Session 6: Atherosclerosis Flashcards
Define arteriosclerosis.
Hardening of arteries. Walls of arteries are thickened and lose their elasticity.
Arteriosclerosis includes three diseases. Which?
Atherosclerosis Arteriolosclerosis Monkeberg’s Disease
Define atherosclerosis.
Disease of large and medium sized arteries that begins in the tunica intima. Plaques are formed in the arterial wall and fill with atheroma. It’s the accumulation of intracellular and extracellular lipid in the intima and media of large and medium sized arteries.
Define arteriolosclerosis. Common cause of arteriolosclerosis.
Hardening of arterioles. It has little or no connection with atherosclerosis and usually occurs secondary to severe hypertension or in diabetes mellitus.
Which arterioles in the body does arteriolosclerosis affect in particular?
The kidneys.
What is Monkeberg’s disease?
Uncommon disease where there is calcification of the media of large arteries.
Define atheroma. What does it consist of?
The necrotic core of the atherosclerotic plaque. Consists of dead cells, debris and cholesterol crystals.
What are the three basic components of the atherosclerotic plaque?
Cells like macrophages, leucocytes, smooth muscle cells Intra and extracellular lipid Extracellular matrix like collagen, elastin and proteoglycans.
The formation of the atherosclerotic plaque can be divided five stages. Describe stage 1.
There’s chronic endothelial damage from conditions such as hyperlipidaemia, hypertension, smoking or from haemodynamic factors. This leads to endothelial dysfunction.
Describe stage 2 of atherosclerotic plaque formation.
Lipid droplets mainly from LDLs and monocytes cross endothelium to accumulate in tunica intima. Lipids become oxidised and macrophages ingest the lipid due to the oxidation. This turns the macrophages into foam cells as their cytoplasm now appears bubbly under a microscope.
Describe stage 3 of atherosclerotic plaque formation.
Accumulation of foam cells creates a bulge in the endothelium. Smooth muscle cells migrate into the lesion from the media and start to proliferate. This is now called a fatty streak.
Describe stage 4 of atherosclerotic plaque formation.
Plaque grows due to more accumulation of foam cells and smooth muscle. Some smooth muscle cells will also take up lipid and become foamy. Some smooth muscle cells will lie over the plaque but beneath the endothelium to form a roof over the plaque. The roof that has now formed is then reinforced by collagen, elastin and other matrix proteins to form what is called a fibrous cap. The endothelium stretches over the plaque, this causes gaps to appear between the endothelial cells and platelets will adhere.
Describe stage 5 of atherosclerotic plaque formation.
Cells in the centre of the plaque are walled off and will start to die and necrosis develops. Deads cells release cholesterol and cholesterol crystals appear in the plaque. Small blood vessels can grow into the plaque from the adventitia and the plaque may undergo calcification.
Describe the morphological appearance of atherosclerosis.
(Microscopically)
Earliest lesions are called fatty streak. Flat and cause no disturbance in blood flow.
They consist of foam cells + smooth muscle cells and some extracellular lipid so this is what you would find under the microscope.
As it grows the fatty streak will become a plaque with a yellow to white appearance. Under the microscope you would see fibrosis, necrosis, cholesterol clefts, disruption of the internal elastic lamina, extension into the media and ingrowth of small vessels from the adventitia.
What are cholesterol clefts?
The remains of what’s left when cholesterol crystals are removed during tissue processing. They appear as linear holes.
Where does atherosclerosis usually occur?
In elastic arteries like the aorta, carotid and iliac arteries. Other large and medium sized arteries like coronary, popliteal and abdominal artery.
Give common complications of plaques.
(8 in total)
Explain them briefly.
Ulceration - core of plaque is exposed. The core can be thrombogenic
Thrombosis on plaque
Spasm at site of plaque - vasooconstrictors releaed from thrombi
Embolisation - pieces of exposed atheroma or overlying thrombus
Calcification - in and around the plaque which makes the artery stiffer
Haemorrhage - New vessels can form in the plaque. They can rupture.
Aneurysm formation - Local dilatation can result due to elastic tissue being destroyed by plaque.
Rupture of the atherosclerotic artery - weakened media and aneurysm causing rupture of the vessel
Explain aneurysm.
What is this condition called in veins?
How can aneurysms be shaped?
Local dilatation of the artery because of loss of elastic fibres.
Varices.
As saccular aneurysm shaped like a sac.
As fusiform aneurysm shaped like a spindle.
Where do saccular aneurysms most commonly occur?
In abdomina aorta. Filled or lined by thrombus.
What are the two major complications of an aortic aneurysm?
They may rupture.
Thrombus or plaque material within them may embolise.
Explain dissecting aneurysms.
Usually occur in aorta and major branches of the aorta.
The inner layer of the arterial wall tears open and blood enters that tear which separates the media into two layers. As the tear fills with blood the lumen of the artery can be occluded.
Where do symptoms most commonly occur in atherosclerosis?
In heart, brain, kidneys, legs or bowel.
What kind of conditions are common following atherosclerosis?
Heart - MI, chronic ischaemic heart disease, sudden cardiac failure, cardiac failure
Brain - Trans ischaemic attacks, cerebral infarctions, multi-infarct dementia
Kidneys - hypertension and renal failure
Legs - Peripheral vascular disease and gangrene
Bowel - ischaemic colitis, malabsorption, bowel infarction
What are the theories of atherogenesis.
Response to injury hypothesis
Encrustation hypothesis
Monoclonal hypothesis
