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Renal and GU > AKI, CKD, and Dialysis > Flashcards

AKI, CKD, and Dialysis Flashcards

1
Q

How is AKI defined?

A

ACUTE reduction in function (GFR, UOP) and accumulation of nitrogenous wastes (BUN, creatinine)

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2
Q

According to the RIFLE criteria, changes in labs need to be within how many days to be classified as AKI?

A

7 days

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3
Q

What are the three distinct types of AKI?

A

Pre-renal (most common)
Intra-renal
Post-renal

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4
Q

What is the cause of pre-renal AKI?

A

Hypoperfusion due to: low volume, bad pump, vasodilation, or intra-renal vasoconstriction

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5
Q

What are the causes behind intra-renal AKI?

A
  • 85% due to ATN (Ischemic or nephrotoxic)
  • Glomerulonephritis
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6
Q

What is the cause of post-renal AKI?

A

Obstruction

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7
Q

What drug classes are considered to be nephrotoxic?

A

A LOT! Just to name a few…

ACE
ARBs
Antibiotics (aminoglycocides in particular)
Diuretics
Vancomycin
Contrast
Methotrexate

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8
Q

What is the number one cause of intra-renal AKI?

A

Acute tubular necrosis (ATN)

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9
Q

What are the typical causes of ATN?

A
  • Ischemia
  • Infection (sepsis)
  • Nephrotoxins (direct cellular injury)
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10
Q

What are the response expectations in the three distinct types of AKI to fluids?

A
  • Pre-renal: improve with fluids
  • Intra-renal: no change with fluids
  • Post-renal: no response to fluids
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11
Q

What type of AKI will have symptoms of volume depletion, CHF, and cirrhosis?

A

Pre-renal

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12
Q

What type of AKI will appear euvolemic?

A

Intra-renal and Post-renal

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13
Q

Because intra-renal and post-renal AKI will present similarly, what test should be ordered to differentiate the type of AKI?

A

Fractional excretion of sodium (FENa)

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14
Q

What does fractional excretion of sodium (FENa) help differentiate?

A

Helps differentiate between pre-renal and intra-renal AKI

Normal 1-2%
< 1% = pre-renal
> 2% = intra-renal

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15
Q

What type of AKI will there be abnormal casts?

A

Intra-renal

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16
Q

What type of AKI will there be no casts?

A

Post-renal

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17
Q

What type of AKI will have increased urine osmolality?

A

Pre-renal

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18
Q

What is the treatment for AKI?

A

Supportive
- Avoid additional injury: discontinue offending agents
- Maintain perfusion/volume (fluids)
- +/- renal replacement therapy

19
Q

The rise in what element is used to define AKI?

A

Creatinine

*AKI is defined as an absolute increase in serum creatinine by 0.3 mg/dL or more over 48 hours, or a relative increase of 1.5 times baseline or more that is known or presumed to have occurred within 7 days.

20
Q

Can there be neurologic changes with AKI?

A

Yes, prolonged bleeding time due to platelet dysfunction may occur with uremia. Progressive uremia may also cause neurologic signs such as asterixis, encephalopathy, and seizures

Most commonly associated with pre-renal AKI

21
Q

What are the risk factors associated with chronic kidney disease?

A
  • Hypertension
  • DM
  • Small birth weight
  • Childhood obesity
  • Increasing age
  • Black race
    • FH
22
Q

How is the decline in kidney function measured in CKD?

A

GFR

23
Q

A GRF greater than ______ is considered severe CKD

A

30

24
Q

What is the presentation of stage 1 or 2 of (mild) CKD?

A

Asymptomatic, typically caught on routine labs

25
Q

What symptoms are associated with moderate (stage 3 and 4) CKD?

A
  • Hypertension
  • Anemia
  • Fatigue
  • Decreased appetite
  • Malnutrition
  • Electrolyte and mineral abnormalities
26
Q

What labs should be ordered in the work-up for CKD?

A

BMP/CMP
*Persistant reduced GFR (>3 months) is diagnostic of CKD

27
Q

What is the mainstay of treatment for ESRD?

A

Renal replacement therapy

28
Q

What is the definitive treatment of CKD?

A

Renal transplant

29
Q

What is likely the complication leading to mortality in CKD?

A

CVD

*80% will die of CVD before reaching ESRD

30
Q

What GFR value qualifies a patient for dialysis (RRT)?

A

GRF < 10 if no DM; GFR < 15 in DM

31
Q

In pre-renal AKI there is decreased GFR, what are the downstream effects?

A
  • Elevated creatinine, urea (BUN)
  • Decreased Na+ in distal convoluted tubule which activates RAAS
32
Q

Why does intrarenal AKI more associated with surgery, trauma or burns?

A

Due to the fluid shifts and third spacing –> kidney’s become dry from decreased blood flow

33
Q

What is the pathophysiology of intrarenal AKI?

A

Decreased blood flow –> ischemia –> necrosis –> dead, sad nephrons

34
Q

How do you differentiate prerenal vs. intrarenal AKI?

A

Fluid response

35
Q

True or False: Typically, Post-renal AKI requires bilateral obstruction to occur

A

True

36
Q

What type of casts will be present with kidney tubule injury?

A

Brown casts

37
Q

What are the two most common causes of chronic kidney disease?

A

DM and HTN

38
Q

What is Azotemia?

A

Increased urea, creatinine, nitrogenous compounds

Elevated BUN and creatinine in labs

39
Q

What is uremia?

A

Azotemia with symptoms or signs of renal failure (uremic syndrome)

40
Q

What systemic changes will be seen in CKD?

A

Hyperkalemia
Hypocalcemia
Hyper/onatremia
Hypoalbuminemia

41
Q

What is a simple cyst?

A

Acquired, thin walled cyst (serous fluid) within the surface of the kidney

42
Q

What type of genetic inheritance is polycystic kidney disease?

A

Autosomal dominant

43
Q

What is the pathophysiology of polycystic kidney disease?

A

Ciliary defects will decrease the signaling between cells

Decreased intracellular signaling –> increased cellular division, increased apoptosis, decreased resorptive function

Renal and GU (14 decks)

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