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2155 finals > AKI > Flashcards

AKI Flashcards

1
Q

AKI - urine output categories

A

1) normal: >/= 1200mL/day
2) non-oliguria: > 500 mL/day
3) oliguria: < 500 mL/day
4) aliguria: < 50mL/day

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2
Q

AKI - lab values

A

1) increase SCr by >/= 26.5 micromol/L within 48 h
2) increase SCr to >/= 1.5x baseline within 7 days
3) urine vol < 0.5 mL/kg/h for >/= 6 hr

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3
Q

AKI - categories

A

1) stage 1
- SCr: 1.5 - 1.9 x baseline or >/= 0.3 mg/dL (26.5 micromol/L) increase
- urine output < 0.5 mL/kg/h for 6-12 hr

2) Stage 2
- SCr: 2.0-2.9x baseline
- urine output < 0.5 mL/kg/h for 6012 hr

3) stage 3
- SCr: 3x baseline or increase to >/= 4.0 mg/dL (353.6 micromol/L)
- eGFR for < 18 yo: < 35 mL/min/1.73m^2
- urine output < 0.3 mL/kd/h for >/- 24 hr or anuria for >/= 12 hr

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4
Q

AKI - pathophysiology - prerenal - general

A

kidney still working but drop in perfusion (hospitalised patient)

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5
Q

AKI - pathophysiology - prerenal - cause

A

1) vol depletion: internal bleed, GI loss (N/D), urinary loss (overdiuresis, DI), loss from third space (burn, peritonitis), decreased effective vol (cirrhosis), peripheral vasodilation (sepsis, drug)

2) reduced cardiac output: CHF, MI, pericardial tamponade, acute PE, sepsis

3) renal hypoperfusion: bilateral renal occlusion (thrombosis, emboli, stenosis), meds

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6
Q

AKI - pathophysiology - prerenal - renal & extra renal signals

A
  • indicate contraction of circulating blood volume: compensatory mechanism to preserve blood vol
  • mecahnisms:
    1) Severe but reversible vasoconstriction to maintain BP
    . decrease solute excretion
    . increase tubular reabsorption of glomerular filtrate

2) stimulate thirst: increase fluid uptake

3) promote Na & H2O retention (prevent further drop in BP)
. reduce urine vol = oliguria
. highly concentrated urine (high SG) and low in Na (FeNa< 1%)

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7
Q

AKI - pathophysiology - prerenal - consequences

A

prolonged reduction in renal perfusion - progress to AKI & renal cell damage

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8
Q

AKI - pathophysiology - prerenal - diagnosis & evaluation

A

1) patient hist: GI loss, diuresis
2) physical exam: dehydration, orthostatic HTN (drop in pressure when sit up after lying/stand up), tachycardia, poor skin turgor
3) central venous pressure: heart vol status
4) urine test: SG, osmolarity

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9
Q

AKI - pathophysiology - prerenal - management

A

1) treat pre renal cause
2) vasopressor w fluid in patient w vasomotor shock
3) supportive care

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10
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - non drug cause

A

1) ischaemia: hypotension, vasoconstriction
2) nephrotoxin: contrast dye, heavy metal, amphotericin B, aminoglycoside, organic solvent
3) endogenous toxin: Hb, myoglobin

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11
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - drug cause - radiocontrast media-induced ATN - general

A

dye used for diagnostic purpose

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12
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - drug cause - radiocontrast media-induced ATN - pathophysiology

A

alter renal haemodynamic, cause renal ischaemia, direct toxicity

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13
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - drug cause - radiocontrast media-induced ATN - identifying feature

A

progressive increase in SCr within 24-48h after contrast administration, peak within 5 days

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14
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - drug cause - radiocontrast media-induced ATN - risk factor

A

1) pre-existing renal disease/CKD
2) old
3) comorbidities: HTN, DM, CHF, metabolic-syndrome, pre-DM, hyepruricemia, respi condition
4) vold epletion, hypotension, haemodynamic instability
5) concomitant administration of nephrotoxin: discontinue
6) use high vol or ionic/hyper osmolar contrast media

