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Clinical Pathology > Kidney and Urinary Tract Disease - Diseases (30 & 31) > Flashcards

Kidney and Urinary Tract Disease - Diseases (30 & 31) Flashcards

1
Q

Function of the kidneys

A
  • Eliminating metabolic waste products
  • Regulating fluid and electrolyte balance
  • Influencing acid-base balance
  • Production of hormones (Renin, erythropoietin)
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2
Q

Function of the kidneys

A
  • Eliminating metabolic waste products
  • Regulating fluid and electrolyte balance
  • Influencing acid-base balance
  • Production of hormones (Renin, erythropoietin)
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3
Q

How many people develop acute renal failure in England?

A

26,000/year

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4
Q

Acute renal failure presentation

A

Rapid rise in creatinine and urea, generally unwell

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5
Q

Nephrotic syndrome presentation

A

Oedema, protein uria and hypoalbuminaemia, proteinuria >3g/24 hr (albumin)

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6
Q

Acute nephritis (nephritic syndrome)

A

Oedema, proteinuria, haematuria, renal failure

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7
Q

Chronic renal failure

A

Slow declining renal function

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8
Q

What part of kidney allows filtration?

A

Foot processes, endothelial cells and basement membrane in podocytes in glomerulus i

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9
Q

Blood flow in kidney

A

Renal artery > afferent arterioles > glomerulus > efferent arteriole > proximal convoluted tubule (PCT) > loop of hence > distal convoluted tubule > collecting duct/renal vein

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10
Q

Immunological causes of damage to BM

A
  • Circulating immune complexes deposit in glomerulus
  • Circulating antigens deposit in glomerulus
  • Antibodies to BM/other components of glomerulus
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11
Q

Immunological causes of damage to BM damage the glomeruli via

A

Complement activation, neutrophil activation, reactive oxygen species, clotting factors

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12
Q

Non-Immunological causes of damage to BM > GD

A
  • Hyperglycaemia
  • Inherited disease (abnormal podocytes)
  • Deposition of abnormal proteins (amyloid)
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13
Q

Non-Immunological causes of damage to vessels > GD

A

Injury to endothelium of vessels

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14
Q

Ischaemic mechanisms of tubular damage

A

Hypotension, damage to vessels within kidney, glomerular damage > reduced blood supply

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15
Q

Toxic mechanisms of tubular damage

A

Direct toxins, hypersensitivity reactions (to drugs), deposition of crystals in tubules (gout), deposition of abnormal proteins in tubules

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16
Q

Mechanisms of vascular damage

A

Hypertension, diabetes, atheroma, vasculitis, thrombotic microangiopathy (rare)

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17
Q

Vasculitis

A

Obliteration of lumen by inflammation, inflammation of larger arterioles > hypoxia, adults and children affected e.g. Wegener’s granulomatosis

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18
Q

Thrombotic microangiopathy

A

Thrombi in capillaries and small arterioles, damage endothelium (bacterial toxins, drugs, abnormal clotting) e.g. haemolytic uraemic syndrome

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19
Q

Glomerular diseases

A 
Membranous nephropathy (idiopathic)
FSGS (idiopathic)
Mesangiocapillary glomerulonephritis (idiopathic)
Minimal change disease
Post-infective glomerulonephritis
Anti-GBM disease
IgA nephropathy
Henoch-Schonlein purpura
Lupus nephritis (in SLE)
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20
Q

Cause of nephrotic syndrome

A

Damage to glomerulus

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21
Q

Symptoms of nephrotic syndrome

A

Oedema, proteinuria (>3g in 24hr), hypoalbuminaemia

+/- hypertension, hyperlipidaemia

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22
Q

Complications of nephrotic syndrome

A

Infection, thrombosis

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23
Q

Causes of nephrotic syndrome in Adults

A

Membranous nephropathy, focal segmental glomerulosclerosis, minimal change disease, diabetes, lupus nephritis, amyloid

