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

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

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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
FSGS
Idiopathic, genetic, heroin use, HIV, M>F
26
Minimal change disease
More common in children, biopsy is normal on light microscopy M=F
27
Causes of nephrotic syndrome in children
Minimal change disease (most common), FSGS
28
Acute nephritis symptoms
Oedema, haematuria, proteinuria, hypertension, acute renal failure
29
Causes of acute nephritis in adults
Post-infective glomerulonephritis, IgA nephropathy, vasculitis, lupus
30
Post-infective glomerulonephritis
Occurs few weeks after streptococcal throat infection, most recover completely
31
IgA nephropathy
Most common, teenagers and young adults with haematuria, 20-50% progress to renal failure over 20 years
32
Vasculitis symptoms
Fever, generally unwell, rash, myalgia, arthralgia (fever and weight loss due to inflammation)
33
Lupus
AI disease, typically young women
34
Causes of acute nephritis in children
Post-infective glomerulonephritis (most common), IgA nephropathy, Henoch-Schonlein purport, HUS
35
Henoch-Schonlein purpura
Specific type of IgA nephropathy, M>F, young boys/teenagers with arthralgia, ab pain, rash, haematuria, acute renal failure, most recover completely
36
Haemolytic-Uraemia syndrome
Typically children with E.Coli 0157 enteritis, acute nephritis, haemolysis, thrombocytopenia, children can be v.ill
37
Diagnosis of acute renal failure
Anuria/oliguria and raised creatinine and urea
38
Treatment of acute renal failure
Short term dialysis may be needed
39
Pre-renal causes of acute renal failure
Reduced blood flow to kidney - severe dehydration, hypotension (bleeding, septic shock, LV failure)
40
Post-renal causes of ARF
Tumours of urinary tract, tumours in pelvis, bladder stones, prostatic enlargement
41
Causes of ARF in adults
Vasculitis and acute interstitial nephritis/tubulointerstitial nephritis
42
Acute interstitial nephritis/tubulointerstitial nephritis
Tubular damage with inflammation, caused by drug reactions
43
Causes of ARF in children
Henoch-Schonlein purpura, HUS (gastroenteritis), Acute interstitial nephritis
44
Complications of acute renal failure
Cardiac failure (fluid overload), arrhythmia (electrolyte imbalance K), GI bleeding, Jaundice, Infection (lung and urinary tract)
45
What is chronic renal failure?
Permanently reduced GFR - reduced number of nephrons
46
Stage 1 CRF
>90
47
Stage 2 CRF
60-89
48
Stage 3 CRF
30-59
49
Stage 4
15-29
50
Stage 5
51
Common causes of CRF in adults
Diabetes (commonest), glomerulonephritis, reflux nephropathy
52
Reflux nephropathy
Chronic reflux of urine up the ureter > repeated infections and scarring of the kidney
53
Common causes of CRF in children
Developmental abnormalities, reflux nephropathy, glomerulonephritis
54
Effects of CRF
Reduced excretion of water and electrolytes (oedema/hypertension), reduced excretion of toxic metabolites, reduced production of erythropoietin (anaemia), renal bone disease
55
Myeloma
Tumour of plasma cells, produce large amounts of Ig, accumulate in kidney and block up glomeruli/tubules (irreversible)
56
Isolated haematuria causes
IgA nephropathy, thin basement membrane disease, Alport type hereditary nephropathy
57
Alport type hereditary nephropathy
Inherited abnormalities of collagen type IV > abnormal BM in glomerulus, eye and ear problems (deafness), autosomal/X-linked
58
Isolated proteinuria
Less than nephrotic range, without haematuria, renal failure/oedema
59
Isolated proteinuria benign causes
Postural, pyrexia, exercise
60
Isolated proteinuria causes in adults
FSGS, diabetes, lupus
61
Isolated proteinuria causes in children
Henoch-Schonlein purpura, FSGS
62
Pyelonephritis
Infection of kidney
63
Acute pyelonephritis
More common in women (ascending infection), instrumentation of urinary tract, diabetes, structural abnormalities
64
Complications of acute pyelonephritis
Abscess formation
65
Chronic pyelonephritis
Associated with obstruction of urinary tract and reflex of urine up ureter
66
Complications of chronic pyelonephritis
Scarring of kidney and chronic renal failure
67
Renal artery stenosis causes
Atheroma or material dysplasia
68
Renal artery stenosis complications
Ischaemia of affected kidney, activation of RAAS > hypertension, loss of renal tissue > reduced renal function
69
Hypertension
> Thickening of vessels walls and reduction in lumen > loss of renal tubules and renal function > activation RAAS > increases hypertension
