Diuretics Flashcards

1
Q

Acetazolamide (Diamox) Type& indication

A

Used as a backup diuretic (weak); Glaucoma (reduction of aqueous humor), urinary alkalinization (to treat overdose or some kidney stones), high-altitude sickness.

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2
Q

Acetazolamide (Diamox) site of action

A

PCT, use organic acid transporter to get into lumen, modifies SALT excretion.

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3
Q

Acetazolamide (Diamox) MOA

A

Carbonic anhydrase inhibitor.

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4
Q

Acetazolamide (Diamox) Effects

A

body bicarb is excreted (metabolic acidosis) along with Na. Na/K pump in Collecting Tubule gets extra sodium load and wastes K.

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5
Q

Acetazolamide (Diamox) Route of Admin

A

oral

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6
Q

Acetazolamide (Diamox) Contraindication

A

Cirrhosis–increased urine pH (excretion of bicarb, base) causes less NH3 binding and increases serum NH3

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7
Q

Acetazolamide (Diamox) Adverse Effects

A

metabolic acidosis, hypokalemia, CaP stones (alkalynization of urine), drowsiness, paresthesias and hypersensitivity rxns (allergy and then can’t use similar drugs).

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8
Q

Acetazolamide (Diamox) Notes/Reminder

A

Others we have to know: Dichlorphenamide (30x more potent than aceta); Methazolamide (5x more potent); Dorzolamide (topical for ocular, not systemic absorb)

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9
Q

Acetazolamide (Diamox) Urinary Electrolyte Pattern

A

+NaCl, +++NaHCO3, +K. Alkaline Urine. Alkaline urine can lead cause ppt of Calcium salts and formation of renal stones, also less excretion of ammonia!

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10
Q

Acetazolamide (Diamox) Serum Electrolyte Pattern

A

Acidosis in blood. Hypokalemia. Possible hyperammonemia if pre-existing hepatic issues.

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11
Q

Mannitol Type& indication

A

Osmotic diuretic. Used to maintain or increase urine volume (flush kidney of contrast dye or myoglobinemia, also ACUTE renal failure), reduce ICP (neuro), IOP (glaucoma)

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12
Q

Mannitol site of action

A

filtered at glomerulus, affects salt and water excretion mainly at PCT

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13
Q

Mannitol MOA

A

Osmotic diuretic.

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14
Q

Mannitol Effects

A

volume of urine is increased, will help maintain high urine flow (good if renal blood flow is reduced or overload from hemolysis or rhabdomyolysis). Reduce ICP and IOP.

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15
Q

Mannitol Route of Admin

A

IV

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16
Q

Mannitol PK

A

IV administration causes expansion of IV volume. Powerful diuretic effect in kidney. Is NOT orally absorbed–MUST give IV! Short t1/2!

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17
Q

Mannitol Adverse Effects

A

major toxicity due to increased plasma osmolality. With reduced GFR (CHF or renal failure), mannitol can be retained in ECF where it will draw H2O out of cells–see hyponatremia and pulmonary edema.

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18
Q

Mannitol More notes

A

other drugs classified with Mannitol but rarely used are: Glycerin, Isosorbide and Urea.

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19
Q

Furosemide (Lasix) Type& indication

A

Treatment of severe edematous states like CHF, Ascites, Acute Pulmonary Edema, Severe Hypercalcemia (like in malignancy). Also good for Hypercalcemia.

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20
Q

Furosemide (Lasix) site of action

A

TAL, use organic acid transporter to get into lumen, modifies SALT excretion.

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21
Q

Furosemide (Lasix) MOA

A

inhibits Na/K/Cl- transporter in loop of henle. K+ wasting, Ca wasting, hypokalemia

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22
Q

Furosemide (Lasix) Effects

A

huge diuresis, need to give pt. K+ as well.
Dehydration Hyponatremia
Hypokalemia
Hyperuricemia
Impaired diabetes control
Increased LDL/HDL
Hypomagnesemia Hypocalcemia
Ototoxicity

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23
Q

Furosemide (Lasix) PK

A

Very short 1/2 life–duration of action generally about 4h

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24
Q

Furosemide (Lasix) Contraindication

A

hypocalcemia (will worsen), diabetics (if on sulfonylureas will get hyperglycemic), watch heart patients (interaction w/B-Block, Digoxin and Quinidine), no renal insufficiency (will potentiate hyperkalemia), hyperuricemia (can lead to GOUT)

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25
Q

Furosemide (Lasix) Adverse Effects

A

OTOTOXICITY. Hypokalemic metabolic alkalosis (due to efflux of H+. ) *See note about uric acid handling with thiazides. *note that K-wasters can precipitate hypokalemia which is associated with arrythmias (ectopic pacemakers) and increased AP length can presuppose to EADs. This can mess up digitalis.

