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5th Year > Nephrology/Urology > Flashcards

Nephrology/Urology Flashcards

1
Q

What is the triad of symptoms for renal cell carcinoma?

A

Haematuria
Loin pain
Abdominal mass

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2
Q

What are two other symptoms for renal cell carcinoma (not in the triad)?

A

Pyrexia of unknown origin

Left varicocele - due to occlusion of Left testicular vein

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3
Q

What organism causes Haemolytic Uraemic Syndrome?

A

E coli 0157

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4
Q

What is the triad of HUS?

A

AKI
Normocytic haemolytic anaemia
Thrombocytopenia
(all following diarrhoea)

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5
Q

What is the management of HUS?

A

Supportive + fluids

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6
Q

What happens to phosphate in CKD?

A

Increases

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7
Q

How does osteomalacia occur in CKD?

A

Phosphate increases which ‘drags’ calcium into bones

Formation of new, weak bones

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8
Q

What is the management of osteomalacia in CKD?

A

Alendronic acid - decreases bone tunrover

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9
Q

What is indicated by raised phosphate, with low calcium and vitamin D?

A

Secondary Hyperparathyroidism (to CKD)

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10
Q

When should you refer someone with CKD to a nephrologist from GP? (top 4)

A

eGFR <30
eGFR reducing by >5 per year
ACR >70
ACR >30 with haematuria (after UTI excluded)

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11
Q

What cause of CKD will show large/normal size kidney on USS?

A

HIV-associated nephropathy

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12
Q

What is sevelamer?

A

Non-calcium-based phosphate binder

Treats hyperphosphataemia in CKD patients

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13
Q

What is calcium acetate?

A

Calcium-based phosphate binder

Not appropriate is already hypercalcaemic

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14
Q

How is diabetic nephropathy screened?

A

Yearly early morning urine ACR

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15
Q

Why does diabetic nephropathy screening use an early morning sample?

A

To avoid orthostatic proteinuria giving false +ve

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16
Q

What ACR would be classed as microalbuminaemia?

A

ACR >2.5

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17
Q

When should CKD be diagnosed in diabetes?

A

eGFR persistently <60

ACR persistently >3

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18
Q

What are the features of myeloma?

A 
CRAB
Calcium raised
Renal complications
Anaemia
Bone disease
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19
Q

What are the renal features of ADPKD? (5)

A 
HTN
Recurrent UTIs and stones
Abdo pain
Haematuria
CKD
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20
Q

What are the extra-renal features of ADPKD? (4)

A

Liver cysts -> hepatomegaly (70%)
Berry aneurysms -> increased SAH risk (8%)
CVD eg. mitral valve disease, aortic dissection
Cysts elsewhere

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21
Q

What is the triad of nephrotic syndrome?

A

Proteinuria >3g/24hr
Hypoalbuminaemia <30g/L
Oedema

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22
Q

What are the causes of metabolic acidosis with a NORMAL anion gap?

A 
T-DAP
Renal Tubular necrosis
Diarrhoea
Addison's
Pancreatic fistula
\+ Acetazolamide
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23
Q

What might cause metabolic acidosis with a RAISED anion gap?

A

Sepsis
DKA
Salicylate poisoning

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24
Q

How do you distinguish between Acute Tubular Necrosis and pre-renal uraemia?

A

ATN = urinary sodium >40

Pre-renal AKI = urinary sodium <20

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25
Q

How is does the management of ATN and pre-renal AKI differ?

A

Pre-renal AKIs have good response to fluids, ATN does not

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26
Q

What medication can be used to reduce proteinuria?

A

ACEi

Reduce filter pressure

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27
Q

What is an acceptable reduction in kidney function when starting an ACEi?

A

25% decrease in eGFR

30% increase in creatinine

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28
Q

Nephritic syndrome 1-2 DAYS post URTI?

A

IgA nephropathy

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29
Q

Nephritic syndrome 1-2 WEEKS post URTI?

A

Post-strep glomerulonephritis

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30
Q

What, when found in urine, in pathognomonic for ATN?

