Such assaults are punishable under Sec 354 IPC up to 2 years imprisonment and/or fine.


Seminal stains have to be detected in cases of rape or attempted rape, sexual murder of the female, sodomy and bestiality. Fertility of fluid has to be proved in disputed paternity. Chemical Examination:
(a) Florence test: It is the best test for seminal stains. The stain is extracted by 1% hydrochloric acid and a drop is placed on a glass slide. A drop of florence solution (potassium iodide, iodine and water) is allowed to run under the cover slip. If semen is present, dark-brown crystals of choline iodide appears immediately. They are rhombic crystals resembling haemin. The test is not proof of seminal fluid, but only of presence of some vegetable or animal substance.
(b) Barberio’s test: A saturated aqueous or alcoholic solution of picric acid when added to spermatic fluids produces yellow needle-shaped rhombic crystals of spermine picrate. In Barberio’s test, presence of spermine in semen is detected.
(c) The Acid phosphatase test: The prostatic secretion element of seminal fluid contains very much higher percentage of acid phosphatase. This test is conclusive in the absence of demonstrable sperms or in aspermia.
(d) Creatine phosphokinase: Serological typing of the semen is possible by precipitin method.
(e) Ammonium molybdate test: for semen stains.


Impotence is the inability of a person to perform sexual inter¬course.
Sterility is the inability of the male to beget children, and in the female, the inability to conceive children.
Frigidity is the inability to start or maintain the sexual arousal pattern in the female.
Impotence may be pleaded as a ground for all – Divorce, Adultery, Unnatural sexual offence except rape.

The question of impotence and sterility may arise in:
(A) Civil— (i) nullity of marriage (ii) divorce (S.12, Hindu Marriage Act, 1955; S.24, Special Marriage Act, 1954) (iii) adultery (iv) disputed paternity and legitimacy (v) suits of adoption (vi) claim for damages where loss of the sexual function is claimed as the result of an assault or accident
(B) Criminal— (i) adultery (ii) rape (iii) unnatural offences.
Men with primary impotence associates sex with dirtness and sinfulness. Systemic disease which is most frequently associated with secondary impotence is Diabetes mellitus. Psychogenic or fear of impotence or, fear of inability complete the act are most common causes of temporary impotence.
Impotent quoad is an individual who may be impotent any particular woman (quoad = as regards) but not with others. Vaginismus is involuntary spasm of perineal muscle so that sexual intercourse is not possible. Treatment is psychotherapy. After vasectomy, the person should be advised to abstain from sexual intercourse for about 3 months. A battered child is one who has received injuries as a result of non-accidental violence produced by a parent or guardian.
Sudden infant death syndrome (SIDS or Cot death)—The commonly accepted hypothesis suggests that some infants have prolonged sleep apnoea, which makes them susceptible to hypoxia, which leads to bradycardia and cardiac arrest.

It is artificial introduction of semen into the vagina cervix or uterus to produce pregnancy. One ml. of semen is deposited by means of syringe in or near the cervix.
(i) When the husband is impotent (not an indication for A.I.D).
(ii)When the husband is unable to deposit the semen in vagina due to hypospadias.
(iii) When the husband is sterile.
(iv) When there is Rh-incompatibility between husband and wife,
(v) When husband is suffering from hereditary disease such as colour blindness, sickle cell disease.

Legal problems of Artificial Insemination Donor:
1. Adultery—Donor and recipient cannot be held guilty of adultery in India, as Sec. 497 IPC requires sexual intercourse as necessary part of adultery.
2. Legitimacy—such a child is illegitimate and cannot inherit property.
3. Nullity of marriage and divorce—Artificial insemination is not a ground for nullity of marriage or divorce. However, if A.I is due to impotence, it is a ground. If A.I is done without the consent of the husband, he can sue his wife for divorce and the doctor for damages.
4. Natural birth: if a child is born naturally sometime after a child born by A.I, the status of the child born after A.I remains illegitimate unless it is adopted, and the status of the natural born child remains legitimate.

Test tube baby (IVF):
The ovum is removed from the ovary of the woman and is fertilised outside the body. At the stage of blastocyst, the embryo is returned to the uterus, which gets implanted in the endometrium.

 Surrogate birth:

Artificial insemination with the semen of the barren woman’s husband is carried out in a hired woman.

A virgin (virgo intacta) is a female who has not experienced sexual intercourse. Defloration means loss of virginity. The question of virginity arises in case of (1) nullity of marriage, (2) divorce, (3) defamation, and (4) rape.

Signs of virginity:
A. Genital findings:
(i) Labia majora — firm, elastic and rounded and lies in close contact with each other even in full abduction of the thighs
(ii) Labia minora — soft and elastic, small and pinkish colour. They lie in close contact and are not visible being under the labia majora.
(iii) Clitoris — not enlarged,
(iv) Vestibule — narrow,
(v) Hymen — intact.
(vi) Vagina — narrow and tight with rugosed pinkish walls, ori is slit like due to the apposition of wall, and due to presence of hymen.
(vii) Perineum — entire.
B. Extra genital findings:
(i) Breast — hemispherical, firm, plump and elastic.
(ii) Nipple — small and pointed surrounded by pink areola.

Narrow and tight vagina is not seen in false virgin. Tears on hymen caused by sexual intercourse or by fore body is usually situated postero-laterally.

Causes of rupture of hymen:
1. An accident—Hymen does not rupture by riding, jump dancing etc.
2. Masturbation.
3. Sola pith introduced into vagina.
4. Sanitary tampoon.
Most important sign of defloration is hymen rupture. Important support of uterus preventing prolapse is transverse cervical ligaments. In women who are used to coitus, and in those who have borne children, the hymen is destroyed and different sized small, round,, fleshy projections or tags, known as carunculae hymenales or myrtiformes are formed round the hymenal ring.

Pregnancy is a condition of having a developing embryo or foetus in the female, when an ovum is fertilized by a spermatozoon.
The question of pregnancy has to be determined in the following conditions:
(1) When a woman pleads pregnancy to avoid attendance in Court as a witness.
(2) When a woman convicted of capital crime, pleads that she is pregnant, to avoid execution. The High Court has the power to postpone the execution of death sentence or to commute it as Imprisonment for life (S.416, Cr.P.C).
(3) When a woman feigns pregnancy soon after death of her husband to claim succession to estate.
(4) To assess damage in a seduction or breach of promise of marriage case.
(5) When a woman blackmails a man and accuses that she is pregnant by him, to compel marriage.
(6) In allegations that an unmarried woman, widow, or a wife living apart from her husband is pregnant
(7) When a woman alleges that she is pregnant in order to get greater compensation when her husband dies through the negligence of some person
(8) When pregnancy is alleged to be motive for suicide or murder of unmarried woman or widow
(9) In cases of divorce, the woman may claim to be pregnant to receive more alimony
(10) In cases of alleged concealment of birth of pregnancy and infanticide.

Diagnosis of pregnancy: the signs and symptoms are usually classified into three groups:
(1) The Presumptive signs, (2) The Probable signs, (3) The Positive signs.

(1) The presumptive signs are amenorrhoea, changes in breast, morning sickness, quickening, pigmentation of the skin, changes in the vulva, urinary disturbances, fatigue and sympathetic disturbances.
Amenorrhoea is the earliest and one of the most important symptom of pregnancy. Breast changes are quite characteristic in primi-gravidas but are of less value in multiparas. Morning sickness usually appears about the end of the first month and disappears 6 to 8 weeks later. Nausea and vomiting are usually present in the morning, and pass off in a few hours. From about 16th to 20th week, the pregnant woman feels slight fluttering movements in her abdomen (Quickening). The vulva, abdomen and axillae become darker due to the deposit of pigment, and a dark line extends from the pubis to beyond the umbilicus, the so called linea nigra. The mucous membrane of the vagina changes from pink to violet, deepening to blue as a result of venous obstruction, after the fourth week (Jackquemier’s sign or Chadwick’s sign). Enlarging uterus exerts pressure on the bladder and produces frequent micturition. Easy fatigue is very important. Salivation, perverted appetite and irritable temper are common.

(2) The probable signs of pregnancy are enlargement of the abdomen, Hegar’s sign, Goodell’s sign, Braxton-Hick’s sign, Ballottement, uterine souffle, biological tests and immunological tests.
During pregnancy, abdomen gradually enlarges in size after the 12th week. Hegar’s sign is positive at about the sixth week. This is the most valuable physical sign of early pregnancy. Goodell’s sign is the progressive softening of the cervix from below upwards, well marked from the fourth month. Intermittent, painless uterine contractions are easily felt after the fourth month known as Braxton-Hick’s sign. They are present even when the fetus is dead. Ballottement is positive during the fourth and fifth month of pregnancy as the fetus is small in relation to the amount of amniotic fluid present. This can be negative if the amniotic fluid is scanty. Uterine souffle is a soft blowing murmur, which is synchronous with the mother’s pulse. It is due to passage of blood through the uterine vessels.
The biological tests are (1) The rapid rat test (2) The Aschheim-Zondek test (3) Friedman test (4) Hogben or female toad test (5) male frog test (6) Galli-Mainini test.
The immunological tests are (1) Inhibition (indirect) latex slide test (2) Direct latex slide test.

(3) Positive signs of pregnancy: They are fetal movements, fetal heart sounds, X-ray diagnosis and Sonography.
Fetal movements are felt by placing the hands on the abdomen by 24 weeks. Fetal parts can be identified by abdominal palpation by 36 weeks. Fetal heart sounds are important and definite sign of pregnancy. They are heard between 18 to 20 weeks for the first time. Rate is usually about 160 at fifth and 120 at the ninth month, not synchronous with the mother’s pulse.
Fetal sounds are not heard: (a) when the fetus is dead, (b) when there is excessive amount of liquor amnii, (c) when abdominal wall is very fatty, (d) when examination is made before 18 weeks of pregnancy. At about 15 to 16 weeks, fetal parts can be detected with certainty. Usually the skull and spine are seen at 15 to 16 weeks.
Radiological signs of fetal death are (1) Spalding’s sign, (2) Collapse of the spinal column due to absence of muscle tone, (3) presence of gas in the heart and great vessels.

Pseudocyesis (spurious or phantom pregnancy): is usually observed in patients nearing the menopause or in younger women who intensely desire children.
Signs of pregnancy in the dead: The presence of an embryo, foetus, placental tissue, membranes or any other product of conception is a positive proof.

Period of gestation: Average is 280 days from the first period of the last menstrual period, so that the actual period is about 270 days or less. Maximum period concluded for medico-legal purpose is 354 days from the coitus to live-birth. The maximum period accepted by English courts on medical evidence is 349 days. Child born at or after 210 days of uterine life are viable, i.e., are born and able to survive.
Posthumous child: It is a child born after the death of its father, the mother being conceived by the said father.

Superfecundation: it means the fertilisation of two ova which have been discharged from the ovary at the same period by two separate acts of coitus committed at short intervals.
Superfoetation: This means the fertilisation of a second ovum in a woman who is already pregnant.

Legitimacy and paternity:
Legitimacy is the legal state of a person born in lawful marriage. If a person is born during the continuance of a legal marriage, or within 280 days after the dissolution of a legal marriage by divorce or death of the husband, his birth is presumed to be legitimate (S.112, I.E.A).
Atavism – The child does not resemble its parents, but resembles its grandparents.

Wife battering: A battered wife is a woman who has received a deliberate, severe, and repeated demonstrable physical injuries from her husband. Faulk has categorised the involved men into five groups: (1) Dependent passive, (2) Dependent suspicious, (3) Violent and bullying, (4) Dominating, (5) Stable and affectionate.

Delivery means the expulsion or extraction of the child at birth. The question of delivery arises in (1) abortion, (2) infanticide, (3) concealment of birth, (4) feigned delivery, (5) legitimacy, (6) nullity of marriage, (7) divorce, (8) chastity, and (9) blackmail.

Signs of recent delivery in the living: For the first 2 or 3 days the woman is pale, exhausted and ill-looking with increase in pulse and slight fever. Breasts are full, enlarged and tender with a knotty feeling, and colostrum or milk may be expressed. The areolae are dark, nipples enlarged, and superficial veins prominent, and Montgomery’s tubercles are present. The abdominal walls are pendulous, wrinkled and show striae gravidarum especially in flanks which appear as irregular, pink, subcutaneous scars. The uterus feels like hard muscular tumour, the upper border of which lies about 3 cm. below the umbilicus. It then diminishes in size by about 1.5 cm a day. The labia are tender, swollen and bruised or lacerated. The vagina is relaxed and capacious. Perineum may be lacerated. Cervix is soft and dilated and its edges torn and lacerated transversely.

The lochia is a discharge from the uterus which lasts for 2 or 3 weeks. During the first 4 to 5 days, the discharge is bright-red and contains large clots (lochia rubra). During the next 4 days, it becomes serous and paler in colour (lochia serosa). After the ninth day, colour becomes yellowish-green or turbid (lochia alba) until its final disappearance.
It the blood or urine gives a positive pregnancy test, it is strong corroborative evidence that pregnancy has recently terminated.
Oligohydramnios is seen in renal-agenesis. In pregnancy, trace element not supplemented from diet is iron.
Signs of Remote delivery in the dead include:
1. Uterus is larger, thicker, and heavier.
2. Walls are concave from inside.-
3. Top of the fundus is convex, and at a higher level than that of broad ligaments.
4. The body of uterus is twice the length of cervix (same length in virgin).
5. The cervix is irregular in form, shortened, its edges show cicatrices.
6. External os is enlarged, and Internal os is not so well defined.

Legally, abortion (miscarriage) means the premature expulsion of the fetus from the mother’s womb at any time of pregnancy, before full term of pregnancy is completed.

Classification: (1) Natural: (a) Spontaneous (b) Accidental (2) Artificial (a) Justifiable (b) Criminal.

 Natural abortion
is the abortion occurring at any time due to natural causes.
Justifiable or therapeutic abortion: Abortion is justifiable only when it is done in good faith to save the life of a woman, if it is materially endangered by the continuance of pregnancy. The World Medical Association in 1970, adopted a resolution on therapeutic abortion, known as Declaration of Oslo.
Criminal abortion is the induced destruction and expulsion of the foetus from womb of the mother unlwfully, i.e., when there is no therapeutic indication for the operation.

Under S.312, IPC, whoever voluntarily causes criminal abortion is liable for imprisonment up to 3 years, and/or fine; and if the woman is quick with child, the imprisonment may extend up to 7 years.
If the means used to abort do not succeed, it is punishable under S.511, IPC with imprisonment up to half of the punishment under S.312.
Under S.313, IPC, if the miscarriage is caused without the consent of the woman, the imprisonment may be up to 10 years.
Under S.314, IPC, if a pregnant woman dies from an act intended to cause miscarriage, the offender is liable to be punished with imprisonment up to 10 years.
Under S.315, IPC, a person doing an act intended to prevent the child from being born alive or to cause to die after its birth is liable to be punished with imprisonment up to 10 years.
Under S.316, IPC, causing death of quick unborn child by any act amounts to culpable homicide, and the punishment may extend up to 10 years imprisonment.

The medical termination of pregnancy act was passed in 1971. Under this act, pregnancy can be terminated under the following conditions: (1) Therapeutic (2) Eugenic (3) Humanitarian (4) social.
Therapeutic abortion is indicated when the continuation of pregnancy endangers the life of a woman or may cause serious injury to her physical or mental health.

Eugenic: When there is risk of the child being born with serious physical or mental abnormalities. This may occur: (A) If the pregnant mother in the first three months suffers from German measles, small-pox or chicken-pox, viral hepatitis, toxoplasmosis, any severe viral infection (B) If the pregnant mother is treated with drugs like thalidomide, cortisone, etc (C) Mother is treated by X-rays or radio-isotopes (D) Insanity of the parents

Humanitarian: when pregnancy is caused by rape
Social: (A) Failure of contraceptive techniques in case of a married woman (B) when social or economic environment, actual or reasonably expected can injure the mother’s health.

Only a qualified RMP possessing experience can terminate pregnancy. A RMP can qualify if he has assisted in performance of 25 cases of M.T.P in a recognised hospital. The consent of the woman is required before conducting abortion; written consent of the guardian is required if the woman is a minor or lunatic. Consent of husband is not necessary. The age of women for abortion is over 18 years. MTP act, 1971 allows termination of pregnancy up to 20 weeks. If the period of pregnancy is below 12 weeks, it can be terminated on the opinion of a single doctor. If the period of pregnancy is between 12 and 20 weeks, two doctors must give opinion that there is an indication. The doctor is protected from any legal action for any damage caused or likely to be caused in terminating pregnancy, provided he has acted in good faith and exercised proper care and skill.

Methods of procuring criminal abortion:
(I) Abortifacient drugs: which produce congestion of the uterine mucosa and then uterine bleeding, followed by contraction of the uterine muscle and expulsion of the foetus, or they cause the uterine contraction by stimulating the myometrium directly.
(i) Drugs that act directly on the uterus:
(A) Ecbolics: They increase uterine contraction and are likely to cause abortion. Eg., Ergot, Hydrastis canadensis, Quinine, Lead in the form of pills made from diachylon (lead oleate) or lead palster is commonly used.
(B) Emmenagogues: They produce or increase menstrual flow. The chiel of these are savin, borax, apiol, rue, laburnum, oestrogens, sanguinarin, senacio, caulophyllin, hellebore, etc.
(iii) Irritants of the Genito-urinary tract: They produce reflex uterine contractions, e.g., oil of pennyroyal, oil of tansy, oil of turpentine, cantharides, etc
(iv) Irritants of the Gastro-intestinal tract: Any substance which causes irritation of the colon may produce hyperaemia and contractions of uterus. Saline cathartics, such as magnesium sulphate or drastic purgatives, such as, aloes, calomel, castor oil, croton oil, jalap, colocynth etc are commonly used.
(v) Drugs having poisonous effects on the body: (a) Inorganic irritants: e.g., lead, copper, iron, mercury, and antimony (b) Organic irritants: e.g., cantharides, unripe fruit of pappaya, unripe fruit of pineapple, seeds of moringa, juice of calotropis, bark of plumbago rosea, saffron, etc.
(II) General violence: It acts directly on the uterus, or indirectly producing congestion of pelvic organs, or hemorrhages between uterus and membranes.
(i) Intentional: (1) Severe pressure on abdomen by blows, kicks, jumping, etc and massage of the uterus through the abdominal wall. (2) Violent exercise like horse riding, cycling, jumping from height, running upstairs, etc. (3) Cupping.
(ii) Accidental:
(III) Local violence: (1) Syringing (2) Rupture of the membranes (3) Dilation of the cervix (4) Abortion stick (5) Air insufflations (5) Electricity (6) Curettage (7) Pastes.

Methods for therapeutic abortion: The common methods are
(1) Low rupture of membranes
(2) Utus paste injection
(3) Dilatation of cervix and oxytocic infusion, or a direct injection of 10 units of oxytocin into the uterus causing abortion
(4) Dilatation of the cervix and evacuation of the uterus by curettage, during the first three months.
(5) Prostaglandins
(6) Amniotic fluid replacement therapy
(7) Vaccum aspiration.
(8) Abdominal hysterectomy

Doctor’s duties in a case of criminal abortion:
The doctor should keep all the information obtained by him as a professional secret. He must ask the patient to make a statement about the induction of criminal abortion. He must treat her to the best of his ability. He must consult a professional colleague. If the woman’s condition is serious, he must arrange to record the dying declaration. If the woman dies, he should not issue a death certificate, but he should inform the police.

According to the Infanticide Act of England (1938), infanticide means the unlawful destruction of a child under the age of one year. In India, there is no such special Act, and as such there is no difference between the murder of newborn infant and that of any other individual. Foeticide is the killing of a fetus at any time prior to birth.

A Stillborn child is one, which is born after 28th week of pregnancy, and which did not breathe or show any other signs of life, at any time after being completely born.
Causes of still birth are: prematurity, anoxia of various types, birth trauma especially intracranial hemorrhage due to excessive moulding, placental abnormalities, toxaemias of pregnancy, erythroblastosis foetalis, and many types of congenital defects.

A dead-born child is one which has died in utero, and shows one of the following signs after it is completely born.

Signs of dead-born are: (1) Rigor mortis at delivery (2) Maceration (3) Mummification.

Maceration is a process of aseptic autolysis, and is the usual change. This occurs when the dead child remains in the uterus for about 3 or 4 days surrounded with liquor amnii but the exclusion of air. The earliest sign of maceration is skin slippage, which can be seen in 12 hours after the death of the child in utero. The body of a macerated fetus is soft, flaccid and flattens out when palced on a level surface. It has a sweetish, disagreeable odour.

Spalding’s sign: Loss of alignment and over-riding of the bones of the cranial vault occurs due to shrinkage of the cerebrum after the death of the foetus. The sign will develop within a few days of death of the foetus, but often takes much longer time, sometimes even 2 to 3 weeks.
Mummification occurs when the fetus dies from deficient supply of blood, when liquor amnii is scanty, and when no air enters uterus.

Viability of the infant: Viability means the physical ability of a fetus to lead a separate existence after birth apart from its mother, by virtue of a certain degree of development.
Livebirth means that the child showed signs of life when only part of the child was out of the mother, though the child may not have breathed or completely born. The causing of death of such a child is homicide.

Live-birth is probable when:
(1) All the lobes of the lungs are fully expanded with or without obstructive emphysema
(2) There is oedema of the lungs, especially gross
(3) An alveolar duct membrane is present and has widespread distribution in the lungs
(4) Pulmonary atelectasis due to obstruction of an alveolar duct membrane is present
(5) Contusions of the lung are present.

 Tests for live birth:

(A) Static test o Fodere’s test: Average weight of both lungs before respiration varies; 30 to 40 gm and after respiration 60 to 66 gm.
(B) Hydrostatic test: The specific gravity of lungs before respiration varies from 1040 to 1050 and after respiration about 940, so it floats in water.
(C) Plocquet’s test: Weight of lungs to body. 1:70 – unrespired lung, 1:35 – respired lung
(D) Wredin’s test: For air in the middle ear.
(E) Breslow’s sign: For air in stomach and duodenum.
Still-birth is probable in the presence of:
(1) Maceration of the infant
(2) Flooding of the lung with liquor amnii, and especially evidence of phagocytosis of meconium by the cells lining the cells
(3) Desquamation of the bronchial epithelium
(4) Distension of large bowel with meconium indicating a struggle to breathe.

Meconium is the green viscid substance consisting of thickened bile and mucus.
Caput succedaneum: is an area of soft swelling that forms in the scalp over the presenting part of the head in vertex presentations.

Cephalhematoma: is a localised accumulation of blood deep to the scalp, between the periosteum and bone surface.
Umbilical cord attached to the child shrinks and dries in 12 to 24 hours, and an inflammatory ring forms at the base in 36 to 48 hours. It mummifies on second to third day. The cord falls off on the fifth or sixth day and leaves an ulcer, which heals and forms a scar in 10 to 12 days.
Contraction of the umbilical arteries starts in about 10 hours and is completely closed by third day. The umbilical vein and ductus venous are closed on the fourth day. The ductus arteriosus closes by tenth day, and foramen ovale by second or third month.

Causes of death of the fetus may be due to (1) Natural causes, and (2) Unnatural causes.

Natural causes: (i) Immaturity (ii) Debility due to lack of genera development (iii) Congenital diseases (iv) Malformations (v) Haemorrhage from the umbilical-cord, genital organs, stomach, rectum, etc (vi) Post-maturity (vii) Pre-eclamptic toxaemia (viii) Disease of the placenta or its accidental seperation from the uterine wall (ix) Placenta praevia or abnormal pregnancy (x) Neonatal infection (xi) Intrapartum or ante-partum anoxia (xii) Cerebral birth trauma (xiii) Erythroblastosis foetalis.
Unnatural causes: These may be (1) Accidental, and (2) Criminal

(1) Accidental causes: (a) During birth: Prolonged labour, prolapse of cord or pressure on the cord, twisting of the cord around the neck or knots of the cord, injuries to the mother, death of the mother. (b) After birth: Suffocation.

(2) Criminal causes: These may be (1) Acts of commission, and (2) Acts of omission
(a) Acts of commission: Suffocation, strangulation, drowning, burning, blunt head injury, fracture and dislocation of cervical vertebrae, wounds, poison.
(b) Acts of omission or neglect.

The abandoning of infants: If the father or mother of a child under the age of 12 years, or anyone having the care of such child, leaves such a child in any place with the intention of abandoning the child, shall be punished with imprisonment up to 7 years (S. 317, IPC).

Concealment of birth: Whoever, secretly buries or otherwise disposes of the dead body of a child, whether such child dies before or after or during its birth, intentionally conceals the birth of such child, shall be punished with imprisonment up to 2 years (S. 318, IPC).

 Sudden infant death syndrome
(SIDS), or cot death or crib death is defined as the sudden and unexpected death of seemingly healthy infant, whose death remains unexplained even after a complete autopsy. Accepted hypothesis is sleep apnoea.

Battered baby syndrome: A battered baby is one who has received injuries as a result of non-accidental violence, produced by a parent or guardian. The classical features are the obvious discrepancy between the nature of injuries, and explanation given by the parents, and delay between the injury and medical attention which cannot be explained.

Diagnosis of BBS: (1) Nature of injuries (2) time taken to seek medical advice (3) recurrent injuries.
DD of BBS: Scurvy, congenital syphilis and osteogenesis imperfecta, (except – osteomyelitis).

The source of the blood (human or animal) is determined by the Serologist of the Government of India at Calcutta. All stains should be sent to the SFSL.

The chemical tests depend on the presence in the blood stains of an enzyme peroxidase, which in the presence of hydrogen peroxide, oxidises the active ingredient of the reagent and produces the characteristic coloured compound.

I. Benzidine test: Most reliable chemical test for blood. Add a drop of saturated solution of benzidine in glacial acetic acid and then a drop of 10 volumes hydrogen peroxide. If blood is present, dark blue colour is produced immediately. A positive reaction is given by blood of almost any age, blood that has been exposed to heat or cold. It detects blood when present in a dilution of one part of blood in 3 lakhs. If a negative reaction is obtained it is certain that the stain is not blood. After death, up to 150 years the test which is positive is Benzidine test.

II. Micro chemical examination:
1. Red corpuscles.
2. Haemin crystal test (Teichmann’s Test)—A small crystal of sodium chloride and 2 to 3 drops of glacial acetic acid are placed on a glass slide. Brownish-black rhombic crystals of haemin or haematin chloride arranged singly or in clustors are seen if blood is present.
3. Haemochromogen crystal test (Takayama test) – Place a small piece of suspected material on a glass slide and add 2 or 3 drops of Takayama reagent (sodium hydroxide, pyridine, glucose), and cover with a coverslip. Pink, feathery crystals of hemochromogen or reduced alkaline hematin arranged in clusters, sheaves, etc., appear in one to six minutes. It is delicate and more reliable.

III. Spectroscopic examination:
— It is the most delicate, specific and reliable test for detecting the presence of blood in both recent and old stains.
IV. Serological examination: This determines whether the blood is derived from human being or from a lower animal.
(A) Immunological methods: (1) Precipitin test (2) Antiglobulin consumption test (3) Gel diffusion (4) Double diffusion in agar gel (5) Precipitation-electrophoresis
(B) Isoenzyme methods

For Blood Stains
1. Magrath test—If blood is present, luminescence is seen.
2. Takayama’s test—Haemochromogen crystal test. Delicate and reliable test. Pink, feathery structure.
3. Tiechmann’s test—Haemin crystal test, microscopy test
4. Precipitin test—Confirm blood of human origin.
5. Phenolphthalein test—Kastle-Mayer test -> pink-purple, ex mely delicate.
6. Benzidine test—Best preliminary test, blue colour.
7. Chromatography—Absorption spectroscopy is the best te
8. Guicum test—Deep blue.
9. Leuco malachite test—Peacock-blue colour.


Psychiatry deals with the study, diagnosis and treatment of mental illness. Forensic psychiatry deals with the application of psychiatry in the administration of justice.

Insanity or soundness of mind can be defined as a disease of the mind or the personality, in which there is derangement of the mental or emotional processes.
Aphasia: The loss of ability to express meaning by the use of speech or writing (motor aphasia), or to understand spoken or written language (sensory aphasia).

Delirium: It is a disturbance of consciousness in which orientation is impaired, critical faculty is blunted or lost and thought content is irrelevant or inconsistent. It occurs in physical disease with high fever, overwork, mental stress, metabolic disease, cerebral neoplasm or drug intoxication. Such persons are not responsible for their criminal acts.

Delusion: It is a false belief in something which is not a fact, and which persists even after its falsity has been clearly demonstrated. It is a disorder of thought.

(i) Grandeur or exaltation—A man imagines himself to be very rich while in reality he is a pauper.
(ii) Persecution—Person imagines that attempts are being made to poison him by his near relatives,
(iii) Reference—The person believes that people, things, events etc. refer to him in a special way.
(iv) Influence—His thought, feelings and actions are being influenced and controlled by some outside agencies.
(v) Infidelity—A man imagines his wife to be unfaithful while in fact she is chaste.
(vi) Nihilistic—The person declares that he does not exist or that there is no world seen in major depression.
(vii) Hypochondriacal—The person believes that there is something wrong with his body, though in fact he is healthy.
Such person is not responsible for his antisocial act.

