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32 Cards in this Set
- Front
- Back
Acetazolamide
Dorzolamide |
Diuretic
CA Inhibitor (everywhere) - Decrease bicarbonate reabsorption - Less Na+ recovery (diuresis) - Produce alkaline urine - Produce acidotic blood |
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1) What are the CA Inhibitor diuretics?
2) Where do they work? 3) What are they indicated for? 4) What are adverse effects? |
1) Acetazolamide and Dorzolamide
2) PT 3) Glaucoma, urine alkalization for elimination of toxic/lipid soluble weak acids 4) Metabolic acidosis, elevated renal pH, renal stones Also used for Altitude sickness (stimulates hyperventilation from metabolic acidosis) |
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Furosemide (Lasix)
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Diuretic
Loop Diuretic - Sulfonamide - Used when rapid volume depletion needed (e.g. acute pulmonary edema) - Major side effects (e.g. Hypo- magnesium, calcium, kalemia, chloride) |
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Bumetanide
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Diuretic
Loop Diuretic - Sulfonamide |
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Torsemide
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Diuretic
Loop Diuretic - Sulfonamide |
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Ethacrynic Acid
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Diuretic
Loop Diuretic - NOT Sulfonamide |
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1) What is the MOA of Loop Diuretics?
2) Where specifically do they work? 3) What are Loop Diuretics indicated in? 4) What are the side effects of Loop Diuretics? |
1) Inhibit Na,K,Cl cotransporter (this site is responsible for recovering 30% of filtered Na+)
Also lose Ca, Mg, HOH 2) TAL - thick ascending limb 3) Acute pulmonary edema, CHF, HTN, refractory edemas, Hypercalcemia <---** 4) Hypokalemia (Alkalosis) Hypovolumia-->thirst-->hyponatremia HYPERuricemia HYPERglycemia Ototoxicity (Ethacrynic acid) Sulfa Sensitivity (Other 3) High-Ceiling Diuretics (POWERFUL) |
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Chlorothiazide (Diuril)
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Diuretic
Thiazide |
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Hydrochlorothiazide (HCTZ)
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Diuretic
Thiazide |
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Polythiazide
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Diuretic
Thiazide (DCT) |
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Indapamide
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Diuretic
Thiazide PLUS vasodilator (HCTZ is not also vasodilator) |
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Chlorthalidone
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Diuretic
Thiazide |
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Metolazone
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Diuretic
Thiazide |
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Spironolactone
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Diuretic
Potassium-Sparing - Also aldosterone ANT |
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Eplerenone
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Diuretic
Potassium-Sparing |
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Triamterene
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Diuretic
Potassium-Sparing |
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Amiloride
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Diuretic
Potassium-Sparing |
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Mannitol
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Diuretic
Osmotic |
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Vasopressin (ADH)
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Diuretic
ADH Agonist V1 and V2 |
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Desmopressin
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Diuretic
ADH Agonist V2 only |
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Lithium Ion
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Anti-Diuretic
ADH Inhibitors - Blocks V2 mechanism - Li-induced DB insipidus is treated w/ desmopression |
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1) What drug class / loop diuretic combination can enhance ototoxicity?
2) What drug can enhance hypokalemia if taken w/ Loop Diuretics? |
1) Aminoglycosides and the non-sulfa loop diuretic, ethacrynic acid
2) Digoxin - hypokalemia |
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1) What are the sulfonamides?
2) What Sulfa antibiotics can these drugs cross-react with? 3) What class of diuretic can cross react with the sulfonamide drugs? |
1) Furosemide, bumetanide, torsemide (loop diuretics)
2) Sulfamethoxazole 3) Thiazides (DCT): HCTZ, Indapamide |
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1) What are symptoms of sulfonamide hypersensitivity?
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1) Skin Reactions: hive, photo sensitivity, Stevens-Johnson syndrome (painful rash on mucuous membranes and all over body)
- Hepatitis, kidney failure - Reduced WBC, RBC, Platelets |
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1) What are the thiazides?
2) What is the MOA? 3) What is retained (vs. other diuretics)? |
1) Thiazides: HCTZ, Indapamide, others
2) They work on the DCT. - Inhibit the Na+Cl- cotransporter 3) Ca2+ is retained |
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1) What are thiazides indicated in?
2) What are side effects of thiazides? |
1) CHF, HTN, Nephrogenic DB insipidus (direct stimulus of ADH site)
- Reduces Ca2+ stone formation 2) Hypokalemia / Alkalosis Hyperuricemia Hypercalcemia (<-- ONLY DIFF IN SIDE EFFECTS FROM LOOPS) Hyperglycemia Sulfa Sensitivity |
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1) What drug is used when RAA is high? What class of diuretic is it?
2) What are other classes of K+ sparring diuretics? |
1) Spironolactone: CT, K+ sparing (is an aldosterone ANT)
2) Amiloride and Triamterene |
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1) Describe why loop and thiazide (DCT) may result in hyperuricemia?
2) Describe why some loop diuretics result in hyperglycemia? 3) How does the hypovolemia and hyponatremia occur? |
1) Loop Diuretics / Thiazides are weak acids --> compete for oraganic acid excretion sites in PT --> uric acid buildup
(uric has to compete w/ diuretics, lactate, etc) 2) Hypokalemia -->less K+ for beta cell K+ current -->steeper gradient (faster current)-->less insulin release 3) During Na+ and water loss, compensatory mechanisms kick in (ADH, etc); pt wants water-->unrestricted water intake leads to acute dilutional hyponatremia (CNS, ventricular arrhythmias, convulsions) |
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1) Which K+ sparring diuretic is used specifically against high aldosterone?
2) How does it do this? 3) What are some possible side effects? |
1) Spironolactone
2) Aldosterone receptor competitive ANT (Anti-HTN, Anti-CHF) 3) Hyperkalemia, acidosis (DIFFERENT FROM OTHERS) |
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1) What K+ sparring diuretics are Na+ transport blockers?
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1) Amiloride, Tramterene
Usually combined w/ thiazides or loops to neutralize K+ loss |
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1) What is the major osmotic diuretic?
2) How does it work? 3) What is it indicated in? |
1) Mannitol
2) filtered, not reabsorbed 3) edema, glaucoma, to make nephrotoxic drugs readily excretable |
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1) Why is desmopressin and not vasopressin indicated in neurogenic diabetes insipidus?
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1) Vasopressin acts at V1 AND V2 receptors, producing vasoconstriction and increased BP (V1) and water retention (V2); Desmopressin only works at V2
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