Vascular Disease 1: Atheroms And Its Complications Flashcards Preview

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Flashcards in Vascular Disease 1: Atheroms And Its Complications Deck (21)

Arteriosclerosis definition

Thickening and hardening of an artery


Arteriolosclerosis definition

Thickening and hardening of an arterioles


Atheroma definition

Degenerative disease effecting large and medium arteries
Initially disease of the intima, later effects media
Only occurs in high pressure systems, not venous, rarely pulmonary
Ubiquitous but very mild in young people-> declines with age


Role of hypertension in arterio and arterioloscelerosis

Hypertension is the most common cause of thickening and hardening of the small arteries and arterioles
Also a risk factor for Atheroma
Hypertrophy of the media
Fibroblast thickening of intima
Elastic lamina replication
-> decreased lumen
In arteriolosclerosis-> replacement of wall structures by amorphous hyaline material
-> decrease lumen-> decreased flow-> Ischaemia
->rigidity of vessel wall-> loss of elasticity and contractility-> unresponsive
Problems when demand is increased


Atheroma stage 1

Damage to endothelium
Blood lipids (LDL) can enter intima


Atheroma stage 2

LDL is taken up by macrophages in the in intima
Proliferation of myointimal cells via growth factor attraction by macrophages
Normal receptor mediated lipid is bypassed by oxidation of LDL-> taken up by receptor independent pathway
Lipid accumulates producing a fatty streak-> visible pale bulge


Atheroma stage 3

Macrophages start to release lipid into the intima
Myointimal cells have myofibroblasts properties-> start to secrete collagen
Raised yellow lesion-> lipid plaque
Early damage to elastic lamina and media
Pressure atrophy on muscle layer-> dissolved by proteolytic enzymes


Atheroma stage 4

Increased collagen synthesis forms a dense fibrous cap over the plaque
Plaque becomes fiibrolipid-> hard and white
Muscle in media is replaced by collagen-> weakens walls
Endothelium is fragile-> ulcerates exposing collagen with fibrin-> thrombus formation via platelet aggregation


Atheroma stage 5

Complicated Atheroma
Free lipid as well as lipid in macrophages
Lipid in intima becomes calcified
Surface of fibrolytic plaque ulcerates
Thinning of media leads to weakness and elasticity


Complications of Atheroma, reduction of blood flow through arteries

Enlargement of intima reduces lumen-> decreased blood flow-> Ischaemic damage
Coronary arteries-> angina
Leg arteries-> intermittent claudication
Cerebral and vertebral arteries-> cerebral Ischaemic Events
Tissue may eventually die of hypoxia


Complications of Atheroma, predisposition to thrombus formation

Ulceration of fibrous cap-> exposes collagen to blood
Initiates thrombus formation
Thrombus may suddenly occlude small arteries-> coronary or cerbral arteries
Or thrombus May embolism in distal vessels


Complications of Atheroma, bleeding into a plaque

Breakdown of fibrous cap-> blood seeps in-> dissects centre of plaque-> plaque balloons-> occlusion
Or blood undergoes thrombosis in plaque


Complications of Atheroma, weakening of vessel walls and aneurysm

Muscle and elastic fibres of media replaced by collagen-> media becomes incompetent-> stretches and becomes thin and weak-> dilation of artery
Most common in abdo aorta



Abnormal permanent focal dilation of an artery
Abdo most common
Aortic dissection
Mycotic-> mostly caused by endocarditis, bacterial septicaemia


Pathogenesis of Atheroma, thrombogenic hypothesis

Thrombus is incorporated into intima of vessels
Lipid derived from platelet membranes and cells stimulated to proliferate by platelet derived growth factors


Pathogenesis of Atheroma, clinal proliferation hypothesis

Obese ration that smooth muscle cells in plaques are derived from one clone of cells
-> caused by a primary abnormality in cell growth


Pathogenesis of Atheroma, lipid insudation hypothesis

LDLs taken up by intima
Become chemically oxidised to act as toxic, pro inflam and chemotactic factors


Pathogenesis of Atheroma, response to injury hypothesis

Atheromatous plaque is response to chromic low grade injury to endothelium
Metabolic disturbances to endothelial cells (haemodynamic stress and toxic effects of LDL)-> platelet adhesion, diffusion of plasma protiens, and migration of monocytes in to the intima of arteries
Platelets release PDGF-> proliferation of intimal smooth muscle-> produces excesse collagen and elastin in to intima


Risk factors for Atheroma, constitutional

Increases with age
More common in men than women
Familial traits


Hard Risk factors for Atheroma

Hyperlipidemia-> risk increases as cholesterol increases
High HDL-> reduces the risk
Diabetes mellitus-> hypercholesterolemia
Cigarette smoking


Soft risk factors for atherosclerosis

Exercise-> decreases risk
Stress and personality

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