Page 263 - Concise Pathology for Exam Preparation ( PDFDrive )

248 SECTION II Diseases of Organ Systems

Hyaline
deposits
in vessel
wall

FIGURE 10.4. Hyaline arteriosclerosis showing thickening of the vessel wall and deposition
of hyaline material (H&E; 1003).

Effects on Blood Vessels (Hypertensive Arteriolosclerosis)
Hypertension affecting blood vessels has three main pathological patterns, namely:
1. Hyaline arteriosclerosis:
This pattern may be:
• Physiological in origin when it occurs as a result of ageing.
• Pathological in origin when it occurs due to hypertension or diabetes mellitus.
Pathogenesis: Chronic haemodynamic stress of hypertension induces leakage of compo-
nents of plasma and deposition of immunoglobulins, complement, fibrin and lipid in the
vessel wall. In diabetes, nonenzymatic glycosylation of the basement membrane of small
vessels makes them permeable to proteins, which leak through into the vessel wall to
produce hyaline change.
Pathology (Fig. 10.4): Vessel walls are thickened and lumina narrowed and eosinophilic
hyaline material is deposited in the intima and media.
2. Hyperplastic arteriolosclerosis:
This is usually a consequence of malignant hypertension or toxaemia of pregnancy.
Pathogenesis: Increase in blood pressure causes endothelial injury which in turn leads
to increased vascular permeability and leakage of plasma components. This is thought
to stimulate smooth muscle proliferation and basement membrane duplication.
Pathology: Vessels typically shows intimal thickening, which may manifest as:
• Onion skinning—Concentric layers of hyperplastic intimal smooth muscle cells
(Fig. 10.5)
• Mucinous intimal thickening—Deposition of anhydrous ground salts
• Fibrous intimal thickening—Laying down of collagen, elastic fibres and hyaline depos-
its in intima.
3. Necrotizing arteriolitis:
This pattern of arteriosclerosis is typically associated with severe-or-malignant
hypertension.
Pathogenesis: Sudden elevation of pressure causes direct physical injury to vessel wall
leading to endothelial damage with fibrin deposition and wall necrosis.
Pathology: Hyaline sclerosis and fibrinoid necrosis of vessel wall, along with an infiltrate
of neutrophils in adventitia.

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