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M2 - Pharm > FA Renal Drugs > Flashcards

FA Renal Drugs Flashcards

1
Q

Mannitol drug type

A

osmotic diuretic

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2
Q

Mannitol MOA

A
  • increases tubular fluid osmolarity (plasma osmotic pressure) in PCT
  • increases urine flow
  • decreases intracranial/intraocular pressure
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3
Q

Mannitol Clinical Use

A
  • Drug overdose
  • Elevated ICP/IOP
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4
Q

Mannitol Toxicity

A
  • Excessive plasma volume expansion
  • Pulmonary congestion/edema
  • Dehydration
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5
Q

Mannitol C/I

A
  • Anuria
  • Heart failure
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6
Q

Acetazolamide drug type

A

Carbonic anhydrase inhibitor

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7
Q

Acetazolamide MOA

A
  • Inhibits carbonic anhydrase in brush border and intracellularly in PCT
    • No H+ produced → No Na+/H+ exchg → Na+ stays in lumen
  • Self-limited NaHCO3 diuresis
  • Decrease in total body HCO3- stores
  • Alkalinizes urine
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8
Q

Carbonic Anhydrase does what?

A
  • Catalyzes CO2 + H2O → H2CO3
  • H2CO3 spontaneously decomposes to HCO3- + H+
  • Required for Na+/H+ exchg in PCT, NaHCO3 reabsorption from PCT, and H+ secretion in collecting duct
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9
Q

Acetazolamide Clinical Use

A
  • Glaucoma (reduce aq humor production)
  • Metabolic alkalosis
    • Altitude sickness
  • Pseudotumor cerebri
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10
Q

Acetazolamide Toxicity

A
  • HypERchloremic metabolic acidosis [ACIDazolamide]
    • Increased Cl- reabsorption to compensate for decreased bicarb reabsorption
  • Acidification of CSF → Paresthesias, other CNS effects
  • NH3 toxicity
  • Sulfa allergy
  • Blood cell deficiencies
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11
Q

Sulfa Diuretics

A

FAT:

  • Furosemide
  • Acetazolamide
  • Thiazides
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12
Q

Mannitol location of action

A

PCT

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13
Q

Acetazolamide location of action

A

PCT

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14
Q

Loop Diuretic Drugs

A
  • Furosemide
  • Bumetanide
  • Torsemide
  • Ethacrynic Acid
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15
Q

Loop Diuretic location of action

A

Thick Ascending LOH

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16
Q

Loop Diuretic drug type

A

Sulfonamide (except Ethacrynic Acid)

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17
Q

Loop Diuretic MOA

A
  • Inhibits Na+/K+/2Cl- transporter (out of lumen)
  • Abolishes hypertonicity of medulla
  • Prevents concentration of urine
  • Stim PGE release → afferent arteriole dilation
  • Inhibited by NSAIDs
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18
Q

NSAIDs inhibit which diuretics?

A

Loop diuretics (PGE)

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19
Q

Loop Diuretics increase excretion of which ions?

A
  • Na+
  • K+
  • Cl-
  • Ca2+
  • Mg2+
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20
Q

Loop Diuretics clinical use

A
  • Edematous states (HF, cirrhosis, nephrotic synd, pulm edema)
  • HTN
  • Hypercalcemia
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21
Q

Loop Diuretics Toxicity

A

OHH DANG!

  • Ototoxicity (worsened by aminoglycosides)
  • HypOkalemia
  • HypOcalcemia
  • Dehydration
  • Allergy (sulfa)
  • Nephritis (interstitial)
  • Gout (hyperuricemia)
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22
Q

Preferred diuretics in pts w/renal impairment?

A

Loop Diuretics

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23
Q

Acetazolamide increases excretion of which ions?