Hallucination is a false sense of perception, without any external object or stimulus to produce it. They are purely imaginary and may affect any or all the special sense organs.
(i) Visual: A person imagines of being attacked by a lion when no lion exists (most commonly seen in delirium).
(ii) Auditory: A person hears voices, when no one is present (schizophrenia).
(iii) Olfactory: A person smells pleasant or unpleasant odour when none is present.
(iv) Gustatory: A person feels different types of taste in the mouth though no food actually is present.
(v) Tactile: A man imagines rats and mice crawling into his bed (Magnan symptom or, cocaine bug).
Hallucinations occur in fevers, intoxications and insanity. Visual and auditory hallucinations are most common. A person suffering from unpleasant hallucination may commit suicide or homicide. Olfactory hallucination is seen in temporal epilepsy.

Illusion is a false interpretation by the senses of an external object or stimulus which has a real existence e.g. a lion for a dog, or hears the notes of birds to human voice, imagines a string to be snake, stem of a tree for a ghost in dark. A sane person may experience illusion, but is capable of correcting the false impressions. An insane person continues to believe in the illusions even though the real facts are clearly pointed out.

This is a sudden and irresistible force compelling a person to the conscious performance of some action without motive or fore-thought. A sane person is capable of controlling an impulse, but an in¬sane person may do things on impulse.
(i) Kleptomania—An irresistible desire to steal articles of little value.
(ii) Pyromania—An irresistible desire to set fire to things.
(iii) Mutilomania—An irresistible desire to mutilate animals.
(iv) Dipsomania—An irresistible desire for alcoholic drinks at periodic intervals.
(v) Sexual impulses—including sexual perversions.
(vi) Suicidal and Homicidal impulses.

Obsession: In this, a single idea, thought or emotion is constantly entertained by a person which he recognises as irrational, but persists inspite of all efforts to drive it from his mind. It is a disorder of content of thought. Any attempt to resist makes them appear more insistent. It is a borderline between sanity and insanity e.g. continuous checking of bolting of door of husband’s room, a wife may continuously believe her husband to be unfaithful.

Phobia: It is an excessive or irrational fear of a particular object or situation.

Lucid Interval: This is a period occurring in insanity during which all the symptoms of insanity disappear completely. The individual is able to judge his acts soundly and he becomes legally liable for his acts. If he commits an offence, he cannot be completely held responsible, because it is difficult to know whether he was suffering from some mental abnormality at the time of committing the offence. In mania and melancholia, lucid intervals are common.

Difference between Psychosis and Neurosis
Trait                           Psychosis                                        Neurosis
1. Nature A disease entity with physical basis which determined genetically—— A reaction to stressful circumstances due to adverse childhood experience
2. Severity                   Major                                             Minor
3. Empathy                  Absent                                            Present
4 Contact with reality    Absent                                            Present
5. Insight                     Absent                                            Present

Psychopath: A person who is neither insane nor mentally defective, but fails to conform to normal standards of behaviour.

 Psychopathic disorder:
It is a persistent disorder or disability of mind which results in abnormally aggressive or seriously irresponsible conduct or a part of the person.

Psychopathic personality: An antisocial person who has been emotionally unstable from childhood or adolescence, but has normal intelligence. He lacks foresight and fails to learn from punishment.

Psychoses: They are characterised by a withdrawal from reality; a living in a world of fantasy.
Neuroses: The patient suffers from emotional or intellectual disorders, but he does not lose touch with reality.
Neurasthenia: It is a condition of nervous exhaustion due to physical or mental conditions. There is abnormal fatigue and irritability of the nervous system.

Mutism: It is complete loss of speech. It is seen in hysteria, catatonic schizophrenia, depression, organic brain lesion and malingering.

Causes of Insanity:
(i) Hereditary, e.g. Huntington’s chorea and amaurotic family idiocy.
(ii) Environmental factors e.g. faulty parental attitude and lack of mental hygiene.
(iii) Psychogenic e.g. unsuccessfully repressed mental conflicts.
(iv) Precipitating e.g. financial and business worries, frustrations and disappointment in sexual affairs, death of close relatives, senile degeneration, myxoedema, pernicious anemia etc.

Classification of Insanity (W.H.O. 1965)
(A) Organic psychoses: (1) Senile and presenile dementia (2) Alcoholic psychosis (3) Associated with intracranial infections, e.g. epidemic ence¬phalitis, abscess, meningitis, tuberculosis, G.P.I, etc. (4) Associated with cerebral arteriosclerosis, epilepsy, intra¬cranial tumours, degenerative diseases, brain anomalies etc (5) Associated with other physical conditions such as endocrine, metabolic and nutritional disorders etc.
(B) Functional psychoses:
(a) Schizophrenia: 1. Simple type 2. Hebephrenic type, 3. Catatonic type, 4. Paranoid and other atypical or unspecified form.
(b) Affective type: 1. Involutional melancholia. 2. Manic-depressive 3. Paranoid states 4. Other atypical forms.

II. NEUROSES: 1. Anxiety neurosis 2. Hysterical-neurosis 3. Phobic 4. Obsessive-compulsive 5. Depressive 6. Depersonalisation syndrome 7. Hypochondriacal 8. Unspecified neurosis.


Mental Subnormality: (Oligophrenia, amentia)
1. Idiocy: Idiots are defined as persons so defective in mind from birth or an early age, that they are unable to guard themselves against ordinary physical dangers. Their mental age does not exceed that of a normal of 3 years. Intelligent quotient (I. Q) 0-20 (profound retardation).
2. Imbecility: Imbeciles are persons who are so defective in mind birth or an early age, that they are incapable of mane themselves or their affairs. An imbecile child is incapable of being taught. Their mental age ranges between that of normal child of 3 to 7 years. I.Q. 20-50 (moderate retardation).
3. Feeble minded (Moron): In these mental defects, not amounting to imbecility exists from birth or an early age, and they require care, super¬vision and control for their protection. Mental age 6 to 11 years. I.Q. 50-75 (Mild retardation).
4. Normal I.Q: It is more than 90. Mental retardation is I.Q. less than 70.

I.Q. = M.A/C.A x 100 (M.A.-Mental age; C.A – Chronological age)

Psychosis associated with Organic diseases:
1) Pre-senile dementia: Dementia is a condition in which there is degeneration of mental faculty after they have been fully developed.
2) Senile dementia: It is caused due to arteriosclerosis and old age. It usually starts after 65 years.
3) Cerebral tumours.
4) Cerebral trauma: It causes concussion and post-traumatic automatism.
5) Drug induced Psychosis: Dependence on barbiturates, amphetamines, cannabis, heroin, cocaine etc. lead to Psychosis. Cocaine, LSD, amphetamines and mescaline can produce clinical symptoms similar to schizophrenia.
6) Toxic Psychosis: Heavy metals, such as arsenic and mercury produce mental degeneration.
7) Deficiency states: (i) Deficiency of cyanocobalamin—pernicious anemia, (ii) Nicotinic acid—pellagra. (iii) Thyroxine—myxoedema. (iv) Pituitary hormones—hypopituitarism. (v) Hypoglycemia produces mental degeneration.

8) Alcoholism:
a. Alcoholic blackouts—Amnesia of several hours for events during a drinking session.
b. Delirium tremens—It usually occurs in a chronic drunkard, (i) One-two days after sudden withdrawal of alcohol. (ii) Due to heavy drinking. (iii) Injuries, infection and shock act as precipitating factor. This is the commonest type of Psychosis in the chronic alcoholic. The patient becomes sleepless, restless, irritable and then develops disorders of perception and coarse muscular tremors of face, tongue and hands. Disorientation and hallucinations of sight and hearing are common. He may be incited to commit suicide, homicide or violent assault. Symptoms usually last for 3 to 7 days. Such persons are not criminally responsible.
c. Alcoholic hallucinosis.
d. Korsakov’s psychosis: It is characterised by loss of memory for recent events both retrograde and antero-grade. The physical component of this syndrome consists of ophthalmoplegia, ataxia, and peripheral neuritis and is known as Wernick’s encephalopathy.
9) General Paralysis of insane: This is a chronic progressive condition leading to paralysis and dementia. It is usually associated with meningo-vascular syphilis and tabes dorsalis. The memory is impaired and thought retarded.
10) Epileptic Psychosis.

Functional Psychosis: This is a disease of hereditary origin affecting young adults and forms a major group of all psychiatric illnesses.

I. Schizophrenia: It is a condition of split personality, in which the patient loses his contact with environment. It is primarily a disorder of thinking (cognition).
It is characterised by splitting of different psychic functions: (1) Disorders of behaviour: withdrawal from reality, pre-occupation with the self (narcissism), depersonalization, passivity of thought. (2) Disorders of thought: confused thoughts leading to thought block, neologism. (3) Disorders of affect: depression, elation, inappropriate moods, anxiety and blunting of emotions. (4) Delusions: of grandeur, paranoid, hypochondriac and influence. (5) Hallucinations—commonly auditory, sometimes visual and tactile. (6) Personality deterioration: affecting his work, family and social relationships.

Schizophrenia is the commonest type of insanity in homicidal crimes.
The types are:
(1) Simple schizophrenia: It begins in early adolescence. There is a gradual loss of interest in the outside world from which he withdraws. He becomes emotionally flat and apathetic and has difficulty in forming social relationships.
(2) Hebephrenia: it begins in adolescents or young adults. Thinking process is disturbed. Wild excitement, illusions, hallucinations and bizarre delusions are present.
(3) Catatonia: This is characterised by alternating stages of depression, excitement and stupor, impulsive suicidal or homicidal attacks and auditory hallucinations are common.
(4) Paranoid schizophrenia: Paranoid schizophrenia develops insidiously in the fourth decade. It is characterised by suspicion, delusions of persecution and auditory hallucinations. At first delusions are indefinite, but later they become fixed on some person.

II. Affective types:
Manic-depressive psychosis:— The primary disturbance is of affect. The mood varies between extremes of joy and sadness. It occurs periodically.

In diagnosis of Insanity, person should be kept under observation up to a maximum 30 days.
Feigned Insanity—Insanity may be feigned by criminals to evade sentence of death or long term prison, by soldiers and policemen to leave the service, and by businessmen to avoid contract.

Neurosis: This forms a group of personality disturbances resulting from reactions to life situations. They may occur singly or in combination.

1. Anxiety Neurosis
2. Hysterical Neurosis: It is common in young females but may occur in old ladies whose nervous system starts degenerating. The patient shows deafness, blindness, loss of smell, anaesthesia, paraesthesia, paralysis, aphonia, amnesia, fainting fits, anorexia etc
3. Phobic Neurosis

Type of Phobia Fear of
(i) Agaraphobia —» Fear of open spaces
(ii) Claustrophobia —> closed spaces
(iii) Necrophobia —» dead bodies
(iv) Nyctophobia —> darkness
(v) Phonophobia —» sound
(vi) Thanatophobia —> death
(vii) Pathophobia —> disease
(viii) Toxiphobia —> being poisoned
(ix) Hydrophobia —> fear of water, seen in rabies
(x) Acrophobia —» fear of height
(xi) Sitophobia —> fear of eating
(xii) Social phobia —> public performance
(xiii) Aerophobia —> Air
(xiv) Algophobia —> Pain.
It interferes with daily activity.
4. Depressive Neurosis.
5. Obsessive compulsive neurosis.

Indian Lunacy Act was passed in 1912. It was repealed by the Mental Health Act. 1987. The Mental Health Act was enacted by parliament to consolidate and amend the law relating to the treatment and care of “mentally-ill person” to make better provision with respect to their property and affairs and for matters concerned with”.

Mental Disorder and Responsibility
: Responsibility, in the legal sense, means the liability of a person for his acts or omissions, and if these are against the law, the liability to be punished for them.

Civil responsibility: the question of civil responsibility arises in the following conditions.
(1) Management of property and affairs: If on enquiry, a person is found incapable of managing his property and affairs, but is not dangerous to himself or to others, the Court appoints a manager to look after his property, granting him necessary power.
(2) Insanity and contracts: A contract is invalid if one of the parties at the time of making it was incapable of understanding what he was doing due to insanity. The mental disorder of partner does not itself dissolve the partnership, unless steps are taken for dissolution.
(3) Insanity and marriage contract: A marriage is considered invalid, if at the time of marriage either party (1) is incapable of giving valid consent due to insanity, or (2) though capable of giving valid consent, has been suffering from such a kind or degree of mental disorder as to be unfit for marriage and procreation, or (3) has been suffering from recurrent attacks of insanity or epilepsy.
(4) The competence of insane to be a witness: An insane person is not competent to give evidence if he cannot understand the necessity of telling the truth due to insanity. An insane person is competent to give evidence during the period of lucid interval.
(5) Consent and insanity: Consent to certain acts like sexual intercourse or hurt is not valid if such consent is given by a person who from unsoundness of mind, is unable to understand the nature and consequences of that of which he gives consent.
(6) Insanity and testamentary capacity: Testamentary capacity (testament = will) is the mental ability of a person to make a valid will. The requirements of a valid will are follows. A written and properly signed and witnessed document must exist. The testator must be major, and of sound disposing mind, at the time of making the will. No force, undue influence, or dishonest representation of facts, should have been applied by others. Persons can make valid wills during lucid interval. The most common symptom of absence of legal capacity is impairment of memory. The most important thing to determine is whether at the time of making the will, the testator understood the business in which he was engaged, and knew how he wanted to dispose of his property.

Criminal responsibility:
The law presumes that every person is sane and responsible for his actions. The defense has to prove that the accused is insane. The law presumes that for every criminal act, there must be criminal intent or mind = mens rea (mens = mind; rea = criminal) motivating it.
The following are the tests for detecting criminal responsibility of an insane person.
1. Mc Naughten Rule (the right or wrong test; the legal test): English courts, in dealing with the responsibility of the insane in criminal cases are guided by the rules laid down after the Mc Naughten trial in 1843. The most important of this rule is as follows:—“an accused person is not criminally responsible, if it is clearly proved, that at the time of committing the crime that he was suffering from such a defect of reason from abnormality of mind, that he did not know the nature and quality of act he is doing, or that what he was doing was wrong”. This legal test has also been accepted in India as the law of criminal responsibilities under sec. 84, IPC.
2. Durham rule: “An accused person is not criminally responsible, if his unlawful act is the product of mental disease or mental defect”.
3. Curren’s rule: “An accused person is not criminally responsible, if at the time of committing the act, he did not have the capacity to regulate his conduct to the requirements of the law, as a result of mental disease or defect.
4. The irresistible impulse test: “An accused person is not criminally responsible, even if he knows the nature and quality of his act and knows that it is wrong, if he is incapable of restraining himself from committing the act, because the free agency of his will has been destroyed by mental disease”.
5. The American law institute test: “A person is not responsible for criminal conduct, if at the time of such conduct, as a result of mental disease or defect, he lacks adequate capacity either to appreciate the criminality of his conduct, or to adjust his conduct to the requirements of the law”.

It is the conduct of a person whose consciousness is impaired to such an extent that he is not fully aware of actions. Main factors producing automatism: (i) Epilepsy (ii) Concussion (iii) Hypoglycemia (iv) Somnambulism (Non-insane automatism).

Somnambulism: It means walking during sleep.
Somnolentia (semisomnolence): It is often called sleep-drunkenness and is midway between sleep and walking.

Impulse: Some crimes are committed due to an impulse in which the person loses self control, such as sudden violent anger. Such persons are criminally responsible unless insanity is present.
Hypnotism or Mesmerism: This is a sleep like condition produced by artificial means or, by suggestions
Delirium: A delirious person may commit violent criminal acts due to delusions and hallucinations. He is not legally responsible for the acts committed during delirium.

(i) An intoxicated person (voluntary drunkenness) is criminally responsible if he has intention or knowledge of committing a crime.
(ii) Mental disorder brought about by drugs and delirium tremens due to drink frees one of criminal responsibility. Also in post-traumatic automatism, twilight state and paranoid states, the person is free from criminal responsibilities.

Types of personality disorders:
(a) Paranoid—suspicious
(b) Schizoid—withdrawn, emotional coldness
(c) Schizo-typal—oddities of thinking
(d) Histrionic—attention seeking
(e) Narcissistic—self-centered
(f) Antisocial—flouting norms
(g) Avoidant—low self esteem
(h) Borderline—unpredictable
(i) Dependent—seeking human contact
(j) Compulsive—perfectionist
(k) Passive aggressive—procrastination. — There is no definite treatment.

Psychic dependence: (i) Cocaine (ii) Marijuana (iii) Amphetamine (iv) LSD

Physical dependence and Psychic both: (i) Opiates (ii) Alcohol (iii) Barbiturates.

Clinical toxicity in alcohol: (i) Fatty liver (ii) Cirrhosis (iii) Pancreatitis (acute chronic)
(iv) Wemicke-Korsakoff syndrome (v) Peripheral neuropathy (vi) Gynecomastia (vii) Amenorrhea.

Psychiatric emergencies are: (i) Delirium (ii) Bereavement (iii) Suicide (iv) Mania (iv) Panic attack.

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Forensic Medicine & Toxicology – A comprehensive study -1

stethDr  Sanil Kumar BHMS MD(Hom)
Department of Forensic Medicine & Toxicology
Govt Homeopathic Medical College. Calicut
Email : drsakumkumar@yahoo.co.in

The general public is fast becoming law conscious and the doctors are being sued from time to time in a Court of law for their acts of omission or commission. Therefore, it is incumbent upon doctors must  have a good knowledge of the law governing their profession, in order not to transgress the law.

History: The Code of Hammurabi, King of Babylon (about 4000 to 3000 B.C) is the oldest known medico-legal code. The first medico-legal autopsy was done in Bologna (Italy) in 1302, by Bartolomeo De Varignana. The first book on Forensic Medicine was published in 1602 by an Italian physician, Fortunato Fedele. Orfila (professor of chemistry and legal medicine at Paris) is considered the founder of modern toxicology. Paulus Zacchias — written “medico-legal questions”, questions Medico legalis.”

a. In the 18th century, study in legal Medicine as a subject was established by appointing professorship in Germany.
b. In England Mc Naughten’s (who was aschizophrenic) rule has been established to deal with legal matters in cases of insanity or like situations whatsoever

Forensic medicine: is the application of medical and paramedical knowledge in the administration of law and justice. Legal medicine and state medicine are other names for it.

Medical jurisprudence: deals with the legal rights, privileges, duties and obligations of medical practitioner.

LEGAL PROCEDUREInquest: is the legal or judicial inquiry to ascertain matter or fact. (Cr.P.C. 174)
It is the investigation into the cause of death. It is conducted in cases of murder, suicide, accidents and suspicious deaths.
1) Police inquest: done by the Officer-in-charge of the police station (S.174, Cr.P.C). Medico-legal autopsy is ordinarily done on requisition of the sub-inspector of police. The inquest report is signed by the police officer and two witnesses.
2) Coroner’s inquest: in Bombay till 1999. Coroner’s court is a court of enquiry and not of trial.
3) Magistrate’s inquest: done by an Executive Magistrate (Collector, Deputy collector, Tahsildar, etc) in cases of death in police custody, death due to police firing, death in prison, dowry death & exhumation (S.176, Cr.P.C).

Courts of law: Criminal and Civil.

  1. Supreme Court: is the highest court and has power of supervision over all courts of law. It is purely an appellate court. A supreme court Judge can pass any sentence authorized by law.
  2. High Court: highest court for state. It may try any case and pass any sentence authorized by law.
  3. Sessions Court: can pass any sentence authorized by law, but a death sentence passed by it must be confirmed by the High court (S.366, Cr.P.C). An Assistant Sessions court can pass a sentence of imprisonment up to 10 years.
  4. Magistrate Courts are of 3 types:

a) Chief Judicial Magistrate: can pass a sentence of imprisonment up to 7 years and any amount of fine.
b) I Class Judicial Magistrate: can pass a sentence of imprisonment up to 3 years and fine up to 5000 rupees.
c) II Class Judicial Magistrate: can pass a sentence of imprisonment up to 1 year and fine up to 1000 rupees.

Offence may be Cognisable or non-cognisable.
Cognisable offence: It is an offence in which a police officer can arrest a person without warrant from the Magistrate, e.g., rape, murder, robbery, etc.

The common punishments allowed by law awarded are:
(i) Death (hanged by neck till death)
(ii) Imprisonment for life. (Max. up to 20 years)
(iii) Imprisonment of sometime but less severe than life imprisonment. This may be the form of simple or rigorous imprisonment.
(iv) Monetary fine (Sec.53, I.P.C)
(v) Detentions in reformatories. DRC

The death sentence can be commuted by the President of India (on mercy appeal), by Supreme Court of India (on appeal or by the High Court by merits).

Subpoena or Summons: is a written document issued by the court and served on the witness under a penalty in all cases by the Police officer to attend the court for giving evidence on a particular day and time (S.174, I.P.C; S. 87, Cr.P.C). It may be served from a criminal or civil court. The witness will be excused from attending the court, if he has a valid and urgent reason. If the witness fails to attend the Court: (1) in a civil case, he will be liable to pay damages, and (2) in a criminal case, to fine or imprisonment (S. 172, I.P.C).

Conduct money is fee paid to a witness at the time of serving the summons to cover the expenses for attending the court. Given only in civil cases. In no case the medical practitioner should insist on conduct money when he receives a subpoena from Criminal court because he is liable to be charged with contempt of court.

Perjury means giving willful false evidence while under oath, or failure to tell what he knows or believes to be true (S.191, I.P.C). The witness is liable to be prosecuted for perjury, and the imprisonment may extend to 7 years (S. 193, I.P.C).

Record of evidence: (S. 137, I.E.A)
(1) Oath
(2) Examination-in-chief (direct examination)
This is the first examination of a witness and consists of questions put to him by the lawyer (counsel or advocate) for the side which has summoned him. In government prosecution cases, the public prosecutor first examines the witness. Leading questions are not allowed except when the witness is hostile.
(3) Cross-examination
In this, the witness is questioned by the lawyer for the opposite party, i.e., lawyer for the accused (defense lawyer). Leading questions are allowed. The court has the power to disallow questions which are intended to insult or annoy or offensive in form (S. 152, I.E.A)
(4) Re-examination (Re-direct examination) (S. 137, I.E.A)
This is conducted by the lawyer for the side which has called the witness. The opposite lawyer has the right of re-cross examination on the new point raised. Leading questions are not allowed.
(5) Questions by judge
The court is also empowered (S. 311, Cr.P.C), to recall and reexamine any witness already examined, if his evidence appears to the Court to be essential to the just decision of the Court. The judge may ask any questions at any stage of the examinations to clear up doubts.

Medical evidence: Evidence means all legal means, which help to prove or disprove any matter in question.
Types: Oral, Documentary, Direct, Indirect or circumstantial, Hearsay

A. Documentary evidence. 3 types: MC, DC, Dying declaration.
1. Medical certificate: it refers to ill-health, insanity, death, etc. they are accepted in a Court of law, only when they are issued by a qualified RMP. A medical practitioner is legally bound to give a death certificate, stating the cause of death without charging fee, if a person whom he has been attending during his last illness dies (Registration of Birth and Deaths Act, 1970). The certificate should not be given if the doctor is not sure of the cause of death, or if there is the least suspicion of foul play. In such cases, the matter should be reported to the police. Issuing or signing a false certificate is punishable under S. 197, I.P.C.
Death certificate: In India, the International Statistical Classification of Death,
Injuries and Causes of Death is used.

2. Medico-legal reports: are reports prepared by a doctor on the request of the investigating officer for his guidance, usually in criminal cases, e.g., assault, rape, murder, poisoning, etc. These are admitted as evidence in court only when the doctor gives oral evidence on oath.

3. Dying declaration: It is a written or oral statement of a person, who is dying as a result of some unlawful act, relating to the material facts of cause of his death or bearing on the circumstances. A magistrate should be called to record the declaration. If the patient’s condition is serious, and there is no time to call a Magistrate, the doctor should take the declaration in the presence of two witnesses. The person need not take oath, because of the belief that a dying person tells the truth. Leading questions should not be asked. It should be read over to the declarant, and his signature or thumb impression is taken. The doctor and the witness should also sign the declaration. If the declarant survives, the declaration is not admitted, and the person is called to give oral evidence.

4. Dying deposition is a statement of a person on oath, recorded by a Magistrate in the presence of the accused or his lawyer, who is allowed to cross-examine the witness. It has greater value than dying declaration bcoz the accused has an opportunity of cross-examining the dying person. Not followed in India.

B. Oral evidence: it includes all statements which the Court permits, or which are required to be made before it by the witness, in relation to matters of facts under enquiry (S. 60, I.E.A). it must be evidence of a person who saw, heard or percieved it by that sense or in that manner. Oral evidence is more important than documentary evidence, as it permits cross-examination.
Exceptions to oral evidence:
(1) Dying declaration (S. 32 & 157, I.E.A)
(2) Expert opinion expressed in treatise (S. 60, I.E.A)
(3) Evidence of a doctor recorded in a lower Court (S. 291, I.E.A)
(4) Evidence of a witness in a previous judicial proceeding (S. 33, I.E.A)
(5) Reports of certain govt. scientific experts: Chemical examiner, Chief Inspector of Explosives, Director of Finger Print Bureau, Director of CFSL or SFSL, Director of Haffkine institute, Bombay and Serologist to the Govt. (S. 293, Cr. P.C)
(6) Public records, E.g., Birth and death, certificates of marriage.
(7) Hospital records: Routine entries are admissible without oral evidence.

Types of Witness
Common and Expert.
Common witness: (witness of fact; occurrence witness) is a person who gives evidence about the facts observed or percieved by him. “ First hand knowledge rule”

Expert witness: is a person who has been skilled in technical or scientific subject, and capable of drawing opinions and conclusions from the facts observed by himself, or noticed by others, e.g., doctor, firearms expert, finger prints expert, hand-writing expert, etc (S.45, I.E.A)
Hostile witness: is one who is supposed to have some interest or motive for concealing part of the truth, or for giving completely false evidence (S.191, I.P.C)

The medical profession is governed by legislation and by a Code of ethics and Etiquette. Medical ethics deals with the moral principles which should guide members of the medical profession in their dealings with each other, their patients and state. Enforcement of the code is done by the medical councils. (CCH).

Central Council of Homoeopathy Act, 1973. (19th December, 1973)
Amendment vide Homoeopathy Central Council of Amendment Act, 2002. Gazette of 9th December, 2002.
Schedule I: No: of elected members from each state.
(a) No: of RMP exceeds 100 – not exceeding 10000 = 1 seat
(b) No: of RMP exceeds 10000 – not exceeding 20000 = 2 seats
(c) No: of RMP exceeds 20000 – not exceeding 30000 = 3 seats
(d) No: of RMP exceeds 30000 – not exceeding 40000 = 4 seats
(e) More than 40000 RMP = 5 seats.

Schedule II: Recognized medical qualifications granted by Universities, Board or Medical Institutions in India.
Schedule III: Qualifications granted by medical institutions outside India.

1. Medical Register: the council maintains a register of medical practitioners who are enrolled on any State Medical Register.
2. Medical Education:
3. Recognition of foreign medical qualifications
4. Appeal against disciplinary action
5. Warning notice for serious misconduct.

Serious professional misconduct: (Infamous conduct in professional respect)
It is any conduct of the doctor which might reasonably be regarded as disgraceful or dishonourable. The conduct of the doctor is judged by professional men of good repute and competence. The main cause for penal erasure is serious professional misconduct. It deprives the doctor of all the privileges of a registered practitioner.

Warning notice
The following are some of the offences contained in the warning notice:-
1. Adultery (voluntary sexual intercourse between a married person, and a person married or not, other than his or her spouse)
2. Conviction by a court of law
3. Issuing false certificates
4. Performing criminal abortions or illegal operations
5. Dichotomy or fee splitting, i.e., receiving or giving commission to a professional colleague or a manufacturer or trader in drugs or appliances, or a dentist, chemist etc.
6. Covering, i.e., assisting some person who has no medical qualification to attend, treat or perform an operation on some person.
7. Advertisement – Repeated advertisement in a newspaper by a medical practitioner is an example of ethical negligence.
8. Using touts or agents for procuring patients.

Duties of Medical Practitioners
A. Doctor should:
1. Exercise reasonable degree of skill and knowledge
2. Attend a patient as long as he requires treatment
3. Prescribe or furnish suitable medicines
4. Warn patients of the dangers involved in the use of a prescribed drug or device
5. Inform patient of risk
6. Notify communicable diseases to the health authorities.
7. Maintain professional secrecy.

Privileged communication: It is a statement made bonafide upon any subject matter by a doctor to the concerned authority, due to his duty to protect the interests of the community or of the State.

