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MBChB Year 3 > Week 4 - Female Breast/GU > Flashcards

Week 4 - Female Breast/GU Flashcards

1
Q

When does the reproductive development diverge (differentiate between male & female)?

A

~7 weeks

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2
Q

What is the endocervix lined by prior to puberty?

A

Columnar (glandular) epithelium

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3
Q

Describe what happens to the cervix during its growth after puberty?

A

Squamo-columnar junction is everted into the vagina & the squamous epithelium adapts to the vaginal environment by squamous metaplasia in the ‘transformation zone’

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4
Q

What are the post pubertal cervical changes reversed by?

A

Menopause

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5
Q

Describe the clinical significance of the cervical ‘transformation zone’?

A

Unstable differentiation is where most cervical neoplasia develop

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6
Q

What is thought to be a necessary cause of cervical cancer & precancer?

A

Persisting infection with an oncogenic strain of Human Papilloma Virus (HPV)

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7
Q

What are the 2 prevalent strains of HPV in glasgow?

A

HPV 16 & 18

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8
Q

Where are the cervical cells taken from for cytological screening?

A

Cervical transformation zone

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9
Q

What is a cervical cytological screening designed to detect?

A

Changes associated with HPV infection & Cervical Intraepithelial Neoplasia

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10
Q

What are dyskaryosis?

A

Nuclear abnormalties

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11
Q

What does the presence of dyskaryosis suggest?

A

CIN

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12
Q

What does the presence of dyskaryosis prompt?

A

Referral to colposcopy clinic for biopsy to detect CIN

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13
Q

Does CIN have symptoms?

A

NO

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14
Q

Who should undergo cervical cytology screening?

A

Current policy in Scotland is that women aged 25 -65 are invited. That is inclusive of those that have been vaccinated

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15
Q

How often should women be screened cervically when 25-50 years old?

A

3 yearly

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16
Q

How often should women be screened cervically when 50-65 years old?

A

5 yearly

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17
Q

What colour are the cervical superficial squamous cells stained?

A

Pink

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18
Q

What colour are the cervical intermediate cells stained?

A

Blue

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19
Q

When would you repeat smear screening if it came back negative?

A

Routinely in 3 years

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20
Q

When would you repeat smear screening if it came back with a borderline nuclear abnormality?

A

6 months later (X3 Borderline nuclear abnormality refer colposcopy)

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21
Q

What would you do if a smear screening test came back with a low/high grade dyskaryosis?

A

Refer to colposcopy

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22
Q

What would you do if a smear screening test came back with a glandular abnormality?

A

Refer to colposcopy

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23
Q

What would you do if a smear screening test came back with features suggestive of invasion?

A

Urgent referral to colposcopy

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24
Q

What type of HPV vaccination (aimed at 12/13year old girls) is Scotland now using?

A

Quadrivalent vaccine to cover against HPV 6, 11, 16 & 18

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25
Q

What is HPV testing easier with?

A

Liquid based cytology

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26
Q

What is HPV testing more sensitive than?

A

Cytology

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27
Q

What can HPV testing be used effectively in?

A

Primary screening in women aged over 30 years

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28
Q

HPV tests are very ______, which at present reduced ______?

A
  • Sensitive

- Specificity

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29
Q

What does high risk HPV in the cervix increase the risk of?

A

CIN

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30
Q

What is Gardasil?

A

HPV vaccination that targets high risk HPV 6,11,16,18

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31
Q

What is the downfall of HPV vaccination?

A

Likely to be important in the long run but

cannot be assumed that it will prevent all cervical cancer

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32
Q

Does most HPV infection progress to CIN or cancer?

A

NO

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33
Q

Describe the colposcopy procedure?

A
  • Cervix visualised
  • Washed with acetic acid
  • Application of Iodine
  • Green light filter
  • Abnormal area can be biopsied or treatment performed at the time or at a further appointment
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34
Q

What are more than 99% of cervical carcinomas associated with?

A

HPV infection

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35
Q

Describe what the early genes (E1 –> E7) in HPV infection do?

A

Interact with intracellular molecules to interfere with cell proliferation machinery to replicate the virus

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36
Q

Describe what the late genes (L1 & L2) in HPV infection do?

A
  • Encode capsid proteins

- Disruption of cell cycle checkpoints may contribute to accumulation of oncogenic mutations & carcinogenesis

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37
Q

What does BNA stand for in HPV infection?

A

Borderline nuclear abnormality

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38
Q

What types of cells are commonly found on histology of HPV?

A

Koilocytes

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39
Q

Describe the histology of low grade squamous dyskaryosis?

A
  • Normal
  • Nuclear:cytoplasmic upto 1/2
  • CIN1
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40
Q

Describe the histology of high grade (moderate) squamous dyskaryosis?

A
  • Nuclear:cytoplasmic from 1/2 to 2/3

- CIN2

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41
Q

Describe the histology of high grade (severe) dyskaryosis?

A
  • Nuclear enlargement with dense hyperchromasia & course chromatin clumping
  • CIN3
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42
Q

What are the 2 means of treatment for cervical abnormalities?

A
  1. Bipolar tubal coagulation

2. Post cold coagulation

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43
Q

What are the 2 immediate complications of cervical treatments (bipolar coagulation & post cold coagulation)?

A
  1. Pain

2. Haemorrhage

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44
Q

What are the 4 delayed complications of cervical treatments (bipolar coagulation & post cold coagulation)?

A
  1. Secondary haemorrhage (1-2%)
  2. Infection
  3. Cervical stenosis (~1%)
  4. No good evidence of impact on fertility
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45
Q

What is the cervical screening programmed designed to pick up specifically?

A

Squamous lesions

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46
Q

What is the name given for endocervical glandular epithelium that undergoes premalignant change?

A

Cervical Glandular Intraepithelial Neoplasia (cGIN )

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47
Q

What is the name given for malignant change in glandular epithelium?

A

Adenocarcinoma

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48
Q

What is a histological feature of an endocervical abnormality?

A

Pseudostratification

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49
Q

What else can a smear test pick up?

A

Endometrial abnormalities

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50
Q

What should always happen when a patient presents with post menopausal bleeding?

A

Referred to gynaecology for endometrial biopsy

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51
Q

What are the 5 possible symptoms of cervical cancer?

A
  1. NONE
  2. Pain
  3. Post coital bleeding
  4. Intermenstrual bleeding
  5. Irregular vaginal bleeding
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52
Q

Describe how invasive squamous carcinoma of the cervix develops?

A

Almost always develops from pre-existing CIN, but not all CIN will become squamous cancer

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53
Q

What type of CIN are more likely to progress to cancer?

A

CIN2 & CIN3

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54
Q

What is another term for CIN?

A

Squamous intraepithelial lesion (SIL)

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55
Q

Describe the histology of invasive squamous cell carcinoma?

A
  • Blood & polymorphs
  • Squamous cells take on bizarre shapes
  • Late stage
  • Basement membrane has been breached and malignant cells penetrate the stroma
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56
Q

What can lead to atopic vaginitis?

A

Low oestrogen after menopause

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57
Q

List the 5 signs & symptoms of atopic vaginitis?

A
  1. Discomfort
  2. Dyspareunia (painful sex)
  3. Bleeding
  4. Polyps
  5. Cysts
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58
Q

What does VAIN stand for?

A

Vaginal intra-epithelial neoplasia

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59
Q

What are 2 uncommon vaginal cancers?

A
  1. Vaginal intra-epithelial neoplasia (VAIN)

2. Squamous carcinoma

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60
Q

What can primary cancers of the cervix/ vulva also involve?

A

The vagina

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61
Q

What 5 infections can cervical smear tests also identify?

A
  1. Bacterial vaginosis
  2. Thrush (candida albicans)
  3. Trichomonas vaginalis
  4. Actinomyces
  5. Herpes Simplex
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62
Q

How is Trichomonas vaginalis usually transmitted?

A

Sexually transmitted

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63
Q

What is a common bacteria associated with the IUD contraceptive coil?

A

Actinomyces

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64
Q

List 8 possible pathologies associated with the female vulva?

A
  1. Inflammatory dermatoses
  2. Skin tumours
  3. Skin tags
  4. Melanocytic nevi
  5. Benign cysts
  6. Candidiasis (thrush)
  7. Lichen planus
  8. Lichen sclerosus et atrophicus
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65
Q

Describe Vulva Candidiasis (thrush)?

A
  • Common
  • May be associated with pregnancy or diabetes
  • Bartholin’s vestibular gland cysts may become infected with abscess formation
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66
Q

What are Lichen planus

& Lichen sclerosus et atrophicus?

A

Non-infective inflammations of the vulva

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67
Q

What region is Lichen Sclerosus especially associated with?

A

Anogenital region

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68
Q

What 2 things are Vulval Squamous Cell Carcinoma’s associated with?