A

HCO3-

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24
Q

Only non-sulfa Loop Diuretic

A

Ethacrynic Acid

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25
Q

Diuretic used in pts w/sulfa allergy

A

Ethacrynic Acid

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26
Q

Ethacrynic Acid drug type

A

Phenoxyacetic acid derivative

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27
Q

Thiazide Diuretic drugs

A
  • Hydrochlorothiazide
  • Chlorthalidone
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28
Q

Thiazide Diuretic location of action

A

Early DCT

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29
Q

Thiazide Diuretic MOA

A
  • Inhibit NaCl reabsorption in early DCT
  • Decrease diluting capacity of nephron
  • Decrease Ca2+ excretion (PTH effect)
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30
Q

Thiazide Diuretic Clinical Use

A
  • HTN
  • HF
  • Edema
  • Idiopathic hypERcalciuria
  • Nephrogenic diabetes insipidus
    • helps concentrate urine
  • Osteoporosis
  • Calcium stones
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31
Q

Thiazide Diuretic Toxicity

A
  • HypOkalemic Metabolic Alkalosis
  • HypOnatremia
  • Hyper-GLUC:
    • Glycemia
    • Lipidemia
    • Uricemia
    • Calcemia
  • Sulfa allergy
32
Q

Potassium-Sparing Diuretic Drugs

A

Competitive Aldosterone Receptor Antagonists:

  • Spironolactone
  • Eplerenone

Sodium Channel Blockers:

  • Amiloride
  • Triamterene
33
Q

Competitive Aldosterone Receptor Antagonist Potassium-Sparing Diuretics

A
  • Spironolactone
  • Eplerenone
34
Q

Sodium Channel Blocker Potassium-Sparing Diuretics

A
  • Amiloride
  • Triamterene
35
Q

Amiloride/Triamterene MOA

A

Block sodium channels in cortical collecting tubule

36
Q

Spironolactone/Eplerenone MOA

A

Competitive aldosterone antagonist in cortical collecting tubule

37
Q

Potassium-Sparing Diuretic location of action

A

cortical collecting tubule

38
Q

Spironolactone Clinical Use

A
  • Primary HypERaldosteronism
    • Conn’s Synd
    • Waterhouse-Friedrichsen Synd
  • Polycystic ovary disease
  • Hirsutism
  • K+ depletion
  • HF
39
Q

Amiloride Clinical Use

A
  • Primary HypERaldosteronism
  • HypOkalemia / K+ depletion
  • CHF
40
Q

Potassium-Sparing Diuretic Toxicity

A
  • HypERkalemia → QT interval elongation → arrhythmia
  • Endocrine effects → gynecomastia, antiandrogen effects (spironolactone)
41
Q

ADH Antagonist MOA

A
  • Block ADH at V2 receptor → block insertion of add’l aquaporin channels in collecting tubule
  • Facilitate water excretion w/o electrolyte loss
42
Q

Aquaretic Drug Type

A

ADH Antagonists

43
Q

Aquaretic Drugs

A
  • Conivaptan
  • Tolvaptan
  • Lithium
  • Demeclocycline
44
Q

Aquaretic Drug Clinical Use

A
  • SIADH
  • Nephrogenic diabetes insipidus
  • Euvolemic/hypERvolemic hypOnatremia
45
Q

Aquaretic Drug Toxicity

A
  • Photosensitivity, abnormalities of bone and teeth (demeclocycline)
  • Nephrogenic DI (demeclocycline & lithium)
46
Q

Aquaretic Drug C/I

A

Extensively metabolized by CYP3A4 → do not give w/3A4 inhibitors

  • Can increase serum levels of midazolam, simvastatin, other drugs metabolized by 3A4
47
Q

ADH/Desmopressin MOA

A
  • Activate V2 receptors
  • Insert aquaporin channels to facilitate water reabsorption from collecting tubule
    • Reduce urine volume
    • Increase urine concentration
48
Q

Desmopressin Clinical Use

A
  • Central diabetes insipidus (intranasal)
  • Hemophilia A/B/C
  • von Willebrand Disease
    • releases vWF stored in endothelium
  • Bedwetting (oral)
49
Q

Rx Central Diabetes Insipidus?

A

Desmopressin

50
Q

Rx Nephrogenic Diabetes Insipidus?

A
  • hydrochlorothiazide
  • indomethacin
  • amiloride
51
Q

Rx SIADH?

