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POM unit 5 > acute kidney injury > Flashcards

acute kidney injury Flashcards

1
Q

definition of AKI

A

inability of kidney to maintain homeostasis leading got a buildup of nitrogenous wastes

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2
Q

AKI characteristics

A

occurs over hours to days, there is increased baseline creatinine of more than 50%. decreased Cr clearance of more than 50% deterioration requiring dialysis.

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3
Q

anuria

A

less than 100mL/24

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4
Q

oliguria

A

<500mL

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5
Q

polyuria

A

> 2.5L

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6
Q

most common form of AKi

A

prerenal or functional

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7
Q

if it is intrarenal what is the next step?

A

considering whether it is tubulointerstitial or glomerular.

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8
Q

prerenal causes

A

inadequate perfusion, need to check volume status

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9
Q

renal causes

A

this is despite perfusion and excretion. check urinalysis, full blood count, and autoimmune screen

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10
Q

post-renal causes

A

blocked outflow. check the bladder and catheter and ultrasound

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11
Q

types of intrinsic AKI

A

ATN (ischemia, toxin, tubular factors), AIN (inflammation, edema), glomerulonephritis (damage to the filtering mechanisms, depends on the presentation)

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12
Q

post-renal causes

A

BPH, malignancy, blocked catheter, ureter

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13
Q

what dilates the afferent arteriole?

A

prostacyclin and NO.

this is why NSAIDs block the afferent dilation of auto regulatory

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14
Q

what constricts the afferent arteriolar

A

endothelin, catecholamines, thromboxane

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15
Q

what constricts the efferent arteriole

A

angiotensin II

thus ACEi block this

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16
Q

what are the classifications of ATN

A

nephrotoxic, ischemic

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17
Q

nephrotoxic ATN endogenous toxins

A

heme pigments (myoglobin and hemoglobin) myeloma light chains.

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18
Q

exogenous toxins nephro ATN

A

antibiotics (aminoglycosides), radioconstrast agents , heavy metals. poisons such as ethylene glycol

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19
Q

what are the phases of ATN

A

insult, oliguria, dialysis, polyuria, and recovery. the creatinine increases steadily and then decreases

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20
Q

causes of acute interstitial nephritis

A

allergic interstitial nephritis, due to hypersensitivity to drugs; infections from bacteria and viruses, sarcoidosis

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21
Q

what are the clinical characteristics of allergic interstitial nephritis

A

fever, rash, arthralgias, eosinophilia, urinalysis shows hematuria sterile pyuria, eosinophiluria

22
Q

contrast induced AKI charateristics

A

very uncommon with patients that have normal function. increases significant;y with renal insufficiency
onset 24-48hrs post-exposure, duration is 5-7 days. majority are nonoliguria, dialysis is rarely needed, there is typically a low fractional excretion of sodium.

23
Q

risk factors for contrast induced aki

A

insufficiency, DM, multiple myeloma, high osmolar contrast media, contrast medium volume

24
Q

what can protect against contrast induced

A

IV fluid, mucomyst (N-acetylcysteine), bicarbonate.

25
Q

what is not helpful for contrast induced AKI

A

diuretics, mannitol

26
Q

glomerulonephritis definiton

A

renal disease characterized by inflammation and damage to the glomeruli. this allows for protein and blood in the urine. generally either proliferative or non.

27
Q

common presentations of GN

A

isolated hematuria and proteinuria, nephrotic syndrome, nephritic, acute renal failure, chronic renal failure.

28
Q

nonproliferative types

A

minimal change, membranous, focal segmental

29
Q

proliferative types

A

IgA, membranoproliferative, post-infectious GN, rapidly progressive GN, good pastures, MPA, wegeners

30
Q

minimal change GN

A

abnormal podocytes on EM, there is effacement and nephrotic syndrome. in children.

31
Q

what to treat MCD with?

A

supportive therapy and prednisilone, most have great prognosis

32
Q

focal segmental GN

A

segments of the glomerulus develop sclerosis. presents with nephrotic. steroids are usually worthless, 50% progress to renal failure.

33
Q

membranous glomerulonephritis

A

thickened BM usually idiopathic 1/3 have chronic, 1/3 remission, 1/3 progress to renal failure.

34
Q

IgA nephropathy

A

most common in adults, hematuria, 24-48 hrs post URTI/GI infection. there are deposits in the membrane

35
Q

membranoproliferative GN

A

immune mediated or hepatitis, usually progresses to end stage renal failure.

36
Q

post infectious glomerulonephritis

A

occurs weeks after URTI usually strep pyogenes, supportive treatment will resolve in 2-4 weeks.

37
Q

RPGN different types?

A

crescentic. good pastures, MPA, and wegeners

38
Q

good pastures

A

autoimmune to the GBM there is an autoantibody to the glomerulus and the lung. hematuria and hemoptyosis. treat with steroids.

39
Q

vasculitis disorders that cause crescentic RPGN

A

MPA and wegeners

40
Q

wegeners

A

vasculitis of the lungs, kidneys, and other organs. c-ANCA, need to treat with steroids and cyclophosphamide

41
Q

MPA

A

small vessel vasculitis, p ANCA long term steroids and cytotoxic agents.

42
Q

when will you see RBC casts or dysmorphic RBCs

A

acute glomerulonephritis, and small vessel vasculitis.

43
Q

when will you see WBC and WBC casts

A

acute interstitial nephritis and acute pyelonephritis

44
Q

acute tubular necrosis sediment

A

renal tubular epithelial cells, RTE casts, pigmented granular muddy brown casts.

45
Q

FENa less than 1%

A

prerenal, urine Na <20 because functional tubules reabsorb lots of filtered Na. ATN (rarely), glomerular or vascular injury.

46
Q

FENa 1-2%

A

prerenal sometimes, ATN sometimes,

47
Q

FENa >2

A

ATN. damaged tubules cannot reabsorb Na.

48
Q

clinical signs and symptoms of AKI

A

weight gain, peripheral edema, hypertension, hyperkalemia, NV, ascites, asterixis, encephalopathy

49
Q

labs for AKI

A

rising Cr and urea, rising potassium, decreasing Hb. acidosis, hyponatremia, hypocalcemia.

50
Q

treatment for AKI

A

immediate management of pulmonary edema and hyperkalemia. dialysis. restriction of water, Na, K. provision of protein intake.

51
Q

indications for acute dialysis

A

AEIOU

acidosis, electrolytes, ingestion of drugs/ischemia, overload, uremia

POM unit 5 (12 decks)

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