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Pathology > Histopathology Part 3- p167-182- Urological, Renal + Gynae) > Flashcards

Histopathology Part 3- p167-182- Urological, Renal + Gynae) Flashcards

1
Q

What type of bacteria are >85% of cystitis caused by?

A

Gram -ve bacilli that normally reside in intestine- commonest E.coli but also Proteus, Klebsiella, Enterobacter, Strep faecalis

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2
Q

What predisposing factors are there for cystitis?

A 
Female
Bladder calculi
Urinary obstruction
DM
Sexually active
Instrumentation 
Cyclophosphamide associated with haemorrhagic cystitis
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3
Q

Clinical features of cystitis?

A

Suprapubic pain
Low grade fever
Dysuria
Frequency

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4
Q

Complications of cystitis?

A

Ascending infection causing pyelonephritis

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5
Q

Treatment of cystitis?

A

Trimethoprim

Nitrofurantoin

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6
Q

What cells are affected in 90% of bladder tumours?

A

Transitional cell tumours

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7
Q

What are contributing factors to transitional cell tumours?

A

Cigarette smoking

Industrial exposure to aromatic amines

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8
Q

What are the clinical features of transitional cell tumours?

A

Painless haematuria
Frequency
Urgency
Pyelonephritis

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9
Q

How are transitional cell tumours diagnosed?

A

Cystoscopy and biopsy

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10
Q

What is the pathology of benign prostatic hyperplasia (BPH)?

A

Dihydrotestosterone-mediated hyperplasia of prostatic stromal and epithelial cells, resulting in formation of large nodules

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11
Q

Symptoms of BPH?

A 
Difficulty urinating
Retention
Frequency
Nocturia
Overflow dribbling
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12
Q

Treatment of BPH?

A

TURP

5a reductase inhibitors

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13
Q

What type of cancer is the commonest type of prostate cancer?

A

Adenocarcinoma

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14
Q

Risk factors for prostate cancer?

A

Age
Race
FH
Hormonal and environmental influences

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15
Q

Where does prostate cancer spread to?

A

Bladder locally and spreads to bone haematogenously

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16
Q

How is prostate cancer graded?

A

Gleason system based on degree of differentiation and glandular patterns

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17
Q

How is prostate cancer diagnosed?

A

History
Examination
PSA- over 4ng/ml is indicative

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18
Q

What is the most common type of germinal tumour?

A

Seminoma (Peak age 30s and radiosensitive)

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19
Q

What biomarkers are there for germ cell tumours?

A

AFP
HCG
LDH

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20
Q

What are the two main categories of testicular cancer?

A

Germ cell- 95%

Sex cord- stromal- 5%

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21
Q

What is nephrotic syndrome characterised by?

A

Proteinuria (>3g/24h) + hypoalbuminaemia + oedema (+hyperlipidaemia)

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22
Q

What key words are there for identifying nephrotic syndrome in EMQs?

A

Swelling- facial in kids and peripheral in adults

‘Frothy’ urine

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23
Q

What are the primary causes of nephrotic syndrome?

A

Minimal change disease
Membranous glomerular disease
Focal segmental glomerulosclerosis

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24
Q

Who does minimal change disease most commonly affect?

A

Children (75%)

Second peak in elderly

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25
Q

What do you see on light microscopy for minimal change disease?

A

No changes

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26
Q

What do you see on electron microscopy for minimal change disease?

A

Loss of podocyte foot processes

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27
Q

What do you see on immunofluorescence for minimal change disease?

A

No immune deposits

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28
Q

How does MCD respond to steroids?

A

Well- 90% respond

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29
Q

What would you see on light microscopy for membranous glomerular disease?

A

Diffuse glomerular basement membrane thickening

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30
Q

What would you see on electron microscopy for membranous glomerular disease?

A

Loss of podocyte foot processes, subepithelial deposits- ‘spikey’

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31
Q

What would you see on immunofluorescence for membranous glomerular disease?

A

Ig and complement in granular deposits along entire GBM

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32
Q

How does membranous glomerular disease respond to steroids?

A

Poorly

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33
Q

Who does Focal Segmental Glomerulosclerosis commonly affect?

A

Adults

Most common in Afro-Caribbean people

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34
Q

What would you see on light microscopy for Focal Segmental Glomerulosclerosis?

A

Focal and segmental glomerular consolidation and scarring

Hyalinosis

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35
Q

What would you see on electron microscopy for Focal Segmental Glomerulosclerosis?