70
Diabetes
- Hyperglycaemia damages BM, becomes thicker, glomerulus > excess ECM > nodules - Damages small vessels > ischaemia and damage to renal tubules
71
Obstruction within lumen of urinary tract
Urinary calculi, strictures, neoplasia
72
Abnormalities of wall
Neoplasia, congenital anatomical abnormalities
73
External compression
Tumour outside urinary tract, inflammatory conditions (retroperitoneal fibrosis), pregnancy
74
Functional obstruction
Neurological conditions, severe reflux
75
Complications of obstruction
Infection (cystitis, ascending pyelonephritis), stone/calculi formation, kidney damage
76
Complete obstruction (acute) leads to
- Reduction if GFR > acute renal failure | - Mild dilatation and mild cortical atrophy
77
Partial/intermitten obstruction (chronic) leads to
- 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
78
Clinical features of acute bilateral obstruction
Pain, acute renal failure and anuria
79
Clinical features of chronic unilateral obstruction
Asymptomatic > cortical atrophy and reduced renal function
80
Clinical features of bilateral partial obstruction
Initially polyuric, progressive scarring and impairment
81
Epidemiology of renal calculi/urolithiasis
7-10% population, male, 20-30
82
Pathogenesis of renal calculi
- Excess of substances precipitate out - Change in urine constituents - Poor urine output (supersaturation) - Decreased citrate levels
83
Calcium stones form because
Hypercalcaemia (bone disease, PTH excess, sarcoidosis), excessive absorption of intestinal Ca, inability to reabsorb tubular Ca, idiopathic, gout, hyperoxaluria (excess dietary intake)
84
What are calcium stones formed of?
Calcium oxalate/phosphate
85
Struvite stones form because
Urease producing bacterial infection (increase pH - ammonia), precipitation of magnesium, ammonium, phosphate salts
86
Characteristics of struvite stones
Large staghorn calculi
87
Urate stones form because
Hyperuricaemia (gout/patient with high cell turnover -leukaemia), idiopathic
88
Cystine stones form because
Inability of kidneys to reabsorb amino acids (rare)
89
Investigations for renal calculi
Non-contrast CT, USS, IV urography
90
Complications of stones
Obstruction, haematuria, infection, squamous metaplasia (SCC)
91
Vast majority or renal carcinomas are
Clear cell (papillary and chromophobe)
92
Peak age for renal cell carcinoma
65-80
93
Male/female more likely to get renal cell carcinoma?
Male > female (3:2)
94
Risk factors for renal cell carcinoma
Tobacco (main), obesity, hypertension, oestrogen, acquired cystic kidney disease (chronic renal failure), asbestos exposure
95
Von Hippel-Lindau syndrome
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
Where do tumours develop in Von Hippel-Lindau syndrome
Kidneys, blood vessels, pancreas
97
Presentation of RCC
Haematuria, palpable abdominal mass, costovertebral pain, paraneoplastic syndromes
98
Paraneoplastic syndrome
Clinical syndrome caused by tumours, not related to the tissue that tumour arose from, not related to invasion by tumour itself/metastases
99
3 paraneoplastic syndromes associated with RCC
- Cushing's syndrome (ACTH) - Hypercalacaemia (PTH related peptide) - Polycthaemia (eryhtropoietin)
100
Morphology of RCC - clear cell
Well defined, yellow tumours, haemorrhagic areas, > perinephric fat/into renal vein
101
Morphology of RCC - papillary
More cystic, more likely to be multiple
102
Microscopy of RCC - clear cell
Clear cells, dedicated vasculature, small bland nuclei
103
Microscopy of RCC - papillary tumours
Cuboidal, foamy cells, surrounding fibrovascular cores, containing foamy macrophages/calcium
104
Prognosis of RCC
5yr survival 45%, organ confined >70%, tumours in perinephric fat/renal vein 50%
105
Urothelial cell carcinoma
95% bladder tumours, arising from specialised multilayered epithelium, may arise renal pelvis > urethra
106
Urothelial cell carcinoma risk factors
Age, male, carcinogens (smoking, arylamines, cyclophosphamide, radiotherapy)
107
Urothelial cell carcinoma presentation
HAEMATURIA, urinary frequency, pain on urinary, urinary tract obstruction
108
Histological patterns of Urothelial cell carcinoma
1. Papilloma-papillary carcinoma 2. Flat non-invasive carcinoma 3. Invasive papillary carcinoma 4. Flat invasive carcinoma
109
Urothelial cell carcinoma prognosis
Recurrences are common, low grade 98% still alive at 5 years, stage muscle invasions 60%
110
How many people develop acute renal failure in England?
