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63 Cards in this Set

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