A

Loss of podocyte foot processes

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36
Q

What would you see on immunofluorescence for Focal Segmental Glomerulosclerosis?

A

Ig and complement in scarred areas

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37
Q

How does focal segmental glomeruloscerosis respond to steroids?

A

50%

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38
Q

What would you see in renal histology for diabetes

A

Diffuse glomerular basement membrane thickening

Mesangial matrix nodules- aka Kimmelstiel Wilson nodules

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39
Q

What stain would you use for amyloidosis in the kidney and what would you see if it was present?

A

Apple green birefringence with Congo red stain

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40
Q

What is nephritic syndrome characterised by?

A 
PHAROH
Proteinuria
Haematuria 'coke urine'
Azootemia- high urea and creatinine
Red cell casts in urine
Oliguria
HTN
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41
Q

What are the different causes of nephritic syndrome?

A 
Acute post-infectious (post strep) GN
IgA Nephropathy- Berger disease
Rapidly progressive (crescentic) GN
Hereditary nephritis- Alport's syndrome
Thin basement membrane disease- benign familial haematuria
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42
Q

When does post-infectious GN occur?

A

1-3wk after streptococcal throat infection or impetigo (strep pyogenes usually)

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43
Q

What investigation findings would you see in post-infectious GN?

A 
Haematuria- red cell casts
Proteinuria
Oedema
HTN
Raised ASOT titre
Decreased C3
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44
Q

What would you see in light microscopy in post-infectious GN?

A

Increased cellularity of glomeruli

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45
Q

What would you see in electron microscopy in post-infectious GN?

A

Subendothelial humps

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46
Q

What would you see in fluorescence microscopy in post-infectious GN?

A

Granular deposits of IgG and C3 in GBM

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47
Q

What is the commonest glomerulonephritis worldwide?

A

IgA nephropathy- Berger disease

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48
Q

What is the pathology of IgA nephropathy?

A

Deposition of IgA immune complexes in glomeruli

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49
Q

How does IgA nephropathy present?

A

1-2d after an URTI with frank haematuria or asymptomatic microscopic haematuria

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50
Q

What would you see in fluorescence microscopy in IgA nephropathy?

A

Granular deposition of IgA and complement in mesangium

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51
Q

What is the most aggressive glomerulonephritis which can cause end stage renal failure in weeks?

A

Rapidly progressive crescentic GN

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52
Q

How does crescentic GN present?

A

As a nephritic syndrome but oliguria and renal failure are more pronounced

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53
Q

What are the three types of rapidly progressive (crescentic) GN?

A

Type 1- Anti-GBM antibody
Type 2- Immune complex
Type 3- Pauci-immune/ANCA-associated

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54
Q

What are rapidly progressive (crescentic) GN all characterised by?

A

Presence of crescents in glomeruli on light microscopy

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55
Q

What causes type 1 rapidly progressive GN?

A

Goodpastures syndrome

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56
Q

What would you see in fluorescence microscopy in type 1 rapidly progressive GN?

A

Linear deposition of IgG in GBM

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57
Q

What other organs are involved in type 1 rapidly progressive GN?

A

Lungs- pulmonary haemorrhage

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58
Q

What causes type 2 rapidly progressive GN?

A

SLE
IgA nephropathy
Post-infectious GN

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59
Q

What would you see in fluorescence microscopy in type 2 rapidly progressive GN?

A

Granular (lumpy bumpy)

IgG immune complex deposition on GBM/mesangium

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60
Q

What causes type 3 rapidly progressive GN?

A

c-ANCA- Wegener’s granulomatosis

p-ANCA- microscopic polyangiitis

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61
Q

What would you see in fluorescence microscopy in type 3 rapidly progressive GN?

A

Lack of/scanty significant immune complex deposition

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62
Q

What other organ involvement is there in type 3 rapidly progressive GN?

A

Vasculitis- skin rashes or pulmonary haemorrhage

63
Q

What causes hereditary nephritis (Alport’s)?

A

Mutation in type IV collagen alpha 5 chain

64
Q

What is the inheritance pattern of hereditary nephritis (Alport’s)?

A

X linked

65
Q

What is the presentation of hereditary nephritis (Alport’s)?

A

Nephritic syndrome + sensorineural deafness + eye disorders

66
Q

What causes thin basement membrane disease?

A

Diffuse thinning of GBM caused by mutation in type IV collagen alpha 4 chain

67
Q

What is the inheritance pattern of thin basement membrane disease?

A

Autosomal dominant

68
Q

Which nephritic syndromes cause asymptomatic haematuria?

