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ESA 3- Urinary System > Pathology Of The Urinary System > Flashcards

Pathology Of The Urinary System Flashcards

1
Q

What does the site of glomerular injury determine?

A

A patients clinical presentation

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2
Q

What are the types of glomerular injury?

A

Primary

Secondary

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3
Q

What is a primary glomerular injury?

A

Just affecting the glomerulus

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4
Q

What is a secondary glomerular injury?

A

Systemic injury that has in turn damaged the glomerulus

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5
Q

What are the sites of glomerular injury?

A

Subepithelial
Within glomerular basement membrane
Subendothelial
Mesangial/paramesangial

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6
Q

Where is considered to be sub-epithelial when considering glomerular injury?

A

Anything that affects podocytes/podocyte side of glomerular basement membrane

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7
Q

Where is considered to be subendothelial when considering glomerular injury?

A

Inside the basement membrane

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8
Q

Where is mesangial/paramesagnial tissue found?

A

Supporting the capillary loop

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9
Q

What are the potential pathologies of the glomerulus?

A

Fluid can block

Fluid can leak

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10
Q

What can cause the glomerular filter to block?

A

Renal failure

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11
Q

What are the main symptoms of renal failure causing filter blockage?

A

Hypertensive

Haematuria

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12
Q

What conditions are caused by the leaking of the glomerular filter?

A

Proteinuria

Haemoturia

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13
Q

What protein is found in the urine in proteinuria resulting from the leakage of the glomerular filter?

A

Albumin

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14
Q

Do proteinuria and haemoturia occur separately or together as a result of glomerular filter leakage?

A

Can be either, depending on damage

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15
Q

What is proteinuria?

A

The presence of excess serum proteins in urine

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16
Q

What is the diagnostic criteria of proteinuria?

A

<3.5g filtered every 24 hours

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17
Q

What is presence of proteins in urine due to?

A

Podocyte damage

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18
Q

How does podocyte damage lead to proteinuria?

A

The widening of the fenestration slits causing protein to be leaked when it would normally not be filtered.

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19
Q

What can proteinuria be said to be?

A

A ‘less severe’ nephrotic syndrome

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20
Q

What is nephrotic syndrome?

A

When over 3.5g of proteins is filtered in 24 hours

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21
Q

What is the result of nephrotic syndrome?

A

Generalised oedema

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22
Q

Why does nephrotic syndrome cause generalised oedema?

A

As a lot of protein is being filtered, oncotic pressure is reduced

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23
Q

What is the most likely site of injury in nephrotic syndrome?

A

Podocyte/subepithelial injury

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24
Q

What are the common primary causes of proteinuria/nephrotic syndrome?

A

Minimal change glomerulonephritis
Focal segmental glomerulosclerosis
Membranous glomerulonephritis

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25
Q

What are the common secondary causes of proteinuria/nephrotic syndrome?

A

Diabetes mellitus

Amyloidosis

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26
Q

Why can diabetes mellitus lead to proteinuria/nephrotic syndrome?

A

Microvascular complications affect kidneys

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27
Q

When does minimal change glomerulonephritis present?

A

In childhood/adolesence

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28
Q

What happens to the incidence of minimal change glomerulonephritis (MCG) with age?

A

It reduces with increasing age

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29
Q

What does MCG cause?

A

Heavy proteinuria or nephrotic syndrome

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30
Q

What is the treatment for MCG?

A

Usually responds well to steriods

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31
Q

What is the problem with MCG treatment?

A

May reoccur once weaned off treatment

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32
Q

Does MCG progress to renal failure?

A

Not usually- normally purely protein loss from kidney

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33
Q

Why is MCG named as such?

A

Because when looking at the glomeruli under a light microscope, they appear to be completely normal

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34
Q

How can the changes in MCG be seen?

A

Under an electron microscope

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35
Q

What can be seen under a electron microscope with MCG?

A

Damage to podocytes is evident- widening fenestration slits, which allow protein to lead through

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36
Q

What is the pathogenesis of MCG?

A

Unknown

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37
Q

Why is FSGS considered to be focal?

