Atherosclerosis Flashcards
What is atherosclerosis
The accumulation of intracellular and extracellular lipids in the intima of the medium and the large size artery’s
What are the stages that would form the atherosclerotic plaque
Damage to the endothelium
Platelet aggregation (Activation of the platelet derived growth factor)
Migration of the monocytes to the intima
Migration of the lipids
Macrophages and smooth muscle cells move from media
Fats engulfed by the smooth muscle cells and macrophages
What type of macrophages would be present
Foamy macrophages
(smooth muscle cells become when they engulf the lipids)
What areas of the blood vessels would be involved
Tunica intima
Tunica media
Where would the cells migrate from
The tunica media
What cells would be involved
Macrophages
Endothelial cells
Lymphocytes
Neutrophils
Smooth muscle cells
What is the fibrous cap
Layer of fibrous collagen
Would stabilise the plaque
What is he necrotic centre? Why would it be necrotic?
Necrotic as would have limited blood flow
Within: cholesterol crystals, calcium, cell debris, foam cells
What is a monkenbergs disease
Calcification of the medium artery’s
What is a vulnerable plaque
Whe would have a thin fibrous cap
The wall is easily ruptured
Lesion likely to move to the blood stream
What is a stable plaque
When would have a thick fibrous cap, so there would be a small chance of rupture
What are the most important causes of the endothelial dysfunction leading to atherosclerosis
Inflammation
Hypercholestrolemia
Hemodynamic disturbances (hypertension)
What is a complicated plaque
Late stage Plaques that would cause:
Aneurysms
Thrombosis
Haemorrhage
Calcification (due to necrosis leading to monkebergs disease)
What is a simple plaque
An early stage plaque:
Raised white and yellow
Enlarged and merged vessel
Widely distributed
Irregular outline
What are the clinical presentations
Progressive narrowing leading to stenosis
Acute atherosclerotic occlusion
Ruptured abdominal aneurysm
What can blockage of the abdominal aorta cause
Abdominal aneurysm
Haemorrhage of the abdominal organs (for example the intestines)
What is peripheral vascular disease? what can it cause?
What: the build of the fatty deposits in the arteries, leading to the blockage of the blood vessel and so blood supply to lower limbs
Cause: the decreased blood flow to the lower limbs, gangrene (dry-coagulative)
What is an aneurysm
Weak spots in the vessels would cause them to balloon and then rupture
If in the aorta, death
What can familiar hyperlipidemia cause
Tendon Xanthomas (fatty deposits in the joints)
Arcus (corneal) fatty deposits in the cornea of the eye (forms a ring)
Xanthelasma (fatty deposits around the eyes)
What are the modifying factors
Smoking
Hypertension
Infection
Hyperlipidaemia
Alcohol intake
What are the non-modifying factors
Age
Genetics
Gender
How can diabetes Mellitus lead to atherosclerosis
Increased risk hyperlipidaemia and hypertension
What do endothelial cells do
Haemostasis
Collagen production
Proliferation and migration of the smooth muscle cells
What do the platelets do
Haemostasis
Proliferation and migration of the smooth muscle cells
What do the smooth muscle cells do
Take up the LDL and the other become foam cells
Synthesis of collagen and proteoglycans
What do macrophages do
Oxidise LDL
Take up lipids
Proliferation of the smooth muscle cells
What do the lymphocytes do
Proliferation of the smooth muscle cells
What do the neutrophils do
Secrete proteases leading to continue local damage and inflammation
What can cause the rupture an aneurysm
When the vessel would grown more then 6cm in length
How does the normal vessels stop thrombus
Production of heparin like molecule
Prostacyclin production (produced in the artery walls - anticoagulant)
Thrombomodulin (integral membrane protein, cofactor to thrombin enzyme (protein c, stops procoagulant functions of thrombin)
What are the infections that can cause atherosclerosis
Chlamydia pneumonia
Helicobacter pylori
Cytomegalovirus
How do the smooth muscle cells become foam cells
Taking up LDL and other lipids
What inflammatory mechanism would be stimulated
The chronic inflammatory