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24
Q

Membrane nephropathy

A

Idiopathic, adults 30-60, M>F, 20-30% progress to end stage renal failure

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25
Q

FSGS

A

Idiopathic, genetic, heroin use, HIV, M>F

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26
Q

Minimal change disease

A

More common in children, biopsy is normal on light microscopy M=F

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27
Q

Causes of nephrotic syndrome in children

A

Minimal change disease (most common), FSGS

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28
Q

Acute nephritis symptoms

A

Oedema, haematuria, proteinuria, hypertension, acute renal failure

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29
Q

Causes of acute nephritis in adults

A

Post-infective glomerulonephritis, IgA nephropathy, vasculitis, lupus

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30
Q

Post-infective glomerulonephritis

A

Occurs few weeks after streptococcal throat infection, most recover completely

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31
Q

IgA nephropathy

A

Most common, teenagers and young adults with haematuria, 20-50% progress to renal failure over 20 years

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32
Q

Vasculitis symptoms

A

Fever, generally unwell, rash, myalgia, arthralgia (fever and weight loss due to inflammation)

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33
Q

Lupus

A

AI disease, typically young women

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34
Q

Causes of acute nephritis in children

A

Post-infective glomerulonephritis (most common), IgA nephropathy, Henoch-Schonlein purport, HUS

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35
Q

Henoch-Schonlein purpura

A

Specific type of IgA nephropathy, M>F, young boys/teenagers with arthralgia, ab pain, rash, haematuria, acute renal failure, most recover completely

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36
Q

Haemolytic-Uraemia syndrome

A

Typically children with E.Coli 0157 enteritis, acute nephritis, haemolysis, thrombocytopenia, children can be v.ill

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37
Q

Diagnosis of acute renal failure

A

Anuria/oliguria and raised creatinine and urea

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38
Q

Treatment of acute renal failure

A

Short term dialysis may be needed

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39
Q

Pre-renal causes of acute renal failure

A

Reduced blood flow to kidney - severe dehydration, hypotension (bleeding, septic shock, LV failure)

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40
Q

Post-renal causes of ARF

A

Tumours of urinary tract, tumours in pelvis, bladder stones, prostatic enlargement

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41
Q

Causes of ARF in adults

A

Vasculitis and acute interstitial nephritis/tubulointerstitial nephritis

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42
Q

Acute interstitial nephritis/tubulointerstitial nephritis

A

Tubular damage with inflammation, caused by drug reactions

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43
Q

Causes of ARF in children

A

Henoch-Schonlein purpura, HUS (gastroenteritis), Acute interstitial nephritis

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44
Q

Complications of acute renal failure

A

Cardiac failure (fluid overload), arrhythmia (electrolyte imbalance K), GI bleeding, Jaundice, Infection (lung and urinary tract)

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45
Q

What is chronic renal failure?

A

Permanently reduced GFR - reduced number of nephrons

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46
Q

Stage 1 CRF

A

> 90

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47
Q

Stage 2 CRF

A

60-89

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48
Q

Stage 3 CRF

A

30-59

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49
Q

Stage 4

A

15-29

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50
Q

Stage 5

A
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51
Q

Common causes of CRF in adults

A

Diabetes (commonest), glomerulonephritis, reflux nephropathy

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52
Q

Reflux nephropathy

A

Chronic reflux of urine up the ureter > repeated infections and scarring of the kidney

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53
Q

Common causes of CRF in children

A

Developmental abnormalities, reflux nephropathy, glomerulonephritis

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54
Q

Effects of CRF

A

Reduced excretion of water and electrolytes (oedema/hypertension), reduced excretion of toxic metabolites, reduced production of erythropoietin (anaemia), renal bone disease

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55
Q

Myeloma

A

Tumour of plasma cells, produce large amounts of Ig, accumulate in kidney and block up glomeruli/tubules (irreversible)

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56
Q

Isolated haematuria causes

A

IgA nephropathy, thin basement membrane disease, Alport type hereditary nephropathy

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57
Q

Alport type hereditary nephropathy

A

Inherited abnormalities of collagen type IV > abnormal BM in glomerulus, eye and ear problems (deafness), autosomal/X-linked