A

It involves less than 50% of glomeruli on light microscopy

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38
Q

Why is FSGS considered to be segmental?

A

It involves part of the glomerular tuft

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39
Q

What is the fibrosis aspect of FSGS?

A

Scarring

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40
Q

When does FSGS present?

A

In adulthood

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41
Q

When does FSGS present?

A

Adulthood

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42
Q

How does the FSGS response to steroids differ from that of MCG?

A

It is less responsive to steroids

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43
Q

Why is protein present in the urine with FSGS?

A

Podocytes undergo damage and subsequent scarring, so protein is lost in urine

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44
Q

What is responsible for podocyte damage in FSGS?

A

A circulating factor

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45
Q

What evidence is there for FSGS being caused by a circulating factor?

A

In transplanted kidneys, the same damage occurs

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46
Q

Can minimal change FSGS progress to renal failure?

A

Yes

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47
Q

What is the pathogenesis of FSGS?

A

Unknown

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48
Q

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

A

Membranous glomerulonephritis (MG)

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49
Q

What does MG result from?

A

Immune complex deposits in the sub-epithelial space

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50
Q

What is the basis of MG?

A

Probably an autoimmune basis, however also evidence that it may be secondary

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51
Q

What is the autoimmune basis of MG likely to be?

A

Autoantibody to podocytes

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52
Q

What is the evidence that MG may be a secondary disease?

A

It is associated with other conditions

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53
Q

What other conditions that MG is associated with?

A

Particular malignancies, e.g. Lymphoma

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54
Q

What rule does MG follow?

A

The rule of thirds

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55
Q

What is the rule of thirds with MG?

A

1/3 just get better
1/3 ‘grumble along’ with proteinuria but are fine
1/3 progress to renal failure

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56
Q

What is shown on the micrograph of MG?

A

Capillary loop far too thick

Basement membrane looks specky

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57
Q

What is nephritic syndrome?

A

Renal failure due to blocking of the filter

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58
Q

What is the most common glomerular nephropathy’?

A

IgA nephropathy

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59
Q

When can IgA nephopathy occur?

A

At any age

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60
Q

What is IgA nephropathy characterised by?

A

Deposition of IgA antibody in the glomerulus

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61
Q

How does IgA nephropathy classically present?

A

With visible/invisible haematuria

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62
Q

What has IgA nephropathy been shown to have a relationship with?

A

Mucosal infections

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63
Q

Why does IgA nephropathy have a relationship with mucosal infections?

A

IgA protects mucosal surfaces

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64
Q

In what respects is IgA nephropathy variable?

A

In its histological features and course

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65
Q

How does the course of IgA nephropathy vary?

A

Some, but not all, patients have proteinuria, and a significant proportion of patients, but not all, progress to renal failure

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66
Q

Why does variation in the course of IgA nephropathy occur?

A

Unknown

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67
Q

What histological features may occur in IgA nephropathy?

A

Mesangial proliferation

Scarring

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68
Q

What is the treatment for IgA nephropathy?

A

No effective treatment

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69
Q

What are the hereditary nephropathies?

A

Thin GBM nephropathy

Alport syndrome

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70
Q

What is the problem with distinguishing between the hereditary nephropathies?

A

The two are not completely distinct, with a grey area between them

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71
Q

What are the features of thin GBM nephropathy?

A 
Nephropathy
Benign familial nephropathy
Isolated haemoturia 
Thin GBM
Benign course
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72
Q

What are the features of Alport syndrome?

A 
X linked
Abnormal collagen IV
Associated with deafness
Abnormal appearing GBM
Progresses to renal failure
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73
Q

What renal symptoms can diabetes mellitus lead to?

A

Progressive proteinuria
Progressive renal failure
Mesangial scleorosis

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74
Q

What kind of damage to the kidney occurs in diabetes mellitus?

A

Microvascular (damages glomerulus directly)

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75
Q

What does mesangial sclerosis in diabetes mellitus lead to?

A

Nodules

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76
Q

What happens to the basement membrane of the glomerulus in diabetes mellitus?

