Atheroma, Thrombosis and Embolism Flashcards
what is atheroma
lesion in the intimate layer of blood vessel raised via lipids (cholesterol and esters) and covered by a fibrous cap
what is atherosclerosis
hardening of the blood vessels due to atheroma formation
which types of arteries are commonly affected by atheroma
bifurcations (sites of turbulent flow) abdominal aorta coronary arteries popliteal arteries carotid arteries circle of willis
what are the major risk factors of atheroma formation
non-modifiable - increasing age, male gender, history, genetic s
modifiable - hyperlipidemia, hypertension, C reactive protein (damage vessel walls)
why does atherosclerosis develop
in response to endothelial injury and develops as a chronic inflammatory response in the arterial wall
what is the response to injury hypothesis in atheroma formation
chronic endothelial damage - margination of cells along endothelium - initiates increased vascular permeability
accumulation of lipoproteins in th eintima (high LDL levels)
monocyte adhesion to endothelium, proliferation and ECM production
factor release - recruitment of inflammatory cells
describe the morphological evolution of atherosclerosis
fatty streak - macrophages enter lesion and become foam cells
further accumulation of lipids thickens the intimacy
plaque impinges the vessel lumen
describe the consequences of atherosclerosis
rupture of the plaque exposing intimal surface
induces thrombosis and lumen occlusion which leads to ischeamia, atherothrombelism and aneurysm formation
what is a thrombus
solid mass of blood constituents within an intact vessel which is veinous and arterial
what is a haemostatic plug
forms at site of vascular injury and is not pathological
what is the mechanism, location, associated diseases, composition and treatment of arterial thrombosis
mech - forms from rupture of atheromatous plaque
loc - left heart chambers, arteries
dis - acute coronary syndrome, ischemic stroke
comp - mainly platelets
treatment - anti-platelet agents (clopidogrel)
what is the mechanism, location, associated diseases, composition and treatment of venous thrombosis
mech - combination factors from virchows triad
loc - venous sinusoids of muscles and valves of veins
dis - DVT and pul embolism
comp - mainly fibrin
treat - anticoagulants (heparin and warfarin)
how do we naturally inhibit thrombosis
natural anticoagulants such as protein C (proteolysis of Va and VIIIa, need protein s)
what factors favour thrombosis formation
platelet aggregation, adhesion and clotting factors
a venous thrombosis is determined by what
give examples
virchows triad
- endothelial injury
- hyper coagulability
- abnormal blood flow
immobility and lack of muscle contraction = stasis of blood
polycythaemia - viscous blood and hypercoaguable