Atherosclerosis Flashcards
What is arteriosclerosis and artherosclerosis?
Arteriosclerosis: hardening and thickening of arterial wall (losing elasticity) where the artery wall lumen becomes smaller
Artherosclerosis: an inflammatory type of arteriosclerosis where there is a build up of cholesterol plaques in arteries which narrows the lumen.
Which arteries are most commonly affected by atherosclerosis?
Common in high pressure systemic arteries, never found in low pressure systems such as pulmonary arteries.
- Abdominal aorta
- Coronary artery
- Popliteal artery
- Carotid artery
At what age does atherosclerosis rapidly develop?
from about 50/55 years old, the development of athersclerosis progresses rapidly
What are the risk factors for atherosclerosis? Which is the major risk factor?
AGE is the best known risk factor for CAD/atherosclerosis.
Others:
- cigarette smoking
- HTN
- Obesity
- DM
- High serum cholesterol
- Concentrated in areas with social deprivation
- Family history of first degree relative
- African-American descent.
Explain the structure of an atherosclerotic plaque
Complex lesion consisting of:
- Lipids
- Necrotic core
- Connective tissue
- Fibrous cap
Explain the process of atherogenesis / atherothrombosis
- Inflammatory response to endothelial cell injury (stress in HTN in arterial bifurcation, smoking, increased cholesterol, bacterial or viral infections) leads to endothelial dysfunction
- LDL particles leak and get oxidised
- Oxidised LDLs become pro-inflammatory antigens which induce immune response by macrophages to fight the antigen
- Leukocytes adhere to the endothelial wall, roll and migrate - Macrophages enter the arterial walls and engulf the LDL particles = foam cells
- Build up of foam cells in the arterial wall = fatty streak and fibrous cap formation
- Fatty streaks are not raised so they do not occlude the lumen or produce clinical symptoms such as angina
- Damage to the endothelial wall causes platelets and endothelial cells to release platelet derived growth factor (PDGF), TGF-B and fibroblast growth factor (FGF)
- These factors stimulate smooth muscle cell proliferation and migration from the tunica media to the tunica intima
- (formation of intermediate lesions)
- Smooth muscle cells proliferate and stimulate the production of ECM over the fibrin cap = plaque formation with a lipid core.
- The lipid core is made of cholesterols
- The plaques formed can begin to occlude the lumen of the artery
- Overtime, foam cells undergo necrosis and release matrix metaloproteinases (MMP’s) which destroy the fibrous cap → atheroma now exposed
- Platelets now react and form a fibrin clot at the site of rupture
- This can also occlude the lumen further or occlude other arteries in the brain.
- Symptoms may start at about 40% occlusion - problems exercising or chest pain.
- By age 50 or 60, they will start having serious symptoms, heart attack if it is around the heart or angina with about 20% of lumen left (NSTEMI or STEMI)
- Full occlusion will cause myocardial infarction
What treatment can we give for atherosclerosis?
- Prescribe low dose aspirin
- Ticagrelor or clopidogrel
- Statins
- Colchicine (new antiinflammatoru drug lowers ischaemic risk in patients with recent MI)
- PCI - more than 90% of patients require stent implantation.
What are stents made of?
What drugs are put on stents?
Stainless steal coated in polymers
Taxus brevifolia - immunosuppressive
Sirolimus - stops proliferation of cells onto the stent
What are complications of atherosclerosis?
- Ischaemia (at 70% occlusion)
- Angina if coronary arteries affectes
- Chronic mesenteric ischaemia if mesenteric artery affected
- Claudification if peripheral vascular disease
- Clot formation
- In head = stroke
- In heart - MI - Atheroma can weaken artery wall and cause aortic aneurysm where rupture can cause sudden death or haemorrhage
- Cholesterol emboli where cholesterol plaque is dislodged
Which of the following are not found in artery walls?
- tunica intima
- tunica media
- epithelial cells
- neutrophils
Epithelial cells
