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DRUGS > RENAL - Drugs > Flashcards

RENAL - Drugs Flashcards

1
Q

Mannitol (mechanism)

A

Mechanism:

  • Osmotic diuretic.
  • Increase tubular fluid osmolarity –> increased urine flow, decreased intracranial/intraocular pressure

Use:

  • Drug overdose
  • Elevated intracranial/intraocular pressure

Toxicity:

  • Pulmonary edema
  • Dehydration
  • Contraindicated in anuria, HF
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2
Q

Mannitol (use)

A

Mechanism:

  • Osmotic diuretic.
  • Increase tubular fluid osmolarity –> increased urine flow, decreased intracranial/intraocular pressure

Use:

  • Drug overdose
  • Elevated intracranial/intraocular pressure

Toxicity:

  • Pulmonary edema
  • Dehydration
  • Contraindicated in anuria, HF
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3
Q

Mannitol (toxicity)

A

Mechanism:

  • Osmotic diuretic.
  • Increase tubular fluid osmolarity –> increased urine flow, decreased intracranial/intraocular pressure

Use:

  • Drug overdose
  • Elevated intracranial/intraocular pressure

Toxicity:

  • Pulmonary edema
  • Dehydration
  • Contraindicated in anuria, HF
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4
Q

Acetazolamide (mechanism)

A

Mechanism:

  • Carbonic anhydrase inhibitor
  • Self limited NaHCO3 diuresis
  • Decreased total body HCO3- stores

Use:

  • Glaucoma
  • Urinary alkalinization
  • metabolic alkalosis
  • Altitude sickness
  • Pseudotumor cerebri

Toxicity:

  • Hyperchloremic metabolic acidosis
  • Paresthesias
  • NH3 toxicity
  • Sulfa allergy
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5
Q

Acetazolamide (Use)

A

Mechanism:

  • Carbonic anhydrase inhibitor
  • Self limited NaHCO3 diuresis
  • Decreased total body HCO3- stores

Use:

  • Glaucoma
  • Urinary alkalinization
  • metabolic alkalosis
  • Altitude sickness
  • Pseudotumor cerebri

Toxicity:

  • Hyperchloremic metabolic acidosis
  • Paresthesias
  • NH3 toxicity
  • Sulfa allergy
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6
Q

Acetazolamide (Toxicity)

A

Mechanism:

  • Carbonic anhydrase inhibitor
  • Self limited NaHCO3 diuresis
  • Decreased total body HCO3- stores

Use:

  • Glaucoma
  • Urinary alkalinization
  • metabolic alkalosis
  • Altitude sickness
  • Pseudotumor cerebri

Toxicity:

  • Hyperchloremic metabolic acidosis
  • Paresthesias
  • NH3 toxicity
  • Sulfa allergy
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7
Q

Furosemide (mechanism)

A

Sulfonamide loop Diuretics

Mechanism:

  • Na+/K+/2Cl- cotransporter inhibitor
    • Abolishes concentration gradient of medulla
  • Stimulate PGE release: vasodilation of afferent arteriole (inhibit with NSAIDS)
  • Increase Ca++ excretion

Use:

  • Edematous states (HF, Cirrhosis, nephrotic syndrome, pulmonary edema)
  • Hypertension
  • Hypercalcemia

Toxicity: (OH DANG)

  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy (sulfa)
  • Nephritis (interstitial)
  • Gout
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8
Q

Furosemide (use)

A

Sulfonamide loop Diuretics

Mechanism:

  • Na+/K+/2Cl- cotransporter inhibitor
    • Abolishes concentration gradient of medulla
  • Stimulate PGE release: vasodilation of afferent arteriole (inhibit with NSAIDS)
  • Increase Ca++ excretion

Use:

  • Edematous states (HF, Cirrhosis, nephrotic syndrome, pulmonary edema)
  • Hypertension
  • Hypercalcemia

Toxicity: (OH DANG)

  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy (sulfa)
  • Nephritis (interstitial)
  • Gout
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9
Q

Furosemide (toxicity)

A

Sulfonamide loop Diuretics

Mechanism:

  • Na+/K+/2Cl- cotransporter inhibitor
    • Abolishes concentration gradient of medulla
  • Stimulate PGE release: vasodilation of afferent arteriole (inhibit with NSAIDS)
  • Increase Ca++ excretion

Use:

