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Renal Exam > Pharmacology of Diuretics > Flashcards

Pharmacology of Diuretics Flashcards

1
Q

clinical uses of diuretics

A

*edema tx
*HTN tx
*hyperkalemia, hyponatremia, hypercalciuria, hypercalcemia tx
*prevention of stone precipitation in urinary tract
*increase in urine flow to reduce tubular toxicity of a drug or toxin
*tx of chronic hyponatremia in states of inappropriate antidiuretic hormone excretion
*increase urine glucose excretion and lower plasma glucose in type 2 DM

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2
Q

if ion transporters are expressed in other epithelial, why are diuretics relatively selective for the kidneys?

A

*transporters are drug-specific targets, expressed on apical membranes, and level of expression in kidney is high
*drug concentration is higher in the kidney

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3
Q

mannitol (osmotic diuretic) - MOA

A

*inert sugar, filtered but not reabsorbed
*works in PCT & distal loop of Henle
*causes increased serum osmolality → fluid shift from interstitium to intravascular space → increased urine flow (large volume of dilute fluid) and decreased intracranial/intraocular pressure

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4
Q

mannitol (osmotic diuretic) - uses

A

*cerebral edema
*nephroprotective (diluting renal toxins helps to maintain urine flow in AKI)

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5
Q

mannitol (osmotic diuretic) - ADEs

A

*volume overload; worsening of CHF or cause acute pulmonary edema
*volume depletion
*hypernatremia
*tubule toxicity

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6
Q

SGLT2 inhibitors - MOA

A

*inhibits Na+/glucose symporter in PCT
*results in:
-glycosuria: decreases blood sugar, osmotic diuresis
-natriuresis: increases NaCl delivery to macula densa → downregulation of RAAS

recall: “-gliflozins” are SGLT2 inhibitors

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7
Q

SGLT2 inhibitors - examples

A

*canagliflozin
*empagliflozin
*dapagliflozin

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8
Q

SGLT2 inhibitors - uses

A

*adjunct treatment for type 2 DM
*prevents CKD progression
*HF symptoms
*HTN

recall: “-gliflozins” are SGLT2 inhibitors

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9
Q

SGLT2 inhibitors - ADEs

A

*urinary tract infections
*genital infections (fungal)
*volume depletion
*euglycemic DKA (ketoacidosis with normal blood sugar)

recall: “-gliflozins” are SGLT2 inhibitors

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10
Q

acetazolamide - MOA

A

*inhibits carbonic anhydrase enzyme → decreased reabsorption of Na+, H2O, and HCO3- in the PCT → increased excretion of Na+, HCO3-, K+, and Cl-
*alkalinizes urine
*causes mild metabolic acidosis

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11
Q

acetazolamide - uses

A

*increased urine pH
*glaucoma
*treat/prevent high altitude sickness (acclimatization; by offsetting respiratory alkalosis)
*treat METABOLIC ALKALOSIS IN CHF

recall: acetazolamide is a carbonic anhydrase inhibitor

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12
Q

acetazolamide - ADEs

A

*ceiling effect: bicarb can only drop down so much
*allergy
*tolerance
*metabolic acidosis
*slight increased risk for stones

recall: acetazolamide is a carbonic anhydrase inhibitor

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13
Q

secretion of loop and distal diuretics by PCT S3

A

*loop diuretics & distal diuretics are protein-bound, and need to get into the tubule to work
*in S3 segment of proximal tubule, OAT transporter & MDRP secrete diuretics and other drugs into our tubular lumen

*note - some drugs or conditions interfere with the function of OAT transporter (cimetidine, NSAIDs, probenacid, uremia, and CKD)

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14
Q

loop diuretics - examples

A

*FUROSEMIDE
*bumetanide
*torsemide

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15
Q

loop diuretics - MOA

A

*inhibit Na+/K+/2Cl- (NKCC) symporter in thick ascending loop of Henle
*results in increased Na+, Cl-, K+, Ca2+, and Mg+ delivery and excretion
*MOST POTENT AND EFFECTIVE DIURETICS