A
  1. Vulvar intraepithelial neoplasia (VIN)

2. Dermatoses

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69
Q

What age group is more prevalent for Vulval Squamous Cell Carcinoma’s associated with VIN?

A

Exclusively in females less than 60 years old

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70
Q

What are Vulval Squamous Cell Carcinoma’s associated with VIN usually related to?

A

High risk type HPV 16/18

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71
Q

What is the appearance of Vulval Squamous Cell Carcinoma’s associated with VIN?

A

Warty or Basaloid

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72
Q

What age group is more prevalent for Vulval Squamous Cell Carcinoma’s associated with dermatoses?

A

Older age group- most over 60, many over 70

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73
Q

Describe Vulval Squamous Cell Carcinoma’s associated with dermatoses?

A
  • Well differentiated & keratinising
  • Not associated with HPV infection or VIN
  • Adjacent squamous hyperplasia &/or lichen sclerosus common
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74
Q

Describe the risk of malignancy in Vulval Lichen Sclerosus?

A
  • Generally low

- But subtle non-HPV related entity called ‘differentiated VIN’ may have a much greater risk of progression

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75
Q

What % of vulval cancers are thought to be HPV dependent?

A

20%

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76
Q

What amount of cervical squamous cancer is HPV dependent?

A

Almost all

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77
Q

What may vulval HPV- associated intraepithelial neoplasia (VIN) develop into?

A

Invasive squamous carcinoma

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78
Q

What may the squamous epithelium of the vagina & perianal skin be affected by?

A

Pre-neoplastic field change

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79
Q

What 2 places could you find ectopic breast tissue?

A
  1. Axilla

2. Vulva

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80
Q

How is the nipple formed?

A

Evagination of the mammary pit

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81
Q

What is premature thelarche?

A
  • Girls who develop small breasts typically before the age of 3 years
  • They do not have other signs of puberty
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82
Q

Describe how breasts are developed?

A
  • During puberty
  • Cyclical oestrogen & progesterone
  • Duct elongation & stromal development
  • Lobuloalveolar differentiation
  • Continues for a decade, enhanced by pregnancy
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83
Q

What 3 things does Duct elongation & stromal development dependant on?

A
  1. Oestrogen
  2. Glucocorticoids
  3. Growth hormone
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84
Q

What 3 things is Lobuloalveolar differentiation dependant on?

A
  1. Progesterone
  2. Insulin
  3. Growth Hormone
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85
Q

Describe the hormonal variation of breast development during the 4 phases of the menstrual cycle?

A
  1. Proliferation in Proliferative phase (3-7)
  2. Decreases in Follicular phase (8-14)
  3. Myoepithelial changes & proliferation in Luteal phase (15-20)
  4. Secretory changes in Secretory phase
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86
Q

Describe breast development during pregnancy?

A
  • Early pregnancy lobular enlargement & stromal depletion
  • Continued lobular enlargement & secretory change
  • Post lactational involution (3 months)
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87
Q

What are the 3 breast developmental abnormalities?

A
  1. Hypoplasia/Amastia
  2. Macromastia
  3. Polymastia/Polythelia
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88
Q

Describe Breast Amastia?

A

Condition where breast tissue, nipple, & areola is absent, either congenitally or iatrogenically

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89
Q

Describe Breast Macromastia?

A

Condition of abnormal enlargement of the breast tissue in excess of the normal proportion

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90
Q

Describe Breast Polymastia?

A

Condition of having an additional breast, may appear with or without nipples or areolae

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91
Q

Describe Breast Polythelia?

A

Presence of an additional nipple alone

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92
Q

Describe the population breast screening programme?

A
  • All women 50-70years
  • 2 view mammography
  • Recalled every 3 years
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93
Q

Describe 6 ways to perform breast screening?

A
  1. Xray
  2. Recall
  3. Examination
  4. Lump, asymmetry, distortion, calcification
  5. Needle biopsy
  6. Open biopsy
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94
Q

List the 4 symptomatic reasons why someone would get breast screening?

A
  1. Breast lump
  2. Treat pain
  3. Nipple discharge
  4. Skin changes
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95
Q

What is the breast triple assessment?

A
  1. Clinical history
  2. Examination
  3. Imaging (MMG, US, MRI)
  4. Needle biopsy
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96
Q

What are the 3 PROS of breast fine needle aspirate?

A
  1. Relatively easy
  2. Only mild trauma
  3. Immediate report at clinic
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97
Q

What are the 3 CONS of breast fine needle aspirate?

A
  1. No architecture, insitu or invasive
  2. Requires trained cytologist
  3. False positives/negatives
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98
Q

What are the 2 PROS of breast core biopsy?

A
  1. Differentiates between insitu & invasive

2. Fewer false positives/negatives

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99
Q

What are the 2 CONS of breast core biopsy?

A
  1. Takes 24hrs to process & no immediate report

2. More local trauma

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100
Q

What are the 5 reasons for doing a breast core biopsy?

A
  1. Gives tissue diagnosis with architecture
  2. Allows correlation with Mammogram
  3. Visualises calcification
  4. Allows diagnosis of borderline lesions
  5. Enables accurate planning of definitive surgery
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101
Q

What are the 5 classifications for breast fine needle aspiration (FNA)?

A
  1. C1- insufficient
  2. C2- Benign
  3. C3- Atypia Probably Benign
  4. C4- Atypia probably malignant
  5. C5- Malignant
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102
Q

What are the 5 classifications for breast core biopsy?

A
  1. B1- Normal tissue/ insufficient for diagnosis
  2. B2- Benign
  3. B3- Atypia probably benign
  4. B4- Atypia probably malignant
  5. B5a/b- Malignant
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103
Q

Give 2 examples of benign breast lesion?

A
  1. Fibroadenoma

2. Fibrocystic

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104
Q

Describe a Fibroadenoma benign breast lesion?

A
  • Young women 20-30
  • Discrete mobile lump
  • Lesion of stroma & epithelium
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105
Q

Describe fibroadenomatoid lesions?

A
  • Well defined rounded opacity
  • C2 FNA classification
  • B2/B3 core biopsy classificaiton
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106
Q

Give 3 examples of fibroadenomatoid lesions?

A
  1. Fibrodenoma
  2. Fibroadenomatoid lesion
  3. Phyllodes tumour
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107
Q

Describe a Phyllodes breast tumour?

A
  • Typically large
  • Fast-growing masses
  • Form from the periductal stromal cells of the breast
  • Pleomorphisim
  • Stromal Overgrowth
  • Necrosis
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108
Q

What are the 3 types of Phllodes breast tumour?

A
  1. Benign
  2. Borderline
  3. Malignant (treat as sarcoma)
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109
Q

What should you always remember when treating Phyllodes breast tumour?

A

Never shell out

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110
Q

Describe a fibrocystic benign breast lesion?

A
  • 30-40years
  • Cyclical Variation
  • May be painful
  • Fibrosis, cysts, apocrine change, epithelial hyperplasia & columnar cell change
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111
Q

What is a Radial scar?

A

Form of sclerosing duct hyperplasia/ parenchymal distortion

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112
Q

What 2 ways would you diagnose a radial scar?

A
  1. Core biopsy to exclude carcinoma

2. Excision biopsy

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113
Q

List 5 ways to differentiate between a radial scar and tubular carcinoma?

A
  1. Pattern
  2. Shape of tubules
  3. Myoepithelial cells
  4. CK5, SMA, P63
  5. Calponin, SMM, CD10
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114
Q

What is duct ectasia?

A

Condition in which the lactiferous duct becomes blocked or clogged & can mimic breast cancer

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115
Q

List the 5 signs & symptoms of duct ectasia?

A
  1. Nipple discharge/inversion
  2. Pain
  3. Squamous metaplasia of lactiferous duct
  4. Mammary duct fistula
  5. Micro dilated ducts & inflammation changes
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116
Q

What is duct ectasia linked to?

A

Smoking

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117
Q

Describe the presentation of a breast papillary lesion?

A

Nipple discharge, blood stained +/- epithelial cells

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118
Q

Describe breast papillary lesion?

A
  • Mass often central
  • Microcalcification
  • Cytology C1, 2, 3, 4, 5
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119
Q

What are 2 ways to diagnose a papillary lesion?

A
  1. Core biopsy

2. Papillary lesion excise

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120
Q

Describe a papilloma?

A
  • Small wart-like growth
  • Fibrovascular cores
  • Epithelial & myoepithelial cells
  • Hyperplasia
  • Single/Multiple
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121
Q

Describe Pseudo angiomatous stromal hyperplasia (PASH)?

A
  • Hard palpable lump
  • Usually premenopausal
  • Well defined mass on imaging
  • Gross well circumscribed pseudo encapsulated mass
  • Dense stroma with anatomizing channels lined by myofibroblasts
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122
Q

What is the differential diagnosis of Pseudo angiomatous stromal hyperplasia (PASH)?

