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Urogenital Y2 > L4 - Acute Kidney Injury > Flashcards

L4 - Acute Kidney Injury Flashcards

1. Know the definition of AKI 2. Understand that there are pre-renal, renal and post renal causes of AKI 3. Clinical features and complications of AKI 4. Investigation and general management of AKI 5. Explain how each of pre-renal, renal and post renal causes of AKI cause injury to the kidney in pathophysiological terms. 6. Understand acute tubular necrosis 7. Distinguish between the most common presentations of the different causes of AKI in the clinical setting (this would only be a slid

1
Q

Definition of AKI

results in…

A
  • Abrupt deterioration in renal function, usually over hours or days.
  • Usually but not always reversible.
  • Results in failure to maintain fluid, electrolyte and acid base homeostasis.
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2
Q

Give examples of criteria which may be used to detect AKI?

4

A
  1. Rise in serum creatinine of > 26 μmol/l within 48hrs.
  2. 50% rise serum creatinine within past 7 days.
  3. Fall in urine output, less that 0.5ml/kg/hr for more than 6hr adult and 8hr in kids.
  4. > 25% or greater fall in eGFR in kids and young peeps.
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3
Q

State methods of identifying the cause of AKI?

2

A
  1. Urinalysis

2. USS

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4
Q

Describe how urinalysis may be used to detect cause of AKI?

e.g. what is tested for in urine dipstick test?

A

Perform urine dipstick testing for:

  • blood
  • protein
  • leucocytes
  • nitrites
  • glucose
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5
Q

Creatinine only rises when…

A

50% of kidney function is lost.

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6
Q

Oliguria is …

A

Urine output less than 0.5 ml/kg/hour

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7
Q

Pyonephrosis

A

Infected and obstructed kidneys.

- pus collects in renal pelvis and causes distention of the kidney.

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8
Q

Summarise the importance of studying AKI?

A

Studies show AKI associated with increased risk of CKD which could lead to ESRD (end stage renal disease) and long term dialysis.

Psychological effects on patients, lower quality of life including higher levels of depression.

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9
Q

State what features we might assess for a person with AKI?

5

A
  1. Volume status
  2. Renal function and serum potassium level (to exclude hyperkalaemia)
  3. Take a history (recent symptoms, history of cardiovascular disease…)
  4. Urine dipstick
  5. Stage of AKI
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10
Q

How might we assess the volume status of a patient?

8

A
  1. Monitor fluid intake and losses.
  2. Peripheral perfusion (capillary refill time)
  3. HR, BP
  4. JVP
  5. Moistness of mucous membranes, skin turgor
  6. Changes in urination.
  7. Peripheral oedema
  8. Pulmonary crackles
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11
Q

State the 3 categories of AKI?

A
  1. Pre-renal
  2. Intrinsic renal
  3. Post-renal
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12
Q

Pre-renal AKI is…

due to…

A

Decreased renal perfusion pressure.

Due to:

  • cardiac failure
  • sepsis
  • blood loss
  • dehydration
  • vascular occlusion
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13
Q

Intrinsic renal AKI examples (3)

A
  1. Glomerulonephritis
  2. Small vessel vasculitis
  3. Acute tubular necrosis
    - drugs, toxins
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14
Q

Post renal AKI

A
  1. Obstruction of urinary flow.
    - Retroperitoneal fibrosis
    - benign prostatic enlargement
    - bladder cancer
    - prostate cancer
    - cervical cancer
    - urinary calculi
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15
Q

AKI with negative urinalysis usually indicates …. cause

A

Pre-renal cause

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16
Q

Positive protein and blood indicators on urinalysis may suggest…

A

Glomerular disease

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17
Q

Increased white cells are non-specific but may suggest…

A

Infection.

Most commonly interstitial nephritis.

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18
Q

Why should dipstick analysis of urine from catheterised patients be interpreted with caution?

A
  1. Possibility of false positive results.

2. For example dipstick haematuria as a result of simple trauma.

19
Q

Urinary calculi is…

signs…

A
  1. Solid particles in urinary system.

2. May cause pain, nausea, vomiting, haematuria and possibly chills.

20
Q

Hypovolaemia caused by…

A
  1. Diarrhoea
  2. Vomiting
  3. Haemorrhage
21
Q

Redued cardiac output as a result of …

A

Heart failure

22
Q

Systemic vasodilation due to

A

Sepsis

Anaphylaxis

23
Q

Afferent arteriolar vasoconstriction due to…

A

due to NSAIDS

contrast

24
Q

Failure of efferent arteriolar vasoconstriction

A

ACE inhibitors
ARBS

  • angiotensin converting enzyme inhibitors
  • angiotensin-receptor blockers
25
Q

What may be seen in a renal biopsy showing acute tubular necrosis? (3)

A
  1. Patchy, diffuse erosion of tubular cells with loss of brush border.
  2. Flattening of renal tubular cells due to tubular dilation.
  3. Intratubular cast formation.
    - responsible for formation of granular casts.
26
Q

Describe the reversibility of Acute tubular necrosis?

