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CP - JL > Disease of Reproductive System - Part 1 > Flashcards

Disease of Reproductive System - Part 1 Flashcards

1
Q

What do the majority of the malignancies in the breast arise from

A

Epithelial cells

Hence they are carcinomas

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2
Q

Do malignant tumours from connective tissue in the breast regularly?

A

No relatively rare

They are called sarcomas

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3
Q

What is a VIN

A

Vulval intraepithelial neoplasm

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4
Q

What is a CIN

A

Cervican intraepithelial neoplasm

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5
Q

What is CGIN

A

Cervical glandular intraepithelial neoplasm

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6
Q

What is a VaIN

A

Vaginal intraepithelial neoplasm

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7
Q

What is a AIN

A

Anal intraepithelial neoplasm

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8
Q

What are all the IN related to

A

HPV hence they often occur together

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9
Q

What is dysplasis

A

The earliest morphological manifestation of neoplasia
It is in situ/non-incasive
If left significant change of progressing to invasive

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10
Q

What are features of malignant cells

A

Nuclear pleomorphism

Mitoses not in the basal layer (where they usually are)

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11
Q

How many early and late genes are there in HPV

A

7 early

2 late

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12
Q

What are the low risk HPV types

A

6, 11

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13
Q

What are the high risk oncogenic HPV types

A

16, 18

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14
Q

What type of DNA is in HPV

A

Double stranded DNA

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15
Q

What % of cancers have HPV/DNA

A

99.7%

But the vast majority of HPV infections resolve themselves

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16
Q

What do the low risk HPV viruses cause

A

Lower genital warts
Condylomas = benign, squamous neoplasia
Low grade IN

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17
Q

What is a condyloma

A

benign, squamous metaplasia

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18
Q

What do the high risk HPV viruses causes

A

high grade IN’s, invasive carcinomas

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19
Q

What does the cervavarix vaccine protect against

A

16, 18

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20
Q

What does the gardasil virus protect agains

A

6, 11, 16, 18

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21
Q

Who is vaccinated against HPV

A

12/13 - catch up till 18

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22
Q

How does HPV cause cancer

A

Early genes expressed at infection onset - control viral replication
Late genes code for cashed proteins
High risk HPV integrates itself into the host chromosome
Upregulate E6, and E7

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23
Q

What does E6 do

A

Binds to and inactivates p53

p53 is the fate keeper of the genome - mediates apoptosis in response to DNA damage

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24
Q

What does E7 do

A

Binds to the RB1 gene product

RB1 is a tumour suppressor gene that arrests cells in the G1/S phase

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25
Q

What are the 2 forms of VIN

A

1) Classical

2) differentiated

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26
Q

Describe Classical VIN

A

Warty/baseloid
Related to HPV
Generally younger people
Graded VIN 1-3

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27
Q

Describe differentiated VIN

A

Not graded
not HPV related
Generally older people
OCCURS IN PEOPLE WITH CHRONIC DERMATSOSES especially lichen sclerosus

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28
Q

What is lichen sclerosus

A

Not curable
Affects vulva/penis
Can lead onto VIN

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29
Q

What makes progression in VIN more likely

A

Immunocomprised, post menopausal

Often get spontaneous regression in younger and post partum

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30
Q

What is the most common vulval cancer

A

Squamous cell carcinoma

Associated with VIN and inflammatory dermatoses (non HPV)

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31
Q

What is squamous cell vulval carcinoma

A

Erodes plaque or ulcer
Spreads locally to include vagina and distal urethra
Spreads to ipsilateral inguinal lymph nodes ,then contralateral, then depp iliofemoral

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32
Q

Treatment of squamous cell vulval carcinoma with less than 1mm invasion

A

Wide excision, rarely will metastasis

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33
Q

Risk of metastasis of squamous cell vulval carcinomas

A

1-3mm invasion - 10%

Over 4mm = 40%

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34
Q

What age do malignant melanoma affcts

A

50-60 years old (5% of all vulval cancers)

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35
Q

Describe malignant melanomas

A

Local recurrent in 1/3, frequently spreads to the urethra
Lymph and haematogenous spread
Depth of invasion correlates with lymph node involvement
commonly pigmented but some aren’t
Not sunlight related at all!

