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Year 3 > MedEd renal 1 > Flashcards

MedEd renal 1 Flashcards

1
Q

What is AKI?

A

Sudden rapid reduction in eGFR with or without oligouria

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2
Q

What criteria is used in AKI

A

Kdigo

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3
Q

What is Kdigo’s criteria and what is it used for

A

Used to diagnose AKI
Serum cr= 1.5-1.9 baseline or >26 umol/L increase
Urine output= <0.5mL/kg/h for 6-12 hrs

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4
Q

How much does serum cr rise in AKI?

A

eGFR 1.5-1.9 x baseline

eGFR >26 umol/L increase

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5
Q

What is stage 1 AKI according to Kdigo’s criteria?

A

normal Kdigo criteria
eGFR 1.5-1.9 x baseline or >26 umol/L
urine output <0.5 ml/kh/h for 6-12 hrs

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6
Q

What is AKI stage 2 according to Kdigo’s criteria?

A

eGFR 2-2.9 x baseline

urine output <0.5 l/kh/h for >12 hrs

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7
Q

What is AKI stage 3 according to Kdigo’s criteria?

A

creatinine 3 x baseline or >354 umol/L
urine output <0.3 ml/kh/h for 24 hrs or anuria for 24 hrs
anyone on renal replacement therapy

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8
Q

What is urine output in AKI?

A

<0.5mL/kg/hr for 6-12 hrs

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9
Q

What are the 4 complications of AKI? What symptoms does each cause and how is it managed?

A

Fluid overload- pulmonary oedema, treat with IV furosimide/GTN infusion and heamolysis if refractory
Uraemia- uraemic encephalitis (lethargy and confusion), uraemic pericarditis, treat with haemodialysis
Metabolic acidosis- confusion, tachycardia, jussmaul’s breathing, NV, treat with IV/PO sodium bicarb and dialysis if refractory
Hyperkalemia- asymptomatic, arrhythmia, muscle weakness, cramps, paarsthesia, hypotension, bradycardia, cardiac arrest, treat with connecting to cardiac monitor, calcium gluconate 10% 30 ml IV, 10 units soluble insulin (drives K+ into cells), 50 mls of 50% glucose (to avoid hypo)

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10
Q

What symptom does fluid overload cause in AKI and how is this managed?

A

Causes pulmonary oedema

Treat with IV furosimide/GTN infusion and heamolysis if refractory

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11
Q

What symptom does uraeamia cause in AKI and how is this managed?

A

Causes uraemic encephalitis (lethargy and confusion), uraemic pericarditis
Treat with haemodialysis

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12
Q

What symptom does metabolic acidosis cause in AKI and how is this managed?

A

Causes confusion, tachycardia, jussmaul’s breathing, NV

Treat with IV/PO sodium bicarb and dialysis if refractory

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13
Q

What are mild, moderate and severe levels for hyperkalemia

A 
Mild= 5.5-6
Moderate= 6.1-6.5
Severe= over 6.5 or any level with ECG changes or if symptomatic
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14
Q

What symptom does hyperkaelmia cause in AKI and how is this managed?

A

asymptomatic, arrhythmia, muscle weakness, cramps, paarsthesia, hypotension, bradycardia, cardiac arrest
Treat with connecting to cardiac monitor, calcium gluconate 10% 30 ml IV, 10 units soluble insulin (drives K+ into cells), 50 mls of 50% glucose (to avoid hypo)

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15
Q

What ECG changes are seen in hyperkalemia

A 
Tall tented T waves
Prolonged PR
Wide QRS
Flattened/ absent p wave
Sinusoid rhythm
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16
Q

How do you remember doses for hyperkaelmia treatment?

A

10, 10, 50, 50
10% 30ml IV calcium gluconate
10 units insulin
50ml 50% glucose

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17
Q

What ix are done for AKI?

A

Fluid assessment
ABG/VBG
Bloods: UEs, FBC, CRP, LFTs, CK, clotting
Hep screen, HIV screen, vasculitic screen, myeloma screen, anti GBM, sepsis screen if septic
KUB
ECG
Take a good drug hx!!

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18
Q

What aspect of the hx is really important in AKI?

A

Drug hx

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19
Q

How is AKI managed?

A 
ABCDE approach 
Find and treat cause
Stop any nephrotoxic drugs
Fluid manage (IV fluids or offload with diuretics or dialysis) 
Treat complications
Dialysis if needed
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20
Q

What common abx often causes AKI?

A

Amoxicillin

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21
Q

What causes AKI?

