L9 - Atheroma, thrombosis and embolism Flashcards
what is an atheroma?
Intimal lesion that protrudes into the vessel wall
- raised lesion
- soft core of lipid
- fibrous cap
what cells would you find in the fibrous cap of an atheroma?
- SMC
- macrophages
- foam cells
- lymphocytes
- collagen and elastin
- proteoglycans
- neovascular
what cells would you find in the necrotic centre of an atheroma?
- cell debris
- cholesterol crystals
- foam cells
- calcium,
which vessels are commonly affected by atheroma?
bifications (sites of tubulent flow)
- abdominal aorta
- coronary arteries
- popliteal arteries
- carotid vessels
- circle of willis
which is the most common site of atheroma?
abdominal aorta
what are some non-modifiable risk factors for atheroma?
- increasing age
- male gender
- family history
- genetic abnormalities
are women more or less likely to get atheroma than men?
less likely up until menopause
- then after menopause the risk is equal between men and women
what are some modifiable risk factors for atheroma/atherosclerosis?
- hyperlipidemia
- hypertension
- smoking
- diabetes
- CRP
why is the CRP protein a risk factor in atherosclerosis?
- usually seen in inflammatory conditions
- can cause damamge to vessel walls = atherogenesis
what is atherogenesis?
the formation of fatty deposits in the arteries.
what is atherosclerosis caused by?
- high blood pressure
- high cholesterol
- an irritant, such as nicotine (can release free radicals)
- disease such as diabetes
what is atherosclerosis?
Atherosclerosis is a disease in which plaque builds up inside your arteries.
what is atheroma?
Intimal lesion that protrudes into the vessel wall
why does atherosclerosis develop?
due to chronic inflammatory response of the. arterial wall to endothelial injury
what are the steps of response-to-injury hypothesis?
- Chronic endothelial injury
- Accumulation of lipoproteins
- Monocyte adhesion to the endothelium
- SMC proliferations and ECM production
- factor release
- platelet adhesion
in the response-to-injury hypothesis, what occurs due to chronic endothelial injury?
- increased permeability
- leukocyte adhesion
- thrombosis
in the response-to-injury hypothesis, what occurs due to the accumulation of lipoproteins?
Low-density lipoprotein molecules (LDL) becoming oxidized (LDL-ox) by free
radicals, particularly oxygen free (ROS).
- When oxidized LDL comes in contact with an artery wall, a series of reactions occur
to repair the damage to the artery wall caused by oxidized LDL. - cholesterol can move in the bloodstream, transported by lipoproteins
in the response-to-injury hypothesis, what occurs due to factor release?
Induces SMC recruitment
NB: factors released from activated platelet, macrophages and vascular wall cells
in the response-to-injury hypothesis, what occurs due to SMC proliferations and ECM production?
- artery becomes inflamed
- cholesterol plaque covers affected area causing:
narrowing of artery
what happens as a result of a narrowed artery?
reduced blood flow
increases blood pressure
in the response-to-injury hypothesis, what occurs due to lipid accumulation?
gives rise to fatty streaks
evolves into a fibre fatty atheroma
what is a a fibrofatty atheroma
contains proliferated SMC and has a ECM formed
what is a fatty streak?
The earliest lesion in atherosclerosis
what is a fatty streak composed of?
lipid filled foamy macrophages