A

Angiosarcoma

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123
Q

Describe Granulomatous mastitis?

A
  • Mean age 33 years
  • Distinct hard mass
  • Usually parous
  • Contraceptive pill effect?
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124
Q

What is granulomatous mastitis?

A

Confluent inflammation with abscess formation centred on lobules

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125
Q

List 6 potential causes for granulomatous mastitis?

A
  1. TB
  2. Sarcoid
  3. Fungal/atypical mycobacterial
  4. Cat scratch disease
  5. Vasculitis
  6. Carcinoma associated granulomas
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126
Q

What fine needle aspirate classification is granulomatous mastitis?

A

C5 or false positive

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127
Q

What is the management of Granulomatous mastitis?

A
  • Spontaneous resolution
  • NSAID’s
  • Steroids
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128
Q

What should you avoid in Granulomatous mastitis?

A

Open biopsy

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129
Q

Describe Diabetic mastopathy?

A
  • Ill defined hard mass.
  • Usually < 30yrs
  • Dense keloid like stroma
  • Perilobular & vascular lymphocytes
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130
Q

Give 2 examples of atypical breast proliferations?

A
  1. Atypical ductal hyperplasia

2. Atypical lobular hyperplasia

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131
Q

How many women does breast carcinoma approximately affect?

A

1:10

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132
Q

What are the 3 risk factors for breast carcinoma?

A
  1. Age- 40-70years
  2. Family history- accounts for <5%
  3. Hormone environment- menstruation, pregnancy, breast feeding, hormone replacement
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133
Q

Describe an insitu breast carcinoma?

A
  • Malignant proliferation of epithelial cells contained within the basement membrane
  • NO extension into breast stroma
  • No communication with blood vessels or lymphatics
  • No possibility of metastases
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134
Q

Describe a breast ductal carcinoma in situ?

A
  • Most are mammographically detected

- May present with lump, nipple discharge or Pagets Disease

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135
Q

What happens if breast ductal carcinoma in situ is left untreated?

A

30% will develop invasive carcinoma in 15 years

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136
Q

Describe the prognosis of breast ductal carcinoma in situ?

A

With adequate surgical treatment prognosis is excellent

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137
Q

What is the 3 part treatment for breast ductal carcinoma in situ (DCIS)?

A
  1. Complete Excision
  2. Mastectomy +/- Reconstruction
  3. Local Excision & Radiotherapy
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138
Q

Describe how breast Lobular Carcinomas in situ are detected?

A

Chance finding in breast biopsies no clinical or mammographic features

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139
Q

Describe the presentation of breast Lobular Carcinomas in situ?

A

Usually multifocal & bilateral

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140
Q

What is the risk factor of breast Lobular Carcinomas insitu?

A
  • Developing invasive cancer in either breast

- 10x greater risk than general population

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141
Q

Describe the management of breast Lobular Carcinomas insitu?

A

Regular follow up via Bilateral mastectomy

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142
Q

What is the most common type of breast cancer (>70%)?

A

Invasive ductal carcinoma

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143
Q

Describe the appearance of Invasive ductal carcinoma?

A
  • Variable histology

- Infiltrating cells in sheets cord & tubules

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144
Q

What Invasive ductal carcinoma grading system gives an indication of survival?

A

Bloom & Richardson Grading

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145
Q

What are the 3 morphological features for all types of breast cancers?

A
  1. Tubules
  2. Pleomorphism
  3. Mitoses
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146
Q

What makes up 10% of all invasive breast carcinomas?

A

Lobular carcinoma

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147
Q

Describe the appearance of Lobular carcinoma?

A
  • Signet ring cells & diffusely infiltrative

- Often multicentric & bilateral

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148
Q

Describe the prognosis of Lobular carcinoma?

A

Usually grade 2 & ER positive (85% 5yr survival)

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149
Q

What makes up 3% of all breast carcinomas?

A

Tubular carcinoma

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150
Q

Describe the appearance of Tubular carcinoma?

A
  • Well differentiated

- Grade 1

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151
Q

What % of Tubular carcinoma have a 5 year survival?

A

95%

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152
Q

What is the most common breast cancer in over 75 year olds?

A

Mucinous/Mucoid carcinoma

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153
Q

Describe the appearance of Mucinous/Mucoid carcinoma?

A
  • Well circumscribed tumour with lakes of mucin

- Well differentiated cells

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154
Q

What % of Mucinous/Mucoid carcinoma have a 5 year survival?

A

90%

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155
Q

List the 2 types of routes for breast metastases?

A
  1. Lymphatics- axillary & internal mammary nodes

2. Blood spread- lungs, bone, liver, brain etc

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156
Q

What should you do in all invasive cancers?

A

Ultrasound axilla

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157
Q

What should you do when the ultrasound shows abnormal axillary nodes?

A

Core biopsy

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158
Q

What should you do if the axillary node core biopsy comes back positive?

A

Axillary clearance

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159
Q

What should you do if the axillary node core biopsy comes back negative?

A

Sentinel Node biopsy with isotope & blue dye

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160
Q

What are the 5 pathological prognostic features of breast cancer?

A
  1. Size of tumour
  2. Type of tumour
  3. Grade of tumour
  4. Node status
  5. Hormone receptor status
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161
Q

What are the 2 hormone receptors affected in breast cancer?

A
  1. ER (oestrogen receptor)

2. PR (progesterone receptor)

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162
Q

What scoring system detects which hormone receptors are affected in breast cancer?

A

Allred score

  • Intensity 1-3
  • Proportion 1-5
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163
Q

What is the Nottingham Prognostic index & what does it do?

A
  • Provides an estimate of prognosis in an individual
  • Determines treatment & follow up
  • Application of indices based on significant factors
  • Allows stratification of treatment in controlled trials & evaluation of therapies
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164
Q

Describe the 3 factors involved in the Nottingham Prognostic index?

A
  1. Grade 1-3: grade 1= 1 point, grade 3= 3 points
  2. Nodal status: 0 nodes= 1 point, 1-3 nodes= 2 points, 4+ nodes= 3 points
  3. Size: cm x 0.2
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165
Q

What is the NPI for a good prognostic breast carcinoma group?

A

NPI <3.4

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166
Q

What is the NPI for an intermediate prognostic breast carcinoma group?

A

NPI 3.41 - 5.4

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167
Q

What is the NPI for a poor prognostic breast carcinoma group?

A

NPI >5.4

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168
Q

What are the 6 means of treatment for Invasive breast carcinomas?

A
  1. Mastectomy
  2. Lumpectomy + radiotherapy
  3. Axillary Surgery
  4. Hormone Therapy
  5. Chemotherapy
  6. Targeted Therapy
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169
Q

What does HER2 stand for?

A

Human epidermal growth factor receptor 2

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170
Q

What do 15-20% of breast cancers over-express?

A

HER2 gene

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171
Q

List 3 things that a HER2 over expression is associated with in breast cancer?

A
  1. Poor outcome
  2. May be related with response to chemo
  3. May be associated with poor response to hormone therapy
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172
Q

What treatment is available for HER2 positive breast cancer?

A

Trastuzumab (Herceptin)

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173
Q

What are 4 indicators of increased HER2 production?

A
  1. Increased gene copy number
  2. Increased mRNA transcription
  3. Increased cell surface receptor protein expression
  4. Increased release of receptor extracellular domain
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174
Q

List 4 other breast related malignancies?

A
  1. Metastatic disease
  2. Lymphoma
  3. Sarcoma
  4. Angiosarcoma
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175
Q

What are array studies?

A

Signature a collection of genes taken together to classify a distinct group of tumours

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176
Q

What are the 4 molecular subtypes for breast cancer?

A
  1. Luminal
  2. Her2
  3. Basal
  4. Normal
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177
Q

What are the 5 different oncotype differential diagnoses of breast cancer?

A
  1. ER
  2. HER2
  3. Proliferation
  4. Invasion
  5. House keeping
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178
Q

What is Oncotype Dx?

A

Tumor profiling test that helps determine the benefit of using chemotherapy in addition to hormone therapy to treat some estrogen receptor-positive (ER-positive) breast cancers

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179
Q

What makes the foetus develop reproductively into a male?

A

Sex determining region Y (SRY) on the Y chromosome

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180
Q

Where do the gonads arise from?

A

Embryonic urogenital ridges

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181
Q

Where do the genital ducts arise from?

A

Paired mesonephric & paramesonephric ducts

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182
Q

What do the mesonephric (Wolffian) ducts develop into?

A

Male structures

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183
Q

What do the paramesonephric (Müllerian) ducts develop into?

A

Female structures

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184
Q

What does SRY direct in the male foetus?

A

Gonad to become a testis, with spermatogonia, Leydig & Sertoli cells

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185
Q

What does testosterone from the Leydig cells stimulate in the male foetus?