A

Pre renal= problems with blood supply
Renal= problems with kidney tissue
Post renal= problems with urine outflow

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22
Q

Why might there be decreased kidney perfusion causing pre renal AKI?

A

Hypovolemia eg acute GI loss, haemorrhage, diuresis, burns, third spacing
Low volume eg heart failure or liver failure
Vascular insult- damage to arteries/arterioles supplying kidneys

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23
Q

What 3 things will cause reduced perfusion to the kidneys?

A

Hypovolemia
Low volume
Vascular insult

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24
Q

What might damage arteries/arterioles supplying the kidneys?

A

ACEi/ARBs
NSAIDs
Contrast
Renal artery stenosis

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25
Q

What are the 3 types of obstruction that cause post renal AKI?

A

Luminal- kidney stones (if urethra pain and anuria if ureter renal colin)
Mural- cancers of renal tract or strictures
Extramural- abdo/pelvic cancers or BPH

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26
Q

What is there obstruction of in post renal AKI?

A

Urine flow

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27
Q

What are the 4 types of intrinsic renal AKI?

A

Tubular
Interstitial
Vascular
Glomerular

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28
Q

What are the 2 types of acute tubular necrosis? Explain them

A

Ischaemic- due to lack of oxygen supply

Toxic- tubules are directly damaged by a nephrotoxic drug

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29
Q

What is the mechanism behind tubular renal AKI?

A

Acute tubular necrosis

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30
Q

Is acute tubular necrosis reversible?

A

Yes

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31
Q

What do patients develop after acute tubular necrosis? How is this managed?

A

Severe diuresis- manage w strict urine input and output

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32
Q

What is acute interstitial AKI?

A

Immune mediated damage of renal interstitium
Tyoe 4 hypersensitivity reaction
Usually due to medications eg NSAIDs, thiazide diuretics

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33
Q

How do you recongise intersitial AKI?

A

Rash, fever, arthralgia, eosinophilia

White cell casts on urinalysis

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34
Q

What is are the 2 types of vascular renal AKI?

A

HUS: haemolytic uraemic syndrome
TTP: thrombocytic thrombocytopenia purpura

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35
Q

What is the triad for HUS?

A

Haemolytic anaemia
Thrombocytopenia
AKI

36
Q

What is seen in TTP?

A 
haemolytic anaemia
AKI
Thrombocytopenia
fever
neurological symptoms
37
Q

What will you see in HUS due to haemolytic anaemia?

A

Dark urine

Petechaie

38
Q

How do you differentiate TUP from HUS in vascular AKI?

A

There will be fever and neuro symptoms alongside haemolytic anaemia, thrombocytopenia and AKI

39
Q

How is vascular AKI due to HUS managed?

A

Abx

40
Q

In who is vascular AKI due to HUS more common?

A

Children

41
Q

How is HUS caused and what will it present with?

A

By e coli most commonly

Presents with blood diarrhoea

42
Q

How is TUP vascular AKI mananged?

A
43
Q

What are the 2 presentations of glomerulonephritis?

A

Nephrotic and nephritic syndrome

44
Q

What is glomerulonephritis?

A

Damage to glomerulus

45
Q

Out of nephrotic and nephritic syndrome which is prolif and which is no prolif

A 
Nephrotic= non prolif
Nephritic= prolif
46
Q

What is the main difference in presentation between nephrotic and nephritic syndrome?

A 
Nephrotic= no haemturia
Nephritic= haematuria
47
Q

What is seen on microscopy in nephrotic vs nephritic syndrome?

A 
Nephrotic= fatty cast
Nephritic= red cell cast
48
Q

What are the 5 main cuases of nephrotic syndrome?

A 
Minimal change disease
Membranous GN
FSGS
Diabetic nephropathy
Amyloid nephropathy
49
Q

What cause of nephrotic syndrome is most common in children? What is it associated with?

A

Minimal change disease

Associated with non hodgkin’s lymphoma

50
Q

What are symptoms of nephrotic syndrome?

A

Puffy face and ankles

51
Q

How is nephrotic syndrome diagnosed?

A

Mainly clinical

Do kidney biopsy if treatment doesnt work

52
Q

What is seen on light and electron microscopy in nephrotic syndrome?

A 
Light= no changes seen
Electron= podocyte effacement
53
Q

How is minimal change nephrotic syndrome managed?

A

Corticosteorids

54
Q

What is the most common cause of nephrotic syndrome in adults?

A

Membranous GN

55
Q

What are the 2 categories in Kdigo’s criteria that are used to diagnose AKI/

A

Serum creatinine

Urine output

56
Q

What happens to HR in hyperkalemia?

