Hypertension definition cause pathology clinical future complications for5 marks
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Hypertension - Definition, Causes, Pathology, Clinical Features & Complications
(Harrison's Principles of Internal Medicine 22E | Morgan & Mikhail's Clinical Anesthesiology 7e | Katzung's Basic and Clinical Pharmacology 16e)
1. Definition
Hypertension is defined as a sustained elevation of arterial blood pressure above normal limits, assessed on two or more separate occasions.
ACC/AHA 2017 Classification (adults ≥18 years):
| Category | Systolic (mmHg) | Diastolic (mmHg) |
|---|---|---|
| Normal | <120 | <80 |
| Elevated | 120-129 | <80 |
| Stage 1 Hypertension | 130-139 | 80-89 |
| Stage 2 Hypertension | ≥140 | ≥90 |
| Hypertensive urgency | >180/120 | No organ damage |
| Hypertensive emergency | >180/120 | With organ damage |
High BP is a leading risk factor for cardiovascular disease (CVD), including ischemic and hemorrhagic stroke, coronary heart disease (CHD), heart failure, peripheral arterial disease, chronic kidney disease/end-stage kidney disease (ESKD), dementia, and all-cause mortality.
2. Causes / Etiology
A. Primary (Essential) Hypertension - 90-95% of cases
No identifiable single cause. Contributing factors include:
- Genetic predisposition (familial aggregation)
- High dietary sodium intake
- Obesity and insulin resistance / hyperinsulinemia
- Sedentary lifestyle
- Excessive alcohol intake
- Sympathetic nervous system overactivity
- Activation of the renin-angiotensin-aldosterone system (RAAS)
- Abnormal intracellular calcium and sodium handling in vascular smooth muscle cells
B. Secondary Hypertension - 5-10% of cases
| Cause | Mechanism |
|---|---|
| Chronic kidney disease | Impaired sodium excretion, RAAS activation |
| Renal artery stenosis | Reduced renal perfusion → RAAS activation |
| Primary hyperaldosteronism | Excess aldosterone → Na+/water retention |
| Cushing's syndrome | Excess cortisol → vasoconstriction |
| Pheochromocytoma | Excess catecholamines |
| Acromegaly | Excess GH/IGF-1 |
| Pregnancy / pre-eclampsia | Endothelial dysfunction |
| Oral contraceptives (estrogen) | Na+ retention, vasoconstriction |
| Obstructive sleep apnea | Sympathetic activation, hypoxia |
| Coarctation of the aorta | Mechanical obstruction |
3. Pathology / Pathophysiology
BP = Cardiac Output (CO) × Total Peripheral Resistance (TPR)
Hypertension arises from abnormalities in one or both of these factors.
Key Pathophysiological Mechanisms:
-
Renin-Angiotensin-Aldosterone System (RAAS) activation
- Angiotensin II causes potent vasoconstriction and aldosterone release → increased Na+ and water retention → raised CO and TPR.
-
Sympathetic nervous system (SNS) overactivity
- Increases heart rate, myocardial contractility, and peripheral vasoconstriction.
- Exaggerated vasopressor responses seen in hypertensive patients.
-
Endothelial dysfunction
- Reduced nitric oxide (NO) synthesis → impaired vasodilation.
- Increased endothelin (a potent vasoconstrictor).
- Reactive oxygen species contribute to vascular inflammation.
-
Abnormal renal sodium handling
- Impaired natriuresis → volume expansion → elevated CO.
-
Vascular remodeling
- Vascular smooth muscle hypertrophy → irreversibly elevated TPR.
- Increased intracellular Ca²+ → increased vascular tone.
Pathological Changes in Tissues:
- Blood vessels: Hyaline arteriolosclerosis (benign hypertension) - thickening of arteriolar walls with homogenous eosinophilic material; Hyperplastic arteriolosclerosis ("onion-skin" lesion) - in malignant hypertension; Fibrinoid necrosis of arterioles in accelerated/malignant hypertension.
