Atherosclerosis General

Front 1

Atherosclerosis

Back 1

= slowly progressive disease of arteries

INTIMAL PLAQUES
elevated fibrofatty
lipid deposition
smooth muscle cell proliferation
ECM synthesis

Front 2

Predisposing factors

Back 2

see other set

Front 3

Complications

Back 3

PLAQUE DISRUPTION

ULCERATION of luminal surface

EMBOLISM due to material release from ulcerated atheroma

THROMBOSIS on damaged endothelial surface
--> occludes vessel, EMBOLISES, or organised and incorporated into original plaque

HAEMORRHAGE into plaque, sudden INC. in size; due to influx of blood through ruptured endothelium or to rupture of new vessels (vasa vasorum) formed in the plaque

CALCIFICATION is common and early compx --> vessel wall is rigid

ANEURYSM can follow atrophy + fibrosis of media which stretches

Thrombosis on a plaque, haemorrhage into a plaque or atheromatous embolism may all cause severe narrowing or occlusion of an artery giving rise to ISCHAEMIA or INFARCTION of the part supplied by the affected artery.

Front 4

Clinical Pathology

Back 4

Atherosclerosis is asymptomatic for decades until it causes disease by the following mechanisms

Insidious NARROWING of lumen (e.g. gangrene of the lower leg because of stenosing atherosclerosis in the popliteal artery)

Plaque RUPTURE + superimposed THROMBUS = sudden occlusion of lumen (e.g. MI precipitated by thrombotic occlusion of disrupted coronary arterial atheroma)

Provides a source of embolic debris, know as atheroembolism (e.g. renal infarction resulting from cholesterol emboli originating in an ulcerated atherosclerotic aortic plaque)

WEAKENING of wall --> aneurysm + rupture (e.g. an abdominal aortic aneurysm)

Front 5

Symptomatic atherosclerotic disease most often affects?

Back 5

HEART (infarction)

BRAIN (stroke)

Kidneys (ischaemia)

Lower extremities (gangrene)

SI (ischaemia of mesenteric vessels)

Complications of atheroma are responsible for most of the effects.