SG - Pharm 4 > DIKD > Flashcards

DIKD Flashcards

(44 cards)

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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)
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2
Q

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

A

Increased

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3
Q

How is nephrotoxicity reversible?

A

Offending agent discontinued

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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
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5
Q

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

A
  • afferent (arrives)
  • efferent (exits)
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6
Q

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

A

a pre-renal reduction in renal function

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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
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8
Q

Damage to the glomerular or tubular regions can lead to…

A

intrinsic AKI

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9
Q

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

A

post-renal impairment

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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
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11
Q

3 causes of pre-renal AKI

A
  • Transient renal hypoperfusion:
    • Hypotension
    • Decreased CO
    • Decreased effective arterial blood volume
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12
Q

1 cause of Post-renal AKI

A

Obstruction of urinary tract

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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
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14
Q

Causes of what?

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

Volume Depletion leading to Pre-renal AKI

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15
Q

3 drugs which cause Pre-Renal AKI

A
  • NSAIDS
  • ACE-I
  • ARBs
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16
Q

Cause of what?

  • Exogenous Toxins (nephrotoxic drugs, contrast dyes)
A

Acute Tubular Necrosis

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17
Q

Causes of what?

  • NSAIDS and certain abx
A

Acute Interstitial Nephritis

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18
Q

Causes of what?

  • BPH
  • Malignancy
  • Anticholinergic drugs
  • Displaced bladder catheter
Study These Flashcards
A

Bladder outlet obstruction –> Post-renal AKI

19
Q

____ is the most common presentation of DIKD in hospitalized patients

Study These Flashcards
A

Acute Tubular Necrosis (ATN)

20
Q

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

Study These Flashcards
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
Study These Flashcards
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
Study These Flashcards
A

Acute Allergic Interstitial Nephritis (AAIN)

23
Q

Which 2 drugs cause the majority of allergic rxns?

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
Study These Flashcards
A
  • Edema
  • Multisystem organ failure
25
What 3 medications are affected by Pharmacokinetic Alterations?
* Vancomycin (tx MRSA and gram +) * Aminoglycosides * Low-molecular-weight heparins
26
**Electrolyte Disorders** * Most common electrolyte disorder * \>\_\_% of ___ is renally eliminated * Life-threatening cardiac arrhythmias * Frequent monitoring needed
Hyperkalemia * 90% of K
27
Which 2 elements are both eliminated by the kidneys and are not removed efficiently by dialysis?
Phosphorus & Magnesium
28
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.
* ACE * ARB * K-sparing (spirinolactone)
29
Amphotericin is a terrible drug which kills what?
Fungi
30
**Types of what?** * Acute Tubular Necrosis * Osmotic nephrosis
Tubular Epithelial Cell Damage
31
**Types of what?** * Intratubular obstruction * Nephrolithiasis * Nephrocalcinosis
Obstructive nephropathy
32
**Types of what?** * Acute allergic interstitial nephritis * Chronic interstitial nephritis * Papillary necrosis
Tubulointerstitial disease
33
3 agents causing osmotic nephrosis (Tubular Epithelial Damage)
* Dextran * IV immunoglobulin * Mannitol
34
**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
Aminoglycoside (AG) Nephrotoxicity
35
_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**
Aminoglycoside Nephrotoxicity
36
If an aminoglycoside must be used, which one should be used?
Amikacin
37
3 risk factors of Aminoglycoside Nephrotoxicity
* **Aggressiveness of AG dosing** * large cumulative dose * prolonged therapy * **Synergistic toxicity w/ other nephrotoxins** * **Preexisting clinical conditions** * CKD * DM * Older age * Dehydration
38
How do you prevent Aminoglycoside Nephrotoxicity?
* **Avoid volume depletion\*\*** * Use alternative abx when possible * Limit total dose administered * Avoid concomitant nephrotoxic drugs
39
4 ways to manage Aminoglycosde Nephrotoxicity
* Discontinue AG or revise dosing regimen * Stop other nephrotoxic drugs * Adequate hydration * Renal Replacement Therapy (RRT) DARS
40
_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
Contrast-Induced Nephrotoxicity (CIN)
41
_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\***
Contrast Induced Nephrotoxicity (CIN)
42
What are the 3 main risk factors of Contrast-Induced Nephrotoxicity (CIN)?
* **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
4 ways to prevent Contrast Induced Nephrotoxicity (CIN)
* **Use alternative imaging procedures\*** * Hydration * Antioxidants (ascorbic acid, N-acetylcysteine) * Hemofiltration
44
Management of Contrast Induced Nephrotoxicity (CIN)
* Supportive Care * Monitoring (renal function, electrolytes, volume status) * RRT when indicated (renal replacement therapy)
SG - Pharm 4
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