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L13 Atheroma, Thrombosis & Embolism


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atheroma
intimal lesion that protrudes into the vessel wall. It consists of a raised lesion with a soft core of lipid and is covered by a fibrous cap
non-modifiable
__-________ risk factors for atheroma: increasing age, male gender, family Hx, genetic abnormalities
modifiable
________ risk factors for atheroma: hyperlipidemia, hypertension, smoking, diabetes, C-reactice proteins
atherosclerosis
...develops as a chronic inflammatory response of the arterial wall to endothelial injury
response to injury hypothesis
current theory model on atherosclerosis formation
endothelial injury
response to injury hypothesis, Step 1: chronic _______ ______
lipoproteins
Response to injury hypothesis, Step 2: accumulation of ________
monocyte
Response to injury hypothesis, Step 3: ________ adhesion to endothelium
ECM
Response to injury hypothesis, Step 4: SMC proliferations and ____ production
factor
Response to injury hypothesis, Step 5: _______ release
platelet
Response to injury hypothesis, Step 6: _______ adhesion
fatty streak
earliest lesion in atherosclerosis; composed of lipid filled foamy macrophages; begins as multiple minute flat yellow spots that eventually coalesce into streaks; these lesions are not significantly raised and do not cause flow disturbance
ischaemia
may result if rupture, ulceration or erosion of intimal surface exposes the blood to highly thrombogenic substancesand induces thrombosis -> lumen occlusion --> _______
haemorrhage
sequela of atherosclerosis: ________ into plaque
atheroembolism
sequela of atherosclerosis: movement of plaque to elsewhere in body
aneurysm
sequela of atherosclerosis: ________ formation
haemostatic plug
formed at the site of vascular injury
haemostasis
a consequence of tightly regulated processes that maintain blood in a fluid state in normal vessels yet also permit rapid formation of hemostatic clot at site of vascular injury
arterial thrombosis
typically from rupture of atheromatous plaque; left heart chambers and arteries; acute coronary syndrome, ischaemic stroke, claudication; mainly platelets; TREATMENT: anti-platelet agents (clopidogrel)
venous thrombosis
typically from combination of factors from Virchow's triad; venous sinusoids of muscles and valves of veins; DVT & PE; mainly fibrin; TREATMENT: anticoagulants (heparin, warfarin)
endothelial dysfunction
caused by smoking and hypertension; an element of one part of Virchow's triad
endothelial damage
consequence of surgery, catheter (PICC lines) or trauma; an element of one part of Virchow's triad
hereditary hypercoagulability
Factor V Leiden, Prothrombin G20210A, protein C & S deficiency contribute to this element of Virchow's triad
acquired hypercoagulability
Cancer, chemotherapy, OCR/HRT, pregnancy, obesity or HIT all contribute to this element of Virchow's triad
stasis
immobility and polycythemia all contribute to this element of Virchow's triad
clot
platelets not involved; occurs outside vessel (e.g. test tube/haematoma) or inside (postmortem); red; gelatinous; not attached to vessel wall
thrombus
platelets involved (lines of Zahn); occurs only inside vessel; red (venous), pale (arterial); firm; attached to vessel wall
embolus
a mass of material in the vascular system able to lodge in a vessel and block it; may be end-/exo-genous; solid, liquid or gas