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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
AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - phases - oliguric phase - management
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
AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - phases - diuretic phase
- 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
AKI - pathophysiology - intrinsic - Acute tubular necrosis (ATN) - phases - recovery phase
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
AKI - pathophysiology - intrinsic - Acute interstitial nephritis (AIN) - causes
1) infection (viral/bacteria) 2) immunologic response - penicillin, cephalosporin, quinolone, sulfanoamide, rifampicin
29
AKI - pathophysiology - intrinsic - Acute interstitial nephritis (AIN) - identifying feature
1) lesion in interstitial comprised of monocyte, macrophage, T/B cell 2) increase SCr, eosinophilia, red rash all over body, fever, malaise
30
AKI - pathophysiology - intrinsic - Acute interstitial nephritis (AIN) - management
1) discontinue (prevent permanent fibrosis) 2) treat underlying infection 3) supportive care
31
AKI - pathophysiology - intrinsic - glomerular damage
1) SLE: lupus nephritis 2) rapidly progressive glomerulonephritis (GN) 3) poststreptococcal GN
32
AKI - pathophysiology - intrinsic - vascular damage
vasculitis, polyarteritis nodosa, haemolytic uremic syndrome, thrombotic thrombocytopenic purpura, accelerated HTN, emboli (thrombotic, atheroscelortic)
33
AKI - pathophysiology - post renal - general
mechanical obstruction of urine flow distal to renal parenchyma (bladder/ureteral level)
34
AKI - pathophysiology - post renal - causes
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
AKI - pathophysiology - post renal - identifying feature
- anuria = complete obstruction - polyuria = partial obstruction - elevated BUN/SCr ratio (reabsorption of urea from stagnated urine)
36
AKI - pathophysiology - post renal - treatment
- relieve obstruction - alpha blocker stimulate passage of ureteric stone
37
AKI - risk factor
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
AKI - clinical presentation
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
AKI - effects of NSAID/ACEi/ARB - normal condition
- afferent arteriole dilate (PG) = increase blood flow - efferent arteriole constrict (AG II) = increase pressure - combined to maintain hydrostatic pressure for filtration
40
AKI - effects of NSAID/ACEi/ARB - outcome
1) NSAID & calcineurin inhibitor inhibit PG = afferent arteriole vasoconstriction 2) ACEi/ARB = antagonise AGII effect = efferent arteriole vasodilation
41
AKI - FeNa eqn
FeNa (%) = (Ua/Sna divide by Ucr/Scr) x100
42
AKI - management of AKI
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
AKI - supportive management
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
AKI - maintain water Na balance
diuretics for fluid management Na < 2-3 g/day
45
AKI - electrolyte & acid base management
- Na Bicarbonate/alkalinising agent - dietary restriction, meds
46
AKI - glycemia control
- plasma glucose 6.1 - 8.3 mmol/L - insulin therapy
47
AKI - nutritional support
- 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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