AKI Flashcards

0
Q

AKI can be __ or ___

which is worse?

A

oliguric
non-oliguric
*oliguric is worse

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1
Q

acute kidney injury definition

A

GFR decreases by >/ 25% within hours to days

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2
Q

three categories acute kidney injury

A

hemodynamic or pre-renal-imbalance of blood supply an ddemand
intrinsic or renal-okay blood supply with direct injury
obstructive or post-renal

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3
Q

what phase persists as long as insult is present?

A

apoptosis and sloughing phase

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4
Q

what do sympethetics do in renal injury

A

vasocon–>decrease renal BF–>increase NA reabs

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5
Q

pre-renal azotemia

A

littel, concentrated low Na urine; pre-renal

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6
Q

muddy brown casts

A

acute tubular necrosis

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7
Q

what is the main shift between AKI and ATN

A

urine osmolarity becomes isothenuric to the plasma

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8
Q

clinical causes of hemodynamic acute kidney injury

A

decrease in ECFV

  • -hypobvolemia (hemorrhage, diarrhea)
  • -hypervolemia (edematous state)
  • -euvolemia (sepsis, SIRS, cap leak)
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9
Q

three types of intrinsic (renal) AKI

A

glomerular
tubulo-interstital
vascular

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10
Q

three ways tubular injury causes a decrease in GF

A

sloughing off cells decreases GFR
back-leak- holes in tubule let filtered blood go back
macula densa senses increased Na and Cl flow–>increases afferent tone–> decreases GFR

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11
Q

when does allergic interstital nephritis start

A

7ish days after causative agent

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12
Q

what will you see with AIN

A

WBC in urine

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13
Q

hallmark of rhabdo

A

pink urine + for heme but no blood on microscopy

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14
Q

treat of rhabdo

A

hydration and alkalinization of urine

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15
Q

Ig light chain

A

usually a marker of MM and non-oliguric

16
Q

why do you get hyperuricemia

A

tumor lysis or inherent errors of purine metabolism

17
Q

how does uric acid fuck up the kidney

A

crystallyzes in tubules and reabsorbed by PCT into tubulointerstium–>produces inflammatory rxn with giant cell

18
Q

treatment of uric acid issues

A

volume expansion/alkalosis

xanthien oxidatse inhibitors (allopuritinol)

19
Q

labs for uric acid issue

A

oliguric or non-oliguric
urine sediment bland or with crystals
serum UA >10
increase circulating phoshphatase and LDH

20
Q

exogenous toxins that mess up kidneys

A

NSAIDs
iodinated contrast-moa
calcineurin inhib (cyclosporine, tacrolimus)–vasocon
aminoglycoside antibiotics-moa –>tubulue specific (RTA)
amphotericin B–>distal RTA, nephrogenic DI
Cisplatinum:distal tubular tox

21
Q

crystals taht mess up kidneys

A
acyclovir
idinavir
methotrexate
sodium phosphate 
quinolone
22
Q

what else do aminoglycoside antibiotics cause

A

ototoxicity

23
Q

renal vein occlusion

A

non-oliguric
loin pain
occurs in hypercoag states (cancer, nephrotic syndrome, sepsis)

24
Q

thrombotic microangiopathies

A

occlusion of vessels with proliferating endothelial and platelet/fibrin thrombi

25
Q

what do you see with thrombotic microangiopathies

A

oliguric aki

no cells or casts

26
Q

post-renal AKI

A

obstruvtive

27
Q

how does obstructive aki present

A
NOT oliguric
back pressure is lower than GFR but highte than medullary capillary pressure
nonanion gap acidosis (type IV)
dilute urine
hyperkalemia!
28
Q

obstruction quick word

A

type IV RTA

29
Q

polyuria with medication

A

induced nephrogenic diabetes insipidus

30
Q

proximal RTA

A

myeloma
aminoglycosides
platinum

31
Q

suggestive of bence jones protein

A

elevated urine protein with negative dipstick

32
Q

indications for dialysis

A

volume overload
hyperkalemia
acidosis
uremia

33
Q

multiple organ failure patients

A

cant do dialysis so solution is continuous venous-venous filtration which replaces plasma with electrolyte soln

34
Q

definition of oliguria

A

<30 ml/hr