How do you classify diuretics?



Diuretics vivaHow do you classify diuretics?Osmotic diuretics eg mannitolCarbonic anhydrase inhibitors eg acetazolamideLoop diuretics eg frusemideThiazide diuretics eg hydrochlorothiazide, indapamidePotassium sparing eg amiloride, spironolactoneADH inhibitors eg demeclocycline (act in collecting tubule)Dopamine receptor agonists eg dopamineDraw a nephron and show me where each of these agents work?How does each work?osmotic diuretics:freely filtered but not reabsorbed and excreted unchanged with an osmotic equivalent of waterthe high flow of tubular fluid and increased osmotic load washes out the medullary concentrating gradientcarbonic anhydrase inhibitorsnon-competitive inhibitor of carbonic anhydrase, decreases supply of carbonic acid, decreased H+ secretion, therefore decreased sodium and bicarb reabsorptionloop diureticsblock Na/K/Cl channel, prevent action of counter current multiplier, decreased ability to concentrate urineincreased Na load to distal tubule, so increased exchange and loss of K and H+also induces renal prostaglandin synthesis resulting in renal vasodilation and increased renal blood flow (dilation precedes onset of diuresis)thiazide diureticsinhibit Na/Cl cotransporter on luminal membraneincreased Na load in distal tubule, stimulates Na exchange with K and Hpotassium sparingcompetitive antagonism of aldosterone, increased Na excretion and decreased K secretion and H+ secretion acts on basolateral surface, takes 2-4 days to workamiloride blocks luminal Na channel produced by aldosteroneADH antagonists – self explanatoryDopamineStimulated D1 receptors (Gs) resulting in renal vasodilation and increased renal blood flow and GFR, inhibit sodium reabsorptionD2 receptors inhibit noradrenaline release from postganglionic sympathetic nerve endingsWhich is the most potent?Loop diuretics.What are some adverse effects of loop diuretics? Interactions?Adverse effectsDehydration, hypotensionhyponatraemia, hypokalaemia, hypochloraemiahypercalciuria, hypocalcaemia, nephrocalcinosismetabolic alkalosishyperuracaemia, exacerbations of gout rashGI disturbanceototoxicitynephrotoxicityInteractionsaminoglycosides: possible nephro and ototoxicity with high dosesbilirubin: displace each other from plasma protein bindingACEi: increased risk renal impairment in setting of renal artery stenosisCeftazidime: increases ceftaz levelsDigoxin: monitor K+ and dig levelsHydrocortisone: hypokalaemiaNon-depolarising NMBD: increased muscle blockadePhenytoin: decrease in frusemide effectLithium levels may rise when given with frusemideTell me about the pharmacology of frusemide.P’ceutsulfonamide diureticpresented as tablets or clear, colourless solutiondose: dependent on renal function, prior exposure and indication, can be between 20-300mg, repeated every 4-6hrs, or can be given as infusion: start at 0.1mg/kg/hr and increase until desired urine output achievedindications: fluid overload (iatrogenic, CCF, renal failure), chronic lung diseaseMOA: loop diureticPKA: oral bioavailability 50%, rapidly absorbed from gutD: 99% plasma protein boundM: half life 100 mins, mostly excreted unchangedE: predominantly renal excretion unchangedPDCVSProblems associated with fluid/electrolyte loss: postural hyptension Arteriolar vasodilation, decreased SVR, reduced preload and afterloadRenalDiuresisIncreased renal blood flowbiochemicalElectrolyte disturbance and acid base disturbances as aboveMetabolicHyperglycaemia (but less common than with thiazides)Adverse/interactions as above ................
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