Pathology - Atherosclerosis Flashcards
What is atherosclerosis?
The accumulation of intracellular and extracellular lipid in the intima and media of large/medium arteries leading to thickening and hardening of arterial walls
What is arteriosclerosis?
The thickening of the walls of arteries and arterioles, usually as a result of hypertension or diabetes mellitus
What is the same given to a yellow, slightly raised lipid deposit in the lumen of an artery?
Fatty streak
How does a simple plaque appear in the lumen?
Raised yellow/white, irregular outline, widely distributed, can enlarge and coalesce
Why is a complicated plaque more dangerous than a simple plaque?
- can lead to thrombosis
- can lead to haemorrhage into plaque
- can lead to calcification of arteries
- may cause aneurysm formation
Give some common sites of atherosclerosis
Aorta (especially abdominal), coronary arteries, carotid arteries, cerebral arteries, leg arteries
What are the EALRY microscopic features of atherosclerosis?
Proliferation of smooth muscle cells, accumulation of foam cells, extracellular lipid
What are the ADVANCED microscopic features of atherosclerosis?
Fibrosis, necrosis, cholesterol clefts, inflammatory cells, disruption of internal elastic lamina, damage extends into media, ingrowth of blood vessels, plaque fissuring
Give some clinical effects of atherosclerosis which relate to ischaemic heart disease
Ischaemic heart disease:
- sudden death
- myocardial infarction
- angina pectoris
- arrhyhmias
- cardiac failure
Give some clinical effects of atherosclerosis which relate to cerebral ischaemia
- transient ischaemic attack
- cerebral infarction
- multi-infarct dementia
Give some effects of atherosclerosis which relate to mesenteric ischaemia
Ischaemic colitis, malabsorption, intestinal infarction
Give some clinical effects of atherosclerosis which relate to peripheral vascular disease
- intermittent claudication
- Leriche syndrome
- ischaemic rest pain
- gangrene
Give some pre-disposing factors for atherosclerosis
- age (risk increases as get older)
- gender (women protected before menopause)
- hyperlipidaemia (high plasma cholesterol associated with atherosclerosis)
- cigarette smoking
- hypertension (possibly due to endothelial damage caused by raised pressure)
- diabetes mellitus
- alcohol
- infection (chlamydia pneumoniae, H. Pylori, cytomegalovirus)
- lack of exercise/obesity
- soft water
- oral contraceptives
- stress (uncertain)
How is atherosclerosis associated with apolipoprotein E?
- genetic variations in Apo E are associated with changes in LDL levels
- polymorphisms of these genes can be used as risk markers for atherosclerosis
Give some physical signs of familial hyperlipidaemia
- corneal arcus
- tendon xanthomas
- xanthelasma
What was the thrombogenic theory of atherosclerosis?
Plaques formed by repeated thrombi, lipid is derived from these. Overlying fibrous cap forms
What was the insulation theory of atherosclerosis?
Endothelial injury leads to inflammation and increased permeability to lipid from plasma
What is the reaction to injury hypothesis of atherosclerosis?
- plaques form in response to endothelial injury
- injury increases permeability and allows platelet adhesion
- monocytes penetrate endothelium
- smooth muscle cells proliferate there and migrate
What is the monoclonal hypothesis of plaque formation?
Each plaque is monoclonal, so they may represent abnormal growth control - could be a benign tumour
Which cell types are involved in atherosclerosis?
- endothelial cells
- platelets
- smooth muscle cells
- macrophages
- lymphocytes
- neutrophils
What is the role of endothelial cells in atherosclerosis?
- altered permeability to lipoproteins
- production of collagen
- stimulation of proliferation/migration of smooth muscle cells
What is the role of platelets in atherosclerosis?
Stimulate proliferation and migration of smooth muscle cells
What is the role of smooth muscle cells in atherosclerosis?
Take up LDL and other lipids to become foam cells, synthesise collagen and proteoglycans
What are the roles of macrophages in atherosclerosis?
- oxidise LDL
- take up lipids to become foam cells
- secrete proteases which modify the matrix
- stimulate proliferation and migration of smooth muscle cells
