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MHD Block 5: Renal > Clinical I: Acute Kidney Injury > Flashcards

Clinical I: Acute Kidney Injury Flashcards

1
Q

Define acute kidney injury (AKI)

A
  • Dramatic decrease in renal function
  • Increases in BUN + plasma creatinine + oliguria
  • *its purpose is to compensate for other pathology in the body by decreasing the kidneys functionality
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2
Q

Which pt populations are commonly affected by AKI?

A
  • chronically ill
  • sepsis pts
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3
Q

Name the three types of AKI

A

pre-renal: azotemia

intrinsic: ATN

post-renal: prostatic or solitary kidney disease

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4
Q

Which ratio can we use to help determine what type of AKI we have?

A

BUN: creatinine ratio

>10.1 : prerenal

10.1: intrinsic

<10.1: postrenal

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5
Q

Which drugs are associated with pre-renal azotemia?

A

NSAIDs and ARBs/ACEinhib

they cause an abolition of autoregulation and can lead to more kidney damage in pts with decrease ECF

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6
Q

What are the causes of pre-renal azotemia?

A

Think of systemic stuff that would lead to decrease renal blood (RBF):

  • CHF
  • hemorrhage
  • stenosis or occlusion
  • NSAIDs/ARBs + ECV
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7
Q

Consequences of pre-renal azotemia?

A
  • may progress to acute tubular necrosis
  • decrease in GFR and FENa*
  • increase BUN & BUN:creatinine ratio

*(body holds on to BUN and Na to perserve volume)

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8
Q

What are the general causes of acute post-renal failure?

A

blockage of outflow from the kidney

commonly caused by:

  • stones
  • solitary kidney diseaese
  • intraabdominal: pelvic cancer
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9
Q

Ways to diagnose post-renal failure?

A

phys: fullness in abdomen and urge to urinate upon palpation

imaging: ultrasound and volume scanner

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10
Q

What is post obstruction diuresis and with which type of AKI is associated?

A
  • after clearing a post-renal obstruction, pts may become volume depleted as the body attempts to normalize the volume overload
  • may lead to altered electrolyte status: hyperK and tubular acidosis
  • pts must be monitored closely and catheters clamped if loosing too much fluid
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11
Q

Name the types of intrinsic AKI

A

Acute tubular necrosis

Acute interstitial necrosis

Acute glomerular disease

Vascular

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12
Q

Which type of intrinsic AKI has phasic nature? Name the phases.

A

ATN: injury phase > repair phase

oligouric/injury phase = HTN + volume overload + brown urine

polyuric/repair phase: after necrosis and casts clear tublue = urine flows

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13
Q

What are the most common causes of ATN?

A
  • sepsis
  • IV contrast
  • nephrotoxic exposure
  • high risk: elderly, diabetics, and HTN pts
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14
Q

How does BUN:creatinine and GFR change in intrinsic AKI?

A

GFR: decreases

BUN:creatinine ratio: increases

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15
Q

What are the vascular conditions that can lead to intrinsic AKI?

A
  • malignant HTN: found in critically ill pts
  • scleroderma
  • may also be caused by: encephalopathy, hemorrhage, ACS, eclampsia
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16
Q

Which kidney disease rarely leads to AKI?

A

acute glomerular disease: nephrotic and nephritic syndrome

17
Q

What are the common causes of acute interstitial nephritis?

A
  • *Meds: antimicrobials, NSAIDs
  • autoimmune
  • infection

*most common cause

18
Q

What are the classic symptoms associated with interstitial nephritis?

A
  • fever
  • rash
  • peripheral + URINE eosinophilia
19
Q

What findings may you see on phys exam of people with AKI?

A

dry status: skin tinting, dry mucosal membranes, neck veins flat when @ zero degrees

wet status:

  • abdominal jugular reflux: press on stomach and examine jugular impulse; if yes = + finding
  • S3 gallop
  • peripheral edema/ascities
20
Q

What diagnostic tools are helpful to diagnose AKI?

A
  • careful patient hx
  • labs: URINALYSIS, renal indices (BUN&creatinine) , urine indices (electrolytes)
  • renal ultrasound
  • BUN:creatinine ratio
  • intrinsic vs pre-renal chart
21
Q

Treatment for AKI

A
  • find cause and fix it: increase ECV!
  • discontinue nephrotoxic drugs
  • supportive therapy: nutritional support, manage infections
22
Q

Differences between prerenal and intrinsic/ATN AKI?

A

prerenal:

  • hyaline casts
  • >500 urine osm
  • <20 urine Na
  • < 1% Na excretion
  • <35% urea excretion
  • more concentrated urine: 1.020

intrinsic:

  • abnormal
  • >300 urine osm
  • >40 urine NA
  • >2% Na excretion
  • >35% urea excretion
  • less concentrated urine: 1.010
23
Q

What are the indications for hemodialysis?

A

AEIOU:

Acidosis

Electrolytes

Intoxication: Meds

Overload: pulm edema?

Uremia

24
Q

Prevention of AKI?

A
  • Avoid nephrotoxic drugs in volume depleted patients: ACEinhb and ARBs*
  • prophylax tumor lysis patient** and IV contrast*** patients

*remember they prevent autoregulation!

**tumor lysis = leads to uric acid build up

***

MHD Block 5: Renal (13 decks)

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