26,000/year
111
Acute renal failure presentation
Rapid rise in creatinine and urea, generally unwell
112
Nephrotic syndrome presentation
Oedema, protein uria and hypoalbuminaemia, proteinuria >3g/24 hr (albumin)
113
Acute nephritis (nephritic syndrome)
Oedema, proteinuria, haematuria, renal failure
114
Chronic renal failure
Slow declining renal function
115
What part of kidney allows filtration?
Foot processes, endothelial cells and basement membrane in podocytes in glomerulus i
116
Blood flow in kidney
Renal artery > afferent arterioles > glomerulus > efferent arteriole > proximal convoluted tubule (PCT) > loop of hence > distal convoluted tubule > collecting duct/renal vein
117
Immunological causes of damage to BM
- Circulating immune complexes deposit in glomerulus - Circulating antigens deposit in glomerulus - Antibodies to BM/other components of glomerulus
118
Immunological causes of damage to BM damage the glomeruli via
Complement activation, neutrophil activation, reactive oxygen species, clotting factors
119
Non-Immunological causes of damage to BM > GD
- Hyperglycaemia - Inherited disease (abnormal podocytes) - Deposition of abnormal proteins (amyloid)
120
Non-Immunological causes of damage to vessels > GD
Injury to endothelium of vessels
121
Ischaemic mechanisms of tubular damage
Hypotension, damage to vessels within kidney, glomerular damage > reduced blood supply
122
Toxic mechanisms of tubular damage
Direct toxins, hypersensitivity reactions (to drugs), deposition of crystals in tubules (gout), deposition of abnormal proteins in tubules
123
Mechanisms of vascular damage
Hypertension, diabetes, atheroma, vasculitis, thrombotic microangiopathy (rare)
124
Vasculitis
Obliteration of lumen by inflammation, inflammation of larger arterioles > hypoxia, adults and children affected e.g. Wegener's granulomatosis
125
Thrombotic microangiopathy
Thrombi in capillaries and small arterioles, damage endothelium (bacterial toxins, drugs, abnormal clotting) e.g. haemolytic uraemic syndrome
126
Glomerular diseases
``` 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
Cause of nephrotic syndrome
Damage to glomerulus
128
Symptoms of nephrotic syndrome
Oedema, proteinuria (>3g in 24hr), hypoalbuminaemia | +/- hypertension, hyperlipidaemia
129
Complications of nephrotic syndrome
Infection, thrombosis
130
Causes of nephrotic syndrome in Adults
Membranous nephropathy, focal segmental glomerulosclerosis, minimal change disease, diabetes, lupus nephritis, amyloid
131
Membrane nephropathy
Idiopathic, adults 30-60, M>F, 20-30% progress to end stage renal failure
132
FSGS
Idiopathic, genetic, heroin use, HIV, M>F
133
Minimal change disease
More common in children, biopsy is normal on light microscopy M=F
134
Causes of nephrotic syndrome in children
Minimal change disease (most common), FSGS
135
Acute nephritis symptoms
Oedema, haematuria, proteinuria, hypertension, acute renal failure
136
Causes of acute nephritis in adults
Post-infective glomerulonephritis, IgA nephropathy, vasculitis, lupus
137
Post-infective glomerulonephritis
Occurs few weeks after streptococcal throat infection, most recover completely
138
IgA nephropathy
Most common, teenagers and young adults with haematuria, 20-50% progress to renal failure over 20 years
139
Vasculitis symptoms
Fever, generally unwell, rash, myalgia, arthralgia (fever and weight loss due to inflammation)
140
Lupus
AI disease, typically young women
141
Causes of acute nephritis in children
Post-infective glomerulonephritis (most common), IgA nephropathy, Henoch-Schonlein purport, HUS
142
Henoch-Schonlein purpura
Specific type of IgA nephropathy, M>F, young boys/teenagers with arthralgia, ab pain, rash, haematuria, acute renal failure, most recover completely
143
Haemolytic-Uraemia syndrome
Typically children with E.Coli 0157 enteritis, acute nephritis, haemolysis, thrombocytopenia, children can be v.ill
144
Diagnosis of acute renal failure
Anuria/oliguria and raised creatinine and urea
145
Treatment of acute renal failure
Short term dialysis may be needed
146
Pre-renal causes of acute renal failure
Reduced blood flow to kidney - severe dehydration, hypotension (bleeding, septic shock, LV failure)
147
Post-renal causes of ARF
Tumours of urinary tract, tumours in pelvis, bladder stones, prostatic enlargement
148
Causes of ARF in adults