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58
Q

Isolated proteinuria

A

Less than nephrotic range, without haematuria, renal failure/oedema

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59
Q

Isolated proteinuria benign causes

A

Postural, pyrexia, exercise

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60
Q

Isolated proteinuria causes in adults

A

FSGS, diabetes, lupus

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61
Q

Isolated proteinuria causes in children

A

Henoch-Schonlein purpura, FSGS

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62
Q

Pyelonephritis

A

Infection of kidney

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63
Q

Acute pyelonephritis

A

More common in women (ascending infection), instrumentation of urinary tract, diabetes, structural abnormalities

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64
Q

Complications of acute pyelonephritis

A

Abscess formation

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65
Q

Chronic pyelonephritis

A

Associated with obstruction of urinary tract and reflex of urine up ureter

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66
Q

Complications of chronic pyelonephritis

A

Scarring of kidney and chronic renal failure

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67
Q

Renal artery stenosis causes

A

Atheroma or material dysplasia

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68
Q

Renal artery stenosis complications

A

Ischaemia of affected kidney, activation of RAAS > hypertension, loss of renal tissue > reduced renal function

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69
Q

Hypertension

A

> Thickening of vessels walls and reduction in lumen > loss of renal tubules and renal function > activation RAAS > increases hypertension

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70
Q

Diabetes

A
  • Hyperglycaemia damages BM, becomes thicker, glomerulus > excess ECM > nodules
  • Damages small vessels > ischaemia and damage to renal tubules
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71
Q

Obstruction within lumen of urinary tract

A

Urinary calculi, strictures, neoplasia

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72
Q

Abnormalities of wall

A

Neoplasia, congenital anatomical abnormalities

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73
Q

External compression

A

Tumour outside urinary tract, inflammatory conditions (retroperitoneal fibrosis), pregnancy

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74
Q

Functional obstruction

A

Neurological conditions, severe reflux

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75
Q

Complications of obstruction

A

Infection (cystitis, ascending pyelonephritis), stone/calculi formation, kidney damage

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76
Q

Complete obstruction (acute) leads to

A
  • Reduction if GFR > acute renal failure

- Mild dilatation and mild cortical atrophy

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77
Q

Partial/intermitten obstruction (chronic) leads to

A
  • Continued GFR > dilatation of pelvis and calyces
  • Filtrate passes back into interstitial > compression of medulla > impaired concentrating ability

Both leads to cortical atrophy, fall in renal filtration and renal failure

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78
Q

Clinical features of acute bilateral obstruction

A

Pain, acute renal failure and anuria

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79
Q

Clinical features of chronic unilateral obstruction

A

Asymptomatic > cortical atrophy and reduced renal function

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80
Q

Clinical features of bilateral partial obstruction

A

Initially polyuric, progressive scarring and impairment

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81
Q

Epidemiology of renal calculi/urolithiasis

A

7-10% population, male, 20-30

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82
Q

Pathogenesis of renal calculi

A
  • Excess of substances precipitate out
  • Change in urine constituents
  • Poor urine output (supersaturation)
  • Decreased citrate levels
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83
Q

Calcium stones form because

A

Hypercalcaemia (bone disease, PTH excess, sarcoidosis), excessive absorption of intestinal Ca, inability to reabsorb tubular Ca, idiopathic, gout, hyperoxaluria (excess dietary intake)

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84
Q

What are calcium stones formed of?

A

Calcium oxalate/phosphate

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85
Q

Struvite stones form because

A

Urease producing bacterial infection (increase pH - ammonia), precipitation of magnesium, ammonium, phosphate salts

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86
Q

Characteristics of struvite stones

A

Large staghorn calculi

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87
Q

Urate stones form because

A

Hyperuricaemia (gout/patient with high cell turnover -leukaemia), idiopathic

88
Q

Cystine stones form because

A

Inability of kidneys to reabsorb amino acids (rare)

89
Q

Investigations for renal calculi

A

Non-contrast CT, USS, IV urography

90
Q

Complications of stones

A

Obstruction, haematuria, infection, squamous metaplasia (SCC)

91
Q

Vast majority or renal carcinomas are

A

Clear cell (papillary and chromophobe)

92
Q

Peak age for renal cell carcinoma

A

65-80

93
Q

Male/female more likely to get renal cell carcinoma?

