Artherosclerosis

Question 1

4 Features of Artherogenesis

Answer 1

Endothelial dysfunction
Inflammation and foam cell formation
Smooth muscle proliferation
Thrombosis

Question 2

Endothelial Dysfunction

Answer 2

LDL comes into cell, free radicals (endothelium supposed to get rid of) oxidize it into modified LDL which increases production of MCP-1 and other adhesion prots on outside which attract/pull in monocytes, and modified LDL inhibits NO synth so lose vasodilation and NO’s ability to suppress adhesion prots as well

Question 3

Inflammation and Foam Cell Formation

Answer 3

Monos come in, develop into macs which activate cytokines and other IS components. Also express non-downreg’able scavenger Rs which take up lipoprots/cholesterol and swell up to become foam cells

Question 4

3 Mechanisms of HDL Antiatherogenic Activites

Answer 4

Transport chol out of cell
Inhibit OxLDL’s pro-inf actions
Cleave oxidized shit to prevent OxLDL from forming

Question 5

Smooth Muscle Proliferation

Answer 5

Macs and foam cells express GFs that stimulate smooth muscle growth to kinda wall off the area, as well as matrix metalloproteinases which digest matrix/collagen and stuff to allow its growth, but may compromise integrity

Question 6

Angiotensin II

Answer 6

Produced by all vascular tissue, upon the same artherosclerotic stimulating factors released and basically exacerbates everything (ox stress, adhesion molecules, inf stuff, smooth muscle prolif)

Question 7

Fibrinolysis

Answer 7

Plasminogen activators convert plasminogen to plasmin, which degrades fibrin

Question 8

PAI-1

Answer 8

Inhibits plasminogen activators. Is stimulated by ATII so that inhibits fibrinolysis

Question 9

Original Theory vs. Evidence Theory of MI Development

Answer 9

Originally thought plaque just builds up overtime until it cuts off blood flow. Actually eccentric remodeling (one side bulges out) and plaque rupture

Question 10

Stable vs. Vulnerable Plaque

Answer 10

Progressive lipid accumulation, but well controlled by fibrin so its stable and won’t rupture. Maybe cause angina. vs. Very eccentric, not well walled off and tons of inflammatory cells. Might rupture and release coagulation factors, coagulating everything in sight and causing MI

Question 11

Main Determinant of Rupture or Not

Answer 11

Integrity of fibrous cap