A

Thin basement membrane disease
IgA nephropathy- Berger
Alport syndrome

69
Q

What is the pathology of acute tubular injury (ATI)/necrosis (ATN)

A

Damage to tubular epithelial cells -> cells shed and block off tubules as casts -> reduced flow and increased haemodynamic pressure in the nephron -> reduced pressure gradient across BM -> acute renal failure -> tubular glomerular feedback reduces blood supply further

70
Q

What is the most common cause of acute renal failure?

A

ATI or ATN

71
Q

What causes ATI/ATN?

A

Hypovolaemia -> pre-renal ARF -> ischaemia of nephrons

Nephrotoxins- drugs (aminoglycosides, NSAIDs), radiographic contrast agents, myoglobin, heavy metals

72
Q

What would you see in histopathology of ATI/ATN?

A

Necrosis of short segments of tubules

73
Q

What is acute pyelonephritis and what commonly causes it?

A

Bacterial infection of the kidney, usually a result of ascending infection, most commonly caused by E. coli

74
Q

How does acute pyelonephritis commonly present?

A 
Fever
Chills
Sweats
Flank pain
Renal angle tenderness
Leucocytosis
\+/- frequency, dysuria + haematuria
Leukocytic casts seen in urine
75
Q

What is chronic pyelonephritis?

A

Chronic inflammation and scarring of the parenchyma caused by recurrent and persistent bacterial infection

76
Q

What can cause chronic pyelonephritis?

A

Chronic obstruction- posterior urethral valves, renal calculi
Urine reflux

77
Q

What causes acute interstitial nephritis?

A

A hypersensitivity reaction, usually to a drug (abx, NSAIDs, diuretics)

78
Q

How does acute interstitial nephritis present?

A 
Fever
Skin rash
Haematuria
Proteinuria
Eosinophilia
79
Q

When is chronic interstitial nephritis seen?

A

Also known as analgesic nephropathy

Seen in elderly with long term analgesic consumption

80
Q

Name two thrombotic microangiopathies?

A

Haemolytic uraemic syndrome (HUS)

Thrombotic thrombocytopenic purpura (TTP)

81
Q

What are thrombotic microangiopathies characterised by?

A

Thrombosis (Generally renal in HUS and widespread in TTP)

Triad of MAHA, thrombocytopenia + sometimes renal failure

82
Q

What is the pathophysiology of thrombotic microangiopathies?

A

Widespread fibrin deposition in vessels associated with ADAMTS3 (platelet surface protein) -> formation of platelet-fibrin thrombi which damage passing platelets and RBCs -> platelet and RBC destruction (thrombocytopenia and MAHA)

83
Q

Who does HUS usually affect?

A

Children

84
Q

Who does TTP usually affect?

A

Adults

85
Q

What is HUS associated with?

A

Diarrhoea caused by E.Coli O157:H7- ‘Children visiting petting zoos’
Non-diarrhoea associated– abnormal proteins in complement pathway/endothelium

86
Q

Where are the thrombi found in HUS?

A

Kidneys

87
Q

Where are the thrombi found in TTP?

A

Throughout circulation esp in CNS- headaches, LOC, seizures, comas)

88
Q

What are the signs and symptoms of thrombotic microangiopathies?

A

Decreased platelets -> bleeding (petechiae, haematemesis, melaena)
MAHA -> pallor and jaundice

89
Q

How are thrombotic microangiopathies diagnosed?

A

Decreased Hb and Plts
Signs of haemolysis- increased bilirubin, reticulocytes and LDH
Fragmented RBCs on blood smear
Coomb’s test negative (as not AIHA)

90
Q

What is acute renal failure?

A

A rapid loss of renal function manifesting as an increased serum creatinine and urea

91
Q

What are the complications of acute renal failure?

A 
Metabolic acidosis
Hyperkalaemia
Fluid overload
HTN
Decreased calcium 
Uraemia
92
Q

What are the different causes of acute renal failure?

A

Pre-renal- caused by renal hypoperfusion e.g. hypovolaemia, sepsis, burns, acute pancreatitis and renal artery stenosis
Renal- ATN, acute glomerulonephritis, thrombotic microangiopathy
Post-renal- obstruction to urine flow as a result of stones, tumours, prostatic hypertrophy + retroperitoneal fibrosis

93
Q

What are the commonest causes of chronic renal failure in the UK?

A 
Diabetes
Glomerulonephritis
HTN + vasc disease
Reflux nephropathy
Polycystic kidney disease
94
Q

How is chronic renal failure classified?