Examples of privileged communication
1. A syphilitic taking bath in public pool
2. Engine or bus driver found to be colour blind
3. A person with infectious diseases working as a cook.
4. A doctor’s duty is to notify birth, death, infectious disease to public health authority.

Professional negligence (Malpraxis)
It is defined as absence of reasonable care and skill, or willful negligence of a medical practitioner in the treatment of a patient, which causes bodily injury or death of the patient. Negligence is defined as doing something that is not supposed to do, or failing to do something that one is supposed to do.

Medical negligence falls under following section – sec. 304 A, IPC 312, Indian contract act. (except – IPC 351.)
I. Civil negligence: Liability for negligence arises if the following conditions are satisfied:
a) Duty – Existence of a duty of care by the doctor
b) Dereliction – Failure of the doctor to maintain care and skill
c) Direct causation – The failure to exercise a duty of care must lead to damage
d) Damage – the damage which results must be reasonable anticipated.
A civil wrong is known as – ‘Tort”

The doctrine of res ipsa loquitor: It means the thing or fact speaks for itself.

Novus actus interveniens: It means an unrelated action intervening. A person is responsible for his actions and also for its consequences. This principle applies to cases of assault and accidental injury. If the doctor is negligent, which results from the logical consequence of events, then the responsibility for the subsequent disability or death may pass from the original incident to the later negligent action of the doctor by the principle of “novus actus interveniens”.

II. Criminal negligence: (Sec. 304A IPC). It occurs when the doctor shows lack of competency, gross inattention, criminal indifference to the patient’s safety, or gross negligence in the selection and application of remedies. It is practically limited to cases in which the patient has died. The doctor may be prosecuted by the police and charged in criminal court with having caused the death of the patient by a rash or negligent act not amounting to culpable homicide. The doctor can be punished with imprisonment up to 2 years, or with fine, or with both.

Contributory negligence: It is any reasonable conduct or absence of ordinary care on the part of the patient, or his personal attendant, which combined with the doctor’s negligence.

Therapeutic misadventure: It is a case in which an individual has been injured or had died due to some unintentional act by a doctor or agent of the doctor or hospital.
It may be subdivided into:
1) Therapeutic (when treatment is being given)
2) Diagnostic (where diagnosis only is the objective at the time)
3) Experimental (where the patient has agreed to serve as a subject in an experimental study).

Vicarious liability: (liability for act of another) An employer is responsible not only for his own negligence but also for the negligence of his employees, if such acts occur in the course of the employment and within its scope, by the principle of respondent superior (let the master answer).

Euthanasia (Mercy killing): It means producing painless death of a person suffering from hopelessly incurable and painful disease. It has no legal sanction in India.

Consent: means voluntary agreement, compliance or permission.
It may be: (i) Express (verbal or written) or (ii) Implied.

Reasons for obtaining consent:
(i) To examine, treat or operate upon a patient without consent is assault in law.
(ii) If there is no informed consent the doctor may be charged for negligence.

Rules for consent:
1. Oral consent should be obtained in the presence of a third party, e.g., nurse.
2. Written consent should be taken for court presentation.
3. The consent should be free, voluntary, clear, intelligent, informed, direct, and personal.
4. In medico-legal cases such as rape, pregnancy, delivery, abortion the woman should not be examined without her consent.
5. In case of a female, the examination should be made only by a or under the supervision of a female medical practitioner (S. 53, IPC)
6. An arrested person at his request may be examined by a doctor to detect evidence in his favour (S.54, IPC)
7. A person above 18 years can give consent to suffer any harm, which may result from an act not intended or not known to cause death or grievous hurt (Sec. 87, IPC).
8. A person can give valid consent to suffer any harm which may result from an act, not intended or not known to cause death, done in good faith and for its benefit (S.88 IPC)
9. Consent is not a defense in cases of professional negligence.
10. A child under 12 years cannot give valid consent to suffer any harm which may result from an act done in good faith and for its benefit. The consent of parent or guardian is taken (S. 89, IPC)

Malingering or shamming means conscious, planned feigning or pretending a disease for the sake of gain. Malingering can be diagnosed by keeping the patient under observation and watching him without his knowledge.

Consumer Protection Act (COPRA) passed on 1986, came into force in 1987.

Identification is the determination of the individuality of a person based on certain physical characteristics, i.e., exact fixation of personality.

Corpus delicti: (body of offence, essence of crime) means, the elements of any criminal offence. E.g., murder. The main part of corpus delicti is the establishment of identity of the dead body, and infliction of violence in a particular way, at a particular time and place, by the person or persons charged with the crime and none other.

Race: It can be determined by complexion, colour of eyes, hair, clothes and skeleton.
Cephalic index = Maximum breadth of skull / Maximum length of skull x 100.
It divides skull into (DOMBA)
1. Dolico-cephalic (long-headed) C.I. 70 to 85 – seen in pure Aryans, Aborigines and Negroes.
2. Mesati-cephalic (medium-headed) C.I. 75 to 80 – seen in Europeans and Chinese.
3. Brachy-cephalic (short-headed) C.I. 80 to 85 – seen in Mongolisms (Max C.I)

Sex: It has to be determined in cases of (1) Heirship, (2) Marriage, (3) Divorce, (4) Legitimacy, (5) Impotence, (6) Rape, etc.

Sex chromatin: is a small plano-convex mass, lying near nuclear membrane (Barr body).
Accuracy of sex determination from pelvis and skull is 98%. Barr body was first demonstrated by Dixon and Tarr. In buccal smear, barr body is present in 20 to 80 % of cells in the female (more than 25% cells are determined) and 0 to 4% in males. Buccal smear is used in determination of sex. Examination of blood is used in determination of sex. Neutrophil leucocytes contain a small nuclear appendage of drumstick form (Davidson body – help in sexing) in upto 6% of cells in the female but is absent in males.
Sex of a developing foetus can be determined at the end of 4th month of I.U life.

Intersex: It is an intermingling in one individual of characters of both sexes, in varying degrees, including physical form, reproductive organs and sexual behaviour. It results from some defect in the embryonic development.
It can be divided into four groups:
1) Gonadal agenesis – In this the testes or ovaries have never developed. The nuclear sex is negative.
2) Gonadal dysgenesis – External sexual structures are present, but at puberty the testes or ovaries fail to develop.
a) Klinefelter syndrome – The anatomical structure is male but the nuclear sexing is female. Sex chromosome is XXY (47 chromosomes). There is delay in onset of puberty, behavioral disorders and mental retardation. Small testis, infertility, gynaecomastia, azoospermia. Increased urinary gonadotropins.
b) Turner’s syndrome – The anatomical structure is female but the nuclear sexing is male. The sex chromosome pattern is XO (45 chromosomes). Earliest feature in newborn girl is oedema of hands and feet and loose nuchal folds. Other features – short stature, webbed neck – shield chest, renal defects – horse shoe kidney and duplication of renal pelvis, cardio-vascular defect – co-arctation of pelvis, skeletal disorder – cubitus vulgus, gonodal streaks – seen in turner’s syndrome, mental status – normal.
3) True hermaphroditism – In this an ovary and testis or two ovotestis are present within the external genitalia of both sexes.
4) Pseudo-hermaphroditism – Internally gonadal tissue of only one sex is seen, but external appearance is of the opposite sex.
a) Male pseudohermaphroditism: Nuclear sex is XY, but sex organs and sexual characteristics deviate to female form, because of testicular feminisation.
b) Female pseudohermaphroditism: Nuclear sex is XX, but deviation of sex organs and sexual characteristics towards male are seen, due to adrenal hyperplasia.
Skeleton: Recognizable sex differences do not appear until puberty except in pelvis, and the accuracy from this bone is about 75 to 80%. The determination of sex is based mainly upon the appearance of the pelvis, skull, sternum and the long bones.

Age can be determined from teeth, ossification of bones, secondary sexual characteristics, and general development in case of children.

1. Teeth: Teeth are useful for age determination (a) by the stage of development, and (b) by secondary changes.
Temporary teeth: these are 20 in number – 4 incisors, 2 canines, 4 molars in each jaw.
In ill-nourished children and in rickets, dentition may be delayed. In syphilis, dentition appears premature or even present at birth. Eruption of temporary teeth is for 2 – 2½ years. The temporary teeth begin to fall at about the sixth or seventh year after the eruption of first permanent molar. In children mixed dentition remains at 6 – 12 years of age.
Age 9: 12 permanent teeth, 8 I, and 4 1st molars + deciduous molars and canines.
Age 11: 20 permanent teeth, 8 I, 8 Pm and 4 M.
Age 14: 28 permanent teeth, and no deciduous teeth.
Permanent teeth are 32 in number: 4 incisors, 2 canines, 4 premolars, and 6 molars in each jaw.
Developmentally, teeth are divided into two sets:
(1) Superadded permanent teeth: Are those which do not have deciduous predecessors. (all permanent molars, 6 in each row)
(2) Successional permanent teeth: are those which erupt in place of deciduous teeth. (Permanent premolars in place of deciduous molars, 10 in each row).
Temporary teeth eruption (in months) – Total 20.
Eruption of permanent teeth (in years) – Total 32.

Gustafson’s method – The age estimation of adult over 21 years 9between 25 – 60 years) depends on the physiological age changes in each of the dental tissues such as attrition, pqaradentosis, secondary dentin, cementum apposition, root resorption, transparency of the root (The most reliable criteria).

2. Growth of individual bones:
The bones of skeleton are performed in hyaline cartilage. The earliest centres of ossification appear at the end of second months of pregnancy. At the eleventh intrauterine week, there are 806 centres of bone growth, at birth about 450, while the adult skeleton has 206 bones. Tarsus and carpus bones ossify from a single centre. Typically, a long bone such as tibia, has become ossified throughout its shaft (diaphysis) at birth; whereas its two ends (epiphysis) are later ossified by secondary centres. The process of union of epiphysis and diaphysis is called fusion. In an individual bone once union has begun, it will be completed by 12 to 18 months.

For determining the age, skiagrams of the shoulder, elbow, wrist, hip, knees, ankle, pelvis and skull, should be taken in antero-posterior position. Union of epiphysis in cartilaginous bones occurs slightly earlier by about 1 year in the female than in the male, but reverse is seen in the closure of the sutures of the skull.
The symphysis pubis is probably the single best criterion for determining age from third to fifth decades. If male criterion is used for females, the age would be underestimated by about 10 years.

Sternum: Four pieces of body of the sternum fuses with one another from below upwards between 14 and 25 years. At about 40 years the xiphoid unites with the body. The manubrium fuses with the body in old age.

The greater cornu of the hyoid bone unites with the body between 40 and 60 years.
Skull: Bones of calvaria are 8 in number: parietal 2, frontal 1, temporal 2, occipital 1.
Bones of the face and jaw are 14 in number: maxilla 2, zygomatic 2, nasal 2, lacrimal 2, palatine 2, inferior nasal concha 2, mandible 1, and vomer 1. Lateral and occipital fontanelles usually close within the first two months. The anterior fontanelles and the two halves of the mandible unite at the second year. The basioccipital fuses with the basisphenoid at about 18 to 21 years. In the vault of the skull, closure of the sutures begins on the inner side 5 to 10 years earlier than on the outer side. Closure of all sutures indicates age more than 60 years. Suture closure in skull occurs later in females than in males.
Sacrum: the sacrum becomes a single bone between 21 and 25 years.

3. Secondary sexual characters:
In males:
(i) At about 14 years – fine hair begins to appear at pubis.
Testes – large, firmer.
Penis – begins to enlarge.
(ii) At about 15 years – pubic hair thick, extends upto umbilicus, dark
– axillary hair appears.
(iii) At about 16 years – appearance of hair at face.
(iv) Between 16 – 18 years – voice becomes deep.
In females:
(i) At 13 – 14 years – Sequence of puberty is (i) breast begins to develop (ii)
hair on mons veneris (iii) menstruation starts.
(ii) At 14 – 15 years – Female public hair thin; straight tops above mons veneris;
hair appears in axilla.

Doctor’s estimation of age is not proof but merely an opinion.

Medico-legal importance of age:
1) Criminal responsibility: Any act done by a child under 7 years is not an offence (S. 82, IPC). It is an offence if done before 7 years according to Railways act. A child between 7 and 12 years is presumed to be capable of committing an offence, if he attains sufficient maturity (S. 83, IPC).

2) Judicial punishment: According to the Juvenile Justice Act, 1986, “juvenile” means a boy who is below the age of 16 years, or a girl who is below 18 years. No delinquent juvenile shall be sentenced to death or imprisonment.

3) Rape: Sexual intercourse by a man with a girl under 15 years even if she is his own wife, or with any other girl under 16 years even with her consent is rape (S. 375, IPC)

4) Kidnapping: It is an offence
(a) to kidnap a child with the intention of taking dishonestly any movable property, if the age of child is under 10 years (S. 369, IPC)
(b) to kidnap a minor from lawful guardianship if the age of a boy is under 16 and that of a girl under 18 years (S. 361, IPC)
(c) to procure a girl for prostitution, if her age is under 18 years (S. 366-A, IPC), and
(d) to import into India from a foreign country a female for the purpose of illicit intercourse, if her age is less than 21 years (S. 366-B, IPC).

5) Employment: A child below 14 years cannot be employed to work in any factory or mine or in any other risky employment. A person completing 15 years (adolescent) is allowed to work in a factory as an adult.
6) Attainment of majority: A person attains majority on the completion of 18 years. (S. 3, Ind. Majority Act, 1875)
7) Evidence: A child of any age can give evidence if the court is satisfied that the child is truthful (S. 118, IEA)
8) Marriage contract: A female under 18 years and a male under 21 years, cannot contract marriage (Child marriage restraint act, 1978)
9) Infanticide: The charge of infanticide cannot be supported, if the infant can be proved under the age of 6 months of intra-uterine life.
10) Criminal abortion: A woman who has passed the child-bearing age cannot be charged of procuring criminal abortion.

Rule of Haase: A rough method of calculating the age of the foetus.
(1) Upto 5 months, age of foetus = √length (in months)
(2) › 5 months = length (in cm)/ 5 = (months).
Length of an infant: At birth = 50 cm, end of 6 months = 60 cm, end of 1st year = 68 cm, end of 4 years = 100 cm (double).
Birth weight doubles by 5months, triples by 1 year.
For the confirmation of age between 6 and 12, best means is dental examination.

Fusion of bones / joints:
(ii) 15 to 16 years – Elbow joint.
(iii) 16 to 17 years – Ankle joint
(iv) 17 to 18 years – Hip joint
(v) 18 to 19 years – Knee, shoulder, knee joint. Centre appears for inner end of clavicle.
(vi) 18 to 20 years – Iliac crest fuses.
(vii) 21 years – Fusion of ischial tuberosity and inner end of clavicle. Patella completely ossifies at 14 years.
(viii) 2nd and 5th decades – Age of 20 years is determined by pubis.
(ix) 14 to 25 years – Sternum fusion takes place below upwards.
(x) Bertellion system – for greater than 21 years.
(xi) Epiphseal union of sternal end of clavicle occurs at the age of 22 years.

1st ossification centre to appear is clavicle, and lower jaw at 2nd week of intra uterine life.
In post – maturity, ossification centres appear in capitate, hamate.

Stature: By applying Karl – pearson formula, we will be able to calculate stature of the individual from long bones. Multiplying factor of estimating stature: from femur (males) is 3.6 to 3.8, from humerus (males) is 5 to 6.

Dactylography, (finger-print system, dermatoglyphics, Galton system)
Most reliable method of identification of a person. Finger prints are impressions of pattern formed by the papillary ridges of the fingertips.
Finger prints are classified primarily as: (i) Loops 67%, (ii) whorls 25%, (iii) arches 6 to 7% (iv) composite forms – 1 to 2% (least common).

In practice, 16 to 20 points of fine comparison are accepted as proof of identity. The patterns are not inherited. The pattern is different in identical twins.
Ridge alterations occurs in eczema, acanthosis nigricans and scleroderma.
Permanent impairment of the finger print pattern occurs in leprosy, electric injuries, and after exposure to radiation.

Poroscopy – This is the further study of fingerprints described by Locard.
(i) Recognition of impression at the scene of crime.
(ii) Identification in case of accidental exchange of new-born infants.
(iii) Prevention of impersonation
(iv) Cheques, bank notes and other legal documents.

Cheiloscopy: is the study of lip-prints.
Superimposition: It is the technique applied to determine whether the skull is that of the person in the photograph. A life sized negative of the skull is prepared. The negatives of the photograph and the skull are superimposed by aligning the characteristic point in negative. A negative result is having more credibility because, it can definitely be stated that the skull and the photograph are not those of the same person.

Hair: Study of hair is known as Trichology.
Medullary index of hair is used to determine the species.
Human hair is fine, thin, cuticular scales are short, broad, not continuous; cortex – thick, 4 to 10 times as broad as medulla; medulla – thin, pigment evenly distributed; precipitin test specific for human.
Animal hair is coarse, thick, cuticular scales very large, step-like projection; cortex thin.

Scalp hair grows at 3 mm a week.
Hair becomes loose after 72 hours of death.
ABO groups can be determined in a single hair from any part of the body by a modified absorption – elution technique with 100 % accuracy.

Thanatology deals with death in all its aspects. Death is of two types: (1) somatic, systemic or clinical, and (2) molecular or cellular.
Somatic death is the complete and irreversible stoppage of the circulation, respiration and brain functions, but there is no legal definition of death.
Autopsy means, post-mortem examination of a body (whole body).

(1) To find out the time since death.
(2) To find out the cause of death.
(3) To find out the manner of death, whether accidental, suicidal or homicidal.
(4) To establish the identity.
(5) In new-born infants to determine live birth and viability.

Rokitansky’s method is autopsy technique for infants.
Before doing the post-mortem, body should be identified by policeman.
Exhumation: is the digging out of an already buried body from the grave. There is no time limit for exhumation in India. The body is exhumed only when there is a written order from the First Class Magistrate (Chief Judicial Magistrate). It should be conducted in natural light in early morning. Average number of sample of earth taken is 6 to 7. Disinfectants should not be sprinkled on the body. In suspected mineral poisoning, hair, nails and long bones, e.g., femur should be preserved for chemical analysis. It is not done for Hindus. Performed for Christians, Muslims and Parsies.

Molecular death means the death of cells and tissues individually, which takes place usually one to two hours after the stoppage of vital functions.

Braindeath consists of: (1) Deep unconsciousness with no response to external stimuli or internal need; (2) No movements, no spontaneous breathing; (3) Cessation of spontaneous cardiac rhythm without assistance; (4) No reflexes (except occasionally spinal reflexes), (5) Bilateral dilatation and fixation of pupils; (6) Flat iso-electric EEG; provided that (a) all of the confirmatory mentioned are present for a 24 hour period; (b) patient’s body temperature should not be below 320C. (c) metabolic and endocrine disturbances, which can be responsible for coma should be excluded.

Modes of death: (1) Coma, (2) Syncope, (3) Asphyxia.
Coma is the insensibility, which involves the central portion of the brain stem, and may result in death.
Syncope is sudden stoppage of action of the heart, which may prove fatal. It is due to vaso-vagal attacks resulting from reflex parasympathetic stimulation.

Asphyxia is a condition caused by interference with respiration or due to lack of oxygen in respired air due to which the organs and tissues are deprived of oxygen. (together with the failure to eliminate CO2 ), causing unconsciousness or death.

The cause of death is the disease or injury responsible for starting a sequence of events, which are brief or prolonged and which produce death. It may be divided into: (1) Immediate cause, (2) Basic cause, (3) Contributory cause.

Negative autopsy:
When gross and microscopic examination, toxicological analysis and laboratory investigations fail to reveal a cause of death, the autopsy is considered as negative. It may be due to (1) Inadequate history, (2) Inadequate external examination, (3) Inadequate or improper internal examination, (4) Insufficient laboratory examinations, (5) Lack of toxicological analysis, (6) Lack of training of the doctor.

Obscure autopsies: are those which do not show a definite cause for death, in which there are minimal, indefinite or obscure findings, or even no positive findings at all.
Sudden death: Death is said to be sudden or unexpected, when a person not known to have been suffering from any dangerous disease, injury or poisoning is found dead or dies within 24 hours after the onset of terminal illness.

Natural death means that the death was caused entirely by the disease, and the trauma or poison did not play any part in bringing it about.

The signs of death appear in the following order:
(I) Immediate (somatic death).
(1) Insensibility and loss of voluntary power
(2) Cessation of respiration
(3) Cessation of circulation.
(II) Early (cellular death).
(4) Pallor and loss of elasticity of voluntary power
(5) Changes in the eye
(6) Primary flaccidity of muscles
(7) Cooling of the body
(8) Post-mortem lividity
(9) Rigor mortis
(III) Late (decomposition and decay)
(10) Putrfaction
(11) Adipocere formation
(12) Mummification.

Complete stoppage of respiration for more than 4 minutes usually causes death.
Suspended animation: In this condition, signs of life are not found, as the functions are interrupted for sometime, or are reduced to minimum. However, life continues and resuscitation is successful in such cases. Voluntarily, practitioners of yoga can pass into a trance, death like in character. Involuntary suspension of animation lasting from a few seconds to half-an-hour may be found in new-born infants, drowning, electrocution, cholera, after anesthesia, shock, sunstroke, cerebral concussion, insanity, etc.

Changes in skin: Skin becomes pale and ashy-white and loses elasticity within a few minutes of death. Lips appear brownish, dry and hard due to drying.
Changes in eye: Loss of corneal reflex is not a reliable sign of death. Opacity of cornea may occur in diseases like cholera, wasting diseases before death. If the lids are open, cornea remains clear for about 2 hours. The retina is pale for the first 2 hours. At about 6 hours, the disk outline is hazy and becomes blurred in 7 to 10 hours.

Cooling of the body (Algor mortis): The body heat is lost by conduction, convection and radiation. The curve of cooling is sigmoid in pattern. Internal organs take 24 hours to cool. The temperature of the body rises up for the first two hours after death by sunstroke, septicemia, tetanus, strychnine poisoning called post-mortem caloricity.

A rough idea of time in hours after death can be obtained by the formula, (Normal body temperature – Rectal temperature) / Rate of temperature fall per hour.

The rate of cooling of the body in first six hours is 2.50F per hour, the rate in next hours is 1.5 – 20F.
Factors affecting rate of cooling: In India, during summer, cooling is very slow. In tropical climates, the heat loss is roughly 0.5 to 0.70C per hour. Children and old people cool more rapidly than adults. Fat bodies cool slowly than lean bodies. Cooling is more rapid in humid atmosphere than in dry atmosphere. A body immersed in cold water cools rapidly; the rate of fall being almost twice as fast as by air cooling. Bodies buried in earth cool rapidly than that in air, but more slowly than those in water.

Post-mortem hypostasis: This is the bluish-purple or purplish-red discoloration which appears under the skin of the dependent parts of the body after death, due to capillo-venous distension. Also called post-mortem staining, sub-cutaneous hypostasis, livor mortis, cadaveric lividity, suggilations, vibices and darkening of death. The intensity of the colour depends on the amount of reduced haemoglobin in the blood.

Post-mortem lividity begins shortly after death, but it may not be visible for about half to one hour after death in normal individuals, and for about one to 4 hours in anaemic persons. It is usually well developed within 4 hours and reaches a maximum between 6 and 12 hours. It is more marked in asphyxia and is less marked in death from wasting diseases, hemorrhage and from anaemia and lobar pneumonia.

In a body lying on its back, it first appears in the neck, and then spread over the entire back except parts directly pressed on, i.e., shoulder-blades, buttocks, calves and heel.

Post-mortem stains can occur in some cases before death in cholera. The location of the lividity indicates the position of the body during post-mortem interval. Hypostasis lasts for hours. Blood clots after ½ hour of death.

Post-mortem staining gets fixed after 5 – 6 hours. A contusion can be differentiated from post-mortem staining by doing incision test.

  •  In carbon-monoxide poisoning, the colour is cherry-red.
  •  In hydrocyanic acid poisoning, the colour of stain is bright-red.
  •  In poisoning by nitrates, potassium chlorate, potassium bicarbonate, nitrobenzene and aniline (causing methaemoglobinaemia) the colour is red-brown, or brown
  •  In poisoning by phosphorus, the colour is dark – brown. (Blue in P.V.Chadha)
  •  In case of aniline or CO2 poisoning, it is deep blue, due to excess of reduced Hb.
  •  In asphyxia, the colour of stains is deeply bluish-violet or purple.
  •  In septic abortion caused by Cl. Welchii, the colour is often greyish-brown.
  •  In hanging, hypostasis, will be most marked in the legs, and hands. In drowning, PM staining is usually found on the face, the upper part of chest, hands, lower arms, feet and calves, as they are the dependent parts. If the body is constantly moving its position, as after drowning in moving water, the staining may not develop.
  • As decomposition progresses, the lividity becomes dusky in colour and turns brown and green before finally disappearing with destruction of the blood.

Muscular changes: After death, muscles of body pass through three stages:
(1) Primary relaxation or flaccidity,
(2) Rigor mortis or cadaveric rigidity,
(3) Secondary flaccidity.
Primary flaccidity: During this stage, death is somatic only, and it lasts for one or two hours.

Rigor mortis (cadaveric rigidity): This is a stage of stiffening of muscles, sometimes with slight shortening of the fibres. Individual cell death takes place at this stage.

ATP is responsible for elasticity and plasticity of muscle. The lost ATP (during muscle contraction) during life is resynthesized. After death there is no resynthesis of ATP. The PM alteration of ATP is due to dephosphorylation and deamination. When ATP is reduced to a critical level (85% of the normal) the overlapping portions of myosin and actin filaments combine as a rigid link of actomyosin, which is viscous and inextensible, and causes hardness and rigidity of muscle rigor. The rigidity is maximum, when the level of ATP is reduced to 15%. Rigor persists until decomposition of the proteins of the muscle fibres makes them incapable of any further contraction.

The order of appearance of rigor mortis:
All the muscles of the body, both voluntary and involuntary are affected. It first appears in involuntary muscles; the myocardium becomes rigid in an hour. It begins in the eyelids, neck, and lower jaw, and passes upwards to the muscle of the face, and downwards to the muscles of the chest, upper limbs, abdomen and lower limbs. It passes off in same order.

When rigor is fully developed, the entire body is stiff, the muscles shortened, hard and opaque. Rigor of erector pilae muscles may cause roughness of skin – known as cutis anserina or goose skin. Rigor is tested by trying to lift the eyelids, depressing the jaw, and gently bending the neck and various joints of the body. RM may occur in amputated limbs and diseased parts.

Time of onset of RM:
In India, it begins 1 to 2 hours after death and takes further 1 to 2 hours to develop.
Duration of RM:
In India, usually it lasts for 24 to 48 hours in winter and 18 to 36 hours in summer. When rigor sets in early, it passes off quickly and vice versa.

Conditions altering duration and onset:
In death from diseases causing great exhaustion and wasting, e.g., cholera, typhoid, tuberculosis, cancer, etc and in violent deaths as by cut-throat, firearms or by electrocution, the onset of RM is early and duration is short.
In Strychnine and other spinal poisons, the onset is rapid and the duration is longer. In deaths from asphyxia, severe haemorrhage, apoplexy, pneumonia, nervous disease causing paralysis of muscle, and perfusion with normal saline, the onset is delayed.
The onset is slow and duration is long in cold weather. The onset is rapid due to heat, because of the increased breakdown of ATP but the duration is short. RM may persist for 3 to 4 days in refrigerated conditions.

Conditions simulating RM:
(1) Heat stiffening: When a body is exposed to temperatures above 650C rigidity is produced, which is much more marked than that found in RM. It is seen in deaths from burning, high voltage electric shocks and from falling into hot liquid. The stiffening remains until the muscles soften from decomposition.
(2) Cold stiffening: When the body is exposed to freezing temperatures, the tissues become frozen and stiff, simulating rigor.
(3) Cadaveric spasm or Instantaneous rigor or cataleptic rigidity: In this condition, the muscles that are contracted during life, become stiff and rigid immediately after death without passing into the stage of primary relaxation. It occurs especially in cases of sudden death, excitement, fear, severe pain, exhaustion, sudden asphyxial death, cerebral haemorrhage, injury to the nervous system, firearm wound of the head, etc. this is usually limited to a single group of muscles and frequently involves the hands. No other condition simulates cadaveric spasm and it cannot be produced by any method after death. It may be explained on the basis of diminished or exhausted ATP in the affected muscles.

MLI: in case of suicide the weapon, e.g., pistol or knife is seen firmly grasped in victim’s hand which is a strong presumptive evidence of suicide. In case of drowning, materials such as grass, weeds or leaves may be found firmly grasped in the hand which shows ante mortem drowning.

Secondary relaxation: Muscle becomes soft and flaccid due to breaking down of actinomyosin due to putrefaction

Putrefaction: It is the final stage following death, mainly by the action of bacterial enzymes, mostly anaerobic organisms derived from the bowel.
Putrefaction is delayed after death due to poisoning by: Carbolic acid, Zinc chloride, Strychnine, Heavy metal poisoning e.g. Arsenic, Antimony.