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26
Q

Furosemide (Lasix) Drug interactions

A

Aminoglycosides (potentiate oto and nephrotoxicity), Anticoagulants (increased activity, prone to bleeds), B-Blockers (hyperglycemia /lipidemia /uricemia as well as increased levels of propranolol, Digoxin (risk of hypokalemia and increased action), NSAIDS (reduced effect, increased risk of salicylate toxicity), Quinidine (increased risk of torsades de pointes), Steroids (increased risk of hypokalemia)

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27
Q

Furosemide (Lasix) Notes/Reminder

A

Bumetanide (40X more potent, shorter t 1/2), Torsemide (Longer 1/2 life, longer duration, oral absorb), Ethacrynic Acid (last resort, no CA inhibition, can be nephro/oto toxic)

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28
Q

Furosemide (Lasix) More notes

A

Thick ascending limb is impermeable to H20! Note that loop diuretics increase blood sugar if pts on sulfonylureas (problem for diabetics, insulin resistance).

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29
Q

Furosemide (Lasix) Urinary Electrolyte Pattern

A

++++NaCl, ++K, +H Acidotic urine. Increased Ca in urine which can lead to CaP kidney stones.

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30
Q

Furosemide (Lasix) Serum Electrolyte Pattern

A

Alkalosis in blood. Hypokalemia. Decreased Ca/Mg. (Ca is coupled to K+ reabsorption in Loop of Henle).

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31
Q

Hydrochlorothiazide Type& indication

A

Used for HTN, CHF, reduce Ca excretion to prevent kidney stones. Also: Nephrogenic Diabetes Inspidus.

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32
Q

Hydrochlorothiazide site of action

A

DCT, use organic acid transporter to get into lumen, modifies SALT excretion.

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33
Q

Hydrochlorothiazide MOA

A

inhibits Na/Cl cotransporter in distal tubule. Not as strong because most Na has already been pumped. Protective against kidney stones.

34
Q

Hydrochlorothiazide Effects

A

Thiazide, K+ wasting, Ca2+ saver. increase volume of urine moderately. K+ wasting due to increased Na presented to collecting duct. hyperglycemia, increased LDL/HDL, hyponatremia, hypokalemia, hypercalcemia

35
Q

Hydrochlorothiazide Route of Admin

A

oral

36
Q

Hydrochlorothiazide PK

A

good oral absorption and LONG half life, duration of action is 6-12 hours which is much longer than loop diuretics.

37
Q

Hydrochlorothiazide Contraindication

A

hypercalcemia (will worsen), watch heart patients (interaction w/B-Block, Digoxin and Quinidine), no renal insufficiency (will potentiate hyperkalemia), hyperuricemia (can lead to GOUT),

38
Q

Hydrochlorothiazide Adverse Effects

A

Metabolic alkalosis due to efflux of H+. Uric acid handling is mainly in proximal tubule but Thiazide (DCT) and Loop Diuretics (LOH) increase net reabsorption or reduce secretion leading to hyperuricemia in some cases.

39
Q

Hydrochlorothiazide Drug interactions

A

Anticoagulants (decreased activity, prone to clots), B-Blockers (hyper glycemia/lipidemia/uricemia as well as increased levels of propranolol), Carbamazapine/Chlorpropamide (hyponatremia), Digoxin (risk of hypokalemia and increased action), NSAIDS (reduced effect, increased risk of salicylate toxicity), Quinidine (increased risk of torsades de pointes), Steroids (increased risk of hypokalemia)

40
Q

Hydrochlorothiazide Notes/Reminder

A

Cholorothiazide (1/10 the potency), Cholorthalidone (same potent, 1/2 life 44 h) Metolozone (10x more potent), Indapamide (20x more potent),

41
Q

Hydrochlorothiazide More notes

A

Metolozone & Indapamide are the only ones that can be used if GFR is low. Remember Ca mech going on at DCT.

42
Q

Hydrochlorothiazide Urinary Electrolyte Pattern

A

++NaCl, +H+, +K Acidotic Urine. Decreased Ca in urine which is protective against kidney stones.

43
Q

Hydrochlorothiazide Serum Electrolyte Pattern

A

Alkalosis in blood. Hypokalemia. Increased Ca (Na affect on Calcium transporters in DCT)

44
Q

Spironolactone Type& indication

A

Used for primary (Conn’s Syndrome)/secondary hyperaldosteronism, drug of choice for edema assoc w/liver cirrhosis, As a combination therapy for HTN.

45
Q

Spironolactone site of action

A

Aldo-R inhibitor, Collecting Tubule. Gets into cell via basolateral (blood) side-no transporter needed.

