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Year 3 Renal > AKI > Flashcards

AKI Flashcards

1
Q

What is AKI?

A

Sudden rapid reduction in eGFR with/without oliguria/anuria

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2
Q

What is oligouria?

A

Reduced urine ouptue

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3
Q

What criteria is used to diagnose AKI?

A

KDIGO Criteria
Serum Cr
- Baseline x1.5
- > 26 micromol/L (>0.3mg/dL) increase

Urine output
- <0.5mL/kg/h for 6-12 hours

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4
Q

What are the 3 stage of the KDIGO criteria?

A

Stage 1
Cr increase 1.5x-1.9x
or >26micromol/L
UO <0.5mL/kg/h for 6-12 hours

Stage 2
Cr increase 2x-2.9x
UO <0.5mL/kg/h for more than12 hours

Stage 3 
Cr increase 3x
or >354 micromol/L (>4mg/dL)
UO <0.3mL/kg/h for 24 hours
Anuria 12h

If conflicting go with most severe

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5
Q

What are 4 main complications of the kidney injury?

A
  1. Fluid Overload
    - Pulmonary/Peripheral Oedema
  2. Uraemia
  3. Metabolic acidosis
  4. Hyperkalaemia
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6
Q

What in the management for fluid overload?

A

IV furosemide
GTN infusion (vasodilation)
Haemodialysis if refractory

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7
Q

What is the outcome of high urea?

A 
Uraemic encephalitis (lethargy, confusion)
Uraemic pericarditis
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8
Q

What is the management of uraemia?

A

Haemodialysis

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9
Q

What are the symptoms of metabolic acidosis?

A

Confusion
Tachycardia
Kussmaul’s breathing (drive of CO2 to increase pH)
Nausea and vomiting

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10
Q

What is the treatment for metabolic acidosis>

A

IV Sodium Bicarb

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11
Q

What are the symptoms of hyerpkalaemia?

A 
Can be asympto
Arrthymias
Muscle weakness
Cramps
Paraesthesia
Hypotension
Bradycardia
Cardiac arrest
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12
Q

How is severity of hyperkalaemia assessed?

A

5.5-6 Mild
6.1-6.5 Moderate
>6.5 Severe OR any K with ECG changes or symptomatic

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13
Q

What are the ECG changes seen in hyperkalaemia? (increasing severity)

A 
Peaked T waves
Wide PR interval
Wide QRS duration
Loss of P wave 
Sinusoidal wave

’ Hyperkalaemia box’

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14
Q

What is the treatment for hyperkalaemia?

A

Cardiac monitoring

If ECG changes are seen:
Calcium gluconate 10% 30mls IV
10U of soluble insulin
50mls of 50% glucose

Adjunct:
Salbutamol
IV furosemide
IV sodium bicarb

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15
Q

Why is inuslin used in hyperkalaemia?

A

Drives K into cells

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16
Q

What is calcium gluconate given in hyperkalaemia?

A

Cardioprotective

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17
Q

Why is glucose used in hyperkalaemia?

A

Avoid hypoglycaemia

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18
Q

What investigations are done for AKI? (diagnose)

A

Fluid assessment
(Pitting oedema, JVP etc.)

ABG/VBG, Potassium & Bicarb

Bloods: U&Es, CRP,

US KUB

ECG

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19
Q

What investigations are done for AKI? (cause)

A

Bloods: FBC, LFTs, CK, Clotting

Hepatitis/HIC scree, Vasculitic screen, Myeloma screen, sepsis screen etc.

Thorough medications history

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20
Q

How is AKI managed?

A

ABCDE approach (medical emergency)

Stop Nephrotoxic drugs if IV you need to stop ASAP even before results are back

Find and treat cause

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21
Q

What are the three categories of AKI causes?

A

Pre-renal: Problems with blood supply

Renal: Problems with kidney tissue

Post-renal: Problems with urine outflow

22
Q

What are the pre-renal causes of AKI?

A

Hypovolaemia - losing fluid

Low volume - low fluid to begin with

Vascular insult

23
Q

What are some causes of hypovolaemia?

A 
Acute haemorrhage
GI losses
Diuresis
Burns
Third-spacing (water inside cells move out - sepsis, acute pancreatitis)
24
Q

What are some causes of a low circulating volume?

A

Heart Failure
AKI + HF = Cardiorenal syndrome

Liver Failure
AKI + LF = Hepatorenal syndrome

25
Q

Why can liver failure cause AKI?