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36
Q

Who does Paget’s disease usually affect

A

over 80

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37
Q

What type of cancer is page’s disease

A

In situ adenocarcinoma of squamous mucosa

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38
Q

What happens in Paget’s disease

A

Adenocarcinoma but usually no underlying tumours

Can develop invasive adenocarcinoma - same prognosis as squamous cell vulval carcinoma

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39
Q

What other tumours can cause paget’s

A

Bladder, cervix, primary rectal

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40
Q

What epithelium is the vagina

A

stratified squamous

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41
Q

what epithelium is the cervix

A

simple columnar

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42
Q

What is the acquired transformational zone

A

Physiological area of metaplasia in the vagina
Where squamous cell metaplasia has occurred
it is susceptible to HPV infection

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43
Q

What happens to the cervix in menopause

A

Decreased oestrogen
SCJ moves back up the cervix - but no metaplasia occurs
Difficult to swab here hence difficult to diagnose cancers post menopausal

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44
Q

What is CIN

A

The pre-invasive stage of squamous cell carcinoma - detect in the cervical screening programme

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45
Q

How do we treat grade I CIN

A

No treatment just observe as high rates of regression but low rates of regression

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46
Q

How do we treat grade II and III CIN

A

Treat these with cancer treatment etc.

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47
Q

Who do we test in the cervical screening programme

A

First call at age 25, every 3 years till 50, then every 5 years until 65

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48
Q

Why don’t we screen under 25’s in the cervical screening programme

A

High carriers of HPV - 70-80% will be eliminated
Relative changes due to normal reactions in young people produce confusing cytology
Unnecessary LLETZ can cause obstetric ocmplications

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49
Q

What is LLETS

A

Large loop excision of the transmission zone - to get rid of CIN

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50
Q

What do we do if the cervical screening test shows low grade change

A

HPV test

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51
Q

When do we do a colposcopy

A

If high grade cervical change or positive HPV test

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52
Q

What are the risk factors for cervical squamous cell carcinoma

A

HPV (most important)
Multiple sexual partners, male with multiple sexual partners, young age at first intercourse, high parity, low socioeconomic group, smoking (DNA adducts), immunosuppression

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53
Q

How do we treat cervical adenocarcinoma

A

CIN/SCC

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54
Q

Why is the stage for stage prognosis of cervical adenocarcinoma worse than cervical squamous cell carcinoma

A

Due to radioresistance

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55
Q

Where do cervical carcinomas metastasise too

A

Pelvic and para-aortic lymph nodes

Via blood to lungs/bones

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56
Q

How do we stage cervical carcinomas

A

Use FIGO staging

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57
Q

What is endometriosis

A

Spread of the endometrium into the pelvis

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58
Q

What are the theories explaining endometriosis

A

Regurgitation theory
Metaplasia theory
Stem cell theory
Metastasis theory - lymphatic spread