The chief destructive bacterial agent is Cl. Welchii which causes marked hemolysis, liquefaction of post-mortem clots and of fresh thrombi and emboli, disintegration of tissue and gas formation in blood vessels and tissue spaces. Enzyme Lecithinase produced by Cl. welchii is most important.

The characteristic features of putrefaction are : (i) changes in the colour of the tissue,
(ii) collection of gases in the tissues, (iii) liquefaction of tissues.
(i) changes in the colour of the tissue: The first external sign of putrefaction in a body lying in air is a greenish discolouration of skin over caecum i.e. right iliac fossa, where the contents of the bowel are more fluid and full of bacteria.

The colour appears in 12 to 18 hours in summer and one to two days in winter. The greenish discoloration then spreads over the entire abdomen, external genitals and then patches appear successively on the chest, neck, face, arms and legs. The patches become dark-green and later purple and dark blue. The marbled appearance is prominent in 36 to 48 hours. The earliest internal change is reddish brown discolouration of the inner surface of the vessels, especially the aorta.

(ii) Collection of gases in the tissue: Gases collect in the intestines in 6 to 12 hours in summer. From 18 to 36 hours after death, the gas collects in the tissues, cavities and hollow viscera under pressure and the features become bloated and distorted. After 3 days, the face is so discoloured and bloated that identification becomes difficult. The hair becomes loose and is easily pulled out.

(iii) liquefaction of the tissues: Colliquative putrefaction begins from 5 to 10 days or more after death.

Skeletonisation: In India, an unconfined buried body is reduced to a skeleton within a year.
Internal phenomenon:
The organs show putrefactive changes in the following order :
1. Larynx and trachea, 2. Stomach, intestines, spleen, 3. Liver and lungs, 4. Brain,
5. Heart, 6. Uterus, prostate, kidney, 7. Skin, muscle, tendon, 8. Bone.
In putrefaction, when bubbles appear the organ has a honey combed, foamy appearance. Prostate and virgin uterus resists putrefaction for a very long time. Putrefaction begins above 10°C and optimum between 21 °C and 38°C. A body decomposes in air twice as rapidly as in water and eight times as rapidly as in earth; formula is given by Taylor. Putrefaction is the surest sign of death. After death, the onset of putrefaction is in the stage of secondary relaxation. Gas rigidity appears after 72 hours.

Entomology of cadaver: Is the study of insects and maggots that infest the dead body.
Bones begin to decompose after death in 3-10 years. Less than 7 amino acids in bone suggest the age of bone to be (after death) more than 100 years. Total ultraviolet fluorescence of cut surface of bones is seen in 35-100 years. Foamy liver is due to bubbling up of gas. Putrefaction is affected by age, clothing and moisture. Maggots in a dead body do not appear before 48 hours.

Adipocere (Saponification)
In this, the fatty tissues of the body changes into a substance known as adipocere. The change is due to gradual hydrolysis and hydrogenation of pre-existing fat such as olein, into higher fatty acids, which combine with calcium and ammonium ions to form insoluble soaps, which being acidic, inhibit putrefactive bacteria. Adipocere is delayed by cold and formed rapidly by warm humid climate and moist damp soil.

Fresh adipocere
is soft, moist, whitish and translucent but old samples are dry, hard, cracked, yellowish and brittle. It is inflammable and burns with a faint yellow flame. It floats in water and dissolves in alcohol and ether. It is formed first in subcutaneous tissue. The face, buttocks, breast, abdomen are the usual sites. In temperate country, the shortest time for its formation is about 3 weeks in summer. Foetuses under 7 months do not show this change. In India, it has been observed within 3 days.

Mummification: It is a modification of putrefaction.

Dessication or, Dehydration or drying and shrivelling of the cadaver occur due to evaporation of water but the natural appearance and features of the body are preserved. It begins in the exposed parts of the body such as face, hands and feet and then extends to the entire body including the internal organs. A mummified body is practically odourless. The time required for complete mummification of a body varies from three months to a year or two. Two factors are necessary for the production of mummification: (1) The absence of moisture in the air, and (2) The continuous action of dry or warmed air.

In this, the contents of the body cavities are removed and the vascular system is injected with an embalming fluid containing 40% formaldehyde and 10% methyl alcohol.

Mechanical injuries (wound) are injuries produced by physical violence.

An injury is any harm, whatever illegally caused to any person in body, mind, reputation or property (S. 44, IPC)
A wound or injury is a break of the natural continuity of any of the tissues of the living body.


(I). Mechanical:
1. Abrasions 2. Contusions 3. Lacerations 4. Incised wounds 5.Stab wounds 6. Firearm wounds 7. Fractures and dislocations

(II) Thermal:
1. Due to cold-
(a) Frost bite (b) Trench foot (c) Immersion foot.
2. Due to heat—
(a) Burns (b) Scalds.

III. Chemical: (a) Corrosive acid (b) Corrosive alkalies.

IV. Injuries due to lightning, electricity, X-ray and radio-active substances..

An abrasion is a destruction of the skin, which involves super¬ficial layers of epidermis only. They are caused by a blow, a fall on a rough surface, by being dragged in a vehicular accident, finger nails, thorns or teeth-bite. The exposed raw surface is covered by exudation of lymph and blood, which produces a protective covering known as scab or crust. They are simple injuries, bleed slightly, heal rapidly and leave no permanent scar.

Types: Abrasions are of four types.
1. Scratches: These are caused by a sharp object passing across the skin, such as finger nails, pin or thorn.
2. Grazes (sliding, scraping or grinding abrasion): They are most common type of abrasions. They show uneven, longitudinal parallel lines (grooves or furrows) with the epithelium heaped up at the ends of these lines, which indicate the direction in which the force is applied.
An abrasion caused by violent friction against a broad rough surface as in dragging over the ground is called brush burn.
3. Pressure abrasion (Crushing or friction abrasion): Ligature mark. They are caused by crushing of the superficial layers of the epidermis and are associated with a bruise of the surrounding area.
4. Impact abrasions or Imprint abrasions— they are caused by impact of a rough object, such as a person knocked down by a motor car. They are also called pattern abrasions.

Age of Abrasions:
1. Fresh — Bright red.
2. 12 to 24 hours — Lymph and blood dries up leaving a bright scab.
3. 2 to 3 days — Reddish-brown scab.
4. 4 to 7 days — Epithelium grows and covers defect under the scab.
5. After 7 days — Scab dries, shrinks & falls off.
In ante-mortem abrasions, intravital reaction and conges¬tion is seen.

Erosion of the skin produced by ants, excoriations of the skin by excreta and pressure sores resemble abrasions.

Contusions (BRUISES)
A contusion is an effusion of blood into the tissues, due to rupture of the subcutaneous vessels, caused by blunt trauma. This is accompanied by a painful swelling and crushing or, tearing of the subcutaneous tissues usually without destruction of the skin. A contusion is a superficial injury. When a large blood vessel is injured, a tumour-like mass called haematoma is formed. The size of the bruise is slightly larger than the surface of the agent which caused it, as blood continues to escape into the area.

If the part is vascular and loose, such as face, vulva, scrotum, a slight degree of violence may cause a large bruise. If the tissues are strongly supported and covered by thick dermis, such as abdomen, back, scalp, palm and soles, moderate violence may produce a small bruise.

Bruising is more marked on tissue overlying bone. Children and old people bruise more easily. Hemorrhages in the soft tissues around the eyes and in the eyelids (black-eye) may be caused by blunt impact to the forehead.

The Age of Bruise:
A bruise heals by destruction and removal of the extra-vasated blood.
At first (1-2 hours)—Red.
Few hours to 3 days—Blue
4th day — Bluish-black to brown (haemosiderin).
5 to 6 days — Greenish (haematoidin).
7 to 12 days—Yellow (bilirubin).
2 weeks—Normal.

In ante-mortem bruising there is swelling, damage to epithelium, extravasation, coagulation and infiltration of the tissue with blood and colour changes.
Bruises are of less value than abrasions. In self inflicted bruises, typical colour changes are not seen.
Artificial bruises: Some irritant substances when applied to skin produce injuries, which simulates bruises. Artificial bruises are dark brown and true bruises show typical colour change.

Incised wounds
An incised wound (cut, slash or slice) is a clean cut through the tissues, which is longer than it is deep. It is produced by pressure and friction against the tissue by object having a sharp cutting edge such as knife, razor, scalpel, sword, etc.

Incised wound appears lacerated on testes. Incised wounds are deeper at their beginning, because more pressure is exerted on the knife at this point, known as the head of the wound.
Towards the end of the cut, the wound becomes shallow, called tailing of the wound.

Age of incised wound:
Fresh—Hernatoma formation.
12 hours—Edges are red, swollen, adherent with blood and-lymph.
24 hours—A continuous layer of endothelial cells cover the surface.
36 hours—The capillary network is complete.
48 to 72 hours—The wound is filled with fibroblasts.
3 to 5 days—Definite fibrils running parallel to the vessels are seen; vessels show thickening and obliteration.
1 to 2 weeks—Scar tissue is formed.

Hesitation marks or tentative cuts or trial wounds—They are cuts which are multiple, small and superficial, often involving the skin and seen at the beginning of the incised wound. They are seen in suicidal wounds.
Chop wounds: They are wounds caused by a blow with the sharp cutting edge of a fairly heavy weapon like a hatchet, axe, a sword etc.
Wound produced by a curved weapon such as sickle is both stab & incised wound.

Stab or Puncture Wounds
Stab wound is a penetrating injury caused by sharp-pointed objects, such as knife, dagger, nail, needle, arrow, screw driver, etc. penetrating the skin and underlying tissues that is deeper than its length and width of the skin.
Most important dimension in stab wound is depth. Punctured wound is deeper than its width and length on skin. The length of wound is less than width. If a single edged weapon is used, the surface, triangular or wedge shaped, one angle of the wound will be sharp, the other blunt or torn.

Harakiri: It is an unusual type of suicide, in which the victim inflicts a single large wound on the abdomen with a short sword while in a sitting position or falls forward upon a ceremonial sword and pulls out intestines. The sudden evisceration of the internal organs causes a sudden decrease of intra-abdominal pressure and cardiac return, producing sudden cardiac collapse.

They are open wound.
Lacerations are tears or splits of skin, mucous membrane, muscle or internal organs produced by application of blunt force to the broad area of the body. Displacement of tissues occurs most commonly when soft tissues are crushed against bone, e.g., scalp, shins, shoulders, and face. They are caused by blows from blunt objects, by falls on hard surfaces, by machinery, traffic accidents, etc.

If the force produces bleeding into adjacent tissues, the injury is a ‘contused-laceration’ or ‘bruised tear’. If the blunt force produces extensive bruising and laceration of deeper tissues, it is called ‘crushing’ injury.
Incised like or incised looking wounds: Lacerations produced without excessive skin crushing may have relatively sharp margins. The sites are the scalp, eyebrows, cheek bones, lower jaw, iliac crest, perineum, and shin.

Stretch lacerations: is seen in the running over by a motor vehicle, and the flap may indicate direction of the vehicle.

Avulsion is a laceration produced by sufficient force (shearing force) delivered at an acute angle to detach (tear off) a portion of a traumatised surface or viscus from its attachments.

Defense wounds
It results due to immediate and instinctive reaction of the victim to save himself, either by raising the arm to prevent the attack or by grasping the weapon.
Self-inflicted wounds are those inflicted by a person on his own body.
Fabricated wounds (fictitious, forged or inverted wound) are those which may be produced by a person on his own body or by another with his consent.

Most fragile bone in the skull to get fractured is — temporal bone.
Depressed fractures -» The outer table is driven into the diploe and inner table is fractured irregularly. Depressed fracture is also called signature fracture. Localised depressed fracture are caused by blows from heavy weapon with a small striking surface e.g. stone, stick, axe. hammer etc.
Pond or Indented fractures —> They occur only in skulls which are elastic i.e. the skulls of infants.
Gutter fractures – They are formed when part of the thickness of the bone is removed so as to form a gutter e.g. oblique bullet wound.
Countre-coup lesions fracture means that the lesion is present in an area opposite the side of impact in head injury.
Concussion is a state of temporary unconsciousness, which results from violence applied to the skull. Concussion of the spinal cord is called railway spine.
In fracture, X-ray examination, callus is not readily visible for 3 weeks.
Whip lash injury is due to violent acceleration or deceleration force.
In Boxing injuries fracture of the skull is rare but sub-dural hemorrhage occurs. It is most common type of hemorrhage. Deterioration of speed and co-ordination are the chief symptoms of the onset of punch-drunk (traumatic encephalopathy) condition. Repeated blows to the head produce small hemorrhages and degenerative changes in brain.
— The specific pulmonary injury of air blast is called ‘blast lung’.
— Most common mechanism of fracture of spine is hyperflexion.
— Most common site of spinal cord injury is thoracolumbar junction (T10- L1).
— Best method of assessing spinal cord injury is MRI.

Intracranial Hemorrhage
1. Extradural hemorrhage: — It is caused always due to trauma.
Most common artery causing extradural hemorrhage is anterior branch of middle meningeal artery. Most common site of extradural hemorrhage is Temporo-parietal area where main source of bleeding is middle meningeal artery. There is a history of head injury which causes the bleeding and temporary unconsciousness usually. This is followed by a period of normal consciousness, the lucid interval of few hours to a week.

2. Subdural hemorrhage:
May occur from relatively mild trauma. It is essentially venous or capillary, not arterial.
3. Subarachnoid hemorrhage
This is the most common form of traumatic intracranial hemorrhage.

4. Intracerebral hemorrhage
Most common cause of intracerebral hemorrhage is hypertension.
Most common site of intracerebral hemorrhage is putamen (corpus striatum).
Most common blood vessel leading to intracerebral hemorrhage is lenticulo striate branch of middle cerebral artery.                                                                                                                                                                                                                                                                                                                       MEDICO-LEGAL ASPECTS OF WOUNDS

Homicide: is killing of a human being by another human being.

Types of homicide:
(1) Lawful (a) Excusable (b) Justifiable
(2) Unlawful (a) Murder (b) Culpable homicide (not amounting to murder/ amounting to murder) (c) Rash or negligent homicide.
Justifiable homicide: This is the homicide which is justified in the circumstance which led to the killing of a person. This may occur; (a) In the administration of justice, like execution of sentence of death (b) The maintenance of justice, e.g., in suppressing riots, or executing arrest, or killing in course of violent crime, e.g., a woman who kills a person who attempts to rape her.

Excusable homicide: This is the homicide caused unintentionally by an act done in good faith. This includes: (a) Killing in self-defense when attacked, provided there is no other means of defense (b) Causing death by accident or misadventure (c) Death following a lawful operation (d) Homicide committed by an insane person.

Murder: S. 300, IPC
Culpable homicide: S. 299, IPC
Punishment for murder: S. 302, IPC – Imprisonment for life, and also fine.
Punishment for culpable homicide: S. 304, IPC – Imprisonment for life, or for a term which may extend to 10 years and also fine.
Causing death by negligence: S. 304 – A, IPC – Imprisonment for a term, extend to 2 years or/with fine, or with both.

Grievous Injury
According to 320 I.P.C., anyone of the following injuries is grievous:
1. Emasculation (Ioss of potency).
2. Permanent privation (loss) of sight of either eye.
3. Permanent privation of hearing of either ear.
4. Privation of any member or joint.
5. Destruction or permanent impairing of the power of a member or joints
6. Permanent disfiguration of the head and face.
7. Fracture or dislocation of a bone or tooth.
8. Any hurt which endangers life or, which causes the victim to be in the severe bodily pain or, unable, to follow his ordinary pursuits for a period of 20 days.

Hurt means bodily pain, disease or infirmity caused to any person (S. 319, IPC)
Punishment for voluntarily causing hurt: Imprisonment up to one year, or with fine up to one thousand rupees or both (S. 323, IPC)
Injury is any harm whatever illegally caused to any person in body, mind, reputation or property (S. 44, IPC)
Punishment for voluntarily causing grievous hurt: Imprisonment for a term extending to seven years and also fine (S. 325, IPC)
Punishment for voluntarily causing grievous hurt by dangerous weapons or means: Imprisonment for a term up to 10 years and also fine (S. 326, IPC)

Dangerous weapons or means: According to Sec. 324 and 326, IPC, dangerous weapons or means include any instrument for shooting, stabbing or cutting or any instrument, which used as a weapon of offence, is likely to cause death; fire or any heated substance; poison or any corrosive substance; explosive substance or any substance which are harmful to human body to inhale, to swallow, or to receive in to the blood or by means of any animal.

Voluntarily causing hurt by dangerous means:
Imprisonment for a term up to 3 years or with fine, or both (S. 324, IPC)
Assault is an offer or threat or attempt to apply force to body or another in a hostile manner (S. 351, IPC)

Dowry death

Sec. 304 B, I.P.C., where death of the women occurs under abnormal circumstances within seven years of her marriage. Punishment: imprisonment not less than 7 years, but may extend to life imprisonment. Sec. 498-A, IPC “Whoever, being the husband or relatives of the husband of a woman, subjects such women to cruelty shall be punished with imprisonment up to 3 years”.

Causes of death from wounds: (1) Immediate or direct (2) Remote or indirect
(1) Immediate causes: (a) hemorrhage (b) reflex vagal inhibition (c) shock (d) mechanical injury to a vital organ
(2) Remote causes: (a) infection (b) gangrene or necrosis (c) crush syndrome (d) neglect of injured person (e) surgical operation (f) natural disease (g) supervention of disease from a traumatic lesion (h) thrombosis (i) fat embolism (j) air embolism.
Causes of fat embolism: (1) Fracture of a long bone (2) an injury to adipose tissue which forces liquid fat into the damaged blood vessels, (3) injecting oil into circulation, e.g., in criminal abortion (4) occasionally due to natural disease without trauma as in sickle cell anaemia (5) in case of burns.

A firearm is any instrument which discharges a projectile by the expansive force of the gases produced by burning of an explosive substance. Forensic ballistics is the science dealing with the investigation of firearms, ammunition and the problem arising from their use.

(I) Rifled weapons: (1) Rifles: (a) Air and gas-operated rifles (b) 0.22 rifles (c) Military and sporting rifles (2) Single-shot target practice pistols (3) Revolvers (4) Automatic pistols (5) True automatic weapons (machine guns)
(II) Smooth-bored weapons (shotgun) (1) Single barrel (2) Double barrel (3) Slide action (4) Bolt – action (5) Semi-automatic (6) Automatic.

Choking is a constricting device at the muzzle end of shot gun.

Muzzle-loading guns are loaded entirely from muzzle end with the help of a rod using gunpowder, pieces of cloth, stones, metal fragments, seeds, bolts, wood, screws, etc. When the entire barrel from breech to the muzzle end is of same diameter, it is called cylinder-bore. In choke-bore, the distal 7.5 to 10 cm. of the barrel is narrow. There are some shotguns which have small portion of their bore near the muzzle end rifled, which are called “paradox guns”. A musket is a military shoulder arm. It has a long fore-stock and usually takes a bayonet at the muzzle. Shot guns are effective up to 30 metres (30-40 yards). 12 bore gun means that a sphere of 1/12 pound of lead will exactly fit the bore of the gun. Markings in projectile occur in Rifle.

A Rifle is a gun with a long barrel, the bore of which is rifled. A Carbine is a short barrelled rifle or a musket. It is effective upto 300 metres. The military rifle has a magazine and bolt action and can kill at a range of 3,000 metres. The pressure in the firing chamber is about 20 tonnes per square inch. The bullet as it leaves the barrel rotates at about 3,000 revolutions persecond. Rifles may be single-shot, repeating, semi-automatic and automatic.

Revolvers are so called because the cartridges are put in chambers in a metal cylinder, which revolves or rotates before each shot, to bring the next cartridge opposite the barrel, ready to be fired. It has a cylindrical magazine situated at the back of the barrel, which is capable of revolving motion. The bores vary from 5.6 to 11.4 mm (0.22 to 0.45 inch). The muzzle velocity is 150 to 180 metres per second. The effective range is 100 metres.

Air rifle and Air pistol

In these compressed air is used to fire lead slugs. Their range is about 40 metres.
Cartridge: is used in shot gun. Detonator cap is situated at the base of the rim. Soiling in a gun shot wound is due to lead content, more marked in distant shot gun wound. Ring of grease occurs at a distance beyond 2 feet.

1. Black gun powder—It consists of potassium nitrate 75%, sulphur 10% and charcoal 15%.
Except— Lead peroxide.
2. Smokeless: it consists of nitrocellulose (single base) or, nitroglycerine and nitrocellulose (double base) powder which produces much less flame and smoke and are more completely burnt than black powder.


The traditional bullet is made of soft metal and has a round nose. This is known as the round-nose soft bullet, and is usually used in rifles and revolvers. In revolver and pistol, the bullet is short and the point usually round or ogival. In rifle, the bullet is elongated with pointed end. Rifle bullet weight ranges from 2 to 33 grams. The extent of muscle damage by a bullet depends primarily on the velocity.

A dumdum bullet,
so called because tip is chiselled out, is one which fragments extensively upon striking and produces extensive wounds with ragged margins.

Incendiary bullets contain phosphorus. Gun shot wound is a perforated wound. Glance bullet causes gutter fracture. In case of shot by bullet, the presence of singeing (of hair) and charring (of skin) indicates a distance up to 6 inches.

Near wound caused by fire-arms is characterised by— (i) Tattoing by unburnt powder,
(ii) Presence of grease collar and abrasion collar, (iii) Presence of carbon monoxide in the blood of the injured tissues in the track of the bullet.
Bevelling of the skull in bullet injury:
(i) At broad end of the entry point, inner table shows bevelling, (ii) At exit point of bullet, outer table shows bevelling.

In close shot, the victim is within the range of the frame i.e. few feets.
The term point blank is used when the range is very close to or in contact with the surface of the skin. Blasting effect is usually seen.

The entrance wound is circular, with inverted edges and is surrounded by blackened and singed area. Abraded collar and grease or, dirt collar are present in gun shot entrance injury. Some contusion is present in abraded collar, called contusion collar. The abrasion collar and contusion collar are proof of an entrance wound.

Skull—In the skull, the wound of entrance shows a punched hole in the outer table. Opening in the inner table is large and shows beveling (sloping). At the point of exit, a punched-out opening is produced in the inner table and beveled opening on the outer table. Greater damage is produced by Dumdum bullet, larger bullet and round bullet.

A bullet traveling in an irregular fashion instead of traveling nose-on is called a yawning bullet. A bullet that rotates end-on-end during its motion is called a tumbling bullet.

Ricochet bullet is one which before striking the object aimed at, strikes some intervening object first, and then after ricocheting and rebounding from these, hits the object.

Tandem bullet or piggyback bullet (one behind the other).

Souvenir bullets: if a bullet is present for a long time in the body, there will be no fresh bleeding in the surrounding area.
Trench foot and Immersion foot are the result of prolonged exposure to severe cold (5 to 8°C) and dampness. The term Immersion foot is used for cases with frost bite. In frost bite, skin becomes hard & black in about 2 weeks. Frost bite occurs due to exposure to extremes of cold (- 2.5°C).

1. Heat cramps (miner’s cramps or, fireman’s cramps): They are caused by rapid dehydration of body through the loss of water and salt in the sweat.
2. Heat hyperpyrexia or Heat stroke: The term thermic fever or sunstroke is used when there has been direct exposure to the sun. High temperature, increased humidity, minor infections, muscular activity, and lack of acclimatisation are the principal factors of the initiation. Failure of cutaneous blood flow and sweating leads to breakdown of heat regulating centre of hypothalamus.

C/F: In some cases, symptom are headache, giddiness, nausea, vomiting, weakness, staggering gait, mental confusion, muscle cramps, restlessness and excessive thirst occur. The skin is dry, hot and flushed with complete absence of sweating.

3. Heat prostration (heat exhaustion and heat syncope): Heat prostration is a condition of collapse without increase in body temperature, which follows exposure to excessive heat. Main cause of death is vascular collapse and syncope. Muscle cramp is due to loss of Na+ ion.

A burn is an injury which is caused by application of heat or chemical substances to the external or internal surfaces of the body.

Burns due to X-rays and radium vary from redness of the skin to dermatitis, with shedding of hair (epilation) and pigmentation of surrounding skin. Curling ulcer is seen in burn patient.

Degrees of Burns
Dupuytren recognised six degrees of burns but they were merged into three groups by Wilson.
1. Epidermal (First and Second degree Dupuytren): Usually a blister (vesicle or bulla) is formed which is covered by white, avascular epidermis, bordered by red, hyperaemic skin. These burns are very painful. Repair is complete without scar formation.
2. Dermo-epidermal (Third and Fourth degree Dupuytren): Whole thickness of skin is destroyed. Skin and subcutaneous tissue is affected. In Dermo-epidermal, pain and shock are greater than in first degrees burns (most painful).
3. Deep (Fifth and Sixth degree Dupuytren): In this, there is gross destruction not only of the skin and subcutaneous tissue but also of muscles and even bone. Nerve endings are also destroyed and as such, the burns are relatively painless.

The extent of the surface
The estimation of the surface area of the body involved is worked out by the ‘rule of nine by Wallace.

  • 9% for head and each upper limb,
  • 9% for front of each lower limb,
  • 9% for back of each lower limb,
  • 9% for front of chest,
  • 9% for back of chest,
  • 9% for front of abdomen,
  • 9% for back of abdomen i.e. 99% of the body.
  • Remaining 1% for external genitalia.
  • Involvement of 50% of burn proves fatal, even of first degree.

Causes of death in burns
(i) Primary (neurogenic) shock due to pain,
(ii) More, than half of deaths from burns occur from secondary shock due to fluid loss from burnt surface.
(iii) Toxaemia.
(iv) Sepsis —> It is late cause of death due to burn.
(v) Acute renal failure,
(vi) Pyemia.
(vii) Suffocation.

Flash burns refer to thermal burns due to sudden exposure to flame.
Presence of carbon particles in trachea and an elevated CO saturation together are absolute proof that the victim was alive when fire occurred. The exudate begins to dry in 12-24 hrs. from dry brown crust within 2-3 days; pus may form under slough in 36 to 72 hours; slough falls off in 4 to 6 days.

Pugilistic attitude (boxing, fencing, or defence attitude)
Pugilistic attitude is due to heat stiffening, seen both in AM and PM burns. This stiffening is due to coagulation of protein albumin of the muscles which causes contraction. Heat stiffening is due to exposure of the body to temperature above 75°C. Pugilistic attitude is seen in those dying due to burns, and sudden immersion in boiling liquid. In heat stiffening, body assumes a posture of generalised flexion.

A scald is an injury which is caused by application of liquid above 60°C or from stream.
Electrical injuries: The electric mark (Joule burn) is specific and diagnostic of electrical bum. Joule burn is both exogenous and endogenous burn. High tension electric currents may produce multiple burns or punched out lesions due to arching from conductor to the body without contact, which present crocodile flash burns. Crocodile flash burn is due to high voltage flash burn. Most common cause of death in electrocution is ventricular fibrillation.
Death may occur from paralysis of medullary (respiratory centre) or from ventricular fibrillation and cardiac arrest.

Lightning stroke
A flash of lightning is due to an electrical discharge from a cloud to the earth. The burns may be Arborescent or Filigree burns (Lichtenberg’s flowers). Arborescent burns are superficial, irregular, thin, resembling the branches of a tree.

In acute starvation, there is a feeling of hunger for the first 30 to 48 hours, followed by pain in the epigastrium which is relieved by pressure. After 4 to 5 days of starvation, general emaciation and absorption of the subcutaneous fat begins to occur. The tongue is coated and dirty and thirst is intolerable. Usually the loss of 40% of body weight is fatal. The intellect remains clear till death. Death occurs from exhaustion, circulatory failure due to brown atrophy of the heart, or intercurrent infection. Ammonia in brain is detoxified in to Glutamine. During starvation the substance which heart uses as energy source is acetoacetate. If starvation exceeds 7 days then the major nutritional supply of brain comes from ketone-bodies. Absorption of Vit. B12 occurs in ileum.

The changes in starvation seen are Hypoglycemia, Hyper-triglyceremia and Ketoacidosis. (except—Hyper cholesterolemia). Iron absorption is decreased by phosphates, phytates, oxalates (except—ascorbic acid).

Fatal period: If both water and food are completely stopped, death occurs in 10 to 12 days.
If food alone is stopped, death occurs in 6-8 weeks or even.
On P-M examination, the heart is small (from brown atrophy), and chambers are empty. The gall bladder is distended with bile.

Asphyxial deaths:
1. Suffocation—Mechanical obstruction to airways other than by hanging, strangulation and throttling. MC cause is inhalation of irritant gas.
2. Smothering—Closing the external respiratory orifice by hand or by other means.
3. Gagging—Closing mouth and nose with cloth etc. and tying around head or stuffing it into mouth.