A

Few proteins reduces

Osmotic effect

26
Q

What causes vascular insults/poor perfusion of kidneys?

A

ACEi/ARBs
NSAIDS
Contrast used for scans
Renal artery stenosis

27
Q

What are the three categories of post-renal AKI?

A

Luminal
Mural
Extramurla

28
Q

What causes luminal, post-renal AKI?

A

Stones

  • Urethra
  • Ureters
29
Q

What causes mural, post-renal AKI?

A

Cancers of renal tract

Strictures

30
Q

What causes extramural, post-renal AKI?

A

Abdominal/Pelvic cancers

BPH

31
Q

What are the four categories of renal AKI?

A

Tubular
Interstitial
Vascular
Glomerular

32
Q

What tubular issues cause AKI?

A

ATN (Acute Tubular necrosis)
1. Ischaemic
2. Toxic
(Endogenous or Exogenous)

33
Q

What are some toxins that harm the tubules?

A

Myoglobin, Uric acid

Cisplatin, NSAIDS

34
Q

What is the management of tubular AKI?

A

Reversible, recovery in 21 days (cell turnover)

35
Q

What is acute interstitial necrosis?

A

Immune mediated damage of renal interstitium

Will present with signs of allergy e.g. rashes, fever
High eosinophil count
White cell casts on urinalysis

36
Q

What are vascular causes of renal AKI?

A

Haemolytic Uraemic Syndrome

Thrombotic Thrombocytopenia Purpura

Both damage the renal capillaries leading to the formation of microthrombi

37
Q

What is the cause of HUS?

A

Most common in children is secondary to EHEC infection (E. Coli strain)

Presents with bloody diarrhoea

Managed with ABs

38
Q

What causes TTP?

A

ADAMTS 13 deficiency
(Enzyme responsible for vWF breakdown)

Associated with pregnancy/HIV

39
Q

What is the treatment of TTP?

A

Plasmapherisis to remove excess vWF

Rituximab

40
Q

What are the two types of glomulonephritis?

A

Nephrotic - Non-proliferative

Nephritic - Proliferative

41
Q

What are the features of nephrotic syndrome?

A

Non-proliferative
Massive protienuria >3.5g/d (foamy urine)

Hypoalbuminaemia <25g/L

Oedema

Hyperlipidaemia

Protein COAL (Proteinuria, cholesterol, oedema, albumin down, lipids up)

42
Q

What are the features of nephritic syndrome?

A

Haematuria
Proteinuria
Oedema
BP increase

43
Q

What are the 5 causes of nephrotic syndrome?

A 
Minimal change disease
Membranous GN 
FSGS
Diabetic nephropathy
Amyloid nephropathy
44
Q

What is minimal change disease?

A

Common form of nephrotic syndrome in children

Idiopathic, associated with non-hodgkins lymphoma

Podocyte effacement on electron microscopy

Treated with corticosteroids - full recovery

45
Q

What is membranous GN?

A

Common form of nephrotic syndrome in adults

Deposition of immune complexes on basement membrane

Diagnosis by exclusion:
BM thickening on light microscopy
Renal biopsy definitive

Conservative management e.g. low salt/protein diet, corticosteroids though low response

46
Q

What are some RFs for membranous GN?

A 
Autoimmune disease
Hep B/C
Syphilis
Malignancy
Medications (NSAIDS, gold, lithium)
47
Q

What are symptoms of membranous GN?

A

asympto
oedema
xanthelasma
foamy urine

48
Q

How is membranous GN diagnosed?

A

Light/Electron microscopy of renal biopsy

you can visualise basement membrane thickening

49
Q

What is FSGS?

A

Focal segmental glomerulosclerosis

Caused by injury to podocytes

RFs: HIV, heroin

50
Q

What is diabetic nephropathy?

A

Kidney damange caused by diabetes

Excess glucose eventually leads to BM thickening, matrix deposition which causes K-W nodules and glomerular damage

Microalbuminuria

Management: diabetic control, ACEi/ARBs to lower pressure

51
Q

What is amyloid nephropathy?

A

Abnormal amyloid protein deposits

Tissue damage in kidneys

Congo red stain + polarising light will show apple green birefringence

52
Q

What is the difference between nephritic and nephrotic syndrome?

A

Nephritic - hameaturia and some proteinuria

Nephrotoic - lots of proteinuria (frothy)

Year 3 Renal (7 decks)

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