Adrenal (suprarenal) Gland – applied anatomy

Dr Sunila BHMS,MD(Hom)
The suprarenal (adrenal) glands are two small bodies of a yellowish colour, flattened anteroposteriorly and situated one on each side of the median plane, behind the peritoneum, and immediately anterosuperior to the superior pole of each kidney. These are a pair of important endocrine glands situated on the posterior abdominal wall. They are enclosed, together with the kidneys, in the renal fascia, but are separated from the kidneys by a little fibro-alveolar tissue. 

Each gland lies in the epigastrium at the upper pole of the kidney, in front  of the crus of the diaphragm, opposite the vertebral end of the 11th  intercostal space and the   12t h rib.


Adrenal glands are made up of two parts:

  • 1)      An outer cortex, mesodermal in origin, consists of lipids only.
  • 2)      An inner medulla, neural crest origin, consist of chromaffin cells, secrete adrenalin and nor adrenalin.

The two parts are absolutely distinct from each other structurally, functionally, and developmentally. Each gland measures 50mm in height, 30mm in breadth, and 10mm in thickness. It weighs about 5 gm, the medulla forming one tenth of the gland. It is approximately one third of the kidney at birth and about one thirtieth of it in adults. The right suprarenal gland is pyramidal ‘cock’s hat” in shape .The left supra renal is semilunar in shape and is a bit higher in level than the right.


Right suprarenal gland:

  •  a) Apex
  •  b) Base: Related to upper pole of the right kidney.

Two surfaces:

 Anterior surface: is devoid of peritoneum except for a small part inferiorly.

  • Medially it is related to inferior venecava.
  • Laterally it is related to liver.
  • Inferiorly it is related to duodenum.

 Posterior :  Related to right crus of the diaphragm

c) Three borders:

  • Anterior border: A little below the apex it presents the hilum where the supra renal vein emerges.
  • Medial border: Related to right coeliac ganglion & Right inferior phrenic artery.
  • Lateral border

Left suprarenal gland:

Two ends:

  • Upper narrow end
  • Lower rounded end

Two borders:

  • Medial; convex border; related to the left coeliac ganglion, left inferior phrenic artery & left gastric artery.
  • Lateral; concave border.

Two surfaces

  • Anterior: From above downwards it is related to the cardiac end of stomach, the splenic artery & the pancreas. The upper end may be related to the posterior extremity of the spleen. Near the lower end there is a hilum through which the left supra renal vein emerges.
  • Posterior: Related to the kidney laterally & the left crus of the diaphragm medially.


Each gland is supplied by

  • Superior supra renal artery: branch of inferior phrenic artery.
  • Middle supra renal artery: branch of the abdominal aorta.
  • Inferior supra renal artery: branch of the renal artery.


  • Right supra renal vein drains into inferior venecava.
  • Left supra renal vein drains into the left renal vein.


Lymphatics from the supra renal glands drain into the lateral aortic nodes.


The supra renal medulla has a rich nerve supply through myelinated preganglionic fibres. The chromaffin cells in it are considered homologous with post ganglionic sympathetic neurons.


CORTEX is divided into

  • Zona glomerulosa: secretes mineralocorticoids- aldosterone.
  • Zona fasiculata: secretes glucocorticoids.
  • Zona reticularis: secretes sex steroids(androgens and  estrogens)

MEDULLA: secretes adrenaline and noradrenaline



  • Glucocorticoid excess: Cushing’s syndrome (Hypercortisolism)
  • Mineralocorticoid excess:  Hyper aldosteronism (Conn’s syndrome)
  • Sex corticoid excess: Adrenogenital syndrome


  • Adreno cortical insufficiency: Primary (Addison s disease) & Secondary.
  • Adrenal crisis


  • Phaeochromocytoma


It is caused by persistent over secretion of glucocorticoids.


