Lecture 31 Flashcards
Which type of vessels are most vulnerable to compression, occlusion, neoplastic invasion, and bystander injury by extension of inflammation from adjacent tissues?(2)
veins and lymphatics
How is the inner half of the wall of a blood vessel supplied with O2 and nutrients
-outer half?
the inner part is avascular and relies on diffusion from the vessel lumen
-vasa vasorum
how do VSM cells respond to sustained inc in blood vol or pressure?
by undergoing hypertrophy and (lesser) hyperplasia
Myointimal cells
smooth myocytes stimulated by growth factors they migrate through pores in the internal elastic lamina into the subendothelial layer (will synthesize and deposit collagen and elastin fibers here)
what causes hypertrophy of SMC of arterioles? Possible consequences?
response to sustained hypertension or hyperperfusion
could dec vessel lumen and inc vascular resistance
When does sustained arteriolar vasoconstriction occur? Consequences?
systemic hypertension->vasoconstriction->exacerbation of hypertension->downstream ischemic tissue injury(ex frostbite)
Arteriosclerosis
hardening of the arteries-chronic degenerative disease, loss of elasticity
Atherosclerosis
arteriosclerosis in which there is significant lipid deposition and fatty degeneration of vessel wall
what does arteriosclerosis look like grossly
lesions may or may not be grossly obvious
slightly raised, thickened wrinkled intima or flat white oval or linear plaques
Clinical significance of arteriosclerosis
rarely of clinical significance
advanced lesions predispose to thrombosis
characteristic lesions of athersclerosis
atheroma (fibrofatty plaque)- focal raised intima of plaque with lipid core covered by fibrous cap
circumstances atherosclerosis likely to develop? (species) clinical significance?
rabbits, chickens, and pigs
pigs are common- high fat diets (do not cause thrombosis in pigs)
clinically significant atherosclerosis is rare
arteriolosclerosis
non fatty degeneration of arterioles of small to medium size
Hyaline degeneration
spectrum of arteriolosclerotic lesions involving depsotion of collagen, elastin, glycosaminoglycans or amyloid in the tunica intima
Fibrinoid change
extracellular degenerative change in damaged small arteries and arterioles (injury to vascular endothelium)