aki Flashcards

1
Q

what is an acute kidney injury?

A

A sudden decline in function & rapid progressive

Ischemic injury
- Related to volume depletion and decreased perfusion
- Toxic injury from chemicals
- Sepsis
Injury initiates an inflammatory response, vascular response, and cell death

3 classifications for AKI
Prerenal
Intrarenal
Postrenal

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2
Q

is an acute kidney injury reversible?

A

it can be

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3
Q

what labs would you find with an acute kidney injury

A

decreased GFR so <90
decreased uOP so <30 mL/ hour, or <400 mL/day
increased BUN so >20
Increased creatinine so >1.2

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4
Q

what does AKI often follow?

A

severe, prolonged hypotension, hypovolemia, or exposure to nephrotoxic agents

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5
Q

what is the most common cause of pre-renal AKI

A

Most common cause is inadequate perfusion

decreased cardiac output, so hypotension, hypovolemia, decreased perfusion to kidneys

Decreased GFR due to low glomerular filtration pressure

Failure to restore blood volume, blood pressure, and oxygen delivery can cause ischemic cell injury and necrosis

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6
Q

what is the most common cause of intrarenal AKI

A

acute tubular necrosis

  • Related to prerenal AKI, nephrotoxic agents, acute glomerulonephritis, & vascular disease
nephrotoxic ATN
Antibiotics
Heavy Metals
Contrast Dye
Rhabdomyolysis
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7
Q

post renal AKI

A
A rare condition that usually occurs with urinary tract obstruction
Bladder outlet obstruction
Prostatic hyperplasia
Bilateral ureteral obstruction
Tumor
Neurogenic bladder

BPH (benign prostatic hypertrophy)

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8
Q

what are the clinical manifestations for aKI

A
  • oliguria <400 ml/day
  • begins 1 day after hypotensive event and lasts 1-3 days
  • fluid volume excess (Why? you aren’t peeing)-metabolic acidosis
  • hyponatremia (disoriented, confused)
  • hyperkalemia
  • waste product accumulation (BUN & cr)
  • neurologic disorders
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9
Q

Treatment for aKI

A

Correct fluid and electrolyte imbalances, especially hyperkalemia and excess fluid volume

  • manage BP
  • prevent/treat infections
  • maintain nutrition
  • avoid nephrotoxic drugs
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10
Q

how to lower serum potassium?

A
  • dietary restriction
  • potassium binders (patiromer, sodium zirconium cyclosilicate, and sodium polystyrene sulfonate)
  • Calcium gluconate IV (lessens risk of dysrhythmias)
  • dextrose and insulin – pushes into cells
  • sodium bicarbonate– correct acidosis & pushes k into cells
  • hemodialysis
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11
Q

when should you NOT give sodium polystyrene sulfonate (kayexalate)

A
  • do not use for emergency life threatening hyperkalemia due to delayed onset
  • do not give if paralytic ileus
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12
Q

AKI labs

may be reversible

A
Decreased GFR (> 90 ml/min)
Decreased UOP (> 30 ml/hr)
Increased BUN (10-20 mg/dL)
Elevated creatinine (0.5 – 1.2 mg/dL)
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13
Q

pharm tx

A

Goal of treatment is to stabilize patient until kidney function is returned
Management includes:
- Correct fluid, electrolyte imbalance (particularly hyperkalemia)
- Lasix to try to push kidneys to function and remove potassium
- Dextrose and insulin to help move K back into cells

Binders

  • sodium polystyrene sulfonate (Kayexalate)
  • patiromer(Veltassa)
  • sodium zirconium cyclosilicate (Lokelma)

Correct Acid-base imbalance (metabolic acidosis)
- Sodium bicarbonate

Manage blood pressure
Avoid drugs that are nephrotoxic

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