Hanging is that form of asphyxia which is caused suspension of the body by a ligature, which encircles the neck, the constricting force being the weight of the body.
In partial hanging, the bodies are partially suspended; the weight of the head (5-6 kg) acts as the constricting force.
Typical hanging: In typical hanging, the ligature runs from the midline above the thyroid cartilage symmetrically upward on both sides of neck to the occipital region.

Causes of Death:
1. Asphyxia: A tension of 15 kg on ligature blocks the trachea.
2. Venous congestion: The jugular vein is closed by a tension in the rope of 2 kg.
3. Combined asphyxia and venous congestion: this is the commonest cause.
4. Cerebral anemia: A tension of 4 to 5 kg on ligature blocks carotid arteries, and 20 kg
blocks the vertebral arteries.
5. Reflex vagal inhibition from pressure on the vagal sheath or carotid bodies.
6. Fracture or dislocation of the cervical vertebrae.
Fatal period: The usual period is 3 to 5 minutes.

Post-mortem appearance:
The ligature mark in the neck is the most important and specific sign of death from hanging. The ligature mark is situated above the level of thyroid cartilage between the larynx and the chin in 80 percent cases. In partial hanging, the feet touch the ground. Le facie sympathique (it the ligature knot presses on cervical sympathetic, the eye on the same side may remain open and its pupils dilated) is seen in ante-mortem hanging. The eyes are frequently protruded and firmer and the conjunc¬tiva congested, the pupils are usually dilated. Saliva may be found dribbling from the angle of the mouth (due to stimulation of the salivary glands by the ligature). Seminal emission is common. In rare cases (5 to 10%), the intima of the carotid arteries show transverse split. Hyoid bone is fractured in 15 to 20% cases. Are seen in persons above 40 years; involves the great horn at junction of the inner two-thirds and outer one-third.

Judicial hanging: Justifiable homicide is judicial hanging and death of a suspected criminal while executing arrest. Legal death sentence is carried out by hanging the criminal. The cause of death in judicial hanging is fracture dislocation at the level of second and third or third and fourth cervical vertebra.
Lynching is a type of homicidal death by hanging by large group of people.

Strangulation is that form of asphyxia, which is caused from constriction of the neck by a ligature without suspending the body.
It is of two types: (1) Strangulation by ligature, and (2) manual strangulation or throttling.
Cause of death: Death may be due to (1) asphyxia, (2) cerebral anoxia or venous congestion (3) combined asphyxia and venous congestion, and (5) rarely fracture – dislocation of cervical vertebrae.
The mark in strangulation completely encircles the neck transversely. Classical signs of asphyxia are seen in about 50% of victims.

Doing a post-mortem on a suspected case of strangulation in situ examination of neck structures is done after opening the skull and the chest, to allow blood to drain from the neck blood vessels. Most important sign of strangulation is ligature mark. Hyoid bone may be fractured in older persons in 10 to 15% cases.

The common methods of homicidal strangulation are: (1) Strangulation by ligature, (2) Throttling, (3) Bansdola, (4) Garrotting, and (5) Mugging
Mugging is homicidal strangulation caused by holding the neck of the victim in the bend of the elbow.
Bansidola is a type of homicidal strangulation caused with sticks.
Garroting is type of homicidal strangulation caused by twisting a lever like torniquet.

(Signs of Strangulation) Signs of Asphyxia:
Intense maximum congestion and deep cyanosis of the head and neck is seen in strangulation. The eyes are wide open and pupils dilated. The tongue is swollen and protruded. Petechial hemorrhages are common in to the skin of the eyelids, face, forehead, behind the ears and scalp. Blood stained froth may escape from the mouth and nostrils and there may be bleeding from nose and ears. There is severe congestion and hemorrhage into the subcutaneous tissue in and above the area compressed. The intima of the carotid artery are not usually damaged. Injury of hyoid bone is not common in strangulation because the level of constriction is below the bone. Fracture of the thyroid cartilage is more common. Pulmonary oedema may be present.

Throttling is manual strangulation. Fracture of the hyoid bone in 30-50% cases. Fracture of the thyroid cartilage and hyoid bone are usually found in above 40 years. Hyoid bone fracture does not occur in choking. It is always homicidal.

Hyoid bone fractures can be classified in to three groups: (1) Inward compression fractures, (2) Antero-posterior compression fractures, (3) Avulsion fractures.

Inward compression fracture is seen in throttling, where the main force is an inward compression acting on the hyoid bone. Antero-posterior compression fractures is seen in case of hanging, the hyoid bone is forced directly backwards, due to which the divergence of greater horns is increased which may fracture with outward displacement of the posterior small fragment. Avulsion fractures occur due to muscular over-activity, without there being direct injury to the hyoid bone. They are also called “tug” or “traction” fractures.

Suffocation is a general term to indicate that form of asphyxia, which is caused by deprivation of oxygen, either due to lack of oxygen in the environment or from obstruction of the air-passages.

Smothering is a form of asphyxia which is caused by closing the external respiratory orifices either by the hand or by any other means, or blocking up the cavities of the nose and mouth by the introduction of a foreign substance, such as mud, paper, cloth, etc.

Gagging: is a form of asphyxia which results from forcing a cloth into the mouth, or the closure of mouth and nose by a cloth or similar material, which is tied around the neck.

Overlaying:It is a type of smothering. Overlaying or Compression suffocation results due to compression of the chest, so as to prevent breathing. Overlaying by mother is common in European countries. The usual findings are those of asphyxia.

Burking:It is a method of homicidal smothering and traumatic asphyxia.

In choking, there is obstruction within airways. It is very rare and is practicable only when the victim is an infant or suffering from disability or, disease or, under the influence of alcohol.

Cafe Coronary:
This is a condition in which a healthy but grossly intoxicated person, who begins a meal, suddenly turns blue, coughs violently, then collapse and dies due to asphyxia. Death appears to be due to sudden heart attack. A blow on the back or on the sternum may cause coughing and expel the foreign body.

Traumatic Asphyxia
Traumatic asphyxia results from respiratory arrest due to mechanical fixation of the chest, so that the normal movement of the chest wall is prevented. Common cause is crushing by falls of earth in a coal mine or during tunneling or in a building collapse. An intense cyanosis of deep purple or purple-red colour of the head, neck and upper chest, above the level of compression is the prominent feature.

Sexual Asphyxia
Partial asphyxia causes cerebral disturbance with feeling of sexual gratification. These cases are associated with some form of abnormal sexual behavior, usually masochism and transvestism.

Drowning is a form of asphyxia due to aspiration of fluid into air-passages, caused by submersion in water or other fluid. Commonest type of drowning is accidental.

In immersion syndrome, death occurs by vagal inhibition and cardiac arrest. Cold water drowning causes immersion syndrome. In secondary drowning, death occurs in half an hour to two days after resuscitation due to secondary changes in lungs. In secondary drowning, sign of asphyxia absent. Victim of drowning in a state of suspended animation can be revived in as long as 10-20 minutes. The extent and direction of the exchange through the alveolar lining depends on the difference between osmotic pressure of the blood and the water.

The drowning in fresh water, water passes rapidly from the lungs to the blood, leading to hemolysis and dilution of the blood with an abrupt increase in blood volume. Fresh water alters or denatures the protective surfactant which lines the alveolar wall. When water is inhaled, vagal reflexes cause increased peripheral airway resistance with pulmonary vaso-constriction, development of pulmonary hypertension, decreased lung compliance and fall of ventilation perfusion ratios. The concentration of serum electrolytes (sodium and calcium) decreases, serum potassium increases. The heart is subjected to hypoxia, overfilling, sodium deficit and potassium excess. Cardiac arrhythmias leading to ventricular tachycardia and fibrillation occur, probably due to hypoxia and hemodilution. Hemodilution leads to hemolysis, haemoglobinemia, and haemoglobinuria, marked hyponatraemia and hyperkalaemia. The potassium and chloride content of the left side of the heart is decreased.

Drowning in Sea water — Due to high salinity of sea water (usually over 3% NaCI), water is drawn from the blood into the lung tissue, and produces severe pulmonary oedema and hypernatraemia and increase in magnesium ion. This causes haemoconcentration. In sea water drowning, chloride content of the left side of the heart is higher (as is Mg concentration).

Causes of Death: (1) Asphyxia, (2) Ventricular fibrillation (3) Laryngeal spasm (4) Vagal inhibition (5) Exhaustion (6) Injuries.

Fatal period: Death usually occurs in 4 to 8 minutes of complete submersion. Hyper-ventilation before drowning can cause death.

Post-mortem appearance:
Gettler’s test is used in drowning. Gettler’s test is based on the biochemical changes in blood in a case of typical drowning. Gettler devised, a test to estimate the chloride content of blood from both sides of the heart. A difference of 25 percent in chioride content is considered significant.

— Limitations of Gettler’s test:
1. There is progressive loss of chloride from blood after death. To be maximal value therefore the test has to be made within a reasonably short time after death.
2. Has no value in atypical drowning.
3. Has no value in congenital cardiac defects such as shunts & patent foramen ovale where admixture of blood freely occurs between two sides of the heart.
4. Has no value if drowning medium and blood contain the same amount of chloride.

In homicidal drowning, multiple injuries may or may not be present. Chloride estimation is not of any help after 12 hours. Absence of foam in drowning can be found in death due to laryngeal spasm and immersion syndrome.

Regurgitation of gastric contents into the larynx and trachea in cases of drowning is due to vomit reflex due to medullary hypoxia. Cutis-anserina is seen in drowning. Cutis-anserina proves that molecular death present at the time of drowning. Wrinkling of limbs indicate that body was in water. Most important evidence for drowning is water in lungs and stomach. In drowning in unconscious state, there is no ballooning of lungs. Water can be absent in stomach in cases of drowning due to sudden death due to vagal inhibition. Presence of water in stomach in case of drowning is found in 70% cases. Deep inspiration above the water level and air pockets in clothing may cause early floatation of the body. Post-mortem staining is usually found on the face, the upper part of chest, hands, lower arms, and feet. The colour of PM stain is light-pink due to oxygenation, but in some cases it is dusky and cyanotic. Petechial hemorrhages are seen in subpleural tissues of lungs.

A fine white leathery froth is seen at mouth and nostrils, most characteristic external sign of drowning. The inhalation of water irritates the mucous membrane of air passages; mucous gland produces large quantity of tenacious mucous. Froth without mucous is seen in death due to strangulation, acute pulmonary oedema, electrical shock, during an epileptic fit, in opium poisoning and putrefaction.

Cutis anserina (goose skin or. goose flesh) in which the skin has granular and puckered appearance may be seen. Weeds, grass, sticks, leaves etc. floating in water may be firmly grasped in the hands due to cadaveric spasm. It indicates antemortem drowning. Bleaching of the cuticle becomes quite evident after 12 hours of immersion. The skin becomes sodden, thickened, wrinkled and white in colour, known as “Washer-women’s” hands, within 12-18 hours.

Wet drowning is due to entry of water into lungs. In wet drowning, lungs are overdistended and alveolar walls are torn. On section, an oedematous condition is seen. This has been described as “emphysema aquosum”.

In dry drowning, death occurs due to laryngeal spasm. There is no water entry into lungs. The alveolar walls may rupture due to increased pressure during forced expiration and produce sub-pleural haemorrhage known as ‘Paltauf’s haemorrhages’. They are shining, pale bluish – red, and may be minute or 3 – 5 cm in diameter. Usually present in the lower lobes.

The stomach contains water in 70% of cases. The small intestine may contain water in 20% cases. This sign is regarded as positive evidence of death by drowning as it depends on peristaltic movement which is a vital act. Haemorrhages are found in middle ear and temporal bone. Temporal bone haemorrhages are also seen in deaths due to hanging, head injury and CO poisoning.

Diatoms : Presence of  of diatoms in tissue is a sign of ante-mortem drowning. Diatoms are microscopic, unicellular, silica coated algae. The bone marrow of long bones such as femur, tibia, and humerus or sternum is examined for diatoms. Diatoms are examined by acid digestion technique.

The reliable signs of drowning at autopsy are:
1. Antemortem drowning is best demonstrated by fine, white froth at the mouth and nose.
2. The presence of weeds, stones etc. grasped in hand, shows ante-mortem drowning.
3. The presence of fine froth at lungs and air passages.
4. The voluminous water-loaded lungs.
5. The presence of water in stomach and intestine.
6. Finding of diatoms in the tissues.
The above signs are not found if death occurs due to vagal-inhibition. In dry – drowning, the PM appearances are those of asphyxia.
The body floats in about 12 to 18 hours in summer and 18 to 36 hours in winter in India.

…….Continued in Part.II

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Allen’s Keynotes & Characteristics with Comparisons Full text

books1Allen’s Keynotes And Characteristics with  Comparisons   of some of the Leading Remedies  of the Materia Medica  – Full text

By   H. C. Allen, M. D.

Author of  The Therapeutics of Fevers, Boenninghausen’s Repertory Slips,Materia Medica of the Nosodes.

Fourth Edition   Philadephia    Boericke and Tafel – 1916

Preface : Fourth Edition

Henri Clay ALLEN M.D. 1836-1909

What applied to the third edition applies to this, the   fourth. The facet that a fourth is demanded is onvincing proof that Dr. Allen left an  indestructible monument of homeopathic materia  medica, on that is true to Homeopathy an     immensely helpful to every physician who consults  it.

Preface : Third Edition 

The first edition of this book was only about half   the size of the second, as it was prepared somewhat hastily for a special purpose, but Dr. Allen took his   time to the second edition and gave the world a well rounded out and complete standard book on   homeopathic materia medica. We do no mean that the first edition was faulty as to its matter, for is was   used unchanged in the later edition, but it did not embrace a sufficient number of remedies. As Dr. Allen died before a third edition was needed we concluded to bring it out unchanged. It is a   masterpiece of materia medica work: its   symptomatology is made up of the unchanging   landmarks of our remedies that are in constant use;  it is, in short, a book that needs no revision.

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A quick review of all the aphorisms of Organon of Medicine

hahnem04Dr. Nihal kumar, BHMS, Pune

Dear Candidates,

If you don’t have  enough  time to read the entire aphorism

Or as a part of last moment revision on Aphorisms

You can use this notes for a quick review on all the aphorisms at a glance 

Download link : www.homeobook.com/pdf/organon-aphorism-quick-review.pdf

Organon – Aphorism with footnote (Full)

Organon55th Edition translated by Dudgeon

6th Edition translated by Boericke

                                                       § 1

The   physician’s   high   and   only   mission   is   to   restore   the   sick   to  health,   to   cure,   as   it   is termed.1

1  His   mission   is   not,   however,   to   construct   so-called   systems,  by   interweaving   empty speculations and hypotheses concerning the internal essential nature of the vital processes and   the   mode   in   which   diseases   originate   in the   interior   of   the   organism,   (whereon   so many physicians have hitherto ambitiously wasted their talents and their time); nor is it to attempt   to   give   countless   explanations   regarding   the   phenomena   in   diseases   and   their proximate   cause   (which   must   ever   remain  concealed),   wrapped   in  unintelligible   words and an inflated abstract mode of expression, which should sound very learned in order to astonish the ignorant – whilst sick humanity sighs in vain for aid. Of such learned reveries (to which the name of theoretic medicine is given, and for which special professorships are   instituted)   we   have   had   quite   enough,   and   it   is   now   high   time   that   all   who   call themselves   physicians   should   at   length   cease   to   deceive   suffering   mankind   with   mere talk, and begin now, instead, for once to act, that is, really to help and to cure.

                                                       § 2

The   highest   ideal   of   cure   is   rapid,   gentle  and   permanent   restoration   of   the   health,   or removal and annihilation of the disease in its whole extent, in the shortest, most reliable, and most harmless way, on easily comprehensible principles.

                                                       § 3

If the physician clearly perceives what is to be cured in diseases, that is to say, in every individual case of disease (knowledge of disease, indication), if he clearly perceives what is   curative    in  medicines,     that  is  to  say,   in  each   individual     medicine     (knowledge      of medical powers), and if he knows how to adapt, according to clearly defined principles, what is curative in medicines to what he has discovered to be undoubtedly morbid in the patient, so that the recovery must ensue – to adapt it, as well in respect to the suitability of the   medicine   most   appropriate   according   to   its   mode   of   action   to   the   case   before   him (choice of the remedy, the medicine indicated), as also in respect to the exact mode of preparation and quantity of it required (proper dose), and the proper period for repeating the dose; – if, finally, he knows the obstacles to recovery in each case and is aware how to remove them, so that the restoration may be permanent, then he understands how to treat judiciously and rationally, a nd he is a true practitioner of the healing art .

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Mnemonic or Medical Students

 students9Diaphragm apertures: spinal levels        

  •  Aortic hiatus = 12 letters = T12
  • Oesophagus = 10 letters = T10
  • Vena cava = 8 letters = T8

 Duodenum: lengths of parts                                                                                                                

  • “Counting 1 to 4 but staggered”:
  • 1st part: 2 inches
  • 2nd part: 3 inches
  • 3rd part: 4 inches
  • 4th part: 1 inch

 Liver inferior markings showing right/left lobe vs. vascular divisions

There’s a Hepatic “H” on inferior of liver. One vertical stick of the H is the dividing line for anatomical right/left lobe and the other vertical stick is the divider for vascular halves. Stick that divides the liver into vascular halves is the one with vena cava impression (since vena cava carries blood, it’s fortunate that it’s the divider for blood halves).

Meckel’s diverticulum details

  • 2 inches long.
  • 2 feet from end of ileum.
  • 2 times more common in men.
  • 2% occurrence in population.
  • 2 types of tissues may be present.

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Anatomy Mnemonics

AnatomyBRACHIAL PLEXUS: Roots, Trunks, Divisions, Cords, Branches

Randy Travis Drinks Cold Beers.

Robert Taylor Drinks Cold Beer.

CRANIAL NERVES: I-optic, II-olfactory, III-oculomotor, IV-trochlear, V-trigeminal, VI-abducens, VII-facial, VIII-acoustic (vestibulocochlear), IX-glossophrayngeal, X-vagus, XI-spinal accessory, XII-hypoglossal

  • On Old Olympus Towering Tops, A Finn And German Viewed Some Hops
  • You have I nose. You have II eyes. (I – Olfactory; II — Optic)

Innervation of Extraocularmotor Muscles:

  • LR6 (SO4) 3
  • LR6–Lateral rectus–> VI abductens
  • SO4–Superior Oblique–> IV Trochlear
  • 3–The remaining 4 eyeball movers = III
  • Some Say Marry Money, But My Brother Says Big Bras Matter More (what cranial nerve is Motor, Sensory, or Both)

BRANCHES OF FACIAL NERVE: Temporal, Zygomatic, Buccal, Masseteric, Cervical

  • Ten Zebras Bought My Car
  • To Zanzibar By Motor Car


  • c345 keeps the phrenic alive (innervation of phrenic nerve)
  • c345 keep the diaphragm alive (innervation of diaphragm)
  • c5-6-7 raise your arms to heaven (nerve roots of long thoracic nerve innervate serratus anterior)


  • The duck is between two gooses (duck = thoracic duct)
  • 2 gooses = azyGOUS and esophaGOUS


  • A lady between two majors.
  • Pectoralis major attaches to lateral lip of bicipital groove.
  • Teres major attaches to medial lip of bicipital groove.
  • Latissimus dorsi attaches to the floor of bicipital groove.
  • The “lati” is between two “majors.”


  • Parasympathetic puts it up; sympathetic spurts it out
  • “S2, 3, 4 keep the penis off the floor”
  • Innervation of the penis by branches of the pudental nerve, derived from spinal cord levels S2-4

“Lateral is less, medial is more.”

Lateral pectoral nerves goes through pectoralis major while medial p.n. goes though both pec major and minor


  • ABC’S
  • Aortic arch gives off the Bracheiocephalic trunk, the left Common Carotid, and the left Subclavian artery


  • “NAVEL”
  • nerve, artery, vein, empty space, lymphatics

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2.  Irving’s Anatomy Mnemonics

Virology for competitive examinations

virus2Dr. Sabitha Vijayan BHMS, MD

Interferon – antiviral substances, it is a family of host coded proteins produced by cells on induction by viral or non viral substances
Pox virus:- small pox- last detected case of small pox – sarban devi , a bengladeshi woman on 24th may 1975.


  • Herpes simplex virus  type I causes oral and cutaneous lesions spreading by direct contact
  • Herpes simplex type II causes genital tract infection transmitted venerally.
  • Occupational variety of cuteneous lesion is herpetic whitlow seen in doctors, nurses and dentists.

Eczema herpeticum
Generalized eruption occurs in children suffering from eczema
Crops of vesicles appear around the ulcer;clinically indistinguishable from vaccinia virus infections . both designated as Kaposi’s varicella form eruptions.

In chicken pox eruptions are centrifugal in distribution. (small pox rashes are centripetal in distribution)

In chicken pox patients , secondary bacterial infection due to streptococci or staphylococci occurs. This is called Reyes syndrome. Clinically characterized by acute hepatic failure, encephalopathy and hypoglycemia.

Herpes zoster (syn; shingles, zona)

  • Occurs in patients affected with chicken pox years later.
  • Ramsay hunt syndrome:- rare form of zoster affecting facial nerve with eruption on areas of tympanic membrane and external auditory canal with facial palsy.

Epstein – Barr virus
Causes IMN (infectious mono nucleosis)

Associated with

  • Burkitt’s lymphoma
  • Immunodeficiencies
  •  Naso pharyngeal carcinoma

IMN (glandular fever) – acute self limited illness seen in non immune adults following primary infection with EB virus. Incubation period is 4- 8 weeks . standard diagnostic test is Paul –  Bunnel test

Adenovirus causes respiratory infection , usually picorno virus includes

–  enterovirus –  coxachie virus and polio virus

Poliomyelitis is mainly 3 types

  1. Minor illness :- called abortive polio with head ache, sore throat, and malaise
  2. Non paralytic illness:- it does not progress beyond asceptic meningitis
  3. 5-10% causes paralytic polio

Vaccine:- 2 types

a.     Salk’s killed polio vaccine

b.     Live polio vaccine is oral polio vaccine

  • Orthomyxovirus causes influenza.
  • Paramyxovirus  Eg. Mumps virus
  • Measles (Rubiola) – genus morbiliform virus
  • Multinucleated giant cells called Warthin – Finkelclay cells are found in lymphoid tissue of patients.
  • Koplik’s spots developon buccal mucosa two or three days before the appearance of rash.


  1. Japanese encephalitis (vector- culex tritaneorynchus)
  2. Yellow fever – Vector – Aedes aegypti
  3. Dengue fever –  Vector  – Aedes aegypti

Tick borne encephalitis eg. KFD (Kyansur forest disease)

 Eg. Rabies virus  causes hydrophobia

  • Diagnosis is confirmed by negri bodies (inclusion bodies) in brain in post mortem examination mostly in hippocampus and cerebellum
  • PAPOVA virus include papilloma virus group and polyoma virus group.
  • The common human disease produced by papova virus is papilloma or wart. (verruca vulgaris)
  • A special type of wart is condylom accuminatum or genital wart found on external genitalia. This may be transmitted venerally and may occasionally turn malignant.
  • Parvo virus cause erythema infectiosum –‘the fifth disease’ a contagious disease of children characterized by erythematous rash first appearing on cheeks. – slapped cheek appearance.


  1. Caused by genus rubivirus of family toga viridae
  2. Koplik’s spot absent
  3. Rash is discrete and coalesce and disappear on 3rd day
  4. Non tender enlargement of post cervical glands is characteristic
  5. If Rubella occurs in early pregnancy, the foetus may die
  6. Congenital malformations are common during first trimester.
  7. Infected babies constitute an important source of infection for about 6 months (virus may persist for years in tissues such as cataractous lenses)
  8. Diagnosis of Rubella in early pregnancy is an indication for therapeutic abortion.
  9. Cruzfelt – Jacob disease is sub acute encephalopathy with progressive incoordination and dementia caused by group b prion virus.

Haemorrhagic fever with renal syndrome(HFRS)- also known as epidemic haemorrhagic nephrosonephritis is caused by Huntaan virus of family Bunya viridae.

HIV – human immunodeficiency virus – retro virus now called Human T cell lymphotrophic virus

  • RNA virus attacks CD4 cells.
  • A. Envelops antigens – 1. spicks antigen, 2. transmembrane
  • B. Shell antigen
  • C. Core antigen
  • D. Polymerase antigen

            Incubation period varies from 2-6 weeks to 15 years.

Features characaterising AIDS

  • 1.     Lymphopenia
  • 2.     Selective T cell deficiency – reduction in numbers of T4 (CD4) cells, inversion of T4: T8 ratio
  • 3.     Decreased delayed hypersensitivityon skin testing
  • 4.     Hypergammaglobulinaemia – predominantly IgG and Ig A; also IgM in children.
  • 5.     Polyclonal activation of B cells an dincreased spontaneous spontaneous secretion Ig.
  • Common malignancies associated with HIV infection is Kaposi’s sarcoma and lymphoma- hodgkin’s and Non hodgkin’s types.

HIV- Elisa for detection :  Western blot for confirmation

Ergotoxicosis (ergotism) is due to claviceps purpura growing on fruiting heads of rye.


            Hepatitis A – incubation period  –   2- 6 weeks

            Hepatitis B  – I P                                     4 – 8 weeks

            Hepatitis C  –      I P                                2 – 22 weeks

            Hepatitis D         I p                                4 – 8 weeks

            Hepatitis E          I P                               2 – 9 weeks

  1. Hepatitis B – DNA virus ; all others are RNA virus
  2. Spreads by faeco oral route –  hepatitis A and E
  3. Spreads by percutaneous route –  Hepatitis B,C and D
  4. Hepatitis B also spread by vertical and sexual route
  5. Oncogenicity present in Hepatitis B especially after neonatal infection.
  6. Carrier state present in Hepatitis B only
  7. Hepatitis B virus may present in blood and other body fluids and excretions such as saliva, breast milk,semen, vaginal secretions, urine , bile etc.
  8. Feces not known to be infectious
  9. HBs Ag is the first viral marker to appear in blood after infection; it remains in circulation throughout icteric course of disease. In a typical case it disappear within roughly 2 months but may last for 6 months.
  10. HBsAg is not demonstrable in circulation but antibody, antiHBe appear in serum a week or two after appearance of HbSAg
  11. So anti-HbeAg is the antibody marker to be seen in blood.
  12. HBeAg (HB envelop antigen) appears in blood concurrently with HBsAg. HbeAg is an indicator of intrahepatic viral replication and its presence in blood indicates high infectivity.
  13. For diagnosis of HBV infection, simultaneous presence of IgM, HBC indicates recent infection and presence of IgG ;anti H-Be indicates remote infection.
  14. Type E hepatitis : enterically transmitted.
  15. Non A – non B hepatitis caused by Hep. C virus

Inclusion body inviruses

a.     Intracytoplasmic

Guarnieri body –  Varicella, Vaccinia

Negri body – Rabies

Henderson – Paterson body –  Molluscum contagium

  • b. Intranuclear
  • a. Lipschutz bodies –  herpes fibrilis, herpes zoster, varicella
  • b. Councilmann’s bodies –  yellow fever, virus B encephalitis
  • c. Nicolau’s bodies – herpes fibrilis, herpes zoster , polio, Rift valley fever

Association of virus with human cancer

Virus family Virus genus Human cancer
Herpes virus E-b Virus Nasopharyngeal carcinomaAfrican Burkitt’s lymphomaB- cell lymphoma
Herpes 2 virus Cervical carcinoma
Papova viridae Papilloma virus Urogenital tumourSquamous cell carcinoma
Hepadne virus Hep B virus Primary Hepatocellular carcinoma
Retrovirus HTL virus Adult T Cell Leukaemia

 Viral infections associated with associated with maculopapular rash

  1. Adenovirus infection
  2. Arbovirus infection
  3. Measles
  4. Cytomegalovirus infections
  5. Enterovirus
  6. Hep-B virus
  7. IMN (kissing disease)
  8. Rubella
  • Haemolytic uraemic syndrome caused by virotoxin producing e-coli
  • Brazilian purpuric fever caused by Haemphilus aegypticus
  • Cryptospridum causes diarrhea
  • Cat scratch disease is caused by cat scratch bacillus


Superficial mycosis(cutaneous ) or dematophytis

  1. Microsporum –  attacks skin and hair ; not nail
  2. Tricophyton attacks skin , hair and nails. Most important human parasites are T. rubrum and T. tonsuran
  3. Epidermophyton  – e.floccosum attacks skin and nails but not hair.


