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302 SBM: Metabolic & Renal > AKI > Flashcards

AKI Flashcards

1
Q

Briefly outline the function of the bowmans capsule and the other part of the nephron

A

Bowmans capsule produces 100% of filtrate

PT- 80% reabsorption back into capillary by active and passive absorption

LoH- 6% absorption of H20 and salt

DT- 9% filtrate absorbed: active secretion, variable reabsorption

CT- 4% filtrate absorption: variable salt and H2O reabsorption

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2
Q

Describe the criteria for the three stages of AKI

A

Stage 1
- Serum creatinine: 1.5-2x increase from baseline
Or 26micromol/L increase in <48hrs
- Urinary output: <0.5ml/kg/hr for 6 hours (8 hours in kids)

Stage 2

  • Serum creatinine: 2-3x increase from baseline
  • Urinary output: <0.5ml/kg/hr for 12 hours

Stage 3
- Serum creatinine: >3x increase from baseline
OR SC>354micromol/L with an acute increase ≥44
- Urinary output: <0.3ml/kg/hr for 24 hours

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3
Q

What is creatinine and how is it used to calculate eGFR?

Describe some natural variations in serum creatinine

A
  • it is a product of muscle turnover
  • its transported in the blood and excreted via the kidneys
  • creatinine clearance, therefore, gives us an indication. of filtration rate (if serumCr rises, the filtration rate is falling)
  • People with lower muscle mass have lower (range of normal) creatinine e.g. elderly, double amputee
  • Higher muscle mass in athletes
  • Dilution effect in pregnancy
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4
Q

What is oliguria?

What is anuria?

A
  • Oliguria: <0.5ml/kg/hr (equates to about 500ml in 24 hours in adults)
  • Anuria: no urine production but a soft definition is <100ml in a day
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5
Q

Consider the natural course of the development of AKI

Describe the onset phase

  • triggers
  • what happens
  • how long does it last
A
  • Triggers: significant blood loss, burns, diabetes insipidus, fluid losses
  • renal blood flow and tissue perfusion drop to 25% of normal
  • Urine output drops <0.5ml/kg/hr
  • Lasts hours -days
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6
Q

Consider the natural course of the development of AKI

Describe the oliguric/anuric phase

  • what happens
  • how long does it last
A
  • UO<400ml per day
  • Theres an increase in BUN (blood urea nitrogen) and SC
  • Electrolyte disturbances, acidosis, fluid overload (kidneys cant excrete)
  • Lasts 8-14 days (longer depending on when dialysis treatment is started)
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7
Q

Consider the natural course of the development of AKI

Describe the diuretic phase

  • what happens
  • how long does it last
A
  • Occurs as AKI is corrected
  • Cells in tubules die as a result of injury –>oedema and scar formation
  • Eventually, produce transport proteins
  • Patient passes urine >400ml/day as GFR increases
  • Lasts 7-14 days
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8
Q

Consider the natural course of the development of AKI

Describe the recovery phase

  • what happens
  • how long does it last
A
  • reduction in oedema
  • the normalisation of fluid balance and electrolytes
  • GFR returns to 70/80%
  • lasts months- 1 year
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9
Q

State the 7 functions of the kidney

A
  1. excretes toxins e.g. urea
  2. electrolyte balance
  3. acid and base balance
  4. fluid balance
  5. BP control
  6. Control of bone metabolism: Vitamin d activation and phosphate excretion
  7. Erythropoiten production
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10
Q

Dysfunction of the kidney can kill.

Describe two ways in which this will happen the fastest and how it may present

A
  1. Hyperkalaemia (>6 = bad, >6.5 medical emergency)
    ECG changes: flatten of P wave and widening of QRS, tented T waves, sinus wave pattern (precardiac arrest)
    Changes occur as K+ increase —->
  2. Fluid Overload (Shortness of breath, Orthopnoea, Limb swelling)
    - the danger is pulmonary oedema which leads to severe tissue hypoxia
    - Remember that patients that are oliguric/anuric cannot get rid of excess water
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11
Q

When is haemodialysis indicated for AKI?

