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M2 - Pharm > FA Renal Drugs > Flashcards

FA Renal Drugs Flashcards

(75 cards)

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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
Diuretic used in pts w/sulfa allergy
Ethacrynic Acid
26
Ethacrynic Acid drug type
Phenoxyacetic acid derivative
27
Thiazide Diuretic drugs
* Hydrochlorothiazide * Chlorthalidone
28
Thiazide Diuretic location of action
Early DCT
29
Thiazide Diuretic MOA
* Inhibit NaCl reabsorption in early DCT * Decrease diluting capacity of nephron * Decrease Ca2+ excretion (PTH effect)
30
Thiazide Diuretic Clinical Use
* HTN * HF * Edema * Idiopathic hypERcalciuria * Nephrogenic diabetes insipidus * helps concentrate urine * Osteoporosis * Calcium stones
31
Thiazide Diuretic Toxicity
* HypOkalemic Metabolic Alkalosis * HypOnatremia * Hyper-GLUC: * Glycemia * Lipidemia * Uricemia * Calcemia * Sulfa allergy
32
Potassium-Sparing Diuretic Drugs
Competitive Aldosterone Receptor Antagonists: * Spironolactone * Eplerenone Sodium Channel Blockers: * Amiloride * Triamterene
33
Competitive Aldosterone Receptor Antagonist Potassium-Sparing Diuretics
* Spironolactone * Eplerenone
34
Sodium Channel Blocker Potassium-Sparing Diuretics
* Amiloride * Triamterene
35
Amiloride/Triamterene MOA
Block sodium channels in cortical collecting tubule
36
Spironolactone/Eplerenone MOA
Competitive aldosterone antagonist in cortical collecting tubule
37
Potassium-Sparing Diuretic location of action
cortical collecting tubule
38
Spironolactone Clinical Use
* Primary HypERaldosteronism * Conn’s Synd * Waterhouse-Friedrichsen Synd * Polycystic ovary disease * Hirsutism * K+ depletion * HF
39
Amiloride Clinical Use
* Primary HypERaldosteronism * HypOkalemia / K+ depletion * CHF
40
Potassium-Sparing Diuretic Toxicity
* HypERkalemia → QT interval elongation → arrhythmia * Endocrine effects → gynecomastia, antiandrogen effects (spironolactone)
41
ADH Antagonist MOA
* Block ADH at V2 receptor → block insertion of add'l aquaporin channels in collecting tubule * Facilitate water excretion w/o electrolyte loss
42
Aquaretic Drug Type
ADH Antagonists
43
Aquaretic Drugs
* Conivaptan * Tolvaptan * Lithium * Demeclocycline
44
Aquaretic Drug Clinical Use
* SIADH * Nephrogenic diabetes insipidus * Euvolemic/hypERvolemic hypOnatremia
45
Aquaretic Drug Toxicity
* Photosensitivity, abnormalities of bone and teeth (demeclocycline) * Nephrogenic DI (demeclocycline & lithium)
46
Aquaretic Drug C/I
Extensively metabolized by CYP3A4 → do not give w/3A4 inhibitors * Can increase serum levels of midazolam, simvastatin, other drugs metabolized by 3A4
47
ADH/Desmopressin MOA
* Activate V2 receptors * Insert aquaporin channels to facilitate water reabsorption from collecting tubule * Reduce urine volume * Increase urine concentration
48
Desmopressin Clinical Use
* Central diabetes insipidus (intranasal) * Hemophilia A/B/C * von Willebrand Disease * releases vWF stored in endothelium * Bedwetting (oral)
49
Rx Central Diabetes Insipidus?
Desmopressin
50
Rx Nephrogenic Diabetes Insipidus?
* hydrochlorothiazide * indomethacin * amiloride
51
Rx SIADH?
* fluid restriction * IV hypertonic saline * conivaptan * tolvaptan * demeclocycline
52
ACE Inhibitor Drugs
* Captopril * enalapril * lisinopril * ramipril
53
ACE Inhibitor MOA
* 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
ACE Inhibitor Clinical Use
* HTN * HF * Prevention of unfavorable heart remodeling from chronic HTN * Proteinuria * Diabetic nephropathy * decreases intraglomerular pressure → slows GBM thickening
55
ACE Inhibitor Toxicity
* Cough * Angioedema * Teratogen (fetal renal malformations) * Increased Creatinine (decreased GFR), * HypERkalemia * HypOtension
56
ACE Inhibitor C/I
* 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
ATII Receptor Blocker (ARB) Drugs
* Losartan * candesartan * valsartan
58
ARB Drug MOA
* Selectively block binding of ATII to AT1 receptor. * Effects similar to ACE inhibitors, but ARBs **do not** increase bradykinin (no cough)
59
ARB Drug Clinical Use
* HTN * HF * proteinuria * diabetic nephropathy w/intolerance to ACE inhibitors (e.g., cough, angioedema)
60
ARB Drug Toxicity
* HypERkalemia * Decreased renal function * HypOtension * Teratogen
61
Aliskiren MOA
* 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
Aliskiren Clinical Use
HTN
63
Aliskiren Toxicity
* HypERkalemia * Decreased renal function * HypOtension
64
Aliskiren C/I
diabetics taking ACE inhibitors or ARBs
65
Which drugs cause urine alkalinization?
Carbonic anhydrase inhibitors
66
Which drugs increase urine NaCl?
All diuretics except Acetazolamide * Note: increasing naturiesis means serum NaCl may decrease
67
Which drugs increase urine potassium?
* Loop diuretics * Thiazide diuretics * Acetazolamide Note: serum K+ may decrease as result
68
Which drugs decrease blood pH (cause acidemia)?
* **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
Which drugs increase blood pH (cause alkalemia)?
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
Which drugs increase excretion of Ca2+?
Loop diuretics * decreased paracellular Ca2+ reabsorption → hypOcalcemia
71
Which drugs decrease excretion of Ca2+?
Thiazides: * Enhanced Ca2+ reabsorption in DCT
72
Which drugs increase excretion of Mg2+?
Loop diuretics * loss of lumen positive potential reduces ion reabsorption
73
Which drugs increase excretion of HCO3-?
Acetazolamide
74
Which drugs decrease excretion of HCO3-?
Loop diuretics
75
Which drugs increase excretion of phosphate?
Acetazolamide * reduced reabsorption in acidosis

M2 - Pharm (10 decks)

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