Atherosclerosis Flashcards
What builds up in atherosclerosis?
Lipids (fats), cholesterol, calcium and cellular debris.
What are the layers of the artery?
Intima: Smooth endothelium, inner lining.
Media: Middle layer with smooth muscle, providing elasticy.
Externa: Connective tissues and blood vessels.
Put these in order…
Plaque progression and Calcification, lipid accumulation and foam cell formation, plaque development, endothelium injury and plaque rupture and thrombosis.
- Endothelium Injury
- Lipid accumulation and foam cell
- Plaque development
4.plaque progression and calcification
5.plaque rupture and thrombosis
What can cause endothelium damage?
Hypotension (mechanical stress), hyperlipidemia (high bad cholesterol ldl), smoking (toxins damage cells), diabetes (high glucose damages endothelium), chronic inflammation (obesity or autoimmune disease).
What does LDL stand for?
Low density lipo protein.
How does cholesterol (LDL) infiltrate the arterial Wall?
Through damaged endothelium, cholesterol then becomes oxidised causing an inflammatory response.
What is the role of monocytes in atherosclerosis?
They migrate into the arterial wall, transform into macrophages and engulf cholesterol cells.
How do foam cells form?
Lipid laden macrophages die and form foam cells, these then build up into a fatty streak.
Plaque development, stage 1.
Over time (normally many years) foam cells accumulate and smooth muscle cells migrate from the media to the intima.
Plaque development, 2.
These smooth muscle cells proliferate and excrete extracellular matrix proteins, leading to plaque growth.
Plaque development, 3.
A fibrous cap forms over the plaque, consisting of smooth muscle cells and collagen, which stabilises the plaque.
Plaque development, 4.
The core of the plaque contains lipids, dead cells, and inflammatory debris.
What happens when plaque enlarges?
Narrows the artery, restricting blood flow.
What causes arteries to become rigid and loose there elasticness?
Calcium deposits within the plaque.
What happens when the fibrous cap on plaque ruptures?
This triggers platelet aggregation and thrombus formation.
A thrombus can partially or completely block blood flow, which can lead to what?
Myocardial infarction, ischaemia stroke, and pulmonary embolism.
What are the non-modifiable risk factors?
Age, gender (men are higher risk and postmenstrual women), family history (genetic predisposition).
What ate the modifiable risk factors?
Dyslipidemia, hypertension, smoking, diabetes, obesity, sedentary lifestyle and poor diet.
What are the symptoms when coronary arteries are blocked?
Angina, chest pain and MI when fully blocked.
Cartoid artery symptoms?
TIA and ischaemia stroke if a clot blocks a cerebral artery.
Renal arteries symptoms?
Hypertension due to reduced blood flow to the kidneys and kidney dysfunction leading to renal failure.
What lifestyles changes can be made for the better?
Diet, exercise, stop smoking, and weight management.
What medication can be taken?
Statins to lower cholesterol, antiplatelets reduce clot formation, antihypertensives to control BP, and diabetes management (tight glycemic control).
What interventions can be done?
Angioplasty and stents.
Coronary artery bypass grafting (CABG).