A

Bradycardia

57
Q

What additional treatment might you give for hyperkalemia?

A

Salbutamol nebulisers
IV furosemide
IV sodium bicarb (if they are acidotic)
If refractory start haemodialysis

58
Q

What drugs might cause vascular insult and lead to AKI?

A

ACEi/ARBs

NSAIDs

59
Q

What exogenous and endogenous toxins cause acute tubular necrosis?

A 
Endogenous= myoglobulin, uric acid, monoclonal light chains 
Exogenous= aminoglycosides, cisplatin, NSAIDs, heavy metals, radiocontrast agents
60
Q

How long does it take to recover from acute tubular necrosis?

A

It is reversible, takes around 21 days to recover

61
Q

What is seen on urinalysis in acute tubular necrosis?

A

Granular muddy brown casts

62
Q

What is seen on urinalysis in acute interstitial necrosis?

A

White cell casts

63
Q

What causes thrombocytic thrombocytopenia purpura?

A

ADAMTS 13 deficiency (can be congenital or autoimmune)

64
Q

What is ADAMTs 13 and what does deficiency of it cause?

A

It is the enzyme responsible for vWF breakdown, deficiency of it causes thrombocytic thrombocytopenic purpura

65
Q

How is thrombocytic thrombocytopenia purpura treated?

A

Plasmapherisis

Rituximab

66
Q

How does nephrotic syndrome present?

A

Massive proteinuria (>3.5 g/day)
Foamy urine
Oedema
Hyperlipidaemia and lipiduria

67
Q

What is seen on urine microscopy in nephrotic syndrome?

A

Fatty casts

68
Q

What are proteinuria levels in nephrotic syndrome?

A

> 3.5 g/day

69
Q

How does nephritic syndrome present?

A 
Haematuria 
Proteinuria (1-3.5g) 
Oedema
Progressive renal impairment 
HTN
70
Q

How does proteinuria levels differ between nephrotic and nephritic syndrome?

A 
Nephrotic= 3.5 g/day (very high)
Nephritic= 1-3.5 g/day
71
Q

What acronym is used to remember how nephrotic vs nephritic syndrome present and what does it stand for?

A 
Nephrotic= protein coal= proteinuria, cholesterol up, oedema, albumin down, lipids up
Nephritic= protein hob= proteinuria, haematuria, oedema, blood pressure up
72
Q

How is nephrotic syndrome due to minimal change disease managed?

A

Corticosteroids

73
Q

What is glomerular nephropathy?

A

Subepithelial deposition of immune complexes on the basement membrane causing nephrotic syndrome

74
Q

Where are immune complexes deposited in membranous glomeulonehropathy?

A

Subepithelium of basement membrane

75
Q

What are some RF for membranous glomerulonephropathy?

A 
Autoimmune disease
Hep b/c
syphillis
malignancy
medications like lithium, nsaids
76
Q

What is immunoflourescence in minimal change disease/

A

Negative

77
Q

How is membranous glomerulonephropathy diagnosed?

A

renal biopsy for definite diagnosis
light microscopy will show basement thickening
electron microscopy will show spike and dome appearance and podocyte effacement

78
Q

What antibodies are seen in membranous glomerulonephropathy and what are they against?

A

IgG4 antibodies against phospholipase A2 receptors

79
Q

How is membranous glomerulonephropathy treated?

A

symptomatic management
low response to corticosteroids but they might still be offered
cytotoxic/immunosupressive therapy

80
Q

What is focal segmental glomerulosclerosis (FSGS)

A

Injury to podocytes causing nephrotic syndrome

81
Q

What are RF for FSGS?

A

HIV, heroin use, congenital malformations, INF treatment

82
Q

How is FSGS diagnosed?

A

Renal biopsy- focal segmental areas of collapse and sclerosis
Electron microscopy- effacement of foot processes of podocytes

83
Q

How is FSGS managed?

A

Corticosteroids and symptomatic management

84
Q

What nodules are present in the kidney in diabetic nephropathy?

A

Kimmelstiel Wilson nodules

85
Q

What is seen on light microscopy in diabetic nephropathy?

A

Mesangial expansion
GBM thickening
Kimmelstiel Wilson nodules

86
Q

How is diabetic nephropathy treated?

A

Good control of diabetes

ACEi/ARB

87
Q

What are the 2 causes of nephritic syndrome?

A

MPGN

RPGN/ cresenteric glomerulonephropathy

Year 3 (104 decks)

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