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59
Q

How does endometriosis cause disease

A

Bleeding into tissues causing fibrosis

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60
Q

History of endometriosis

A

25% asymptomatic
Dysmennorhoea, dysparenunia, pelvic pain, subfertility

Late symptoms are pain on passing stool and dysuria

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61
Q

What investigations do you do for endometriosis

A

Laproscopy

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62
Q

Treatment of endometriossi

A

COCP, GnRH Agonists/antagonists, progesterone agents

Surgical - ablation or TAH-BSO depending on wish to remain fertile

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63
Q

What is endometriosis linked to

A

Ectopic pregnancy, ovarian cancer, IBD

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64
Q

What is endometriris

A

Inflammation of the endometrium

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65
Q

What causes acute endometritis

A

Retained POC/placenta, prolonged ROM, complicated labour

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66
Q

What do we see in acute endometritis

A

Neutrophils

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67
Q

What causes chronic endometritis

A

PID, retained gestational tissues, endometrial TB, IUCD infection

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68
Q

What do we see in chronic endometritis

A

Lymphocyes/plasma cells

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69
Q

History of endometriris

A

Abdominal pain, pyrexia, discharge, dysuria, abdnormal vaginal bleeding

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70
Q

Investigations of endometritis

A

biochemistry/microbiology, USS

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71
Q

Treatment of endometritis

A

Analgesia to remove cause

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72
Q

What are endometrial polyps

A

Sessile/polypod oestrogen dependent uterine overgrowths

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73
Q

History of endometrial polyps

A 
Often asymptomatic
Intermenstrual bleeding
Post menopausal bleeding
Menorrhagia
Dysmenorrhagia
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74
Q

Treatment of endometrial polyps

A

Expectant
Progesterone
GnRH agents
Surgical Cutterage

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75
Q

What % of endometrial polyps are malignant

A

Less than 1%

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76
Q

What investigations do we do of endometrial polyps

A

USS, hysteroscopy

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77
Q

What is a leimyomata

A

Benign myometrial tumours with oestrogen/progesterone dependent growth

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78
Q

Risk factors for leimyomata

A

Genetics, nullparity, obestiy, PCOS, HTN

79
Q

Symptoms of leimyomata

A

Asymptomatic
Menometorrhagia (become iron deficient)
Sub-fertility/pregnancy problems
Pressure sx

80
Q

Investigations of leimyomata

A

Bimanual examination

USS

81
Q

Treatment of leimyomata

A

NSAIDS, IUS, OCP/Fe2+
Or
Artery embolization, ablation, TAH

82
Q

What is endometrial hyperplasia

A

Excessive endometrial proliferation

High oestrogen but low progesterone

83
Q

Types of endometrial hyperplasia

A

Atypical (unto 48% are carcinomas) or non-atypical (1-3% progress to carcinomas)

84
Q

History of endometrial hyperplasia

A

Abnormal bleeding (IMB, PCB, PMB)

85
Q

Investigations of endometrial hyperplasia

A

USS, hysteroscopy +/- biopsy

86
Q

Treatment of endometrial hyperplasia

A

IUS, progesterone, surgical (TAH

87
Q

How does malignant hyperplasia progress

A

Normal
Non-atypical hyperplasi
Atypical hyperplasia
Endometrial carcinoma

88
Q

What do we see in atypical hyperplasia

A

Complex patterns of proliferating glands with nuclear atypia

89
Q

What do we see in non-atypical hyperplasia

A

Whole overgrowth of the endometrium with simple tubular gland
Dilated and high gland to storm ratio

90
Q

What is the most common cancer of the female genital trct

A

Endometrial carcinoma

91
Q

History of endometrial carcinoma

A

PMB/IMB, pain if late

92
Q

investigation of endometrial carcinoma

A

USS, biopsy, hyterescopy

93
Q

Staging of endometrial carcinoma

A

FIGO (1-4)

94
Q

Treatment of endometrial carcinoma

A

Progesterone
Surgery (TAH-BSO)
Adjuvant therapy (chemo/radio)

95
Q

Prognosis of different stages of endometrial carcinoma

A

Stage 1 - 90%

Stage 2 -3 :