A

Development of mesonephric duct structures

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186
Q

What happens if the foetus does not have testosterone from the Leydig cells?

A

Mesonephric ducts atrophy

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187
Q

What does Dihydrotestosterone promote in the male foetus?

A

Development of prostate, penis & scrotum

188
Q

What causes the regression of paramesonephric ducts in the male foetus?

A

Anti-Müllerian Hormone / Müllerian Inhibiting Substance from Sertoli cells

189
Q

What 6 structures does the Mesonephric ducts in the male foetus produce?

A
  1. Rete testis
  2. Efferent ducts
  3. Epididymis
  4. Vas deferens
  5. Seminal vesicle
  6. Trigone of bladder
190
Q

What 4 structures does the Urogenital sinus in the male foetus produce?

A
  1. Bladder (except trigone)
  2. Prostate gland
  3. Bulbourethral gland
  4. Urethra
191
Q

What happens without the SRY gene in the female foetus?

A
  • Gonad develops into an ovary with oogonia & stromal cells
  • Without testosterone, mesonephric ducts regress
192
Q

What 4 structures does the paramesonephric ducts in the female foetus produce?

A
  1. Oviducts
  2. Uterus
  3. Cervix
  4. Upper 1/3 of the vagina
193
Q

What 5 structures does the urogenital sinus in the female foetus produce?

A
  1. Bulbourethral glands
  2. Lower 2/3 of vagina
  3. Vestibule
  4. Bladder (except trigone)
  5. Urethra
194
Q

What structure does the Mesonephric ducts in the female foetus produce?

A

Trigone of bladder

195
Q

What do the Primordia of the external genitalia in males develop into?

A
  • Body & glans penis

- Corpora cavernosum

196
Q

What do the Primordia of the external genitalia in females develop into?

A
  • Body & glans of clitoris

- Labia

197
Q

What are the 3 foetal Primordia of the external genitalia?

A
  1. Genital tubercle
  2. Genital folds
  3. Genital swellings
198
Q

Describe the appearance of the fallopian tubes?

A
  • Lined by ciliated columnar epithelium
  • Complex plicae
  • Layers of smooth muscle
  • Peritoneum external surface
199
Q

Give an example of fallopian (ovarian) tube pathology?

A

Salpingitis

200
Q

What spectrum of diseases does Salpingitis come under?

A

Pelvic inflammatory disease

201
Q

List the potential infective causes of Salpingitis?

A
  1. Chlamydia trachomatis
  2. Mycoplasma
  3. Coliforms
  4. Streptococci
  5. Staphylococci
  6. Neisseria gonorrhoeae
202
Q

Describe Tuberculous salpingitis?

A
  • Uncommon

- Usually associated with tuberculosis of the endometrium

203
Q

Describe the signs & symptoms of Salpingitis?

A
  • Fever
  • Lower abdominal or pelvic pain
  • Pelvic masses if tubes distended with exudate
    or secretions
204
Q

List the 3 possible complications of Salpingitis?

A
  1. Adherence of tube to ovary: tubo-ovarian abscess
  2. Adhesions involving tubal plicae increase risk of tubal ectopic pregnancy (rupture of ectopic is life-threatening)
  3. Damage or obstruction of tube lumen may produce infertility which may not be easy to treat
205
Q

What can occur when endometriosis is also present in salpingitis?

A

Compromise ovarian tube function

206
Q

List 3 tubal malignancies?

A
  1. Primary adenocarcinomas (Papillary serous carcinoma)
  2. Endometrioid carcinoma
  3. Fallopian tube carcinoma
207
Q

When can Fallopian tube carcinomas occur?

A

BRCA1 mutations

208
Q

Where is about 10% of occult tubal malignancy present?

A

Fimbria of prophylactic salpingo-oophorectomies

209
Q

What do fallopian tube carcinomas often involve at the time of presentation?

A

Omentum & peritoneal cavity

210
Q

Where may the origin of some ovarian carcinomas be?

A

Fallopian tube

211
Q

What does STIC stand for?

A

Serous Tubal Intraepithelial Carcinoma

212
Q

Describe (STIC) Serous Tubal Intraepithelial Carcinoma?

A
  • Abnormal epithelium distal Fallopian tube
  • Limited by basement membrane (B) so in situ
  • Nuclear atypia (N) clearly seen
  • Likely precursor for high grade serous carcinoma
213
Q

What is mutation in (STIC) Serous Tubal Intraepithelial Carcinoma similar to?

A

Invasive tumour, including p53

214
Q

Describe the normal structure of an ovary?

A
  • Flat surface epithelium
  • Cortex: compact ovarian stroma, small functional cysts, germ cells
  • Medulla: hilus cells, vessels, nerves
215
Q

List 2 pathologies of ovaries?

A
  1. Non-neoplastic cysts

2. Polycystic ovaries (stein-leventhal syndrome)

216
Q

What are the 3 types of ovarian Non-neoplastic cysts?

A
  1. Inclusion
  2. Follicular
  3. Luteal
217
Q

List the 7 signs & symptoms of polycystic ovary disease (stein-leventhal syndrome)?

A
  1. Oligomenorrhea
  2. Hirsutism
  3. Infertility
  4. Obesity
  5. Over-production of androgens
  6. LH high
  7. FSH low
218
Q

Describe the appearance of polycystic ovaries (stein-leventhal syndrome)?

A
  • Enlarged
  • Multiple subcortical cysts 5-15mm in diameter
  • Thickened, fibrotic outer surface
  • Lined by granulosa cells with hypertrophic & hyperplastic luteinised theca interna
  • Absence of corpora lutea
  • Corpora albicantes (ovulation not occurring)
219
Q

What may polycystic ovaries (stein-leventhal syndrome) result in & why?

A

Type 2 diabetes due to insulin resistance

220
Q

What are the 3 cell types that make up the normal ovary?

A
  1. Surface (coelomic) epithelium
  2. Germ cells
  3. Sex cord/stromal cells
221
Q

What are the 2 risk factors for epithelial ovarian cancers?

A
  1. Nulliparity

2. Family history

222
Q

What may reduce the risk of epithelial ovarian cancers?

A

Prolonged oral contraceptive use

223
Q

What % of ovarian cancers are familial?

224
Q

What are ovarian cancers mostly related to?

A

BRCA1 & BRCA2 gene mutations

225
Q

What is the % lifetime risk of ovarian cancer in BRCA1 carriers?

226
Q

Is the risk of ovarian cancer higher in BRCA1 or BRCA2 carriers?

A

BRCA1 carrier

227
Q

What % of sporadic ovarian cancers have a BRCA mutation?

228
Q

What % of ovarian cancers have HER2 over expression?

A

35% (poor prognosis)

229
Q

What % of ovarian tumours have a KRAS mutation & what specific type of tumour is most prevalent for this?

A
  • ~30%

- Mucinous cystadenocarcinomas

230
Q

What % of ovarian cancers have a p53 mutation & what type of tumour is most prevalent for this?

A
  • ~50%

- High grade serous cancer

231
Q

What are the 4 genetic alterations associated with sporadic ovarian cancer?

A
  1. BRCA mutation
  2. HER2 over-expression
  3. KRAS mutation
  4. p53 mutation
232
Q

What are surface epithelial ovarian tumours classically thought to arise from?

A

Coelomic mesothelium on the surface of the ovary

233
Q

What are benign surface epithelial ovarian lesions usually?

A

Cystic (cystadenoma) with or without a solid stromal component (cystadenofibroma)

234
Q

What do surface ovarian epithelial tumours also have?

A

Intermediate, borderline category currently referred to as tumours of low malignant potential

235
Q

Describe a factor of ovarian tumours of low malignant potential?

A

Limited invasive potential & a much beter prognosis than overtly malignant ovarian carcinomas

236
Q

What are the 2 types of malignant epithelial ovarian tumours?

A
  1. Cystic (cystadenocarcinoma)

2. Solid (adenocarcinoma)

237
Q

What are the 5 types of ovarian carcinomas?

A
  1. High grade serous (HGSC, 70%)
  2. Endometrioid (10%)
  3. Clear-cell (10%)
  4. Low grade serous (LGSC, 5%)
  5. Mucinous (3%)
238
Q

Where are High grade serous carcinomas (HGSC) of the ovary though to often arise from?

A

Epithelial precursor lesions in the ovarian end of the Fallopian tubes

239
Q

Where are Endometrioid and clear cell carcinomas of the ovary probably from?

A

Ovarian endometriosis

240
Q

What is an Ovarian endometrioma also known as?

A

Chocolate cysts

241
Q

Describe the genetics of High grade serous carcinomas (HGSC)?

A
  • p53 & BRCA1 are typically abnormal

- Inability to repair double stranded DNA breaks leads to chromosomal instability & genomic chaos

242
Q

What are ovarian carcinomas in patients with BRCA1 almost always?