A

Muddy brown casts of epithelial cells

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31
Q

Which antibiotic class may cause acute interstitial nephritis?

A 
Penicillins
Cephalosporins
Macrolides
Sulfonamides
Fluoroquinolones
Anti-TB drugs
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32
Q

What are the symptoms of acute interstitial nephritis?

A

Back/abdo pain
Dysuria
Haematuria

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33
Q

What is present on urinalysis in acute interstitial nephritis?

A 
Eosinophilic casts
(sometimes have raised eosinophils on FBC)
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34
Q

Which renal patients are at risk of squamous cell carcinomas and skin cancers?

A

Those on long-term immunosuppression suppression eg. transplant patients

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35
Q

What could new onset confusion and a pericardial rub indicate in a CKD patient?

A

Uraemic encephalopathy and pericarditis

These are indications for dialysis

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36
Q

What would salicylate poisoning show on an ABG?

A

Metabolic acidosis with RAISED anion gap

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37
Q

What is Goodpasture’s syndrome?

A

Type II Hypersenitivity reaction

Anti-GBM Abs vs Type IV collagen mainly in lungs and kidneys

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38
Q

What are the features of Goodpasture’s syndrome?

A

Haemoptysis and haematuria

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39
Q

What is the management of hyperkalaemia?

A

IV calcium glunconate 30mls over 2mins
Nebulised salbutamol 5mg B2B 2-4
Actrapid 10 units + 125ml 20% Dextrose infusion

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40
Q

How long does an A-V fistula take to start working?

A

6-8 weeks

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41
Q

What are the daily fluid replacement requirements?

A

Glucose 50-100g/day
Water 25-30ml/kg/day
Na, K, Cl = 1mmol/kg/day

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42
Q

What medication can be used to treat ascites?

A

Spironalactone

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43
Q

When is a micturating cystography used?

A

If you suspect reflux nephropathy

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44
Q

What may be a knock-on effect of renal artery stenosis?

A

Renal artery stenosis -> increased plasma renin
Increased renin -> secondary hyperaldonsteronism
Hyperaldosteronism -> Refractory HTN

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45
Q

What is eplereone?

A

Alternative to spironalactone

Used in those who experience gynaecomastia

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46
Q

What do the kidneys of someone with diabetic nephropathy appear like on USS?

A

Bilaterally enlarged

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47
Q

What are the criteria for URGENT haematuria urology referrals?

A

> 45yrs with visible haematuria + no UTI

>60yrs with non-visible haematuria + dysuria/rasied WCC

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48
Q

What is the criteria for ROUTINE haematuria urology referrals?

A

> 60yrs with recurrent/persistent UTI

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49
Q

Where should someone <40yrs with haematuria be referred?

A

Nephrology (not urology)

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50
Q

What are the causes of metabolic acidosis with a RAISED anion gap?

A 
LUKA
Lactate - shock/hypoxia/sepsis
Urate - renal failure
Ketones - DKA
Acid poisoning - paracetamol/methanol
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51
Q

What is the prognosis of minimal change disease?

A

1/3 single episode
1/3 few relapses
1/3 frequent relapses (these stop before adulthood)

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52
Q

What is the management of minimal change disease?

A

Steroids (80% responsive)

Ciclophosphamide = 2nd line

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53
Q

What results would indicate diabetes insipidus?

A

Raised plasma osmolality
Reduced urine osmolality
Urine osmolality >700 excludes DI

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54
Q

How do you differentiate between cranial and nephrogenic diabetes insipidus?

A

Water deprivation test - cranial DI responds to exogenous vasopressin, nephrogenic does not

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55
Q

Which psychiatric medication can result in nephrogenic diabetes insipidus?

A

Lithium

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56
Q

What is an important DDx in an elderly patient who has had a long lie?

A

Rhabdomyolysis

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57
Q

What measures should be taken if someone with CKD requires a contrast-CT?

A

12hrs IV fluids at 1ml/kg/hr pre- and post-CT

Consider temporary stop of ACEi if eGFR <40

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58
Q

Why are those with nephrotic syndrome at increased risk of clotting?

