Arterial Thrombosis and Anti-platelet drugs Flashcards
arterial thrombotic events
coronary, cerebral, peripheral
arterial thrombosis treatment
- aspirin and other anti-platelet drugs
- modify risk factors for atherosclerosis (smoking, BP, diabetes)
atherosclerosis- what happens/pathophysiology
damage to endothelium
‘foamy’ macrophages rich in cholesterol are recruited to the damage
forms plaques rich in cholesterol
stable atherosclerotic plaques
Hyalinised and calcified
Stable plaques: stable angina (coronary artery), intermittent claudication (leg artery)
unstable atherosclerotic plaques
Plaques rupture, platelets are recruited and cause acute thrombosis
Sudden onset of symptoms
Unstable angina or myocardial infarction (coronary arteries)
Stroke (cerebral arteries)
Unstable atherosclerotic plaques - gradual or sudden onset of symptoms?
sudden
are plaque ruptures more likely in veins or arteries
Plaque ruptures – more likely in the high pressure environment of arteries
Factors that cause damage to endothelium, increase in foamy macrophages and platelet activation:
Factors that cause damage to endothelium, increase in foamy macrophages and platelet activation:
- Hypertension (damage to endothelium,
platelet activation)
- Smoking (endothelium, platelets) - High cholesterol (accumulated in plaque) - Diabetes mellitus (endothelium, platelets, cholesterol)
prevention of arterial thrombosis
Stop smoking
Treat hypertension
Treat diabetes
Lower cholesterol
Anti-platelet drugs
platelets are formed in the ____ _____ by ‘budding’ from ___________
bone marrow
megakaryocytes
what is the mean lifespan of platelets
7-10 days
what do platelets releasee to further stimulate platelet activation in order to recruit more platelets
Thrombin,Thromboxane A2 and ADP
Aspirin inhibits __________ which is necessary to produce Thromboxane A2 (a platelet agonist released from granules on activation).
cyclo-oxygenase
Aspirin inhibits cyclo-oxygenase which is necessary to produce ____________ (a platelet agonist released from granules on activation).
Thromboxane A2
side effects of aspirin
- Bleeding
- Blocks production of prostaglandins:
- GI ulceration
- Bronchospasm
how does clopidogrel work
blocks ADP receptor
Dipyridamole mechanism of action
Phosphodiesterase inhibitor - increases production of cAMP which inhibits platelet aggregation.
GP IIb/IIIa inhibitors example
abciximab
GP IIb/IIIa inhibitors mechanism of action
inhibit aggregation
Platelets attach to each other via ________ and _________.
GPIIbIIIa
fibrinogen
How long before elective operations should anti-platelet agents be stopped
7 days
If serious bleeding, how could we potentially reverse
platelet transfusion
arterial thrombosis conclusions
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 conclusions
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