Thyroid and Adrenal Glands

2.5. Clinical Relevance

1. Addison’s Disease (Primary Adrenal Insufficiency)

• Cause: Destruction or dysfunction of the adrenal cortex (autoimmune, infection, or injury).

• Hormonal Effect: ↓ Cortisol and ↓ Aldosterone → ↑ ACTH due to loss of negative feedback.

• Clinical Features: Fatigue, hypotension, dehydration, hyperpigmentation, hyponatremia, and hyperkalemia.

• Physiological Insight: Loss of RAAS and HPA regulation leads to impaired stress response and fluid imbalance.

2. Cushing’s Syndrome (Glucocorticoid Excess)

• Cause: Chronic excess of cortisol (often due to ACTH-secreting pituitary tumor or prolonged steroid therapy).

• Hormonal Effect: ↑ Cortisol → ↓ CRH and ACTH (if exogenous or adrenal source).

• Clinical Features: Central obesity, muscle wasting, hypertension, hyperglycemia, and “moon face.”

• Physiological Insight: Breakdown of HPA negative feedback control results in cortisol overproduction and metabolic dysregulation.

3. Conn’s Syndrome (Primary Hyperaldosteronism)

• Cause: Aldosterone-secreting adrenal adenoma or hyperplasia of the zona glomerulosa.

• Hormonal Effect: ↑ Aldosterone → Na⁺ retention, K⁺ loss, and water retention.

• Clinical Features: Hypertension, muscle weakness, hypokalemia, and metabolic alkalosis.

• Physiological Insight: Excessive aldosterone secretion occurs independent of RAAS, disrupting electrolyte and fluid balance.

4. Congenital Adrenal Hyperplasia (CAH)

• Cause: Genetic enzyme defects (most commonly 21-hydroxylase deficiency) impair cortisol synthesis.

• Hormonal Effect: ↓ Cortisol → ↑ ACTH → adrenal hyperplasia and excess androgen production.

• Clinical Features: Ambiguous genitalia in females, early virilization in males, and electrolyte disturbances.

• Physiological Insight: Lack of cortisol feedback drives overproduction of adrenal androgens.