A

It thickens to 4-5x normal

77
Q

How common is Goodpasture syndrome?

A

Relatively uncommon

78
Q

Why is Goodpasture syndrome clinically important?

A

It is very rapidly progressing Glomerular Nephritis

79
Q

What is Goodpasture syndrome bought about by?

A

An autoantibody to collagen IV in basement membranes

80
Q

Where does Goodpasture syndrome affect?

A

Only the kidney

81
Q

Why does Goodpasture syndrome only affect the kidney?

82
Q

How is Goodpasture syndrome treated?

A

Immunosuppresion

Plasmophoresis

83
Q

What is the limitation of the treatment of Goodpasture syndrome?

A

It can only be treated if caught early

84
Q

What is Goodpastures syndrome characterised by?

A

IgG deposition, but no extracellular matrix deposit

85
Q

What is vasculitis?

A

Inflammation of the blood vessels

86
Q

Why does vasculitis affect the kidney?

A

Because its highly vascularised

87
Q

What happens in vasculitis?

A

Blood vessels are attacked directly in the glomerulus by anti-neutrophil cytoplasmic antibody (ANCA)

88
Q

Is vasculitis treatable?

A

Yes, if caught early

89
Q

What are the mechanisms responsible for the different expression of immune complex mediated disease?

A

Subepithelial deposits

Mesangial deposits

90
Q

Give an example of an immune complex mediated disease that leads to subepithelial deposits

A

Membranous glomerulonephritis

91
Q

What happens in the subepithelial deposits mechanism of immune complex mediated disease?

A

Antigen abnormally recognised on podocytes, circulating IgG binds to it, forming immune complexes in the glomerulus

92
Q

Are circulating immune complexes causing damage in subepithelial deposits?

93
Q

Give an example of an immune complex mediated disease that leads to mesangial deposits

A

IgA nephropathy

94
Q

What happens in the mesangial deposits mechanism of immune complex mediated disease?

A

Immune complexes can be deposited in the mesangium, as there is no podocytes or basement membrane to act as a barrier

95
Q

What is the most common cancer in men in the UK?

A

Prostate cancer

96
Q

Is prostate cancer the most common cause of death from cancer in men?

A

No, it is the second most common

97
Q

What happens to most men who are diagnosed with prostate cancer?

A

They are more likely to die with it than of it

98
Q

What are the risk factors of prostate cancer?

A

Age
Family
History
Race

99
Q

What is the relationship between prostate cancer and age?

A

There is a correlation with increasing age

100
Q

Who is prostate cancer uncommon in?

A

Men younger than 50

101
Q

What is the relationship between family history and prostate cancer?

A

4x increased risk

102
Q

What is considered to be a family history of prostate cancer when considering risk?

A

If one 1st degree relative is diagnosed with prostate cancer before age 60

103
Q

Why is family history only considered when a family member is diagnosed before age 60?

A

Any diagnosis after 60 was probably age related

104
Q

How does the incidence of prostate cancer differ between the races?

A

Incidence in asian < caucasian < afro-caribbean

105
Q

What is the usual clinical presentation of prostate cancer?

A

Vast majority asymptomatic
Urinary symptoms
Bone pain

106
Q

What urinary symptoms are usually seen in prostate cancer?

A

Benign enlargement of the prostate
Bladder over activity
+/- CaP

107
Q

When is bone pain seen in prostate cancer?

A

Advanced metastatic prostate cancer

108
Q

What is an unusual clinical presentation of prostate cancer?

A

Haematuria

109
Q

When is haematuria seen in prostate cancer?

A

In advanced prostate cancer

110
Q

What is the first stage in diagnosis of prostate cancer?

A

A digital rectal examination (DRE) and serum PSA (prostate specific antigen) is used to assess wether or not a biopsy of the prostate is necessary

111
Q

What happens if a biopsy of the prostate is necessary?

A

It is carried out via a TRUS (transrectal ultrasound) guided biopsy of prostate

112
Q

How are lower urinary tract symptoms (LUTS) caused by prostate cancer treated?