Vasculitis and acute interstitial nephritis/tubulointerstitial nephritis
149
Acute interstitial nephritis/tubulointerstitial nephritis
Tubular damage with inflammation, caused by drug reactions
150
Causes of ARF in children
Henoch-Schonlein purpura, HUS (gastroenteritis), Acute interstitial nephritis
151
Complications of acute renal failure
Cardiac failure (fluid overload), arrhythmia (electrolyte imbalance K), GI bleeding, Jaundice, Infection (lung and urinary tract)
152
What is chronic renal failure?
Permanently reduced GFR - reduced number of nephrons
153
Stage 1 CRF
>90
154
Stage 2 CRF
60-89
155
Stage 3 CRF
30-59
156
Stage 4
15-29
157
Stage 5
158
Common causes of CRF in adults
Diabetes (commonest), glomerulonephritis, reflux nephropathy
159
Reflux nephropathy
Chronic reflux of urine up the ureter > repeated infections and scarring of the kidney
160
Common causes of CRF in children
Developmental abnormalities, reflux nephropathy, glomerulonephritis
161
Effects of CRF
Reduced excretion of water and electrolytes (oedema/hypertension), reduced excretion of toxic metabolites, reduced production of erythropoietin (anaemia), renal bone disease
162
Myeloma
Tumour of plasma cells, produce large amounts of Ig, accumulate in kidney and block up glomeruli/tubules (irreversible)
163
Isolated haematuria causes
IgA nephropathy, thin basement membrane disease, Alport type hereditary nephropathy
164
Alport type hereditary nephropathy
Inherited abnormalities of collagen type IV > abnormal BM in glomerulus, eye and ear problems (deafness), autosomal/X-linked
165
Isolated proteinuria
Less than nephrotic range, without haematuria, renal failure/oedema
166
Isolated proteinuria benign causes
Postural, pyrexia, exercise
167
Isolated proteinuria causes in adults
FSGS, diabetes, lupus
168
Isolated proteinuria causes in children
Henoch-Schonlein purpura, FSGS
169
Pyelonephritis
Infection of kidney
170
Acute pyelonephritis
More common in women (ascending infection), instrumentation of urinary tract, diabetes, structural abnormalities
171
Complications of acute pyelonephritis
Abscess formation
172
Chronic pyelonephritis
Associated with obstruction of urinary tract and reflex of urine up ureter
173
Complications of chronic pyelonephritis
Scarring of kidney and chronic renal failure
174
Renal artery stenosis causes
Atheroma or material dysplasia
175
Renal artery stenosis complications
Ischaemia of affected kidney, activation of RAAS > hypertension, loss of renal tissue > reduced renal function
176
Hypertension
> Thickening of vessels walls and reduction in lumen > loss of renal tubules and renal function > activation RAAS > increases hypertension
177
Diabetes
- Hyperglycaemia damages BM, becomes thicker, glomerulus > excess ECM > nodules - Damages small vessels > ischaemia and damage to renal tubules
178
Obstruction within lumen of urinary tract
Urinary calculi, strictures, neoplasia
179
Abnormalities of wall
Neoplasia, congenital anatomical abnormalities
180
External compression
Tumour outside urinary tract, inflammatory conditions (retroperitoneal fibrosis), pregnancy
181
Functional obstruction
Neurological conditions, severe reflux
182
Complications of obstruction
Infection (cystitis, ascending pyelonephritis), stone/calculi formation, kidney damage
183
Complete obstruction (acute) leads to
- Reduction if GFR > acute renal failure | - Mild dilatation and mild cortical atrophy
184
Partial/intermitten obstruction (chronic) leads to
- 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
Clinical features of acute bilateral obstruction
Pain, acute renal failure and anuria
186
Clinical features of chronic unilateral obstruction
Asymptomatic > cortical atrophy and reduced renal function
187
Clinical features of bilateral partial obstruction
Initially polyuric, progressive scarring and impairment
188
Epidemiology of renal calculi/urolithiasis
7-10% population, male, 20-30
189
Pathogenesis of renal calculi
- Excess of substances precipitate out - Change in urine constituents - Poor urine output (supersaturation) - Decreased citrate levels
190
Calcium stones form because
Hypercalcaemia (bone disease, PTH excess, sarcoidosis), excessive absorption of intestinal Ca, inability to reabsorb tubular Ca, idiopathic, gout, hyperoxaluria (excess dietary intake)
191
What are calcium stones formed of?
