Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 4 - Toxicology > 21 - Nephrotoxicity > Flashcards

21 - Nephrotoxicity Flashcards

1
Q

Diagnostic criteria of acute kidney injury

A
  • Abrupt decline in GFR
    • sCr by 0.3 mg/dL or more w/in 48 h, OR
    • sCr to 1.5 times or more baseline w/in 7 days, OR
    • Urine volume < 0.5 mL/kg/h for 6 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pre-renal AKI means ____

A

Impaired renal perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Causes of pre-renal AKI

A
  • Volume depletion (diuretics, cathartics, emetics)
  • Bleeding (anticoagulants)
  • Cardiac dysfunction (beta-blockers, cardiotoxins)
  • Vasoconstriction (NSAIDs, calcineurin inhibitors, ex: cyclosporine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Renal AKI means ____

A

Intrinsic damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Causes of renal AKI

A
  • Vascular -> cyclosporine, tacrolimus, quinine, clopidogrel
  • Glomerular (ACE inhibitors, NSAIDs)
  • Acute tubular necrosis (acetaminophen, aminoglycosides, antifungals, chemotherapeutic agents, iodinated contrast media)
  • Acute interstitial nephritis (hypersensitivity) -> antimicrobials, NSAIDs, diuretics, antihistamines, PPI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the most common cause of AKI?

A

Pre-renal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Post-renal AKI means ____

A

Obstruction of urine flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes of post-renal AKI

A
  • Bladder dysfunction (anticholinergics, antipsychotics)
  • Crystal forming (acyclovir, ciprofloxacin, methotrexate, sulfonamides)
  • Retro-peritoneal fibrosis (beta-blockers, bromocriptine, hydralazine, methyldopa)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Risk factors for chronic kidney disease

A
  • Pre-existing renal impairment
  • Dehydration (diuresis, vomiting or diarrhea, hemorrhage)
  • Medical conditions (cirrhosis, HF, DM)
  • Multiple nephrotoxic agents
  • Seriously ill (septic shock, hypotension)
  • Advanced age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which NSAIDs are most nephrotoxic?

A

All equally nephrotoxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Mechanism of NSAID nephrotoxicity

A
  • Pre-renal (decreases vasodilatory prostaglandins => vasoconstriction => decreased renal blood flow)
  • Acute interstitial nephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Clinical manifestations of NSAID nephrotoxicity

A
  • Increased plasma creatinine
  • Decreased renal blood flow and GFR
  • Oliguria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Prevention of NSAID nephrotoxicity

A
  • Avoid NSAIDs among high-risk px
  • Monitor creatinine levels closely
  • Avoid NSAIDs prior to procedures involving radiocontrast
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Mechanism of aminoglycoside nephrotoxicity

A
  • Proximal tubular necrosis

- Interstitial nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Clinical manifestations of aminoglycoside nephrotoxicity

A
  • Increased plasma creatinine
  • Increased BUN
  • Non-oliguric
  • Electrolyte abnormalities (infrequent)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Aminoglycoside-related risk factors for nephrotoxicity

A
  • Elevated serum drug concentrations
  • Prolonged duration of therapy
  • Type of aminoglycoside (gentamicin > tobramycin > amikacin)
    • B/c gentamicin has highest affinity
  • Frequency of dosing (once daily vs. traditional dosing)
17
Q

Prevention of aminoglycoside nephrotoxicity

A
  • Avoid in px w/ risk factors
  • Adjust dose for renal function
  • Correct hypokalemia and hypomagnesemia
  • Limit duration of therapy to 7-10 days
  • Minimize concomitant nephrotoxic medications
  • Choose aminoglycoside w/ less nephrotoxicity
  • Monitor aminoglycoside serum concentration
  • Utilize a once-daily dosing regimen
18
Q

Mechanism of iodinated contrast media nephrotoxicity

A

High osmolality => acute tubular necrosis and vasoconstriction

19
Q

What are properties of the newest iodinated contrast media?

A
  • Non-ionic dimers

- Iso-osmolal

20
Q

Clinical manifestations of iodinated contrast media nephrotoxicity

A
  • Within 24-48 h after exposure
  • Mild increase in sCr
  • Usually non-oliguric
  • Hyperkalemia, acidosis, hyperphosphatemia
21
Q

Dye-related risk factors for iodinated contrast media nephrotoxicity

A
  • Dose of contrast agent
  • Type of contrast agent
  • Specific procedure (intra-arterial vs. IV and interventional vs. diagnostic angiography)
22
Q

Pt-related risk factors for iodinated contrast media nephrotoxicity

A
  • GFR < 60 mL/min + significant proteinuria (proteinuria > 500 mg/day)
  • GFR < 60 mL/min + comorbidities (DM, HF, liver failure, or multiple myeloma)
  • GFR < 45 mL/min
  • GFR < 30 mL/min (highest risk)
23
Q

Prevention of iodinated contrast media nephrotoxicity

A
  • Avoid volume depletion
  • Withhold NSAIDs for 24-48 h prior to procedure
  • Dose and type of contrast agent:
    • Use lowest effective dose
    • Avoid high osmolality agents, use iso-osmolal agent or nonionic low-osmolal agents (2nd or 3rd gen agents)
  • For at-risk px/risky procedures -> hydrate w/ IV isotonic saline

Year 4 - Toxicology (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions