Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology Exam #4 > DIKD > Flashcards

DIKD Flashcards

1
Q

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

A
  • Decline in GFR
  • Rise in serum creatinine (Scr)
  • Rise in BUN (blood urea nitrogen)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

BUN is a marker of reanl health. If GFR and blood volume are decreased, will BUN be elevated or decreased?

A

Increased

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

How is nephrotoxicity reversible?

A

Offending agent discontinued

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

6 things to look out for in DIKD

“HE A PUP”

A
  • Hematuria
  • Electrolyte imalances
  • Acid-base abnormalities
  • Proteinuria
  • Urine sediment abnormalities
  • Pyuria-neutrophils (pus) in urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Blood flows through the ___ arteriole, to the glomerulus, and exits through the __ arteriole.

A
  • afferent (arrives)
  • efferent (exits)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

A decrease in blood flow and renal perfusion can lead to _____.

A

a pre-renal reduction in renal function

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

Under conditions in which renal blood flow is diminished, the kidney maintains glomerular ultrafiltration by _____ the _____ arterioles and _____ the _____ arterioles.

A
  • vasodilating the afferent
  • vasoconstricting the efferent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Damage to the glomerular or tubular regions can lead to…

A

intrinsic AKI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Obstruction of urine flow in the collecting tubule, ureter, bladder, or urethra is termed _____

A

post-renal impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

3 parameters to assess for possible drug-induced AKI

A
  • Abrupt (48 hrs) reduction in kidney function defined as absolute increase in Scr of greater than or equal to 0.3mg/dL
  • Percentage increase in Scr of greater than or equal to 50% (1.5 fold from baseline) within 7 days
  • Reduction in urine output (documented oliguria of less than 0.5 mL/kg/h for more than 6 hrs), when correlated temporally w/ the initiation od drug
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

3 causes of pre-renal AKI

A
  • Transient renal hypoperfusion:
    • Hypotension
    • Decreased CO
    • Decreased effective arterial blood volume
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

1 cause of Post-renal AKI

A

Obstruction of urinary tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

3 causes of Intrinsic AKI

A
  • Acute glomerulonephritis (inflammation/damage to glomerular membrane)
  • Acute interstitial nephritis (allergic rxn may be caused by drugs)
  • Acute tubular necrosis (accounts for more than 50% of cases of AKI)
    • nephrotoxic agents
    • prolonged renal hypoperfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Causes of what?

  • drug-induced osmotic diuresis
  • Diabetes Insipidus
  • burns
  • 3rd space losses (hypoalbuminemia)
A

Volume Depletion leading to Pre-renal AKI

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

3 drugs which cause Pre-Renal AKI

A
  • NSAIDS
  • ACE-I
  • ARBs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cause of what?

  • Exogenous Toxins (nephrotoxic drugs, contrast dyes)
A

Acute Tubular Necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Causes of what?

  • NSAIDS and certain abx
A

Acute Interstitial Nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Causes of what?

  • BPH
  • Malignancy
  • Anticholinergic drugs
  • Displaced bladder catheter
A

Bladder outlet obstruction –> Post-renal AKI

19
Q

____ is the most common presentation of DIKD in hospitalized patients

A

Acute Tubular Necrosis (ATN)

20
Q

What are the 6 primary agents causing ATN –> DIKD in hospitalized pts?

A

RAACO

  • Radiocontrast media**
  • Aminoglycoside abx**
  • Amphotericin B**
  • Cisplatin
  • Osmotically active agents
21
Q

Pathogenesis is a decrease in glomerular capillary hydrostatic pressure

  • ACI-I
  • NSAIDS
A

Hemodynamically mediated kidney injury

22
Q
  • 27% of kidney biopsies performed for hospitalized pts w/ unexplained AKI
  • Clinical manifestations present approximately 14 days after initiation of therapy:
    • fever, maculopapular rash, eosinophilia
    • arthralgia, pyuria, hematuria
    • proteinuria, oliguria
A

Acute Allergic Interstitial Nephritis (AAIN)

23
Q

Which 2 drugs cause the majority of allergic rxns?

A
  • PCN
  • Sulfa
24
Q

Pharmacokinetic Alterations

  • What can significantly increase the volume of distribution of many drugs
  • What is often an accompanying problem resulting in: -reduction in CO -reduction in liver function
A
  • Edema
  • Multisystem organ failure
25
Q

What 3 medications are affected by Pharmacokinetic Alterations?

A
  • Vancomycin (tx MRSA and gram +)
  • Aminoglycosides
  • Low-molecular-weight heparins
26
Q

Electrolyte Disorders

  • Most common electrolyte disorder
  • >__% of ___ is renally eliminated
  • Life-threatening cardiac arrhythmias
  • Frequent monitoring needed
A

Hyperkalemia

27
Q

Which 2 elements are both eliminated by the kidneys and are not removed efficiently by dialysis?

A

Phosphorus & Magnesium

28
Q

What 3 drugs can cause hyperkalemia?

We don’t “recycle” potassium. But we can prevent the excretion. It is NOT well regulated by the kidneys.

A
  • ACE
  • ARB
  • K-sparing (spirinolactone)
29
Q

Amphotericin is a terrible drug which kills what?

A

Fungi

30
Q

Types of what?

  • Acute Tubular Necrosis
  • Osmotic nephrosis
A

Tubular Epithelial Cell Damage

31
Q

Types of what?

  • Intratubular obstruction
  • Nephrolithiasis
  • Nephrocalcinosis
A

Obstructive nephropathy

32
Q

Types of what?

  • Acute allergic interstitial nephritis
  • Chronic interstitial nephritis
  • Papillary necrosis
A

Tubulointerstitial disease

33
Q

3 agents causing osmotic nephrosis (Tubular Epithelial Damage)

A
  • Dextran
  • IV immunoglobulin
  • Mannitol
34
Q

Pathogenesis of what?

  • Accumulation of high drug concentrations within proximal tubular epithelial cells
  • Produces reactive oxygen species causing mitochondrial injury
  • LEADS TO KIDNEY NECROSIS**
  • Toxicity is related to the # of cationic groups on the molecule
    • Neomycin>Gentamicin>Tobramycin>Amkacin
A

Aminoglycoside (AG) Nephrotoxicity

35
Q

Clinical presentation of what?

  • Nonoliguria
  • Evidence of injury seen within 5-10 days after initiation of therapy*** (not abrupt)
  • Gradual progressive rise in Scr and BUN and decrease in CrCl
  • Full recovery of renal function is common if therapy is immediately discontinuted
A

Aminoglycoside Nephrotoxicity

36
Q

If an aminoglycoside must be used, which one should be used?

A

Amikacin

37
Q

3 risk factors of Aminoglycoside Nephrotoxicity

A
  • Aggressiveness of AG dosing
    • large cumulative dose
    • prolonged therapy
  • Synergistic toxicity w/ other nephrotoxins
  • Preexisting clinical conditions
    • CKD
    • DM
    • Older age
    • Dehydration
38
Q

How do you prevent Aminoglycoside Nephrotoxicity?

A
  • Avoid volume depletion**
  • Use alternative abx when possible
  • Limit total dose administered
  • Avoid concomitant nephrotoxic drugs
39
Q

4 ways to manage Aminoglycosde Nephrotoxicity

A
  • Discontinue AG or revise dosing regimen
  • Stop other nephrotoxic drugs
  • Adequate hydration
  • Renal Replacement Therapy (RRT)

DARS

40
Q

Pathogenesis of what?

  • Renal ischemia from systemic hypotension and acute vasoconstriction**
  • Disruption of normal renal blood flow may last for several hours
  • Increased contrast in renal tubules, exacerbating direct toxicity
    • extent of cellular toxicity directly related to contrast exposure
A

Contrast-Induced Nephrotoxicity (CIN)

41
Q

Presentation of what?

  • Nonoliguria (>500ml urine/ day)
  • Injury present within first 24-48 hrs after administration*
  • Scr usually peaks between 3 and 5 days after exposure*
  • Recovery after 7 - 10 days*
A

Contrast Induced Nephrotoxicity (CIN)

42
Q

What are the 3 main risk factors of Contrast-Induced Nephrotoxicity (CIN)?

A
  • Pre-existing kidney disease* (GFR<60)
  • Decreased renal blood flow* (CHF, dehydration/volume depletion, hypotension, diabetes)
  • Concurrent use of nephrotoxins* (NSAIDs, ACEIs)

(as # of risk factors increase, mortality increases)

43
Q

4 ways to prevent Contrast Induced Nephrotoxicity (CIN)

A
  • Use alternative imaging procedures*
  • Hydration
  • Antioxidants (ascorbic acid, N-acetylcysteine)
  • Hemofiltration
44
Q

Management of Contrast Induced Nephrotoxicity (CIN)

A
  • Supportive Care
  • Monitoring (renal function, electrolytes, volume status)
  • RRT when indicated (renal replacement therapy)

Pharmacology Exam #4 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions