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Renal > Diuretics + B&B > Flashcards

Diuretics + B&B Flashcards

1
Q

what kind of drug is acetazolamide and what is its mechanism of action? (renal)

A

acetazolamide: carbonic anhydrase inhibitor in PCT —> blocks HCO3- reabsorption and inhibits ability of NHE exchanger to reabsorb Na+ (relies on H+ from CA reaction)

also recall acetazolamide can be used to treat acute mountain sickness

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2
Q

what is the effect of caffeine on renal function?

A

caffeine: adenosine A1 receptor antagonist —> diuresis

adenosine A1 receptor enhances Na+/H2O reabsorption in PCT and activates tubuloglomerular feedback (TGF) to induce vasoconstriction and decrease GFR

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3
Q

what toxicities are associated with carbonic anhydrase inhibitors such as acetazolamide, dorzolamide, and brinzolamide? (one of them is an acid-base disorder!)

A

(side effects uncommon)

  • hyperchloremic metabolic acidosis (due to bicarb loss)
  • allergic reactions, skin toxicity (due to sulfonamide groups)
  • drowsiness, paresthesias
  • calcium kidney stones (due to reduced urinary citrate excretion)

*avoid in patients with hepatic cirrhosis (because of decreased NH4+ excretion)

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4
Q

what is the use of topical carbonic anhydrase inhibitors such as dorzolamide and brinzolamide?

A

useful for ocular glaucoma via decreased production of aqueous humor

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5
Q

what effect does mannitol have on the kidneys?

A

mannitol: osmotic diuretic, increase water excretion in PCT and descending limb of loop of Henle (where cells are freely permeable to water)

also promotes removal of renal toxins (such as after use of radiocontrast agents)

basically, mannitol increases the osmolarity in the tubule lumen, but doesn’t get reabsorbed, so it pulls more water out

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6
Q

what are the therapeutic uses of mannitol? considering this, what are the associated toxicities?

A

mannitol: osmotic diuretic, increases extracellular volume by pulling water out of cells - can be used to reduce intracranial/ocular pressures (cerebral edema, glaucoma)

toxicity: disruption of sodium balance via extracellular volume expansion and diuresis - can complicate CHF or cause headache, N/V

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7
Q

what kind of drug is furosemide and what is its mechanism of action?

A

furosemide: loop diuretic, blocks NKCC (Na/K/Cl cotransporter)

—> blocks tubuloglomerular feedback by inhibit Na+ transport to the macula densa
—> induces PGE2 synthesis by increasing COX-2 expression, increasing renal blood flow

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8
Q

explain why loop diuretics such as furosemide, ethacrynic acid, and bumetanide cause an increase in Mg2+ and Ca2+ excretion

A

loop diuretics block NKCC in the thick ascending limb (TAL) —> disrupts negative lumen potential, leading to lumen positive electro-potential

positive potential drives excretion of Mg2+ and Ca2+ (it’s a charge thing)

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9
Q

which renal transporters are blocked by loop diuretics such as furosemide, ethacrynic acid, and bumetanide?

A

blocks NKCC (Na/K/Cl cotransporter) in thick ascending limb (TAL)

—> blocks tubuloglomerular feedback by inhibit Na+ transport to the macula densa

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10
Q

explain why NSAIDs interfere with the function of loop diuretics such as furosemide, ethacrynic acid, and bumetanide?

A

loop diuretics block NKCC in TAL, but also induce synthesis of renal prostaglandins (PGE2) by increasing expression of COX-2 —> increasing renal blood flow

recall NSAIDs inhibit COX-2 —> can interfere with loop diuretics

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11
Q

what type of acid-base disorder can be caused by loop diuretics such as furosemide, ethacrynic acid, and bumetanide?

A

loop dietetics: block NKCC in TAL

can cause hypokalemic metabolic alkalosis via decreased ECF which concentrates HCO3- (“contraction alkalosis”)

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12
Q

what is the mechanism of action of thiazide diuretics such as hydrochlorothiazide, indapamide, chlorthalidone, and metolazone?

A

thiazide diuretics: block NCC (Na+/Cl- cotransporter) in the DCT

also enhance Ca2+ reabsorption

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13
Q

what are 5 indications of thiazide diuretics such as hydrochlorothiazide, indapamide, chlorthalidone, and metolazone?