A

High grade serous carcinomas (HGSC)

243
Q

What are Low grade serous (LGSC) often associated with?

A

Borderline serous component

244
Q

What % of serous ovarian tumours are benign, borderline or malignant?

A
  • 60% benign
  • 15% borderline
  • 25% malignant
245
Q

What age group are benign serous ovarian tumours most prevalent?

A

30-40 years

246
Q

What age group are malignant serous ovarian tumours most prevalent?

A

45-65 years

247
Q

What % of ovarian cancers does HGSC account for?

248
Q

What 2 types of tumours are BRAF & K-RAS mutations common in?

A
  1. Borderline tumours

2. Low grade serous carcinomas (LGSC)

249
Q

Describe the morphology of benign serous tumours?

A
  • Large
  • Cystic (up to 30 - 40 cm) & filled with clear serous fluid
  • May be bilateral
  • Smooth shiny serosal covering
  • Lined by a single layer of tall columnar epithelium
  • Some cells ciliated
250
Q

Describe the morphology of borderline serous tumours?

A
  • Complex architecture
  • Mild cytologic atypia but no stromal invasion
  • Peritoneal implants may be present
251
Q

Describe the morphology of Serous carcinomas?

A
  • Anaplasia of cells

- Obvious stromal invasion

252
Q

What are Psammoma bodies?

A

Concentrically laminated calcified concretions

253
Q

Where are Psammoma bodies common?

A

Papillae of serous tumours in general

254
Q

What is the prognosis of benign & borderline serous tumours?

A

Excellent outcome (borderline tumours almost 100% survival, & even with peritoneal involvement nearly 75%)

255
Q

What is the prognosis for invasive serous carcinomas?

A

Poor & depends on stage at diagnosis

256
Q

What are the 3 types of mucinous ovarian tumours & how common are they?

A
  1. 10% Malignant (cystadenocarcinoma)
  2. 10% of Low malignant potential (borderline)
  3. 80% Benign
257
Q

What 2 factors is the diagnosis of mucinous ovarian tumours dependant on?

A
  1. Architectural complexity

2. Cytological atypia

258
Q

What can mimic primary ovarian mucinous carcinomas?

A

Metastases to the ovary from GI tract (‘Krukenberg tumours’)

259
Q

What type of tumours are more likely to be primary ovarian mucinous carcinomas?

A

Large unilateral tumours

260
Q

Describe the morphology of mucinous ovarian tumours?

A
  • Large
  • Multilocular
  • No psammoma bodies
  • Cysts lined by cells with abundant mucinous cytoplasm
261
Q

What is the prognosis of mucinous cystadenocarcinoma compared to serous?

A

Slightly beter than serous, but stage is more important than histologic type

262
Q

What are ovarian endometrioid carcinomas microscopically characterised by?

A

Neoplastic tubular glands, similar to those of the endometrium

263
Q

What is the most common type of ovarian endometrioid carcinoma?

264
Q

What % of ovarian endometrioid carcinomas are bilateral?

265
Q

~15-20% of women with ovarian endometrioid carcinomas also have what?

A

Endometrial carcinoma (most are low grade & many arise from endometriosis)

266
Q

How are endometrioid carcinomas like endometrial cancer?

A

Often lost the PTEN (‘phosphatase and tensin homolog’) tumour suppressor gene

267
Q

What is ovarian clear cell carcinoma also associated with?

A

Endometriosis

268
Q

95% of ovarian germ cell tumours are what?

A

Mature cystic teratomas (‘dermoid cysts’)

269
Q

What do totipotent germ cells differentiate into?

A

Mature cells of all 3 germ cell layers:

  1. Ectoderm
  2. Endoderm
  3. Mesoderm
270
Q

What is the most common presentation of germ cell tumours?

A
  • Young women as ovarian masses or are found incidentally on abdominal scans
  • May contain foci of calcification associated with bone or teeth
  • ~10% bilateral
271
Q

Describe the gross appearance of germ cell tumours?

A
  • Smooth capsule
  • Often filled with sebaceous secretion & matted hair
  • Sometimes, foci of bone & cartilage, nests of bronchial or GI epithelium, teeth & other recognisable lines of development also present
272
Q

What are 5% of ovarian teratomas in adults?

A

Immature cystic teratomas with immature neuroectodermal elements, associated with more aggressive behaviour

273
Q

What are teratomas in children?

A

Rare but much more often immature than in adults

274
Q

What occurs in 1% of ovarian teratomas?

A

Malignant transformation of one of the tissue elements (squamous carcinoma, adenocarcinoma, sarcomas etc)

275
Q

What are cystic ovarian teratomas prone to?

A

Torsion (presentation of 10% - 15% of cases), producing an acute surgical emergency

276
Q

What are 4 rare ovarian tumours?

A
  1. Dysgerminoma
  2. Embryonal carcinoma
  3. Yolk-sac tumour
  4. Choriocarcinoma
277
Q

What 3 things do ovarian sex cord-stomal tumours include?

A
  1. Granulosa cell tumours
  2. Theca cell tumours
  3. Sertoli-Leydig cell tumours
278
Q

When do granulosa cell tumours usually occur?

A

Postmenopausal women & are not rare

279
Q

What may granulosa cell tumours lead to & why?

A

Oestrogen over-production may lead to endometrial hyperplasia or endometrial carcinoma

280
Q

Describe Ovarian fibromas & thecomas?

A
  • Benign
  • Rare
  • Can over-produce oestrogens, esp thecomas
281
Q

What is Meig’s syndrome?

A

Combination of an ovarian fibroma with ascites & pleural effusion

282
Q

What cures Meig’s syndrome?

A

Removal of the tumour

283
Q

What is an ovarian tumour with ascites likely to be?

284
Q

Describe Brenner tumours?

A
  • Uncommon mixed surface epithelial-stromal tumours
  • Usually benign, unilateral, size variable, solid, circumscribed, yellowish
  • Often found incidentally
285
Q

Describe Brenner tumours histologically?

A

Nests of transitional epithelial cells with longitudinal nuclear grooves & abundant fibrous stroma

286
Q

What are the 5 clinical challenges for all ovarian tumours?

A
  1. Often asymptomatic until well advanced
  2. Clinical presentations often similar despite biological diversity
  3. Torsion common, producing severe abdominal pain
  4. Functioning ovarian tumours often come to attention because of the hormones they produce
  5. Abdominal swelling due to ascites is common of ovarian malignancy but is also seen in benign tumours
287
Q

List 5 common endometrial pathologies?

A
  1. Adenomyosis
  2. Endometriosis
  3. Endometrial polyps
  4. Endometrial hyperplasia
  5. Endometrioid adenocarcinoma
288
Q

List 3 other uterine pathologies?

A
  1. Leiomyoma
  2. Leiomyosarcoma
  3. Endometrial stomal sarcoma
289
Q

What happens to the foetal coelomic lining epithelium at around 6 weeks?

A

Forms the lateral müllerian ducts, which grow downwards into the pelvis & fuse with the urogenital sinus

290
Q

What does the fused portion of the müllerian ducts become?

291
Q

What does the remaining unfused portion of the müllerian ducts become?

A

Fallopian tubes

292
Q

What 3 gynaecological organs are derived from the coelomic lining?

A
  1. Endometrial cavity
  2. Linings of fallopian tubes
  3. Peritoneal covering
293
Q

What are abnormalities of the uterus related to?

A

Foetal abnormalities in the fusion of the müllerian ducts

294
Q

List the 5 classes of uterine developmental abnormalities?

A
  1. Class U1- dysmorphic uterus
  2. Class U2- septet uterus
  3. Class U3- bicorporeal uterus
  4. Class U4- hemi uterus
  5. Class U5- aplastic uterus
295
Q

Describe the basic histology of the uterine endometrium?

A

Consists of glands & stroma & has a variety of normal appearances depending on the phase of the menstrual cycle, menopausal status etc

296
Q

Describe the basic histology of the uterine myometrium?

A

Smooth muscle comprising much of the uterus

297
Q

Describe the 3 stages of the normal menstrual cycle?

A
  1. Proliferative phase: stratification in basal area, mitotic activity in dividing area
  2. Secretory phase: ovum released from ovary & corpus luteum formed in ovary at day 14, glands are enlarged. Secretion during the progesterone development of vacuoles
  3. Menstrual phase: occurs when we don’t have implantation of a fertilised egg, the cells in stroma are close together, there is apoptosis
298
Q

Describe the histological appearance of endometrium in a post-menopausal woman?

A
  • Endometrium becomes very thin
  • Less glands
  • Nucleus takes over the small cells
299
Q

What is endometriosis?

A

The presence of endometrial tissue outside of the uterus

300
Q

What is adenomyosis?

A

The presence of endometrial tissue within the myometrium

301
Q

List 8 sites of endometriosis?

