Drugs Used In IHD Flashcards
Aspirin
- cyclo-oxygenase inhibitor
- irreversibly binds to cycle-oxygenate by actylating a serine residue on the active site
- reduced synthesis of thromboxane - a susbstance that promotes platelet aggregation
- secondary prevention IHD and mortality reduction post MI
Clopidogrel
- thienopyridine derivative
- irreversibly prevents ADP from binding to its receptor on the platelet surface
- thereby preventing glycoprotein IIb\IIIa receptor transforming into its active form.
Used for prevention of atherothrombotic events in all known cases of ACS.
Glycoprotein 2b/3a antagonists
Used in treatment of IHD, eg. Abiciximab, tirofiban, eptifibatide
inhibit glycoprotein receptor on platelets and this block the final common pathway for platelet aggregation.
Short term prevention of early acute MI in patients with ACS and recent chest pain who are not responding to conventional treatment.
Which antiplatelets must be stopped before elective surgery?
Theinpyridines have greater antiplatelet activity than salicylates. Markedly increase surgical bleeding.
Also not recommended for regional anaesthesia if taking anything other than aspirin only.
Fibrinolytic mechanism action
Act as thrombolytics by activating plasminogen to form plasmin, which degrades fibrin, and so breaks up thrombi
Ie streptokinase, alteplase
Streptokinase
Enzyme produced by group C beta-haemolytic streptococci, which activates the fibrinolytic system by forming a complex with plasminogen.
Allergic reactions are common.
Alteplase
Glycoprotein that becomes activated only when bound to fibrin, and thus results in less systemic fibrinolysis.
Ca channel blockers mechanism a
Block Ca entry through L-type slow channels of active cell membranes.
In the myocardium, this causes depletion of ATP stores and thus reduces contractility and subsequently O2 consumption. Coronary and peripheral vasodilation.
Used to treat angina, HTN, post MI ischaemia in IHD.
Classes of Ca channel blockers, and examples
Class 1 - phenylalklamimes (verapamil)
Class 2 - dihydropyridines (amlodipine, nifedipine)
Class 3 - benzothiazepines (diltiazem)
All myocardial depressants.
Nitrates mechanism of action
Side effects?
Cause vasodilation by production of nitric oxide, thus acts by promotion of coronary blood flow and more significantly by reduction of venous return and subsequent reduction in LVF work.
Side effects- flushing, headaches, postural hypotension. Tolerance may occur.
Nicorandil
Anti-aginal
- K channel activator with a nitrate component.
- Causes arterial and venous vasodilation.
- prevention and treatment of long standing angina.
Ivabradine
- anti-anginal
- acts on mixed Na/K channel, which is highly expressed in SA node.
- slows heart rate, allows time for more diastolic filling.
- useful adjunct with b-blockers for patients with stable angina with sinus rhythm.
Ranolazine
- anti-anginal
- does not alter heart rate or blood pressure.
- adjunctive therapy in angina is not adequately controlled by first line anti-anginal drugs
How do ACE inhibitors work?
- inhibit angiotensin converting enzyme
- reduces production of angiotensin II (potent vasoconstrictor)
- blocks the break down of the kinins, naturally occurring vasodilators
- accumulation of bradykinin leads to side effect of cough
How do ARB2 antagonists work?
Inhibit ARB2 binding time angiotensin receptor, do not inhibit breakdown bradykinin so no cough side effects.
