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USMLE/COMLEX 1 - Hypertension Definitions & Etiologies

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Here are key facts for USMLE Step 1 & COMLEX-USA Level 1 from the Hypertension Overview tutorial, as well as points of interest at the end of this document that are not directly addressed in this tutorial but should help you prepare for the boards. See the tutorial notes for further details and relevant links.
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VITAL FOR USMLE/COMLEX 1
1. Definition of Hypertension: Sustained elevation in blood pressure due to increased cardiac output and/or total peripheral resistance.
2. Classification (2017 ACC/AHA Guidelines):
    • Normal: <120/<80 mmHg
    • Elevated: 120–129/<80 mmHg
    • Stage 1: 130–139 or 80–89 mmHg
    • Stage 2: ≥140 or ≥90 mmHg
3. Primary Hypertension:
    • Accounts for 90–95% of adult cases.
    • No single identifiable cause; multifactorial and influenced by genetic and lifestyle factors.
4. Secondary Hypertension:
    • 5–10% of cases.
    • Caused by identifiable conditions (e.g., renal artery stenosis, primary aldosteronism, pheochromocytoma).
5. Key contributors to Primary Hypertension:
    • Obesity
    • High salt intake
    • Sedentary lifestyle
    • Genetics and epigenetics
6. Renovascular Hypertension:
    • Caused by renal artery stenosis, leading to activation of the renin-angiotensin-aldosterone system (RAAS).
    • Common causes: atherosclerosis (older adults) and fibromuscular dysplasia (younger women).
Renal Artery Stenosis
7. Primary Aldosteronism:
    • Increased aldosterone → sodium and water retention → increased BP.
    • Causes: aldosterone-producing adenoma or bilateral adrenal hyperplasia.
8. Coarctation of Aorta:
    • Consider in children or young adults with hypertension and weak femoral pulses.
9. Pheochromocytoma:
    • Catecholamine-secreting tumor of adrenal medulla.
    • Presents with paroxysmal hypertension, sweating, headache, and palpitations.
10. Cushing Syndrome:
    • Excess cortisol → increased BP via mineralocorticoid effects.
11. Obstructive Sleep Apnea:
    • Intermittent hypoxia → sympathetic activation → sustained hypertension.
12. Drug-induced Hypertension:
    • NSAIDs, oral contraceptives, decongestants, amphetamines, cocaine.
13. Gestational Hypertension:
    • Develops after 20 weeks of gestation.
    • Risk of pre-eclampsia (new-onset proteinuria, organ damage).
14. Pathophysiology of BP:
    • BP = CO × TPR; both cardiac output and peripheral resistance contribute to blood pressure.
15. Mean Arterial Pressure (MAP):
    • MAP = Diastolic BP + 1/3 (Systolic − Diastolic).
    • Key determinant of tissue perfusion.
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HIGH YIELD
16. Demographic Patterns:
    • Highest prevalence in African Americans, American Indians, and Alaskan Natives.
    • Post-menopausal women have higher BP than premenopausal women and age-matched men.
17. Masked vs White Coat Hypertension:
    • White coat HTN: elevated in clinic, normal at home.
    • Masked HTN: normal in clinic, elevated at home.
18. Salt Sensitivity:
    • Enhanced in African Americans, elderly, and post-menopausal women.
    • Tied to impaired sodium excretion.
19. Diet and HTN:
    • Excess salt, low intake of potassium, calcium, fiber, and vegetable protein contribute.
20. Chronic Stress:
    • Sustained sympathetic activation can lead to elevated blood pressure.
21. Total Peripheral Resistance (TPR):
    • Major determinant of diastolic pressure.
    • Regulated by arteriolar tone and sympathetic nervous system activity.
22. Cardiac Output (CO):
    • Major determinant of systolic pressure.
    • Affected by heart rate and stroke volume.
23. Clinical Evaluation:
    • BP measurements must be repeated under standardized conditions, including ambulatory monitoring if needed.
24. Fibromuscular Dysplasia:
    • Non-atherosclerotic, non-inflammatory vascular disease that causes renovascular hypertension in younger women.
25. Hypertension Complications (clinical consequences — previewed in Step 2+):
    • Coronary artery disease, stroke, aneurysms, renal failure, retinopathy.
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Beyond the Tutorial
26. Baroreceptors:
    • Located in carotid sinus and aortic arch.
    • Short-term BP regulation via autonomic nervous system.
27. RAAS System Activation:
    • Triggered by renal hypoperfusion → ↑ renin → ↑ angiotensin II → vasoconstriction and aldosterone release.
28. JNC 8 vs ACC/AHA Guidelines:
    • Step 1 focuses on basic understanding; current exam favors the ACC/AHA guidelines presented in the tutorial.
29. Hypertensive Urgency vs Emergency (Step 2+):
    • Urgency: Severe BP without end-organ damage.
    • Emergency: Severe BP with signs of damage (e.g., encephalopathy, AKI, chest pain).