Acute Kidney Injury Flashcards

1
Q

acute kidney injury/ acute renal failure definition

A

sudden impairment of kidney function resulting in the retention of nitrogenous and other waste products normally cleared by the kidneys
BUN and SCr increased
oliguria/anuria

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2
Q

BUN

A

blood urea nitrogen
LIVER= protein metabolism
So the substances that increase protein will also increase BUN

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3
Q

classification of AKI

A

• Prerenal= assoc with decreased amt of blood that is flowing to the kidney
○ When there is prob outside kidneys which affects blood flow
• Renal= acute injury inside kidneys
• Postrenal= blockage of urine outflow

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4
Q

prerenal

A
  • increased BUN= increased reabsorption and decreased filtration
  • increased SCr= ONLY due to decreased filtration
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5
Q

renal

A
  • increased BUN= ONLY due to decreased filtration

* SCr mostly stays the same

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6
Q

things that cause prerenal

A

anything that causes hypoperfusion
○ Hypovolemia= burns, severe diarrhea, elderly if they are dehydrated
○ Liver failure= reduced effective amt of circulating blood
§ Blood has been moved to certain areas and is not accessible to kidneys (if blood is trapped)
○ Congestive heart failure
○ Impaired renal autoregulation (NSAIDS, ACE-I/ARB, cyclosporine)

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7
Q

things that cause renal/ instrinsic

A

○ Important one= sepsis= presence of bact in the blood → leads to destruction of tubules and interstitium
○ Ischemia= occurs when you have hypoperfusion ○ Nephrotoxins= a lot of meds and/or contrast agents that are nephrotoxic but you also have endogenous nephrotoxins (hemolysis)
○ Vascular diseases

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8
Q

things that cause postrenal

A

bladder outlet obstruction

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9
Q

what is the most common form of AKI?

A

prerenal azotemia

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10
Q

prerenal azotemia

A

inadequate renal plasma flow and intraglomerular hydrostatic pressure (no parenchymal damage to kidney except if it goes on for long enough)

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11
Q

drop in BP with NSAIDS

A

○ Meds affect prostagladin prod
○ Vessel cannot dilate since meds are inhibiting prostaglandins
○ Hydrostatic pressure drops and increases angiotensin

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12
Q

drop in BP w/ ACE-I/ARB

A

○ Vessel cannot be narrowed

○ Increased perfusion which decrease ANG II

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13
Q

hepatorenal syndrome (prerenal azotemia)

A

caused by advanced liver cirrhosis (liver failure)
• Blood is trapped in splanchnic circulation
○ So don’t have loss of blood but blood is moved in circulation → kidney doesn’t have enough blood → activation of vasoconstrictor responses
○ Fragmentation of renal parenchyma → blood cannot go through the liver

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14
Q

ex of endogenous toxins that affect kidneys

A

myoglobin, hemoglobin, uric acid, myeloma ligh chains

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15
Q

postrenal

A

anything that causes obstruction in the urinary tract
• Common causes= kidney stones, prostatic enlargement (in older men), cancer/ tumors
• Hydronephrosis= kidney will be replaced with urine to where it is just a big sac of urine

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16
Q

diagnosis of AKI

A
  • SCr= rise in at least 0.3 mg/dL or 50% higher than baseline w/in 24-48 HOUR PERIOD or a reduction in urine output to 0.5 mg/kg per hour for longer than 6 hours
  • red/ brown urine color, mild proteinuria
  • hyaline casts= prerenal azotemia
  • BUN/creatinine
  • excretion of sodium (FeNa)
  • kidney biopsy
  • biomarkers (KIM-1, NGAL)
17
Q

important to distinguish AKI from CKD

A

Chronic kidney injury will not have rapid increase in SCr whereas AKI will change w/in like 24 hours

18
Q

oligouria diagnosis

A

urine <400 mL/24h

19
Q

diagnosis for postrenal AKI

A

radiologic evaluation (ultrasound and CT)

20
Q

complications of AKI

A
  • uremia (BUN extremely high!)
  • hypervolemia (pulmonary edema!!= vol overload & hemorrhage in pulmonary-renal syndrome –> acute lung injury)
  • hypovolemia
  • hypoNatremeia
  • hyperkalemia, arrhythmias
  • metabolic acidosis
  • hyperphosphatemia & hypoCaemia
  • bleeding
  • plt dysfunction
  • infections