Diuretics

Question 1

MOA furosemide

Answer 1

blocks Na-K-2Cl cotransporter in thick ascending limb, directly inhibiting reabsorption of Na+ and Cl-

Question 2

spironolactone effects

Answer 2

K+ sparing diuretic

• blunts ability of aldosterone to promote Na+/k+ exchange

Question 3

spironolactone MOA

Answer 3

competitive antagonist of aldosterone receptors

Question 4

spironolactone clinical app

Answer 4

• counteracts K+ loss induced by other diuretics
• tx of primary aldosteronism

Question 5

toxicities of spironolactone

Answer 5

• hyperkalemia
• amenorrhea, hirsutism, gynecomastia, impotence

Question 6

furosemide effects

Answer 6

increased excretion of water, sodium, potassium, chloride, magnesium, Ca2+

Question 7

furosemide clinical app

Answer 7

• manages edema
• decreases preload
• rapid dyspnea relief
• HTN
• ACUTE DECOMPENSATED HEART FAILURE

Question 8

toxicities of furosemide

Answer 8

• hypokalemia
• hyponatremia
• hypocalcemia
• hypomagnesemia
• hyperglycemia
• hyperuricemia
• ***it’s a sulfa drug so watch for allergies

Question 9

hydrochlorothiazide MOA

Answer 9

blocks Na/Cl cotransporter in distal convoluted tubule

Question 10

hydrochlorothiazide effects

Answer 10

increases urinary excretion of sodium and water, potassium, and magnesium

Question 11

hydrochlorothiazide clinical app

Answer 11

• HTN
• edema

Question 12

toxicities of hydrochlorothiazide

Answer 12

• orthostatic hypotension
• hypokalemia
• hypomagnesemia
• hyponatremia
• hypochloric metabolic alkalosis

Question 13

compare torsemide with furosemide

Answer 13

longer half life, better oral absorption, works better in heart failure

Question 14

compare bumetanide with furosemide

Answer 14

more predictable oral absorption

Question 15

when would you use ethacrynic acid instead of furosemide

Answer 15

non-sulfonamide loop diuretic reserved for those with sulfa allergies

Question 16

MOA amiloride

Answer 16

blocks epithelial sodium channels (ENaC) in collecting ducts

Question 17

effects amiloride

Answer 17

• causes small increase in Na+ excretion
• blocks major pathway for K+ elimination so K+ is retained (K+ sparing)
• H+, Mg2+, and Ca2+ excretion decreased

Question 18

clinical app amiloride

Answer 18

counteracts K+ loss induced by other diuretics in tx of HTN or HF

Question 19

half life and administration amiloride

Answer 19

given orally

half life 6-9 hours

Question 20

toxicities amiloride

Answer 20

hyperkalemia

• hyponatremia
• hypovolemia
• hyperchloremic metabolic acidosis
• dizziness, fatigue, HA
• n/v/d

Question 21

MOA triamterene

Answer 21

similar to amiloride (K+ sparing diuretic)

Question 22

MOA eplerenone

Answer 22

aldosterone receptor antagonist

(more selective aldosterone antagonist than spironolactone)

Question 23

clinical app eplerenone

Answer 23

approved for use in post-MI HF and alone or in combo for tx of HTN

Question 24

MOA conivaptan

Answer 24

non-peptide arginine casopressin receptor antagonist

affinity for V1A and V2 receptors

Question 25

effects conivaptan

Answer 25

promotes excretion of free water (without loss of serum electrolytes) - increases urine output - decreases urinary osmolality - increases plasma osmolality

Question 26

clinicap app conivaptan

Answer 26

tx of euvolemic and hypervolemic hyponatremia in pts who are hospitalized, symptomatic, and not responsive to fluid restriction

Question 27

problems with too rapid serum Na+ correction when using conivaptan

Answer 27

can lead to seizures, osmotic demyelination, coma, or death

Question 28

administration of conivaptan

Answer 28

IV

Question 29

toxicities conivaptan

Answer 29

- orthostatic hypotension - fatigue - thirst - polyuria, bedwetting

Question 30

MOA tolvaptan

Answer 30

V2 receptor antagonist

Question 31

what patients do you give tolvaptan to

Answer 31

only patients in a hostpial where plasma sodium can be closely monitored

Question 32

how long do you treat with tolvaptan

Answer 32

less than 30 days for hyponatremia because longer use can cause potentially fatal hepatotoxicity

Question 33

clinical app tolvaptan

Answer 33

tx for hyponatremia used to slow progression of adult PKD

Question 34

mannitol MOA

Answer 34

osmotic diuretic - it is unabled to be reabsorbed --\> keeps water in the PCT lumen --\> water is delivered to the distal portions of the nephron --\> much of it is ultimately excreted - acts throughout body to pull water out of cells

Question 35

adverse effects mannitol

Answer 35

ECF volume acutely increased --\> exacerbates HF HA, nausea, vomiting, electrolyte imbalances

Question 36

therapeutic uses of mannitol

Answer 36

prophylaxis of renal failure reduction of intracranial and intraocular pressure

Question 37

MOA acetazolamide

Answer 37

carbonic anhydrase inhibitor bicarbonate ion remains in PCT --\> H+ cycling is lost --\> inhibits Na+/H+ exchange --\> **Na+ bicarbonate diuresis**

Question 38

therapeutic uses carbonic anhydrase inhibitors

Answer 38

urinary alkalinization metabolic alkalosis glaucoma acute mountain sickness

Question 39

adverse effects acetazolamide

Answer 39

hyperchloremic metabolic acidosis nephrolithiasis potassium wasting

Question 40

MOA and therapeutic use metolazone

Answer 40

thiazide diuretic used as adjunct diuretic in tx of CHF

Question 41

MOA and therapeutic uses chlorthalidone

Answer 41

thiazide diuretic often preferred by hypertension specialists