  • Tinea capitis – ring worm of scalp
  • Tinea circinata – ringworm of glabrous skin
  • Tinea barbae –  ringworm of beard
  • Tinea pedis – Athletes foot
  • Tinea cruris – Dhobi itch or Jock itch
  • Tinea unguum  – ring worm of nails

Systemic mycosis

  • Candid albicans – yeast like fungi
  • Histoplasma capsulatum –  Darling’s disease
  • Cryptococcus neoformans – yeast
  • Aspergillus  –  fungus ball
  • Cocciodes immitis – desert rheumatism

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Microbiology notes for competitive examinations

virus1Dr. Sabitha Vijayan BHMS, MD

  1. The first person to observe bacteria – Anton von leuwen hock
  2. The earliest discovery of pathogenic micro organism was probably made by – Augustino Bassi
  3. The development of bacteriology as a scientific discipline date from Louis Pasteur
  4. The kingdom Protista has been divided into two groups – prokaryotes and Eukaryotes
  5. Bacteria and blue green algae are Prokaryotes while fungi, algae, slime moulds and protozoa are Eukaryotes.
  6. The types of staining that may be toxic and that which kills bacteria is called supravital staining.
  7. Bacteria have an affinity to basic dyes due to acidic nature of protoplasm.
  8. Acid fast staining discovered by Ehrlich and modified by Zeil and Neelssen.

According to shape bacteria are classified into

  • 1. Cocci –  spherical shaped bacteria
  • 2. Bacilli –  rod shaped cells
  • 3. Vibrio –  comma shaped cells
  • 4. Spirilla- rigid spiral forms
  • 5. Spirochetes- flexuous spiral forms
  • 6. Actinimycetes –  branching filamentous form.
  • 7. Mycoplasma – lacks cell wall. Hence do not possess stable morphology.

Cultural media may be a complex medic if ingredients are added for special purpose of growth.


  •  Refers to resistance exhibited by host towards injury caused by microorganisms and their products.
  • Innate immunity is inborn.
  • Acquired immunity may passive and active immunity.
  • Active immunity developed by an individual due to antigenic stimulus . once developed it is long lasting.
  • In PASSIVE immunity no antigenic stimulus; preformed ontibodies are administered.
  • An antigen has been defined as any substance when introduced parenterally into the body stimulates the production of antibodies. The smallest unit of antigenicity is called an epitope
  • Antibodies are immunoglobulins 
  • IgG :- this is major serum immunoglobulin. Its level is raised in chronic malaria, kala azar, or myeloma. IgG is only maternal immunoglobulin that is normally transported across the placenta and provides natural passive immunity in newborn.
  • IgA:-it is the second most abundant class of immunoglobulin seen in body fluids such as colostrums, saliva and tears. 
  • IgM:- is called ‘millionaire” molecule. It is not transported across the placenta hence presence of IgM in the foetus or newborn indicates diagnosis of congenital infection such as syphilis, rubella, HIV and toxoplasmosis.
  • IgM antibodies are short lived, hence their presence in serum indicates recent infection. 
  • IgE:- greatly elevated in atopic (Type I allergy) conditions such as asthma, hay fever, eczema, and also in children having high load of intestinal parasites. 
  • In general
  •             IgM – protects body fluids
  •             IgA – protects body surfaces
  •             IgM – protects blood stream
  •             IgE –  mediates reagenic hypersensitivity
  • Bence jones proteins are abnormal light chain immunoglobulins seen in multiple myeloma.
  • Coomb’s test – antiglobulin test- dirct commb’s test is positive in haemolytic disease of newborn due to Rh incompatibility
  • Idirect commb’s test is positive in Brucellosis 
  • Wasserman reaction (Serodiagnosis of syphilis) is a complement fixation test
  • The term hypersensitivity means injurious consequence in sensitized host following contact with specific antigens. Mainly classified into
  • Immediate – B-cell or antibody mediated and Delayed – t cell mediated 
Immediate hypersensitivity Delayed hypersensitivity
1. Appears rapidly and recedes rapidly2. Induced by antigens or happens by any route3. Circulating antibodies are present and responsible for reaction4. So antibody mediated reaction 1. Appears slowly and lasts longer2. Induced by infection, ingestion of antigen or happen intradermally3. Antibodies absent4. Cell mediated reaction 
  1. In anaphylactoid reactions there is no immunological basis.
  2. Shwartzan reaction is not an immune reaction but reaction resembles immune inflammation.
  3. Auto immunity is a condition in which structural or functional damage is produced by action of immunologically competent cells or antibodies against normal components of body.
  4. Rose water test is used for the detection of rheumatic fever.


  • Gram positive
  • Occurs in ‘grape like clusters’
  • Enzyme coagulase present

Common culture media is nutrient ogar and organization shows ‘oil –paint’ appearance in medica. Main exotoxins of S.aureus are cytolytic toxin, enterotoxin and exfoliative toxins. Entero toxin causes staphylococcal food poisoning (milk and milk products are responsible for common food items)

Exfoliative toxins causes TSS (toxic shock syndrome)

And SSSS  – Staphylococcal scalded skin syndrome- seen in infants – Ritter’s disease


  1. Localized skin lesions including furuncles, styes, boils, abscesses, carbuncles, impetigo.
  2. Sepsis in burns and wounds
  3. Acute osteomyelitis
  4. Tonsillitis, pharyngitis, pneumonia, especially bronchopneumonia secondary to some respiratory infections
  5. Breast abscess in lactating mothers
  6. Tropical myositis- in young adults of tropics multiple abscess in voluntary muscles.
  7. In staphylococcal food poisoning diarrhea and vomiting starts with in 6 hours of taking contaminated food
  8. Exfoliative diseases such as impetigo, pemphigus neonatorum, Ritter’s disease, toxic epidermal necrolysis.
  9. Non pathogenetic staphylococci- staphylococcus epidermitidis


  • Gram positive
  • It causes SPREADING PYOGENIC INFECTIONS  and non suppurative lesions sucj as rheumatic fever and glomerulonephritis
  • 3 types
  • Alpha haemolytic s.cocci
  • Beta haemolytic s.cocci
  • Gamma haemolytic s.cocci (non haemolytic)
  • Streptococci form several exotoins and ensumes. The two haemolysins are haemolysin ‘O’ and ‘S’.
  • Streptolysin ‘O’ is oxygen labile. Streptolysin regularly appear in sera following streptococcal infection –  ASO tite
  • Strepto lysine S is not antigenic
  • Erythrogenic toxin is also called Dick , scarlatinal or pyrogenic toxin.

DICK TEST:- this test is used to identify children susceptible to scarlet fever (scarlet fever is a type of acute pharyngitis with extensive rash caused by str.pyogens

SCHULRZ CHARTON reaction:- blanching of rash on localinfection convalescent serum. This is used as a diagnostic test in scarlet fever.

The enzyme sternodornase present in the str.cocci helps to liquefy pus and hence responsible for serous character of pus.


  • Respiratory infection including sore throat, tonsillitis, pharyngitis
  • Extension of infection from  throat to surrounding tissues causes ASOM, mastoiditis , quinsy, Ludwig’s angina, suppurative adenitis
  • Skin and subcutaneous infection –  Variety of suppurative infection including infection of wounds or burns.
  • 2 typical streptococcus infections are Erysipelas and impetigo (impetigo are vesicular pin head like infection with exfoliation.)
  • Streptococcal subcutaneous infection range from cellulites to necrotizing fascitis.
  • Genital infection including puerperial sepsis and abscess in internal organs such as brain, kidneys etc.
  • Non suppurative leisions such as rheumatic fever and acute glomerualonephritis.
  • In rheumatic fever, a connective tissue degeneration of heart valve and inflammatory myocardial leisions causes Aschoff nodules
  • Str. Viridans normally residing in mouth and upper respiratory tract


  • It is gram positive
  • Single most prevalent bacterial genera in pneumonia, otitis media, acute sinusitis, meningitis, and other infectious processes
  • Cultural characters :- on blood agar draughtsman or carom coin appearance. It exhibits capsule swelling reaction called quelling reaction.
  • The toxins are oxygen labile haemolysin and a leucosidin


  • Lobar pneumonia
  • Bronchopneumonia following viral infections
  • Acute exacerbation of chronic bronchitis (haemophilus influenza also causes this)
  • Empyema, pericarditis, ASOM, otitis media, sinusitis, conjunctivitis, suppurative arthritis


  • Gram negative cocci
  • N.meningitidis
  • Causes meningococcal meningitis or cerebrospinal fever
  • Oval or spherical in shape
  • Grows only on enriched media such as blood agar, chocolate agar
  • Modified  Thayer-Martin media is a useful selective media 


  • Cerebrospinal meningitis
  • Meningococcal septicemia
  • In meningococcal septicemia there occurs adrenal haemorrhage and shock. This is Water house – Frederickson syndrome

N. gonorrhoea

            Causes veneral disease gonorrhoea. Here also Thayer – Martin media is used.


            Gonorrhoea is acquired by sexual contact. c/c urethritis lead to stricture formation. The may spread to periurethral tissue causing abscess and multiple discharging sinuses. (Water can perineum)

  • In women causes Bartholinitis and salpingitis
  • Proctitis, conjunctivitis, arthritis, ulcerative endocarditis and meningitis
  • Non veneral infection is gonococcal ophthalmia in newborn


Causative organisms are

  1. Chlamydia trachomatis
  2. Ureaplasma urealyticum
  3. Mycoplasma hominis 


  • Gram positive
  • Non acid fast, non motile rods
  • C.diphtheria :- syn. (Loffler’s bacillus)
  • Having Chinese letter of cuneiform arrangement
  • Usual media –  Loeffler’s serum slope and tellurate blood agar

3 types –

  • Gravis – most fatal infections
  • Intermediate
  • Mitis

Universally used strain is Park william’s strain


Site of infection

  1. Faucial
  2. Laryngeal
  3. Nasal
  4. Otitic
  5. Conjunctival
  6. Genital
  7. Cutaneous
  • Faucial diphtheria is the commonest type. Classified into malignant or hyper toxic diphtheria in which there is sever toxaemia with marked adenitis – bull neck. Death occurs due to circulatory failure.
  • Septic- which leads to ulceration, cellulitis, gangrene
  • Haemorrhagic – characterized by bleeding from edge of membranes
  • Common complication – asphyxia, acute circulatory failure, post diphtheritic paralysis
  • SHICK TEST- susceptibility test for diphtheria


  • Rod shaped bacteria
  • 2 types
  • Aerobic bacilli and anaerobic bacillus
  • Gram positive

B.anthracis :- first pathogenic bacteria observed under microscope and it is the first bacillus to be isolated in pure culture and first bacterium used for preparation of attenuated vaccine.

M-Fayden’s reaction:- used for presumptive diagnosis of anthrax in animals

Culture media:- on agar media frosted glass appearance with locks of matted hair called medusa head appearance, on gelatin slab having ‘inverted fir tree’ appearance when grown on solid media ‘ strings of pearl reaction’.

ANTRAX is a zoonosis

3 types

1. Cutaneous 2. Pulmonary 3. Intestinal

  • All types leads to fatal septicemia.
  • Cutaneous anthrax
  • Follows infection through skin. Leisions are called ‘malignant pustule’ or black eschar
  • Disease is common in dock workers carrying loads of hides and skins on bare back. Hence called hide porter’s disease.


Wool sorter’s disease due to inhalation of dust from infected wool. There is haemorrhagic pneumonia. Haemorrhagic meningitis is a complication.

Intestinal anthrax is rare. Occurs mainly in primitive communities which uses undercooked meat.

Lab diagnosis is by immunofluoroscence

Bacillus cereus – causes food borne disease characterized by diarrhea and abdominal pain associated with consumption of cooked rice, usually fried rice from Chinese restaurant.

Gram positive

  • Anaerobic sphere forming bacilli
  • Genus responsible for  3 major diseases : 1.     Gas gangrene. 2. Food poisoning 3. Tetanus
  • Spores may be central or equatorial.  Eg. Cl. Bifermingens
  • Oval or terminal   Tennis racket  eg. Cl. Tertian
  • Spherical and terminal – drum stick appearance eg. Cl. Tetani

Useful media :   Robertson’s cooked meat broth

cl. perfingens –  Gas gangrene (malignant oedema)

  • Wound contamination
  • Septic abortion
  •  Anaerobic myositis
  • Food poisoning and
  • Necrotizing enteritis

In litmus reaction fermentation of lactose causes stormy fermentation

cl. perfingens show ‘Nagler reaction’ due to specific lecithinase effect

Food poisoning starts between 8-24 hours – self limiting illness

cl.noviji (cl.oedematiens)

Also causes gangrene characterized by high mortality and large amount of oedema fluid with little or no observable gas.

Clostridium tetani

  1. Drumstick appearance
  2. Media: robertson’s cooked meat broth
  3. 2 toxins: tetanolysin which is haemolysin and tetanospasmin which is a powerful  neurotoxin
  4. Tetanus toxins block synaptic inhibitors in spinal cord. While  strychnine acts post synaptically.
  5. Abolition of spinal inhibition causes uncontrolled spread of impulses initiated any where in CNS. This results in muscle rigidity and spasm.
  6. Sometimes tetanus may be due to local suppuration called otogenic tetanus.

Clostridium botulinum
Causes food poisoning – exotoxin is responsible for pathogenicity. It acts by blocking acetylcholine at synapse and neuromuscular junction. Hence onset marked by diplopia, dysphagia and dysarthria

Botulinum – 3 type

  1. Food borne botulism
  2. Wound botulism
  3. Infantile botulism

Food borne botulism– 12- 36 hours after ingestion

  •  Vomiting, thirst, constipation, ocular paresis, difficulty in swallowing, speaking, breathing, coma or delirium
  • Death is due to respiratory failure.
  • Wound botulism – Rare. Symptoms similar to food borne botulism except GIT symptoms
  • Infant botulism –  Infants less than 6 months are affected. Manifestations are constipation, poor feeding, lethargy, weakness, pooled oral secretion, weak or altered cry, loss of head control.


Enterobacteria – proteus

Mc conkeney’s medium

E coli- pathogenesis

  • Neonatal meningitis
  • Septicemia

Clinical features:

  1. UTI
  2. Pylonephritis and hypertension in pregnant women
  3. For diagnosis –  Mid stream urinalysis
  4. Diarrhea – traveller’s diarrhea
  5. Enterohaemorrhagic colitis – frank dysentery
  6. Pyogenic infection and septicemia

KLEBSIELLA (fried –landler’s bacillus)

            -Pneumonia, UTI, septicemia and rarely diarrhea 


            Shigella causes bbacillary dysentery

            Short incubation period – 1-7 days; usually 48 hours

  • Enterobacteria  – Salmonella
  • Salmonella typhi:- causes typhoid fever.
  • Enteric fever :- typhoid and paratyphoid fever- salmonella paratyphi A,B,C
  • Widal reacton
  • Leucopenia
  • Diazo test of urine

Slamonella gastroenteritis

Poultry, meat, milk, cream and eggs

Short incubation period – less than 24 hours


  • Gram negative; comma shaped
  • Described by Koch as ‘fish in stream’ vibrio colonies are identified by ‘string test’
  • Biochemical reaction- cholera rod reaction
  • In cholera – watery diarrhea, vomiting with hypovolumic shock and death in less than 2 hours
  • Stool has fishy odour and it is described as ‘rice watery’ stool.


  1. Bacillus pyocyanius
  2. Gram negative
  3. Pyocyanis forms blue pus ; self limiting illness –  shanghai fever
  5. Yersinia safety pin appearance
  6. On nutrient agar –  stalactile growth
  7. Yersinia causes plague
  8.  Pandemic plague causes black death due to extensice cutaneous haemorrhage and gangrene.
  9. 3 forms :     Bubonic, pneumonic and septicemic
  10. Vector is rat flea – xenophilla cheopis


  • Gram negative bacillus
  • Cultural media is blood agar and shows Satelletism in media


  • Meningitis
  • Otitis media
  • Pneumonia
  • Arthritis
  • Endocarditis, pericarditis
  • Bronchitis

Haemophilus ducreyi

Cause chancroid or soft sore. Veneral disease. Bacilli are arranged in groups called school of fish or rail road track appearance

BORDETELLA PERTUSIS ( bordet- gengou glycerine –potatoe blood agar

‘Bisected pearls’ or mercury drops’ with ‘aluminium paint’ appearance

Pathogenesis: Pertusis  or whooping cough.


Acute brucellosis ; undulant fever

                        Malta fever

                        Relapsing fever

Caused by B. melitensis – Brucellosis is primarily a disease of reticuloendothelial system

Lab investigation:- castinada method of blood culture.


  • Gram positive
  • Acid fast bacillus
  • In children it causes primary complex.
  • Ghon’s focus :- subpleural focus of tuberculous pneumonia in lung parenchyma
  • Adult type TB is due to reactivation of primary infection.
  • In mantoux test 0.1 ml. purified protein derivative is injected intracutaneously on flexor aspect of forearm. Site is examined after 48-72 hours
  • If induration of diameter 10mm or more – positive mantoux test
  • If induration is 5 mm. or less than 5mm. – negative
  • If induration is between 6-9 mm it is doubtful case. 

Caused by gram positive mycobacterium leprae. Organism is arranged in parallel rows are having ‘cigar bundle’ appearance. Masses of bacilli are called globi. The globi appear in virchow’s lepra cell or foamy cell.

Leprosy is a chronic granulomatous disease.

4 types

  1. Lepromatous
  2.  Tuberuloid
  3. Dimorphous
  4. Indeterminate
  • Lepromatous variety is most infectious type. Lepromin test is negative in lepromatous leprosy due to deficient cell mediated immunity.
  • In Tuberculoid leprosy patient is having high resistance. Good prognosis. Lepromin test is positive. Few skin lesions but neurological symptoms are more and deformity occurs early.
  • The term borderline or dimorphous refers to lesions possessing characteristic of both tuberculoid and lepromatous type.
  • The indeterminate type is early unstable tissue response to the microorganism. Lesions undergo spontaneous healing.
  • Classification according to Reiding & jopteng scale of classification
  • Lepromin test is described by metsuda
  • Biphasic events
  • First phase –  early reaction –  Fernandes reaction. Ie. Erythema and induration developing in 24-48 hours.
  • Late phase –  Mitsuda reaction –  starting 1 or 2 weeks later. It consists of indurated skin nodule which may ulcerate.
  • Lepromin test is positive in Tuberculoid leprosy
  • Lepromin test is negative in lepromatous leprosy
  • Lepromin test is variable in dimorphous and indeterminate varieties


  1.  Treponema pallidum causing syphilis
  2.  Treponema pertenue  causes yaws
  3.  Treponema carateum  causes pinta
  • Staining reaction is silver impregnation method
  • Syphilis is a veneral disease
  • Primary lesion is chancre
  • Lymph nodes are characteristically rubbery in consistency
  • Secondary syphilis starts after 2-6 weeks, characterized by roseolar skin rashes
  • After secondary syphilis there is a stage of latent syphilis. During this period diagnosis is possible by serological test. There occurs cardiovascular lesions including aneurysm.
  • Tertiary syphilis – delayed hypersensitivity reaction mainly tabes dorsalis and general paralysis of insane.

Serological test for diagnosing syphilis

  • A.    Reagin test
  • B.    Kahn test (floaculation test)
  • C.    VDRL test (veneral disease research laboratory test)
  • D.    Rapid plasma regain test is the first modified VDRL

First reagen test is Wasserman reaction


Causes relapsing fever

2 types

  • Louse borne relapsing fever
  •  Tick borne relapsing fever
  • Louse borne relapsing fever is caused by Borellia recurrentis
  • Borellia vincenti causes ulcerative gingivostomatitis or oropharyngitis called – vincent’s angina or cancre oris
  • Borellia burgdorferi causes lyme disease
  • Rat bite fever caused by spirillum minus or streptobacillus moniliformis


  1. Leptospira icterohaemorrhagica causes Weil’s disease which causes hepatorenal damage.
  2. Antibodies appear in serum towards the end of first week of disease and increase till 4th week. Caonicola fever is caused by leptospira canicola.


  •  Smallest free living microorganism. Organism in colony have ‘fried egg’ appearance.
  • Mycoplasma causes pneumonia and genital infection especially of children and adolescents.


  • Gram positive. Between bacteria and fungi
  • It causes ‘lumpy jaw’ in cattle.

Actinomycosis is a chrnic granulomatous infection characterized by development of indurated swelling mainly in connective tissue with suppuration and discharge of sulphur granules. Actinomycosis in human being is an endogenous infection. Actinomycetes Israeli is the causative organism.

3 forms

1. Cervico fascial

2. Thoracic

3. Abdominal

Pelvic actinomycosis is associated with the use of IUCD (intra uterine contraceptive device)

Actinomycetes mycetoma( Madura mycosis)
It is a localized chronic granulomatous involvement of subcuteneous and deeper tissue affecting foot and less commonly hands and presenting as a tumour with multiple discharging sinuses.

Helicobacter pylori associated with antral gastritis and peptic ulcer disease.

Legionella pneumonia is caused by Legionella pneumophilia. Human infection is typically caused by inhalation of aerosols produced by airconditioners and shower heads.


Gram negative organism

Weil – Felix raction used for diagnosis of rickettsial infection.

Scrub typhus –   Rickettsiae tsu tsu gambusti

Epidemic typhus

            Rickettsiae prowazekii (vector is louse or pediculus humanis)

  • Recrudescent typhus is activated latent infection called Brill- Zeinsser disease
  • Rocky mountain spotted fever  – Rickettsia rickettsi
  • Endemic typhus is caused by rickettsiae typhi  ( r. mooseri)
  • Transmitted by xenopsyla cheopis or rat flea
  • Trench fever  is caused by Rickettsiae Quintana
  • Transmitted by body louse
  • Q fever is caused by coxellia burnetti


  • Main pathogenitic varieties are
  • Chlamydiae psittaci
  • hlamydiae pneumoniae

Trachomatis causes

  1. Trachoma which is a chronic keratoconjunctivitis  (lab diagnosis by Hp bodies)
  2. Inclusion benorrhoea (neonatal form of inclusion conjunctivitis)
  3. Pool conjunctivitis
  4. Lymphogranuloma venerum

Chlamydia psittaci
Causes psittacosis – consumption of infected poultry products leads to this disease

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Parasitology for competitive examinations

virusDr. Sabitha Vijayan BHMS, MD

Parasites are organisms that infect other living beings. Medical parasitology deals with the parasites which infect man and diseases they produce.
Human parasites may be either unicellular microbes – the protozoa or larger organisms – the metazoan.
Parasites may be either ecto or endo parasites.
Ectoparasites inhabits body surfaces only without penetrating into tissues   Eg. Lice, tick, mites

They are important as vectors Transmitting pathogenic microbes.

The term infestation is employed for parasitation with ectoparasites while infection for endoparasites.

The host in which the adult stage lives or sexual mode of reproduction take place is called definitive host. The species in which larval stage of parasites live or asexual reproduction takes place is called intermediate host.

Paratenic host– a vertebrate host in which a parasite remains viable without development or multiplication is called paratenic host. Such a host may serve to pass on the infection to another is called a transport host.

Anthroponosis : Infection with a parasitic species that are maintained in man alone.Eg. Malaria, filaria

Premunition –  once a parasitic infection is completely eliminated, host become again susceptible to re infection, this type of immunity to re infection depends on the continued presence of residual parasites . this is called premunition.

The PROTOZOA are classified into 4 groups

  • Amoeba –  can assume any shape and crawl by means of pseudopodia
  • Flagellates – possess whip like appendages called flagella for locomotion
  • Sporozoa – production of spore like oocysts
  •  Ciliates – motile by means of cilia which covers entire body surface.


Entamoeba histolytica :- found in human colon. Infection is acquired though contaminated food and water containing mature cyst. Entire life cycle is completed in one host. Lumen dwelling amoeba when invade intestinal tissue cause disease.

Amoebic penetration of colon causes necrosis and abscesses. The abscesses breaks down into form an ulcer numerous in caecum. Superficial ulcers heal without scarring and deep ulcers form scars leading to strictures. Chronic ulcer leads to granuloma mistaken for malignant tumour

Parasite invade portal vein leading to multifocal hepatic invasion with liver enlargement. This is the stage of amoebic hepatitis. Peripheral extension leads to amoebic abscess. The centre of abscess contain thick chocolate brown pus  ‘ the anchovy sauce pus’ with liquefied necrotic tissues.

Amoebiasis of lung usually occurs in right lung. A hepatobronchial fistula develops with chocolate brown sputum.

Cutaneous amoebiasis occurs by direct spread from rectum ,perianally and colostomy openings and sinuses draining liver abscesses. Trophozoets can be demonstrated in leisions. Also occurs as a venereal infection of penis following anal intercourse.

The typical presentation of intestinal amoebiasis is amoebic dysentery, similar to bacillary dusentery.

Charcot-Leyden crystals are demonstrable in stool.

If diarrhea does not occur there may be vague abdominal symptoms called uncomfortable belly’ or growling abdomen’


1. Charcot-leyden crystals are found in microscopic faecal examination. ( also occur in malignancy  and ulcerative colitis)

2. In extraintestinal amoebiasis, LATEX agglutination and ELISA

Entamoeba gigivalis

Is a commensal in unhygienic mouths. Not reported to cause any disease.

Two pathogenic free living amoeba are 1. Naegleria and 2. acanthamoeba.

Species Naegleria fowleri causes acute purulent meningitis acquired by swimming in contaminated ponds.

Acanthamoeba causes acute meningoencephalitis and granulomatous leisions in skin, lungs, eyes or gastric mucosa; transmitted through inhalation, ingestion, or traumatized skin.

Both Naegleria and Acanthamoeba cause allergic pneumonitis acquired from amoeba growing in humidifiers of air conditioning plants.


 Intestinal flagellates

  • Giardia lamblia
  • Trichomonas vaginalis
  • Giardia lamblia was first observed by Leuwenhook in his own stool. It is the only protozoan parasite in the lumen of human small intestine.
  • Infection acquired by ingestion of cyst in the contaminated food and water.
  • Giardia L do not invade tissues but remain tightly attached by means of sucking disc.usually no clinical illness result but mucous diarrnoea, dull epigastric pain and flatulence.
  • But children may develop spruce like symptoms with chronic diarrhea.
  • Enhanced susceptibility to giardia associated with blood group A, achlorhydria, use of cannabis, chronic pacreatitis and AIDS.

Trichomonas vaginalis

Occurs in vagina and cervix and Bartholin’s gland, urethra and bladder in female and in anterior urethra, prostate and preputial sac in male.

Usually asymptomatic but may cause pruritic vaginitis in female and urethritis in male.

Haemoflagellates :  Lives in blood and tissues of man and  vertebrae and gut of insect vectors.

Haemoflagellates infecting man belong to 2 genera – Trypanosoma,  Leishmania

Haemoflagellates have two or more morphological stages such as amastigote, promastigote, epimastigote and trypomastigote

Trypomastigote stage lacking in leishmania

The important trypanosomes are the following

            1.T. brucci Gambians

            2. T. brucci rhodensis

            3. T. cruzi

  • T.brucei causes Nagana in cattle
  • T. gambiens –  west African sleeping sickness
  • T. rhodensis –  East African sleeping sickness
  • The human infection acquired by metacyclic trypomastigote form.
  • West African sleeping sickness(Gambian)
  • Vectors are glossina palpate and g. tachinoides
  • Incubation period – 1-2 weeks

Illness is chronic

Initial parasitemia following which they are predominantly located in lymph nodes.

Intermittent fever, chills, headache mark the stage.  There is hepatosplenomegaly with lymphadenopathy particularly in the post cervical region. With the invasion of CNS which occur after several months a sleeping sickness stage starts. Patient falls into coma and death.

East African (Rhodesian ) sleeping sickness

It is more acute form and may end fatally with in one year before involvement of CNS. Fever, weakness, rapid loss of weight and myocarditis.

Typical sleeping sickness not seen.

South American Trypansomiasis (Chaga’s disease) 

T.cruzi  Vector –  reduviid bug

These are night biting bug which defaecate while feeding. The faeces of infected bugs contain mitocyclic trypomastigote which are infective forms. Trypomastigote induce local inflammatory reaction called chogomas. When they enter through conjunctiva, unilateral oedematous swelling of eyelids results. This is Romana’s sign.

This disease ends fatally with myocarditis or meningoencephalitis.


Named after Sir. William leishman. Leishmania produce 2 broad type of clinical diseases. – Visceral and Cutaneous.

Mainly 4 type are parasitic to man

L. donovani- kala azar/ visceral leishmaniasis/ dumdum fever/ tropical splenomegaly.

L. tropica –  oriental sore/ old world cutaneous leishmaniasis.

L. braziliensis  or L. mexicana – new world cutaneous leishmaniasis or epsundia

Amastigote form of Leishmania donovani are seen smears of patients called L.D bodies, in giemsa or wright stain. Habitat is reticuloendothelial system.

Kala azar

Visceral leishmaniasis –  first characterized in India.

Vector- sand fly (phlebotomus argentipes)

PKDL – post kala azar dermal leishmaniasis –  is characterized by depigmented macules and erythematous patches on face- butterfly patches. Cut surface of liver shows nutmeg appearance. Leucopaenia , anaemia, neutropenia and thrombocytopaenia are common.

