Disease of Reproductive System - Part 1 Flashcards Preview

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Flashcards in Disease of Reproductive System - Part 1 Deck (193):
1

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

Epithelial cells
Hence they are carcinomas

2

Do malignant tumours from connective tissue in the breast regularly?

No relatively rare
They are called sarcomas

3

What is a VIN

Vulval intraepithelial neoplasm

4

What is a CIN

Cervican intraepithelial neoplasm

5

What is CGIN

Cervical glandular intraepithelial neoplasm

6

What is a VaIN

Vaginal intraepithelial neoplasm

7

What is a AIN

Anal intraepithelial neoplasm

8

What are all the IN related to

HPV hence they often occur together

9

What is dysplasis

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

10

What are features of malignant cells

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

11

How many early and late genes are there in HPV

7 early
2 late

12

What are the low risk HPV types

6, 11

13

What are the high risk oncogenic HPV types

16, 18

14

What type of DNA is in HPV

Double stranded DNA

15

What % of cancers have HPV/DNA

99.7%
But the vast majority of HPV infections resolve themselves

16

What do the low risk HPV viruses cause

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

17

What is a condyloma

benign, squamous metaplasia

18

What do the high risk HPV viruses causes

high grade IN's, invasive carcinomas

19

What does the cervavarix vaccine protect against

16, 18

20

What does the gardasil virus protect agains

6, 11, 16, 18

21

Who is vaccinated against HPV

12/13 - catch up till 18

22

How does HPV cause cancer

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

23

What does E6 do

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

24

What does E7 do

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

25

What are the 2 forms of VIN

1) Classical
2) differentiated

26

Describe Classical VIN

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

27

Describe differentiated VIN

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

28

What is lichen sclerosus

Not curable
Affects vulva/penis
Can lead onto VIN

29

What makes progression in VIN more likely

Immunocomprised, post menopausal
Often get spontaneous regression in younger and post partum

30

What is the most common vulval cancer

Squamous cell carcinoma
Associated with VIN and inflammatory dermatoses (non HPV)

31

What is squamous cell vulval carcinoma

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

32

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

Wide excision, rarely will metastasis

33

Risk of metastasis of squamous cell vulval carcinomas

1-3mm invasion - 10%
Over 4mm = 40%

34

What age do malignant melanoma affcts

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

35

Describe malignant melanomas

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!

36

Who does Paget's disease usually affect

over 80

37

What type of cancer is page's disease

In situ adenocarcinoma of squamous mucosa

38

What happens in Paget's disease

Adenocarcinoma but usually no underlying tumours
Can develop invasive adenocarcinoma - same prognosis as squamous cell vulval carcinoma

39

What other tumours can cause paget's

Bladder, cervix, primary rectal

40

What epithelium is the vagina

stratified squamous

41

what epithelium is the cervix

simple columnar

42

What is the acquired transformational zone

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

43

What happens to the cervix in menopause

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

44

What is CIN

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

45

How do we treat grade I CIN

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

46

How do we treat grade II and III CIN

Treat these with cancer treatment etc.

47

Who do we test in the cervical screening programme

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

48

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

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

49

What is LLETS

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

50

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

HPV test

51

When do we do a colposcopy

If high grade cervical change or positive HPV test

52

What are the risk factors for cervical squamous cell carcinoma

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

53

How do we treat cervical adenocarcinoma

CIN/SCC

54

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

Due to radioresistance

55

Where do cervical carcinomas metastasise too

Pelvic and para-aortic lymph nodes
Via blood to lungs/bones

56

How do we stage cervical carcinomas

Use FIGO staging

57

What is endometriosis

Spread of the endometrium into the pelvis

58

What are the theories explaining endometriosis

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

59

How does endometriosis cause disease

Bleeding into tissues causing fibrosis

60

History of endometriosis

25% asymptomatic
Dysmennorhoea, dysparenunia, pelvic pain, subfertility

Late symptoms are pain on passing stool and dysuria

61

What investigations do you do for endometriosis

Laproscopy

62

Treatment of endometriossi

COCP, GnRH Agonists/antagonists, progesterone agents
Surgical - ablation or TAH-BSO depending on wish to remain fertile

63

What is endometriosis linked to

Ectopic pregnancy, ovarian cancer, IBD

64

What is endometriris

Inflammation of the endometrium

65

What causes acute endometritis

Retained POC/placenta, prolonged ROM, complicated labour

66

What do we see in acute endometritis

Neutrophils

67

What causes chronic endometritis

PID, retained gestational tissues, endometrial TB, IUCD infection

68

What do we see in chronic endometritis

Lymphocyes/plasma cells

69

History of endometriris

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

70

Investigations of endometritis

biochemistry/microbiology, USS

71

Treatment of endometritis

Analgesia to remove cause

72

What are endometrial polyps

Sessile/polypod oestrogen dependent uterine overgrowths

73

History of endometrial polyps

Often asymptomatic
Intermenstrual bleeding
Post menopausal bleeding
Menorrhagia
Dysmenorrhagia

