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Cardiopulm/Renal Exam 2 > Diuretic Drugs > Flashcards

Diuretic Drugs Flashcards

1
Q

Where do Carbonic Anhydrase Inhibiters exert their effects?

A

Proximal tubule

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2
Q

Where do Osmotic Diuretics exert their effects?

A

Proximal tubule and Thin descending limb of Henle

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3
Q

Where do Loop Diuretics exert their effects?

A

Thick Ascending limb of Henle

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4
Q

Where do Thiazide Diuretics exert their effects?

A

Distal Convoluted Tubule

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5
Q

Where do Na+ channel blockers and Spironolactone exert their effects?

A

Cortical collecting duct

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6
Q

Where do Vaptans exert their effect?

A

Collecting Duct

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7
Q

Furosemide: MOA

A
  • In the TAL, it blocks the Na+-K+-2Cl- cotransporter

- Indirectly inhibits reabsorption of Ca2+ and Mg2+

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8
Q

Furosemide: Effects

None emphasized

A

Causes increased excretion of water, sodium, potassium, chloride, magnesium, and calcium

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9
Q

Furosemide: Clinical Applications

A
  • Management of edema
  • Acute pulmonary edema by decreasing preload
    • Decreases EC volume
    • Rapid dyspnea
  • Treatment of hypertension (that is unresponsive to other diuretics)
  • Also works in patients with low GFR and low RBF
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10
Q

Furosemide: Toxicities

A

• hypokalemia
• hyponatremia
• hypocalcemia (increases kidney stone risk)… Opposite of thiazides
• hypomagnesemia
• hypochloremic metabolic alkalosis
• hyperglycemia
• hyperuricemia (increases risk of gout)
• increased cholesterol and triglycerides (increases atherosclerosis risk)
• ototoxicity: vertigo, hearing impairment, tinnitus
- Dangerous to use during pregnancy (crosses placenta)
• sulfonamide, so risk of hypersensitivity

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11
Q

sulfonamide similar to furosemide with longer t1/2, better oral absorption and some evidence that it works better in heart failure

A

torsemide

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12
Q

sulfonamide similar to furosemide, but more predictable oral absorption

A

bumetanide

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13
Q

non-sulfonamide loop diuretic reserved for those with sulfa allergy

A

ethacrynic acid ****

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14
Q

Furosemide: Drug Interactions

A
  • Digoxin
  • Ototoxic drugs
  • Potassium-sparing diuretics - can counterbalance potassium-wasting effects
  • Can also increase lithium toxicity, potentiate effects of other antihypertensive agents and have diuretic effects antagonized by NSAIDs
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15
Q

Hydrochlorothiazide: MOA

A

Blockade of Na+-Cl- cotransporter in the distal tubule

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16
Q

Hydrochlorothiazide: Effects

A

K+ losing

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17
Q

Hydrochlorothiazide: Clinical Applications

A

• Management of mild-to-moderate hypertension, alone or in combination with other antihypertensive agents
- Not effective in patients with low GFR or low RBF

• Off-Label: Calcium nephrolithiasis (decreases calcium excretion which decreases risk of kidney stones); treats nephrogenic diabetes insipidus

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18
Q

Hydrochlorothiazide: Toxicities

A
  • hypovolemia
  • K+ losing
  • hypokalemia
  • hypomagnesemia ** (may be severe)
  • hyponatremia
  • hypochloremic metabolic alkalosis **
  • sulfonamide drug, so hypersensitivity reactions possible
  • increase plasma glucose, urate (risk of gout), and lipid levels
  • Avoid starting during pregnancy
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19
Q

Hydrochlorothiazide: Pharmacokinetics (None emphasized)

A

Well absorbed via oral administration

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20
Q

Similar to HCTZ, but poor oral absorption

A

chlorothiazide

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21
Q

similar to HCTZ, but half-life of 40-60 hrs… prolonged/stable response with proven benefits, often preferred by hypertension specialists

A

chlorthalidone

22
Q

Another long-acting thiazide diuretic, this is a favorite of cardiologists for use as an adjunct diuretic in the treatment of congestive heart failure

A

metolazone

23
Q

Hydrochlorothiazide: Drug Interactions

A
  • often combined with antihypertensive medications from other drug classes to potentiate the blood pressure lowering effects
  • K+ loss can be offset by combining with K+-sparing diuretics
  • Increases risk of digoxin and lithium toxicity
24
Q

Amiloride: MOA

A

Blocks epithelial sodium channels (E Na C) in the collecting ducts (and adjacent upstream nephron region known as the “connecting tubule”) responsible for Na+-K+ exchange

  • so it increases urinary Na+ excretion and decreases urinary K+ excretion
25
Q

Amiloride: Clinical Applications

A
  • Counteracts K+ loss

* Used to treat hypertension and edema, often in combination with a loop or thiazide diuretic

26
Q

Amiloride: Pharmacokinetics

A

since channel is blocked directly, effects are seen more rapidly than with spironolactone (e.g., <2 hrs) but smaller and therefore harder to detect, last 12- 16 hrs

27
Q

Amiloride: Toxicities

A
  • hyperkalemia

* nausea, vomiting, leg cramps, and dizziness are common; blood dyscrasias are rare

28
Q

used similar to amiloride for edema and off-label for hypertension, rapidly absorbed, duration of action 6-9 hrs, eliminated as drug metabolites

A

triamterene

29
Q

Spironolactone: MOA

A
  • competitive antagonist of aldosterone receptors
  • leads to increased sodium excretion and decreased potassium excretion
  • side effects due in part to it being a partial agonist at androgen receptors
30
Q

