Stable coronary heart disease - clinical pharmacology Flashcards
(26 cards)
What is the spectrum of ACS
Unstable angina
Non-ST elevation myocardial infarction (NSTEMI)
ST-elevation myocardial infarction (STEMI)
Sudden cardiac death
What is the goal of clinical pharmacology in ACS
Increase myocardial supply
Reduces myocardial demand
Through which mechanisms does drug therapy increase myocardial supply
through coronary vasodilation
Through which mechanism does drug therapy reduces myocardial demand
Decrease in heart rate,
Decrease blood pressure,
Decrease preload or myocardial contractility
When would thrombolysis treatment be administrated
If PCI is not available within 2 hours
How do Thrombolytic agents work
and what is the outcome
Serine proteases convert plasminogen to plasmin which lyses clot by breaking down the fibrinogen and fibrin contained in a clot
Resulting in bursting up of the clot but not dealing with the atheroma
What is the two categories of Thrombolytic agents
Fibrin-specific agents such as
Non–fibrin-specific agents
What are examples of fibrin specific agents
alteplase,
reteplase,
tenecteplase
What is an examples of a non fibrin specific agent
streptokinase
What further reduces mortality in combination with thrombolysis
aspirin
What are the possible contradictions to consider before performing thrombolysis
Prior intracranial hemorrhage (ICH)
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Ischaemic stroke within 3 months
Suspected aortic dissection
Active bleeding or bleeding diathesis (excluding menses)
Significant closed-head trauma or facial trauma within 3 months
what is the ACS medical protocol treatments if no evidence of a STEMI
Aspirin Tigagrelor/Clopidogrel Fondaparinux/LMW heparin Intravenous nitrate Analgesia Beta Blockers prasugrel GIIbIIIa receptor blockers Statins
What the management to reduce the risk of a STEMI
PCI or CABG Aspirin Clopidogrel, prasugrel, ticagrelor, ticlopidine or cilostazol Heparin (LMWH) Fondaparinux GIIb/IIIa receptor blockers Statins B blockers
What is the normal dosage of aspirin used
and why is this
75-150mg
Aspirin is just as effective at low dose than high, slow dose used to reduced adverse reaction of bleeding
How does aspirin work in the treatment of ACS
As a preventer
Inhibit platelet thromboxane A2
Preventing platelet aggrevation and vasoconstriction
What is examples of ADP receptor inhibitors
Clopidogrel
Prasugrel
How does clopidogrel (ADP receptor) work in the treatment of ACS
As a preventer
Inhhibits GP IIb/IIIa pathway therefore preventing binding of fibrinogen, so platelets aren’t activated
(glycoprotein IIb/IIIa pathway receptor found on platelets)
What is ADP receptor inhibitors used in combination with
Aspirin
What is the disadvatages of clopidogrel
Adverse reaction of G bleeding
Interact and reduces affect of proton pump inhibitors
Can show resistance
Why could some patients show a resistance to clopidogrel
Clopidogrel is a prodruf, therefore some patients may have low levels of CYP 2C19 hepatic enzymes, so isn’t metabolised
what is the benefit of prasugrel over clopidogrel
More effective
More rapid and consistent inhibits ADP induced platelet aggravation
How does Low molecular weight heparin work
preventing certain cofactors, namely thrombin and fibrin, from working correctly
What is examples of LMWH
Enoxaparin
dalteparin
Tinzeparin
Fondaparinux - most effective
Beta blockers is used post MI as secondary prevention how does this work in treating ACS
Inhibit sympathetic system, reducing myocardial oxygen consumption , lowers heart rate and reduces contracility