A

Loss of antithrombin III, protein C and protein S in urine
This increases fibrinogen levels which increases clotting risk
Require LMWH prophylaxis

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59
Q

What is Alport syndrome?

A

X-linked abnormality in Type IV collagen -> abnormal GBM

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60
Q

What are the triad of features of Alport syndrome?

A

Progressive renal failure
Bilateral sensorineural deafness
Occular abnormalities

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61
Q

What does electron microscopy of the glomerulus show in Alport syndrome?

A

Basket-weave appearance

Longitudinal splitting of lamina densa of GBM

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62
Q

What is the causative organism of peritonitis secondary to peritoneal dialysis?

A

S. epidermidis

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63
Q

What is the management of diabetes insipidus?

A

Cranial DI = vasopressin

Nephrogenic DI = thiazide diuretic eg. Chlarothiazide

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64
Q

What is the most important infection post-organ transplant?

A

CMV

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65
Q

What are the symptoms of post-transplant CMV infection?

A

Few days unwell + anorexia
Hepatitis + jaundice
Widespread LNs

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66
Q

What is the treatment of post-transplant CMV infection?

A

Ganciclovir

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67
Q

What is alfacalcidol?

A

Vitamin D analogue

Used in end-stage CKD as does not need kidney reactivation

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68
Q

What are the ECG features of hypokalaemia?

A

Flattened T waves

U waves

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69
Q

What is the cut-off for severe hypokalaemia?

A

<2.5

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70
Q

What are the symptoms of hypokalaemia?

A

Muscle weakness

Palpitations

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71
Q

What is the management of hypokalaemia?

A

Replacement in infusion

Should not exceed 20mmol/hr

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72
Q

Which diagnoses are important to consider in someone developing an AKI after starting ACEi?

A

Young female = fibromuscular dysplasia

Older patients = atherosclerosis

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73
Q

What is a hallmark feature of fibromuscular dysplasia?

A

‘String of beads’ renal arteries

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74
Q

What ABG will Addison’s show?

A

Hyperkalaemic metabolic acidosis

Decreased aldosterone -> increased K retention and increased Na excretion which causes increase H+ retention

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75
Q

What should be considered if a patient has persistent sterile pyuria with negative cultures?

A

Renal TB

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76
Q

What may falsely show a decreased eGFR?

A

Large muscle mass

Due to increased creatinine

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77
Q

What do those with nephrotic syndrome require to prevent complications?

A

LMWH prophylaxis

Low threshold for Abx

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78
Q

What are the stages of AKI in terms of urine productions?

A

Stage 1 = <0.5ml/kg/hr for >6hrs
Stage 2 = <0.5ml/kg/hr for >12hrs
Stage 3 = <0.3ml/kg/hr for >24hrs OR anuric for >12hrs

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79
Q

When does minimal change disease require a biopsy?

A

When not steroid-responsive
Child with nephrotic syndrome only gets biopsy if don’t respond to steroids
ALL adults get biopsy

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80
Q

What is the hallmark feature on biopsy of Rapidly Progressive GN?

A

Epithelial crescent formation

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81
Q

What are 3 causes of RPGN?

A

Goodpasture’s
Wegner’s
SLE

82
Q

What renal(ish) complication might haemochromatosis cause?

A

Cranial diabete insipidus

83
Q

What are the features of amyloidosis?

A

50-65yr old
Decreased renal function with proteinuria
Hepatosplenomegaly
COPD

84
Q

How might an amyloidosis patient present?

A

50-65yrs old with progressive breathlessness and weakness

85
Q

How is amyloidosis diagnosed? (3)

A
  1. Congo red staining = apple green birefringence
  2. Serum amyloid precursor (SAP) scan
  3. Rectal biopsy
86
Q

What are the features of nephrotic syndrome? (5)

A 
Proteinuria >3.5g/day
Hypoalbuminaemia
Oedema
Hyperlipidaemia
Lipiduria
87
Q

How does SELECTIVE proteinuria develop in minimal change disease?