A 
Stage 1- GFR>90
Stage 2- mild- GFR  60-89
Stage 3- moderately- GFR 30-59
Stage 4- severely- GFR 15-29
Stage 5- Renal failure- GFR<15
95
Q

What causes adult polycystic kidney disease (APCKD)?

A

Autosomal dominant inheritance- 85% due to mutations in PKD1 on chromosome 16 (encoding polysystin-1), remainder in PKD2 on chromsome 4 (encoding polycystin-2)

96
Q

What are the pathological features of APCKD?

A

Large multicystic kidneys with destroyed renal parenchyma, liver cysts and berry aneurysms

97
Q

What are the clinical features of APCKD?

A

Haematuria
Flank pain
UTI
Features are often due to cyst complications- rupture, infection and haemorrhage

98
Q

Different types of renal cell carcinoma?

A

Clear cell carcinoma- well differentiated
Papillary carcinoma- dialysis-associated
Chromophobe renal carcinoma- pale, eosinophilic

99
Q

RFs for renal cell carcinoma?

A 
Smoking
Obesity
HTN
Unopposed oestrogen
Heavy metals
CKD
100
Q

Clinical features of renal cell carcinoma?

A

Costovertebral pain
Palpable pain
Haematuria
Paraneoplastic syndrome- polycythaemia, hypercalcaemia, HTN, Cushing’s, amyloidosis

101
Q

What is pelvic inflammatory disease?

A

Infection ascending from vagina and cervix up to uterus and tubes, leading to inflammation (endometritis, salpingitis) and formation of adhesions

102
Q

Most common organisms causing PID in UK?

A

Chlamydia trachomatis

Neisseria gonorrhoea

103
Q

Clinical features of PID?

A 
Lower abdo pain
Dyspareunia
Vaginal bleeding/discharge
Fever
Adnexal tenderness
Cervical excitation
104
Q

Complications of PID?

A 
Fitz Hugh Curtis syndrome- RUQ from peri-hepatitis + violin string peri-hepatic adhesions
Infertility
Risk of ectopic pregnancy
Tubo-ovarian abscess
Chronic pelvic pain
Peritonitis
105
Q

What is endometriosis?

A

Presence of endometrial glands or stroma in abnormal locations outside the uterus e.g. ovaries, uterine ligaments, rectovaginal septum, Pouch of Douglas, pelvic peritoneum

106
Q

How does endometriosis present clinically?

A 
Pelvic pain 
Dysmenorrhoea
Deep dyspareunia
Decreased fertility
Cyclical PR bleeding
Haematuria
Umbilical bleeding
Nodules/tenderness in vagina, posterior fornix or uterus
107
Q

What does endometriosis macroscopically present as?

A

Red-blue to brown nodules- ‘powder burns’

‘Chocolate cysts’ in ovaries

108
Q

What does endometriosis microscopically present as?

A

Endometrial glands and stroma

109
Q

What is adenomyosis?

A

Presence of ectopic endometrial tissue deep within the myometrium

110
Q

How does adenomyosis present clinically?

A

Heavy menstrual bleeding
Dysmenorrhoea
Deep dyspareunia
Globular uterus

111
Q

What is a leiomyoma (fibroid)?

A

A benign tumour of smooth muscle origin

112
Q

What is the most common tumour of the female genital tract?

A

Leiomyoma/fibroid (20% of women >35)

113
Q

What has a strong influence over leiomyoma size?

A

Oestrogen

Grow during pregnancy and regress post-menopause

114
Q

What do leiomyomas look like macroscopically?

A

Sharply circumscribed, discrete, round, firm, gray-white tumours

115
Q

What do leiomyomas look like microscopically?

A

Bundles of smooth muscle cells

116
Q

How do leiomyomas present clinically?

A

Heavy menstrual bleeding
Dysmenorrhoea
Pressure effects (urinary freq, tenesmus)
Sub fertility

117
Q

What complications are associated with leiomyomas in pregnancy?

A

Red degeneration of fibroids- haemorrhagic infarction -> severe abdo pain
Post-partum torsion

118
Q

What is postmenopausal bleeding until proven otherwise?

A 
Endometrial cancer
(10% with PMB have malignancy)
119
Q

How is endometrial cancer staged?

A

FIGO system

120
Q

What are the two types of endometrial cancer?

A

Endometrioid- 80% (look like normal endometrial glands and mainly adenocarcinomas)
Non-endometrioid- 20% (include papillary, serous and clear cell)

121
Q

What is the pathophysiology of endometrioid endometrial cancer?