96
Q

What are the 2 types of endometrial carcinoma

A

Type 1 - endometrial

Type 2 - serous

97
Q

What % of cases are type 1 and type 2 endometrial carcinoma

A

Type 1 - 75%

Type 2 - 25%

98
Q

Age of type 1 endometrial carcinoma

A

Pre/peri menopausal

99
Q

Age of type 2 endometrial carcinoma

A

Post menopausal

100
Q

Pre-existing state of type 1 endometrial carcinoma

A

Endometrial hyperplasia

101
Q

Pre-existing state of type 2 endometrial carcinoma

A

Ednometrial atrophy

102
Q

Mutation in type 1 endometrial carcinoma

A

Kras, PTEN

103
Q

Mutation in type 2 endometrial carcinoma

A

p53

104
Q

Oestrogen status of type 1 endometrial carcinoma

A

Oestrogen +ve

105
Q

Oestrogen status of type 2 endometrial carcinoma

A

Oestrogen -ve

106
Q

Grades of type 1 endometrial carcinoma

A

1-3

107
Q

Grades of type 2 endometrial carcinoma

A

3

108
Q

What is polycystic ovary syndrome

A

A complex endocrine disorder

109
Q

What is the rotterdam criteria

A

A set of 3 symptoms, of which you must have 2 to have polycystic ovary disease

110
Q

What are the 3 rotterdam criteria

A 
Polycystic ovaries (20% f women have this)
Hyperanddrogenism (hirsuitism/biochemical)
Menstrual abnormalities (cycles over 35 days)
111
Q

Investigations of polycystic ovary disease

A

USS, bioschemical screen

112
Q

Biochemical results of polycystic ovary disease

A

Low FSH

High LH, testosterone, DHEAS

113
Q

Treatment of polycystic ovary disease

A

Weight loss
Metformin, OCP, clomiphene
Ovarian drilling surgery

114
Q

Links of polycystic ovary disease

A

Infertility, endometrial hyperpalsia, adenocarcinoma

115
Q

What is primary gonadal failure

A

Hypertrophic hypogonadism

High LH and FSH to try and stimulate the gonads

116
Q

Congenital causes of primary gonadal failure

A

45XO

47XXY

117
Q

Acquired causes of primary gonadal failure

A

Infection
Surgery
Chemo/radiotherapy
Toxins/drugs

118
Q

What is secondary gonadal failure

A

Hypotrophic hypogonadism

119
Q

Causes of secondary gonadal failure

A

Sheehans syndrome, pituitary tumour, brain injury, empty sella syndrome, PCOS

120
Q

Presentation of gonadal failure

A

Amenorrhea/absent menarche
Delayed puberty
Decreased sex hormones
Increased LH/FSH in primary

121
Q

Investigation of gonadal failure

A

Hormonal and karyotyping

122
Q

What are the 3 origins of ovarian neoplasms

A

Surface epithelium
Germ cell tumours
Sex cord stromal stumours

123
Q

What are the 3 types of surface epithelium ovarian tumours

A

Serous (tubular)
Mucinous (endocervical)
Endometrial (endometrial)

Each type can be benign or malignant

124
Q

Name th benign tumours of surface epithelium ovarian neoplasm

A

Cystic - cystadenoma
Fibrous - adenofibroma
Cystic and fibrous - cystadenofibroma