A

Male > female (3:2)

94
Q

Risk factors for renal cell carcinoma

A

Tobacco (main), obesity, hypertension, oestrogen, acquired cystic kidney disease (chronic renal failure), asbestos exposure

95
Q

Von Hippel-Lindau syndrome

A

Most common cancer syndrome in RCC, VHL gene required for breakdown of hypoxia inducible factor-1 (HIF-1) oncogene, loss of gene function > cell growth and increased cell survival

96
Q

Where do tumours develop in Von Hippel-Lindau syndrome

A

Kidneys, blood vessels, pancreas

97
Q

Presentation of RCC

A

Haematuria, palpable abdominal mass, costovertebral pain, paraneoplastic syndromes

98
Q

Paraneoplastic syndrome

A

Clinical syndrome caused by tumours, not related to the tissue that tumour arose from, not related to invasion by tumour itself/metastases

99
Q

3 paraneoplastic syndromes associated with RCC

A
  • Cushing’s syndrome (ACTH)
  • Hypercalacaemia (PTH related peptide)
  • Polycthaemia (eryhtropoietin)
100
Q

Morphology of RCC - clear cell

A

Well defined, yellow tumours, haemorrhagic areas, > perinephric fat/into renal vein

101
Q

Morphology of RCC - papillary

A

More cystic, more likely to be multiple

102
Q

Microscopy of RCC - clear cell

A

Clear cells, dedicated vasculature, small bland nuclei

103
Q

Microscopy of RCC - papillary tumours

A

Cuboidal, foamy cells, surrounding fibrovascular cores, containing foamy macrophages/calcium

104
Q

Prognosis of RCC

A

5yr survival 45%, organ confined >70%, tumours in perinephric fat/renal vein 50%

105
Q

Urothelial cell carcinoma

A

95% bladder tumours, arising from specialised multilayered epithelium, may arise renal pelvis > urethra

106
Q

Urothelial cell carcinoma risk factors

A

Age, male, carcinogens (smoking, arylamines, cyclophosphamide, radiotherapy)

107
Q

Urothelial cell carcinoma presentation

A

HAEMATURIA, urinary frequency, pain on urinary, urinary tract obstruction

108
Q

Histological patterns of Urothelial cell carcinoma

A
  1. Papilloma-papillary carcinoma
  2. Flat non-invasive carcinoma
  3. Invasive papillary carcinoma
  4. Flat invasive carcinoma
109
Q

Urothelial cell carcinoma prognosis

A

Recurrences are common, low grade 98% still alive at 5 years, stage muscle invasions 60%

110
Q

How many people develop acute renal failure in England?

A

26,000/year

111
Q

Acute renal failure presentation

A

Rapid rise in creatinine and urea, generally unwell

112
Q

Nephrotic syndrome presentation

A

Oedema, protein uria and hypoalbuminaemia, proteinuria >3g/24 hr (albumin)

113
Q

Acute nephritis (nephritic syndrome)

A

Oedema, proteinuria, haematuria, renal failure

114
Q

Chronic renal failure

A

Slow declining renal function

115
Q

What part of kidney allows filtration?

A

Foot processes, endothelial cells and basement membrane in podocytes in glomerulus i

116
Q

Blood flow in kidney

A

Renal artery > afferent arterioles > glomerulus > efferent arteriole > proximal convoluted tubule (PCT) > loop of hence > distal convoluted tubule > collecting duct/renal vein

117
Q

Immunological causes of damage to BM

A
  • Circulating immune complexes deposit in glomerulus
  • Circulating antigens deposit in glomerulus
  • Antibodies to BM/other components of glomerulus
118
Q

Immunological causes of damage to BM damage the glomeruli via

A

Complement activation, neutrophil activation, reactive oxygen species, clotting factors

119
Q

Non-Immunological causes of damage to BM > GD

A
  • Hyperglycaemia
  • Inherited disease (abnormal podocytes)
  • Deposition of abnormal proteins (amyloid)
120
Q

Non-Immunological causes of damage to vessels > GD

A

Injury to endothelium of vessels

121
Q

Ischaemic mechanisms of tubular damage

A

Hypotension, damage to vessels within kidney, glomerular damage > reduced blood supply