  • Edematous states (HF, Cirrhosis, nephrotic syndrome, pulmonary edema)
  • Hypertension
  • Hypercalcemia

Toxicity: (OH DANG)

  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy (sulfa)
  • Nephritis (interstitial)
  • Gout
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10
Q

Bumetanide (mechanism)

A

Sulfonamide loop Diuretics

Mechanism:

  • Na+/K+/2Cl- cotransporter inhibitor
    • Abolishes concentration gradient of medulla
  • Stimulate PGE release: vasodilation of afferent arteriole (inhibit with NSAIDS)
  • Increase Ca++ excretion

Use:

  • Edematous states (HF, Cirrhosis, nephrotic syndrome, pulmonary edema)
  • Hypertension
  • Hypercalcemia

Toxicity: (OH DANG)

  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy (sulfa)
  • Nephritis (interstitial)
  • Gout
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11
Q

Bumetanide (use)

A

Sulfonamide loop Diuretics

Mechanism:

  • Na+/K+/2Cl- cotransporter inhibitor
    • Abolishes concentration gradient of medulla
  • Stimulate PGE release: vasodilation of afferent arteriole (inhibit with NSAIDS)
  • Increase Ca++ excretion

Use:

  • Edematous states (HF, Cirrhosis, nephrotic syndrome, pulmonary edema)
  • Hypertension
  • Hypercalcemia

Toxicity: (OH DANG)

  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy (sulfa)
  • Nephritis (interstitial)
  • Gout
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12
Q

Bumetanide (toxicity)

A

Sulfonamide loop Diuretics

Mechanism:

  • Na+/K+/2Cl- cotransporter inhibitor
    • Abolishes concentration gradient of medulla
  • Stimulate PGE release: vasodilation of afferent arteriole (inhibit with NSAIDS)
  • Increase Ca++ excretion

Use:

  • Edematous states (HF, Cirrhosis, nephrotic syndrome, pulmonary edema)
  • Hypertension
  • Hypercalcemia

Toxicity: (OH DANG)

  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy (sulfa)
  • Nephritis (interstitial)
  • Gout
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13
Q

Torsemide (mechanism)

A

Sulfonamide loop Diuretics

Mechanism:

  • Na+/K+/2Cl- cotransporter inhibitor
    • Abolishes concentration gradient of medulla
  • Stimulate PGE release: vasodilation of afferent arteriole (inhibit with NSAIDS)
  • Increase Ca++ excretion

Use:

  • Edematous states (HF, Cirrhosis, nephrotic syndrome, pulmonary edema)
  • Hypertension
  • Hypercalcemia

Toxicity: (OH DANG)

  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy (sulfa)
  • Nephritis (interstitial)
  • Gout
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14
Q

Torsemide (use)

A

Sulfonamide loop Diuretics

Mechanism:

  • Na+/K+/2Cl- cotransporter inhibitor
    • Abolishes concentration gradient of medulla
  • Stimulate PGE release: vasodilation of afferent arteriole (inhibit with NSAIDS)
  • Increase Ca++ excretion

Use:

  • Edematous states (HF, Cirrhosis, nephrotic syndrome, pulmonary edema)
  • Hypertension
  • Hypercalcemia

Toxicity: (OH DANG)

  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy (sulfa)
  • Nephritis (interstitial)
  • Gout
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15
Q

Torsemide (toxicity)

A

Sulfonamide loop Diuretics

Mechanism:

  • Na+/K+/2Cl- cotransporter inhibitor
    • Abolishes concentration gradient of medulla
  • Stimulate PGE release: vasodilation of afferent arteriole (inhibit with NSAIDS)
  • Increase Ca++ excretion

Use:

  • Edematous states (HF, Cirrhosis, nephrotic syndrome, pulmonary edema)
  • Hypertension
  • Hypercalcemia

Toxicity: (OH DANG)

  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy (sulfa)
  • Nephritis (interstitial)
  • Gout
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16
Q

Ethacrynic acid (mechanism)

A

Loop Diuretic: Phenoxyacetic acid derivative

Mechanism_:_

  • Inhibit Na/K/2Cl

Use:

  • Diuresis in patients with sulfa alergies

Toxicity:

  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy (sulfa)
  • Nephritis (interstitial)
  • Gout
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17
Q

Ethacrynic acid (Use)

A

Loop Diuretic: Phenoxyacetic acid derivative

Mechanism_:_

  • Inhibit Na/K/2Cl

Use:

