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RENAL II Exam 3 > Diuretics DSA I > Flashcards

Diuretics DSA I Flashcards

1
Q

topical ophthalmic CAIs

A

brinzolamide

dorzolamide

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2
Q

diuretics

A

increase sodium excretion and amount of urine produced by kidney

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3
Q

diuretic

A

increases urine volume

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4
Q

natriuretic

A

increased renal sodium excretion

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5
Q

K in proximal tubule

A

paracellular pathway

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6
Q

HCO3 reabsorption in PCT

A

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

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7
Q

straight segment of proximal tubule

A

acid secretory systems

-organic acids to lumen from blood

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8
Q

thin descending loop

A

water reabsorption

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9
Q

thin ascending loop

A

water and ion/solute impermeable

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10
Q

thick ascending limb

A

Na/K/2Cl cotransporter

NKCC2 or NK2Cl

dilutes luminal fluid

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11
Q

thick ascending loop potassium?

A

increased K in cell - back diffusion of K out of cell

  • lumen positive charge - drive reabsorption of Mg and Ca
  • paracellular pathway
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12
Q

distal convoluted tubule

A 
Na/Cl cotransporter
calcium channels (regulated by PTH)
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13
Q

diuretic induced changes in K

A

occur in collecting tubule

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14
Q

ENaC

A

Na channels in collecting tubule

-more Na to CT > more K out of cell > hypokalemia

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15
Q

aldosterone

A

increases ENaC and Na/K ATPase

-more Na reabsorption and K secretion

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16
Q

ADH

A

aquaporins to apical membrane in collecting tubule
-V2 receotpr

regulated by serum osmolality and volume status

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17
Q

alcohol

A

decreased ADH release and increases urine production

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18
Q

CAI pharmacy

A
  • 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
Q

CAI toxicity

A
  • metabolic acidosis and bicarbonatirua
  • renal stones - calcium salts insoluble basic pH
  • hypokalemia
  • drowsiness and parasthesias
  • sulfa allergy
20
Q

CAI contraindications

A

-cirrhosis - decreased urine pH - less ammonia released-
>hyperammonemia and hepatic encephalopathy

-hyperchloremic acidosis or COPD
>worsen metabolic or respiratory acidosis

21
Q

CAI clinical use

A

-rarely as diuretics
-glaucoma - reduces aqueous humor formation
> decreased IOP
>topical formulations

-also used for urinary alkalinization, metabolic alkalosis, acute mountain sickness, epilepsy

22
Q

loop diuretic pharmacy

A
  • oral administration
  • eliminated by kidney - flitration/secretion
  • half life correlates with secretion (act luminal side)
  • coadmin with acids - reduced activity (same secretion)
23
Q

loop diuretic mechanism

A

(-) Na/K/2Cl cotransporter

  • block Na, K, Cl, Mg, Ca transport
  • induce prostaglandin synthesis
  • increased K excretion
24
Q

loop diuretic toxicity

A
  • 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
Q

sulfa loop diuretics

A

furosemide, bumetanide, torsemide

-cause sulfa allergies

26
Q

contraindications for loop diuretics

A
  • sulfa allergy
  • hepatic cirrhosis, renal failure, heart failure
  • postmenopause osteopenia - hypocalcemia
  • aminoglycoside interaction
  • lithium interaction
  • digoxin interaction
27
Q

loop diuretic drug interactions

A

aminoglycoside - ototoxicity
lithium
digoxin

28
Q

loop diuretics clinical use

A
  • edematous states
  • HTN and heart failure
  • mild hyperkalemia
  • ARF
  • anion overdose - bromide fluoride, iodide
  • hypercalcemic states
29
Q

thiazide diuretics pharmacy

A
  • oral admin
  • secreted in PCT (competes uric acid)
  • enhanced Ca reabsorpion (PCT volume contraction/DCT enhanced Na/Ca basolateral exchange)
  • weak CAI
30
Q

chlorothiazide

A

not lipid soluble - given IV

31
Q

chlorthalidone

A

long acting thiazide diuretic

-T1/2 - 47 hours

32
Q

thiazide diuretic toxicity

A

hypokalemic metabolic acidosis and hyperuricemia

  • decrease glucose tolerance - hyperglycemia (impaired insulin release from pancreas)
  • hyperlipidemia
  • hyponatremia
  • weak, fatigable, paresthesia, impotence
  • sulfa allergy
33
Q

contraindiciations for thiazide diuretics

A
  • diabetics
  • efficacy reduced when NSAIDs and COX-2 inhibitors co-administered
  • hepatic cirrhosis, renal failure, heart failure
34
Q

thiazide diuretic clinical use

A
  • HTN and heart failure
  • nephrolithiasis (due to hypercalciuria)
  • diabetes insipidus
35
Q

HCTZ in diabetes insipidus

A

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
Q

K-sparing - MR antagonists pharmacy

A

spironolactone and eplerenone

  • oral admin
  • first pass effect
  • eplerenone - greater affinity for MR
37
Q

K-sparing - Na channel inhibitor pharmacy

A

amiloride and triamterene

  • oral admin
  • triamterene - first pass (give more than amiloride)
  • amiloride - no first pass
38
Q

K-sparing MR antagonist mechanism

A

competitive (-) of aldosterone binding to MR

  • decreased ENaC and Na/K ATPase activity
  • reduced Na reabsorption in collecting tubule
  • reduced K secretion**
39
Q

only diuretics not requiring access to lumen

A

MR antagonists - K sparing

40
Q

K-sparing ENaC (-)

A

block ENaC in collecting tubule

-reduced K secretion**

41
Q

K-sparing toxicity

A

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
Q

K-sparing contraindications

A

chronic renal insufficiency

  • use with NSAIDs, beta-blockers, ACE (-), ARB
  • liver disease
  • strong (-) of CYP3A4 - increased levels of eplerenone
43
Q

K-sparing clinical use

A

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

RENAL II Exam 3 (17 decks)

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