74

Treatment of endometrial polyps

Expectant
Progesterone
GnRH agents
Surgical Cutterage

75

What % of endometrial polyps are malignant

Less than 1%

76

What investigations do we do of endometrial polyps

USS, hysteroscopy

77

What is a leimyomata

Benign myometrial tumours with oestrogen/progesterone dependent growth

78

Risk factors for leimyomata

Genetics, nullparity, obestiy, PCOS, HTN

79

Symptoms of leimyomata

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

80

Investigations of leimyomata

Bimanual examination
USS

81

Treatment of leimyomata

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

82

What is endometrial hyperplasia

Excessive endometrial proliferation
High oestrogen but low progesterone

83

Types of endometrial hyperplasia

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

84

History of endometrial hyperplasia

Abnormal bleeding (IMB, PCB, PMB)

85

Investigations of endometrial hyperplasia

USS, hysteroscopy +/- biopsy

86

Treatment of endometrial hyperplasia

IUS, progesterone, surgical (TAH

87

How does malignant hyperplasia progress

Normal
Non-atypical hyperplasi
Atypical hyperplasia
Endometrial carcinoma

88

What do we see in atypical hyperplasia

Complex patterns of proliferating glands with nuclear atypia

89

What do we see in non-atypical hyperplasia

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

90

What is the most common cancer of the female genital trct

Endometrial carcinoma

91

History of endometrial carcinoma

PMB/IMB, pain if late

92

investigation of endometrial carcinoma

USS, biopsy, hyterescopy

93

Staging of endometrial carcinoma

FIGO (1-4)

94

Treatment of endometrial carcinoma

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

95

Prognosis of different stages of endometrial carcinoma

Stage 1 - 90%
Stage 2 -3 :

96

What are the 2 types of endometrial carcinoma

Type 1 - endometrial
Type 2 - serous

97

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

Type 1 - 75%
Type 2 - 25%

98

Age of type 1 endometrial carcinoma

Pre/peri menopausal

99

Age of type 2 endometrial carcinoma

Post menopausal

100

Pre-existing state of type 1 endometrial carcinoma

Endometrial hyperplasia

101

Pre-existing state of type 2 endometrial carcinoma

Ednometrial atrophy

102

Mutation in type 1 endometrial carcinoma

Kras, PTEN

103

Mutation in type 2 endometrial carcinoma

p53

104

Oestrogen status of type 1 endometrial carcinoma

Oestrogen +ve

105

Oestrogen status of type 2 endometrial carcinoma

Oestrogen -ve

106

Grades of type 1 endometrial carcinoma

1-3

107

Grades of type 2 endometrial carcinoma

3

108

What is polycystic ovary syndrome

A complex endocrine disorder

109

What is the rotterdam criteria

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

110

What are the 3 rotterdam criteria

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

111

Investigations of polycystic ovary disease

USS, bioschemical screen

112

Biochemical results of polycystic ovary disease

Low FSH
High LH, testosterone, DHEAS

113

Treatment of polycystic ovary disease

Weight loss
Metformin, OCP, clomiphene
Ovarian drilling surgery

114

Links of polycystic ovary disease

Infertility, endometrial hyperpalsia, adenocarcinoma

115

What is primary gonadal failure

Hypertrophic hypogonadism
High LH and FSH to try and stimulate the gonads

116

Congenital causes of primary gonadal failure

45XO
47XXY

117

Acquired causes of primary gonadal failure

Infection
Surgery
Chemo/radiotherapy
Toxins/drugs

118

What is secondary gonadal failure

Hypotrophic hypogonadism

119

Causes of secondary gonadal failure

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

120

Presentation of gonadal failure

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

121

Investigation of gonadal failure

Hormonal and karyotyping

122

What are the 3 origins of ovarian neoplasms

Surface epithelium
Germ cell tumours
Sex cord stromal stumours

123

What are the 3 types of surface epithelium ovarian tumours

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

Each type can be benign or malignant

124

Name th benign tumours of surface epithelium ovarian neoplasm

Cystic - cystadenoma
Fibrous - adenofibroma
Cystic and fibrous - cystadenofibroma

