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pharmacology > Renal > Flashcards

Renal Flashcards

1
Q

What are the most common manifestation of drug induced kidney disease? (3)

A
  1. reduced GFR (most important)
  2. serum creatinine
  3. increased BUN
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2
Q

Which parts are damaged in the intrinsic AKI?

A

Glomerulus and tubular regions

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3
Q

Which part of the kidney is damaged in the post renal impairment?

A

obstruction of urine flow in bladder, ureter, collecting tubules and urethra

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4
Q

Which part of the kidney is damaged in prerenal AKI?

A

vasodilaton of afferent arteriole

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5
Q

What are the parameters to access for suspected drug induced kidney disease?

A
  1. abrupt (48 hrs) reduction in kidney function, noted by an increase of serum creatinine greater than 0.3 mg/dL
  2. % increase of serum creatinine by 50% within 7 days
  3. reduced urine output (0.5 mg/kg/h for more than 6 hrs after initiation of drug)
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6
Q

Causes for prerenal AKI?

A

Hypoperfusion….

  1. Hypotension
  2. decreased cardiac output
  3. decreased arterial blood volume
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7
Q

Post renal cause?

A

obstructed urine flow

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8
Q

Intrinsic AKI categories? (3)

A

Acute glomerular nephritis
Acute interstitial nephritis
Acute tubular necrosis

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9
Q

What is the most common cause of DIKD in hospitalized patients?

A

ATN

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10
Q

Name two pharmacokinetic alterations? (2)

A

edema -affects volume distribution

multisystem organ failure-reduced liver function

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11
Q

What is the most common electrolyte disorder?

A

hyperkalemia

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12
Q

Name 4 drugs that cause ATN?

A

Aminoglycosides
Radiographic contrast media
Amphotericin B
Cyclosporine

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13
Q

Causes of osmotic nephrosis (3)?

A

Mannitol
Dextran
IV immunoglobulin

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14
Q

What is Aminoglycoside pathogenesis?

A
  • causes ATN

- high concentrations of drug= cationic groups=reactive oxygen species =nephrotic necrosis

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15
Q

What is clinical presentation of ATN with aminoglycoside toxicity?

A
  • nonoliguria >500mL per day
  • occurs 5 to 7 days after starting therapy
  • gradual progressive rise serum creatinine and BUN and decrease in Cr Cl
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16
Q

T/ F Full recovery of renal function achieved with immediate discontinuation of AG?

A

TRUE

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17
Q

Name the 4 aminoglycosides from most to least toxic?

A

Neomycin>Gentamicin>Tobramycin>Amikacin

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18
Q

Risk factors for AG nephrotoxicity?

A
  • Aggressive AG dosing
  • synergistic effect with other toxins
  • CKD, DM, dehydration, and increased age
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19
Q

How do you prevent AG toxicity? (3)

A
  • limit dosing
  • avoid volume depletion!
  • fluoroquinolones or 3rd gen cephalosporins
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20
Q

How do you manage AG toxicity?(3)

A
  • hydration
  • stop all nephrotoxic drugs and AG
  • renal replacement therapy
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21
Q

What is pathogenesis of contrast induced nephrotoxicty?

A

-renal ischemia from systemic hypotension and acute vasoconstriction

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22
Q

What is clinical presentation of CIN? (3)

“NISR”

A
  • injury presents 24-48hrs after
  • serum creatinine peaks at 3-5 days
  • recovery in to 10 days
  • non oliguria
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23
Q

Risk factors for CIN?(3)

A
  • reduced renal blood flow
  • GFR <60
  • concurrent use of NSAIDS and ACE-I
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24
Q

Prevention of CIN? (2)

A
  • use of low or iso-osmolar contrast agents

- hydration

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25
Q

What is management of CIN? (2)

A
  • supportive care

- RRT

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26
Q

What is pathogenesis of Amphotericin B? (2)

A
  • reduction in renal blood flow

- increased permeability and necrosis in tubular epithelium

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27
Q

What is clinical presentation of amphotericin B? (5)

A
  • nonoliguria
  • Na, K, and Mg wasting
  • dysfunction appears in 1-2 weeks
  • decrease in GFR, rise in creatinine, and BUN
  • damage may be irreversible
28
Q

What is prevention of Amphotericin B toxicity? (3)

A
  • use azoles
  • increase infusion time
  • switch to liposomal form in high risk patients
29
Q

What is pathogenesis of Cyclosporine?

A
  • distal tubular acidosis with vasoconstriction

- renal function improves after removing the drug

30
Q

name the 3 hemodynamically induced kidney injury?

A

ACE
ARB
NSAIDS

31
Q

What is pathogenesis of ACE and ARBS?

A
  • decreased angiotensin II
  • dilated efferent arteriole
  • reduced hydrostatic pressure in glomerular capillaries
  • already hypotension
32
Q

What is the clinical presentation ACE and ARB toxicity? (5)

RASSO mnemonic

A
  • oliguria
  • acutely reduced GFR
  • Scr rise by 30%
  • stabilizes in 1 -2 weeks
  • reversible upon stopping
33
Q

What are risk factors for ACE and ARB’s?