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16
Q

loop diuretics - uses

A

*edema (pulmonary, systemic)
*heart failure
*hypercalcemia
*hypertension (thiazides are better)

17
Q

loop diuretics - ADEs

A
  1. electrolyte abnormalities:
    -volume depletion, metabolic alkalosis
    -hypokalemia, hypomagnesemia, hypocalcemia, hyponatremia
  2. hyperglycemia, hyperuricemia
  3. allergy (sulfa drug)
  4. ototoxicity: NKCC cotransporters in inner eras
  5. diuretic resistance
18
Q

starting dose of furosemide =

A

*20x creatinine
*the lower the GFR, the higher dose is needed

19
Q

thiazide diuretics - examples

A

*hydrochlorothiazide (HCTZ)
*chlorthalidone
*indapamide
*metolazone

20
Q

thiazide diuretics - MOA

A

*inhibit Na+/Cl- symporter in DCT → increased delivery and excretion of Na+, Cl-, and K+

21
Q

thiazide diuretics - uses

A

*HYPERTENSION
*edema
*prevention of kidney stones
*hypercalciuria

22
Q

thiazide diuretics - ADEs

A

*electrolyte abnormalities:
-volume depletion
-HYPONATREMIA
-hypokalemia
-metabolic alkalosis
*hyperglycemia, hyperuricemia
*allergy

23
Q

hyperuricemia in loop & thiazide diuretics

A

*uric acid is freely filtered but it it both reabsorbed and secreted
*parallel relationship between Na+ and urate reabsorption in proximal tubule

24
Q

HYPERCALCIURIA in loop diuretics

A

*Loops LOSE calcium (increased urinary excretion)
*Ca2+ absorption is dependent on voltage generated by NKCC and K+ backleak
*loop diuretics turn off NKCC → no positive lumen → NO REABSORPTION OF Ca2+ → hypercalciuria

25
Q

decreased calcium excretion (hypercalcemia) in thiazide diuretics

A

*increased reabsorption of Ca2+ with THIAZIDE diuretics due to less NCC action → more calcium reabsorption

26
Q

hypokalemia with loop & thiazide diuretics

A
  1. higher delivery of Na+ and Cl- to distal nephron (principal cell) enhances K+ secretion by DCT2 and CD
  2. volume depletion leads to secondary hyperaldosteronism enhancing K+ secretion by ROMK
27
Q

metabolic alkalosis with loop & thiazide diuretics

A

*diuretics result in increased distal Na+ and Cl- delivery, leading to:
-increased Cl- excretion
-increased K+ excretion
-increased H+ excretion
-decreased ECV
*results in hypokalemic, hypochloremic alkalosis

28
Q

potassium-sparing diuretics - MOA

A
  1. ENaC inhibitors: epithelial Na+ channel inhibitors (amiloride, triamterene)
  2. mineralocorticoid antagonists (spironolactone, eplerenone)

*all work in the late DCT and the cortical collecting duct

29
Q

potassium-sparing diuretics - uses

A

*adjunct agent HTN/edema
*prevent hypokalemia
*refractory edema
*ascites with secondary hyperaldosteronism

30
Q

potassium-sparing diuretics - ADEs

A

*HYPERKALEMIA
*GYNECOMASTIA (from spironolactone)
*volume depletion
*stones (triamterene)

31
Q

aquaretics - MOA

A

*V2 receptor antagonists; inhibit ADH response
*selective WATER DIURESIS without effect on Na+ or K+
*excrete dilute urine
*increase thirst, need to monitor Na+

32
Q

aquaretics - examples

A

*tolvaptan
*satavaptan
*lixivaptan
*conivaptan

33
Q

aquaretics - uses

A

*hyponatremia with SIADH
*cirrhosis with ascites
*CHF
*ADPKD

Renal Exam (44 decks)

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