122
Q

Toxic mechanisms of tubular damage

A

Direct toxins, hypersensitivity reactions (to drugs), deposition of crystals in tubules (gout), deposition of abnormal proteins in tubules

123
Q

Mechanisms of vascular damage

A

Hypertension, diabetes, atheroma, vasculitis, thrombotic microangiopathy (rare)

124
Q

Vasculitis

A

Obliteration of lumen by inflammation, inflammation of larger arterioles > hypoxia, adults and children affected e.g. Wegener’s granulomatosis

125
Q

Thrombotic microangiopathy

A

Thrombi in capillaries and small arterioles, damage endothelium (bacterial toxins, drugs, abnormal clotting) e.g. haemolytic uraemic syndrome

126
Q

Glomerular diseases

A 
Membranous nephropathy (idiopathic)
FSGS (idiopathic)
Mesangiocapillary glomerulonephritis (idiopathic)
Minimal change disease
Post-infective glomerulonephritis
Anti-GBM disease
IgA nephropathy
Henoch-Schonlein purpura
Lupus nephritis (in SLE)
127
Q

Cause of nephrotic syndrome

A

Damage to glomerulus

128
Q

Symptoms of nephrotic syndrome

A

Oedema, proteinuria (>3g in 24hr), hypoalbuminaemia

+/- hypertension, hyperlipidaemia

129
Q

Complications of nephrotic syndrome

A

Infection, thrombosis

130
Q

Causes of nephrotic syndrome in Adults

A

Membranous nephropathy, focal segmental glomerulosclerosis, minimal change disease, diabetes, lupus nephritis, amyloid

131
Q

Membrane nephropathy

A

Idiopathic, adults 30-60, M>F, 20-30% progress to end stage renal failure

132
Q

FSGS

A

Idiopathic, genetic, heroin use, HIV, M>F

133
Q

Minimal change disease

A

More common in children, biopsy is normal on light microscopy M=F

134
Q

Causes of nephrotic syndrome in children

A

Minimal change disease (most common), FSGS

135
Q

Acute nephritis symptoms

A

Oedema, haematuria, proteinuria, hypertension, acute renal failure

136
Q

Causes of acute nephritis in adults

A

Post-infective glomerulonephritis, IgA nephropathy, vasculitis, lupus

137
Q

Post-infective glomerulonephritis

A

Occurs few weeks after streptococcal throat infection, most recover completely

138
Q

IgA nephropathy

A

Most common, teenagers and young adults with haematuria, 20-50% progress to renal failure over 20 years

139
Q

Vasculitis symptoms

A

Fever, generally unwell, rash, myalgia, arthralgia (fever and weight loss due to inflammation)

140
Q

Lupus

A

AI disease, typically young women

141
Q

Causes of acute nephritis in children

A

Post-infective glomerulonephritis (most common), IgA nephropathy, Henoch-Schonlein purport, HUS

142
Q

Henoch-Schonlein purpura

A

Specific type of IgA nephropathy, M>F, young boys/teenagers with arthralgia, ab pain, rash, haematuria, acute renal failure, most recover completely

143
Q

Haemolytic-Uraemia syndrome

A

Typically children with E.Coli 0157 enteritis, acute nephritis, haemolysis, thrombocytopenia, children can be v.ill

144
Q

Diagnosis of acute renal failure

A

Anuria/oliguria and raised creatinine and urea

145
Q

Treatment of acute renal failure

A

Short term dialysis may be needed

146
Q

Pre-renal causes of acute renal failure

A

Reduced blood flow to kidney - severe dehydration, hypotension (bleeding, septic shock, LV failure)

147
Q

Post-renal causes of ARF

A

Tumours of urinary tract, tumours in pelvis, bladder stones, prostatic enlargement

148
Q

Causes of ARF in adults

A

Vasculitis and acute interstitial nephritis/tubulointerstitial nephritis

149
Q

Acute interstitial nephritis/tubulointerstitial nephritis

A

Tubular damage with inflammation, caused by drug reactions

150
Q

Causes of ARF in children

A

Henoch-Schonlein purpura, HUS (gastroenteritis), Acute interstitial nephritis

151
Q

Complications of acute renal failure

A

Cardiac failure (fluid overload), arrhythmia (electrolyte imbalance K), GI bleeding, Jaundice, Infection (lung and urinary tract)

152
Q

What is chronic renal failure?

