103114 acute kidney injury Flashcards

1
Q

acute kidney injury is also called

A

acute renal failure

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2
Q

acute kidney injury

A

reduction in GFR resulting in azotemia developing over days

usually reversible
absence of symptoms of chronic uremia
kidney size usually preserved

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3
Q

what are the common causes of acute kidney injury

A

renal ischemia or toxins

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4
Q

diagnositic criteria for AKI

A

abrupt (48 hr) reduction in kidney fxn defined as

an absolute increase in serum creatinine level of 0.3 mg/dl or

percentage increase in serum creatinine of greater than 50% or

reduction in urine output to

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5
Q

oliguria

A

urine output under 400-500 mL/day

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6
Q

azotemia

A

elevation of nitrogen waste products related to insufficient filtering of blood by kidneys

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7
Q

uremia

A

illness accompanying kidney failure which results from toxic effects of abnormally high concnetrations of nitrogenous substances in blood

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8
Q

what tests can be used in AKI?

A

serum creatinine
blood urea nitrogen
urinalysis

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9
Q

urinalysis testing for AKI can look for what?

A

casts-caused by trapping of cellular elements in a matrix of protein secreted by renal tubule cells

granular casts (muddy brown urine) are seen in acute tubular necrosis

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10
Q

how does autoregulation of GFR occur under decreased perfusion pres?

A

increased vasodilatory prostaglandins at afferent arteriole
increase angiotensin II at efferent arteriole

some cases of kidney injury can be precipitated when there’s a loss of these autoregulatory mechanisms

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11
Q

how can autoregulation of GFR be altered?

A

elderly, NSAIDs, CKD–do not have normal vasodilatory prostaglandin response

ppl taking ACEi and ARBs cannot mount the normal angiotensin II constriction response

so for these ppl, even at modest decrease in MAP, they will have a decrease in GFR

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12
Q

what are possible causes of pre-renal AKI?

A

volume depletion
heart failure
liver failure

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13
Q

possible causes of renal AKI

A

acute tubular necrosis
interstitial nephritis
glomerulonephritis
vascular diseases

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14
Q

possible causes of post-renal AKI

A

obstruction-prostate, bladder, stones, tumors

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15
Q

prerenal AKI definition

A

due to decreased effective renal perfusion

decreased GFR WITHOUT ischmemic or nephrotoxic injury to tubules

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16
Q

pathogenesis of prerenal AKI

A

decreased effective renal perfusion, leading to increased ang II and vasopressin, leading to increased reabosprtion of Na at proximal tubule and water, leading to CONCENTRATED URINE AND OLIGURIA

increased reabsorption of urea, leading to elevation of BUN out of proportion to creatinine (>20:1)

17
Q

renal AKI

A

acute injury involving tubules, glomeruli, interstitium or vasculature

ex:
acute tubular necrosis: ischemic, toxic, both

inflam: glomerulonephritis, tubulointerstitial neprhitis, vasculitis

embolism, thrombosis, thrombitc microangiopathy

neoplasms: infiltrating tumors

18
Q

most common cause of “renal” AKI

A

acute tubular necrosis

19
Q

mechanisms of acute tubular necrosis

A

if ischemic-can cause endothelial cell dysfxn and vasoconstriction. can cause tubule cell injury and reversible or irreversible damage. ultimately all of the above lead to reduced GFR and oliguria

20
Q

morphologic features of ATN

A
tubular dilatation
attenuation of tubular epithelium
loss of epithelial cell brush border
granular cast material
mitotic figures (regenerative change)
21
Q

how does tubule regeneration occur in ATN?

A

sublethally injured tubular epithelial cells dedifferentiate, proliferate, migrate, and reestablish cell polarity

22
Q

morphology of post renal AKI

A

hydronephrosis-distension and dilation of renal pelvis calyces

23
Q

how can you distinguish prerenal AKI from acute tubular necrosis (both have oliguria)

A

changes in urine sodium reabsoprtion–look at urine sodium excretion

in volume depletion–urine Na reabsoprtion should be increased in proximal tubules—FENa2%

24
Q

eqn for FENa

A

UNa * PCr / (PNa * UCr) multiplied by 100

25
Q

symptoms of ECF volume depletion

A

hypotension

oliguria

26
Q

in chronically hypertensive individuals, what happens to GFR autoregulatory curve?

A

shifted to the right. so when lower their BP, their BP falls out of the regulatory range even when it’s a normal BP

also, if they are on lisinopril (ACEi), they don’t have maintained efferent arteriolar tone, so can’t keep up good GFR

27
Q

is acetaminophen nephrotoxic?

A

no

28
Q

what is septic shock an ex of in terms of AKI?

A

acute tubular necrosis