  • ACTH –dependent conditions:
  • Bilateral adrenal hyperplasia: 70% of these are secondary to a small adenoma involving the basophils (cushing’s disease) or chromophobes in the pituitary. Sometimes the abnormality is in the production and release of CRF from the hypothalamus.
  • Ectopic ACTH secretion: This is seen as a paraneoplastic syndrome in bronchogenic caricinoma, medullary carcinoma of thyroids, pancreatic carcinoma, nonteratogenic ovarian carcinoma, neuroblastoma, and ganglioma.
  • Iatrogenic: Regular therapeutic administration of exogenous ACTH leads to Cushing‘s syndrome. This is the most common cause at present.
  • ACTH –independent conditions
  • Adenomas or carcinomas of the adrenal cortex and micro nodular hyperplasia: These are rapidly growing with local invasion and distant metastases early in course.
  • Iatrogenic: Use of pharmacological doses of glucocorticoids

Clinical features:

  • The affected person is plethoric with rounded appearance of the face (moon face).
  • There is characteristic obesity with deposition of fat over the neck, shoulders, abdomen, and hips. This is called the “buffalo type” of obesity.
  • Hirsutism is seen in some cases.
  • Painless reddish striae are seen over thighs, gluteal regions, abdomen, axillae, and arms.
  • Other features include acne, delayed wound healing, bruising, pigmentation, hypertension, myopathy, psychiatric symptoms like depression, melancholy, amenorrhea, and osteoporosis.
  • Diabetic complications, hypernatremia, hypokalemia, and fluid retention are also seen.

Treatment: Surgical removal of the adrenal tumours is the main treatment.

Nelson’s syndrome
Some patients who undergo bilateral adrenalectomy develop enlargement of the pituitary, pressure effects on the optic chiasma and raised intra cranial tension. They also show increased pigmentation due to hypersecretion of MSH. This syndrome follows bilateral adrenalectomy after a few years.


Primary hyperaldosteronism (Conn’s syndrome)

This is a rare disorder caused by a primary increase in the production of aldosterone. Around 60-75% of cases are due to aldosterone producing adenoma. This is common in women.

Idiopathic hyperaldosteronism: Probably due to due to bilateral adrenal hyperplasia .In men it is common.

Secondary hyperaldosteronism: Due to high rennin production occurring in renal artery stenosis, congestive heart failure, prolonged use of diuretics and others.

Clinical features:
Include hypertension, unprovoked hypokalemia, low plasma rennin activity. The triad of low serum potassium, low plasma rennin activity, alkalosis, and high non suppressible plasma aldosterone confirms the diagnosis.

Demonstration of raised aldosterone levels in the adrenal venous blood obtained by selective catheterization helps to identify the side of lesion. Tumours can be detected by C T scanning, MRI & isotoping imaging.

Bartter’s syndrome
Hyperplasia of juxtaglomerular cells of the kidney associated with hypokalaemic alkalosis and hyperaldosteronism without hypertension, named after Frederic Bartter, US physicion. It is primary hyper-reninemia, inherited as an autosomal recessive. It presents with polyuria, polydipsia, failure to thrive, hypokalemia, alkalosis. The blood pressure is normal and there is no edema. Urinary excretion of potassium and chlorides is elevated.

ADRENOGENITAL SYNDROME (Congenital adrenal hyperplasia)
This rare disorder is characterized by virilization in female and precocious puberty in male children .The underlying defect is congenital deficiency of enzymes leading to metabolic block in hormone synthesis. This results in the accumulation of intermediary metabolites with androgenic activity.

Aetiology: The enzyme defect is transmitted as an autosomal recessive disorder. Females are affected more than females.

Clinical featuresThey include failure to thrive, vomiting, hyponatremia, and hypotension. Milder cases manifest as virilization in girls and sexual precocity in boys. Due to premature fusion of epiphyses, growth is stunted. Hyperandrogenism causes testicular atrophy and inferitily in adult males.

Diagnosis is confirmed by estimation of the products of androgens in urine.

Hypo function of the adrenal cortex may be due to a primary disorder of the gland or secondary to hypo secretion of the tropic hormone.