A

Permanently reduced GFR - reduced number of nephrons

153
Q

Stage 1 CRF

A

> 90

154
Q

Stage 2 CRF

A

60-89

155
Q

Stage 3 CRF

A

30-59

156
Q

Stage 4

A

15-29

157
Q

Stage 5

A
158
Q

Common causes of CRF in adults

A

Diabetes (commonest), glomerulonephritis, reflux nephropathy

159
Q

Reflux nephropathy

A

Chronic reflux of urine up the ureter > repeated infections and scarring of the kidney

160
Q

Common causes of CRF in children

A

Developmental abnormalities, reflux nephropathy, glomerulonephritis

161
Q

Effects of CRF

A

Reduced excretion of water and electrolytes (oedema/hypertension), reduced excretion of toxic metabolites, reduced production of erythropoietin (anaemia), renal bone disease

162
Q

Myeloma

A

Tumour of plasma cells, produce large amounts of Ig, accumulate in kidney and block up glomeruli/tubules (irreversible)

163
Q

Isolated haematuria causes

A

IgA nephropathy, thin basement membrane disease, Alport type hereditary nephropathy

164
Q

Alport type hereditary nephropathy

A

Inherited abnormalities of collagen type IV > abnormal BM in glomerulus, eye and ear problems (deafness), autosomal/X-linked

165
Q

Isolated proteinuria

A

Less than nephrotic range, without haematuria, renal failure/oedema

166
Q

Isolated proteinuria benign causes

A

Postural, pyrexia, exercise

167
Q

Isolated proteinuria causes in adults

A

FSGS, diabetes, lupus

168
Q

Isolated proteinuria causes in children

A

Henoch-Schonlein purpura, FSGS

169
Q

Pyelonephritis

A

Infection of kidney

170
Q

Acute pyelonephritis

A

More common in women (ascending infection), instrumentation of urinary tract, diabetes, structural abnormalities

171
Q

Complications of acute pyelonephritis

A

Abscess formation

172
Q

Chronic pyelonephritis

A

Associated with obstruction of urinary tract and reflex of urine up ureter

173
Q

Complications of chronic pyelonephritis

A

Scarring of kidney and chronic renal failure

174
Q

Renal artery stenosis causes

A

Atheroma or material dysplasia

175
Q

Renal artery stenosis complications

A

Ischaemia of affected kidney, activation of RAAS > hypertension, loss of renal tissue > reduced renal function

176
Q

Hypertension

A

> Thickening of vessels walls and reduction in lumen > loss of renal tubules and renal function > activation RAAS > increases hypertension

177
Q

Diabetes

A
  • Hyperglycaemia damages BM, becomes thicker, glomerulus > excess ECM > nodules
  • Damages small vessels > ischaemia and damage to renal tubules
178
Q

Obstruction within lumen of urinary tract

A

Urinary calculi, strictures, neoplasia

179
Q

Abnormalities of wall

A

Neoplasia, congenital anatomical abnormalities

180
Q

External compression

A

Tumour outside urinary tract, inflammatory conditions (retroperitoneal fibrosis), pregnancy

181
Q

Functional obstruction

A

Neurological conditions, severe reflux

182
Q

Complications of obstruction

A

Infection (cystitis, ascending pyelonephritis), stone/calculi formation, kidney damage

183
Q

Complete obstruction (acute) leads to

A
  • Reduction if GFR > acute renal failure

- Mild dilatation and mild cortical atrophy

184
Q

Partial/intermitten obstruction (chronic) leads to

A
  • Continued GFR > dilatation of pelvis and calyces
  • Filtrate passes back into interstitial > compression of medulla > impaired concentrating ability

