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FA17 Nephrology > AKI 2 > Flashcards

AKI 2 Flashcards

1
Q

renal failure

A

kidney fails to remove end products of metabolism from blood, regulate fluid, electrolyte and pH balance of extracellular fluid

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2
Q

AKI is _____ risk factor for…

A

independent risk factor for MORBIDITY and MORTALITY of hospitalized patients

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3
Q

diagnostic criteria of AKI

A

abrupt reduction in kidney function (48hrs) , on e of:

  1. increase in serum Cr by 0.3 mg/dL+ in 48hrs
  2. increased serum Cr by 150% + in 48hrs
  3. Oliguria less than 0.5 mL/kg/hr for more than 6 hrs
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4
Q

when is serum Cr unreliable

A
  1. when pt is not in steady state (hasn’t accumulated properly)
  2. Dialysis patients
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5
Q

pre-renal azotemia def + cause (5)

A

decrease in renal blood flow - kidney is STILL being perfused, just not filtered

  1. Heart failure
  2. blood loss (surgery, trauma, GI)
  3. shock
  4. renal artery stenosis
  5. dehydration (vomiting, diarrhea, sweat)
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6
Q

renal azotemia

A

disease of renal parenchyma (Kidney is also not being perfused)

tubular necrosis , caused by
1. HoTN (severe decrease in blood flow)

  1. Nephrotoxins
  2. glomerulonephritis and acute interstitial nephritis
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7
Q

most cases of intrinsic AKI are due to

A

acute tubular necrosis

caused by ischemia and nephrotoxins

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8
Q

post renal azotemia

A

diseases that involve remainder of urinary tract excluding kidney (down stream obstruction)

  1. kidney stone
  2. BPH
  3. neurogenic bladder
  4. retroperitoneal fibrosis
  5. tumor (pelvis - cancers)
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9
Q

best way to diagnose AKI

A

good history and PE

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10
Q

history questions (7)

A
  1. hx of renal fxn and labs
  2. urinary output (amnt, color, incontinence)
  3. infection
  4. HoTN, volume loss
  5. nephrotoxic agents
  6. recent sx, anesthesia
  7. evidence of obstruction
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11
Q

PE findings indicative of AKI

A
  1. orthostasis (pre-renal, severe intrinsic)
  2. fluid overload
  3. weight loss
  4. palpable, full bladder (post renal)
  5. rectal exam/prostate (post renal)
  6. post void straight cath or bladder scan
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12
Q

s/s of aki

specific for kidney

A
  1. decreased/absent urine output
  2. flank pain
  3. edema
  4. HoTN
  5. discolored urine
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13
Q

General S/s of AKI

A

weakness/easy fatiguability

anorexia, n/v

mental status change

systemic: fever, arthralgia, pulmonary lesions, lived reticularis

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14
Q

symptoms of AKI suggesting vasculitis

A

fever, arthralgia, pulmonary lesions

this indicates systemic disease

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15
Q

causes of livedo reticularis in AKI

A

aortic cat or atheromatous or cholesterol emboli

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16
Q

diagnostic eval of of AKI

A

plasma CR

serum bicarb, K

urine volume (anuria, can be oliguric, non-oliguric)

urine sediments (cells and casts)

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17
Q

pre-renal azotemia casts

A

moderate hyaline and finely granular casts but cellular casts are infrequent

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18
Q

ATN casts

A

dirty brown granular casts

renal tubular epithelial cells, free and in casts

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19
Q

urinary indicies use

A

helpful in distinguishing ATN and pre-renal azotemia

urine sodium, urine CR, urine osmolarity, FE Na)

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20
Q

urinary indices in prerenal azotemia

A

can’t filter, so decreased volume therefore

Urine Na = LOW (not as much water out)
Urine Cr = HIGH
Urine osmolarity = HIGH (more concentration)

Fe Na = < 1

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21
Q

urinary indices in ATN

A

not enough blood flow, decreased function (unable to pull the water in so diluted)

Urine Na = HIGH
Urine Cr = LOW
Urine osmolarity = LOW

Fe Na = > 2

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22
Q

when are imaging tests indicated in AKI ?

