Arteriosclerosis is the hardening and thickening of arteries. It affects both small arteries and arterioles. There are two main types - hyaline arteriolosclerosis and hyperplastic arteriolosclerosis. Hyaline arteriolosclerosis involves homogeneous thickening of arterioles and narrowing of the lumen. It is more common and severe in hypertension and diabetes. Hyperplastic arteriolosclerosis occurs in severe hypertension and shows concentric, layered thickening of arterial walls. Mönckeberg medial sclerosis involves calcific deposits in muscular arteries centered on the internal elastic lamina, typically in individuals over 50.
Arteriosclerosis is the hardening and thickening of arteries. It affects both small arteries and arterioles. There are two main types - hyaline arteriolosclerosis and hyperplastic arteriolosclerosis. Hyaline arteriolosclerosis involves homogeneous thickening of arterioles and narrowing of the lumen. It is more common and severe in hypertension and diabetes. Hyperplastic arteriolosclerosis occurs in severe hypertension and shows concentric, layered thickening of arterial walls. Mönckeberg medial sclerosis involves calcific deposits in muscular arteries centered on the internal elastic lamina, typically in individuals over 50.
Arteriosclerosis is the hardening and thickening of arteries. It affects both small arteries and arterioles. There are two main types - hyaline arteriolosclerosis and hyperplastic arteriolosclerosis. Hyaline arteriolosclerosis involves homogeneous thickening of arterioles and narrowing of the lumen. It is more common and severe in hypertension and diabetes. Hyperplastic arteriolosclerosis occurs in severe hypertension and shows concentric, layered thickening of arterial walls. Mönckeberg medial sclerosis involves calcific deposits in muscular arteries centered on the internal elastic lamina, typically in individuals over 50.
• hardening of the arteries • arterial wall thickening and loss of elasticity. Arteriolosclerosis affects small arteries and arterioles may cause down stream ischemic injury. E.g hyaline and hyperplastic arteriolosclerosis Hyaline arteriolosclerosis • Arterioles show homogeneous, pink hyaline thickening with associated luminal narrowing • . These changes reflect both plasma protein leakage across injured endothelial cells, • as well as increased smooth muscle cell matrix synthesis in response to the chronic hemodynamic stresses of hypertension. • Although the vessels of older patients (either normotensive or hypertensive) also frequently exhibit hyaline arteriosclerosis, it is more generalized and severe in patients with hypertension. The same lesions are also a common feature of diabetic microangiography; in that case, the underlying etiology is hyperglycemia-induced endothelial cell dysfunction (Chapter 24). In nephrosclerosis due to chronic hypertension, the arteriolar narrowing of hyaline arteriosclerosis causes diffuse impairment of renal blood supply and glomerular scarring (Chapter 20). Hyperplastic Arteriolosclerosis. This lesion occurs in severe hypertension; vessels exhibit concentric, laminated (“onion-skin”) thickening of the walls with luminal narrowing (Fig. 11-6B). The laminations consist of smooth muscle cells with thickened, reduplicated basement membrane; in malignant hypertension, they are accompanied by fibrinoid deposits and vessel wall necrosis (necrotizing arteriolitis), particularly in the kidney . Mönckeberg medial sclerosis is characterized by – the presence of calcific deposits in muscular arteries usually centered on the internal elastic lamina – typically in individuals older than 50 years of age. – The lesions do not encroach on the vessel lumen and usually are not clinically significant. • Fibromuscular intimal hyperplasia is – a non-atherosclerotic process – occurs in muscular arteries larger than