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diuretics
drugs and review of nephron
| Question | Answer |
|---|---|
| define diuretics | increase water and solute excretion in urine |
| define naturetics | increase excretion of sodium in urine |
| define diuresis | increase urine flow rate |
| what is secretion? | movement of substance from blood(interstitium) to tubule lumen |
| what is reabsorption? | movement of substances from tubule lumen into blood(interstitium) |
| what is the equation to determine excretion? | excretion=filtration across glomeruli+ secretion into tubule-reabsorption from tubule |
| what is RBF? | renal blood flow; 25% of CO; ~1200 ml/min |
| what is RPF? | renal plasma flow; 50% of RBF; ~660 ml/min |
| what is GFR? | volume of filtrate formed each min by ~2 million glomeruli(1 million per kidney); 125 ml/min |
| what is the renal clearance of a substance? | volume of plasma that is completely cleared of a substance by the kidneys in a given unit of time (L/min) |
| what is creatinine clearance used for? | used to estimate the GFR; ages 30-39(males 59-137;females 71-121); ages 70-79(males 49-79;females 37-61); creatinine is cleared from blood almost entirely by glomeruli filtration |
| what is the defintion of an osmotic pressure of a solute? | it is the amount of pressure that must be applied to a semipermeable membrane to stop osmosis of water |
| what are the percentages of sodium and water reabsorption in the nephron? | PCT (Na: 67%, water: 65%), thin descending (water:15%), thick ascending (Na: 25%), DCT & collecting tubule (Na: 8%, water: 20%) |
| On the nephron, where do carbonic anhydrase inhibitors work? | early PCT |
| On the nephron, where do thiazides/thiazide-like work? | primary: early DCT,bind to Cl site of Na/Cl pump -> decrease Na reabsorption; secondary: PCT,bind Cl site on Na/Cl pump |
| On the nephron, where do osmotic agents work? | primary:descending limb, secondary:PCT, tertiary: DCT & collecting duct |
| On the nephron, where do the loop agents work? | ascending loop -> inhibit Na/K/2Cl cotransporter -> increase delivery of Na and Cl to DCT where the extra ions are NOT reabsorbed |
| On the nephron, where do the aldosterone antagonists work? | collecting duct -> inhibit Na and water reaborption; peak effect is seen 2-3 days due to time required to metabolize to active metabolite |
| On the nephron, where do the ADH agonists work? | collecting duct -> agonist of V2 receptors; 4000 times that of ADH;increase plasma levels of factor VIII |
| On the nephron, where do the Na channel blockers work? | late DCT & collecting duct -> block Na channels of lumen cell -> reduces negative charge on apical membrane -> less diffusion of K into lumen |
| What is the MOA of osmotic diuretics? | descending limb: hypotonic interstitium reduces reabsorption of water from descending limb; PCT: increased osmotic pressure within lumen opposes water reabsorption, DCT & collecting duct: inhibit action of ADH, cannot reabsorb increased Na and water load |
| What are the indications of osmotic diuretics? | closed(narrow) angle glaucoma(reduce IOP prior to surgery),reduced intracranial pressure assoc. head trauma, hemorrhage, or cerebral mass; prevent/treat acute renal failure when GFR is greatly reduced; edema; not reliable |
| What are ADRs, precaution, and contraindications assoc. with osmotic diuretics? | worsening of CHF & pulmonary edema, hyponatremia, seizures; precautions: excessive & rapid diuresis may exacerbate preexisting hyponatremia & hypovolemia; contraindications: severe dehydration, CHF, pulmonary congestion |
| What is the MOA of carbonic anhydrase inhibitors? | inhibit carbonic anhydrase at apical and interior of PCT cell; inhibit Na/H exchange pump due to reduced amount of H in lumen cell, limited diuretic effect since increased luminal Na is reabsorbed "downstream" |
| What are the indications of CA inhibitors? | edema, metabolic alkalosis assoc. with heart failure & excessive use of diuretics; epilepsy; alkalanize urine; open-angle glaucoma; closed-angle glaucoma; acute mtn. sickness |
| What are the ADR's and precautions of CA inhibitors? | metabolic acidosis due to reduced HCO3 in blood, hypokalemia, aplastic anemia & thrombocytopenia (both limit use of drugs); precautions: cross-sensitivity with sulfonamide antibiotics & thiazide diuretics |
