Pharmacology of ACS Flashcards
mechanism of action of thrombolytic therapy
most effective within 2 hours of symptoms, serine proteases that work by converting plasminogen to the natural fibrinolytic agent plasmin. plasmin lyses clot by breaking down the fibrinogen and fibrin contained in a clot
the potential adverse drug reactions which a patient may suffer following drug treatment of ischaemic heart disease.
increased risk of bleeding, clopidogrel resistance,
the strengths and weaknesses of low dose aspirin.
strengths- reduces non fatal MI, non fatal stroke and cardiovascular death by nearly a third. don’t need a lot to be effective. all patients should be maintained on long term aspirin therapy following acute coronary syndrome
weaknesses- combination therapy more effective (happens for 6 months after ACS)
the strengths and weaknesses of beta adrenoceptor antagonists.
used in treatment of acute MI, for secondary prevention in survivors, reduces rate of progression of NSTEMI and unstable angina, however increase in cardiac shock and no effect on death, reinfarction or cardiac arrest
fibrin specific agents
catalyse plasminogen to plasmin. alteplase, reteplase, tenecteplase
non fibrin specific agents
catalyse systemic fibrinolysis. streptokinase. not used in acute coronary syndrome in uk
P2Y12 inhibitors
always used in combination with aspirin. inhibits the P2Y12 ADP receptor which is important in aggregation of platelets and cross linking by fibrin. prasugrel, ticagrelo, clopidogrel (added alongside aspirin)
DAT
ticagrelor better combination than copidogrel but chance of bleeding is the same
patients with acute coronary syndrome should be treated with
long term beat blocker therapy, long term statin therapy prior to hospital discharge
patients with unstable angina or myocardial infarction should be commenced on
long term angiotensin converting enzyme inhibitor therapy