A

thiazide diuretics: block NCC (Na+/Cl- cotransporter) in the DCT

  1. HTN
  2. heart failure
  3. osteoporosis
  4. nephrolithiasis due to idiopathic hypercalciuria
  5. nephrogenic diabetes insipidus (ADH insensitivity) - reduce plasma volume to lower GFR, which enhances proximal reabsorption of NaCl/H2O, decreasing delivery of fluid to collection ducts
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14
Q

what are the toxicities associated with thiazide diuretics such as hydrochlorothiazide, indapamide, chlorthalidone, and metolazone? (5)

A

thiazide diuretics: block NCC (Na+/Cl- cotransporter) in the DCT

  1. hypokalemic metabolic alkalosis and hyperuricemia
  2. impaired carbohydrate tolerance
  3. hyperlipidemia
  4. hyponatremia
  5. allergic reactions (thiazides are sulfonamides)
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15
Q

what is the mechanism behind K+ wasting dietetics? (why is K+ lost)

A

collecting duct is major site of K+ secretion, via principal cells and aldosterone secretion

diuretics that act upstream of collecting tubule will increase Na+ to collecting duct, enhancing K+ secretion

diuretic-mediated volume depletion will also enhance aldosterone secretion, further enhancing K+ secretion

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16
Q

what kind of drugs are spironolactone, eplerenone, amiloride, and triamterene?

A

potassium-sparing diuretics

spironolactone and eplerenone: competitive antagonists of aldosterone receptor

amiloride and triamterene: block ENaC Na+ channel in apical cells of collecting tubule

17
Q

what is the mechanism of action of amiloride and triamterene?

A

potassium-sparing diuretics, block ENaC Na+ channels in collecting tubule

18
Q

amiloride can be used to treat HTN in patients with ______, characterized by GOF mutation in ENaC Na+ channel

A

amiloride - blocks ENaC Na+ channel, can be used to treat HTN in Liddle’s syndrome (GOF ENaC mutation)

19
Q

what are the toxicities and contraindications associated with K+ sparing diuretics such as spironolactone (aldosterone antagonist) and amiloride (blocks ENaC)?

A

toxicities:
- hyperkalemia (esp. in patients with renal disease or drugs that inhibit RAAS system)
- hyperchloremic metabolic acidosis (via inhibiting H+ secretion)

contraindications: patients with chronic renal insufficiency

20
Q

what kind of drugs are conivaptan, lixivaptan, and tolvaptan? what is their clinical indication?

A

“vaptan” = ADH receptor antagonist

used for treatment of euvolemic hyponatremia (like SIADH)

conivaptan: IV, non-selective (V1 and V2 receptors)
lixivaptan, tolvaptan: oral, selective for V2

21
Q

what is the therapeutic use of lithium and demeclocycline?

A

non-selective ADH antagonists (bind V1 and V2)

used to treat SIADH or other causes of elevated ADH

22
Q

demeclocycline

A

non-selective ADH antagonists (bind V1 and V2)

used to treat SIADH or other causes of elevated ADH

23
Q

what major toxicities (2) are associated with ADH antagonists such as conivaptan, lithium, and demeclocycline?

A
  1. nephrogenic diabetes insipidus* - ADH antagonists can cause severe hypernatremia
  2. renal failure (lithium, demeclocycline - limited therapeutic use)

*recall nephrogenic DI can be treated with thiazide diuretics or amiloride

24
Q

what are the clinical uses of carbonic anydrase inhibitors such as acetazolamide? (4)

A
  1. severe metabolic alkalosis - causes metabolic acidosis due to HCO3- loss
  2. glaucoma - blocks formation of aqueous humor
  3. pseudotumor cerebri - blocks formation of CSF
  4. prevention of altitude sickness - reverses symptoms of respiratory alkalosis
25
Q

which loop diuretic is NOT a sulfa drug, and therefore can be used in allergic patients?

A

ethacrynic acid

26
Q

what toxicities are associated with loop diuretics such as furosemide, bumetanide, torsemide, and ethacrynic acid? (3)

A
  1. ototoxicity - tinnitus, hearing loss, usually reversible
  2. acute interstitial nephritis - elevated BUN/Cr, WBC casts, urine eosinophils
  3. gout - via increased uric acid reabsorption
27
Q

describe the mechanism of “contraction alkalosis” caused by loop diuretics and thiazides

A

diuretics increase urine output, which lowers the ECV —> RAAS is activated, which causes an increase in H+ secretion —> metabolic alkalosis

28
Q

blood levels of which molecules are elevated by thiazide diuretics (hint, there’s an acronym)?

A

HyperGLUC:
Glucose
Lipids
Uric acid
Calcium

29
Q

what are the specific side effects of spironolactone?

A

spironolactone: aldosterone antagonist

similar structure to testosterone (blocks action) —> gynecomastia in males

derivative of progesterone (activates receptors) —> amenorrhea in females

30
Q

which 2 classes of diuretic drugs cause acidosis and why?

A
  1. carbonic anhydrase inhibitors: acidosis via HCO3- excretion
  2. K+ sparing diuretics: acidosis via decrease aldosterone and hyperkalemia (H+/K+ exchanger)
31
Q

what is the effect of loop vs thiazide diuretics on calcium?

A

lOOp diuretics: hypOcalcemia

thiaZides: hYpercalcemia (x, Y, Z)

Renal (28 decks)

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