Diagnostic test for kala azar

  • Napier’s aldehyde test
  • Chopra’s antimony tes
  • Montenegro skin test(leishmanian skin test) this is negative in kala azar positive in dermal leishmaniasis and in persons who have recovered from kala azar. But not in active cases( the first two diagnostic tests are based on the increased globulin content of serum in the disease)

The antigen used in the serological test for non-leishmanial antigen is WKK antigen.

Three distinct patterns of old world cutaneous leishmaniasis are

1. Zoonotic rural type causing moist ulcers which are inflamed and often multiple- L. tropica major

2. Anthroponotic urban type causing painless dry ulcerating lesions often single leading to desquamating scars –  L. tropica minor

3. Non ulcerative  often diffuse lesions caused by L. aethiopica.

Leishmaniasis recidivans :- is a type of leisions seen in persons with a high degree of cell mediated immunity to the parasite . it resemble lupus or tuberculoid leprosy. Parasites are very scanty in the leisions, leishmanian test is strongly positive.

Mucocutaneous leishmaniasis or Epsundia is a late consequence of the cutaneous leishmaniasis due to L. brazieliensis. 


Syn; paludism in latin ; palus = marsh

Causative agent discovered in 1880 by Laveran , French army surgeon.

In 1886 Golgi described asexual development in the RBC – Golgi cycle

Romanowsky in Russia developed method of staining malarial parasite in blood films. Human malaria transmitted by female Anopheles mosquito. Chimpanzees act as reservoir hosts .

Mainly 4 species

  1. Plasmodium vivax
  2. Plasmodium malaria
  3. Plasmodium falciparum
  4. Plasmodium ovale
  • In life cycle of malaria parasite, asexual phase occurs in man and sexual phase occurs in mosquito. (the sexual phase takes place in female anopheles mosquito, even though sexual forms of the parasite origin in human RBC
  • In falciparum malaria ecrudescences are seen for one or two years;while in P.malariae infections they may last for even 50 years.
  • The periodicity of malarial fever depends on the erythrocytic schizogenic cycles to become synchronized so that all the mature shizonts in the body burst at the same time releasing merozoites and other pyrogens into the circulation causing febrile paroxysms.
  • P. vivax- benign tertian or BT malaria.fever recur after 48 hours
  • P. falciparum –  malignant tertian or MT malaria (also called subtertian. Fever paroxysm recur at less than the expected 48 hours. It is called pernicious malaria because of its lethal nature and active autumnal referring to its seasonal prevalence)
  • p.malariae –  Quartan malaria – 72 hours periodicity
  • P.ovale –  ovale tertian – 48 hours periodicity

Note:- sometimes in early P.vivax infection, there may be two independent broods of parasites with overlapping cycles so that there may be daily paroxysms. This is called quotidian periodicity

  • The infected erythrocytes show Schoffner’s dots on the surface in p.vivax infections.
  • Shortest incubation period is in P.falciparum infections
  • Longest incubation period is seen in p. malariae infections.
  • The minimum level of parasitaemia for their microscopic detection, is called microscopic threshold
  • The typical picture of malaria consist of periodic bouts of fever with rigor, followed by anaemia and splenomegaly.
  • All clinical manifestations  in malaria are due to the products of erythrocytic shizogony and host’s reactions to them.
  • The new malarial attack that appear after a period of latency, usually within eight weeks after the culmination of primary attack and resulting from persistence of erythrocytic cycle of parasite is called ecrudescence.
  • The most serious and fatal type of malaria MT malaria caused by P. falciparum . they may present in various forms, the most important of which are cerebral, algid, and septicaemic varieties.
  • Cerebral malaria is characterized by hyperpyrexia, coma, and paralysis.
  • Algid malaria resembles surgical shock.
  • In septicaemic malaria, characterized by high degree of prostration, high fever with involvement of various organs.
  • A syndrome called Black water fever is seen in falciparum malaria particularly in patients who have experienced repeated infections and inadequate treatment with quinine. It is malarial haemoglobunuria, seen in P.falciparum infections. It is due to massive intravascular haemolysis.
  • TSS- tropical splenomegaly syndrome- is a chronic benign condition seen in endemic areas. It is an abnormal immunological response to malaria characterized by splenomegaly, high titres of circulatory antimalarial antibody and absence of malarial parasite in peripheral blood smear.
  • National Malaria Eradication Programme – 1958
  • The immune depression caused by endemic malaria is responsible for the Buckett’s  lymphoma seen in African children.
  • Diagnosis :    ISB stain, Field’s stain
  • Several serological tests include immunofluorescence test, indirect haemagglutination, ELISA.


  •  Toxoplasma gondi
  • Cat is the definitive host
  • Congenital toxoplasmosis results when infection is transmitted trasplacentally from mother to foetus. Clinical manifestation may be developed after months or years, such as chorioretinitis, strabismus, blindness, deafness, epilepsy or mental retardation.
  • Sometimes acute disease manifestation occur such as fever, jaundice, hydrocephalus, pneumonitis or myocarditis.
  • Post nasal infection is usually asymptomatic. Commonest manifestation of acquired toxoplasmosis is lymphadenopathy particularly in post cervical lymph nodes
  • May become fatal in immunodeficiency diseases.
  • Diagnostic test is Sabin –Fieldman dye test.
  • Cryptosporidium causes intractable diarrhea in AIDS patients.
  • Pneumocystis carini causes pneumonia which become fatal in immuno compromised patients.
  • The only ciliate protozoan parasite of man is Balantidium coli. – largest protozoan parasite in man. It lives in large intestine. Infection acquired from pigs. Clinically resembles amoebiasis.
  • Helminthes are metazoan parasite with an outer covering
  • Trimatodus (flukes) are unsegmented helmiths which are flat and broad.
  • Flukes are hermaphrodites except schistostomes.

Clinically important trematodes infecting man are

1.     Schistosomes (which live inside veins)
a.     s. haematobium – in vesical or pelvic venous plexus
b.     s. mansoni – in inferior mescenteric vein
c.     s. japonicum –  in superior mescenteric vein

B. In various locations

            a. Biliary tract –    clonorchis sinensis

            b. fasciola hepatica

s. haematobium

            Formerly known as Bilharzia haematobium.

Endemic in Egypt. Adult worm lives in vesical and pelvic plexus of vein. Eggs passed to lumen of urinary bladder and discharged in urine particularly at the end of urination.

  • Intermediate host is snail
  • Man is the definitive host
  • Clinical illness result by skin penetration, egg deposition, tissue proliferation.
  • Clinical picture include local ——-carial dermatitis or general anaphylactic or toxic symptoms with fever, head ache, malaise, and urticaria. This is called katayama fever.
  • Typical manifestation is endemic haematuria or painless terminal haematuria.
  • In chronic cases, there is hyperplasia and fibrosis of vesical mucosa with granular appearance – sandy patch.
  • Schistosomiasis favours urinary carriage of typhoid bacilli
  • Diagnosis is by intradermal allergic test called fairley’s test.
  • S. mansoni causes intestinal Bilharziasis or Schistosomal dysentery.
  • S. japonicum- seenin superior mesenteric vein and intrahepatic portal vein.
  • Disease is otherwise called oriental schistosomiasis or katayama disease.
  • Acute illness include fever, abdominal pain, diarrhea, allergic manifestation called Katayama fever.
  • In chronic illness liver is maximally infected with hepatomegaly and fibrosis. There occurs periportal cirrhosis called Simmer’s pipestem fibrosis with portal hypertension and splenomegaly.

Liver fluke

Clonorchis sinensis – Chinese liver fluke . dogs and fish eating canines acts as reservoir host.

Migration of larva to bile duct causes hyperplasia and adenomatous change leading to cholangitis. Chronic infection leads to calculus formation, primary biliary cirrhosis and portal hypertension.

Fasciola hepatica

Sheep liver fluke –  first trematode to have been discovered and it is the largest and commonest liver fluke.

Intermediate host is snail of genera Lymnae. Present with fever, oesinophils, tender hepatomegaly.  cholelithiasis is a late complication.

Halzoun- ingestion of raw liver of infected sheep results insuffocation.

Lung fluke:-  Paragonimus westermani

Chronic disease resembles tuberculosis


  1. Fish tapeworm – diphyllobothrium latum
  2. Taenia saginata –  beef tape worm
  3.  Taenia solium – pork tape worm
  4. Echinococcus granulosus –  dog tape worm. Larval form causes hydatid disease in man
  5. Hymenolepis nana –  dwarf tape worm
  6. Hymenolepis diminuta  –  rat tape worm

Fish tape worm infection usually asymptomatic but sometimes causes mechanical obstruction. It causes a kind of pernicious anaemia called Bothrioceps anaemia.

Sparganosis – Ectopic infection by Sparganum (plerocercoid) larvae of tapeworm in abnormal host.

Taenia Saginata –  Beef tapeworm

            Mainly in small intestine

Larvae – bladder worm or cysticercus bovis

Human infection follows consumption of raw or undercooked beef

Taenia solium : When eggs are ingested by man or pig larval stage develops in muscles called cysticercus cellulosae. Pig flesh containing larvae is called measly pork.

Cysticercosis of brain cause epileptic manifestations

Ocular cysticercosis causes blurring of vision, uveitis, iritis and blindness ultimately.

Echinococcus granulosus :   Dog tapeworm or hydatid worm causes hydatid cyst.

Diagnostic test is Casoni’s intradermal test

When hydatid cyst forms inside bones, erode bony tissue and form osseous hydatid. Primary site is liver.

Trichinella spiralis :   Trichinia worm –  trichinosis

Infection acquired through consumption of inadequately cooked pork.

Trichuris trichuria :  Whipworm – infective larvae is rhabdiform larvae. Mechanical effect due to heavy infection is appendix causes appendicitis and in children cause rectal prolapse.

Strongyloides stercoralis : Causes strongyloidasis – usually benign but severe form is seen in immunocompromised persons called hyper infection.

Cutaneous form –  dermatitis, erythrema and itching 

Hook worms

  • Ancylostoma duodenale and necator americanus
  • Ancylostoma duodenale – infection is acquired when walking barefooted on soil containing filariform larvae
  • No multiplication in host
  • Necator americanus – is smaller than Ancylostoma duodenale.
  • When filariform larva enter the skin, they give rise to severe itching  at the site; scratch causes bacterial infection and forms the ground itch
  • Larva sometimes causes creeping eruption called cutaneous larva migricans.
  • When larva break out in pulmonary capillaries and enter alveoli causing minute local haemorrhages. Pulmonary lesion is called loeffler’s syndrome.(more common in ascariasis)
  • Adult worm in intestine sucks the blood and cause ulceration , second degree anaemia, hypoproteinaemia, odema and effusion
  • Single ancylostoma sucks 0.2 ml blood a day and necator 0.03 ml/day 

Enterobius vermicularis

  • Pinworm, thread worm or seatworm
  • Formerly called oxyuris vermicularis
  • Enterobiasis is usually a group  infection.
  • Diagnosis :- NIH swab

 Round worms

  • Ascaris lumbricoides- largest nematode parasite in human intestine
  • Larval migration causes allergic reaction. Migrating larvae in lungs cause ascaris pneumonia with fever, cough and wheezing.  Sputum contains charcto-leyden crystals. Larva may occur in sputum but more in gastric  washings. This is called loeffler’s syndrome
  • Ascaris contribute to PEM, Vit. A deficiency.



Mainly classified into

1.     Lymphatic filariae           site of adult       site of microfilaria          vector

Wuchereria bancrofti   lymph nodes           blood                          culex mosquito

Brugiya malay               lymph nodes      blood                mansoni

Brugiya timori                lymph node       blood

2.     Subcutaneous filarial

Loa loa                          connective tissue            blood                chrysops

Onchocercha volvularis   subcutaneous     skind and          similium

                                                nodule               eyes

3.     Serous cavity

Mansonilla ozadis

Mansonilla pestani

Occult filariasis
In some persons immune process to filarial antigens may produce clinical conditions unrelated to lymphatic lesions. Microfilaria not demonstrable in blood

Clinical features
Worms inside lymphnode and vessel causes granuloma formation with subsequent scarring and even calcification, increased permeability of vessel wall causes leakage of protein rich lymph into tissue causing typical hard pitting or brawny oedema.

Clinical features include lymphadenitis, lymphangitis, filarial fever, lymphorrhagia, hydrocele, lymphoedema, elephantiasis

Diagnostic kit : DEC provocation test

Small quantity of diethyl carbazine induce microfilaria to appear in peripheral blood even during day time. (microfilaria usually have a nocturnal periodicity in peripheral circulation being seen only at night, between 10 pm and 4 am)

Onchocerca volvulus :  Convoluted filaria

Or blinding filaria- causes blindness

Here subcutaneous nodule called onchocercoma occurs due to fibroblastic reaction around worms.


  • Fiery serpent
  • Incubation period – 1 year
  • No illness until gravid female worm comes to lie under skin ready to discharge embryos.
  • A few hours before blister formation there is constitutional symptoms of nausea, vomiting, intensive pruritus and urticarial rash.
  • The term Larva currens (racing larva) has been applied to rapidly progressing linear urticarial track caused by migrating larvae
  • Larvae migrans – sometimes nematode larvae appear to lose their way and wander aimlessly. Infections are abortive.
  • Cutaneous larva migrans are mainly due to Ancylostoma braziliensis and A. caninum.

All rights reserved @ similima

Pathology – Frequently asked questions

diseasesDr.Amir Khalid
BHMS, MD(Hom)  Calicut.

This notes may be used for Group discussion which is also an important factor in preparation.One among you asks questions in haphazard/ rapid manner and others try to answer. This will quicken or sharpen your memory and reflexes. But not conceal any points for fear of others knowing it.  It is always said to be good to do group study.

  1. Rudolf Virchow is known as the Father of Modern Pathology
  2. Deletion of long arm of chromosome 13 in — Retinoblastoma.
  3. Loss of chromosome 22 n — Meningioma.
  4. 8- 14 Chromosomal translocation in — Burkitis lymphoma.
  5. Normal nuclear cytoplasmic ratio is 1:4.
  6. Cancer suppressor genes are located on chromosomes 13 and 11
  7. Glycoprotein that acts as tumor marker for colon cancer and pancreatic cancer is CA-19-9
  8. In CEA positive colon cancers, the period after which elevated levels of CEA indicate residual disease s 6 weeks.
  9. Marker for Ca breast is CA-i5-3.
  10. Schwannomas are associated with somatic mutations in gene NF-1.
  11. Total coagulative necrosis in M w loss of nuclei is not apparent until about 72 hours.
  12. Retinoblastoma is associated with deletion in Chromosome 13.
  13. After initial acute attack, chronic RED appears at least after 10 years.
  14. ‘Wedge shaped’ infiltrates on X-ray are diagnostic of pulmonary infarction. It appears 12-36 hours after.
  15. Length of oesophagus in newborn is 10 cm .
  16. Toxic injury of liver affects most often Zone 1.
  17. Macronodular cirrhosis is considered once nodule is greater than 3 mm.
  18. The oncogene amplified in Down’s syndrome leading to mental retardation is Ets-2.b
  19. The percentage of total cholesterol that freely circulates in plasma is 7%.
  20. For teratogenesis, peak sensitivity during embryonic period is 4-5 week.
  21. DNA sequence in any two persons reveal variation in one nucleotide for every 200-500 nucleotides.
  22. Thè  perinatal infection to erythroid precursor in bone marrow is Parvovirus C-19.
  23. In a newborn with normal surfactant production, the residual volume retained by kings after first breath is 40%.
  24. Normal human deploid fibroblasts stop proliferating in culture after 5O doublings
  25. Gaucher’s cells are glucocorebroside filled cells measuring 20-1OO mm,-and are fat negative
  26. Glucogonomas arise from the Alpha -cells of the pancreatic islets
  27. Craniopharyngiomas are tumors that arise from remnants of Rathke’s pouch.
  28. The 21-hydroxylase deficiency is most commonly found form of the adrenogenital  syndrome.
  29. Malignant hypertension is microscopically characterized by fibrinoid necrosis of arteriolar wall
  30. The most common site for intestinal amoebiasis  is caecum
  31. Fibrosis is evident by light microscopic examination when a thrombus is more than one week old.
  32. Both systemic and pulmonary embolism is seen in septal infarction.
  33. The commonest malignancy seen in immune deficiency state is lymphoreticular malignancy.
  34. Pseudomyxoma peritonei is seen with mucus secreting ovarian carcinoma.
  35. The most common complication of infective endocarditis is thromboembolism.
  36. The commonest site for amyloid deposition in intestine is colon.
  37. Villous atrophy is diagnostic of coeliac disease.
  38. The thyroid cancer most frequently metastasises to lymph nodes is papillary.
  39. Alzheiniers disease is degenerative disease which typically shows progressive atrophy of the brain particular the frontal, parietnal occipital cortex.
  40. Multiple endocrine neoplasia (MEN) are familial disorders with autosomal dominant mode of transmission
  41. MEN 11 syndrome is characterized by the occurrence of medullary carcinoma thyroid. pheochromocytomas and parathyroid hyperplasia.
  42. Affection of terminal ileum in Crohns disease is called as back wash ileitis?
  43. Ulcerative colitis is primarily a disease of mucosa.
  44. The most common lesion in Wernicke’s encephalopathy is found in the mamillary bodies.
  45. The lesion of atherosclerosis occurs mainly in abdominal aorta.
  46. A tumor arising from hum scar is most likely squamous cell carcinoma.
  47. Duct papilloma is the commonest cause of blood stained nipple discharge.
  48. Thyroid appearance of renal tubules is considered pathognomonic of chronic pyelonephritis.
  49. Periglomerular fibrosis is considered typical of chronic pyelonephritis.
  50. A reliable screening test for platelet function is clot retraction test.
  51. Exposure to vinyl chloride may develop angiosarcoma of liver.
  52. Haematuria  is characteristically seen in proliferative glomerulonephritis.
  53. ‘Russel bodies are seen in plasma cells.
  54. The cells most sensitive to ischaemia is cortical neurons.
  55. Keloids predominantly consist of dense collagen fibres.
  56. The epithelial cells of tubercle are derived from monocytes.
  57. Rosette formation is characteristically seen in Retinoblastoma.
  58. Laminin is the most abundant glycoprotein in the basement membranes
  59. Chancroid is also called “ulcus molle.’
  60. Lipoid nephrosis of the most common cause of nephrotic syndrome in childhood.
  61. Budd-chiari syndrome is produced by occlusive lesions of the Hepatic veins.
  62. Glomeruloid bodies or Schiller-Duval bodies, are commonly found in endodermal sinus tumour.
  63. K.W syndrome comprises diabetes mellitus, hypertension, albuminuria and edema.
  64. Monodermal teratomas are very uncommon and most frequently take the forms of struma ovarii or carcinoids. .
  65. Nodular melanoma is the most aggressive type of melanoma and hence carries the worst prognosis.
  66.  “Lafora syndrome” is a progressive familial myoclonic degenerative disease affecting predominantly the basal ganglia, most patients dying by the age of 30 years.
  • Lutembacher’s disease consist of a combination of an atrial septal defect and mitral stenosis
  • Almost all lysosomal storage diseases are transmitted as autosomal recessive genes.
  • Philadelphia chromosome (ph) is identifiable in more than 90% of patients with chronic myelogenous leukaemia.
  • Patients with ph-negative CML respond poorly to chemotherapy and have shorter survival than those with ph-positive CML
  • Chloromas  are tumorous masses of acute myeloblastic leukaemia.
  • Auer rods are abnormal lysosomal structures visualized as reddish rods in myeloblasts and promyelocytes.
  • Medullary carcinoma of the thyroid gland arises from parafollicular “c’ cells.
  • Achalasia of esophagus is associated with “Chagas’ disease.
  • Hyperacute rejection occurs within minutes after u and is due to cytotoxic complement dependent. pre existing antibodies in the host.
  • Papillary carcinoma is the most common malignancy of thyroid.
  • Aschoff bodies are pathognomonic of rheumatic carditis.
  • Most carcinomas of pancreas originate from the epithelial cells lining the ducts and are most often located in the head
  • Most breast tumors originate in the ducts and have the histologic appearance of infiltrating duct carcinoma.
  • The serum TSH is the most sensitive indicator of primary hypothyroidism
  • Mixed tumors e.g.mixoid parotid tumour
  • Teratomas arise from totipotential cells that retain the ability to form endodermal, ectodermal, ectodermal and mesenchymal tissue. Such tumors are found in testis and ovary.
  • Two non-neoplastic  lesions simulating tumours.
  • Choristomas Ectopic, sometimes nodular, rests of non transformed tissues (e.g Pancreatic cells under of the small bowel mucosa).
  • Hamartomas Malformations that present as a mass of disorganized tissue indigenous to the particular site (i.e. a hamartomatous nodule in the lung may contain islands of cartilage, bronchi, and blood (vessels).
  • Metastasis is the single most important feature distinguishing benign from malignant turnouts. Exception being I. Brain tuinours 2.Basal cell carcinoma of skin
  • Grading is based on the degree of differentiation and the number of mitoses within the tumour. Cancers are classified as grades   1 to IV with increasing anaplasia.
  • Staging is based on the anatomic extent of the tumour. Two methods of staging are in use now-a-days. .TNM (Tumour, Node & metastases). 2. AJC (American joint committee).
  • In Philadelphia chromosome a reciprocal balanced translocation between chromosomes 22 and usually 9(9, 22)is seen in more than 90% of cases of CML.
  • In more than 90% of cases of Burkiti’s lymphoma at (8; 14) translocation is present.
  • Deletion of chromosome 13, band q 14 is associated with retinoblastoma.
  • Deletion of chromosome II band q 13. is associated with Wilm’s tumour.
  • Gene amplification associated with cytogeneüc changes is best exemplified by neuroblastomas
  • Cancers of lung, colon and prostate are the leading causes of cancer deaths in males while in females lung, breast and colon cancers are morn common.
  • Japanese are prone to develop gastric cancer
  • In xeroderma pigmentosum, affected patients develop Ca skip in areas exposed to the ultraviolet light.
  • Clinical conditions associated with increased risk of developing cancers.
  • Cinhosis of liver—hepatocellular Ca.
  • Atrophic gastritis of pernicious anemia—stomach cancers.
  • Chronic ulcerative colitis—Ca colon.
  • Leukoplakia (oral/genital mucosa)—squamous cell carcinoma
  • Villous adenoma colon—colonic Ca.

Carcinogenic chemicals.

  1. Alkylating agents e.g. cyclophosphamide and Busulphan induced cancer.
  2. Aromatic hydrocarbons present in cigarette smoke induces lung cancer.
  3. Azodyes ( naphthylamines) induces bladder cancer
  4. Aflatoxin BI—hepato cellular carcinoma
  5. Nitrosamines and amides—gastric cancer.
  6. Asbestos—mesotheloma
  7. Vinyl chloride—angiosarcoma
  8. Saccharin & cyclamates—bladder cancer promoter,
  9. Oestrogen—endometrial carcinoma.

Radiation carcinogenesis

  1. UVR—Carcinoma & Melanoma
  2. Ionizing radiation
  3. Miners f radioactive ores have an increased risk of lung cancer.
  4. Increased risk of leukaemia in atomic bomb survivors in Japan.
  5. Therapeutic radiation of the neck in children has been associate with the later development of thyroid cancer (papillary).
  6. Note: In man there is a hierarchy of vulnerability of radiation induced neoplasms;
  7. Most common are myeloid leukaemias, followed by thyroid cancer in children.
  8. Cancer of the breast and lung are less commonly radiation induced.
  9. Skin, bone and gut are least susceptible to radiation to cause cancer lies in their ability to induce mutations. Paniculate radiations (alpha & beta Neutrons) are more carcinogenic than electromagnetic radiation (X-rays. gama Viral oncogenesis)

Causes of cachexia in cancer.

  •  Loss of appetite
  • Infections due to immunosuppression
  • Bleeding froth ulcerative lesions
  • Production of cachectin (TNE-a) by activated macrophages cachectin moblilizes body fat

Paraneoplastic syndromes It may be the earliest clinical manifestation of a neoplasm and may mimic distant spread. The most common syndromes are

  • Endocrinopathies -ectopic hormone production—(ACTH)
  • Hypercalcemia (PTH like peptide)
  • Squamous cell carcinoma lung
  • T cell leukemias or lymphomas.
  • Note—Cancer associated hypercalcemia also results from osteolysis induced by bony metastases.
  • Acanthosis nigricans—Verrucous pigmented lesion of skin is frequently associated with visceral malignancy.
  • Clubbing of fingers and hypertrophic osteoarthropathy are associated with lung cancers. e. Thromhotic diatheses resulting from production of thromboplastic substances by tumour cells may manifest as m or as vegetations in non-bacterial thrombotic endocarditis.
  • Heart failure cells are seen in pulmonary edema.
  • In the development of these cells, the initial pulmonary edema (due to LVF) leads to dilatation of intra-alveolar capillaries which in turn rupture. The minute intra-alveolar haemorrhages breakdown and phagocytosis of red blood cells leads to the formation of haemosiderin laden macrophages which are termed Heart Failure Cells.
  • Brown Induration of Lung—Name given to firm, heavy, dark brown appearance of Lungs due to long standing pulmonary congestion e.g. in mitral stenosis or CHF.

Nut-Meg Liver—A descriptive term for congestive red-blue central region of a lobule in liver parenchyma, surrounded by a zone of uncongested liver substance-due to CPC liver conditions associated.

  • Right Heart Failure
  • Obstruction to IVC
  • Obstruction to hepatic vein less common

Organs Affected in Generalised Primary Amyloidosis

  • I.Heart  5. Tongue
  • 2.Kidney            6.Larynx
  • 3.Intestine         7.Skin etc.
  • 8. Skeletal muscles

Staining reaction of amyloid material

  1. Iodine gives brown- colour and I2 followed by H2S04 gives blue colour Congo red  -red
  2. Methyl violet—rose red while other tissue becomes blue (metachromatic stain).
  3. Von-Gieson’s stain—Khaki shade
  4. PAS stain—red.
  5. Iodide green—(metachromatic stain)—violet red other stained green.
  6. H- & E stain—faintly eosinstained homogenous material.
  7. Fluorescent dyes—to demonstrate amyloid in juxta glomerular area of kidney.
  8. Immunohistological stain—to distinguish between AL and AA.

Predisposing factor for secondary amyloidosis. 1. TB of lungs, bone, joints etc

  • Chronic suppuration in lungs, bones and joints etc.
  • Syphilis
  • Rheumatic fever and rheumatoid arthritis.
  • Ulcerative colitis, Hodgkin’s disease.
  • Advanced malignancy.
  • Hansen’s disease (leprosy).

Lab diagnosis of amyloidosis

  • Congo red test
  • Rectal mucosa biopsy.
  • Gingival biopsy.
  • Biopsy of bone marrow, liver, spleen, kidney and intestine.
  • Peripheral smear examination.
  • Serum and urinary protein by immuno-electrophoresis.
  • Demonstration of Bence-Jones protein.
  • Demonstration of calcitonin.
  • Note Amyloid can be differentiated from hyaline connective tissue by its characteristic staining  with Congo red, with which it appears red and shows apple-green bipolar refringence.  Aschoff bodies are found in, Heart, Synovia of joints, Joint capsules, Tendons (Extensor aspect), Subacutaneous tissues.

Diagnosis of Acute Ml

  • ECO—Presence of pathologic Q-waves usually indicates transmural MI Also present are ST-Segment and T wave changes with alone indicate subendocardial infarct.
  • lsoenzyrne studies
  • MB isoenzyme of creatinine Kinase-highly specific and sensitive marker for MI, Elevated within 48-72 his, of M and peaks at 12-24 hours after Ml.
  • SGOT levels—begin to rise in 8 hrs after MI and peak at 18 to 36 hours to return to baseline within 3 to 4 days
  • Lactic dehydrogenase—Begins to rise 24 hours after Ml, peaks in 3 to 6 days and returns to normal only after two weeks
  • Most sensitive is LDH I: LDH 2 ratio which in inverted in MI.
  1. Ring granuloma in —Q-fever.
  2. The main feature of rapidly progressive giomenilonephritis—Epithelial crescents.
  3. The Tram track (Thickened or split) basement membrane in —Membrano-prolitèrative  glomerulonephritis.
  4. Thyroldisation of Renal tubules (Atrophic tubules with casts) in —Chronic pyelonephritis.
  5. Periglomemlar fibrosis in —Chronic pyelonephritis
  6. Michaelis Gutman bodies (Giant cells containing calcium and Iron inclusion) in Melakoplakia of urinary body (a variant of cystitis).
  7. Nebothian follicle in — Chronic Cervicitis.
  8. Flea bitten kidney —Focal Globerulonephritis.
  9. Onion skin appearance of spleen in—SLE.
  10. Hurthle cells in — Hashimatos thyroiditis.
  11. Lipofusein — wear and tear pigment.
  12. Karyorrhexia — Nuclear fragmentation.
  13. Hassel’s corpuscles in —Thymus.
  14. In oncocytoma, the oncocytes have sac like mitochondria.
  15. Left ventricular hypertrophy is said to present when the thickness of left ventricular wall is more than 15mm.
  16. Melanin like pigment in liver is — Dubin Johnson syndrome.