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15
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - drug cause - radiocontrast media-induced ATN - prevention

A

1) lowest dose possible contrast medium in risk patient
2) iso/hypo osmolar contrast media
3) IV hdyration: 1 hr before & continue for 3-6 hr after
4) N-acetylcysteine: antioxidant, 600-1200mg PO BID pre & post procedure or higher dose/IV

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16
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - drug cause - Aminoglycoside (AG) induced ATN - types of AG

A

amikacin, gentamicin, tobramycin

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17
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - drug cause - Aminoglycoside (AG) induced ATN - pathophysiology

A

accumulate in renal cortex = tubular epi cell damage & obstruction

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18
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - drug cause - Aminoglycoside (AG) induced ATN - risk factor

A

1) elderly
2) CKD, renal disease, DM
3) vol depletion, hypotension, sepsis, shock, hepatorenal syndrome
4) concomitant nephrotoxin adminsitration
5) AG therapy > 3 day, multiple dose, high serum trough conc, recent AG therapy
- gentamicin > 2mcg/mL

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19
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - drug cause - Aminoglycoside (AG) induced ATN - prevention

A

1) lower drug exposure
2) only use AG as last line
3) extend interval in normal kidney func
4) further prolong dosing for CKD patient
5) TDM
- single dose > 48h
- multiple dose > 24h

20
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - drug cause - Amphotericin B induced nephrotoxicity - general

A

fungicidal, standard for life threatening systemic mycoses

21
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - drug cause - Amphotericin B induced nephrotoxicity - dose limiting nephrotoxicity

A

ischaemic injury: vasoconstriction of afferent arteriole = direct tubular/glomerular toxicity

22
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - drug cause - Amphotericin B induced nephrotoxicity - prevention

A

1) continuous infusion instead of 2-4h infusion
2) alternate dat dosing
3) lipid formulation

23
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - phases - initiating

A
  • ischaemia/exposure to nephrotoxic agent
  • PG protective role on renal autoregulation during vasoconstrictive insult
24
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - phases - oliguric phase - general

A
  • lower urine vol than necessary to excrete nitrogenous waste product = accumulation of toxic products
  • 1-2 wks
25
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - phases - oliguric phase - management

A

1) diuretics
- non oliguria less extensive damage, better able to maintain fluid/electrolyte balance = better prognosis
- frusemide, bumetanide, torsemide, ethacrynic acid (if sulfa llergy and anaphylactic to others)
- increase urine ourput, facilitate fluid management
- diuretic resistance in aggressive Na restriction
- avoid diuresis in early AKI

2) CCB: reverse renovascular constriction, increase renal blood flow & GFR

3) supportive management: water, Na, K, P, acidbase balance

4) nutrition, dose adjustment, short term dialysis

26
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - phases - diuretic phase

A
  • identifying feature: sig increase in urine output (start to cutdown diuretic)
  • gradual increase in renal blood flow & GFR followed by increase concentrating ability of tubules to reabsorb Na & concentrating urea
27
Q

AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - phases - recovery phase

A

1) regenerate new tubular cell
2) continue increase diuresis
3) Azotemia resolve 5-60 days after onset
4) gradual incease GFR to normal
5) sometimes permanent loss in renal func (fibrosis/atrophy)

28
Q

AKI - pathophysiology - intrinsic - Acute interstitial nephritis (AIN) - causes

A

1) infection (viral/bacteria)
2) immunologic response
- penicillin, cephalosporin, quinolone, sulfanoamide, rifampicin

29
Q

AKI - pathophysiology - intrinsic - Acute interstitial nephritis (AIN) - identifying feature

A

1) lesion in interstitial comprised of monocyte, macrophage, T/B cell
2) increase SCr, eosinophilia, red rash all over body, fever, malaise

30
Q

AKI - pathophysiology - intrinsic - Acute interstitial nephritis (AIN) - management

A

1) discontinue (prevent permanent fibrosis)
2) treat underlying infection
3) supportive care

