Flashcards in Diuretics Deck (16):
MOA of osmotic diuretics
increase RBF, alter medullary tonicity so that tubular water reabsorption is osmotically blocked
Uses of osmotic diuretics (mannitol)?
localised oedema, glaucoma
ADRs of osmotic diuretics?
GI upset, injection site reactions, chills/fever, acute renal failure, CNS toxicity
MOA of CA inhibitors?
inhibit recycling of H+ secretion and Na+ reabsorption
Uses of CA inhibitors?
localised oedema e.g. glaucoma
MOA of loop/high ceiling diuretics?
acts at thick ascending limb, blocks Na+/K+/2Cl- symporter, block 15-25% of Na+ reabsorption
ADRs of loop diuretics
K+ wasting (dysrhythmias, ECG changes, increased digoxin toxicity, muscle weakness, constipation, drowsiness, irritability, confusion, dizziness), Na+ Mg2+ Ca2+ loss, impaired uric acid excretion, dose-related hearing loss
Uses of loop diuretics
APO, CHF, liver cirrhosis, renal failure, hypertension, in drug overdose, in combination with thiazides or K-sparing diuretics
MOA of thiazide and related diuretics?
increased Na+ excretion 5-10%, increased K+ excretion, decreased Ca2+ excretion
ADRs of thiazides and related diuretics?
hypokalaemia, hyperuricaemia, hypomagnesaemia, hypercholesterolaemia, hyperglycaemia, acid-base imbalance, erectile dysfunction, digoxin toxicity increased
K+ sparing diuretic drug groups?
aldosterone antagonists and Na+ channel blockers, act on late distal tubule and collecting ducts
MOA of aldosterone antagonists (spironolactone)
inhibit 3Na+/2K+ exchanger on basolateral membrane and luminal membrane Na+ channel
uses of aldosterone antagonists (like spironolactone)
with thiazides and loop diuretics to produce diuresis without hypokalaemia, used in conditions associated with hyperaldosteronism/Cushing's, improves survival in CHF
MOA of Na+ channel blockers (amiloride)
blocks Na+ channel on luminal membrane
Uses of Na+ channel blockers (amiloride)
to spare K+ in the absence of aldosterone, used with thiazide and loop diuretics