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

Flashcards in Drug-Induced Kidney Disease Deck (44)
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1

Causes for prerenal AKI

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

2

List causes for Acute tubular necrosis

Exogenous toxins:
1. Nephrotoxic drugs
2. Contrast

3

List causes for post renal AKI

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

4

What is the MC presentation of DIKD in hospitalized patients?

Acute Tubular Necrosis (ATN)

5

List the nephrotoxic agents that cause AKI

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

6

Pathogenesis in hemodynamically mediated kidney injury

Decrease in glomerular capillary hydrostatic pressure

7

List the agents that cause hemodynamically mediated kidney injury

1. ACE-1
2. NSAIDs

8

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

14 days
1. Fever
2. Maculopapular rash
3. Eosinophilia
4. Arthralgia
5. Hematuria, proteniuria, oliguria

9

What is the most common electrolyte disorder?

Hyperkalemia

10

What other electrolyte disorders do we see in kidney disease?

1. Hyperglycemia and insulin resistance
2. Hypertriglyceridemia

11

What is the pathogenesis of ATN with Aminoglycosides abx

Accumulation of high drug concentration in tubular epithelial cells leads:
1. Tubular damage
2. Kidney necrosis

12

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

5-10 days

13

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

Pre-existing clinical condition
1. Dehydration*
2. CKD
3. DM

14

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

Avoid volume depletion

15

Pathogenesis of Contrast-Induced Nephrotoxicity (CIN)

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

16

Clinical presentation of Contrast-Induced Nephrotoxicity (CIN)

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

17

Risk factors in Contrast-Induced Nephrotoxicity (CIN)

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

18

Prevention of Contrast-Induced Nephrotoxicity (CIN)

Use alternative imaging procedures

19

Pathogenesis of ATN with the use of Amphotericin B

1. Increased permeability and necrosis
2. Decreased RBF exacerbates necrosis

20

What electrolytes will you see wasting with Amphotericin B?

1. Potassium
2. Sodium
3. Magnesium

21

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

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

22

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

Liposomal form

23

Amphotericin B prevention

1. Increase infusion time
2. Alternative antifungals: Azoles, Caspofungin

24

What do patients take Cyclosporine for?

Prevent kidney graft rejection

25

What is unique about Cyclosporine toxicity?

Dose-Dependent

26

Presentation of nephrotoxicity with use of ACE-1 and ARBs

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

27

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

1-2 weeks

28

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

1. Renal artery stenosis
2. Decrease arterial blood flow: CHF, volume depletion

29

When should you discontinue an ACE-1 or ARB?

SCr increases >30% in 1-2 weeks

30

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

Inhibits synthesis of vasodilatory prostoglandins=unopposed vasoconstriction of afferent arteriole

31

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

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

32

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

Indomethacin

33

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

Sulindac

34

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

Beta-lactacm abx
14 days after initiation

35

Clinical presentation of Methicillin-induced AIN

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

36

How do you treat/manage Methicillin-induced AIN

Immediate corticosteroids

37

List the cause for chronic interstitial nephritis

1. Cyclosporine

38

List the cause for papillary necrosis

NSAIDs

39

What drugs can cause intratubular obstruction (obstructive nephropathy)?

1. Acyclovir
2. Sulfonamides

40

what conditions can cause intratubular obstruction (obstructive nephropathy)?

1. Hyperuricemia
2. Rhabdomyolysis

41

What drugs increases your risk for Rhabdomyolysis?

1. HMG-CoA reductase inhibitors (statins)
2. Concurrent CYP3A4 drugs

42

What drugs cause renal vasculitis and thrombosis

1. Hydralazine
2. Methamphetamine

43

What drugs cause a cholesterol emboli

1. Warfarin
2. Thrombolytic agents

44

What drugs cause glomerular disease?

1. NSAIDs
2. COX-2 inhibitors