100. Pathophysiology of Hypertension and Hypotension – Quiz

📌 Professor’s Notes: Quick Revision

  • Hypertension is a sustained elevation of systemic arterial blood pressure documented on repeated measurements. Persistent blood pressure of ≥130/80 mmHg is considered hypertension in many current guidelines. Long-standing hypertension increases the risk of stroke, myocardial infarction, heart failure, and chronic kidney disease.
  • Hypertension is classified into:
    • Primary (essential) hypertension: Accounts for 90–95% of cases and has no single identifiable cause. It results from increased sympathetic activity, activation of the renin–angiotensin–aldosterone system (RAAS), increased blood volume, obesity, excess salt intake, genetic factors, and reduced nitric oxide production.
    • Secondary hypertension: Caused by identifiable disorders such as renal diseases, endocrine disorders (hyperaldosteronism, Cushing syndrome, pheochromocytoma), coarctation of the aorta, neurological disorders, drugs, and pregnancy-induced hypertension.
  • Major risk factors for essential hypertension include family history, advancing age, obesity, high salt intake, stress, smoking, excessive alcohol intake, sedentary lifestyle, hyperlipidemia, and environmental factors. Blood pressure increases with age because of reduced arterial compliance.
  • Experimental hypertension is produced in animal models to study disease mechanisms. Important models include renal artery constriction (Goldblatt model), neurogenic hypertension, steroid-induced hypertension, reduced renal mass, and salt-induced hypertension.
  • Chronic hypertension causes left ventricular hypertrophy due to increased afterload. Persistent pressure overload eventually leads to ventricular dilatation, heart failure, increased myocardial oxygen demand, and ischemic heart disease. It also causes arterial wall thickening, reduced vascular compliance, accelerated atherosclerosis, stroke, hypertensive encephalopathy, retinopathy, and progressive chronic kidney disease due to renal vascular sclerosis.
  • Management is based on correcting the physiological abnormalities:
    • Weight reduction lowers blood pressure.
    • Dietary sodium restriction reduces extracellular fluid volume.
    • A diet rich in fruits, vegetables, whole grains, and fiber improves cardiovascular health.
    • Regular aerobic exercise decreases sympathetic activity and improves endothelial function.
    • Stress reduction, adequate sleep, smoking cessation, and limiting alcohol intake are essential lifestyle measures.
    • Drug therapy includes diuretics, calcium channel blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, vasodilators, and anti-adrenergic drugs. Lifestyle modification should continue even after drug therapy is started.
  • Hypotension is usually defined as systolic blood pressure below 90 mmHg. It is classified as:
    • Chronic hypotension: Common causes include adrenal insufficiency, hypopituitarism, malnutrition, chronic diarrhea, and prolonged bed rest.
    • Acute hypotension: Caused by hemorrhage, dehydration, myocardial infarction, septic shock, or anaphylaxis.

📝 Practice MCQs

Welcome to your Physiology – Chapter 100 – Pathophysiology of Hypertension and Hypotension

🎙️ Frequently Asked Viva Questions

Q1. What is the physiological basis of essential (primary) hypertension?
Answer: Essential hypertension is mainly due to persistent sympathetic overactivity, along with increased RAAS activity, sodium retention, expanded blood volume, and reduced nitric oxide production.

Q2. Why is isolated systolic hypertension common in elderly people?
Answer: Aging causes reduced arterial compliance (arterial stiffness), increasing systolic pressure while diastolic pressure may remain normal.

Q3. Why does excessive dietary salt increase blood pressure?
Answer: Excess sodium promotes water retention, expands extracellular fluid volume, and increases vascular reactivity, leading to hypertension in susceptible individuals.

Q4. How does obesity contribute to hypertension?
Answer: Obesity increases sympathetic activity, insulin resistance, and blood volume, all of which raise arterial blood pressure.

Q5. Why does chronic stress increase blood pressure?
Answer: Chronic stress causes persistent sympathetic activation, producing vasoconstriction and sustained elevation of arterial pressure.

Q6. What are the common causes of secondary hypertension?
Answer: Major causes include renal diseases, endocrine disorders, renal artery stenosis, coarctation of the aorta, pregnancy-induced hypertension, and certain drugs.

Q7. Why does long-standing hypertension produce left ventricular hypertrophy?
Answer: Persistent hypertension increases afterload, forcing the left ventricle to work harder, resulting in concentric hypertrophy.

Q8. How does hypertension damage the kidneys?
Answer: Hypertension causes renal arteriolar sclerosis and glomerular damage, reducing glomerular filtration rate and leading to chronic kidney disease.

Q9. Why does hypertension increase the risk of stroke?
Answer: Chronic hypertension accelerates cerebral atherosclerosis and may cause intracerebral hemorrhage, increasing the risk of stroke.

Q10. Why is weight reduction recommended in hypertension?
Answer: Weight loss decreases sympathetic activity, blood volume, and cardiovascular workload, resulting in lower arterial blood pressure.

Q11. How does regular aerobic exercise lower blood pressure?
Answer: Regular exercise reduces sympathetic activity, increases parasympathetic tone, improves endothelial function, and helps weight reduction.

Q12. Why are ACE inhibitors effective antihypertensive drugs?
Answer: They reduce angiotensin II formation and increase bradykinin, producing vasodilation and lowering blood pressure.

Q13. What is orthostatic (postural) hypotension?
Answer: It is a fall in systolic blood pressure of at least 20 mmHg within a few minutes of standing, usually due to impaired autonomic compensation.

Q14. Why does orthostatic hypotension occur on standing?
Answer: Standing causes venous pooling in the lower limbs, reducing venous return and cardiac output. Inadequate reflex vasoconstriction leads to hypotension.

Q15. What is the physiological basis of beta-blockers in hypertension?
Answer: Beta-blockers decrease heart rate, cardiac output, and renin release, thereby reducing arterial blood pressure.

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