A
  1. Ovaries
  2. Peritoneal surfaces (including uterine ligaments & rectovaginal septum)
  3. Large & small bowel
  4. Appendix
  5. Mucosa of cervix,
  6. Vagina
  7. Fallopian tubes
  8. Laparotomy scars
302
Q

What are the 3 clinical symptoms of Endometriosis and adenomyosis?

A
  1. Dysmenorrhoea
  2. Pelvic pain
  3. Infertility
303
Q

What are the 2 pathogenesis theories regarding Endometriosis & adenomyosis?

A
  1. Metastatic theory

2. Metaplastic theory

304
Q

Describe the Metastatic theory for Endometriosis & adenomyosis?

A

Retrograde menstruation or surgical procedures introduce endometrium to sites outwith the uterine cavity

305
Q

Describe the Metaplastic theory for Endometriosis & adenomyosis?

A

Endometrium arises directly from the coelomic epithelium (i.e. peritoneum) of the pelvis, as this is where endometrium originates from during embryological development

306
Q

Describe the histological appearance of Endometriosis & adenomyosis?

A
  • Endometrial gland & stroma tissue embedded into the omentum
  • Scarring
  • Blood irritates the perineum –> scarring –> strictures –> pain
307
Q

What are endometrial polyps?

A

Exophytic masses of variable size which project into the endometrial cavity

308
Q

What drug is endometrial polyps associated with?

309
Q

How can endometrial polyps present?

A

Abnormal bleeding

310
Q

How can endometrial polyps be treated?

A

Hysteroscope in outpatient clinic

311
Q

Describe the histology of endometrial polyps?

A
  • Haphazardly arranged glands with preservation of a low gland to stroma ratio
  • Often thick walled blood vessels & fibrous stroma
  • The glands are usually inactive, but can also show
    proliferation, secretory changes or metaplasias
312
Q

What 2 things can be occasionally found in endometrial polyps?

A
  1. Cytological atypia

2. Frank adenocarcinoma

313
Q

What is Endometrial hyperplasia & adenocarcinoma associated with?

A

Prolonged oestrogenic stimulation of the endometrium

314
Q

List 3 possible underlying causes for Endometrial hyperplasia & adenocarcinoma?

A
  1. Anovulatory cycles
  2. Endogenous sources of oestrogen: obesity, PCOS,
    oestrogen secreting ovarian tumours
  3. Exogenous sources of oestrogen such as oestrogen only HRT
315
Q

What is the usual symptom for Endometrial hyperplasia & adenocarcinoma?

A

Postmenopausal bleeding

316
Q

Describe the histological appearance of endometrial hyperplasia?

A
  • Increased gland to stroma ratio

- Can be seen with or without cytological atypia

317
Q

What is atypical endometrial hyperplasia a known precursor of?

A

Endometrioid adenocarcinoma

318
Q

How would you manage endometrial hyperplasia?

A

Progesterone therapy such as Mirena IUS, or hysterectomy

319
Q

How would you manage endometrial adenocarcinoma?

A

Hysterectomy, with subsequent management depending on tumour grade & stage

320
Q

What is a Leiomyoma?

A

Benign smooth muscle tumour of the myometrium (maybe single or multiple)

321
Q

Describe the prevalence of Leiomyoma?

A
  • Very common
  • Atleast 25% of women, mostly of reproductive age
  • Incidence is over 70% by age 50
322
Q

List the 4 symptoms associated with Leiomyomas?

A
  1. Asymptomatic
  2. Abnormal bleeding
  3. Urinary frequency if large
  4. Impaired fertility
323
Q

Describe the histology of Leiomyomas?

A
  • Variable size
  • Sharply demarcated round grey-white tumours with a whorled cut surface
  • Well circumscribed
  • Don’t have areas of haemorrhage or necrosis
  • Don’t invade into myometrial surface
324
Q

How would you manage Leiomyomas?

A
  • Varies depending on number, size & symptoms
  • Medical: progesterone secreting IUS, hormonal
    therapies, tranexamic acid, GnRH agonists
  • Surgical: uterine artery embolisation, myomectomy,
    hysterectomy
325
Q

What is a Leiomyosarcoma?

A

Uncommon malignant smooth muscle tumour of the myometrium (1-2% of uterine malignancies, commonest uterine sarcoma)

326
Q

Describe the prevalence of Leiomyosarcoma?

A

Peak incidence age 40-60 years, can be pre- or post- menopausal

327
Q

Describe the symptoms of Leiomyosarcoma?

A

Initially none, then bleeding or pain

328
Q

Describe the macro-pathology of Leiomyosarcoma?

A

Bulky invasive masses or polypoid, necrosis, haemorrhage & variable cut surface

329
Q

Describe the micro-pathology of Leiomyosarcoma?

A

Overt cytological atypia, necrosis, mitotic

activity, infiltrative margin

330
Q

Describe the prognosis for Leiomyosarcoma?

A
  • Spread to lungs, liver & brain

- 40% 5 year survival

331
Q

What are Endometrial stromal sarcomas (ESS)?

A

A group of rare tumours of the endometrial stroma (can be low or high grade)

332
Q

Describe the growth pattern of Endometrial stromal sarcomas (ESS)?

A

Diffusely infiltrative “worm like” growth pattern macroscopically & microscopically

333
Q

Describe the microscopic appearance of Endometrial stromal sarcomas (ESS)?

A

Low grade tumour cells resemble cells of proliferating endometrial stroma, with mitoses

334
Q

Why are products of conception sent to a pathology lab in some situations?

A
  • Usually to confirm intrauterine pregnancy & look for placentally derived chorionic villi/implantation site
  • Identify gestational trophoblastic disease: partial & complete hydatidiform moles & choriocarcinoma
335
Q

What is gestational trophoblastic disease?

A

Umbrella term for several conditions including hydatidiform moles (partial & complete) & malignant tumours including choriocarcinoma

336
Q

How to hydatidiform moles present?

A

Either spontaneous miscarriage or abnormalities detected on ultrasound

337
Q

Describe how a partial mole is formed?

A

Fertilisation of 1 egg by 2 sperm, resulting in a triploid karyotype

338
Q

Describe the microscopic appearance of a partial mole?

A

Oedematous villi & subtle trophoblast proliferation

339
Q

What is the risk of a partial mole?

A

Invasive mole, which invades & destroys the uterus

340
Q

How is a complete mole formed?

A
  • Fertilisation of an egg with no genetic material, usually by 1 sperm which duplicates its chromosomal material
  • 10% occur when an egg with no genetic material is fertilised by 2 sperm
  • Diploid karyotype, usually 46 XX
341
Q

What is the microscopic appearance of a complete mole?

A

Markedly enlarged oedematous villi with central cisterns & circumferential trophoblast proliferation

342
Q

Describe the 2 risks of a complete mole?

A
  • 10% risk of invasive mole

- 2.5% risk of choriocarcinoma

343
Q

Describe choriocarcinoma & how its treated?

A
  • Frankly malignant, rapidly invasive & metastastises widely
  • Treatable with chemotherapy
344
Q

What are the 4 special characteristics of cancer cells?

A
  1. Uncontrolled proliferation
  2. Loss of original function (anaplasia)
  3. Invasiveness
  4. Metastasis (malignant cells)
345
Q

What are the 3 treatments available for cancer therapy?

A
  1. Surgical removal- only for solid tumours & non-metastasised
  2. Irradiation- only if localised
  3. Chemotherapy with anticancer drugs- selective toxicity required
346
Q

Describe how normal cells become cancer cells?

A
  • DNA change
  • Multi-stage process
  • Usually regulatory genes become mutated
347
Q

What are the 2 main categories of genetic change in cancer cells?

A
  1. Inactivation of tumour suppressor genes

2. Activation of proto-oncogenes to oncogenes

348
Q

What do cancer chemotherapy drugs mainly effect?

A

Cell division (affect all rapidly dividing normal tissue)

349
Q

What 3 things do anticancer drugs not reverse?

A
  1. De-differentiation
  2. Invasiveness
  3. Metastasis
350
Q

List 7 general toxic effects of anticancer drugs?

A
  1. Bone marrow suppression
  2. Loss of hair
  3. Damage to GI epithelium
  4. Liver, heart, kidney
  5. In children, depression of growth
  6. Sterility
  7. Teratogenicity (damage to embryo)
351
Q

What are 4 effects of anticancer’s bone marrow suppression?

A
  1. Anaemia
  2. Immune depression
  3. Prone to infection
  4. Impaired wound healing
352
Q

What are the 4 phases in the normal cell division cycle?

A
  1. G1 phase
  2. S-phase
  3. G2 phase
  4. Mitosis
353
Q

What happens in the mitosis phase of the normal cell division cycle?

A
  • Nuclear division
  • Cytokinesis
  • Can lead to G0 phase which is irreversible differentiation
354
Q

What are the anticancer drugs called that are active only on dividing cells?