A

Related to oestrogen excess- peri-menopausal women

122
Q

Risk factors for endometrioid endometrial cancer?

A

E2 excess- obesity, anovulatory amenorrhoea (PCOS), nulliparity, early menarche, late menopause, tamoxifen
DM, HTN

123
Q

What is the pathophysiology of non-endometrioid endometrial cancer?

A

Unrelated to oestrogen excess- elderly women with endometrial atrophy

124
Q

What is normal vulval histology?

A

Squamous epithelium

125
Q

What is vulval intraepithelial neoplasia (VIN) associated with?

A

HPV-16

126
Q

How does the usual type of VIN present?

A

Warty and basaloid in women 35-55y

127
Q

What is the main type of vulval carcinoma?

A

Squamous cell carcinoma- can arise from VIN or from other skin abnormalities

128
Q

What is the leading cause of death from gynae malignancy in the UK?

A

Ovarian carcinoma

129
Q

What is the main cell type in ovarian carcinoma?

A

Epithelial- 70%

130
Q

At what age group is the peak incidence of ovarian cancer?

A

75-84

131
Q

Subtypes of epithelial ovarian cancer?

A 
Serous cystadenoma- most common (Psammoma bodies common)
Mucinous cystadenoma (No psammoma and in younger women)
Endometrioid
Clear cell (hobnail appearance)
132
Q

How do germ cell tumours usually differ in severity between children and adults?

A

Children- malignant

Adults- benign

133
Q

What is treatment for dysgerminoma?

A

Radiotherapy

134
Q

What are the different types of teratoma and how do they differ?

A

Mature (95%)- e.g. dermoid cyst, benign

Immature- malignant, solid, can secrete AFP

135
Q

What can choriocarcinomas secrete?

A

hCG

136
Q

What are the different types of ovarian germ cell tumours?

A

Dysgerminoma
Teratoma
Choriocarcinoma

137
Q

What are the three main cell types of ovarian cancer?

A

Epithelial- 70%
Germ cell- 20%
Sex cord/stroma- 10%

138
Q

Three different types of sex cord/stroma tumour and how do they differ in production?

A

Fibroma- no hormone production and 50% associated with Meig’s syndrome (ascites+pleural effusion)

Granulosa-theca cell tumour- produce E2 (oestrogenic effects)

Sertoli-Leydig cell tumour- secrete androgens- look for defeminisation and virilisation

139
Q

What staging system is used for ovarian cancer?

A

FIGO

140
Q

What are the different stages of FIGO?

A

1- limited to ovaries
2- limited to pelvis
3- limited to abdo including regional LN metastases
4- Distance metastases outside abdo cavity

141
Q

What is normal cervical histology? (outer and endocervical canal)

A

Outer cervix covered by squamous epithelium
Endocervical canal lined by columnar glandular epithelium
Squamocolumnar junction separates them

142
Q

What is the transformation zone?

A

Area where columnar epithelium transforms into squamous cells (squamous metaplasia). Normal physiological process. This area is susceptible to malignant change.

143
Q

What is cervical intraepithelial neoplasia (CIN)?

A

Dysplasia at TZ as result of infection by HPV 16 + 18

144
Q

How is CIN graded on both cytology and histology?

A

Cytology: mild, moderate or severe dyskaryosis
Histology-
CIN 1- dysplasia confined to lower 1/3 of epithelium
CIN2- lower 2/3
CIN 3- Full thickness but basement membrane intact

145
Q

What percentage of CIN1 reverts to normal over 10-23m?

A

60-90%

146
Q

What percentage of CIN3 progresses to cervical cancer over 10yrs?

A

30%

147
Q

What are the risk factors for CIN?

A 
Early age at first intercourse
Multiple partners
Multiparity
Smoking
HIV 
Immunosuppression
148
Q

What is the second most common cancer in women worldwide?

A

Cervical carcinoma

149
Q

Which age groups are at most risk of cervical carcinoma?

A

2 peaks
30-39
>70

150
Q

RF for cervical cancer?

A

Early exposure to HPV
COCP + high parity
Smoking
Immunosuppression

151
Q

Most common type of cervical cancer?

A

Squamous (70-80%)

152
Q

What marks the change from CIN to carcinoma?

A

Invasion through the basement membrane

153
Q

Clinical presentation of cervical cancer?

A 
PCB
Intermenstrual bleeding
PMB
Discharge
Pain
154
Q

How is cervical cancer staged?

A

FIGO

Pathology (13 decks)

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