A

T-cells release cytokines
Podocyte foot effacement
Loss of -ve charge barrier
CanNOT repel albumin but CAN repel immunoglobulins

88
Q

What type of malignancy is minimal change disease associated with?

A

Hodgkin’s lymphoma

89
Q

What do LM, EM and IF show in minimal change disease?

A

LM: No change
EM: Podocyte effacement
IF: -ve

90
Q

What is the management of minimal change disease?

A

Steroids

Kids respond well, adults also but slower

91
Q

What is Focal Segmental Glomerulosclerosis?

A

PARTS of SOME glomeruli develop scarring and SCLEROSIS

92
Q

Who is FSGS more common in?

A

African-americans

Hispanics

93
Q

What are the features of primary (idiopathic) FSGS?

A

Damaged podocytes become leaky over time
Some proteins get trapped in mesangium
This causes HYALINOSIS = glassy appearance
This turns to SCLEROSIS over time

94
Q

What are the causes of secondary FSGS? (5)

A 
Sickle cell disease
HIV-associated nephropathy
Heroin
Kidney hyperperfusion
Increased glomerular capillary pressure
95
Q

What do LM, EM and IF show in FSGS?

A

LM: Segmental sclerosis and hyalinosis
EM: Foot process effacement
IF: Non-specific focal IgM and complement deposits

96
Q

What is the management of FSGS?

A

Steroids
Inconsistent response
<10% spontaneously remiss

97
Q

What is membranous GN?

A

Damage to GBM due to immune complex deposition

98
Q

Who gets membranous GN?

A

Caucasian adults
Generally primary/idiopathic
3rd most common ES-RF cause
Lots of causes including SLE

99
Q

What are the two mechanisms of immune complex deposition in membranous GN?

A
  1. AutoAb tageting GBM

2. Complexes form outside kidneys and carried to GBM

100
Q

What are the two types of AutoAbs targeting the GBM in membranous GN?

A

M-type phospholipase A2 receptor
Neutral endopeptidase

Both expresses on podocyte surface

101
Q

What is the main protein involved in immune complex formation outside the kidneys in membranous GN?

A

Cationic Bovin Serum Albumin

Found in cow’s milk and beef protein

102
Q

Where are the immune complex deposits in membranous GN?

A

Subepithelial

103
Q

How do the immune complex deposits cause kidney damage in membranous GN?

A

They cause complement activation which forms MACs which damages podocytes and mesangial cells
This causes GBM thickening and ‘spike and dome’ appearance on EM

104
Q

What are the LM, EM and IF features of membranous GN?

A

LM: GBM thickening
EM: Spike and dome appearance
IF: Granular complex deposits

105
Q

What is the management of membranous GN?

A

ACEi
Steroids
Treat underlying cause

106
Q

What is the prognosis for membranous GN?

A

1/3 spontaneous remission
1/3 remain proteinuria
1/3 ESRF

107
Q

What is membranoproliferative GN?

A

Subendothelial immune complex deposition causing inflammation
May present as mixed nephrotic/nephritic picture
Poor prognosis

108
Q

What are the causes of type 1 membranoproliferative GN?

A

Cryoglobulinaemia

Chronic Hep C/B

109
Q

What is the pathophysiology of membranoproliferative GN?

A

SUBENDOTHELIAL deposits by 2 mechanisms:

  1. Overactivation of classical complement pathway
  2. Inappropriate activation of alternative complement pathway
110
Q

How does over activation of the classical complement pathway cause Type 1 MPGN?

A

Immune complex formation secondary to chronic infection (eg. HepB/C) deposit in glomerulus
This activates the classical complement pathway
Results in complex AND complement deposits

111
Q

How does inappropriate activation of the alternative complement pathway occur in Type 1 MPGN?

A

Nephritis factor (C3NeF) stabilises C3 convertase
This causes inappropriate activation
Results in complement deposits ONLY

112
Q

What is the difference between the classical and alternative pathway activation causing Type 1 MPGN?

A 
Classical = complex AND complement deposits
Alternative = complement deposits ONLY
113
Q

What is the hallmark feature of MPGN?