Spironolactone: Effects

A

K+ sparing diuretic

31
Q

Spironolactone: Clinical Applications

A

• Off-label:
- reduce fibrosis post-MI heart failure

• used to treat hypertension and edema, often in combination with a loop
or thiazide diuretic

  • primary hyperaldosteronism
  • greatly reduces mortality rate in patients with severe heart failure… e.g., decreases myocardial fibrosis, reduces early morning rise in HR
32
Q

Spironolactone: Pharmacokinetics

A
  • can take 48 hours to work
  • steroid hormones produce effects with a slow onset (i.e., takes time for protein synthesis) and slow offset (proteins last for awhile)
33
Q

Spironolactone: Toxicities

A
  • hyperkalemia

* amenorrhea, hirsutism, gynecomastia, impotence, menstrual irregularities, and deepening voice

34
Q

Spironolactone: Drug Interactions

A

• often combined with thiazide and loop diuretics to counteract their
potassium loss **

• should “never” be given with drugs that increase plasma potassium levels… but still used cautiously with ACE inhibitors in heart failure

35
Q

Vapatans: MOA

A

vaptans

block the antidiuretic hormone receptor in the collecting duct

36
Q

more selective aldosterone antagonist (also lacks sulfur), approved for use in post-MI heart failure and alone or in combination for treatment of hypertension; less gynecomastia, etc. … but ~10x more expensive than generic spironolactone

A

eplerenone

37
Q

Conivaptan: MOA

A
  • non-peptide arginine
    vasopressin receptor antagonist
  • prevents ADH-mediated insertion of the aquaporin water channels into luminal membrane of principal cells in collecting duct
  • Prevents the reabsorption of water, therefore increases water excretion
  • Decreased plasma volume and increased plasma osmolality, primarily due to an increase in plasma sodium concentration
38
Q

Conivaptan: Effects

A

promotes the

excretion of free water

39
Q

Conivaptan: Clinical Applications

A

• Treatment of euvolemic and hypervolemic hyponatremia in patients who are…

  • hospitalized
  • symptomatic
  • not responsive to fluid restriction

• Monitor closely plasma sodium and neurological status
- too rapid serum sodium correction (>12 mEq/L/24 hours) can lead to seizures, osmotic demyelination, coma, or death

• autosomal dominant polycystic kidney disease (slow progression)

40
Q

Conivaptan: Pharmacokinetics

A
  • Administered IV

* conivaptan not available, t1/2 of 5.3 – 8.1 hrs

41
Q

Conivaptan: Toxicities

A

– orthostatic hypotension
– fatigue
– thirst
– polyuria, bedwetting

42
Q

Conivaptan: Drug Interactions

A
  • metabolized by CYP3A4, so inhibitors and inducers of this enzyme can alter its half-life and potential for toxicity
  • selective water loss means:
  • possibility of hypovolemia
  • other electrolytes and drugs can become concentrated… e.g., hypernatremia, hyperkalemia, hyperuricemia
  • toxic levels of drugs
43
Q

selective V2 receptor antagonist administered orally…
• initiate and reinitiate tolvaptan in patients only in a hospital where plasma sodium can be closely monitored

•must use < 30 days for hyponatremia, longer use can lead to potentially fatal hepatotoxicity
- used to slow progression of adult polycystic kidney disease (must monitor liver)

A

tolvaptan

44
Q

Carbonic Anhydrase Inhibitors (Acetazolamide): MOA

A
  • bicarbonate ion remains in early proximal tubule
  • H+ cycling lost, inhibiting Na+ /H+ exchange

• pharmacological effect
- sodium bicarbonate
diuresis
- hyperchloremic acidosis

45
Q

Carbonic Anhydrase Inhibitors (Acetazolamide): Therapeutic Uses

A 
These are now quite limited 
• urinary alkalinization
• metabolic alkalosis
• glaucoma: acetazolamide, dorzalamide 
• acute mountain sickness
46
Q

Carbonic Anhydrase Inhibitors (Acetazolamide): Adverse Effects

A
  • hyperchloremic metabolic acidosis
  • nephrolithiasis: renal stones
  • potassium wasting
47
Q

Mannitol: MOA

A

– the inability to reabsorb this solute keeps water in the proximal tubule lumen; this water is delivered to the distal portions of the nephron where much of it is ultimately excreted

– mannitol acts throughout the body to PULL WATER OUT OF THE CELLS

– the net effect after administering mannitol is to EXCRETE TOTAL BODY WATER IN EXCESS OF PLASMA ELECTROLYTES

48
Q

Mannitol: Pharmacokinetics

A

– distributes in extracellular fluid, must give IV in large amounts sufficient
to raise its osmolality (e.g., 50-200 grams over 24 hours)

– effects are noticeable within 30–60 minutes, and mannitol is eliminated unchanged in the urine over a period of 6-8 hours

49
Q

Mannitol: Adverse Effects

A

– extracellular volume is acutely increased because mannitol sucks water out of the cells, which can exacerbate heart failure

– headache, nausea, vomiting, and fluid and electrolyte imbalances also occur

50
Q

Mannitol: Therapeutic Uses

A

– PROPHYLAXIS OF RENAL FAILURE, keeps some fluid volume in the tubules to prevent them from collapsing when the glomerular filtration rate is very low

– REDUCTION OF INTRACRANIAL PRESSURE

– REDUCTION OF INTRAOCULAR PRESSURE (treating glaucoma) when patients haven’t responded to other therapy

51
Q

Alternative Medicine?

A

• herbal diuretics

• licorice (contains GLYCYRRHIZIC ACID)
- potentiates aldosterone effects in kidney and dose-dependently increases systolic blood pressure (~3-14 mm Hg)

Cardiopulm/Renal Exam 2 (3 decks)

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