125
Q

Name the malignant tumour of surface epithelium neoplasia

A

Cystadenocarcinoma

126
Q

What % of ovarian tumours are surface epithelium tumours

A

90%

127
Q

What % of ovarian tumours are germ cell tumours

A

15-20%

128
Q

What are the two types of germ cell tumours

A

Germinatous or non-germinatous

129
Q

Name the type of germinatous germ cell tumours of the ovary

A

Dysgerminosa - differentiate towards again
Malignant
Respond to chemo

130
Q

Do dysgerminosas respond to chemo

A

Yes

131
Q

Name the type of non-germinatous germ cell tumours of the ovary

A

Teratomas
Yolk Sac
Choriocarcinomas

132
Q

What do teratomas differentiate towards

A

Differentiated towards multiple germ layers

133
Q

What do yolk sac tumours differentaite towards

A

The extramembryonic yolk sac

134
Q

What do choriocarcinomas differentiate towards

A

Placenta

135
Q

Describe mature teratomas

A

Benign, dermatoid cysts

Only 1% malignant

136
Q

Describe immature teratomas

A

Malignant

Often contain immature fetal/embryonic tissue

137
Q

Are yolk sac tumours responsive to chemo

A

Yes

138
Q

Are choriocarcinomas responsive to chemo

A

No

139
Q

Are choriocarcinomas malignant

A

Yes

140
Q

Treatment of germ cell tumours of the ovary

A

Surgery +/- chemo if they are malignant

141
Q

Where do sex cord stromal tumours arise from

A

They are rare but arise from ovarian stroma which was derived from the sex cord of an embryonic gonad

142
Q

What are the types of sex cord stromal tumours

A

Thecomas/fibromas/fibrothecomas
Granulosa cell tumours
Sertoli/Leydig Cell tumours

143
Q

What do thermos and fibrothecomas produces

A

Oestrogen and also rarely androgens

144
Q

What do fibromas produce

A

Nothing they are hormonally inactive

145
Q

What are thecomas/fibrothecomas/fibromas comprised of?

A

Comprised of spindle cells with lipid droplets - thecoma appearance

146
Q

What is Meig’s syndrome

A

Ovarian tumour (thecoma/fibroma) with RS hydrothorax and ascites

147
Q

What are granulosa cell tumours

A

Sex cord stromal cell tumours
They are low grade malignant
Produce oestrogen

148
Q

What do granulosa cells do

A

Convert testosterone to oestrogen (thecoma cells also help)

149
Q

What do setoli/leydig cells do

A

Produce androgen

150
Q

What happens in sertoli/leydig cell tumours

A

Produce androgens and 10-25% of them are malignant

151
Q

What increases your risk of ovarian cancer

A

FH, Elderly, PMH Breast cancer, oestrogen only HRT, Lynch II syndrome

Weak - obestiy and nullparity

152
Q

What is protective from ovarian cancer

A

OCP, breast feeding, hysterectomy

153
Q

History of ovarian cancers

A 
Non-specific symptoms (difficult to diagnose)
Pain
Bloating
Weight Loss
PV bleeding
Urinary frequenct 
Anorexia
154
Q

What is the staging for ovarian tumours

A

FIGO

155
Q

Treamtnet for ovarian tumours

A

Stage 1 - TAH/BSO
Amenectomy, appendectomy, lymphadenectomy and adjuvant chemom

Chemo in sensitive germ cell tumours

156
Q

Prognosis of ovarian tumours

A

5 years survival - 43%

157
Q

What are the metastatic mullerian tumours of ovarian cancer (most common)

A

Uterus
Fallopian tubes
Pelvic peritoneum
Contralateral ovary

158
Q

What are the metastatic extra mullerian metastatic tumours of ovarian cancer

A

Haematogenous and lymphatic spread to:

GI Tract: large bowel, stomach (called Krukenburg Syndrome), pancreatobilliary

Breast, melanoma (kidneys and lungs less common)

159
Q

Direct extension of ovarian tumours to where

A

Bladder and rectal

160
Q

Prognosis of ovarian metastatic tumours

A

generally poor prognosis

161
Q

Where do the majority of breast malignancies arise from

A

Epithelial cells hence carcinomas

Sarcomas are relatively rare

162
Q

What type of tissue to tumours have more of

A

Fibrous tissue - makes them hard and lumpy/radioopaque so we can see them more

Fat is soft and translucent

163
Q

What are the main priniciple ingredients of breast tissue

A

Fat
Fibrous tissue
Epithelial cells

164
Q

What diffference in structure is there in younger breasts

A

Have more fibrous tissue

More opaque and lumpy therefore more difficult to find tumorus

165
Q

What increaeses the risk of breast cancer

A 
Alcohol
Oestrogen containing pills
Body fatness
Height
Digoxin
Shiftwork - it disrupts the circadian rhythm
Smoking
166
Q

