Pathophysiology · MU Plovdiv

37. Arterial hypertensions – essential hypertension. Etiology, pathogenesis. Secondary (symptomatic) hypertensions.

Inside: 23 sections · 7 labelled pictures · 9 tables · 29 flashcards · 19 min

Topic 37 of 63 in the MU Plovdiv syllabus for Pathophysiology (Medicine, Year 3). The free AceMed note covers it in 22 sections, about 2,063 words (19 min of reading), with 29 flashcards.

In this note

  1. Definition and epidemiology
  2. Aetiology and pathogenesis
  3. Classification
  4. Measurement and diagnosis
  5. Clinical features
  6. Hypertension-mediated organ damage (HMOD)
  7. Complications
  8. Hypertensive crises: urgency and emergency
  9. Prognosis
  10. Arterial Hypertension
  11. Definition
  12. Blood Pressure Categories
  13. Primary Hypertension
  14. Pathophysiology
  15. Symptoms of Hypertension
  16. Physical Examination Findings
  17. Secondary Hypertension
  18. Types of Secondary Hypertension
  19. Hypertensive Crisis
  20. Symptoms
  21. Laboratory Tests
  22. Instrumental Tests

Definition and epidemiology

  • Arterial hypertension: a persistent rise in blood pressure (BP) to a level at which lowering it clearly reduces cardiovascular risk. ESC 2024: office BP ≥ 140/90 mmHg (systolic and/or diastolic), confirmed by out-of-office readings or by repeated office visits.
  • ESC 2024 adds the category elevated BP (office 120–139/70–89 mmHg): not yet hypertension, but treated with lifestyle measures and, if the cardiovascular risk is high, with drugs.
  • About 1.3 billion adults worldwide (30–45% of adults, over 60% after 60 years); the leading modifiable risk factor for death. Only about one patient in five is controlled.
  • Risk rises continuously from about 115/75 mmHg: each extra 20 mmHg systolic (or 10 mmHg diastolic) roughly doubles the risk of death from stroke and coronary disease. After 50, systolic BP predicts risk better than diastolic.

Aetiology and pathogenesis

BP = cardiac output × total peripheral resistance; hypertension results when either rises without a matching fall in the other.

Primary (essential) hypertension — about 90%

  • No single cause: a polygenic background interacting with the environment.
  • Risk factors: age, family history, high salt intake (> 5 g of salt a day), obesity and the metabolic syndrome, inactivity, alcohol, low potassium intake, chronic stress, Black African or Caribbean ancestry.
  • Mechanisms: impaired renal sodium excretion (a higher pressure is needed to excrete the same salt load), sympathetic overactivity, renin–angiotensin–aldosterone system (RAAS) activation, endothelial dysfunction (less nitric oxide, more endothelin), insulin resistance, small-artery remodelling.
  • Young patients often have a high cardiac output and heart rate; in older patients stiffening of the large arteries raises systolic and lowers diastolic BP → isolated systolic hypertension, the commonest form after 60.

Secondary hypertension — about 10% (5–15%)

An identifiable and sometimes curable cause. Primary aldosteronism is the most common endocrine cause (5–10% of all hypertensives, up to 20% of resistant hypertension); renal disease and obstructive sleep apnoea are also common.

When to look for a secondary cause

  • Onset before 40 years (especially grade 2–3); any hypertension in childhood.
  • Resistant hypertension; sudden onset or worsening of previously controlled BP.
  • Grade 3 hypertension, a hypertensive emergency, or organ damage out of proportion to the BP history.
  • Clues: spontaneous or diuretic-induced hypokalaemia, adrenal incidentaloma, paroxysms, kidney disease, symptoms of sleep apnoea.
  • ESC 2024 advises considering screening for primary aldosteronism (aldosterone and renin) in all adults with confirmed hypertension. Beta-blockers lower renin (false-positive ratio); diuretics, ACE inhibitors, ARBs and mineralocorticoid receptor antagonists raise it (false-negative). Correct hypokalaemia first.

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