Page 568 - Concise Pathology for Exam Preparation ( PDFDrive )

20 Endocrinology 553

Morphology

Main lesion of Cushing syndrome is found in pituitary and adrenal glands.
• Pituitary glands:
• Changes regardless of the cause of Cushing syndrome
• Most common alteration due to high levels of glucocorticoids is labelled Crooke hyaline
change in which the normal granular basophilic cytoplasm of the ACTH-producing cells
in the anterior pituitary is replaced by homogenous lightly basophilic material; the altera-
tion is because of accumulation of intermediate keratin filaments in the cytoplasm.
• Adrenals: Morphology varies depending on the cause of hypercortisolism. The adrenals
have one of the following abnormalities:
• Cortical atrophy (exogenous glucocorticoids cause suppression of endogenous
ACTH)
• Diffuse hyperplasia
• Nodular hyperplasia
• Adenoma
• Carcinoma
Q. Write briefly on the pathogenesis, clinical features and
morphology of hyperaldosteronism.
Ans. Hyperaldosteronism is a generic term for a group of many closely related syndromes,
characterized by excessive aldosterone secretion. Excessive aldosterone secretion causes
sodium retention and potassium excretion resulting in hypertension and hypokalaemia.
Types

• Primary
• Secondary (due to an extra-adrenal cause)
1. Primary hyperaldosteronism
(a) Autonomous overproduction of aldosterone
(b) Resultant suppression of renin–angiotensin system and decreased plasma renin
activity
(c) Caused by:
(i) Adrenocortical neoplasm

Adenoma (80%) Carcinoma (20%)
or
Conn syndrome
(ii) Primary idiopathic adrenocortical hyperplasia, which is characterized by bilat-
eral nodular enlargement.
(iii) Glucocorticoid-remediable hyperaldosteronism (familial), which is caused by
a chimeric gene, resulting from fusion of CYP11B1 (11 b-hydroxylase) and
CYP11B2 (aldosterone synthase).
2. Secondary hyperaldosteronism (Flowchart 20.11): Aldosterone release occurs sec-
ondary to activation of renin–angiotensin system.

• Decreased renal perfusion • Arterial hypovolaemia and oedema • Pregnancy
• Arteriolar nephrosclerosis • Congestive cardiac failure • Increased
• Renal artery stenosis • Cirrhosis oestrogen levels

Increased plasma renin

Release of aldosterone
FLOWCHART 20.11. Pathogenesis of secondary hyperaldosteronism.

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