Primary adrenocortical insufficiency (Addison’s disease)

  • Atrophy of the adrenal cortex due to autoimmune adrenalitis
  • Tuberculosis
  • Infiltration by metastatic carcinoma
  • Hemochromatosis
  • Amyloidosis
  • Post-surgical(total or subtotal adrenalectomy)

Secondary adrenocortical insufficiency

  • Hypothalamic causes: Tumours of third ventricle, meningitis, encephalitis, injury to the base of the brain, corticosteroid therapy, sarcoidosis, and histiocytosis.
  • Pituitary causes: Tumours, basal meningitis, hypophysectomy, after irradiation, empty sella syndrome.

It is the most common disease, mostly in women. Generally, the onset is slow and may be unnoticed but many patients present for the first time in acute adrenal failure precipitated by stress.

Clinical features:
Initial symptoms may be vague such as weakness, tiredness, lethargy, weight loss, gastrointestinal upset. Pigmentation occurs in face, palms, extensor aspects of limbs, flexure, mucous membranes of the mouth, tongue, and genitalia, vitiligo, premature greying of hair, amenorrhea & impotence in males. Other features include hypoglycemia, hypotension, diminution in size, psychiatric symptoms like depression or melancholia is seen.

Investigations include hypoglycemia, hyponatremia, hyperkalemia, low plasma cortisol levels, high plasma ACTH levels.

ADRENAL CRISIS (Acute adrenal insufficiency, Adrenal apoplexy)
Sudden development of adrenal cortical failure leads to adrenal crisis. It is a medical emergency which is fatal if undiagnosed. Adrenal crisis may complicate chronic adrenal insufficiency or it may occur acutely in subjects who develop fulminant infections.

Sudden withdrawal of ACTH of steroid therapy, infections, surgery, drugs, stress, obstetric accidents precipitate acute adrenal failure in patients with chronic adrenal cortical insufficiency.

Clinical features include severe vomiting, diarrhea, profound shock, blotchy purpura, if untreated coma supervenes and death occur.

Phaeochromocytomas are tumours of the chromaffin tissues of medulla. They produce excess of catecholamines which causes hypertension and other effects. Of these tumours 90% are benign and 10% malignant.

Clinical features include paroxysmal hypertension, headache, excessive sweating, tachycardia, flushing, fever, glycosuria and postural hypotension.

Demonstrating raised levels of VMA which is the excretory product of catecholamines present in urine or total or free urinary Meta –adrenalines (Normal VMA- 6mg/ day)

  • Plasma catecholamine levels.
  • Localization of tumor by CT, MRI, ultrasonography, & adrenal angiography.


  • Measurement of  adrenal steroids11-hydroxy corticosteroid:
  • Levels of these hormones in plasma, urine or adrenal tissue can be estimated.

Urinary cortisol

Normal:  55-193 nmol/24 h

Urinary17-hydroxy corticosteroids

Normal:  5-17mg/24hr in men,   5-15mg/24hr in women

Aldosterone and its derivatives

  • Normal plasma concentration: 10 ng/ dl
  • Normal Urinary excretion: 5-19 ng/dl

Metabolites of sex hormones 17 KS(keto steroids)

Normal urinary excretion

  • 5-25mg/24 h in men
  • 3-20mg/24 h in women

17 ketogenic steroids

Normal excretion 5-22 mg in men        5-15 mg in women

  • Secretory activity of the adrenal cortex    
  • It is estimated isotopically.
  • Normal value is 15-30 mg cortisol in 24 hrs

Test for pituitary –adrenal interaction:

  • To evaluate the adrenal reserve, ACTH secreting capacity and normal pituitary-adrenal feedback control.
  • Metyrapone test
  • Dexamethasone suppression test
  • Demonstration of lesion by CT, MRI etc


  • Essentials of Human Anatomy- Thorax and Abdomen by A K Datta
  • B D Chaurasia’s Human Anatomy- Thorax and Abdomen
  • Clinically oriented anatomy by Keith. L.Moore
  • Gray’s Anatomy
  • Clinical Anatomy by Richard S Snell
  • Grant’s method of anatomy by Basmajian and Slonecker
  • Text book of Medicine by K V Krishna Das

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