Diuretics Flashcards

1
Q

what are the loop diuretics

A

furosemide and torsemide

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2
Q

how do the loop diuretics work

A

-inhibit Na/K/2Cl (cotransporter) pump in the thick ascending loop hence inhibiting the reabsorption of NaCl

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3
Q

why are loop diuretics called high ceiling diuretics

A

they are the most efficacious diuretic agent available since thick ascending loop has a large absorptive capacity and no other part of the nephron after it has the same ability

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4
Q

in the presence of loop diuretics, what is occurring with the other ions located in the distal portion of the nephron

A
  • due to inhibition of reabsorption of NaCl, the lumen positive potential created by reabsorption of the K+ (Na/K/Cl pump) is diminished; this potential drives the reabsorption of Mg2+ and Ca2+ so without it, more of these ions are excreted
  • also in distal tubule there is an increased exchange of Na+ for K+ so increased excretion of K+ will lead to hypokalemia
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5
Q

what are loop diuretics used to treat

A
  • management of edema associated with heart failure and hepatic or renal disease
  • acute pulmonary edema
  • hypertension (though not first line for this)
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6
Q

adverse effects of loop diuretics

A

OH DANG!
Ototoxicity (tinnitus, hearing impairment, etc)
Hypokalemia (cardiac arrhythmias)
Dehydration (acute hypovolemia due to hyponatremia –> hypotension)
Allergy to sulfa
Nephritis (intersitial)
Gout (due to hyperuricemia)

also hypomagnesia and hypocalcemia

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7
Q

what are the thiazides

A

Chlorthalidone, Hydrochlorothiazide, Metolazone

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8
Q

how do thiazides work

A

they inhibit NaCl reabsorption in the distal convoluted tubule by blocking the Na/Cl cotransporter

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9
Q

in the presence of thiazides, what is going on with the other ions in the nephron

A
  • increased excretion of K+ from the distal tubule
  • increased reabsorption of Ca2+
  • mild magnesuria (don’t know why)
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10
Q

what are thiazides used to treat

A
  • mild to moderate hypertension
  • edema from heart failure
  • hypercalcuria (help with kidney stones)
  • nephrogenic diabetes insipidus
  • osteoporosis (hypercalcemia effect)
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11
Q

how long does it take for thiazides to work

A

1-3 weeks since their half life is about 40 hours

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12
Q

adverse effects of thiazides

A
HyperGLUCS
hyperGlycemia
hyperLipidemia
hyperUricemia
hyperCalcemia
hyperSensitivity (sulfa allergy)

HypoKNT
hypoKalemia
hypoNatremia
hypoTension (orthostatic hypotension)

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13
Q

what are the potassium sparing drugs

A
potassium SEAT
Spironolactone
Eplerenone
Amiloride
Triameterene
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14
Q

how would you further classify the potassium sparing drugs

A

spironolactONE and eplerenONE are aldosterONE antagonist

amiloride and triameteren act at same part of the tubule as the above but they block the Na+ channels in the cortical collecting tubule

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15
Q

what spironolactone and eplerenone used to treat

A
  • edema in those with excessive aldosterone excretion or CHF
  • hypertension
  • primary hyperaldosteronism
  • hypokalemia
  • cirrhosis of liver accompanied with edema/ascited
  • nephrotic syndrome
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16
Q

off label use of spironolactone

A

female acne and hirsutism

17
Q

spironolactone has an affinity to what other receptors not including aldosterone hence leading to what issues

A

progesterone and androgen receptors antagonist leading to gynecomastia, impotence, and menstrual irregularities

18
Q

adverse effects of spironolactone and eplerenone

A

spironolactone - gastric upset and peptic ulcers, endocrine effects (gynecomastia, impotence, decreased libido etc), hyperkalemia, metabolic acidosis (H+ excreted in parallel with K+), CNS effects

eplerenone - GI upset and hyperkalemia

19
Q

potassium sparing diuretic (those in the aldosterone antagonist class) are contraindicated in who?

A

those who are hyperkalemia
those who are at risk for developing hyperkalemia like those with chronic kidney disease, on other K+ sparing diuretics, ACE inhibitors, ARBs)

20
Q

why are amiloride and triamterene usually given

A

for their antikaliuretic effects to offset effects of other diuretics that increase K+ excretion

inhibit ENAC in late distal tubules

21
Q

advantage of amiloride and triamterene in comparison to spironolactone and eplerenone

A

they do not depend on aldosterone to exert their effects of being an antikaliuretic

22
Q

what is triamterene and amiloride metabolized by

A

triamterene is metabolized by the liver before being excreted by the kidney while amiloride is excreted as an intact drug

23
Q

adverse effects of triamterene and amiloride

A

hyperkalemia and hyponatremia

triamterene –> glucose intolerance, renal stones, interstitial nephritis, photosensitivity

TRIAMTERENE GRIP

24
Q

what is the carbonic anhydrase inhibitor

A

acetazolamide

25
Q

what does carbonic anhydrase do

A

reduction of absorption of HCO3- in proximal convoluted tubule hence decreasing the amount of sodium absorbed there (but it increases the amount of sodium absorbed in the rest of the nephron so not really efficient)

26
Q

uses of carbonic anhydrase inhibitor

A

not usually used for its diuretic property since it is not very efficient at that

Glaucoma (decreases formation of aqueous humor)
Mountain Sickness (blood becomes more acid due to excretion of bicarb hence more blood stimulates more ventilation and increased O2 in the blood)
Metabolic Alkalosis
Epilepsy

27
Q

when is dosing of acetazolamide reduced

A

in renal insufficiency since it is excreted unchanged in the proximal tubule

28
Q

adverse effects of acetazolamide

A

metabolic acidosis, hyponatremia, hypokalemia, renal stones, sulfa allergy, paresthesia, malaise, fatigue, depression

29
Q

what is an osmotic diuretic

A

mannitol

30
Q

what do osmotic diuretics do

A

expand extracellular fluid volume, decrease blood viscosity, inhibit renin release, and urinary excretion of almost all electrolytes

31
Q

what is mannitol used for

A
  • reduction of increased intracranial pressure associated with edema
  • reduction of increased intraocular pressure
  • promotion of urinary excretion of toxic substances
  • genitourinary irrigant in transurethral prostatic resection or other transurethral surgical procedures
32
Q

adverse effects of mannitol

A

extracellular volume expansion and hyponatremia

tissue dehydration

33
Q

what type of people is mannitol contraindicated in

A

those with active cranial bleeding

34
Q

what is an ADH antagonist

A

conivaptan

35
Q

who is conivaptan given to

A
  • euvolemic and hypervolemic hyponatremia in hospitalized patients
  • SIADH patient
  • heart failure pts when benefit is greater than risk
36
Q

adverse effects of conivaptan

A

nephrogenic DI (due to hypernatremia)
infusion site reactions
atrial fibrillations, GI, and electrolyte disturbances

37
Q

who is conivaptan contraindicated in

A

hypovolemic hyponatremia

renal failure

38
Q

what does conivaptan inhibit

A

CYP 3A4 inhibitor