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Pharmacology- Exam #4 > Drug-Induced Kidney Disease > Flashcards

Drug-Induced Kidney Disease Flashcards

1
Q

Causes for prerenal AKI

A

Volume Depletion

  1. Hemorrhagic
  2. GI losses
  3. Renal losses: Drug-induced, osmotic diuresis, diabetes insipidus
  4. Skin losses: Burns
  5. Third spacing (hypoalbuminemia)

Functional

  1. ACE-1, ARB
  2. NSAIDs
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2
Q

List causes for Acute tubular necrosis

A

Exogenous toxins:

  1. Nephrotoxic drugs
  2. Contrast
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3
Q

List causes for post renal AKI

A

Obstruction:

  1. BPH
  2. Tumor (malignancy)
  3. Anticholinergic drugs
  4. Displaced bladder catheter
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4
Q

What is the MC presentation of DIKD in hospitalized patients?

A

Acute Tubular Necrosis (ATN)

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5
Q

List the nephrotoxic agents that cause AKI

A
  1. Aminoglycosides
  2. Contrast
  3. Amphotericin B
  4. Osmotically active agents
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6
Q

Pathogenesis in hemodynamically mediated kidney injury

A

Decrease in glomerular capillary hydrostatic pressure

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7
Q

List the agents that cause hemodynamically mediated kidney injury

A
  1. ACE-1

2. NSAIDs

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8
Q

How many days after you initiated therapy would you see clinical manifestations of acute allergic interstitial nephritis (AIN)? Sx’s?

A

14 days

  1. Fever
  2. Maculopapular rash
  3. Eosinophilia
  4. Arthralgia
  5. Hematuria, proteniuria, oliguria
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9
Q

What is the most common electrolyte disorder?

A

Hyperkalemia

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10
Q

What other electrolyte disorders do we see in kidney disease?

A
  1. Hyperglycemia and insulin resistance

2. Hypertriglyceridemia

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11
Q

What is the pathogenesis of ATN with Aminoglycosides abx

A

Accumulation of high drug concentration in tubular epithelial cells leads:

  1. Tubular damage
  2. Kidney necrosis
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12
Q

How many days after initiation of Aminoglycosides do we see evidence of injury?

A

5-10 days

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13
Q

What is one of the main risk factors in ATN with the use of Aminoglycosides?

A

Pre-existing clinical condition

  1. Dehydration*
  2. CKD
  3. DM
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14
Q

What is the main preventative strategy in ATN with the use of Aminoglycosides?

A

Avoid volume depletion

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15
Q

Pathogenesis of Contrast-Induced Nephrotoxicity (CIN)

A

Renal ischemia from systemic hypotension and acute vasoconstriction (contrast is a vasoconstrictor) d/t disruption of normal RBF

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16
Q

Clinical presentation of Contrast-Induced Nephrotoxicity (CIN)

A
  1. Injury present w/in 24-48 hrs of administration
  2. Serum Cr peaks w/in 3-5 days
  3. Recovery in 7-10 days
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17
Q

Risk factors in Contrast-Induced Nephrotoxicity (CIN)

A
  1. Pre-existing kidney dz, GFR <60 mL/min
  2. Decreased RBF: CHF, dehydration
  3. Concurrent use of nephrotoxins: NSAIS, ACE-1
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18
Q

Prevention of Contrast-Induced Nephrotoxicity (CIN)

A

Use alternative imaging procedures

19
Q

Pathogenesis of ATN with the use of Amphotericin B

A
  1. Increased permeability and necrosis

2. Decreased RBF exacerbates necrosis

20
Q

What electrolytes will you see wasting with Amphotericin B?

A
  1. Potassium
  2. Sodium
  3. Magnesium
21
Q

When does the dysfunction become apparent with the use of Amphotericin B? Lab findings?

A

1-2 weeks
Decrease in GFR
Increase in Serum Cr and BUN

22
Q

What should you switch to for high risk patients in place of with the use of Amphotericin B?

A

Liposomal form

23
Q

Amphotericin B prevention

A
  1. Increase infusion time

2. Alternative antifungals: Azoles, Caspofungin

24
Q

What do patients take Cyclosporine for?

A

Prevent kidney graft rejection

25
Q

What is unique about Cyclosporine toxicity?

A

Dose-Dependent

26
Q

Presentation of nephrotoxicity with use of ACE-1 and ARBs

A
  1. Decrease in UO
  2. Acutely reduces GFR
  3. Rise in Serum Cr up to 30% in 3-5 days
27
Q

How long after discontinuing the ACE-1 or ARB do you stabilize?

28
Q

Risk factors for nephrotoxicity with the use of an ACE-1 or ARB

A
  1. Renal artery stenosis

2. Decrease arterial blood flow: CHF, volume depletion

29
Q

When should you discontinue an ACE-1 or ARB?

A

SCr increases >30% in 1-2 weeks

30
Q

Pathogenesis of NSAIDs and COX-2 in pre-renal AKI

A

Inhibits synthesis of vasodilatory prostoglandins=unopposed vasoconstriction of afferent arteriole

31
Q

Presentation of NSAIDs and COX-2 in pre-renal AKI

A
  1. Decreased UO
  2. Weiht gain/edema
  3. HTN
  4. Elevated SCr, BUN, K+
32
Q

What is a a potent compound you should avoid in high risk patients with NSAIDs/COX-2 pre-renal AKI

A

Indomethacin

33
Q

What NSAID can you consider that has a shorter half life for prevention management in pre-renal AKI?

34
Q

What is Methicillin-induced AIN associated with? When do you see injury after initiation of these drugs?

A

Beta-lactacm abx

14 days after initiation

35
Q

Clinical presentation of Methicillin-induced AIN

A 
1. Fever
2, Maculopapular rash
3 Eosinophila
4. Arthralgia 
5. Oliguria
36
Q

How do you treat/manage Methicillin-induced AIN

A

Immediate corticosteroids

37
Q

List the cause for chronic interstitial nephritis

A
  1. Cyclosporine
38
Q

List the cause for papillary necrosis

39
Q

What drugs can cause intratubular obstruction (obstructive nephropathy)?

A
  1. Acyclovir

2. Sulfonamides

40
Q

what conditions can cause intratubular obstruction (obstructive nephropathy)?

A
  1. Hyperuricemia

2. Rhabdomyolysis

41
Q

What drugs increases your risk for Rhabdomyolysis?

A
  1. HMG-CoA reductase inhibitors (statins)

2. Concurrent CYP3A4 drugs

42
Q

What drugs cause renal vasculitis and thrombosis

A
  1. Hydralazine

2. Methamphetamine

43
Q

What drugs cause a cholesterol emboli

A
  1. Warfarin

2. Thrombolytic agents

44
Q

What drugs cause glomerular disease?

A
  1. NSAIDs

2. COX-2 inhibitors

Pharmacology- Exam #4 (6 decks)

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