A
  1. obstructive pathology
  2. determine if renal failure is acute or chronic

ultrasound of Kidney or CT scan of abdomen/pelvis

if CKD: small, shrunken kidney

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23
Q

when is a renal biopsy indicated in AKI?

A
  1. vascular pathology suspected
  2. progressive AKI and no reason why (non responsive to meds)
  3. oliguria greater than 4 weeks
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24
Q

early renal bx looks for

A

vasculitis, TTP, glomerulonephritis, HUS

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25
Q

what might suggest duration of disease if previous labs are unavailable?

A
  1. recent onset of symptoms
  2. little to no urine
  3. progressively increasing Cr
  4. rate of rise in Cr (ATN = 0.3-0.5/day, rapid)
  5. small, echogenic kidney on US (chronic dz)
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26
Q

lab abnormalities of AKI

A

Hyperkalemia (K > 5.5)

BUN > 80

bicarb levels fall (< 15)

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27
Q

emergent action in AKI

deadly complications

A

arrhythmias (due to hyperK)

fluid overload

acidosis

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28
Q

emergent AKI complications (8)

A
  1. cogaulopathy
  2. confusion, coma
  3. pericarditis
  4. severe itching
  5. infection
  6. seizures
  7. drug toxicity
  8. nausea/vomiting
29
Q

indications for “urgent” hemodialysis

A
  1. metabolic acidosis
  2. fluid overload (unresponsive to med)
  3. hyperkalemia
  4. affects of uremia (pericarditis, confusion, coma, seizures, coagulopathy, n/v, GIB
30
Q

pre-renal AKI tx

A

drop in perfusion pressure

fluids (0.9 NS, LR)

pressers (dobutamine)

31
Q

post renal AKI tx

A

imagining and restoration of urine flow

foley cath
stent urethra
nephrostomy tube placement

32
Q

stages of ATN

A

ignition phase

mantainence phase

recovery phase

33
Q

pathophysiology of ATN

A

due to initiation and injury of tubular cells

  1. loss of barrier, back leak of filtrate
  2. damage to Na+/K+ ATPase pump
  3. sloughing of tubular cells = granular casts
  4. decreased vasodilator production
  5. increased free radicals
34
Q

maintenance phase

A

stabilization of GFR at low level (1-2 weeks)

uremic complications

35
Q

recovery phase

A

cells regenerate

abnormal diuresis can occur - salt and water loss

36
Q

ischemic ATN cause

A

low perfusion to parenchyma

can be due to progression of prerenal phase

caused by HoTN, hypoxemia, shock, sepsis, dehydration, hypovolemia

37
Q

effects of major surgical procedures and ischemia ATN

A

prolonged hypoperfusion worsened by vasodilation anesthetic agents and narcotics

38
Q

when is ATN most likely to occur?

A

surgery
shock (esp. sepsis)
contrast

39
Q

which patients are susceptible to ATN

A

underlying CKD
elderly
people on medications (ACE, ARB, diuretics, metformin)

dehydration

40
Q

how to prevent ATN

A

correct underlying electrolyte abnormalities

hydration

avoid nephrotoxic drugs

41
Q

antibiotics that likely cause ATN (class and drug names)

A

aminoglycosides

Gentamycin
Tobramycin
Amacaine/Neomycin

42
Q

aminoglycosides and ATN

A

older patients and those with renal disease are concerns

occurs 5-10 days after exposure (mild and non oliguric)

43
Q

treatment of ATN caused by aminoglycosides

A

stop medications

hydrate gently

monitor renal function

44
Q

NSAIDs/COX-2 and ATN

A

inhibit prostaglandin synthesis by endothelial cells

not an issue in people with normal function, but some patients depend on constant prostaglandin induced vasodilation of renal arterioles