  • Diuresis in patients with sulfa alergies

Toxicity:

  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy (sulfa)
  • Nephritis (interstitial)
  • Gout
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18
Q

Ethacrynic acid (Toxicity)

A

Loop Diuretic: Phenoxyacetic acid derivative

Mechanism_:_

  • Inhibit Na/K/2Cl

Use:

  • Diuresis in patients with sulfa alergies

Toxicity:

  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy (sulfa)
  • Nephritis (interstitial)
  • Gout
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19
Q

Chlorthalidone (Mechanism)

A

Thiazide diuretic

Mechanism:

  • Inhibit NaCl reabsorption in DCT
    • Also Decrease Ca++ excretion

Clinical Use:

  • Hypertension
  • HF
  • Idiopathic hypercalciuria
  • Nephrogenic DI
  • Osteoporosis

Toxicity (hyper GLUC)

  • Hypokalemic metabolic alkalosis
  • Hyponatremia
  • hyperglycemia
  • Hyperlipidemia (increase LDL/Cholesterol)
  • Hyperuricemia
  • Hypercalcemia
  • Sulfa alergy
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20
Q

Chlorthalidone (clinical use)

A

Thiazide diuretic

Mechanism:

  • Inhibit NaCl reabsorption in DCT
    • Also Decrease Ca++ excretion

Clinical Use:

  • Hypertension
  • HF
  • Idiopathic hypercalciuria
  • Nephrogenic DI
  • Osteoporosis

Toxicity (hyper GLUC)

  • Hypokalemic metabolic alkalosis
  • Hyponatremia
  • hyperglycemia
  • Hyperlipidemia (increase LDL/Cholesterol)
  • Hyperuricemia
  • Hypercalcemia
  • Sulfa alergy
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21
Q

Chlorthalidone (Toxicity)

A

Thiazide diuretic

Mechanism:

  • Inhibit NaCl reabsorption in DCT
    • Also Decrease Ca++ excretion

Clinical Use:

  • Hypertension
  • HF
  • Idiopathic hypercalciuria
  • Nephrogenic DI
  • Osteoporosis

Toxicity (hyper GLUC)

  • Hypokalemic metabolic alkalosis
  • Hyponatremia
  • hyperglycemia
  • Hyperlipidemia (increase LDL/Cholesterol)
  • Hyperuricemia
  • Hypercalcemia
  • Sulfa alergy
22
Q

Hydrochlorothiazide (Mechanism)

A

Thiazide diuretic

Mechanism:

  • Inhibit NaCl reabsorption in DCT
    • Also Decrease Ca++ excretion

Clinical Use:

  • Hypertension
  • HF
  • Idiopathic hypercalciuria
  • Nephrogenic DI
  • Osteoporosis

Toxicity (hyper GLUC)

  • Hypokalemic metabolic alkalosis
  • Hyponatremia
  • hyperglycemia
  • Hyperlipidemia (increase LDL/Cholesterol)
  • Hyperuricemia
  • Hypercalcemia
  • Sulfa alergy
23
Q

Hydrochlorothiazide (clinical use)

A

Thiazide diuretic

Mechanism:

  • Inhibit NaCl reabsorption in DCT
    • Also Decrease Ca++ excretion

Clinical Use:

  • Hypertension
  • HF
  • Idiopathic hypercalciuria
  • Nephrogenic DI
  • Osteoporosis

Toxicity (hyper GLUC)

  • Hypokalemic metabolic alkalosis
  • Hyponatremia
  • hyperglycemia
  • Hyperlipidemia (increase LDL/Cholesterol)
  • Hyperuricemia
  • Hypercalcemia
  • Sulfa alergy
24
Q

Hydrochlorothiazide (Toxicity)

A

Thiazide diuretic

Mechanism:

  • Inhibit NaCl reabsorption in DCT
    • Also Decrease Ca++ excretion

Clinical Use:

  • Hypertension
  • HF
  • Idiopathic hypercalciuria
  • Nephrogenic DI
  • Osteoporosis

Toxicity (hyper GLUC)

  • Hypokalemic metabolic alkalosis
  • Hyponatremia
  • hyperglycemia
  • Hyperlipidemia (increase LDL/Cholesterol)
  • Hyperuricemia
  • Hypercalcemia
  • Sulfa alergy
25
Q

