IM8.1-7 | Hypertension Foundations — Summary & Reflection

KEY TAKEAWAYS

Hypertension foundations — key facts:

• Definition and staging: ACC/AHA 2017 (≥130/80 = hypertension; Stage 1: 130–139/80–89; Stage 2: ≥140/≥90) vs JNC 7 (≥140/90 = hypertension; Stage 1: 140–159/90–99). Always cite which system. Indian guidelines (IGH-IV) use JNC 7 threshold for treatment decisions.
• Epidemiology: 220 million hypertensive Indians; ~28% prevalence; only ~15% controlled. India's burden reflects urbanisation, dietary sodium, and reduced physical activity.
• Genetics: Polygenic (heritability 30–50%); rare monogenic forms include Liddle syndrome, GRA, Gordon syndrome. GWAS identify RAAS, sodium-transport, and NO-pathway variants.
• Pathophysiology (primary HTN): RAAS activation, SNS overactivity, renal sodium-handling defect, endothelial NO deficit, vascular remodelling, and adipose/metabolic contributions. Each mechanism maps to a drug class.
• Secondary HTN (5–10% overall; up to 30% in young/resistant): Key causes — primary aldosteronism (ARR screening), renovascular HTN (renal Doppler/CT angiography), phaeochromocytoma (urinary metanephrines), Cushing syndrome (UFC/overnight DST), coarctation (radio-femoral delay, CXR rib notching), OSA, drugs (OCP, NSAIDs).
• Urgency vs Emergency: Same BP level; the distinction is acute end-organ damage. Emergency = acute TOD (encephalopathy/PRES, stroke, ACS, pulmonary oedema, aortic dissection, AKI, papilloedema, eclampsia) → IV agent, MAP ↓20–25% in 1h. Urgency = no acute TOD → oral agents, 24–48h reduction.
• Target organ damage: Heart (LVH, diastolic dysfunction, HFpEF, HFrEF, AF); Brain (lacunar infarcts, haemorrhagic stroke, vascular dementia, PRES); Kidney (microalbuminuria, nephrosclerosis, ESRD); Retina (KWB grades I–IV; grade III–IV = emergency); Vessels (aortic aneurysm, PAD).

REFLECT

Consider Ramesh from the opening hook — a 52-year-old with asymptomatic, untreated hypertension who already has cardiac, renal, and retinal target organ damage at the time of first diagnosis. He represents millions of Indians who are silent carriers of organ-damaging hypertension. What structural features of the Indian healthcare system — access barriers, symptom-driven care-seeking, lack of routine screening, cost of medications — could explain this delayed diagnosis? If you were designing a community hypertension detection programme for a semi-urban district in Tamil Nadu, which three interventions would you prioritise, and how would you ensure that those detected actually remain on treatment? These questions bridge the clinical science of hypertension with the public health and social determinants of disease — a perspective the final-year student and future physician must integrate.