Arterial thrombosis Flashcards
what is an arterial thrombosis
blood clot which forms in an artery
risk factors for arterial thrombosis
Factors that cause damage to endothelium, increase in foamy macrophages and platelet activation:
* Hypertension
* Smoking
* High cholesterol
Diabetes mellitus
management of arterial thrombosis
aspirin and other anti platelets
modify risk factors for atheroscleoriss
clinical presetation of arterial thrombosis
Peripheral arterial thrombosis: Sudden pain, pallor, coldness, pulselessness, and potential tissue necrosis in the limb.
Coronary thrombosis: Chest pain, shortness of breath, sweating, and possible heart attack (myocardial infarction).
Cerebral thrombosis: Sudden onset of weakness, speech difficulty, and loss of vision, possibly leading to a stroke.
atherosclerosis steps
damage to endothelium causes recruitment of foamy macrophages rich in cholesterol resulting in cholesterol rich plaques
what do stable plaques resul;t in
stable angina and intermittent claudicationwh
what do unsatble plaques result in
stroke, unstable angina or MI
durgs for arterial thrombosis
anti platelets
drugs for venous thrombosis
anti coags
characterisitcs of stable atherosclerotic plaques
hyalinsed and calcified
unstable atherosclerotic plaques steps
Plaques rupture, platelets are recruited and cause acute thrombosis
Sudden onset of symptoms
Unstable angina or myocardial infarction (coronary arteries)
Stroke (cerebral arteries)
leads to acute organ ischaemia and infarctionn
platelets and arterial thrombosis
Plaque ruptures – more likely in the high pressure environment of arteries
Platelet adheres to it – exposed endothelium and release of Von Willebrand factor
Platelets becomes activated - release granules that activate coagulation and recruit other platelets to developing platelet plug
Platelet aggregation via membrane glycoproteins
what are foamy macrophages rich in
cholesterol
what do platelets bind to subendothelial collagen via
glycoprotein 1b and vwf
what do platelets attach to each other via
GPIIbIIIa and fibrinogen
activation stage steps
Platelets alter their shape to expose more phospholipid on the surface-provides a greater surface area for coagulation activation and fibrin production to stabilise the clot.
Process is augmented by release of granules that further stimulate platelet activation eg Thrombin,Thromboxane A2 and ADP in order to recruit more platelets to the process.
This occurs via receptors to ADP etc on the platelet surface.
MOA of aspirin
inhibits coco oxygenase which is necessary to produce thromboxane a2
side effects of aspirin
. Bleeding
Blocks production of prostaglandins:
GI ulceration
Bronchospasm
ADP receptor antagonists
clopidogrel, prasugrel
Phosphodiesterase inhibitor
dipyridamole
increases production of camp which inhibits platelet aggregation
GP IIb/IIIa inhibitors
abciximab
inhibit aggregation
when should antiplatelets be stpped
7 days prior to elective operations
arterial thrombosis conclusion
Causes organ ischaemia and is an inflammatory disorder instigated by damage to the endothelium
Platelets are central and are recruited to ruptured plaques
Antiplatelet drugs are useful in prevention
venous thrombosis conclusion
Occurs in a low pressure system mainly by stasis
Platelets are not largely involved, and clots are rich in fibrin
Anticoagulants are useful in prevention