Studydroid is shutting down on January 1st, 2019

by kuc


keywords:
Bookmark and Share



Front Back
Aciclovir - Mechanism
Virus infected cells convert aciclovir to aciclovir triphosphate, terminating DNA chain growth
Aciclovir - s/e
Renal failure, neurotoxicity (hallucinations, convulsions)
NSAIDs - preparations [5]
Aspirin, ibuprofen, diclofenac, indometacin, mefanamic acid
NSAIDs - mechanism
Inhibition of COX, which catalyzes prostaglandin synthesis
NSAIDs - s/e [4]
GI toxicity, renal impairment, hypersensitivity (bleeding - aspirin)
Coxibs - preparations [1]
Etoricoxib,
Coxibs - mechanism
Selective inhibition of COX-2 isoform
Coxibs - s/e [3]
Dry mouth, dyspepsia, cough
Bisphosphonates - mechanism
Adsorbed onto hydroxyapatite crystals in bone, reducing bone turnover
Bisphosphonates - preparations [4]
Disodium etidronate, alendronic acid, risedronate, disodium pamidronate
Bisphosphonates - s/e [3]
GI disturbance, flu-like symptoms, bone pain
Diuretics - mechanism
Reduce sodium and chloride reabsorption in the nephron, increasing urinary sodium and water loss (thiazide - DCT, loop - ascending loop of Henle, K+sparing - cortical CT, spironolactone inhibits aldosterone)
Thiazide diuretics - preparations [2]
Bendroflumethiazide, metolazone,
Thiazide diuretics - s/e [5]
Postural hypotension, hypokalaemia, hyponatraemia, profound diuresis, caution in renal/hepatic impairment
Loop diuretics - preparations [2]
Furosemide, bumetanide,
Loop diuretics - s/e [4]
Hyponatraemia, hypokalaemia, hypomagnesaemia, GI
Potassium-sparing diuretics - preparations [2]
Amiloride, spironolactone
Potassium-sparing diuretics - s/e [2]
Hyperkalaemia, gynaecomastia (spironolactone)
Beta-blockers - mechanism
Block beta-adrenoceptors in heart and peripheral vasculature, decreasing heart rate and contractility
Beta-blockers - preparations [4]
Propanolol, Atenolol, Metoprolol, Sotalol,
Beta-blockers - s/e [4]
Bradycardia, claudication exacerbation, lethargy, hallucinations
ACE inhibitors - mechanism
Inhibition of angiotensin I to II conversion, reducing angiotensin II mediated vasoconstriction
ACE inhibitors - preparations [3]
Perindopril, lisinopril, ramipril
ACE inhibitors - s/e [4]
Initial HTN, dry cough, hyperkalaemia, renal failure in renal artery stenosis
A2 receptor antagonists - mechanism
Antagonist of angiotensin II receptors (AT1), reducing angiotensin II mediated vasoconstriction
A2 receptor antagonists - preparations [4]
Olmesartan, candesartan, valsartan, losartan
A2 receptor antagonists - s/e [3]
Postural hypotension, rash, hyperkalaemia
Nitrates - mechanism
Increase in cGMP in vascular smooth muscle decreases intracellular calcium, promoting smooth muscle relaxation in vasculature
Nitrates - preparations [2]
Glyceryl trinitrate, isosorbide mononitrate
Nitrates - s/e [3]
Flushing, headache, postural hypotension
Calcium channel blockers - mechanism
Block calcium channels, modifying uptake into myocardium and vasculature, depressing cardiac conduction and contractility, and promoting vasodilatation
Calcium channel blockers - preparations [4]
Amlodipine, verapamil, nifedipine, diltiazem
Calcium channel blockers - s/e [6]
Flushing, dizziness, tachycardia, hypotension, ankle swelling, headache
Potassium channel activators - mechanism
Action of nitrates and K-channel activator - increased K+ flow into cell causes calcium-channel blockade and arterial dilatation
Potassium channel activators - preparations [1]
Nicorandil
Potassium channel activators - s/e [5]
Headache, flushing, nausea and vomiting, hypotension, tachycardia
Cardiac glycosides - mechanism
Inhibition of myocardial cell Na+/K+ ATPase increases intracellular sodium and calcium, increasing contraction force and reducing AV node conductivity
Cardiac glycosides - preparations [1]
Digoxin
Cardiac glycosides - s/e [6]
Anorexia, nausea & vomiting, diarrhoea, visual disturbance, heart block, confusion
Adenosine - mechanism
Acts on adenosine receptors, enhancing outflow of K+ from myocardium, slowing heart rate and AV node conduction
Adenosine - s/e [5]
Bradycardia, AV block, flushing, headache, chest pain
Amiodarone hydrochloride - mechanism
Class III - prolongs AP increasing refractory period, inhibits repolarisation, b-adrenoceptor antagonist activity
Amiodarone hydrochloride - s/e [2]
Hypo-/hyper-thyroidism, liver toxicity
Disopyramide - mechanism
Class Ia - blocks Na+ channels, increasing refractoriness of cell
Disopyramide - s/e [3]
GI disturbance, -ve inotropic, avoid in HF and heart block
Lidocaine hydrochloride - mechanism
Class Ib - blocks Na+ channels, and increases AP duration
Lidocaine hydrochloride - s/e [5]
Dizziness, paraesthesias, confusion, convulsions, hypotension
LMW-heparins - mechanism
Mainly anti-Xa activity
LMW-heparins - preparations [2]
Enoxaparin, tinzaparin
LMW-heparins - s/e [3]
Haemorrhage, immune thrombocytopaemia, hyperkalaemia
x of y cards Next > >> >|