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Renal Care > AKI > Flashcards

AKI Flashcards

1
Q

What is AKI?

A
  • Syndrome
  • rapid decrease GFR
  • accumulation nitrogenous waste products
  • decrease/ urine output
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2
Q

What is criteria of AKI?

A
  • increase SCr atleast 27mol/L within 48 hrs
  • increase baseline SCr by 1.5 times / more within 7 days
  • Urine output < 0.5ml/kg/h atleast 6 hrs
    = ONLY ONE CRITERIA MET FOR DIAGNOSIS
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3
Q

What is Pre-renal?

A

Pre-renal:

  • reduced BF to kidneys
  • due volume depletion - haemorrhage, dehydration/ GI fluid loss
  • reduce CO - CHF, MI, septic shock, hypotension - reduce renal BF + glomerular perfusion
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4
Q

What medications cause pre-renal? how to manage?

A 
Nsaids - naproxen:
- impair pg -mediated 
inhibit angiotensin II mediated efferent arteriole - vasoconstriction 
- ACE-I - enalpril 
-ARB -

= decrease intraglomerular pressure + GFR
= discontinue

with mild-moderate decrease in renal BF - intraglomerular pressure is maintained

  1. dilation afferent arterioles
  2. constriction efferent arterioles
  3. redistribution renal bf –> oxygen-sensitive renal medulla

early volume restoration to prevent progression needed before structural damage

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5
Q

What is intrinsic AKI?

A
  • diseases affect structure nephron - tubules, glomerulus, intersititium, BV
  • ATN = necrosis tubular epithelial cells - nephrotoxins (aminogl, constrast agents, amphotericin B) , sepsis / ischemia
  • less commonly caused by glomerular , interstitial and BV diseases - glomerulonephritis, SLE , intersititial nephritis and vasculitis
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6
Q

Can pre-renal AKI progress to intrinsic AKI?

A

yes

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7
Q

What is postrenal AKI?

A
  • obstruction urinary flow
  • prostate disease / bladder tumour
  • causes BPH, tumours, renal calculi
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8
Q

Clinical presentation and diagnosis

What is criteria for stage 1 and 3?

A

stage 1: increase SCr 27umol/L / increase

Stage 3: patients receive RRT

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9
Q

what is presentation of urinary output ?

A

sensitive marker than SCr in AKI

  • Oliguria - production small vol urine - daily urine output < 400ml/day
  • Anuria - failure to produce urine - daily urine output < 50ml/day
  • Non-oliguria AKI - urrine output > 400ml/day
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10
Q

How to determine prerenal AKI using BUN and SCr?

A
  • elevated SCr + BUN (> protein + GIT bleeding due to AA breakdown in gut)
  • Urea product AA met
  • BUN < sensitive marker than SCr
  • increase blood urea reabs at lower urine flow rates
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11
Q

What is fractional excretion of Na and what drug affects it?

A
  • measure of % Na excreted by kidney

- Loop diruetic - furosemide - increase FENa

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12
Q

What is rhe FENa in pre-renal AKI?

A
  • enhanced Na reabs
  • decreased FENa + urine [Na]
    <1% = decreased renal perfusion + Na excretion
  • urine > concentrated in pre-renal than post and intrinsic due higher osmolality + urine-to plasma creatine ratio
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13
Q

symptoms of AKI

A
  1. weight gain
  2. N, V, D, anorxia
  3. fatigue
  4. shortness of breath
  5. pruritis
  6. PRE-RENAL - weight loss
  7. Postrenal - anuria alternating polyuria + clocky abdominal pain radiating from flank to groin
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14
Q

physical examination AKI

A
  • increased BP
  • peripheral odema
  • change mental status
  • JVD
  • pulmonary oedema
  • crackles
  • asterixis
  • pericardial or pleural friction rub
  • hypotension/ orthostatic hypoyension - pre-renal
  • rash - instrinsic due to acute intersitial nephritis
  • bladder distention + prostatic enlargement - postrenal
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15
Q

what are treatment goals?

A
  • find identifiable cause
    1. hypovolaemia
    2. nephrotoxic drugs
    3. ureter obstruction

pre-renal + post-renal can be reversed
instrinc - supportive therapy

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16
Q

Hydration therapy

A
  1. Isotonic colloidal solns = 0.9% normal salinr
    - expand extravascular vol
    - return volume status
    - neural fluid balance - euvolaemia
    = ensure tissue perfusion
  2. Crystalloids - normal saline / balanced solns - ringers lactate / plasma - lyte A
    - preffered over colloidal - albumin, hydroxyethyl starch for fluid resucitation
  3. 0.9% normal saline PREFFERRED over lower tonicity saline due smaller fraction of hypotonic fluid remains in intravascular space
  4. Dextrose 5% in water = isotonic = its absorbed ONLY H20 left intravascular space

= too much fluid = pulmonary oedema, increased postoperative complications, increased mortality
= excess chloride from 0.9% normal saline = hyperchloraemic metabolic acidosis

17
Q

Loop diuretics

A
  1. bumetanide
  2. furosemide
  3. torasemide
    MIDE
    = worsen kidney function
  • improved urine ouput
  • no improvement in survival / need dialysis
  • reserved treating volume overload
  • NOT given prevent AKI/ hasten recovery of kidney func in euvolAEMIC/ HYPOVOlaemic individuals
18
Q

Purpose RRT

A
  1. treat pulmonary oedema + volume overload = unresponsive diuretics
  2. minimize accum nitrogenous waste
  3. correct electrolyte + a-b balance - hyper + metabolic acidosis
19
Q

Name 2 process and explain of solute removal in RRT

A

Diffusion - move from [high] to [low] in dalysate across SP dialysis membrane

Convection - removal solutes secondarily to fluid removal of ultrafiltration = solute drag

20
Q

2 modalities of RRT

A
  1. intermittent haemodialysis - IHD
    - higher efficiency form
    - fluid removal by ultrafiltration
    - solute removal by diffusion
    several hrs - daily 3/5 times a week
  2. continous renal replacement therapy - CRRT
    - slow fluid/ solute removal on continous basis - 24hrs
21
Q

what is continos venovenous haemodialfiltration

CVVH-DF?

A

type of CRRT allows for fluid removal + removal of solutes - small-large mol via diffusion

22
Q

Advantage of CCRT

A

haemodynamic stability

better volume control in patients unable tolerate rapid fluid removal

23
Q

disadvantage of CCRT

A

continous nursing requirements + anticoagulation
frequent clotting dialyzer
patient immobility
increase cost

Renal Care (1 decks)

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