A

Tram-track appearance

Due to splitting of GBM

114
Q

How does GBM occur in MPGN?

A

Subendothelial deposits cause mesangial proliferation
This causes mesangial INTERPOSITION
Results in splitting of GBM

115
Q

What do EM and IF of MPGN show?

A

EM: Tram-track appearance
IF: Granular complex deposits

116
Q

What is the hallmark feature of Type 2 MPGN?

A

‘Dense deposits’

Due to complement (NOT complex) deposits

117
Q

What associated features are found in Type 2 MPGN?

A

Partial lipodystrophy = lose submit tissue from face

Low C3 levels

118
Q

What is the pathophysiology of Type 2 MPGN?

A

Persistent activation of the ALTERNATIVE complement pathway due to NEPHRITIC FACTOR causes complement deposition and low C3 levels

119
Q

Where are the complement deposits in Type 2 MPGN?

A

WITHIN the GBM, NOT subendothelial

120
Q

What does EM show in Type 2 MPGN?

A

INTRAMEMBRANOUS complement deposits = DENSE DEPOSITS

121
Q

What is the hallmark feature of Type 3 MPGN?

A

Deposits and sub endothelial AND subepithelial

122
Q

What is the management of MPGN?

A

Steroids = often poor response

123
Q

Why is diabetic nephropathy important?

A

Leading cause of ESRF in developed world

124
Q

What is the pathophysiology of diabetic nephropathy?

A

Initial hyperfiltration with increased GFR
This causes GBM thickening
Results in widened podocyte gaps -> protein can pass
Decreases GFR over time

125
Q

Why does initial hyper filtration occur in diabetic nephropathy?

A

Excess glucose causes glycation of efferent arteriole -> atherosclerosis -> increased glomerular pressure
Also afferent arteriole dilates -> increased glomerular pressure
Together = hyperfiltration

126
Q

What is the screening for diabetic nephropathy?

A

Yearly U+E and first-pass ACR

127
Q

When should CKD be diagnosed in diabetic nephropathy?

A

ACR >3 or eGFR <60 for >3 months

128
Q

What is the management of diabetic nephropathy? (4)

A 
Protein restriction
Tight glycemic control
ACEi - keep BP <130/80
(ARB in Afro-caribbeans)
Statin
129
Q

What are the features of nephritic syndrome? (6)

A 
PHAROH
Proteinuria (non-selective)
HAEMATURIA
Azotemia (increased creatinine and urea)
RBC casts in urine
OLIGURIA
HTN
130
Q

What blood tests should be done for someone with nephritic syndrome?

A 
Usuals = FBC, U+E, LFT, ESR, CRP
Losses = Igs electrophoresis, C3/4 levels
Causes = AutoAbs (eg. ANA, ANCA etc), cultures, ASOT, HBsAg, anti-HCV
131
Q

What urine tests should be done for someone with nephritic syndrome?

A

MC&S
RBC casts
ACR
Bence-Jones protein

132
Q

What is ASOT?

A

Anti-streptolysin O = used for Dx of post-strep GN

133
Q

What is the general management for all nephritic syndromes?

A

Early nephrology referral
Keep BP <130/80
(<125/75 if proteinuria)
ACEi

134
Q

What is IgA nephropathy?

A

Type III hypersensitivity reaction

Mesangial deposits of IgA immune complexes

135
Q

What is another name for IgA nephropathy?

A

Berger’s disease

136
Q

Why is IgA nephropathy important?

A

Commonest GN worldwide

137
Q

How does IgA nephropathy present?

A

Macroscopic haematuria in young male 1-2 days following URTI

Nephrotic protein and renal failure are rare

138
Q

What will LM, EM and IF show in IgA nephropathy?

A

LM: Mesangial proliferation
EM: Immune complex deposition
IF: IgA and C3 deposits

139
Q

What is the management of IgA nephropathy?

A

ACEi for HTN control

Steroids are not helpful

140
Q

What is the prognosis for IgA nephropathy?

A

20% develop ESRF in 20yrs

141
Q

What would suggest a good prognosis in IgA nephropathy?