A

Cell-cycle specific drugs

355
Q

What are the anticancer drugs called that are active on diving and resting cells?

A

Cell cycle-non specific

356
Q

What cells are less sensitive to anticancer drugs?

A

Resting (G) phase cells

357
Q

What 3 things does a solid tumour consist of?

A
  1. Dividing cells: progressing through cell cycle
  2. Resting cells: not dividing but could do so
  3. Cells which can no longer divide but contribute to tumour size (not a problem)
358
Q

What cells cause many relapses of cancer?

A

Resting cells (insensitive to many drugs)

359
Q

What can lead to severe cumulative toxicity?

A

Prolonged treatment required to reduce chance of relapse from resting cells

360
Q

List the 5 main classes of cancer chemotherapy drugs?

A
  1. Alkylating agents
  2. Antimetabolites
  3. Cytotoxic antibiotics
  4. Microtubule inhibitors
  5. Steroid hormones & antagonists
361
Q

Describe how Alkylating agents work (chemotherapy)?

A
  • Form covalent bonds with DNA
  • Interfere with both transcription & replication
  • Most have 2 reactive groups
  • Allow the drug to cross-link
362
Q

Give 5 examples of Alkylating agents (chemotherapy)?

A
  1. Nitrogen mustards
  2. Cysplatin
  3. Temozolomide
  4. Lomustine
  5. Busulphan
363
Q

Give 4 examples of Nitrogen mustards (alkylating chemotherapy agents)?

A
  1. Melphalan
  2. Chlorambucil
  3. Cyclophosphamide
  4. Ifosfamide
364
Q

What should you remember about Lomustine (alkylating chemotherapy agents)?

A

Can penetrate brain

365
Q

What should you remember about Busulphan (alkylating chemotherapy agents)?

A

“Selective” effect on bone marrow

366
Q

Describe the anticancer drug Mechlorethamine (Nitrogen mustards)?

A
  • First anticancer chemotherapy drug
  • Blister agent
  • Used to treat Hodgkin’s lymphoma, non-Hodgkins lymphoma
  • Highly reactive: must be given IV
367
Q

What is phenylalanine a precursor for?

368
Q

Describe Melphalan (Nitrogen mustards)?

A
  • Much more stable, less agressive
  • Absorption & distribution possible without extensive alkylation
  • Oral drug
369
Q

What 3 things is Melphalan (Nitrogen mustards) used to treat?

A
  1. Myeloma
  2. Ovarian cancer
  3. Breast cancer
370
Q

Describe Cyclophosphamide (Nitrogen mustards)?

A
  • Prodrug, with activation in the liver by phosphoramidase

- Much less toxic

371
Q

What protects against Cyclophosphamide (Nitrogen mustards) toxicity?

A

Aldehyde dehydrogenase (ALDH)

372
Q

Where is Aldehyde dehydrogenase (ALDH) present?

A
  • Bone marrow cells
  • Hepatocytes
  • Intestinal epithelium
373
Q

What does Cisplatin (other DNA cross-linker) target?

A

N7 of purine nucleotides

374
Q

What 2 things are Cisplatin (other DNA cross-linker) resistant from?

A
  1. Nucleotide excision repair mechanisms

2. Efflux transporters for Copper

375
Q

How to antimetabolites (anticancer drugs) work?

A

Interfere with nucleotide synthesis or DNA synthesis

376
Q

Give 3 examples of nucleotide synthesis: antifolates (antimetabolites)?

A
  1. Methotrexate
  2. Ralitrexed
  3. Pemetrexed
377
Q

Give 5 examples of Nucleotide analogues (antimetabolites)?

A
  1. 5-fluorouracil
  2. Cytarabine (Ara-C)
  3. Gemcitabine
  4. Fludarabine
  5. Capecitabine
378
Q

Describe Folate antagonists: Methotrexate?

A
  • Higher affinity for Dihydrofolate reductase than folic acid
  • Inhibition of dihydrofolate formation
  • Inhibition of purine/pyrimidine nucleotide synthesis
  • Ultimately, halt to DNA & RNA synthesis
379
Q

Describe Pyrimidine analogues: Fluoro-uracil?

A
  • Prevents thymidine formation

- Stops DNA synthesis

380
Q

Describe Purine analogues: Mercaptopurines?

A
  • Converted into false nucleotides
  • Disrupts purine nucleotide synthesis
  • Maybe incorporated into DNA, disrupting helix
381
Q

What does the incorporation of Cytarabine (nucleotide analogue) into DNA cause?

A

Inhibits DNA polymerases & causes chain termination

382
Q

What do cytotoxic antibiotics (anticancer) mainly act by?

A

Direct action on DNA as intercalators

383
Q

What is Dactinomycin (cytotoxic Antibiotics) isolated from?

A

Streptomyces

384
Q

Describe how Dactinomycin (cytotoxic Antibiotics) works?

A
  • Inserts itself into the minor groove in the DNA helix

- RNA polymerase function is disrupted

385
Q

What is Doxorubicin (cytotoxic antibiotic) from?

A

Streptomyces

386
Q

Describe how Doxorubicin (cytotoxic antibiotic) works?

A
  • Inserts itself between base pairs
  • Binds to the sugar-phosphate DNA backbone
  • Local uncoiling
  • Impaired DNA & RNA synthesis
387
Q

Give an example of a microtubule inhibitor anticancer drug?

A

Vinca alkaloids (Vincristine)

388
Q

Describe how Vinca alkaloids (Vincristine) works?

A
  • Bind to microtubular protein
  • Block tubulin polymerisation
  • Block normal spindle formation
  • Disrupt cell division
389
Q

Give 2 examples of steroid hormones that you can use in cancer?

A
  1. Prednisone

2. Prednisolone

390
Q

Describe Prednisone?

A
  • Synthetic adrenocortical steroid hormone

- Converted in the body to active form

391
Q

Describe how Prednisolone works?

A

Suppresses lymphocyte growth

392
Q

Give an example of hormone antagonists that you can use in breast cancer?

393
Q

How does Tamoxifen work?

A

Antagonist of oestrogen receptor

394
Q

What else can Tamoxifen treat, other than breast cancer?

A

Ovulatory infertility

395
Q

What are 2 ways of treating prostate cancer?

A
  1. Testosterone receptor antagonist

2. Pituitary downregulators

396
Q

Give 2 examples of Testosterone receptor antagonist used to treat prostate cancer?

A
  1. Flutamide (Drogenil)

2. Now replaced by Bicalutamide (Casodex)

397
Q

Give an example of Pituitary downregulators used to treat prostate cancer?

A

Luteinising hormone releasing hormone (LHRH) agonist (Prostap)

398
Q

Describe how Prostap drug works for treating prostate cancer?

A
  • Inhibit release of Luteinising Hormone (LH) which normally stimulates testes to produce testosterone
  • Most prostate cancers are dependent on testosterone
399
Q

What are the 4 common conditions of the ovaries?

A
  1. Cysts
  2. Polycystic ovaries syndrome
  3. Tumors- benign & malignant
  4. Torsion
400
Q

What are the 5 common symptoms of ovarian pathology?

A
  1. Menstrual irregularities
  2. Pain
  3. Hirsuitism/Metabolic syndrome (PCOS)
  4. Asymptomatic
  5. Bloated abdomen (ascites)
401
Q

What are 3 ways to investigate ovarian pathology?

A
  1. Physical examination- normal (ascites)
  2. Serology- CA 125
  3. Ultrasound
402
Q

What is a Krukenberg tumour?

A

Malignancy in the ovary that metastasized from a primary site, classically the gastrointestinal tract

403
Q

Describe a Dermoid cyst?

A

Abnormal growth (teratoma) containing epidermis, hair follicles, & sebaceous glands, derived from residual embryonic cells

404
Q

What would a ultrasound colour doppler image appear like for ovarian torsion?

A
  • Absence of blood flow

- Whirlpool sign

405
Q

What are 2 common fallopian tube conditions?

A
  1. Tubo-ovarian abscess

2. Ectopic pregnancy

406
Q

List the signs & symptoms of Tubo-ovarian abscess?

A
  • Pelvic pain
  • WCC/CRP increased
  • Temperature
  • Discharge
407
Q

List the signs & symptoms of ectopic pregnancy?

A
  • Pain
  • Missed period
  • bHCG increased
  • Circulatory collapse
408
Q

Describe the appearance of a Tubo-ovarian abscess on transabdominal ultrasound scan?

A
  • Bilateral complex cystic adnexal masses
  • No ovary can be identified that is separate from this collection
  • Air in the endometrium & endometritis
409
Q

What are 3 common condtions of the uterus?

A
  1. Uterine fibroids
  2. Endometriosis
  3. Uterine cancer
410
Q

What are the 4 signs & symptoms of uterine fibroids?