A

Transurethral resection of prostate

113
Q

What factors influence treatment decisions in prostate cancer?

A 
Age
Digital rectal exam
PSA level
Biopsies
MRI scan and bone scan
114
Q

What can be determined from the digital rectal exam with prostate cancer?

115
Q

What are the potential stages of prostate cancer?

A

Localised (T1/2)
Locally advanced (T3)
Advanced (T4)

116
Q

What is used to judge biopsies in prostate cancer?

A

Gleason Grade

117
Q

What is being looked for on a MRI scan and bone scan with prostate cancer?

A

Nodal/visceral metastases

118
Q

How are established prostate cancers treated?

A

Surveillance
Radical prostatectomy
Radiotherapy

119
Q

When is surveillance appropriate in treatment of established prostate cancers?

A

If the cancer is low risk

120
Q

How can it be determined that a cancer is low risk?

A

The Gleason score is quite low

121
Q

Why may surveillance be more appropriate than treatment in established prostate cancers?

A

Treatment may do more harm than good

122
Q

How is an radical prostatectomy conducted?

A

Open
Laparoscopic
Robotic

123
Q

What form of radiotherapy is conducted to treat established prostate cancers?

A

External beam or low dose brachytherapy (implanted beads)

124
Q

How are developmental prostate cancers treated?

A

High intensity focused ultrasound (HIFU)
Primary cryotherapy
Brachytherapy

125
Q

What happens in primary cryotherapy?

A

Freeze the prostate

126
Q

What kind of brachytherapy is given in developmental prostate cancer?

127
Q

How is metastatic prostate cancer treated?

A

Hormones

Pallitation

128
Q

What are the hormone based treatments for metastatic prostate cancer?

A

Surgical castration

Medical castration

129
Q

How is medical castration performed?

A

LHRH agnoists

130
Q

What are the palliation based treatments for metastatic prostate cancer?

A

Single-dose radiotherapy
Bisphosphonates
Chemotherapy

131
Q

How is locally advanced prostate cancer treated?

A

Surveillance
Hormones
Hormones and radiotherapy

132
Q

How is haematuria classified?

A

Visible

Non-visible

133
Q

What is the change of malignancy on investigation if haemoturia is visible?

134
Q

What malignancies might cause haemoturia?

A

Kidney

Ureter

135
Q

Is non-visible haemoturia symptomatic?

A

Can be symptomatic or asymptomatic

136
Q

How is non-visible haematuria detected?

A

Via microscopy or urine dipstick

137
Q

How is haematuria detected using urine dipstick?

A

Perioxidation of haem

138
Q

What are the urological differential diagnoses of haemoturia?

A 
Cancer
Stones
Infection 
Inflammation
Benign prostatic hyperplasia (large)
Nephrological (glomerular)
139
Q

What cancers can can haematuria?

A

Renal cell carcinoma
Upper tract transition cell carcinoma
Bladder cancer
Advanced prostate cancer

140
Q

What needs to be asked about when taking a history for haematuria?

A 
Smoking
Occupation 
Painful or painless
Other lower urinary tract symptoms
Family history
141
Q

What should be looked for on examination with haematuria?

A 
BP 
Abdominal mass
Variocele 
Leg swelling
Assess prostate by DRE
142
Q

What is a varicocele?

A

Collection of veins in the scrotum

143
Q

What should be looked for on prostate assessment?

A

Size

Texture

144
Q

What investigations should be done with haematuria?

A

Urine culture and cytology (abnormal cells)
FBC
Ultrasound
Flexible cystoscopy

145
Q

How common is bladder cancer, compared to other cancers, in the UK?

A

7th most common cancer

146
Q

What is happening to the incidence of bladder cancer?

A

Decreasing

147
Q

What is the male to female ratio of bladder cancer?

148
Q

What % of bladder cancers are transitional cell carcinomas (TCC)?

149
Q

What are the risk factors for bladder cancer?

A

Smoking
Occupational exposure
Schistosomiasis

150
Q

By how much does smoking increase the risk of bladder cancer?

