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63 Cards in this Set
- Front
- Back
Name the carbonic anyhydrase inhibitors
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Acetazolamide and Dorzolamide
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Name the thiazides and congeners
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Hydrochlorothiazide and Indapamide
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Name the loop diuretics
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Furosemide and Ethacrynic acid
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Name the K sparing diuretics
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Triamterene, amiloride, and spirinolactone
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Name the osmotic diuretics
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Mannitol
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Name the ADH antagonists
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Conivaptan
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S.O.A/M.O.A of carbonic anhydrase inhibitors
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Proximal Tubule, inhibits NaHCO3 reabsorption
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S.O.A/M.O.A of loop diuretics
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TAL of Henle Loop, block the Na/K/Cl symport
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SOA/MOA of thiazides
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EDT, block the Na/Cl symport
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SOA/MOA of K sparing diuretics
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LDT, CCT, blocks Na channels and blocks aldosterone receptors
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SOA/MOA of osmotic diuretics
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TDL of Henle Loop and prox tubule, increases osmolarity of tubular fluid
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Carbonic Anhydrase Inhibitors MOA
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inhibits membrane bound CA in cells of prox tubule
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Renal effects of Carbonic anhydrase inhibitors
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metabolic acidosis because hyperchloremia
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Other effects of carbonic anhydrase
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block CA in ciliary body(decreases production of aqueous humor)
-block CA in choroid plexus, decreases prodn of csf |
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A/Es of carbonic anhydrase inhibitors
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paresthesias, **SULFA type allergic rxns
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therapeutic uses of carbonic anhydrase inhibitors
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open angle glaucoma, acute mountain sickness, edema from heart failure, epilepsy
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what are all thiazide and congeners
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sulfonamides
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what are thiazides MOA
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inhibit Na/Cl cotransporter on luminal surface of early DCT
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with the exception of indapamide and metolazone, what value of GFR does the diuretic effect of thiazides disappear?
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less than 30 ml/min
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what affect do thiazides have on vasculature?
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arteriolar vasodilation
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A/Es of thiazides
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hypokalemia, hyperuricemia, sexual dysfunction,
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therapeutic uses of thiazides
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HTN(first choice diuretics), edema associated with heart, liver, kidney, ascites,
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which of the loop diuretics are sulfonamides
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furosemide, bumetanide, torsemide
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MOA of loops diuretics
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inhibits Na/K/Cl of TAL leads to decreased lumen positive potentially, decreased hypertonicity of medulla therefore decreased ability of kidney to concentrate the urine, and inhibition of mac densa sensitivity
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does the diuretic effect of loop diuretics remain when GRR less than 30 ml/min?
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yes
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what are the vascular effects of loop diuretics
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vasodilation in venous bed
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A/E of loop diuretics
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tinnitus, hearing loss, SULFA rxn
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therapeutic uses of loop diuretics
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acute pulmonary edema, heart failure, edema assoc with chronic renal failure or nephrotic syndrome, ascites, HTN
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what can be used with loops to increase effectiveness when loop alone not working
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thiazide
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which of the K sparing diuretics is a steroid?
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spironolactone
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what is the MOA of spironolactone?
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blocks aldosterone receptors in late distal tubule and cortical collecting tubules
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what is the MOA of triamterene and amiloride?
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directly block Na channels in luminal membrane of late distal tubule and cortical collecting tubule
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A/E of all K sparing
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hyperkalemia
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A/E of spironolactone
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sexual dysfunction
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A/E of loop diuretics
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tinnitus, hearing loss, SULFA rxn
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C/I of all K sparing diuretics
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beta blockers and ACEI
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therapeutic uses of loop diuretics
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acute pulmonary edema, heart failure, edema assoc with chronic renal failure or nephrotic syndrome, ascites, HTN
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therapeutic uses of spironolactone
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primary hyperaldosteronism(adrenal adenoma, adrenal hyperplasia), secondary hyperaldosteronism(hepatic cirrhosis, CHF), heart failure
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what can be used with loops to increase effectiveness when loop alone not working
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thiazide
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which of the K sparing diuretics is a steroid?
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spironolactone
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what is the MOA of spironolactone?
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blocks aldosterone receptors in late distal tubule and cortical collecting tubules
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what is the MOA of triamterene and amiloride?
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directly block Na channels in luminal membrane of late distal tubule and cortical collecting tubule
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A/E of all K sparing
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hyperkalemia
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A/E of spironolactone
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sexual dysfunction
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C/I of all K sparing diuretics
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beta blockers and ACEI
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therapeutic uses of spironolactone
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primary hyperaldosteronism(adrenal adenoma, adrenal hyperplasia), secondary hyperaldosteronism(hepatic cirrhosis, CHF), heart failure
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Therapeutic uses of amiloride
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lithium induced nephrogenic diabetes insipidus
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therapeutic uses of K sparing
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treatment and prevention of hypokalemic states with therapy with loop diuretics and thiazides
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MOA of osmotic diuretics
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limit water reabsorption in thin descending limb and prox tubule
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A/E of osmotic diuretics
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extracellular volume contraction with high doses when kidney normal(hypovolemia, dehydration), extracellular volume expansion in pts with cardiac or renal disease which can cause hypervolemia
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C/I of osmotic diuretics
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severe renal failure, heart failure, pulm edema, severe dehydration
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therapeutic uses of osmotic diuretics
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reduce cerebral edema pre/post surgery, reduce intraocular pressure in acute angle closure glaucoma, reduce intraocular pressure before and after iridotomy
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MOA of ADH antagonists
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antagonists at vasopressin receptors, conivaptan at v1a and v2, and tolvaptan at v2
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what is conivaptan a strong inhibitor of
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cyp34a
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therapeutic uses of ADH antagonists
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SIADH
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what is the value for hypokalemia
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less than 3.5mEq/L
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what are some causes of hypokalemia
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excess renal loss, GI losses, ecf to icf shifts, insufficient intake, drugs
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S/S of hypokalemia
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skeletal muscle weakness, flaccid muscle paralysis, resp failure, disturbances in cardiac repol
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treatment of hypokalemia
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potassium chloride orally or IV
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what is the value of hyperkalemia
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greater than 5.3mEq/L
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causes of hyperkalemia
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diminished renal excretion, transcellular shift, increase in intake, drugs
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s/s of hyperkalemia
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disturbances in cardiac excitability and conduction, flaccid paralysis
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treatment of hyperkalemia
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insulin and glucose, calcium gluconate
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