Vascular Flashcards
Describe arteriosclerosis
Thickening of arterial walls due to plaque formation
Two main cholesterol
- LDL = bad cholesterol, pro- atherogenic
- HDL = good cholesterol, anti-atherogenic
pathophysiology of atherosclerosis
LDL’s in blood stream + damaged endothelium = macrophages releases chemicals = causing oxidation of LDL’s and engulf oxidized LDL’s = macrophages releasing more inflammatory chemicals = repeats cycle
= Once engulf enough oxidized LDL’s = macrophages become foam cells = multiple foam cells form a fatty streak in blood vessel wall = smooth muscle cell proliferate and migrate to fatty streak = produce collagen = forms plaque
pathophysiology of peripheral artery disease
- Atherosclerosis within peripheral arteries
- Arterial narrowing/blockage = ischemia and possible tissue infarction (death) = pain, ulceration(tissue loss) , gangrene (infected dead tissue)
S+S of peripheral artery disease
- skin changes
- ulcers
-decrease pulse - pain
pathophysiology of deep vein thrombosis
Thrombus abnormally formed = localised inflammation = may resolve OR 3 ways causes of DVT
Endothelial damage (possibly due to smoking, surgery)
Blood stasis= decrease blood flow/increase blood pooling (e.g. immobility, damaged valves, dehydration)
Hypercoagulation = increase clotting activity (e.g. pregnancy, coagulopathies)
Risk factor of DVT
after localised formation-
may become organised = infiltrate blood vessel wall = may become dislodged
pathophysiology of pulmonary embolism,
Due to blood clot embolism (DVT that becomes dislodged)
Embolus eventually blocks pulmonary artery/arterials due to being too big
Small embolism S+S
Cough
Pain
SOB
Increase RR
Increase HR
Large s+S
hemodynamic compromise
Shock, respiratory or cardiac failure