Calcium oxalate/phosphate
192
Struvite stones form because
Urease producing bacterial infection (increase pH - ammonia), precipitation of magnesium, ammonium, phosphate salts
193
Characteristics of struvite stones
Large staghorn calculi
194
Urate stones form because
Hyperuricaemia (gout/patient with high cell turnover -leukaemia), idiopathic
195
Cystine stones form because
Inability of kidneys to reabsorb amino acids (rare)
196
Investigations for renal calculi
Non-contrast CT, USS, IV urography
197
Complications of stones
Obstruction, haematuria, infection, squamous metaplasia (SCC)
198
Vast majority or renal carcinomas are
Clear cell (papillary and chromophobe)
199
Peak age for renal cell carcinoma
65-80
200
Male/female more likely to get renal cell carcinoma?
Male > female (3:2)
201
Risk factors for renal cell carcinoma
Tobacco (main), obesity, hypertension, oestrogen, acquired cystic kidney disease (chronic renal failure), asbestos exposure
202
Von Hippel-Lindau syndrome
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
Where do tumours develop in Von Hippel-Lindau syndrome
Kidneys, blood vessels, pancreas
204
Presentation of RCC
Haematuria, palpable abdominal mass, costovertebral pain, paraneoplastic syndromes
205
Paraneoplastic syndrome
Clinical syndrome caused by tumours, not related to the tissue that tumour arose from, not related to invasion by tumour itself/metastases
206
3 paraneoplastic syndromes associated with RCC
- Cushing's syndrome (ACTH) - Hypercalacaemia (PTH related peptide) - Polycthaemia (eryhtropoietin)
207
Morphology of RCC - clear cell
Well defined, yellow tumours, haemorrhagic areas, > perinephric fat/into renal vein
208
Morphology of RCC - papillary
More cystic, more likely to be multiple
209
Microscopy of RCC - clear cell
Clear cells, dedicated vasculature, small bland nuclei
210
Microscopy of RCC - papillary tumours
Cuboidal, foamy cells, surrounding fibrovascular cores, containing foamy macrophages/calcium
211
Prognosis of RCC
5yr survival 45%, organ confined >70%, tumours in perinephric fat/renal vein 50%
212
Urothelial cell carcinoma
95% bladder tumours, arising from specialised multilayered epithelium, may arise renal pelvis > urethra
213
Urothelial cell carcinoma risk factors
Age, male, carcinogens (smoking, arylamines, cyclophosphamide, radiotherapy)
214
Urothelial cell carcinoma presentation
HAEMATURIA, urinary frequency, pain on urinary, urinary tract obstruction
215
Histological patterns of Urothelial cell carcinoma
1. Papilloma-papillary carcinoma 2. Flat non-invasive carcinoma 3. Invasive papillary carcinoma 4. Flat invasive carcinoma
216
Urothelial cell carcinoma prognosis
Recurrences are common, low grade 98% still alive at 5 years, stage muscle invasions 60%

Clinical Pathology (60 decks)

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