Flashcards in Diuretics DSA I Deck (43)
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1
topical ophthalmic CAIs
brinzolamide
dorzolamide
2
diuretics
increase sodium excretion and amount of urine produced by kidney
3
diuretic
increases urine volume
4
natriuretic
increased renal sodium excretion
5
K in proximal tubule
paracellular pathway
6
HCO3 reabsorption in PCT
initiated by action of Na/H exchanger
-luminal membrane of proximal tubule epithelial cell
membrane and cytoplasm carbonic anhydrase catalyze
> H2CO3 to CO2 and H2O at luminal membrane
> and CO2 and H2O H2CO3 in cytoplasm
7
straight segment of proximal tubule
acid secretory systems
-organic acids to lumen from blood
8
thin descending loop
water reabsorption
9
thin ascending loop
water and ion/solute impermeable
10
thick ascending limb
Na/K/2Cl cotransporter
NKCC2 or NK2Cl
dilutes luminal fluid
11
thick ascending loop potassium?
increased K in cell - back diffusion of K out of cell
-lumen positive charge - drive reabsorption of Mg and Ca
-paracellular pathway
12
distal convoluted tubule
Na/Cl cotransporter
calcium channels (regulated by PTH)
13
diuretic induced changes in K
occur in collecting tubule
14
ENaC
Na channels in collecting tubule
-more Na to CT > more K out of cell > hypokalemia
15
aldosterone
increases ENaC and Na/K ATPase
-more Na reabsorption and K secretion
16
ADH
aquaporins to apical membrane in collecting tubule
-V2 receotpr
regulated by serum osmolality and volume status
17
alcohol
decreased ADH release and increases urine production
18
CAI pharmacy
-oral administration
-secreted prox tubule (dosing change renal insufficiency)
-no first pass
-carbonic anhydrase (-) and NHE3 (-)
-45% bicarb reabsorption inhibited > acidosis (30 mins)
-decreased efficiency after multiple days of use
19
CAI toxicity
-metabolic acidosis and bicarbonatirua
-renal stones - calcium salts insoluble basic pH
-hypokalemia
-drowsiness and parasthesias
-sulfa allergy
20
CAI contraindications
-cirrhosis - decreased urine pH - less ammonia released-
>hyperammonemia and hepatic encephalopathy
-hyperchloremic acidosis or COPD
>worsen metabolic or respiratory acidosis
21
CAI clinical use
-rarely as diuretics
-glaucoma - reduces aqueous humor formation
> decreased IOP
>topical formulations
-also used for urinary alkalinization, metabolic alkalosis, acute mountain sickness, epilepsy
22
loop diuretic pharmacy
-oral administration
-eliminated by kidney - flitration/secretion
-half life correlates with secretion (act luminal side)
-coadmin with acids - reduced activity (same secretion)
23
loop diuretic mechanism
(-) Na/K/2Cl cotransporter
-block Na, K, Cl, Mg, Ca transport
-induce prostaglandin synthesis
-increased K excretion
24
loop diuretic toxicity
-overuse - hyponatremia, reduced GFR, circ collapse, thrombohemolysis, hepatic encephalopathy
-hypokalemic metabolic alkalosis (K and H loss)
-precipitate gout attacks (hyperuricemia)
-hearing loss (ototoxicity)
-sulfa allery (furosemide, bumetanide, torsemide)
-hypomagnesemia
25
sulfa loop diuretics
furosemide, bumetanide, torsemide
-cause sulfa allergies
26
contraindications for loop diuretics
-sulfa allergy
-hepatic cirrhosis, renal failure, heart failure
-postmenopause osteopenia - hypocalcemia
-aminoglycoside interaction
-lithium interaction
-digoxin interaction
27
loop diuretic drug interactions
aminoglycoside - ototoxicity
lithium
digoxin
28
loop diuretics clinical use
-edematous states
-HTN and heart failure
-mild hyperkalemia
-ARF
-anion overdose - bromide fluoride, iodide
-hypercalcemic states
29
thiazide diuretics pharmacy
-oral admin
-secreted in PCT (competes uric acid)
-enhanced Ca reabsorpion (PCT volume contraction/DCT enhanced Na/Ca basolateral exchange)
-weak CAI
30
