Pathophysiology · MU Sofia

110. Hemodynamic damage from arterial hypertension. Clinical course.

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Topic 110 of 168 in the MU Sofia syllabus for Pathophysiology (Medicine, Year 3). The free AceMed note covers it in 1 section, about 259 words (2 min of reading), with 15 flashcards.

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  1. Hemodynamic damage from arterial hypertension. Clinical course.

Hemodynamic damage from arterial hypertension. Clinical course.

Arterial hypertension exerts chronic increased pressure load on arteries and target organs, leading to structural and functional changes called hypertensive (hemodynamic) damage.

Target organs and types of damage

  1. 1 Heart

Left ventricular hypertrophy (LVH)

Due to increased afterload (pressure overload).

Concentric hypertrophy → reduced compliance → diastolic dysfunction.

Can progress to heart failure (especially HF with preserved ejection fraction).

Coronary artery disease

Accelerated atherosclerosis → increased risk of myocardial infarction.

Arrhythmias

Due to LV remodeling and atrial dilation.

  1. 2 Blood vessels

Large arteries

Accelerated atherosclerosis → increased risk of aneurysms, dissections.

Small arteries and arterioles

Hyaline arteriolosclerosis (in benign hypertension).

Hyperplastic arteriolosclerosis ("onion-skin" changes, in severe or malignant hypertension).

  1. 3 Brain

Stroke (ischemic and hemorrhagic ).

Transient ischemic attacks (TIAs).

Hypertensive encephalopathy.

  1. 4 Kidneys

Nephrosclerosis → progressive chronic kidney disease.

Proteinuria.

Renal failure in advanced cases.

  1. 5 Eyes (retina)

Hypertensive retinopathy:

  • Arteriolar narrowing.
  • AV nicking.
  • Cotton-wool spots, hemorrhages.
  • Papilledema (in malignant hypertension).

Pathogenesis (mechanisms)

  1. Increased shear stress on vessel walls → endothelial dysfunction → smooth muscle proliferation and extracellular matrix deposition.
  2. Arteriolosclerosis reduces lumen diameter → ischemia of downstream tissues.
  3. Left ventricular overload due to increased systemic resistance → compensatory hypertrophy.
  4. Atherosclerosis acceleration due to vessel wall damage and lipid infiltration.

Clinical course

Benign (chronic) hypertension

Slowly progressive.

Target organ damage develops over years (e.g., LVH, nephrosclerosis).

Often asymptomatic initially ("silent killer").

Malignant (accelerated) hypertension

Rapid BP rise (>180/ 120 mmHg).

Severe vascular injury (fibrinoid necrosis, hyperplastic arteriolosclerosis).

Acute end- organ damage:

  • Encephalopathy.
  • Acute renal failure.
  • Retinal hemorrhages and papilledema.

Medical emergency — requires urgent treatmen t

Summary table

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