Chronic hemodynamic stress leads to plasma protein leakage across endothelium and smooth muscle cells, resulting in which arteriolosclerosis?

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Multiple Choice

Chronic hemodynamic stress leads to plasma protein leakage across endothelium and smooth muscle cells, resulting in which arteriolosclerosis?

Explanation:
Chronic hemodynamic stress injures small vessel walls, causing endothelial damage and increased permeability. Plasma proteins leak into the arteriolar wall and, with smooth muscle cell–driven matrix synthesis, create a homogeneous, eosinophilic (hyaline) thickening of the vessel wall. This results in luminal narrowing typical of hyaline arteriolosclerosis. It’s the pattern you see with long-standing hypertension and also with diabetes mellitus, where protein leakage and extracellular matrix deposition produce the characteristic smooth, pink hyaline on histology. By contrast, malignant hypertension would cause hyperplastic arteriolosclerosis with onion-skinning from smooth muscle proliferation; atherosclerosis involves lipid plaques in larger arteries; Monckeberg medial sclerosis is calcification of the media with less luminal impact.

Chronic hemodynamic stress injures small vessel walls, causing endothelial damage and increased permeability. Plasma proteins leak into the arteriolar wall and, with smooth muscle cell–driven matrix synthesis, create a homogeneous, eosinophilic (hyaline) thickening of the vessel wall. This results in luminal narrowing typical of hyaline arteriolosclerosis. It’s the pattern you see with long-standing hypertension and also with diabetes mellitus, where protein leakage and extracellular matrix deposition produce the characteristic smooth, pink hyaline on histology. By contrast, malignant hypertension would cause hyperplastic arteriolosclerosis with onion-skinning from smooth muscle proliferation; atherosclerosis involves lipid plaques in larger arteries; Monckeberg medial sclerosis is calcification of the media with less luminal impact.

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