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37 Cards in this Set

  • Front
  • Back
PT diuretics mOA
CA inhibitors
CA inhibitors
Acetazolamide
dichlorphenamide
methazolamide
methazolamide
SEs
Met acid (loss hco3)
renal stones (incr pH)
hypokalemia (upsteam of CD thus when lots of na arrives will crazy exchange for K)
encephalopathy- nh3 reabsorbed easier)
methazolamide
uses
= PT CA inhibitor
glaucoma (CA inc aqueous hum)
epilepsy
produce met. acid (altitude)
prod. alk urine (excr. weak acids)
TAL diuretics mOA
Na/K/cl symport inh.
TAL Diur. named
furosemide
bumetamide
Ethacrynic Acid
Torsemide
Lasix =
Furosemide
effect of NKCC2 inh
usually most K recycles back through ROMK thus creating the + lumenal charge alowing mg,ca,na to come in paracellularly. inhibition abolishes this as well as na reabsorption bigtime
Loop diuretics effect on blood electrolytes
pH ?
dec K,Na,Ca,Mg in blood

High [na] arriving in CT drives high na/K exchange
(K loss)but high []in lumen
which drives high k/H
(H secretion) equals
Met. ALKALOSIS
Loop Diur
SEs
HYpovolemia
HYpo-kal/calc/magnes-emia
met Alkalosis
ototoxicity-NKCC1 inner ear
hyperglycemia (and lipids)
hyperuricemia (OAT scene)
ca stones
loop diuretics
uses
HTN- not 1st choice
but PGs help
DOC in acute severe
pulm/syst edema
hypercalcemia, drug OD
Hyponatremia ( with hypertonic saline post abolishing kidneys ability to dilute & CONCENTRATE urine)
DCT diuretics mOA
and class
Na/Cl symporter Inh.(NCC)
= thiazides and Thia-like
DCT diuretics Named and prototype
all end in Thiazide
Hydrochlorothiazide is the Prototype
Thiazide like diuretics
Chlorthalidone
Metholazone
Indapamide
Thiazides effect on E-lytes

ph
dec na,k,
increase Ca
inc na/k exchange then k/H exchange with H secretion
= met. ALKALOSIS
HYdroclorothiazide
SEs
Hypokalemia
Metabolic alkalosis
Hyperuricemia (OAT)
inc glucose/lipids
HYPERCALCEMIA (oppos of loops
vol depletion
hyponatremia (more than LOOP)
sex dysfun
Thiazides uses
mild/mod edema
idiopathic hyperCalcURIA (stones)
dec Ca loss in osteoporosis
HTN--------DOC often combo
Nephrogenic Dia INsipidus (paradoxical-create hyperosmotic urine)
Collecting Tubule Diuretics
mOA
Na Channel Inhibitors (ENAC)
&
Aldo Receptor Antagonists
(the K sparing)
K sparing Diuretics
types
Na Channel (ENAC)Inhibitors (CD)
&
Aldo Receptor Antagonists
Na Channel Inhibitors (ENAC)
&
Aldo Receptor Antagonists
named
Na Channel Inhibitors-
amiloride, triamterene
Aldo Receptor Antagonists-
Spironolactone, Epleronone (SARA)
Triamterene mOA
ENAC inhibitor in DCT
thus K sparing
amiloride mOA
ENAC inhibitor in DCT
thus K sparing
ENAC inhibitors
USES
Amiloride,Triamterene

Mild edema and combo with K wasting diuretics
Enac role in K secretion
na/k pumps keeps intra Na down
Na enters ENAC in DCT depolarizing apical membrane and activating the ROMK k secreting channel. Thus coupling na absorption and K secretion in the DCT.
Thus Enac inhibitors ANd SARA's abolish this and spare K
ENAC inhibitors
SE
Amiloride,Triamterene

hyperkalemia
met ACIDOSIS (Na absorption in the DCT drives Acid Secretion)
Renal Stones (esp TRiam)
Amiloride,Triamterene

USes
Enac Inh.( K spare)

weak diur, adjunct to K wasting
Aldo Rec Antagonists

SE
Spirono, Eplero

Hyperkalemia
Met ACIDosis (enac drives H+ secretion in DCT)
Spironolactone -gynecomastia impotence
SARA uses
adjunct to k wasting

Hyperaldosteronism

ESPECIALLY in Hep Cirrhosis
Probenecid and Diuretics
Prob inh OAT thus decreasing delivery of diuretics to the ductular LUmen
NSAIDS and Diuretics
inh. PGs = Dec. diuretic response
Aminoglycosides and Diuretics
with LOOP diuretic (REMEmBER NKCC) = increased OTOtoxicity
Diuretics and DIGitalis
Watch K wasting = Dig toxicity
K sparing watch out for
ACEI contribute to hyperKalemia
OSMOTIC DIUretics
Named
Mannitol and Urea (IV)
Glycerin and ISosorbide (Oral)
OSMOTIC DIUretics
uses
Maintain urine Flow in ACUTE Renal failure (plus flush casts)

Draw fluid out of eyes and BRAIN

Restore Osmolality in DIALYSIS DISEQU. SYND.
ADH R antagonists
named
Conivaptan
Tolvaptan
Vaptan uses
Conivaptan,Tolvaptan
cause aquaresis in
hypervol. hyponatremia