109. Secondary hypertension - classification, etiology, pathogenesis.

Secondary hypertension - classification, etiology, and pathogenesis.

Secondary hypertension is elevated systemic blood pressure due to a specific, identifiable, and potentially reversible underlying cause.

It accounts for 5–10% of all hypertension cases.

Classification and etiology

1. 1 Renal (most common cause of secondary hypertension)

Renovascular hypertension

Renal artery stenosis (atherosclerosis in elderly men, fibromuscular dysplasia in young women).

Parenchymal renal disease

Chronic glomerulonephritis.

Polycystic kidney disease.

Diabetic nephropathy.

Chronic pyelonephritis.

1. 2 Endocrine causes

Primary hyperaldosteronism (Conn's syndrome)

Adrenal adenoma or bilateral adrenal hyperplasia → excessive aldosterone → sodium and water retention, hypokalemia.

Pheochromocytoma

Catecholamine-producing tumor of adrenal medulla → episodic or sustained hypertension.

Cushing’s syndrome

Glucocorticoid excess (ACTH-producing tumor or adrenal adenoma) → increased vascular sensitivity and volume expansion.

Thyroid disorders

Hyperthyroidism: increased cardiac output → systolic hypertension.

Hypothyroidism: increased diastolic BP due to increased PVR.

Acromegaly

GH and IGF- 1 excess → sodium retention and vascular changes.

1. 3 Cardiovascular causes

Coarctation of the aorta → upper limb hypertension with lower limb hypotension.

1. 4 Neurogenic causes

Increased intracranial pressure (Cushing reflex).

Autonomic dysfunction.

1. 5 Drug- induced

Oral contraceptives ( estrogens → RAAS activation).

NSAIDs.

Steroids.

Sympathomimetics.

Cyclosporine, erythropoietin.

1. 6 Other causes

Obstructive sleep apnea (sympathetic overactivity).

Pregnancy- related hypertension (preeclampsia/ eclampsia).

Pathogenesis

Renal hypertension

1. Reduced renal perfusion (stenosis or disease) → increased renin release.
2. Activation of RAAS → increased angiotensin II → vasoconstriction and aldosterone- mediated sodium and water retention → increased BP.

Endocrine hypertension

Hormone excess (aldosterone, catecholamines, cortisol, thyroid hormones) → increased blood volume, vasoconstriction, or increased cardiac output → hypertension.

Coarctation of aorta

Narrowing → increased proximal BP (upper limbs), reduced distal BP → activation of RAAS due to renal hypoperfusion → further raises BP.

Drug- induced hypertension

Various mechanisms: sodium retention (NSAIDs), increased sympathetic tone (decongestants), hormonal effects (OCPs).