Atheroma Flashcards
What is an atheroma?
Accumulation of intra and Extracellular lipid in the tunica media of large and medium sized arteries.
What is atherosclerosis?
Thickening and hardening of the walls of arteries as a result of atheroma.
What is a simple plaque?
This is a raised yellow or white area which has an irregular outline. It is widely distributed.
What properties does a complicated plaque possess?
There is haemorrhage into the plaque, calcification and aneurysm formation.
What are the most common sites for atheroma formation?
Aorta, coronary artery, carotid artery, cerebral artery and leg arteries.
What microscopic changes are seen early in atheroma formation?
There is proliferation of smooth muscle cells, accumulation of foam cells and Extracellular lipid.
Name three microscopic changes which occur later in atheroma formation.
Fibrosis, necrosis and Cholestrol clefts.
What is plaque fissuring?
This is when material within the plaque moves.
What problem can atheroma cause to the heart?
Ischaemic heart disease.
What can be seen on a post mortem of heart tissue which indicates ischaemic heart disease?
There will be areas of white fibrotic tissue.
Name three things that cerebral ischaemia can lead to
Transient ischaemia attack, cerebral infarction and multi-infarct dementia.
What can mesenteric infarction cause?
Malabsorption, ischaemic collitis and intestinal infarction.
What is peripheral vascular disease?
This is when there is problem with the blood supply to the legs.
What is intermittent claudication?
This is when there is pain in the legs and it gets worse on exercise, causing the person to have to stop.
State risk factors of atheroma.
Age, gender, hyperlipidaemia, smoking, alcohol, diabetes, infection, lack of exercise, hypertension, obesity, stress
What is the thrombogenic theory for atheroma formation?
This suggest that repeated thrombi formation in the smooth muscle tissue is where the lipid is derived from.
What is insudation theory of atheroma formation?
When there is endothelial injury, this causes inflammation and increased permeability of the membrane to lipid.
What is the reaction to injury hypothesis for atheroma formation?
This proposes that oxidised LDL causes the initial damage. This injury increases permeability and platelet adhesion occurs. Smooth muscle cells proliferate and migrate.
What is the monoclonal hypothesis for atheroma formation?
This proposes that each plaque is monoclonal and displays abnormal growth control.
Name the cell types involved in atheroma formation.
Endothelial cells, platelets, smooth muscle cells, neutrophils, lymphocytes and macrophages.
How do the smooth muscle cells change during atheroma formation?
They take up lipid and become foam cells.
How do macrophages contribute to atheroma formation?
They take up LDL and become foam cells, and then secrete proteases which cause modification to the matrix and stimulate smooth muscle cell proliferation.
Name four causes of endothelial injury.
Raised LDL, hypertension, toxins and haemodynamic stress.
What happens after endothelial injury in atheroma formation?
Platelet adhesion and smooth muscle cell proliferation and migration. This is followed by insudation of lipid and then uptake into the smooth muscle cells and macrophages.
What preventative strategies can be employed for atheroma formation?
No smoking, treat hypertension, reduce fat and alcohol intake, take regular exercise and control weight.
What interventions are employed with atheroma formation?
Modify diet, stop smoking, treat diabetes, lower lipids and treat hypertension.