31
Q

AKI - pathophysiology - intrinsic - glomerular damage

A

1) SLE: lupus nephritis
2) rapidly progressive glomerulonephritis (GN)
3) poststreptococcal GN

32
Q

AKI - pathophysiology - intrinsic - vascular damage

A

vasculitis, polyarteritis nodosa, haemolytic uremic syndrome, thrombotic thrombocytopenic purpura, accelerated HTN, emboli (thrombotic, atheroscelortic)

33
Q

AKI - pathophysiology - post renal - general

A

mechanical obstruction of urine flow distal to renal parenchyma (bladder/ureteral level)

34
Q

AKI - pathophysiology - post renal - causes

A

1) bladder obstruction: prostatic hypertrophy, infection, cancer
2) improperly placed catheter, anticholinergic
3) ureteral: Cancer w abdominal mass, retroperitoneal fibrosis, nephrolithiasis (Stone/crystal)
4) renal pelvis/tubules: nephrolithiasis (oxalate, uric acid)

35
Q

AKI - pathophysiology - post renal - identifying feature

A
  • anuria = complete obstruction
  • polyuria = partial obstruction
  • elevated BUN/SCr ratio (reabsorption of urea from stagnated urine)
36
Q

AKI - pathophysiology - post renal - treatment

A
  • relieve obstruction
  • alpha blocker stimulate passage of ureteric stone
37
Q

AKI - risk factor

A

1) > 60 yo
2) female
3) acute infection
4) pre-existing CVS/chronic respi disease
5) dehydration/vold epletion
6) pre-existing CKD -> AoCKD

38
Q

AKI - clinical presentation

A

1) decreased urine output
2) dark pee
3) peripheral oedema
4) flank pain
5) lab abnormalities
- increase SCr, BUN, K
- metabolic acidossi
- urinalysis: cast/cell/crystal/WBC/RBC/protein, abnormal SG, fractional excretion of Na (FeNa), urine osmolarity

39
Q

AKI - effects of NSAID/ACEi/ARB - normal condition

A
  • afferent arteriole dilate (PG) = increase blood flow
  • efferent arteriole constrict (AG II) = increase pressure
  • combined to maintain hydrostatic pressure for filtration
40
Q

AKI - effects of NSAID/ACEi/ARB - outcome

A

1) NSAID & calcineurin inhibitor inhibit PG = afferent arteriole vasoconstriction
2) ACEi/ARB = antagonise AGII effect = efferent arteriole vasodilation

41
Q

AKI - FeNa eqn

A

FeNa (%) = (Ua/Sna divide by Ucr/Scr) x100

42
Q

AKI - management of AKI

A

1) high risk: discontinue nephrotoxic agent, ensure vol status & perfusion pressure, monitor SCr & urine output, avoid hyperglycemia
2) stage 1: high risk stuff + non-invasive diagnostic workup, consider invasive ones
3) stage 2: stage 1 stuff + check for change in drug dosing, consider renal replacement, consider ICU admission
4) Stage 3: stage 2 stuff + avoid subclavian catheter if possible

43
Q

AKI - supportive management

A

1) haemodynamic support, vol replacement
2) remove inciting agent
3) treat underlying disease/condition
4) remove cause of obstruction for postrenal AKI
5) remove cause of obstruction for postrenal AKI

44
Q

AKI - maintain water Na balance

A

diuretics for fluid management
Na < 2-3 g/day

45
Q

AKI - electrolyte & acid base management

A
  • Na Bicarbonate/alkalinising agent
  • dietary restriction, meds
46
Q

AKI - glycemia control

A
  • plasma glucose 6.1 - 8.3 mmol/L
  • insulin therapy
47
Q

AKI - nutritional support

A
  • maintain calorie intake, minimise hypercatabolic state & increase rate of urea increase
  • goal 20-30 kcal/kg/day
  • protein:
    1) non-catabolic AKI: 0.8-1 g/kg/day
    2) dialysis: 1-1.5 g/kg/day
    3) hypercatabolic/on CRT: up to 1.7g/kg/day

2155 finals (6 decks)

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