Bio 252- atherosclerosis Flashcards
Hyperlipidemia
excessive lipid concentration in blood
all Lipids?
triglycerides, cholesterol, phospholipids
Non modifiable risk factors for coronary heart diease
- men over 45
- postmenopausal women
- family history of cardiovascular disease
- men under 55
- women under 65
Modifiable risk factors for coronary heart disease
- hypertension
- smoking
- dyslipidemia
- Low LDL
- elevated LDL
- diabetes mellitus
- obesity
- left ventricular hypertrophy
Apoprotiens are?
Lipid carriers (transport lipids)
Hyperlipdemia in what percent of canadians?
40%
lipid + apoprotien=
lipoprotien
Proteins are more ____ than liquids
dense
lipoprotiens are differentiated from each other via
individual density
lipids are
insoluble
Lipoprotiens vary in density
VLDL, LDL, HDL
lowest to highest density
Chylomicrons lowest density lower than VLDL
Chylomicrons
Lipid (fat) absorbed into blood (or lymph) through small intestine
sclerosis=
hardening
layers of artery & vein
lumen, tunica intima, tunica media, tunica externa
Athersclerosis
(lesion that develops in wall of artery)
- hardening of blood vessel wall
- fibrofatty (Fibers & lipids) lesion (atheroma) in intima of larger arteries
what does asthersclerosis cause
-impedes blood flow–impedes perfusion –ischemia–MI/stroke/PVD
32% of all deaths are complications of
MI/stroke/PVD from atherosclerosis
ischemia
restriction/reduction of blood supply/ inadequate perfustion to a local area d/t obstruction in a blood vessel
Infarction
necrosis of tissue d/t ischemia
3 lesions/ 3 stages of atherosclerosis
- Fatty streak: -change within intima
-macrophages -foam cells (as soon as macrophages engulf lipids become foam cells)
-smooth muscle cells - Fiborous atheromatous plaque: -clinically significant lesion w necrotic core
-swelling lesion made of fibrous tissue - Complicated lesion: -unstable
-hemmorhage into plaque, bllod form lumen moving into plaque
-risk of part of plaque dislodging
-
pathogenesis of atherosclerosis
- primarily occurs in intima of artery, THEN swells into lumen(area of least resistance) –compromises lumen
- insidious origin: subltle endothelial injury from risk factors cause inflm(CRP will be elevated d/t inflm)
- monocytes & other inflm cells bind to endothelium :adhesion factors aid ( selectins & integrins)
- lipids enter intima (free floating shouldnt be there)
- monocytes enter intima, become macrophages: engluf lipids, become foam cells
- relase free radicals via oxidization of lipids(causes additional damage)
- release growth factors which aid in proliferation of smooth muscle cells in layer below intima (tunica media)
- atheroma continues to swell into lumen
- creates a necrotic core(full of dead lipids ect)
- hemorrhaging into plaque may cause embolus (unstable)
Sites where severe atherosclerosis appears frequently
- Abdominal aorta & iliac arteries
- proximal coronary arteries
- Thoracic aorta, femoral & popliteal arteries
- Internal carotid arteries
- vertebral , basilar & middle cerebral arteries
what lipid do you want in minimal quantities
LDL, lousy lipid, cholesterol