Pharmacology > Renal > Flashcards

Renal Flashcards

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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
What is management of CIN? (2)
- supportive care | - RRT
26
What is pathogenesis of Amphotericin B? (2)
- reduction in renal blood flow | - increased permeability and necrosis in tubular epithelium
27
What is clinical presentation of amphotericin B? (5)
- 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
What is prevention of Amphotericin B toxicity? (3)
- use azoles - increase infusion time - switch to liposomal form in high risk patients
29
What is pathogenesis of Cyclosporine?
- distal tubular acidosis with vasoconstriction | - renal function improves after removing the drug
30
name the 3 hemodynamically induced kidney injury?
ACE ARB NSAIDS
31
What is pathogenesis of ACE and ARBS?
- decreased angiotensin II - dilated efferent arteriole - reduced hydrostatic pressure in glomerular capillaries - already hypotension
32
What is the clinical presentation ACE and ARB toxicity? (5) | RASSO mnemonic
- oliguria - acutely reduced GFR - Scr rise by 30% - stabilizes in 1 -2 weeks - reversible upon stopping
33
What are risk factors for ACE and ARB's?
- volume depletion | - patients dependent on renal vasoconstriction to maintain renal blood flow (renal artery stenosis)
34
How do you prevent ACE ARB toxicity in at risk patients?
-use Captopril, enapiril, lisinopril, shorter acting agent in at risk patients
35
How do you manage ACE and ARB toxicity? (3)
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
What is MOA of NSAIDS ?
- reduces PGA production - blocks afferent vasodilation causes ischemia (unopposed renal vasoconstriction) - reduced GFR
37
What is clinical presentation of NSAID toxicity?
- occurs within days - weight gain - oliguria - elevated Srcr, K and BP
38
Risk factors for NSAID?
age >60
39
How do you prevent NSAID toxicity?
- don't use indomethicin - use APAP - use short half life drugs sulindac
40
What is MOA of methicillin induced allergic interstitial nephritis?
Allergic hypersensitivity response Infiltration of lymphs, eosinophils, and neutrophils Tubular necrosis
41
What is pathogenesis of AAIN?
allergic hypersensitivity response with more changes to renal interstitial than the tubules
42
What is pathogenesis of AIN?
allergic hypersensitivity response with more changes to renal interstitial than the tubules
43
Which drugs account for over 70% of AIN? (5)
- penicllins - cirpo - nsaids - PPI (proton pump inhibitor) - loop diuretics
44
What drug causes chronic interstitial nephritis?
cyclosporine
45
What is pathogenesis of methicillin induced AIN?
diffuse infiltration of lymphs, eosinophils, and neutrophils and tubular necrosis
46
how many days will it take for methicillin induced AIN?
14 days after initiating therapy
47
What are the clinical signs of methicillin induced AIN? (5) | "FEOAM"
``` Fever Eosinophilia Oliguria Arthralgia Maculopapular rash ```
48
How do you tx methicillin induced AIN?
start corticosteroid therapy ASAP | full recovery can be achieved
49
What are the two classifications of obstructive nephropathy?
Crystal nephropathy and nephrolithiasis
50
Name two drugs that cause crystal nephropathy?
sulfonamides | acyclovir
51
Name drugs that causes nephrolithiasis? (4)
sulfonamides nitrofurantoin amoxicillin ciprofloxacin
52
T/F The precipitation of crystal drugs in distal tubular lumens can lead to intratubular obstruction
true
53
What is nephrolithiasis?
formation renal calculi or kidney stones
54
What is side effect of crystal nephropathy? (2)
Rhabdo | Hyperuricemia
55
Is GFR reduced in nephrolithiasis?
NO, GFR is not usually decreased
56
What are drug interaction in crystal nephropathy?
HmG CoA reductase inhibitors (statins) | increased with concurrent CYP3A4 drugs
57
Which drugs cause vasculitis and thrombosis?
Hydralazine | Methamphetamine
58
How do you tx vasculitis and thrombosis?(2)
stop medication | give corticosteroid
59
Which drug causes cholesterol emboli? (2)
Warfarin | thrombotic agents
60
What is pathogenesis of Warfarin and TA?
thrombotic agents cause plaque hemorrhage, cholesterol crystals are released and induce inflammation causing ischemia
61
Is kidney damage reversible with Warfarin/TA?
No, irreversible
62
What is clinical presentation in Warfarin toxicity?
purple discoloration and mottles skin
63
What is tx for Warfarin toxicity?
tx is supportive
64
Name the 3 types of glomerular damage?
mild change disease membranous focal segmental glomerularsclerosis
65
What drug can cause mild change disease?Clinical presentation?
NSAIDS | proteinuria, hyperlipidemia, hypoalbuminuria
66
What drugs can cause membranous disease?(3) Clinical presentation?
gold therapy, peniclliamine, and captopril, NSAID | damage to proximal tubule epithelial, immune complex deposition
67
What can cause focal segmental glomerularsclerosis? (3) | Clinical presentation?
interferon a,b, anabolic steroids, and lithium | patchy areas of glomerularsclerosis with interstitial inflammation
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