Clinical Pathology · MU Sofia

51. Systemic arterial hypertension: vascular and organ-specific pathomorphological changes.

Covers how blood pressure depends on cardiac output and peripheral resistance, then lists the risks hypertension adds, such as cardiac hypertrophy, aortic dissection, stroke and renal failure. It distinguishes primary from secondary hypertension and describes arterial wall changes in large and small vessels. The note separates hyaline arteriolosclerosis from hyperplastic (onion-skin) arteriolosclerosis, with kidney findings and a memory aid contrasting benign and malignant forms, and ends with criteria for hypertensive heart disease.

Inside: 1 section · 2 labelled pictures · 14 flashcards · 2 min

Topic 51 of 138 in the MU Sofia syllabus for Clinical Pathology (Medicine, Year 4). The free AceMed note covers it in 1 section, about 287 words (2 min of reading), with 14 flashcards.

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  1. Systemic arterial hypertension: vascular and organ-specific pathomorphological changes

Systemic arterial hypertension: vascular and organ-specific pathomorphological changes

Blood pressure is determined by Cardiac Output x Peripheral Resistance (image).

Hypertension is when blood pressure is high (>140/90). Hypertension causes increased risk of:

  • Cardiac hypertrophy and heart failure
  • Aortic dissection
  • Multi-infarct dementia
  • Renal failure
  • Atherosclerosis
  • Stroke

Hypertension is generally considered an issue of both genetic and environmental origins, which increase blood volume and/or peripheral resistance. Hypertension can be primary (essential), 95% of cases, or secondary (due to a renal, endocrine, cardiovascular or neurological disorder).

Not only does hypertension increase atherosclerosis, but it also causes arterial wall changes, which can cause aortic dissection and cerebrovascular hemorrhage.

In small vessels (i.e. in the organs), there are two key changes we should be aware of:

  • Hyalinization
  • Hyperplastic arteriosclerosis

Hyaline arteriolosclerosis is the deposition of hyaline into the small vessels and loss of underlying wall structure with luminal narrowing. One organ in which this is most notable is the kidneys, where nephrosclerosis can occur with diffuse vascular compromise.

Hyperplastic arteriosclerosis causes laminated thickening of the arteriolar wall due to smooth muscle cell hypertrophy and reduplication of the basement membrane (looks like an onion skin), in malignant hypertension these changes are accompanied by fibrinoid deposits and wall necrosis (necrotizing arteriolitis). This is again most common in the kidney.

Remember: hyaline arteriolosclerosis (pink, glassy, thickened wall) is seen in benign hypertension, diabetes and old age, and gives small, finely granular kidneys (benign nephrosclerosis). Onion-skin hyperplastic arteriolosclerosis with fibrinoid necrosis marks malignant hypertension (diastolic pressure above about 120 mmHg) and gives "flea-bitten" kidneys with petechial haemorrhages.

Hypertensive heart disease is a slightly separate topic and worth touching on. Mostly note that it requires two conditions to be met for diagnosis:

  • Left ventricular hypertrophy in absence of other cardiovascular pathology
  • And history of hypertension

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