What is protective against breast cancer

A

Breastfeeding

Physical activity

167
Q

When do you get invited to the breast screening programm

A

Every 3 years once you are 50

Some areas extended it from 47 to 73

168
Q

How can breast cancer present

A 
Lumps
Puckered skin/indrawn nipple
Pain (rare)
Inflammation
Nipple discharge
Abnormal/sore nipple
Radiologically
169
Q

What is the triple assessment of breast abnormatlities

A

Clinical - examination/palpation
Radiological
Pathological - cytology or hystopathoogy

Discuss results in MDT meeting

170
Q

What do we look for in radiology of breast abnormalities

A

Calcifications

171
Q

What is fibrocystic change

A

Almost physiological group of changes
Ductal hyperplasia, apocrine metaplasia and cysts
Can mimic cancer clinically and pathologically
May present as a lump and associated with micro calcifications - hard for histopathologists to identify

172
Q

Is fibrocystic change linked to breast cancer

A

Unlikely to be a precursor

BUT some statistical link to breast cancer - probably as both are associated with high levels of oestrogen

173
Q

What is a fibroadenoma

A

Common/mobile lumps - BENIGN

Biosy them - if fine leave them alone

174
Q

What are fibroadomas aka Fibroepithelial neoplasma

A

Coordinated growth of glandular and connective (stromal) tissue

175
Q

What are phyllodes tumours

A

Rare fibroepithelial neoplasms - form a spectrum of lesions
One end of spectrum - looks like firoadomas
Other end of spectrum - may show overgrowth of stromal element - sarcomas so may recur

176
Q

Can benign tumours be moved about

A

Yes as they do not invade - may have sharp edges

177
Q

What colour does cancer appear

A

White

178
Q

Why do we get puckered skin/indrawn nipples

A

Due to fibrous tissue with fibroblasts in

Fibroblasts contract

179
Q

What is Peau D’orange

A

a pitted or dimpled appearance of the skin, especially as characteristic of some cases of breast cancer or due to cellulite.

It is an inflammatory carcinoma blocking the lymphatic capillaries causing oedema

180
Q

Causes of inflammation/infection in the breast

A

Mastitis during breast feeding
Breast abscesses and fistulae
TB
Carcinoma/sarcoma

181
Q

Causes of nipple duct discharge

A

Duct ectasia (dilation/distension)
Intraductal papilloma
In situ papillary carcinoma
INtracystic papillary carcinoma

182
Q

What is Paget’s disease of the nipple

A

Ductal carcinoma in situ

Due to cancer cells growing up through ducts and colonising the skin - looks red

183
Q

Describe pain in best

A

Can be cyclical and difficult to treat

Not a common presentation of breast cancer

184
Q

Why do calcium crystals form in cancer

A

Necrosis in centre of tumour

Causes influx of calcium and formation of calcium crystals (but other benign causes also are linked to cancer)

185
Q

What should pathology reports of malignancy tell you

A

1) in situ/invasive
2) type
3) Grade
4) Vascular Invasion - stage related
5) relationship to margins - close margins and lymph node involvement affect treatment
6) Nodal status
7) Size
8) ER, PR and HER2 status

186
Q

What type of carcinomas produce mucin

A

Mucinous carcinomas

187
Q

What do lobular carcinomas look like

A

Indian files of cancer cells

188
Q

What are the most common type of cancer

A

Ductal - 75%
Lobular - 12%
Tubular/cribiform - 3%

189
Q

What is stage

A

how far a tumour has progressed

190
Q

What is grade

A

How fast a tumour is progressing

191
Q

What are two key stage indicators

A

Nodal status and size

192
Q

If a tumour is oestrogen positive what does this mean

A

Can respond to oestrogen targeting agents

193
Q

Why is HER2 status important

A

Overexpression of HER2 on the membrane means they are likely to respond to Herceptin

CP - JL (14 decks)

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