Both leads to cortical atrophy, fall in renal filtration and renal failure

185
Q

Clinical features of acute bilateral obstruction

A

Pain, acute renal failure and anuria

186
Q

Clinical features of chronic unilateral obstruction

A

Asymptomatic > cortical atrophy and reduced renal function

187
Q

Clinical features of bilateral partial obstruction

A

Initially polyuric, progressive scarring and impairment

188
Q

Epidemiology of renal calculi/urolithiasis

A

7-10% population, male, 20-30

189
Q

Pathogenesis of renal calculi

A
  • Excess of substances precipitate out
  • Change in urine constituents
  • Poor urine output (supersaturation)
  • Decreased citrate levels
190
Q

Calcium stones form because

A

Hypercalcaemia (bone disease, PTH excess, sarcoidosis), excessive absorption of intestinal Ca, inability to reabsorb tubular Ca, idiopathic, gout, hyperoxaluria (excess dietary intake)

191
Q

What are calcium stones formed of?

A

Calcium oxalate/phosphate

192
Q

Struvite stones form because

A

Urease producing bacterial infection (increase pH - ammonia), precipitation of magnesium, ammonium, phosphate salts

193
Q

Characteristics of struvite stones

A

Large staghorn calculi

194
Q

Urate stones form because

A

Hyperuricaemia (gout/patient with high cell turnover -leukaemia), idiopathic

195
Q

Cystine stones form because

A

Inability of kidneys to reabsorb amino acids (rare)

196
Q

Investigations for renal calculi

A

Non-contrast CT, USS, IV urography

197
Q

Complications of stones

A

Obstruction, haematuria, infection, squamous metaplasia (SCC)

198
Q

Vast majority or renal carcinomas are

A

Clear cell (papillary and chromophobe)

199
Q

Peak age for renal cell carcinoma

A

65-80

200
Q

Male/female more likely to get renal cell carcinoma?

A

Male > female (3:2)

201
Q

Risk factors for renal cell carcinoma

A

Tobacco (main), obesity, hypertension, oestrogen, acquired cystic kidney disease (chronic renal failure), asbestos exposure

202
Q

Von Hippel-Lindau syndrome

A

Most common cancer syndrome in RCC, VHL gene required for breakdown of hypoxia inducible factor-1 (HIF-1) oncogene, loss of gene function > cell growth and increased cell survival

203
Q

Where do tumours develop in Von Hippel-Lindau syndrome

A

Kidneys, blood vessels, pancreas

204
Q

Presentation of RCC

A

Haematuria, palpable abdominal mass, costovertebral pain, paraneoplastic syndromes

205
Q

Paraneoplastic syndrome

A

Clinical syndrome caused by tumours, not related to the tissue that tumour arose from, not related to invasion by tumour itself/metastases

206
Q

3 paraneoplastic syndromes associated with RCC

A
  • Cushing’s syndrome (ACTH)
  • Hypercalacaemia (PTH related peptide)
  • Polycthaemia (eryhtropoietin)
207
Q

Morphology of RCC - clear cell

A

Well defined, yellow tumours, haemorrhagic areas, > perinephric fat/into renal vein

208
Q

Morphology of RCC - papillary

A

More cystic, more likely to be multiple

209
Q

Microscopy of RCC - clear cell

A

Clear cells, dedicated vasculature, small bland nuclei

210
Q

Microscopy of RCC - papillary tumours

A

Cuboidal, foamy cells, surrounding fibrovascular cores, containing foamy macrophages/calcium

211
Q

Prognosis of RCC

A

5yr survival 45%, organ confined >70%, tumours in perinephric fat/renal vein 50%

212
Q

Urothelial cell carcinoma

A

95% bladder tumours, arising from specialised multilayered epithelium, may arise renal pelvis > urethra

213
Q

Urothelial cell carcinoma risk factors

A

Age, male, carcinogens (smoking, arylamines, cyclophosphamide, radiotherapy)

214
Q

Urothelial cell carcinoma presentation

A

HAEMATURIA, urinary frequency, pain on urinary, urinary tract obstruction

215
Q

Histological patterns of Urothelial cell carcinoma

A
  1. Papilloma-papillary carcinoma
  2. Flat non-invasive carcinoma
  3. Invasive papillary carcinoma
  4. Flat invasive carcinoma
216
Q

Urothelial cell carcinoma prognosis

A

Recurrences are common, low grade 98% still alive at 5 years, stage muscle invasions 60%

Clinical Pathology (60 decks)

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