- Heart: Concentric left ventricular hypertrophy (LVH) due to chronic increased afterload; diastolic dysfunction; eventually systolic dysfunction.
- Kidney: Nephrosclerosis - hyalinization of glomeruli, tubular atrophy, interstitial fibrosis. In malignant hypertension, necrotizing glomerulitis + fibrinoid necrosis.
- Brain: Microaneurysms (Charcot-Bouchard aneurysms) in small penetrating arteries.
4. Clinical Features
Hypertension is largely asymptomatic ("the silent killer") until organ damage develops.
Symptoms (when present):
- Headache (typically occipital, worse in the morning) - especially in severe hypertension
- Dizziness / tinnitus
- Epistaxis (nosebleeds)
- Visual disturbances (blurring)
- Palpitations
Signs on Examination:
- Elevated blood pressure on repeated measurements
- Fundoscopy (Keith-Wagener-Barker classification):
- Grade I: Silver wiring (arteriolar narrowing)
- Grade II: AV nipping (arteriovenous nicking)
- Grade III: Flame-shaped hemorrhages, cotton-wool spots (soft exudates)
- Grade IV: Papilledema (malignant hypertension)
- Loud A2 (aortic component of second heart sound)
- Sustained apex beat (LVH)
- S4 gallop (impaired LV relaxation)
- Renal bruits (if renovascular hypertension)
5. Complications
Long-standing uncontrolled hypertension accelerates atherosclerosis and causes hypertensive organ damage across multiple systems:
A. Cardiac Complications
- Left ventricular hypertrophy (LVH) - concentric hypertrophy → diastolic dysfunction
- Coronary artery disease / Angina / MI - accelerated atherosclerosis
- Congestive heart failure - initially diastolic, later systolic
- Aortic dissection - especially with severe/uncontrolled hypertension
B. Cerebrovascular Complications
- Ischemic stroke - thromboembolism from atherosclerotic arteries
- Hemorrhagic stroke - rupture of Charcot-Bouchard microaneurysms
- Hypertensive encephalopathy - breakthrough of cerebral autoregulation
- Vascular dementia - chronic microvascular ischemia
C. Renal Complications
- Nephrosclerosis - gradual loss of renal function
- Proteinuria / microalbuminuria - early marker of hypertensive nephropathy
- Chronic kidney disease (CKD) / End-stage renal disease (ESRD) - hypertension is a major cause
- Malignant hypertension → acute renal failure
D. Ocular Complications (Hypertensive Retinopathy)
- Arteriolar narrowing → hemorrhages, exudates → papilledema (Grade IV)
E. Peripheral Vascular Complications
- Peripheral arterial disease (PAD) - 2.5x increased risk in men, 3.9x in women
- Aortic aneurysm formation
Summary Table of Complications:
| System | Complication |
|---|---|
| Heart | LVH, IHD, MI, CCF, aortic dissection |
| Brain | Stroke (ischemic/hemorrhagic), encephalopathy, dementia |
| Kidney | CKD, ESRD, nephrosclerosis |
| Eyes | Hypertensive retinopathy, papilledema |
| Peripheral vessels | PAD, aortic aneurysm |
Key Points for 5 Marks:
- Definition: sustained BP ≥130/80 (ACC/AHA) or ≥140/90 (traditional)
- 90-95% is essential (primary); 5-10% is secondary
- Pathophysiology centers on RAAS activation, SNS overactivity, endothelial dysfunction, and vascular remodeling
- Largely asymptomatic until organ damage - the "silent killer"
- Major complications: stroke, MI, heart failure, CKD, and retinopathy (target organ damage)
Sources: Harrison's Principles of Internal Medicine 22E (2025), Morgan & Mikhail's Clinical Anesthesiology 7e, Katzung's Basic and Clinical Pharmacology 16e
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