46
Q

Spironolactone MOA

A

competitive inhibitor of aldosterone receptor (intra-cytoplasmic R) Anti-androgenic effects as well. (DHT R)

47
Q

Spironolactone Effects

A

K+ sparing diuretic, mild diuresis, interferes directly with action of aldosterone

48
Q

Spironolactone Route of Admin

A

oral

49
Q

Spironolactone PK

A

very SLOW onset (for non-emergent cases), very SLOW offset (24-48h). metabolized in the liver

50
Q

Spironolactone Contraindication

A

hyperkalemia or in patients that can have a state causing hyperkalemia (diabetes, myeloma, renal dx, renal insuff). Or with ACEI’s or ARBS (hyperk risk!)

51
Q

Spironolactone Adverse Effects

A

Hyperkalemic metabolic acidosis (due to sparing of H+.) Gynecomastia, antiandrogenic effects (not w/newer eplerenone)

52
Q

Spironolactone Drug interactions

A

ACE inhibitors/ATII inhibitors (block production of K-waster aldosterone–potentiate hyperkalemia situation), K+ supplements (due to risk of hyperkalemia), NSAIDS (can exacerbate hyperkalemia)

53
Q

Spironolactone Notes/Reminder

A

Eplerenone, a newer one–does not have some of the side effects of Spironolactone.

54
Q

Spironolactone Urinary Electrolyte Pattern

A

+NaCl, -K. Alkalotic urine. Decreased K in urine (interference w/natural site of K wasting, the CCT)

55
Q

Spironolactone Serum Electrolyte Pattern

A

Acidosis in blood. May cause hyperkalemia. Most helpful in combo with a K waster like thiazide.

56
Q

Amiloride Type& indication

A

K+ sparing diuretic, mild diuresis. Used for edema, hypertension. Mainly used in combo with K-wasting diuretics to spare K to treat HTN.

57
Q

Amiloride site of action

A

CCT, use organic base transporter, modifies SALT excretion.

58
Q

Amiloride MOA

A

blocks Na+ channels in the principle cells of collecting duct

59
Q

Amiloride Effects

A

works on the channels that aldosterone promotes in CCT (does not interfere with aldosterone directly though)

60
Q

Amiloride Contraindication

A

hyperkalemia, no ACEI’s or ARBS either.

61
Q

Amiloride Adverse Effects

A

Hyperkalemic metabolic acidosis (due to sparing of H+.)

62
Q

Amiloride Notes/Reminder

A

Also Triamterene which has a shorter 1/2 life than Amiloride.

63
Q

Demeclocycline Type& indication

A

SIADH patients. Has been replaced in use with Tolvaptan.

64
Q

Demeclocycline site of action

A

Collecting Duct: ADH-R, modify water excretion

65
Q

Demeclocycline MOA

A

ADH antagonist.

66
Q

Demeclocycline Adverse Effects

A

see Tolvaptan, selective ADH receptor antagonist.

67
Q

Demeclocycline Drug interactions

A
  • do not confuse these with ADH agonist desmopressin
68
Q

Demeclocycline Notes/Reminder

A

replaced by Tolvaptan group (selective)

69
Q

Lithium Type& indication

A

Main use is in Psych. Can be nephrotoxic, so is not used really to treat SIADH.

70
Q

Lithium site of action

A

Collecting Duct: ADH-R, modify water excretion

71
Q

Lithium MOA

A

ADH antagonist,

72
Q

Lithium Effects

A

can cause nephrogenic diabetes insipidus

73
Q

Lithium Notes/Reminder

A

replaced by Tolvaptan group (selective)

74
Q

Tolvaptan Type& indication

A

Use for patient w/Hyponatremia (dilutional) either Eu or Hypervolumia, where saline will worsen patient. SIADH, hypothyroidism, adrenal insufficiency, congestive HF, cirrhosis, nephrotic syndrome, small cell carcinoma (secretes ADH like substance) are examples.

75
Q

Tolvaptan site of action

A

Collecting Duct: ADH-R, modify water excretion

76
Q

Tolvaptan MOA

A

selective antagonist of Vassopressin (ADH) V2 receptor

77
Q

Tolvaptan Effects

A

increase serum Na (keep Na) but increase H2O output (get rid of excess water)

78
Q

Tolvaptan Contraindication

A

does not alter normal serum electrolyte balance!

79
Q

Tolvaptan Notes/Reminder

A

replaces Demeclocycline/Li, other drugs like it are Lixivaptan and OPC-31260

80
Q

Tolvaptan Urinary Electrolyte Pattern

A

very dilute urine

81
Q

Tolvaptan Serum Electrolyte Pattern

A

increases serum Na