A
  • volume depletion

- patients dependent on renal vasoconstriction to maintain renal blood flow (renal artery stenosis)

34
Q

How do you prevent ACE ARB toxicity in at risk patients?

A

-use Captopril, enapiril, lisinopril, shorter acting agent in at risk patients

35
Q

How do you manage ACE and ARB toxicity? (3)

A

stop if Srcr increases 30% above baseline over 1- 2 weeks

  • Scr and hyperkalemia will resolve in several days
  • can use again once you correct volume depletion
36
Q

What is MOA of NSAIDS ?

A
  • reduces PGA production
  • blocks afferent vasodilation causes ischemia (unopposed renal vasoconstriction)
  • reduced GFR
37
Q

What is clinical presentation of NSAID toxicity?

A
  • occurs within days
  • weight gain
  • oliguria
  • elevated Srcr, K and BP
38
Q

Risk factors for NSAID?

A

age >60

39
Q

How do you prevent NSAID toxicity?

A
  • don’t use indomethicin
  • use APAP
  • use short half life drugs sulindac
40
Q

What is MOA of methicillin induced allergic interstitial nephritis?

A

Allergic hypersensitivity response
Infiltration of lymphs, eosinophils, and neutrophils
Tubular necrosis

41
Q

What is pathogenesis of AAIN?

A

allergic hypersensitivity response with more changes to renal interstitial than the tubules

42
Q

What is pathogenesis of AIN?

A

allergic hypersensitivity response with more changes to renal interstitial than the tubules

43
Q

Which drugs account for over 70% of AIN? (5)

A
  • penicllins
  • cirpo
  • nsaids
  • PPI (proton pump inhibitor)
  • loop diuretics
44
Q

What drug causes chronic interstitial nephritis?

A

cyclosporine

45
Q

What is pathogenesis of methicillin induced AIN?

A

diffuse infiltration of lymphs, eosinophils, and neutrophils and tubular necrosis

46
Q

how many days will it take for methicillin induced AIN?

A

14 days after initiating therapy

47
Q

What are the clinical signs of methicillin induced AIN? (5)

“FEOAM”

A 
Fever
Eosinophilia
Oliguria
Arthralgia
Maculopapular rash
48
Q

How do you tx methicillin induced AIN?

A

start corticosteroid therapy ASAP

full recovery can be achieved

49
Q

What are the two classifications of obstructive nephropathy?

A

Crystal nephropathy and nephrolithiasis

50
Q

Name two drugs that cause crystal nephropathy?

A

sulfonamides

acyclovir

51
Q

Name drugs that causes nephrolithiasis? (4)

A

sulfonamides
nitrofurantoin
amoxicillin
ciprofloxacin

52
Q

T/F The precipitation of crystal drugs in distal tubular lumens can lead to intratubular obstruction

A

true

53
Q

What is nephrolithiasis?

A

formation renal calculi or kidney stones

54
Q

What is side effect of crystal nephropathy? (2)

A

Rhabdo

Hyperuricemia

55
Q

Is GFR reduced in nephrolithiasis?

A

NO, GFR is not usually decreased

56
Q

What are drug interaction in crystal nephropathy?

A

HmG CoA reductase inhibitors (statins)

increased with concurrent CYP3A4 drugs

57
Q

Which drugs cause vasculitis and thrombosis?

A

Hydralazine

Methamphetamine

58
Q

How do you tx vasculitis and thrombosis?(2)

A

stop medication

give corticosteroid

59
Q

Which drug causes cholesterol emboli? (2)

A

Warfarin

thrombotic agents

60
Q

What is pathogenesis of Warfarin and TA?

A

thrombotic agents cause plaque hemorrhage, cholesterol crystals are released and induce inflammation causing ischemia

61
Q

Is kidney damage reversible with Warfarin/TA?

A

No, irreversible

62
Q

What is clinical presentation in Warfarin toxicity?

A

purple discoloration and mottles skin

63
Q

What is tx for Warfarin toxicity?

A

tx is supportive

64
Q

Name the 3 types of glomerular damage?

A

mild change disease
membranous
focal segmental glomerularsclerosis

65
Q

What drug can cause mild change disease?Clinical presentation?

A

NSAIDS

proteinuria, hyperlipidemia, hypoalbuminuria

66
Q

What drugs can cause membranous disease?(3) Clinical presentation?

A

gold therapy, peniclliamine, and captopril, NSAID

damage to proximal tubule epithelial, immune complex deposition

67
Q

What can cause focal segmental glomerularsclerosis? (3)

Clinical presentation?

A

interferon a,b, anabolic steroids, and lithium

patchy areas of glomerularsclerosis with interstitial inflammation

pharmacology (47 decks)

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