Psammoma Bodies in:

  • Psammomatous Meningioma.
  • Papillary carcinoma of Thyroid.
  • Pupillary serous cystadenoma of ovary.
  1. Libman Sacks endocarditis in —SLE.
  2. Amyloidosis is also known as — Beta fibrillosis.
  3. Durck’s granulomas am seen in — Malaria.
  4. Lepra cells encountered in —Lepromatous lepmsy.
  5. Microscopical]y, normal cells or tissues present in abnormal locations are referred to as Choristoma.
  6. Hyaline material consists of—Precipitated plasma proteins.
  7. Glycogen can be confirmed by PAS stain.
  8. Flame cells seen in — Multiple myeloma.
  9. Mc Callums patch is found in — Left Atrium.
  10. Melanin can be stained with Fontana stain.
  11. Bilirubin an be confirmed by —Hall’s stain.
  12. Hemosiderin is golden yellow in colour.
  13. Heart failure cells are seen in lungs, in profound anemia, fatty change in heart is —‘Thush breast or Tigered effect,
  14. In all organs, fatty change appears as Clear Vacuoles within parenchymal cells.   Fatty in growth, fatly change appears as Clear Vacuoles within parenchymal cells.
  15. Fatty in growth is most commonly encountered in Heart and Pancreas.
  16. Fat can be stained with —Sudan IV or Oil Red-O.
  17. Glycogen stained by — Bests Carmine or FAS reaction.
  18. The most common exogenous pigment is — Carbon or coal dust.
  19. Lipofuscin is — Insoluble pigment. also known as Lipochrome.
  20. The tell tale sign of free radical injury and Lipid peroxidation – Lipofuscin.
  21. Homogentisic acid is a — Black pigment, occurs in Alkaptonuria.
  22. Lipofuscin is seen in cells undergoing slow, regressive changes, and is particularly prominent in Liver and heart of ageing or patients or patients with severe malnutrition and cancer cacehxia.
  23. Lipofuscin is usually accompanied by — Organ shrinkage (Brown Atrophy).
  24. Hemosiderin is derived fro Hemoglobin.
  25. In Fenton reaction, Hydroxyl Radicals are generated by interaction of Hydrogen peroxide with Transitional metals like Iron, Copper.
  26. The major antioxidant enzymes are — Superoxide dismutase, catalase, Glutathione peroxidase.
  27. Cells sometimes respond to infection with Measles or herpes virus by the formation of Syncytial or multinucleate giant cells, caused by cell to cell fusion.
  28. Certain virus infected cells develop inclusion bodies which contain — Virions or viral proteins in nuclei or cytoplasm.
  29. Mitochondrial swelling is the first manifestation of almost all forms of injury to cells.
  30. The dead cells usually shows increased eosinophilia.
  31. Necrosis is the sum of the morphological changes that follow cell death in a living tissue or organ.
  32. Apoptosis—Morphological pattern of cell death.
  33. The earliest observed ultrastructural change in necrosis cell —A reversible clumping of the chromatin to create large aggregates attached to the nuclear membrane and to the nucleolus.
  34. Pyknosis—Progressive shrinking of nucleus and becomes transformed to a small, dense mass of tightly packed chromatin.
  35. Karyolysis—Dissolution of chromatin.
  36. Karyorrhexis—Nucleus break into many clumps (Fragmented nucleus).
  37. Acidophil or Councilman body seen in the liver in —Toxic or viral hepatitis.
  38. The most common pattern of necrosis — Coagulation necrosis.
  39. In Coagulation necrosis—Basic cellular shape is preserved with loss of nucleus.
  40. Coagulation necrosis most commonly results from sudden severe ischaemia of organ such as -Kidney, Heart, Adrenal gland.
  41. Liquefaction necrosis is from the action of —Hydrolytic enzyme.
  42. The liquefaction necrosis pattern is characteristic of—ischemic destruction of Brain tissue.
  43. Caseous necrosis is a combination of coagulative and liquefactive necrosis.
  44. Caseous necrosis is attributed to capsule of Mycobact. tuberculosis, which contains — Lipopolysacharides.
  45. Fat necrosis is due to the action of—Lipases.
  46. Fat necrosis induced by trauma, particulaily in — Breast Adipose tissue.
  47. Fat necrosis is most commonly seen in —Acute pancreatitis.
  48. In Gangrenous necrosis — Coagulative necrosis is modified by the liquefactive action of Bacteria and leukocytes.
  49. In dry gangrene—Coagulative necrosis is dominant.
  50. In wet gangrene necrosis is dominant. – –
  51. Fatty change in liver, the mostly accumulated lipid is —Thglycerides.
  52. Acute fatty liver of pregnancy is often fatal.

Fatty change is due to:

  • In alcohol poisoning — Increased esterification of fatty acids to Triglycerides.
  • In carbon tetrachioride, phosphorous poisoning and protein malnutrition —
  • Decreased Apoprotein synthesis.
  • In experimental node! of Fatty liver induced by orotic acid — Impaired secretion of lipoprolein.
  • Starvation, corticosteroids — Excessive entry of free fatty acids into the liver.
  1. Father of Modern Pathology—Virchow.
  2. Fatty change per se is Reversible.
  3. Fatty change is most often seen in —Liver and heart.
  4. Bilirubin do not contain Iron,
  5. In advanced obstructive jaundice, aggregates of pigment creates — Bile lakes.
  6. The organs in which Bilirubin accumulation is evident in Liver and Kidneys.
  7. Heiiiochrormatois of pancreas results in Diabetes mellitus,
  8. Colchcine  block the mitosis in the Metaphase.
  9. In Chediak—Higashi syndrome, there is – Impaired pathocytosis.
  10. The cytoskeleton consists of microtubules, thin actin filaments, thick Myosin filaments, Intermediate filaments.
  11. Intermediate filaments are keratin filaments, neurofilaments, glial elements vimentine, Desmin etc.
  12. In the erythrocyte, the major protein consist of spectrin, actin, protein 4.1 and ankyrin.
  13. In hereditary spherocytosis, the defect in Red cell shape is due to — abnormal or deficient spectrin. –
  14. In hypertrophy of cell. there is increase in the number of mitochondria. In atrophy there is decrease in the number of mitochondria
  15. Compensatory hyperplasia — Hyperplasia that occurs when a portion of liver is removed.
  16. Pathological calcification implies the abnormal deposition of—calcium salts, together with smaller amounts of Iron, magnesium etc.
  17. Ferrugenous bodies (Exotic, beaded dumbel forms) in lung occur in —Asbestosis.
  18. Initiation of intracellular calcification occur in the mitochondria of dead or dying cells.
  19. Metastatic calcification appears to begin in Mitochondria except in — kidney (where it develops in the basement membrane
  20. Alcoholic hyalin (Mallory body) consist of aggregates of Prekeratin Intermediate filaments.
  21. Amyloid with congo Red stain appears—Red and shows Bipolar refringence.
  22. Keratin pearl in —Squamous cell carcinoma.
  23. Pseudocartilage in —Pleomorphic adenoma.
  24. Tadpole cell in —Rhabdomyosarcoma.
  25. Rosette formation in — Neuroblastoma, Retinoblastoma.
  26. Arias Stellas reaction in — Ectopic pregnancy.
  27. One of the causes of Hypercalcemia — Addison’s disease.
  28. Antimitochondrial antibody in — Primary biliary cirrhosis.
  29. Viirucae body in —Neurilemmoma.
  30. In most types of acute inflammation, neutrophils predominate in the first 6 to 24 hours, being replaced by monocytes in 24 to 48 hours.
  31. Opsonic fragment of C3 complement – C3b.

Thromboxane A2

  1. Found in Platelets
  2. Causes platelet aggregation and blood vessel constriction. Prostacyclin: Inhibitor of platelet aggregation and causes vasodilation. Aspirin – indomethacin etc inhibit the enzyme – cyclooxygenase. Macrophages in (Mononuclear phagocytes in)
  3. Blood – Monocytes.
  4. Nervous system – Microglia.
  5. Bone – Osteoclasts.
  6. Liver – Kupffer cells.
  7. Connective tissue – Hiystiocytes.
  8. Bone marrow – Macrophages.
  9. Skin – 1 Langerhan’s cells.
  10. Lymphoid tissue –  Dendritic cells. 
  • Asteroids in giant cells in — Sarcoidosis.
  • Labile cells — Proliferate throughout life.
  • Permanent cells in—Skeletal muscle, cardiac muscle, nervous system.
  •  Commonest tumor of Appendix — Argentaffinoma
  •  Juvenile polyposis supposed to be Retention cysts.
  • Nurse cells in — Trichenella spiralis.
  • Heart failure cells (Hemosiderin laden Macrophages) in Alveolar spaces in —Congestive heart failure. Lisch nodules (pigmented Iris hamanomas) in —Neurofibromatosis.
  • Most of the known carcinogens are metabolized by the— cytochrome P dependent monooxygenases.
  • The most common type of thickening of Glomerular basement membrane is due to extensive subepithelial deposition of immune complexes, as occurs in — Membranous Glomerulonephritis
  •  The classic Glomerular basement membrane antigen is component of collagen type – IV.
  • Kidney (Electron Microscopy):
  • Subepithelial humps in— Post streptococcal Glomerulonephritis
  • Subepithelial deposits in —Membranous G.N.
  • Loss of foot process in — Lipoid nephrosis, Focal segmental Glomerulosclerosis
  • Subendothelial deposits in — Membrano proliferative G.N.
  •  Mesangial and paramesangial dense deposits of IgA nephropathy

Kidney (Light Microscopy):

  • Diffuse capillary wall thickening —Membranous G.N.
  • Lipid in Tubules in — Lipoid nephrosis.
  • Hyalinized Glomeruli in — Chronic Glomerulonephritis.
  • Splitting of basement membrane — Membrano proliferative G.N.
  1. Two Histologic Alterations that Characterise Malignant Hypertension:  Fibrinoid necrosis of arterioles,-lyperplastic arteriolitis
  2. Angiomyolipoma are common in patients with —Tuberous sclerosis.
  3. Fatty streaks appear in the aortas of all children older than one year.
  4. Ring like calcifications in the media of medium sized to small arteries of muscular type in — Monckeberg’s medial sclerosis.
  5. Te most usual site of involvement of polyarteritis nodosa — Kidney (Renal vessels).
  6. Classic polyarteritis nodosa does not affect the pulmonary circulation.
  7. Fibrinoid necrosis in — Malignant hypertension, Polyarteritis nodosa etc.
  8. In inflammation, macrophages originate from — Macrophages.
  9. Bacteria containing Hyaluronidase — Clostridium
  10. Granulation tissue is formed in the process of Healing by Secondary union.
  11. The Amyloidosis that occurs in Multiple myeloma — Primary Amyloidosis.
  12. Rodent ulcer — Basal cell carcinoma.
  13. Centrilobular necrosis of liver in —Congestive heart failure.
  14. Nut meg liver in —Congestive heart failure
  15. Cardiac sclerosis of liver in — Congestive heart failure.
  16. Carcinoid tumors in the ovary or lung may induce carcinoid syndrome without antecedent Hepatic metastases.
  17. The fact that the cardiac changes in carcinoid heart diseases are largely Right sided is explained by —Inactivation off both serotonin and bradykinin in the blood dining passage through lungs by Monoamine oxidase found in pulmonary vascular endothelium.
  18. The most common primary tumor of heart in adults — Myxomas (Commonest site – Left Atrium).
  19. The most frequent primary tumor of heart in infants and children — Rhabdomyomas.
  20. Gandy — Gamma bodies contain – Deposits of Hemosiderin and Calcium. –
  21. Autosplenectomy occur in Sickle cell anemia.
  22. Lacunar cells in Nodular sclerosis type of Hodg disease.
  23. Owl eyed nucleoli in the nucleus of Reed-Sternberg cell.
  24. Chloromas are seen most commonly in —AML.
  25. Myeloblasts are characterised by delicate nuclear chromatin three to live nucleoli and fine  azurphilic granules  in cytoplasm.
  26. Lvmphoblasts  have coarse, clumped chromatin and few nucleoli — Azurophilic granules are not present in cytoplasm.
  27. Auer rods ire Red staining, intracytoplasmic, rod like structures      in granulocytes.
  28. Massive splenomegaly is associated with —CML and hairy cell leukemia.
  29. Spontaneous rupture of spleen seen in — Infectious mononucleosis, Malaria, Typhoid fever, Leukaemia, Acute splenitis
  30. In diabetic nephropathy, the cells of the distal portions of proximal convoluted tubules contain —Glycogen (Armanni ebstien lesion).
  31. The characteristic hail mark of all syphilitic infections — obliterative endarteritis with perivascular cuffing of lymphocytes and plasma cells.
  32. The half mark of cutaneous T cell lymphoma of Mycosis fungdides type histologically is the identification of the Sezary-Lutzner cells.
  33. Polyglucoside bodies — CorDora Amylacea.
  34. Microglia can be stained by special stains like — Hortega carbonate.
  35. Brain has no lymphatic system.
  36. Subdural haemorrhage result from —rupture of bridging veins that connect the venous system of brain to the large intradural  venous sinuses.
  37. Hirano bodies in—Aizheimer’s disease;
  38. Pick bodies in —Picks disease.
  39. The most common congenital malformation of the brain in humans—Anencephaly.
  40. In Schwannomas, no nerve fibres are present in the tumor.
  41. Retinal phlebitis with candle wax drippings in or near Retinal vessels in— Sarcoidosis
  42. Dalen Fuchs nodules between Bruchs membrane and Retinal pigment epithelium in — Sympathetic uveitis.
  43. The most common primary ocular malignancy in Caucasians—Intraocular Melanomas.
  44. Fexner Wintersterier Rossettes in —Retinoblastoma.
  45. Thrombi when formed with a cardiac chamber or Aorta, they may have apparent laminations called— Lines of Zahn.
  46. Lines of Zahn are produced by— Alternating layers of pate platelets admixed with fibrin separated by dark layers containing red cells.
  47. Vericcous endocarditis—Non-bacterial bland Thrombotic vegetations seen in systemic lupus erythematosis.
  48. Chicken fat thrombus — Post mortem thrombus.
  49. Commonest site of Pblebothrombosis — deep leg veins.
  50. Infarct of Zahn — due to occlusion of intrahepatic branch of portal vein.
  51. The two most distinctive features of chronic active hepatitis — piecemeal necrosis and Bridging necrosis.
  52. Ovarian Tumors:
  53.  • Call-Exner bodies in— Granojosa cell tumours.
  54.  • Reinke crystefloids in :— Hilus cell tumor.
  55.  • Alpha fetoprotein in — Endodermal sinus tumor.
  56.  • Chronic gonadotrophin in — Dysgerminomas.
  57.   • Meigs syndrome in — Ovarian fibromas.
  58. The causes of Rapidly progressive Glomerulonephritis are SLE (lupus nephritis), PAN, Post streptococcal glomerulonephritis etc.
  59. Rapidly progressive glomerulonephritis. pathologically characterised by extensive proliferation of cells in the Bowman’s space with the formation of crescents.
  60. Von Hansemann cells in— Melakoplakia of Bladder.
  61. Macrophages containing PAS positive glycoprotein granules typically seen in — Whipples disease
  62. In membranous glomerulonephritis, the kidneys are — large, swollen and pale.
  63. Ascending infection is the most common pathway by which bacteria reach the kidney.
  64. Bazins disease is Erythema induration.
  65. Real papillary necrosis or necrotising papillitis is due to – Diabetes mellitus, analgesics like phenacetin. urinary tract obstruction.
  66. The law that regeneration is more complete in younger individuals than in older ones is Spllanzani law.
  67. Encelitis is inflammation of intra abdominal organ.
  68. Hemophilia C due to defect in synthesis of PTA or factor Xl. It is Mendelian dominant.
  69. In hemophilia, bleeding is from large vessels whereas in thrombocytopenia, it is from small capillaries. Deficiency of factors 1 and II are rarely congenital. Parahemophilia is due to deficiency of factor V.
  70. Indian file pattern of cords in Ca breast is seen in infiltrating lobular type.
  71. Pagets cells arc seen in Pagets disease ofnipple.
  72. ANCA (Anti neutrophilic cytoplasmic antibody) is seen in Polyarteritis nodosa.
  73. Alveolar haemonhage syndrome may be present in Goodpasture’s syndrome, rheumatoid arthritis, SLE, idiopathic pulmonary hemosiderosis and toxin-induced disease from penicillamine.
  74. Anitschkow myocytes (caterpiller cells) are believed to be modified fibroblasts.
  75. Aschoff node is seen in rheumatic fever in myocardium.
  76. In Bowenoid papulosis, there are numerous small velvetly papules on shaft of penis of young men probably caused by HPV.
  77. Burnt out plaques are seen in multiple sclerosis.
  78. Lines of Zahn is a characteristic appearance of laminations in thrombi when formed in aorta.
  79. Adhesion molecules on leucocytes are P-150, MO-I, LEA-I.
  80. Polypoid cells seen in hypertrophy of cardiac muscle cells are arrested 02 phase
  81. Helper T-cells interact with Class-il MHC
  82. In SLE, autoantibodies against red cells, white cells and platelets is mediated by hypersensitivity reaction type I1
  83. Rubber hose inflexibility of GIT in systemic sclerosis is commonest in lower two thirds o esophagus. The lesion most specific for SLE is subendothelial deposit.
  84. Onion skin lesion  concentric periarterial fibrosis in spleen is characteristic of SLE.
  85. Pink to gray pinpoint elevations of endocardium giving Dew drop appearance is seen in amyloidosis TB does not produce granulomas in patients of  HIV
  86. Protoncogene with GTPase activity is H -ras.
  87. Zeebra bodies are seen in Niemann Pick disease.
  88. Hard glassy’ splenomegaly may be seen in amyloidosis.
  89. The dark lines of Zahn are composed of RBC’s.
  90. Amyloid gives apple green birefringence when stained with congored.I
  91. In psoriasis, the turnover of epithelial cells is at least twice as fast that of normal skin.
  92. In situ hybridisation uses biotin to give a colorimetric detection system.
  93. Lads cells are found in Juxta glomerular apparatus.
  94. The only human DNA which lies outside to nucleus is in mitochondria.
  95. Lacunar cells are found in nodular sclerosing lymphoma.
  96. Repetitive necrosis of adjacent regions of several infarcts of varying ages yields progressive extension of an individual infract over a period of days to weeks, called Stuttering infarct.
  97. Popcorn cells or cells like elephant feet are found in lymphocytic predominant Hodgkin’s disease.
  98. Lambl’s excrescences are to aging
  99. Lewy bodies are found in Parkinsonism
  100. Leopard. Lizard or Elephant skin is seen in Oncocerciasis.
  101. Meyers-Kouvenaar bodies are found in Filariasis
  102. Mazzoni reaction is seen in oncocerciasis.
  103. Molluscum body is found in stratum conieum and stratum granulosum.
  104. Residual bodies in a cell are lysosomes.
  105. Ring abscess is found in infective endocarditis.
  106. Bite cells are seen in 0-6-P deficiency.
  107. Pigbel is caused by Cl. perfringens.
  108. In addition to Hodgkin’s disease and infectious mononucleosis, Reed Sternberg cells may be seen in mycosis fungoides. –
  109. Accumulation of RNA in cytoplasm makes it pyroninophilic.
  110. Stiff lung is seen in ARDS.
  111. Collar button lesions are characteristic of bronchia carcinoid,
  112. The oncogerie amplification seen in small cell carcinoma is Myc.
  113. Part of colon with highest wail tension is caecum.
  114. A bizarre map like pattern, leopard spotting of oesophagus is due to postmortem digestion.
  115. Commonest she of origin of lower 01 bleeding due to angiodysplasia is caecum.
  116. Most sensitive indicator of Castro esophageal reflux is pathohistology of esophagitis is intraepithelial eosinophils.
  117. APUD cells are derived from endoderm.
  118. Most abundant substance secreted in bile is bile salts.
  119. Life long immunity in HBV is due to Anti HBS.
  120. LDL clearance independent of LDL receptors occur in mononuclear phagocytic system.
  121. Electron microscopic appearance of prominent lysosomes with whorld appearance is seen in Tay Sach’s disease.
  122.  Technique most used for linkage analysis is variable number of tandem repeats.
  123. Most common cause of false negativity of RELP is Closer linkage.
  124. Uniparental disomy of paternal chromosome 15 causes Angleman syndrome.
  125. Retinoic acid causes teratogenesis by induction of fox gene.
  126. Amniotic bands are classical example of deformation.
  127. Retinoblastoma gene (RB) inactivation is seen in small cell carcinoma of lung, osteosarcoma and carcinoma of bladder
  128. Typhus nodule in brain due to focal microglial proliferation with leukocytic infiltration seen in Typhus fever is limited to grey matter.
  129. The organism with shepperd crook  appearance is leptospira interrogans.
  130. Von Hansemann’s cells are large histiocytes seen in Malakoplakia.
  131. Caplan’s nodoles are seen in rheumatoid pneumoconiosis.
  132. Carre’s osteomyelitis is non suppurative osteomyelitis resulting in increased density of shaft of a long bone. There is new bone formation but no pus cells.
  133. Glomus organ is a convoluted AV anastomosis with modified muscle cells.
  134. Michaelis-Gutmann bodies are targetoid bodies due to defective lysosomal function seen in Malalcoplakia.
  135. Brunu’s nest are rounded collections of urothelial cells found just below the urothelial surface frequently seen in normal bladder..
  136. Carcinoid tumor may also be seen in ovary and stomach in addition to appendix and intestine (SI/LI)
  137. Catheter tumor is proliferated granulation tissue in urinary bladder due to catheter.
  138. In central core disease, there is non-progressive congenital myopathy.
  139. Clear cell sarcoma usually involves foot and knee.
  140. Cytoid bodies axe fluffy white patches in retina seen in accelerated HT, SLE and dlermatomyocytis.
  141. Cytoid body is a nodular swelling in injured axon.
  142. The commonest site from where a nerve biopsy in taken is sun] nerve.
  143. In ‘dying back’ neuropathy, there is axonal degeneration.
  144. Hibernoma is a type of lipoma.
  145. Kiel classiflcation is used to classify lymphoma.
  146. Indirect serologic predictors of HIV infection are beta-2 microglobulin, Neoptrrin,Interleulcin 2- receptor, Net gene markers
  147. Endheim’s medial degeneration is also called cystic medial necrosis
  148. Kumura’s disease is epitheloid hemangioma
  149. Wertlake and Del Guercio were first observers to comment on the diagnostic value of bile cytology
  150. Postmortem clot shows ‘chicken fat’ and ‘currantjelly’ appearances
  151. Mural or parietal thrombus is nonocclusive thrombus adherent to the wall
  152. Saddle or riding thrombus is that which extends into the branches or tributaries of a vessel.
  153. Hyaline thrombus is when thrombus is a homogenous mass.
  154. CNS fungal infections are aspergillosis, candidiasis,cledosporin,cryptococcus and zigomycosis.
  155. In urine cytology. superficial cells are called umbrella cells
  156. Decoy cells’ or ‘comet cells’ with tail like cytoplasmic processes and homogenous degenerated nuclei simulating carcinoma cells
  157. Durck’s granuloma is due to aggregates of reactive astrocytosis and microghat cell proliferation seen in cerebral malaria
  158. HIV wasting syndrome is also called ‘slim diseas ‘
  159. HIV virus contains 3 group of structural proteins-gag (Group specific antigen), p coding and env (codes for envelop proteins)
  160. Gag codes for p and p 1 8, poi codes for reverse transcriptase and Env codes for synthesis of gp l2O and fgp41
  161. Non-structural genes in HIV virus are tat, art and 3’ orf
  162. HIV virus contains LTR (long terminal repeat) segments
  163. In Huntington’s disease, basal ganglia most commonly atrophied is caudate nucleus
  164. Loss of acetyl neurons in nucleus of Meynert is a feature of Alzheimer disease
  165. Verocay bodies are pathognomonic of schwanomma
  166. Hooping on silver staining is characteristic feature of primary brain lymphoma
  167. Bery aneurysm ruptures once diameter is more than 10mm
  168. Rosenthal fibres are pathognomonic of pilocytic astrocytoma
  169. Round cells with perinuclear halos are pathognomonic of oligodendroglioma
  170. Candle quattering appearance of ventricular system is pathognomonic of tuberous sclerosis
  171. Free radicals in reperfusion injury are produced by infiltrating PMN
  172. P53 dependent apoptosis is seen in irradiation
  173. Thrush breast appearance of myocardium is seen in profound anemia
  174. Cell shrinkage in a apoptosis is due to activation of glutathione peroxidase
  175. The cells with longest telomeres are sperms
  176. Feyrter cells are also called Kulchitsky cells or argentaffin cells. They belong to APUD coils or dense core granule (DCG) cells
  177. Frauzen needle is used for prostatic aspiration
  178. Bernard Soulier syndrome is an autosomal recessive taint characterized by a variable thrombocytopenia, IBT, defective
  179. Prothrombin consumption and giant platelets. Defect is in sialic acid rich protein GP I b of platelet membrane. It causes defective adhesion
  180. Gray platelet syndrome is due to abnormalities in platelet secretion
  181. Folded cell index and crowded cell index are also used for hormonal evaluation of vaginal cytology
  182. Joplin I reaction (Gel and coombs type IV) is seen in borderline leprosy and Joplin’s type II (gel and coombs type 3) is seen in lepromatous and borderline leprosy
  183. Myelin enveloping the axon is interrupted at regular intervals by funnel shaped clefts called Schmidt Lauterman clefts
  184. Renau bodies are hyaline bodies occur in endoneural compartment
  185. Mikulicz cells are seen in rhinoscleroma and they am grnular or foamy macrophages
  186. Farmer’s lung is also called Silofiller’s lung
  187. Concentric onion skin lesions is pathohistological feature  of tertiary syphilis is seen in arteri des
  188. Schiller-Duval bodies are found in endodermal sinus tumor
  189. Sherman’s paradox is typically seen in fragile X-syndrome
  190. Tamm Horsfall protein is a glycoprotein
  191. In hereditary spherocytosis, there is chief abnormality in spectrin
  192. Fibroblast proliferation is associated with LOF, FOE and PDCIF
  193. Struvite stones are composed of magnesium ammonium P04
  194. Tamm horsfall protein may be seen in acute tubular necrosis and multiple myeloma
  195. Triton tumors are malignant schwannoma
  196. Lafora bodies are seen in neurons, hepatocytes and myocytes
  197. Ferruginous bodies mainly contain asbestos
  198. Type2 muscle Fibre differs rum type I by widc Z band
  199. Heymann’s  membraneous GN is due to fixed intrinsic tissue antigen
  200. Oncocytes are also known as Hurthiel cells
  201. Parking lot inclusions are found in mitochandrial myopathy
  202. Flame cells or Mon cells are found in trypanosomiasis
  203. Ring chromosome is a type of deletion
  204. Popcorn cells are found in Hodgkin’s disease
  205. Pores of Kohn are found in alveolar wall
  206. Ring fibre is present in myotonic dystrophy
  207. Weibel-Palade bodies are characteristically contain P- selectin and von Willebrand disease
  208. Hydatid cyst is most often seen in liver, followed by lung omentum. mesentry and kidney. Calcification is common spleen liver and lungs.
  209. Oseous types are most often in upper end of femur, tibia or humerus, vertebrae and ribs.
  210. The Bends” (periarticular bubbles); t (bubbles in lungs) and “Staggers’ (involvement of inner ear) are seen in Caisson disease.
  211. Steroid myopathy is muscle fibre atrophy, affecting type 2 fibers.
  212. Sezary-Lutzner cells and Pautrier’s micro abscesses are found in Mycosis fungoides.
  213. Von Mayenburg Complexes are anomalies of biliary tree (small clusters of dilated bite ducts embedded in a fibrous, sorn times hyalinized stroma).
  214. Zebra bodies are seen in mucopolysaccharidoses.
  215. Decay cells or Comet cells with tail like cytoplasmic processes and homogenous degenerated nuclei simulate carcinoma cells
  216. Duret haemorrhages are midline haemorrhages in midbrain and pons seen in brain herniation.
  217. Ferruginous bodies are found in asbestosis.
  218. Heat-shock proteins or stress proteins alt present constitutively in normal cells, where they play an important role in normal cell metobolism. Two familes are HSP 70 and hsp 60 (also called Chaperones or chaperonins).
  219. Soap bubble lesion in brain is seen in cryptococcosis
  220. Brewer’s lung is seen in aspetgillosis
  221. Birbeck granules are found in histiocytosis X
  222. Heinz bodies are seen in C3-6-P-D deficiency.
  223. Flame cells or Mott cells are plasma cells in African trypanosomiasis.
  224. Major Basic protein (MBP) is a cationic protein of eosinophils, which has limited bactericidal activity but is cytotoxic to many parasites.
  225. Asteroid bodies are found in Sarcoidosis.
  226. Antischkow cells are found in rheumatic fever.

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