125

Name the malignant tumour of surface epithelium neoplasia

Cystadenocarcinoma

126

What % of ovarian tumours are surface epithelium tumours

90%

127

What % of ovarian tumours are germ cell tumours

15-20%

128

What are the two types of germ cell tumours

Germinatous or non-germinatous

129

Name the type of germinatous germ cell tumours of the ovary

Dysgerminosa - differentiate towards again
Malignant
Respond to chemo

130

Do dysgerminosas respond to chemo

Yes

131

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

Teratomas
Yolk Sac
Choriocarcinomas

132

What do teratomas differentiate towards

Differentiated towards multiple germ layers

133

What do yolk sac tumours differentaite towards

The extramembryonic yolk sac

134

What do choriocarcinomas differentiate towards

Placenta

135

Describe mature teratomas

Benign, dermatoid cysts
Only 1% malignant

136

Describe immature teratomas

Malignant
Often contain immature fetal/embryonic tissue

137

Are yolk sac tumours responsive to chemo

Yes

138

Are choriocarcinomas responsive to chemo

No

139

Are choriocarcinomas malignant

Yes

140

Treatment of germ cell tumours of the ovary

Surgery +/- chemo if they are malignant

141

Where do sex cord stromal tumours arise from

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

142

What are the types of sex cord stromal tumours

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

143

What do thermos and fibrothecomas produces

Oestrogen and also rarely androgens

144

What do fibromas produce

Nothing they are hormonally inactive

145

What are thecomas/fibrothecomas/fibromas comprised of?

Comprised of spindle cells with lipid droplets - thecoma appearance

146

What is Meig's syndrome

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

147

What are granulosa cell tumours

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

148

What do granulosa cells do

Convert testosterone to oestrogen (thecoma cells also help)

149

What do setoli/leydig cells do

Produce androgen

150

What happens in sertoli/leydig cell tumours

Produce androgens and 10-25% of them are malignant

151

What increases your risk of ovarian cancer

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

Weak - obestiy and nullparity

152

What is protective from ovarian cancer

OCP, breast feeding, hysterectomy

153

History of ovarian cancers

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

154

What is the staging for ovarian tumours

FIGO

155

Treamtnet for ovarian tumours

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

Chemo in sensitive germ cell tumours

156

Prognosis of ovarian tumours

5 years survival - 43%

157

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

Uterus
Fallopian tubes
Pelvic peritoneum
Contralateral ovary

158

What are the metastatic extra mullerian metastatic tumours of ovarian cancer

Haematogenous and lymphatic spread to:

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

Breast, melanoma (kidneys and lungs less common)

159

Direct extension of ovarian tumours to where

Bladder and rectal

160

Prognosis of ovarian metastatic tumours

generally poor prognosis

161

Where do the majority of breast malignancies arise from

Epithelial cells hence carcinomas
Sarcomas are relatively rare

162

What type of tissue to tumours have more of

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

Fat is soft and translucent

163

What are the main priniciple ingredients of breast tissue

Fat
Fibrous tissue
Epithelial cells

164

What diffference in structure is there in younger breasts

Have more fibrous tissue
More opaque and lumpy therefore more difficult to find tumorus

165

What increaeses the risk of breast cancer

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

166

What is protective against breast cancer

Breastfeeding
Physical activity

167

When do you get invited to the breast screening programm

Every 3 years once you are 50
Some areas extended it from 47 to 73

168

How can breast cancer present

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

169

What is the triple assessment of breast abnormatlities

Clinical - examination/palpation
Radiological
Pathological - cytology or hystopathoogy

Discuss results in MDT meeting

170

What do we look for in radiology of breast abnormalities

Calcifications

171

What is fibrocystic change

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

Is fibrocystic change linked to breast cancer

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

173

What is a fibroadenoma

Common/mobile lumps - BENIGN
Biosy them - if fine leave them alone

174

What are fibroadomas aka Fibroepithelial neoplasma

Coordinated growth of glandular and connective (stromal) tissue

175

What are phyllodes tumours

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

Can benign tumours be moved about

Yes as they do not invade - may have sharp edges

177

What colour does cancer appear

White

178

Why do we get puckered skin/indrawn nipples

Due to fibrous tissue with fibroblasts in
Fibroblasts contract

179

What is Peau D'orange

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

Causes of inflammation/infection in the breast

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

181

Causes of nipple duct discharge

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

182

What is Paget's disease of the nipple

Ductal carcinoma in situ
Due to cancer cells growing up through ducts and colonising the skin - looks red

183

Describe pain in best

Can be cyclical and difficult to treat
Not a common presentation of breast cancer

184

Why do calcium crystals form in cancer

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

185

What should pathology reports of malignancy tell you

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

What type of carcinomas produce mucin

Mucinous carcinomas

187

What do lobular carcinomas look like

Indian files of cancer cells

188

What are the most common type of cancer

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

189

What is stage

how far a tumour has progressed

190

What is grade

How fast a tumour is progressing

191

What are two key stage indicators

Nodal status and size

192

If a tumour is oestrogen positive what does this mean

Can respond to oestrogen targeting agents

193

Why is HER2 status important

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