Dr . M.A.Kubtan MD - FRCS
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Anatomy
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 components of the gland: the inner adrenal medulla and the outer adrenal cortex .
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The weight of a normal adrenal gland is approximately 4 g.
They are situated at the upper poles of the kidneys in the retroperitoneum within
Gerota’s capsule.
They are well supplied by blood vessels.
A large adrenal vein drains on the right side into the vena cava and on the left side into the renal vein.
Position of the adrenal glands
(hatched) in the retroperitoneum.
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The cortex and the medulla
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Arise from different blastodermic layers .
Mesodermal cells form the adrenal cortex .
Neuroectodermal cells migrate to the cortex and form the adrenal medulla.
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 Catecholamines adrenalinen(epinephrine) but also noradrenaline
(norepinephrine) and dopamine. are secreted by the adrenal medulla .
 corticosteroids, aldosterone and cortisol are synthesised in the adrenal cortex.
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Act as hormones .
They are secreted directly into the circulation.
Their effects are mediated through α and β receptors on target organs .
Activation of the cardiovascular system .
Increase in blood pressure and heart rate.
Vasoconstriction of vessels in the splanchnic system .
Vasodilatation of vessels in the muscles an bronchodilatation.
Increased glycogenolysis in liver and muscles .
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Cells of the zona glomerulosa produce aldosterone .
The target organs of aldosterone are the kidneys, the sweat and salivary glands and the intestinal mucosa.
Aldosterone promotes sodium retention and potassium excretion.
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 Renin–angiotensin system are the most important regulators of aldosterone secretion .
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Renin produced by the juxtaglomerular cells in the kidneys .
Its substrate angiotensinogen to generate angiotensin 1 .
Angiotensin I is converted by the angiotensin-converting enzyme (ACE) to the octapeptide angiotensin II .
 Angiotensin II, is modified to angiotensin III.
 Both II & III stimulate the secretion of aldosterone from the adrenal cortex
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Cortisol
Cortisol secretion is regulated by adrenocorticotrophic hormone (ACTH)
 The hypothalamus controls ACTH secretion by secreting corticotropinreleasing hormone (CRH).
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Adrenal androgens
Dehydroepiandrosterone (DHEA)
 Dehydroepiandrosterone sulphate
( DHEAS )
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Incidentaloma
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Definition
A clinically unapparent mass detected incidentally by imaging studies conducted for other reasons.
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Incidence
The prevalence of adrenal masses in autopsy studies ranges from
1.4% to 8.7% and increases with age.
 Incidentalomas may be detected on imaging studies in 4% of patients.
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More than 75% are non-functioning adenomas .
Cushing’s adenomas, phaeochromocytomas and even adrenocortical carcinomas may be present .
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Prevalence of non-functioning and functioning tumours in patients with incidentalomas
Tumour Prevalence (%)
Non-functioning adenoma 78
Cushing’s adenoma 7
Adrenocortical carcinoma 4
Phaeochromocytoma 4
Myelolipoma 2
Cyst 2
Metastases 2
Conn’s adenoma 1
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Hormonal evaluation includes:
 Morning and midnight plasma cortisol measurements;
 A 1-mg overnight dexamethasone suppression test;
 24-hour urinary cortisol excretion (optional);
 24-hour urinary excretion of catecholamines, metanephrines
 Plasma-free metanephrines;
 Serum potassium, plasma aldosterone and plasma renin activity;
 Serum Dehydroepiandrosterone sulphate DHEAS, testosterone or 17βhydroxyestradiol (virilising or feminising tumour).
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For evaluation of malignancy computerised tomography (CT) or magnetic resonance imaging (MRI) should be performed in all patients with adrenal masses .
Fine-needle aspiration cytology after a phaeochromocytoma has been excluded.(A pheochromocytoma will often release a burst of catecholamines, with the associated signs and symptoms quickly following ).
The likelihood of an adrenal mass being an adrenocortical carcinoma increases with the size of the mass (25% > 4 cm).
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 Primary hyperaldosteronism (Conn’s adenoma ) .
 Cushing’s syndrome .
 Adrenogenital syndrome (Congenital adrenal hyperplasia ) .
 Adrenal insufficiency (loss of function of the adrenal cortex ).
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(Conn’s adenoma )
 Incidence : Commonly unilateral adenoma , 12% of hypertensive patients have PHA with normal potassium levels.
 Pathology : In 20–40% of cases, bilateral micronodular hyperplasia is causative. 70% have hyperplasia and 30% unilateral adenoma.
 Clinical features : Most patients are between 30 and 50 years of age , female predominance , non-specific symptoms: headache, muscle weakness, cramps, intermittent paralysis, polyuria, polydypsia ( excessive thirst ) and nocturia , hypertension and hypokalaemia .
 Diagnosis : Biochemical diagnosis is the assessment of potassium level and the aldosterone to plasma renin activity ratio , MRI or CT with a sensitivity of 80–90% , selective adrenal vein catheterisation , determination of aldosterone to cortisol ratio (ACR).
 Treatment : Laparoscopic or open surgical resection when indicated .
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Definition : Hypersecretion of cortisol , (85%) ACTH-dependent ,
ACTH-independent (pituitary Adenoma ) or Ectopic ACTH-producing tumours .
Clinical features of Cushing’s syndrome :
1. Weight gain/central obesity
2.Diabetes
3.Hirsutism
4. Hypertension
5.Skin changes (abdominal striae, facial plethora, ecchymosis, acne)
6.Muscle weakness
7.Menstrual irregularity/impotence
8.Depression/mania
9.Osteoporosis
10.Hypokalaemia
Diagnosis : Biochemical , MRI or CT .
Treatment : Surgery when indicated .
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(adrenal paraganglioma)
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This is a tumour of the adrenal medulla, which is derived from chromaffin cells and which produces catecholamines.
Approximately 10% of phaeochromocytomas are malignant.
About 8% of patients with an apparently benign phaeochromocytoma subsequently develop metastases.
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