A
  1. Heavy periods
  2. Pain
  3. Pressure
  4. Anaemia in woman of child bearing age
411
Q

What are the 4 signs & symptoms of uterine endometriosis?

A
  1. Progressively painful periods
  2. Dyspareunia (pain during sex)
  3. Pain with bowel movements
  4. Abdominal pain
412
Q

What are the 2 means of treatment for uterine endometriosis?

A
  1. Hormonal therapy

2. Analgesia

413
Q

How do you diagnose uterine endometriosis?

A

Laparoscopy (imaging not helpful in early disease)

414
Q

What are the 2 signs & symptoms of uterine (endometrial) cancer?

A
  1. Post menopausal bleeding/Abnormal bleeding

2. Pain

415
Q

How would you diagnose cervical cancer?

A

Smear test (also can do ultrasound & MRI)

416
Q

What are the 3 signs & symptoms for cervical cancer?

A
  1. Abnormal bleeding
  2. Discharge
  3. Pain
417
Q

What are the 2 common vaginal pathologies?

A
  1. Bartholin cysts

2. Vaginal cancer

418
Q

Describe an Bartholin cyst?

A
  • Small fluid-filled sac just inside the opening of a vagina
  • Soft, painless lump that doesn’t usually cause problems
  • Caused by a blocked secretory duct
419
Q

What does dyskaryosis imply?

A

Definitely abnormal nuclei & the most likely reason for their presence is significant cervical intraepithelial neoplasia or CIN

420
Q

What is the reason for cervical screening?

A

Detecting CIN (cervical intraepithelial neoplasia)

421
Q

What is CIN?

A

Pre-malignant lesion which can be treated before it becomes a cancer

422
Q

What is the cervix external os?

A

Opening into endocervical canal

423
Q

What is Koilocytes in the cervix a sign of?

A

Viral infection (human papilloma virus) in the epithelial cells of the squamous cervical mucosa

424
Q

Describe Herpes Simplex Virus II (HSV II) and cervical cancer?

A

Common genital infection but there is no definite evidence it has a significant role in cervical cancer

425
Q

Describe Cytomegalovirus (CMV) & Human Herpes virus 8 (HHV-8) and cervical cancer?

A

Other members of the herpes virus family but they are not involved in cervical cancer

426
Q

What does Human Herpes virus 8 (HHV-8) have a role in?

A

Kaposi’s sarcoma, usually in immunocompromised individuals

427
Q

What is the most appropriate treatment for a cervical HPV infection & why?

A
  • Loop excision of the transformation zone (LETZ) treats abnormal epithelium & assesses lesion by histopathology, confirms CIN & makes sure there is no invasive cancer
  • Cone biopsy with scalpel is also effective & appropriate when LETZ is not available
428
Q

What has replaced the a “Pap” smear?

A

Liquid based cytology (LBC)

429
Q

Describe the appearance of normal cervical squamous cells in cervical cytology?

A

Abundant cytoplasm & small regular nuclei

430
Q

What does the different cell cytoplasm colours in a cervical cytology reflect?

A

Differences in keratinisation & are not especially significant, the nuclear changes are more important

431
Q

Describe the appearance of Koilocyte cells in cervical cytology?

A

‘Clearing’ of the cytoplasm around the nucleus of the cell & is a reliable sign of HPV infection

432
Q

Describe the appearance of moderate dyskaryosis cells (likely CIN 2) in cervical cytology?

A

As well as some normal looking nuclei there are also enlarged nuclei with abnormally coarse looking chromatin

433
Q

Describe the appearance of severe dyskaryosis cells (likely CIN 3) in cervical cytology?

A
  • Some normal squamous cells & also scattered cells with similar dyskaryotic nuclei & much less cytoplasm (ie the nucleus-to-cytoplasm ratio is abnormally high) - Also a scattering of inflammatory cells
434
Q

Describe the appearance of invasive squamous carcinoma in cervical cytology?

A

‘Dirty looking’ smear reflects necrosis & inflammation

435
Q

What is the ectocervix (up to the transformation zone) lined by?

A

Non-keratinising stratified squamous

436
Q

Where would simple squamous epithelium be found?

A

Alveoli of lungs

437
Q

Where would simple columnar epithelium be found?

A

Digestive tract

438
Q

Where would pseudostratified columnar epithelium be found?

439
Q

Where would transitional epithelium be found?

A

Urinary tract

440
Q

Describe the shedding process in cervix non-keratinising stratified epithelium?

A

Stem cells in the basal layer divide asymmetrically to yield a cell which remains as a stem cell & a cell which will proliferate to supply the new cells which will mature as they migrate from the bottom of the epithelium to the top where the differentiated cells are finally shed

441
Q

Where are mitoses most likely to be seen in normal cervical stratified squamous epithelium?

A

Proliferative zona just above the basal layer of cells

442
Q

What is the cervical epithelium “transit amplifying” population of cells?

A

A population of cells which is proliferating to make enough new cells to supply the need for renewal of a tissue

443
Q

The cervical epithelial cells _______ towards the surface?

A

Flatten out

444
Q

What is the endocervix lined by?

A

Glandular, columnar mucosa

445
Q

What is cervical glandular intraepithelial neoplasia like?

A

Squamous cervical intraepithelial neoplasia & is also a cancer precursor

446
Q

What cervical neoplasms can both be present in the one patient simultaneously?

A

CIN & CGIN

447
Q

What is the most striking abnormality in a histology of cervical intraepithelial neoplasia (CIN)?

A

Imbalance between the zone of proliferation, which is greatly increased, & the zone of differentiation, which is reduced

448
Q

What are 3 histological signs of HPV infection?

A
  1. Koilocytes
  2. Dyskeratosis
  3. Binucleate or multinucleate cells
449
Q

More than ___ of the epithelium is not differentiating in CIN3?

450
Q

What histological feature has to be apparent for a squamous carcinoma?

A

Invasion through the basement membrane

451
Q

What are 3 treatment options for an established invasive squamous carcinoma?

A
  1. Radical surgery
  2. Lymph node dissection
  3. Radiotherapy may have a role in some cases
452
Q

Describe the histological appearance of a moderately differentiated invasive squamous carcinoma?

A
  • Irregular cords & islands of abnormal squamous cells infiltrate deeply into the subjacent connective tissue of the cervix
  • Associated inflammation
453
Q

What do almost all cervical cancers have?

A

HPV infection (HPV 16, 18)

454
Q

What are genital warts associated with?

455
Q

What are common warts associated with?

456
Q

Describe the histological appearance of a polypoid lesion on the cervix external os?

A

Normal-looking endocervical glandular epithelium covering, fibromuscular & vascular connective tissue core

457
Q

Describe the prognosis of a polypoid lesion?

A

Cause is not understood but is not neoplastic & it has no malignant potential

458
Q

Describe the appearance of uterine fibroids (leiomyomas)?

A
  • Several firm, well-defined masses

- Cut section of these was paler than the surrounding myometrium & had a whorled, ‘watered silk’ appearance

459
Q

Uterine fibroids (leiomyomas) are usually ____?

460
Q

What abnormality is present in 40% of leiomyomas?

A

Clonal cytogenetic abnormalities (ie. Trisomy 12)

461
Q

What are the 3 uses of an MDT?

A
  1. Discuss the diagnosis in all patients who have had a biopsy
  2. Make a treatment plan
  3. To dicuss scan & possible metastatic cases
462
Q

List the 6 people who are at the MDT?

A
  1. Surgeons
  2. Pathologist
  3. Medical Oncologist
  4. Clinical Oncologist
  5. Breast care nurses
  6. Audit facilitator
463
Q

What are the 2 first treatments for breast cancer?

A
  1. Surgery (85%): Breast & Axilla

2. Neo-adjuvant treatment (15%)

464
Q

List 4 examples of Neo-adjuvant treatment?

A
  1. Radiotherapy
  2. Chemotherapy
  3. Endocrine
  4. HER2 target (Herceptin)
465
Q

What are the 3 local surgical treatments for breast cancer?

A
  1. Breast conserving surgery (75%)
  2. Mastectomy (25%)- standard or skin sparing with reconstruction
  3. Axillary surgery
466
Q

What are the 6 indications for mastectomy?

A
  1. 1+ tumour in breast
  2. Diffuse DCIS
  3. Large tumour & small breast
  4. Failed breast conserving surgery
  5. Recurrent breast cancer after previous surgery & radiotherapy
  6. Radiotherapy contraindicated e.g. pregnancy
467
Q

What are the 5 breast cancer post op things we should consider?

A
  1. Is Surgery Complete?
  2. Is Radiotherapy Needed?
  3. Which Adjuvant therapy?
  4. Prognostic Predictor Indices? (Nottingham prognostic index)
  5. Clinical Trials?

MBChB Year 3 (15 decks)

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