A

Frank haematuria

142
Q

What would suggest a worse prognosis in IgA nephropathy? (6)

A 
Male
Proteinuria
HTN
Hyperlipidaemia
Smokers
ACE genotype DD
143
Q

How do you differentiate between IgA nephropathy and HSP?

A

IgA nephropathy = kidneys ONLY

HSP = systemic features

144
Q

What is Post-Strep GN?

A

Type III Hypersensitivity reaction

Immune complex deposition in glomeruli

145
Q

What makes up the immune complexes deposited in Post-Strep GN?

A

IgG, IgM and C3

146
Q

How does Post-Strep GN present? (6)

A 
Malaise
'Cola-coloured haematuria'
Proteinuria
Oliguria
Peripheral and periorbital oedema
7-14 days post-strep infection
147
Q

Who gets Post-Strep GN?

A

Generally young children

148
Q

Which Strep causes Post-Strep GN?

A

Strep pyogenes

Group A beta-haemolytic strep

149
Q

What specific bloods with suggest Post-Strep GN?

A

Low C3
Raised ASO titre
Anti-DNAse B +ve

150
Q

Other than strep-throat, what else can post-strep GN present following?

A

Impetigo - 6 weeks following

151
Q

What is the general prognosis of post-strep GN?

A

Generally mild - resolves within 1 month

152
Q

What will LM, EM and IF shown post-strep GN?

A

LM: Enlarges and hypercellular
EM: ‘Humps’ of subendothelial deposits
IF: ‘Starry sky’ granular appearance along GBM

153
Q

What percentage of SLE patients develop kidney disease?

A

50%

Should be monitored for proteinuria

154
Q

How many WHO classes of SLE-related GN are there?

A

6

155
Q

Which is the worst WHO class of SLE-related GN?

A

Class IV = diffuse proliferative GN

156
Q

What specific appearance does Class IV SLE-related GN have on LM?

A

‘Wire-loop’ appearance

Due to GBM deposits

157
Q

What type of hypersensitivity reaction is SLE-related GN?

A

Type III Hypersensitivity

Immune complex deposition, generally subendothelial

158
Q

How does SLE-related GN usual present?

A

Nephrotic syndrome

But can present as nephritic as well depending on lesion location

159
Q

What is the management of SLE-related GN?

A

Steroids +/- immunosuppression for Tx of SLE

ACEi for Tx of HTN

160
Q

Why is Rapidly Progressive GN important?

A

Can cause ESRF over few days

161
Q

What is a specific feature must be present for it to be RPGN?

A

Glomerular CRESCENTS on LM

162
Q

What causes glomerular crescents in RPGN?

A

Cell proliferation in Bowman’s space

163
Q

What are the 3 types of RPGN?

A

Type 1 = Anti-GBM disease (3%)
Type 2 = Immune complex disease (45%)
Type 3 = Pauci-immune disease (50%)

164
Q

What is an example of an Anti-GBM RPGN?

A

Goodpasture’s syndrome

165
Q

What are 3 examples of immune complex RPGN?

A

SLE-related GN
IgA nephropathy
HSP

166
Q

What are 2 examples of Pauci-immune RPGN?

A 
Granulomatosis with polyangiitis (cANCA +ve)
Microscopic polyangiitis (pANCA +ve)
167
Q

What does LM show for all RPGN?

A

Glomerular crescents

168
Q

What does IF show for each type of RPGN?

A

Type 1 = Linear anti-GBM deposits
Type 2 = Granular deposits
Type 3 = -ve IF as no deposits

169
Q

What is the general management of all RPGN?

A

Anticoagulation - prevent fibrin deposits
Immunosuppression
Plasmaphoresis

170
Q

What is Goodpasture’s syndrome?

A

Type II Hypersensitivity reaction

Anti-GBM Abs vs Type IV collagen

171
Q

What are the features of Goodpasture’s syndrome?

A

Pulmonary haemorrhage then RPGN

172
Q

Who is at increased risk from Goodpasture’s syndrome?

