Anti Platelet drugs Flashcards
what causes artterial thrombosis
lipid deposits in endothelium
damage to endothelium of arteries recruits foamy macrophages rich in cholesterol
forms cholesterol rich plaque
high pressure system causes plaques to rupture
platelets recruited, adhere to expose endothelium and released VWf
platelets become activate - release granules that activate coagulation (more platelets come and form platelet plug)
causes acute thrombosis
how do platelets aggregate
via membrane glycoproteins (GPIIbIIIa) and fibrinogen
what type of thrombus in aterial disease
platelet rich
what is the treatment for arterial thrombosis
aspirin (+ other anti platelet drugs)
modification of risk factors (HPTx, diabetes, smoking)
what are atherosclerotic plaques rich in
cholesterol
what are stable atherosclerotic plaques like
hyalinised and calcified
cause stable angina (in coronary artery), intermittent claudication (leg artery)
what do unstable atherosclerotic plaques cause
when rupture cause: sudden onset of symptoms, unstable angina/ MI
stroke
=acute organ ischaemia and infarction
what are the risk factors for arterial thrombosis
(factors that cause damage to the endoethelium, increase in foamy macrophages and platelet activation)
- hypertension (damage to endothelium, platelet activation)
- smoking (endothelium (raises BP), platelets)
- high cholesterol (accumulated in plaque)
- diabetes (endothelium damage, platelets, cholesterol)
how do you prevent arterial thrombosis
stop smoking
treat hypertension and diabetes
lower cholesterol
anti platelet drugs
how are vessels damaged in Venous thrombosis
valves damaged (not atheromas like in arterial)
what do platelets do in arterial disease
adhere at site of injury to exposed collaged with help of VWf
activate and secrete chemicals (ADP, thromboxan A2) which causes aggregation at site of injury
how do platelets bind to subendothelial collagen
glycoprotein 1b and VWf
what happens in platelet activation
platelets shape alters to expose more phospholipid on the surface-provides a greater surface area for coagulation activation and fibrin production to stabilise the clot
also release of granules (thrombin, thromboxane A2, ADP) which further stimuates platelet activation and recruitment (via ADP receptors on platelet surface)
how does aspirin work
inhibits cyclo-oxygenase which is needed to produce throboxane A2 (platelet agonist released from granules, attracts other to site of injury)
what are the side effects of aspirin
bleeding
blocks production of prostaglandins:
-GI ulceration (prostaglandins provide protective surface in the stomach, blockage of this more likely to get ulcer, and as on antiplatelet more likely to bleed from this)
-bronchospasm (having asthma a CI to aspirin)