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Flashcards in Coronary Artery Disease Deck (26):
1

The body's main lipids

cholesterol, triglycerides and phospholipids

2

Sources of Cholesterol

Dietary, from animal fats
Biosynthesis (primarily by liver) --> this is inhibited by LDL uptake by the liver

3

Metabolism Cholesterol

converted to bile acids in the liver

4

Very low-density lipoprotein (VLDL)

10 - 15% of total cholesterol
essentially your triglycerides
precursor of LDL
Very sensitive to diet

5

Low-density lipoprotein (LDL)

60 - 70% of total cholesterol
major artherogenic lipoprotein
ingestion of cholesterol and saturated fatty acids associated with dec LDL receptor activity, inc LDL production and inc LDL plasma concentrations (all BAD!!)

6

High-density lipoprotein (HDL)

20 - 30% of total cholesterol
levels inversely related to CHD risk
levels tend to be higher in women, and pts on estrogen
dec the amount of cholesterol by taking it from tissues to liver

7

Triglycerides

combo of glycerol and 3 fatty acid chains
make up most of the fat in diet
levels are very sensitive to diet (VLDL)

8

Coronary Atherosclerosis (definition)

development of lipid-rich fibrous plaques in the coronary arteries

9

Coronary Heart Disease (definition)

a.k.a. coronary artery disease (CAD)
atherosclerotic narrowing of at least 1 major coronary artery

10

Ischemic Heart Disease (definition)

imbalance between myocardial oxygen demand and oxygen supply

11

Atherosclerosis Timeline

As we age the build up of atherosclerotic tissue in the vessels inevitably grows

12

Normal Artery Wall

contains inactivated endothelial cells surrounded by smooth muscle cells

13

Early Atherosclerosis

activated endothelial cells recruit inflammatory cells, mostly monocytes
smooth muscle cells then migrate over the lipid build up in order to form a fibrous cap these are of the repair phenotype and do not contract

14

Stable Plaque

after the smooth muscle cells migrate they from a matrix, become fibrous and stay put

15

Unstable Plaque

the smooth muscle cells begin dying due to macrophages being activated, this leads to degradation of the matrix and a poor fibrous cap

16

Rupture/erosion of Plaque

Platelets will aggregate at the site of rupture or erosion and attempt to seal the hole, this narrows and sometimes blocks blood flow in the artery

17

Thrombus formation

1. endothelial damage
2. inflammation
3. Platelet activity
4. clotting cascade activation
5. HUGE thrombus forms

18

consequence thrombus formation

impedes blood flow even more, new smooth muscle cells will cover this as well, leads to further blockage

19

Vulnerable vs. Stable Plaques

1. V take up less space, but have a thinner fibrous cap which is more likely to rupture
2. S take up more space but have a very thick fibrous cap which is very unlikely to rupture

20

Pathogenesis

both stable and unstable plaques will eventually lead to myocardial ischemia if left untreated, stable plaques just take a longer time.

21

Chronic Stable Angina

reduction blood flow and O2 supply due to plaques
symptoms: chest pain, pressure, tight, pain in chest, arm and jaw, shortness of breath

22

Coronary Artery Disease

Unstable angina, acute myocardial infarction

23

Unstable Angina

thrombus partiall occludes artery, body halts thrombus progression, myocardial necrosis does NOT occur

24

Acute MI (NSTEMI)

necrosis of myocardium
thrombus partially occludes vessel
ST elevation, ST depression or T wave inversion on EKG

25

Acute MI (STEMI)

necrosis myocardium
thrombus completely occludes vessel, abrupt cessation of blood flow
worst case scenario!!

26

Complications Acute MI

death
heart failure
cardiogenic shock
arrhythmias
ventricular rupture
papillary muscle rupture
mural thrombus
ventricular aneurysm