A

Males 20-30yrs and 60-70yrs

Smoking and LRTI increases pulmonary haemorrhage risk

173
Q

Which HLA is Goodpasture’s syndrome associated with?

A

HLA DR2

174
Q

What 2 specific investigations will suggest Goodpasture’s syndrome?

A

Renal biopsy = Linear IgG GBM deposits on IF

Raised transfer factor secondary to pulmonary haemorrhage

175
Q

What is the management of Goodpasture’s syndrome?

A

High-dose IV steroids + cyclophosphamide

Plasma exchange

176
Q

What is the most common type of bladder cancer?

A

Transitional cell carcinoma (90%)
SCC (7%)
Adenocarcinoma (2%)

177
Q

What is the most common presentation of bladder cancer?

A

Painless haematuria

178
Q

Who gets bladder cancer?

A

50-80yr old males
Smokers
Aniline dyes

179
Q

What type of bladder tumour is most common?

A

Papillary (70%)

Mixed/sold growths are more prone to invasion

180
Q

What percentage of females over 50yrs with incidental haematuria, after excluding UTI, will have bladder cancer?

A

10%

181
Q

How is bladder cancer staged?

A

Cystoscopy + biopsy
Pelvic MRI for local spread
CT for mets

182
Q

What is the management of bladder cancer?

A

Isolated lesion = TURBT
High-grade isolated lesion = TURBT + adjuvant BCG
PT2+ = radial cystectomy with ill conduit OR radical radiotherapy

183
Q

What is the PT staging system of bladder cancer?

A 
PTA = no invasion
PT1 = mucosal invasion
PT2 = muscle invasion
PT3 = serosal invasion
PT4 = mets
184
Q

What is the 5yr survival of bladder cancer?

A 
T1 = 90%
T4a = 10-25%
N1-2 = 30%
185
Q

Where do renal cell cancers arise from?

A

PCT

Generally upper pole of kidney

186
Q

What is the most common renal cell cancer?

A

Clear cell tumour (75-85%)

These arise from PCT

187
Q

What type of carcinoma would a renal cell caner arising from the renal pelvis be?

A

Transitional cell carcinoma

188
Q

Which two syndromes are associated with renal cell cancer?

A

von Hippel-Lindau

Tuberous sclerosis

189
Q

What is von Hippel-Lindau syndrome?

A

Dysfunction of VHL gene on Chr3 -> increase IGF-1

Often get bilateral renal cell cancers

190
Q

What does the increased IGF-1 in vHL syndrome cause?

A
  1. Dysregulated cell growth

2. Increased VEGF -> angiogenesis

191
Q

What other non-renal cancers is vHL associated with?

A

Tumours/cysts in eyes and CNS

192
Q

What is the classical triad of renal cell cancer?

A

Haematuria
Loin pain
Abdominal mass

193
Q

What 4 endocrine effects are associated with renal cell cancer?

A

EPO -> polycythaemia
PTH -> hypercalcaemia
Renin -> HTN
ACTH -> Cushing’s

194
Q

What non-endocrine paraneoplastic syndrome is associated with renal cell cancer?

A

Stauffer syndrome

Cholestasis and hepatosplenomegaly secondary to increased IL-6

195
Q

What percentage of patients with renal cell cancer have mets at presentation?

A

25%

Lungs and bones primarily

196
Q

Why do renal cell cancers met to lungs preferentially?

A

Grows into renal vein

Lungs are first capillary bed reached

197
Q

How is renal cell cancer staged?

A

CT chest, abdo and pelvis

198
Q

Would you biopsy a renal cell cancer?

A

No

199
Q

Why wouldn’t you biopsy a renal cell cancer?

A

High risk of spread and no change to management

200
Q

What is the name of a benign renal tumour with a ‘spoke-wheel’ pattern on angiography?

A

Oncocytoma

Preoperative distinction near impossible

201
Q

What is the management of renal cell cancers?

A

Partial or Total nephrectomy

202
Q

What type of neoadjuvant chemotherapy can be used to shrink a renal cell cancer preoperatively?

A

Tyrosine kinase inhibitors

5th Year (8 decks)

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