A
  • fluid restriction
  • IV hypertonic saline
  • conivaptan
  • tolvaptan
  • demeclocycline
52
Q

ACE Inhibitor Drugs

A
  • Captopril
  • enalapril
  • lisinopril
  • ramipril
53
Q

ACE Inhibitor MOA

A
  • Inhibit ACE → decrease AT II → prevent efferent arteriole constriction → decrease GFR
  • Loss of feedback inhibition → Renin levels decrease
  • Also prevents inactivation of bradykinin, a potent vasodilator
54
Q

ACE Inhibitor Clinical Use

A
  • HTN
  • HF
    • Prevention of unfavorable heart remodeling from chronic HTN
  • Proteinuria
  • Diabetic nephropathy
    • decreases intraglomerular pressure → slows GBM thickening
55
Q

ACE Inhibitor Toxicity

A
  • Cough
  • Angioedema
  • Teratogen (fetal renal malformations)
  • Increased Creatinine (decreased GFR),
  • HypERkalemia
  • HypOtension
56
Q

ACE Inhibitor C/I

A
  • C1 esterase inhibitor deficiency → Angioedema
    • C1EI def → too much complement activation on self cells
  • Pregnancy → fetal renal malformations
  • Bilateral renal artery stenosis → renal failure
57
Q

ATII Receptor Blocker (ARB) Drugs

A
  • Losartan
  • candesartan
  • valsartan
58
Q

ARB Drug MOA

A
  • Selectively block binding of ATII to AT1 receptor.
  • Effects similar to ACE inhibitors, but ARBs do not increase bradykinin (no cough)
59
Q

ARB Drug Clinical Use

A
  • HTN
  • HF
  • proteinuria
  • diabetic nephropathy w/intolerance to ACE inhibitors (e.g., cough, angioedema)
60
Q

ARB Drug Toxicity

A
  • HypERkalemia
  • Decreased renal function
  • HypOtension
  • Teratogen
61
Q

Aliskiren MOA

A
  • Direct renin inhibitor
  • Blocks conversion of angiotensinogen (liver) → ATI
    • JG cells secrete renin in response to decreased renal blood pressure, increased sympathetic tone (β1), and/or decreased NaCl delivery to macula densa in DCT
62
Q

Aliskiren Clinical Use

A

HTN

63
Q

Aliskiren Toxicity

A
  • HypERkalemia
  • Decreased renal function
  • HypOtension
64
Q

Aliskiren C/I

A

diabetics taking ACE inhibitors or ARBs

65
Q

Which drugs cause urine alkalinization?

A

Carbonic anhydrase inhibitors

66
Q

Which drugs increase urine NaCl?

A

All diuretics except Acetazolamide

  • Note: increasing naturiesis means serum NaCl may decrease
67
Q

Which drugs increase urine potassium?

A
  • Loop diuretics
  • Thiazide diuretics
  • Acetazolamide

Note: serum K+ may decrease as result

68
Q

Which drugs decrease blood pH (cause acidemia)?

A
  • Carbonic anhydrase inhibitors → decrease HCO3- reabsorption
  • K+ sparing: Aldosterone blockade → prevent K+/H+ secretion
    • Hyperkalemia → K+ enters cells in exchange for H+ exiting cells (via K+/H+ exchg)
69
Q

Which drugs increase blood pH (cause alkalemia)?

A

Loop diuretics and Thiazides:

  • Volume contraction → increased ATII → increased Na+/H+ exchg in PCT → increased HCO3- reabsorption (“Contraction alkalosis”)
  • K+ exits cells in exchg for H+ entering cells (via K+/H+ exchanger)
  • Low K+ state → H+ rather than K+ exchg for Na+ in cortical collecting tubule → alkalosis, paradoxical aciduria
70
Q

Which drugs increase excretion of Ca2+?

A

Loop diuretics

  • decreased paracellular Ca2+ reabsorption → hypOcalcemia
71
Q

Which drugs decrease excretion of Ca2+?

A

Thiazides:

  • Enhanced Ca2+ reabsorption in DCT
72
Q

Which drugs increase excretion of Mg2+?

A

Loop diuretics

  • loss of lumen positive potential reduces ion reabsorption
73
Q

Which drugs increase excretion of HCO3-?

A

Acetazolamide

74
Q

Which drugs decrease excretion of HCO3-?

A

Loop diuretics

75
Q

Which drugs increase excretion of phosphate?

A

Acetazolamide

  • reduced reabsorption in acidosis

M2 - Pharm (10 decks)

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