Spironolactone (Mechanism)

A

K+ sparing Diuretics

Mechanism:

  • Competitive aldosterone antagonists in CT

Clinical use:

  • Hyperaldosteronism
  • K+ depletion
  • HF

Toxicity:

  • Hyperkalemia
  • Endocrine effects (gynecomastia, antiandrogen effects)
26
Q

Spironolactone (Clinical use)

A

K+ sparing Diuretics

Mechanism:

  • Competitive aldosterone antagonists in CT

Clinical use:

  • Hyperaldosteronism
  • K+ depletion
  • HF

Toxicity:

  • Hyperkalemia
  • Endocrine effects (gynecomastia, antiandrogen effects)
27
Q

Spironolactone (Toxicity)

A

K+ sparing Diuretics

Mechanism:

  • Competitive aldosterone antagonists in CT

Clinical use:

  • Hyperaldosteronism
  • K+ depletion
  • HF

Toxicity:

  • Hyperkalemia
  • Endocrine effects (gynecomastia, antiandrogen effects)
28
Q

Eplerenone (Mechanism)

A

K+ sparing Diuretics

Mechanism:

  • Competitive aldosterone antagonists in CT

Clinical use:

  • Hyperaldosteronism
  • K+ depletion
  • HF

Toxicity:

  • Hyperkalemia
29
Q

Eplerenone (Clinical use)

A

K+ sparing Diuretics

Mechanism:

  • Competitive aldosterone antagonists in CT

Clinical use:

  • Hyperaldosteronism
  • K+ depletion
  • HF

Toxicity:

  • Hyperkalemia
30
Q

Eplerenone (Toxicity)

A

K+ sparing Diuretics

Mechanism:

  • Competitive aldosterone antagonists in CT

Clinical use:

  • Hyperaldosteronism
  • K+ depletion
  • HF

Toxicity:

  • Hyperkalemia
31
Q

Triamterene (Mechanism)

A

K+ sparing Diuretics

Mechanism:

  • Block Na+ channels in teh cortical CT

Clinical use:

  • Hyperaldosteronism
  • K+ depletion
  • HF

Toxicity:

  • Hyperkalemia (arrythmias)
32
Q

Triamterene (Clinical use)

A

K+ sparing Diuretics

Mechanism:

  • Block Na+ channels in teh cortical CT

Clinical use:

  • Hyperaldosteronism
  • K+ depletion
  • HF

Toxicity:

  • Hyperkalemia (arrythmias)
33
Q

Triamterene (Toxicity)

A

K+ sparing Diuretics

Mechanism:

  • Block Na+ channels in teh cortical CT

Clinical use:

  • Hyperaldosteronism
  • K+ depletion
  • HF

Toxicity:

  • Hyperkalemia (arrythmias)
34
Q

Amiloride (Mechanism)

A

K+ sparing Diuretics

Mechanism:

  • Block Na+ channels in teh cortical CT

Clinical use:

  • Hyperaldosteronism
  • K+ depletion
  • HF

Toxicity:

  • Hyperkalemia (arrythmias)
35
Q

Amiloride (Clinical use)

A

K+ sparing Diuretics

Mechanism:

  • Block Na+ channels in teh cortical CT

Clinical use:

  • Hyperaldosteronism
  • K+ depletion
  • HF

Toxicity:

  • Hyperkalemia (arrythmias)
36
Q

Amiloride (Toxicity)

A

K+ sparing Diuretics

Mechanism:

  • Block Na+ channels in teh cortical CT

Clinical use:

  • Hyperaldosteronism
  • K+ depletion
  • HF

Toxicity:

  • Hyperkalemia (arrythmias)
37
Q

Urine NaCl Changes

A

Increased with all drugs (except acetazolamide)

38
Q

Urine K+

A

Increase with Loop and thiazide diuretics (serum K+ may decrease as well)

39
Q

Blood pH: Renal drugs –> adidemia

A

CA inhibitors, K+ sparing diuretics

40
Q

Renal drugs –> Alkalemia

A

Loop diuretics and thiazides

  • Volume contraction alkalosis
  • K+ loss –> K+/H+ exchanger
  • Exchange of H+ (instead of K+) in cortical collecting tube
41
Q

Urine Ca++: renal drug affects

A

Increase with loops, (decrease paracellular transport)

Decrease with thiazides (enhanced reabsorption

42
Q

Captopril, enalapril, lisinopril, ramipril

(mechanism)