A

4x increased risk

151
Q

What is the latent period for occupational exposure with bladder cancer?

152
Q

What occupational exposures can lead to bladder cancers?

A

Rubber or plastics manufacture (Arylamines)
Handling of carbon, crude oil, combustion (polyaromatic hydrocarbons)
Painters
Mechanics
Printers
Hairdressers

153
Q

Give an example of where schistosomiasis is common

154
Q

What are the stages of bladder cancer?

A

Superficial (Ta/T1)
Tis (in situ)
Muscle invasive

155
Q

What % of bladder cancers are superficial?

156
Q

What % of bladder cancers are Tis?

157
Q

What % of bladder cancers are muscle invasive?

158
Q

What is the treatment for high risk non-muscle invasive TCC?

A

Check cytoscopies

Intravesical chemotherapy/immunotherapy

159
Q

What is the treatment for low risk non-muscle invasive TCC?

A

Check cytoscopies

160
Q

What are the categories of treatment for muscle invasive TCC?

A

Potentially curative

Not curative

161
Q

What are the potentially curative treatments for muscle invasive TCC?

A

Radical cystectomy or radiotherapy, with or without chemotherapy

162
Q

What are the not curative treatments for muscle invasive TCC?

A

Palliative chemotherapy/radiotherapy

163
Q

What is a radical cystectomy/

A

The removal of the urinary bladder

164
Q

How can urine be passed following a radical cystectomy?

A

A piece of ileum may be used to make a conduit from the ureters to the abdomen, where urine can be collected in a bag
May attempt to reconstruct the bladder from a piece of small intestine

165
Q

How common is renal cell carcinoma, compared to other cancers, in the UK?

A

8th most common cancer in UK

166
Q

What % of all upper urinary tract tumours are renal cell carcinomas?

167
Q

What is happening to the incidence and mortality of renal cell carcinomas?

A

It is increasing

168
Q

What is the male to female ratio of renal cell carcinoma?

169
Q

What % of renal cell carcinoma (RCC) have metastases on presentation?

170
Q

What are the risk factors for RCC?

A

Smoking
Obesity
Dialysis

171
Q

By how much does smoking increase the risk of RCC?

A

Doubles it

172
Q

Where can metastases of RCC spread?

A

To lymph nodes, up the renal vein and vena cava, and into the right atrium and sub-capsular fat (perinephric spread)

173
Q

What is the treatment for established RCC?

A

Surveillance
Radical nephrectomy
Partial nephrectomy

174
Q

What is a radical nephrectomy?

A

Removal of kidney, adrenal, surrounding fat, upper ureter

175
Q

What is the treatment for developmental renal cell carcinoma?

176
Q

What is ablation?

A

Removal of tumour from surface of kidney via erosive process

177
Q

What are the palliative treatments for RCC?

A

Molecular therapies targeting angiogenesis

Immunotherapy

178
Q

What % of malignancies of upper urinary tract are upper tract transitional cell carcinoma (TCC)?

179
Q

What can TCC be due to?

A

The spread of cancer from the bladder up the ureter

180
Q

What % of TCC are due to the spread of cancer from the bladder up the ureter?

181
Q

What % of cancers of the upper urinary tract spread to the bladder?

182
Q

What are the investigations for TCC?

A

Ultrasound
CT urogram
Retrograde pyelogram
Ureteroscopy

183
Q

What is being looked for on ultrasound with TCC?

A

Hydronephrosis

184
Q

What is hydronephrosis?

A

Swelling of kidney due to backup of urine

185
Q

What is being looked for on a CT urogram with TCC?

A

Filling defect

Ureteric structure

186
Q

What happens in a retrograde pyelogram?

A

Inject contrast into the ureter

187
Q

What is taken with a ureteroscopy with TCC?

A

Biopsy

Washing for cytology

188
Q

What is the treatment for TCC?

A

Nephro-uretectomy

189
Q

What is a nephro-urecterectomy?

A

Removal of the kidney, fat, ureter, and cuff of bladder

ESA 3- Urinary System (13 decks)

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