| what are some of the CA inhibitors? | acetazolamide (diamox), dichlorphenamide (daranide), methazolamide (neptazone) |
| what are some of the osmotic diuretics? | glycerol (osmoglyn), mannitol (osmitrol) |
| what are the thiazide diuretics? | hydrochlorothiazide (HCTZ, hydrodiuril, esidrex, microzide), chlorothiazide (diuril), methyclothiazide (diuretic), polythiazide (renese) |
| what are the thiazide-like diuretics? | chlorthalidone (hygroton), indapamide (lozol, lozide), metolazone (zaroxolyn), quinethazone (hydromox) |
| what are the indications of thiazide diuretics? | mild/moderate hypertension with normal renal function (except indapamide & metolazone); edema of mild & severe CHF; edema of hepatic necrosis, renal failure, & drug-induced edema; hypercalcuria; diabetes insipidus |
| what are the ADR's, precautions, contraindications of thiazide diuretics? | hyperuricemia -> gouty arthritis; hypokalemia; hypercalcemia; hyperglycemia; hyponatremia; skin photosensitivity; impotence; precautions: diabetes/pre-diabetes; contraindicated: sulfonamide allergy |
| what do thiazide diuretics interact with? | oral hypoglycemics; digitalis; NSAIDs |
| what are the loop diuretics? | furosemide(lasix), bumetanide(bumex), torsemide(demadex), ethacrynic acid(edecrin) |
| what is the "ceiling effect" seen with loop diuretics? | diuretics secreted into PCT must reach a threshold concentration to produce diuresis; further increases in concentration will not result in enhanced diuresis |
| what is post-diuretic Na retention? | due to the short half-life of a dose interval may not maintain the adequate concentration of diuretic in lumen of ascending limb -> previously blocked nephrons reabsorb large amount of Na -> reduces affect of loop diuretic |
| what are the indications of loop diuretics? | CHF, pulmonary edema, renal failure, liver cirrhosis, hypercalcemia, hypertension in patients with reduced renal function (<30ml/min) |
| what are the ADR's with loop diuretics? | ADR's: hypokalemia, hyponatremia, hypocalcemia, hypomagnesemia, orthostatic hypotension, ototoxicity, dehydration |
| what are the warnings assoc. with loop diuretics? | warnings: may cause hyperkalemia(patients with renal impairment, diabetes and the elderly are at greatest risk therefore serum K levels must be monitored frequently); potent diuretics, excess amounts can lead to profound diuresis |
| what are the contraindications and drug interactions assoc. with loop diuretics? | drug interactions: aminoglycosides & other ototoxic drugs, NSAIDs, digitalis, thiazide diuretics; contraindicated: severe electrolyte depletion, anuria |
| what are the potassium sparing(antikaliuretic diuretics)? | Na channel blockers:triamterene,triamterene/HCTZ,amiloride,amiloride/HCTZ; aldosterone receptor antagonists:spironolactone,spironolactone/HCTZ,eplerenone |
| what is the rationale for combination of potassium sparing diuretics and HCTZ? | obtain effect in patients who cannot risk hypokalemia(hisotry of arrhythmia, concomitant digitalis) |
| what is the MOA of potassium sparing diuretics Na channel blockers? | effects the late DCT plus collecting ducts; blocks Na channel of lumen cell -> reduces negative charge at apical membrane -> less diffusion of K into lumen; minor effect on water and Na reabsorption |
| what are the indications for potassium sparing diuretics Na channel blockers? | hypertension in patients with normal renal function(rarely used as monotherapy); edema; hypokalemia assoc with thiazide, loop, or CA inhibitor diuretics |
| what is the black box warning assoc with potassium sparing diuretics Na channel blockers? | hyperkalemia in patients with renal impairment, diabetes, elderly, and severely ill; serum potassium levels must be monitored frequently |
| what are the ADR's of potassium sparing diuretics Na channel blockers? | hyperkalemia; metabolic acidosis; photosensitivity |
| what are the contraindications of potassium sparing diuretics Na channel blockers? | prior or existing hyperkalemia; other potassium sparing diuretics; potassium-rich diet |
| what is the MOA of potassium-sparing diuretics aldosterone receptor antagonists? | aldosterone receptor is blocked in collecting duct -> inhibit Na and water reabsorption; spironolactone is prodrug must be converted to canrenone (active metabolite) -> 2-3 days to peak effect |
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rustie32384
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