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PHARM 343 > Acute Kidney Injury Drugs > Flashcards

Acute Kidney Injury Drugs Flashcards

1
Q

Prerenal
- Drugs

A

ACEi/ARBs
NSAIDS
Celcinerurin Inhibitors

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2
Q

Intrarenal (Acute Tubular Necrosis)
- Drugs

A

Amphotericin B
Aminoglycosides
Radiographic Contrast Dye

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3
Q

Intrarenal (Acute Interstitial Nephritis)
- Drugs

A

Penicillins
Lithium

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4
Q

Intrarenal (Chronic Interstitial Nephritis)
- Drugs

A

Calcineurin Inhibitors
Lithium
NSAIDs

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5
Q

Postrenal
- Drugs

A

Acyclovir
Indinavir
Sulfonamide Antibiotics

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6
Q

AKI and ACE/ARB
- Presentation

A

Therapy causes Serum Creatinine to rise by 25-30% within 2-7 days of initiation of therapy
- Stabilizes within 1 week

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7
Q

AKI and ACE/ARB
- Mechanism

A

ACEi dilute efferent arteriole –> Reduces glomerular hydrostatic pressure
- Lower GFR

Summary: Prevents vasoconstriction of efferent arteriole

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8
Q

AKI and ACE/ARB
- Lab Values

A

Urine
- Low urine
- Low sodium

Very concentrated urine
- High urea, High creatinine

No cells in urine

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9
Q

AKI and ACE/ARB
- Prevention

A

Maintain hydration

Do not use with NSAIDS

Low dose and titrate slowly

Monitor SCr and Potassium

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10
Q

AKI and NSAIDS
- Considerations

A

Do not combine ACE and NSAID, both alter renal blood flow

Low dose ASA does not impair renal function

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11
Q

AKI and NSAIDS
- Presentation

A

Low urine volume
Edema/Weight gain
Elevated SCr, K+ and Urea

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12
Q

AKI and NSAIDS
- Mechanism

A

NSAIDS inhibit COX-2, which normally forms prostaglandins which compensate altered renal perfusion

Without COX-2, PGE2 response is inhibited
- afferent arterial dilation and reduce GFR

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13
Q

AKI and NSAIDS
- Lab Values

A

Low urine volume
Low urine sodium

Concentrated urine
- High Urea, High Creatinine

No cells in urine

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14
Q

AKI and NSAIDS
- Prevention

A

Avoid prolonged NSAID use in elderly patients, Heart failure patients, or CKD patients

Do not use with ACE/ARB

Start with low dose and titrate slowly

Monitor BP and SCr

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15
Q

AKI
- NSAIDS vs ACE/ARB

A

NSAIDS affect PGE2 and afferent arteriole
- Inhibit afferent arteriole dilation = Less Blood = Low GFR

ACE/ARB affect Angiotensin II and efferent arteriole
- Causes dilation of efferent arterioles = Less pressure = Low GFR

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16
Q

Most common intrarenal AKI

A

Acute Tubular Necrosis

17
Q

ATN
- Different phases

A

Oliguric Phase
- Within 24 hours, lasts 1-3 weeks

Diuretic Phase
- Indicates renal recovery

18
Q

ATN
- Different kinds

A

Nephrotoxic ATN
- Endogenous or Exogenous
–> Myoglobin
–> Aminoglycosides (Tobramycin, Gentamicin)
–> CT Contrast Dye

Ischemic ATN
- Ischemia and Toxin related

19
Q

AKI and Aminoglycosides
- Mechanism

A

ATN

Epithelial cell damage at proximal tubular cells
- Caused by cationic charge

20
Q

AKI and Aminoglycosides
- Lab Values

A

ATN

Brown Cast Cells and Epithelial Cells in Urine
High Sodium in urine

21
Q

AKI and NSAIDS
- Management

A

Discontinue
Supportive Therapy

22
Q

AKI and ACE/ARB
- Management

A

Discontinue
Supportive Therapy

23
Q

AKI and Aminoglycosides
- Management

A

Discontinue
Supportive Therapy
- Correct volume derangements
- Correct metabolic acidosis
- Hemodialysis/Renal Replacement Therapy

24
Q

AKI and Aminoglycosides
- Prevention

A

Avoid hypovolemia
Avoid nephrotoxic drugs
Avoid high risk populations
- Elderly
- Pre-existing renal failure

25
Q

AKI and Amphotericin B
- Mechanism

A

ATN

Direct toxicity to cells in distal nephron
- Cell death and necrosis

Kidneys lose ability to filter and concentrate urine

26
Q

AKI and Amphotericin B
- Management

A

Hydration

Use of liposomal formulations

Limit dose

Monitor renal function

Avoid Nephrotoxic drugs

27
Q

AIN
- Presentation

A

Acute Interstitial Nephritis
- Fever,
- Rash
- Pyuria/Hematuria
- Oliguria

  • Metabolic acidosis
  • Hyperkalemia
  • Salt wasting

Occurs 14 days after drug

28
Q

AIN
- Mechanism

A

Hypersensitivity reaction
- Lymphocytes infiltrate the interstitium

29
Q

AIN
- Lab Values

A

Urine
- High Sodium
- WBC
- Protein
- Eosinophils

30
Q

AIN
- Management

A

Discontinue offending drug
- Penicillins, Lithium

Supportive Therapy
- Correct volume derangements
- Prednisone therapy for up to 4 weeks
- Intermittent hemodialysis

31
Q

Obstructive Neuropathy
- Different Kinds

A

All are Postrenal AKI
- Renal Tubular Obstruction
- Extrarenal Urinary Tract Obstruction
- Nephrolithiasis (Kidney Stones)

32
Q

Obstructive Neuropathy
- Renal Tubular Obstruction

A

Precipitation of drug crystals or other tissue degradation products in the tubule
- Acyclovir, Rhabdomyolysis with statins

33
Q

Obstructive Neuropathy
- Extrarenal Urinary Tract Obstruction

A

Males with BPH given Anticholinergic drugs

34
Q

Obstructive Neuropathy
- Nephrolithiasis

A

Precipitation of stone forming components into ureters
- Indinavir

35
Q

Obstructive Neuropathy
- Lab Values

A

RBC and WBC in Urine
Crystals
- Acyclovir = Needle Shaped
- Indinavir = Rectangular plates or rosettes

36
Q

Obstructive Neuropathy
- Management

A

Discontinue drug

Hydration

Loop diuretic

Supportive Therapy

37
Q

Obstructive Neuropathy
- Prevention

A

Aggressive hydration

Avoid rapid infusions and large bolus doses of drugs that crystalize (Ex. Acyclovir)

Urine alkalinzation

38
Q

Drug Induced Stones
- Crystalize in urine

A

Antibacterials
- Sulphonamides

Protease Inhibitors
- Indinavir, Acyclovir

Antihypertensives
- Triamterene

Others
- Methotrexate

39
Q

Drug Induced Stones
- Metabolically induced

A

Change in fluid balance

Change pH

Hypercalcemia

Hypophosphatemia

Hyperoxaluria

PHARM 343 (20 decks)

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