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RENAL - Drugs Flashcards

(51 cards)

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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)

Study These Flashcards
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)

Study These Flashcards
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)

Study These Flashcards
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)

Study These Flashcards
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
Spironolactone (Mechanism)
_K+ sparing Diuretics_ **Mechanism:** * **Competitive aldosterone antagonists in CT** Clinical use: * Hyperaldosteronism * K+ depletion * HF Toxicity: * Hyperkalemia * Endocrine effects (gynecomastia, antiandrogen effects)
26
Spironolactone (Clinical use)
_K+ sparing Diuretics_ Mechanism: * Competitive aldosterone antagonists in CT **Clinical use:** * **Hyperaldosteronism** * **K+ depletion** * **HF** Toxicity: * Hyperkalemia * Endocrine effects (gynecomastia, antiandrogen effects)
27
Spironolactone (Toxicity)
_K+ sparing Diuretics_ Mechanism: * Competitive aldosterone antagonists in CT Clinical use: * Hyperaldosteronism * K+ depletion * HF T**oxicity:** * **Hyperkalemia** * **Endocrine effects (gynecomastia, antiandrogen effects)**
28
Eplerenone (Mechanism)
_K+ sparing Diuretics_ **Mechanism:** * **Competitive aldosterone antagonists in CT** Clinical use: * Hyperaldosteronism * K+ depletion * HF Toxicity: * Hyperkalemia
29
Eplerenone (Clinical use)
_K+ sparing Diuretics_ Mechanism: * Competitive aldosterone antagonists in CT **Clinical use:** * **Hyperaldosteronism** * **K+ depletion** * **HF** Toxicity: * Hyperkalemia
30
Eplerenone (Toxicity)
_K+ sparing Diuretics_ Mechanism: * Competitive aldosterone antagonists in CT Clinical use: * Hyperaldosteronism * K+ depletion * HF T**oxicity:** * **Hyperkalemia**
31
Triamterene (Mechanism)
_K+ sparing Diuretics_ **Mechanism:** * **Block Na+ channels in teh cortical CT** Clinical use: * Hyperaldosteronism * K+ depletion * HF Toxicity: * Hyperkalemia (arrythmias)
32
Triamterene (Clinical use)
_K+ sparing Diuretics_ Mechanism: * Block Na+ channels in teh cortical CT **Clinical use:** * **Hyperaldosteronism** * **K+ depletion** * **HF** Toxicity: * Hyperkalemia (arrythmias)
33
Triamterene (Toxicity)
_K+ sparing Diuretics_ Mechanism: * Block Na+ channels in teh cortical CT Clinical use: * Hyperaldosteronism * K+ depletion * HF **Toxicity:** * **Hyperkalemia (arrythmias)**
34
Amiloride (Mechanism)
_K+ sparing Diuretics_ **Mechanism:** * **Block Na+ channels in teh cortical CT** Clinical use: * Hyperaldosteronism * K+ depletion * HF Toxicity: * Hyperkalemia (arrythmias)
35
Amiloride (Clinical use)
_K+ sparing Diuretics_ Mechanism: * Block Na+ channels in teh cortical CT **Clinical use:** * **Hyperaldosteronism** * **K+ depletion** * **HF** Toxicity: * Hyperkalemia (arrythmias)
36
Amiloride (Toxicity)
_K+ sparing Diuretics_ Mechanism: * Block Na+ channels in teh cortical CT Clinical use: * Hyperaldosteronism * K+ depletion * HF **Toxicity:** * **Hyperkalemia (arrythmias)**
37
Urine NaCl Changes
Increased with all drugs (except acetazolamide)
38
Urine K+
Increase with Loop and thiazide diuretics (serum K+ may decrease as well)
39
Blood pH: Renal drugs --\> adidemia
CA inhibitors, K+ sparing diuretics
40
Renal drugs --\> Alkalemia
Loop diuretics and thiazides * Volume contraction alkalosis * K+ loss --\> K+/H+ exchanger * Exchange of H+ (instead of K+) in cortical collecting tube
41
**Urine** Ca++: renal drug affects
Increase with loops, (decrease paracellular transport) Decrease with thiazides (enhanced reabsorption
42
Captopril, enalapril, lisinopril, ramipril (mechanism)
_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
Captopril, enalapril, lisinopril, ramipril (cliniical use)
_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
Captopril, enalapril, lisinopril, ramipril (toxicity)
_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
Losartan, candesartan, valsartan | (Mechanism)
_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
Losartan, candesartan, valsartan | (Clinical use)
_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
Losartan, candesartan, valsartan | (Toxicity)
_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
Aliskiren | (Mechanism)
**Mechanism** * **Direct Renin inhibitor** Clinical use: * Hypertension Toxicity: * Hyperkalemia * decreased renal function * hypotension * Contraindicated in diabetics taking ACE inhibitors or ARBS
49
Aliskiren | (Clinical use)
Mechanism * Direct Renin inhibitor **Clinical use:** * **Hypertension** Toxicity: * Hyperkalemia * decreased renal function * hypotension * Contraindicated in diabetics taking ACE inhibitors or ARBS
50
Aliskiren | (toxicity)
Mechanism * Direct Renin inhibitor Clinical use: * Hypertension **Toxicity:** * **Hyperkalemia** * **decreased renal function** * **hypotension** * **Contraindicated in diabetics taking ACE inhibitors or ARBS**
51
Bezold Jarisch reflex
ACEi --\> hypotension Exacerbated with other previously used diuretics

DRUGS (41 decks)

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