Diuretics DSA I Flashcards Preview

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Flashcards in Diuretics DSA I Deck (43):
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

chlorothiazide

not lipid soluble - given IV

31

chlorthalidone

long acting thiazide diuretic
-T1/2 - 47 hours

32

thiazide diuretic toxicity

hypokalemic metabolic acidosis and hyperuricemia
-decrease glucose tolerance - hyperglycemia (impaired insulin release from pancreas)
-hyperlipidemia
-hyponatremia
-weak, fatigable, paresthesia, impotence
-sulfa allergy

33

contraindiciations for thiazide diuretics

-diabetics
-efficacy reduced when NSAIDs and COX-2 inhibitors co-administered
-hepatic cirrhosis, renal failure, heart failure

34

thiazide diuretic clinical use

-HTN and heart failure
-nephrolithiasis (due to hypercalciuria)
-diabetes insipidus

35

HCTZ in diabetes insipidus

nephrogenic
-inhibits Na/Cl tranport in DCT
> increased diuresis and reduce ECF volume
> decreased GFR
> tubuloglomerular feedback
> less sodium and water to collecting duct (decrease urine output)

36

K-sparing - MR antagonists pharmacy

spironolactone and eplerenone
-oral admin
-first pass effect
-eplerenone - greater affinity for MR

37

K-sparing - Na channel inhibitor pharmacy

amiloride and triamterene
-oral admin
-triamterene - first pass (give more than amiloride)
-amiloride - no first pass

38

K-sparing MR antagonist mechanism

competitive (-) of aldosterone binding to MR
-decreased ENaC and Na/K ATPase activity
-reduced Na reabsorption in collecting tubule
-reduced K secretion****

39

only diuretics not requiring access to lumen

MR antagonists - K sparing

40

K-sparing ENaC (-)

block ENaC in collecting tubule
-reduced K secretion****

41

K-sparing toxicity

hyperkalemia - increased w/ renal disease, RAAS (-), or when combined with other K-sparing diuretics

-metabolic acidosis
-gynecomastia, impotence, BPH (bc MR antagonists are steroids)
-triamterene > kidney stones with indomethacin

42

K-sparing contraindications

chronic renal insufficiency
-use with NSAIDs, beta-blockers, ACE (-), ARB
-liver disease
-strong (-) of CYP3A4 - increased levels of eplerenone

43

K-sparing clinical use

hyperaldosteronism
-Conn's syndrome, heart failure, hepatic cirrhosis, nephritic

-thiazides and loop diuretics can cause secondary hyperaldosteronism (use K-sparing to stop this)

MR antagonists - heart failure