45
Q

patients depending on prostaglandin for normal kidney function

A 
HTN 
Stage III CKD
Chronic arteriosclerotic dz 
volume depletion 
nephrotic syndrome ESLD 
severe hypercalcemia
46
Q

treatment of ATN due to NSAIDs/COX-2

A

improve in 3-7 days following drug d/c

47
Q

acute interstitial nephritis

A

allergy to NSAIDS (ibuprofen, naproxen, fenoprofen)

reaction occurs in the kidney

causes renal insufficiency and nephrotic range proteinuria

48
Q

other drugs causing ATN

A

amphotericin B (Antifungal)

vancomycin

acyclovir

cephalosporins

ACE inhibitors/ARBs

Foscarnet

Antivirals

synthetic cannabinoids

49
Q

contrast dye and ATN

A

occurs w/in 24-96 hrs of administration

renal function returns in 7-10 days

no effective treatment

50
Q

risk factors for contrast induced ATN

A 
CKD (stage 3+) 
DM 
>65 y/o
Volume depletion 
large volumes/repeated doses
51
Q

prevention of contrast induced ATN

A

lower doses

IV hydration before and after

avoid nephrotoxic agents 224-48hrs before and after

mucomyst/m-acetylcystine

52
Q

exogenous nephrotoxins

A

cyclosporin immunosuppressant (dose dependent, biopsy needed)

antineoplastics, cisplatin

organic solvents

heavy metals (mercury, cadmium, arsenic)

53
Q

endogenous nephrotoxins

A

myoglobin

hemoblogbin

54
Q

myoglobin and nephrotoxin

A

from rhabdo

released into blood causing damage to renal tubules

complain of muscular pain (show signs of muscle injury)

55
Q

myoglobin urine

A

dark brown without RBCs

serum CPK and myoglobin elevated

dark brown and false positive for RBCs (not on dipstick)

56
Q

clinical situations where Rhbadomyolysis is seen

A

statins

elderly people/drugs = fall can’t get up

extreme exercise

crush injuries

57
Q

clinically relevant CK levels

A

20k-50k or more

58
Q

side effects of muscle cell lysis

A

ATN

hyperkalemia, hyperphostphatemia, hyperuricemia

59
Q

treatment of ATN due to rhabdo

A

hydration at high rate

may do alkaline IV

must monitor urine output

60
Q

alkaline IV in rhabdo

A

sodium bicarb in D5

forces metabolic alkalosis that protects kidney and body from hyperkalemia and prevents AKI

61
Q

hemoglobin

A

causes direct injury

due to massive intravascular hemolysis

treament: reversal of cause and hydration

62
Q

causes of massive hemolysis

A

wrong match blood transfusions

hemolytic anemia

63
Q

uric acid as a nephrotoxin

A

occurs in rapid cell turnover and lysis (neoplastic diseases)

esp. in chemo

precipitation of uric acid crystals in tubules (+ hyper K and PO4)

64
Q

prevention of uric acid ATN

A

UOP of 3l/day

prophylactic allopurinol

65
Q

multiple myeloma and ATN

A

nephrotoxicity due to excretion of light chain Igs into urine

light chains are not found on UA so must diagnose with serum electrophoresis

hydration and MM treatment

66
Q

treatment goals of ATN

A

avoid volume overload and hyper kalmia (volume restriction and loop diuretics)

nutritional support (catholic state, keep weight up)

67
Q

indications for hemodialysis in AKI

A
  1. life threating electrolyte issue (hyperK)
  2. volume overload
  3. worsening acidosis
  4. avoidance of uremic complications (BUN > 80)
68
Q

treatment of ATN

A

correct anemia if symptomatic (don’t want to fluid overload)

appropriately dose drugs

be sure to monitor for infection (decrease number of lines)

FA17 Nephrology (13 decks)

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