A
  • Refractory hyperkalaemia*
  • Pulmonary oedema**
  • Refractory acid-base disturbance
  • Uraemic complications (Coma, pericarditis)
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12
Q

State 5 prerenal causes of AKI (the really likely ones)

A
  • Haemorrhage
  • Renal artery stenosis
  • Dehydration
  • MI/ PE
  • Iatrogenic
  • Septic shock
  • Systemic vasodilation as with antihypertensive or in anaphylaxis
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13
Q

State 3 intrinsic causes of AKI

A
  • Nephrotoxicity (e.g. from calcium and other metals, drugs - particularly cisplatin)
  • Overproduction which leads to block tubules e.g. Rhabdomyolysis, myeloma
  • Inflammation of the kidney: GN, Interstitial arthritis, Acute tubular necrosis
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14
Q

State 5 postrenal causes of AKI

A
  • Renal stones
  • Ureteric or Urethral stricture
  • Benign prostatic hypertrophy
  • Prostate cancer (or cervical and bladder cancer)
  • Unary retention (neurogenic, constipation)
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15
Q

What is the prognosis for patients with AKI

A
  • 50% require ITU admission
  • May require haemofiltration
  • Independent risk factor of mortality
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16
Q

What are the acute risk factors?

What are the chronic risk factors?

A 
ACUTE
S- sepsis and hypoperfusion
T- toxins
O- obstruction
P- parenchyma

CHRONIC
- elderly, CKD, DM, nephrotoxic medication, HF, liver disease, vascular disease

17
Q

How do we protect and promote AKI?

A

4 Ms

Monitor: Observations/news, Regular bloods, fluid chart, pathology alerts
Maintain circulation: hydration, resuscitation, oxygenation
Minimise kidney insult: remove nephrotoxic drugs, surgery, contrast, hospital acquired infections
Manage acute illness: sepsis, HF, LF

18
Q

Get five categories of nephrotoxic drugs

A
  • ACEi
  • ARBs
  • Diuretics
  • Chemotherapy agents: cisplatin
  • NSAIDs: ibuprofen, diclofenac
  • Naproxen
  • Metformin
  • Aminoglycosides
19
Q

Outline the management of AKI

A

Is the patient safe

  • A-E approach; [K+]; volume status
  • if volume deplete give 250-500ml bolus of saline

Consider catheter for monitoring

  • patient needs strict fluid input/output
  • check VBG for acid base status

Investigate the cause once stable:

  • Urine stick, bladder scan, ultrasound kidneys, ureter and bladder (KUB)
  • Take detailed Hx + exam + medication review
  • FBC, U&E, VBG
20
Q

What are the red flag features When taking a history family patient presenting with an AKI?

A
  • haemoptysis
  • rashes
  • joint swelling/pain
  • jaundice
  • ENT: crusting of nose/acute hearing impairment
  • significant limb swelling acutely
  • noticeable urine frothiness
21
Q

Draw a table outlining what you might expect to find in a urine dip of a patient with:

a) pre renal AKI
b) renal AKI
c) post renal AKI
d) UTI

A

a) Prerenal: -/+ for blood, - for proteins, nitrates and leukocytes
b) Renal: + for blood, protein, leukocytes; - for nitrites
c) Post renal: + for blood and protein; - for nitrites and leukocytes
d) UTI: + for all

22
Q

Polyuria is a known common phase of AKI (the diuretic phase).

Name four other causes of polyuria

A
  • DM
  • Psychogenic polyuria
  • Beer potomania
  • Rare endocrine causes e.g. diabetes insipidus
23
Q

How do you manage polyuria

A
  • encourage drinking

- IV fluids if dry to match output (once renal function improves, reduce input to 75% of output)

302 SBM: Metabolic & Renal (6 decks)

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