A

ACE inhibitors:

Mechanism:

  • Inhibit ACE –> decrease AT II –> decrease GFR by lowering constriction of efferent arterioles
  • Prevents inactivation of bradykinin (a potent vasodilator)

Clinical use:

  • Hypertension
  • HF
  • Proteinuria
  • Diabetic nephropathy
  • Prevent heart remodelling

Toxicity:

  • Cough
  • Angioedema
  • Teratogen
  • Creatinin (decreased GFR)
  • Hyperkalemia
  • Hypotension
  • (avoid in bilateral renal artery stenosis)
43
Q

Captopril, enalapril, lisinopril, ramipril

(cliniical use)

A

ACE inhibitors:

Mechanism:

  • Inhibit ACE –> decrease AT II –> decrease GFR by lowering constriction of efferent arterioles
  • Prevents inactivation of bradykinin (a potent vasodilator)

Clinical use:

  • Hypertension
  • HF
  • Proteinuria
  • Diabetic nephropathy
  • Prevent heart remodelling

Toxicity:

  • Cough
  • Angioedema
  • Teratogen
  • Creatinin (decreased GFR)
  • Hyperkalemia
  • Hypotension
  • (avoid in bilateral renal artery stenosis)
44
Q

Captopril, enalapril, lisinopril, ramipril

(toxicity)

A

ACE inhibitors:

Mechanism:

  • Inhibit ACE –> decrease AT II –> decrease GFR by lowering constriction of efferent arterioles
  • Prevents inactivation of bradykinin (a potent vasodilator)

Clinical use:

  • Hypertension
  • HF
  • Proteinuria
  • Diabetic nephropathy
  • Prevent heart remodelling

Toxicity:

  • Cough
  • Angioedema
  • Teratogen
  • Creatinin (decreased GFR)
  • Hyperkalemia
  • Hypotension
  • (avoid in bilateral renal artery stenosis)
45
Q

Losartan, candesartan, valsartan

(Mechanism)

A

Angiotensin II receptor

Mechanism:

  • Selectively blcok Angiotensin II binding to AT1 receptor

Clinical use:

  • Hypertension
  • HF
  • Proteinuria
  • Diabetic nephropathy
  • Patients with intolerance to ACE inhibitors

Toxicity:

  • Hyperkalemia
  • Decrease renal function
  • Hypotension
  • Teratogen
46
Q

Losartan, candesartan, valsartan

(Clinical use)

A

Angiotensin II receptor

Mechanism:

  • Selectively blcok Angiotensin II binding to AT1 receptor

Clinical use:

  • Hypertension
  • HF
  • Proteinuria
  • Diabetic nephropathy
  • Patients with intolerance to ACE inhibitors

Toxicity:

  • Hyperkalemia
  • Decrease renal function
  • Hypotension
  • Teratogen
47
Q

Losartan, candesartan, valsartan

(Toxicity)

A

Angiotensin II receptor

Mechanism:

  • Selectively blcok Angiotensin II binding to AT1 receptor

Clinical use:

  • Hypertension
  • HF
  • Proteinuria
  • Diabetic nephropathy
  • Patients with intolerance to ACE inhibitors

Toxicity:

  • Hyperkalemia
  • Decrease renal function
  • Hypotension
  • Teratogen
48
Q

Aliskiren

(Mechanism)

A

Mechanism

  • Direct Renin inhibitor

Clinical use:

  • Hypertension

Toxicity:

  • Hyperkalemia
  • decreased renal function
  • hypotension
  • Contraindicated in diabetics taking ACE inhibitors or ARBS
49
Q

Aliskiren

(Clinical use)

A

Mechanism

  • Direct Renin inhibitor

Clinical use:

  • Hypertension

Toxicity:

  • Hyperkalemia
  • decreased renal function
  • hypotension
  • Contraindicated in diabetics taking ACE inhibitors or ARBS
50
Q

Aliskiren

(toxicity)

A

Mechanism

  • Direct Renin inhibitor

Clinical use:

  • Hypertension

Toxicity:

  • Hyperkalemia
  • decreased renal function
  • hypotension
  • Contraindicated in diabetics taking ACE inhibitors or ARBS
51
Q

Bezold Jarisch reflex

A

ACEi –> hypotension

Exacerbated with other previously used diuretics

DRUGS (41 decks)

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