Pharmacology Flashcards
GTN MOA?
NO release
Activates and increases cGMP
cGMP causes smooth muscle relaxation -> cardiac vasodilation
This reduces venous return (and therefore cardiac output) and therefore reduces LV workload
Beta blocker MOA?
Reduces sympathetic drive -> reduced HR and contractility
Reduced workload = improved exercise tolerance and symptomatic relief
Dihydropyridine MOA?
Smooth muscle relaxation by inhibiting calcium influx -> coronary and peripheral vascular smooth muscle relaxation
(SM relaxation = vasodilation = reduced VR = decreased CO / LV workload)
Non-dihydropyridine aka “rate limiting” MOA
Smooth muscle relaxation by inhibiting calcium influx -> coronary and peripheral vascular smooth muscle relaxation
(SM relaxation = vasodilation = reduced VR = decreased CO / LV workload)
AND SLOWS CONDUCTION AT AV NODE THEREFORE RATE LIMITING EFFECT
Isosorbide mononitrate MOA?
Release of NO -> release and activation of cGMP -> smooth muscle relaxation and subsequent cardiac vasodilation
= reduced VR, CO and therefore LV workload
Nicorandil MOA?
Potassium channel activator
- NO donor to activate cGMP causing arterial and venous vasodilation
- K+ channels open causing K+ efflux which hyperpolarises cell, and reduces Ca entry. This all causes smooth muscle relaxation.
Ivabradine MOA
Blocks a “pacemaker” or “funny” current channel in SAN
Ranolazine MOA
Inhibits “late” sodium channels to reduce calcium overload, leading to smooth muscle relaxation
(calcium overload through sodium dependent calcium currents causes myocardial ischaemia)
What is the first line treatment for chronic stable angina?
Beta blockers
What is the first line treatment for chronic stable angina where beta blockers are contra-indicated?
Non-dihydropyridine (rate limiting) beta blockers
Calcium channel blockers examples?
Dihydropyridines
-dipines
Non-dihydropyridines
Verapamil
Diltiazem
What is added in as second-line to beta-blocker therapy?
Dihydropyridine calcium channel blocker
di-pines
What can be added it to beta-blocker therapy for SYMPTOM CONTROL?
Longer-acting nitrates
e.g. isosorbide mononitrate, GTN sustained release or transdermal patches
Which drug would only be started by a cardiologist as an add-on therapy after all else isn’t working?
Ranolazine
A/Es of GTN
Hypotension
Headache
Flushing
Contraindications of GTN
Hypotension
Aortic or mitral stenosis
Hypertrophic cardiomyopathy