A

Tubular cells have the capacity to regenerate rapidly and to reform the disrupted tubular basement membrane.

27
Q

Summarise Acute tubular necrosis

A

Hypo perfusion overwhelms kidneys auto regulatory defences.

- Decreased GFR from ischaemic injury.

28
Q

Describe the pathophysiology of Acute tubular necrosis

A
  1. Reduced renal BF - hypoxia - endothelial / epithelial injury
  2. Sloughing of live and dead cells causes cast formation and obstruction of lumen.
  3. Apical blebs, loss of brush border, loss of polarity and integrity of tight junctions.
29
Q

Bleb is…

A
  1. Bleb is a blister filled with serous fluid.

2. Often hemispherical.

30
Q

What would ischaemia in ATN result in?

A
  1. Decreased production of vasodilators (nitric oxide and prostacyclin) by tubular epithelial cell.
  2. This leads to further vasoconstriction —> hypoperfusion.
  3. Low ATP and cytosol calcium. Affects AT. Cell vol and electrolyte regulation disrupted. Cell swells, intracellular sodium and calcium accumulates.
31
Q

Describe the maintainence phase of ATN?

A

Stabilisation of GFR at v.low level (often 1-2weeks).

Period where complications develop.

32
Q

How does tuberglomerular feedback play a role in ATN?

A

Constriction of afferent arterioles by macula densa cells, which detect an increased salt load in distal tubule.

33
Q

Describe the recovery stage of ATN?

A

Regeneration of tubular epithelial cells.

34
Q

ANCA associated vasculitis

A
  1. Antineutrophil cytoplasmic antibody associated vasculitis.
  2. AAV occurs when neutrophils attack small and medium vessels of the body.
  3. Characterised by destruction and inflammation of small vessles.
35
Q

Good pasture syndrome

what kind of disease…
brief patho…
damage?

A

aka anti-glomerular basement membrane disease.

  • Rare, autoimmune
  • Antibodies attack basement membrane in lungs and kidneys leading to bleeding.
  • Can lead to permanent damage.
36
Q

IgA nephropathy

occurs when

A

aka Berger’s disease.

  • Occurs when IgA accumulates in kidneys.
  • Results in local inflammation.
37
Q

State subtypes of renal intrinsic causes to AKI

A
  1. Glomerular
    - ANCA associated vasculitis
    - Anti GBM, goodpasture’s disese
    - IgA nephropathy
  2. Vascular
    - Haemolytic uraemic syndrome
    - hypertensive emergency
  3. Tubular
    - acute tubular necrosis
    - acute interstitial nephritis
    - myeloma / tumourlysis / rhabdomyolysis
38
Q

Myeloma

A

Blood cancer arising from plasma cells.

39
Q

Tumourlysis (2)

A
  1. Metabolic abnormality occurring as a complication during treatment of cancer.
  2. Large amount of tumour cells killed off, their contents released into blood stream.
40
Q

Rhabdomyolysis

A
  • Death of muscle fibres
  • and release of their contents into blood stream.
  • Can lead to renal failure.
  • Kidneys cannot remove waste and concentrated urine.
41
Q

Acute interstitial nephritis

A
  • Renal lesion.
  • Characterised by an inflammatory infiltrate in the kidney interstitium.
  • Most often induced by an allergic reaction to certain drugs.
42
Q

Symptoms of AKI

loadssss

A 
Little urine output 
Oedema in legs, ankles, around eyes 
Fatigue 
Shortness of breath 
confusion 
nausea 
seizures or coma 
chest pain or pressure
43
Q

Complications in a patient with AKI

3 main ones

A
  1. Volume overload.
    - may develop as result of obligate intravenous infusions (antibiotics, vasopressors)
  2. Disturbances of Potassium
    - hyperkalemia
  3. Hypoatremia / hypernatremia
44
Q

Hyponatremia

mild symptoms
severe symptoms

A

Low sodium concentration in blood. <135mmol/L

Mild symptoms: decreased ability to think, headaches, nausea and poor balance

Severe: confusion, seizures and coma

Urogenital Y2 (16 decks)

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