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female genital tract pathology Flashcards

1
Q

what is the epidemiology of endometriosis?

A

6-10% of women aged 30-40 years old

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2
Q

what is the presentation of endometriosis?

A

25% are asymptomatic, if symptomatic then pain passing stool, pelvic pain, subfertility, dysparenuria and dysmenorrhoea

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3
Q

what are the investigations for endometriosis?

A

laparoscopy

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4
Q

what is the treatment for endometriosis?

A

medical - progesterone antagonist or GnRH agonists or antagonists or COCP
surgical - ablation or TAH-BSO

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5
Q

what are the associations with endometriosis?

A

ectopic pregnancy, ovarian cancer and IBD

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6
Q

what is the result and how is this reached for endometriosis?

A

ectopic endometrium (regurgitation/metaplasia/stem cell/metastasis theory) leading to bleeding into tissues and then fibrosis ultimately

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7
Q

what is inflammation of the endometrium?

A

chronic endometriosis with a predominant picture of lymphocytes and plasma cells in histology and is caused by foreign bodies or chronic retained products or infection

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8
Q

where is there increasing prevalence of inflammation of the endometrium?

A

with increasing chlamydia

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9
Q

what is the cause of inflammation of the endometrium?

A

retained gestational tissue, endometrial TB, IUCD infection

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10
Q

what is the presentation of inflammation of the endometrium?

A

abdo pain or pelvic pain, dysuria, discharge, abnormal vaginal bleeding and pyrexia

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11
Q

what is the investigations for inflammation of the endometrium?

A

biochemistry, microbiology or USS

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12
Q

what are the treatments for inflammation of the endometrium?

A

medical such as analgesia or ANX or removing the cause

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13
Q

what are endometrial polyps?

A

they are sessile/polypoid E2 dependent uterine overgrowths of which <1% are malignant. They are in less than 10% of women and this is in their 40-50s

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14
Q

what is the presentation of endometrial polyps?

A

often asymptomatic but can present with intermenstrual or post menopausal bleeding, menorrhagia or dysmenorrhoea

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15
Q

what are the investigations for endometrial polyps?

A

USS or hysteroscopy

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16
Q

what are the treatments for endometrial polyps?

A

medical (P4/GnRH agonists) or surgical (curettage)

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17
Q

what are leiyomyomas?

A

they are uterine fibroids - benign myometrial tumours with E2/P4 dependent growth that affect around 20% of women in the 30-50s and can result in menopausal regression and have a malignancy risk of 0.01%

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18
Q

what are the risk factors for leiyomyomas?

A

genetics, nullparity, obesity, PCOS and HTN

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19
Q

what is the history of leiyomyomas?

A

often asymptomatic, menorrhagia (leading to Fe deficienct anaemia), subfertility and pregnancy problems and pressure

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20
Q

what are the investigations for leiyomyomas?

A

bimanual examination or USS

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21
Q

what are the treatments for leiyomyomas?

A

medical or non medial
medical - NSAIDs, IUS, OCP, P4 or Fe2+
non medical - artery embolisation or ablation or TAH

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22
Q

what is endometrial hyperplasia?

A

it is excessive endometrial proliferation where E2 increases and P4 decreases and has a risk of progression to endometrial adenocarcinoma or regression

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23
Q

what are the types of endometrial hyperplasia?

A

there is simple: atypical or non atypical or complex: atypical or non atypical

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24
Q

what are the risk factors for endometrial hyperplasia?

A

obestiy, exogenous E2, PCOS, E2 producing tumours, tamoxifen, HNPCC (PTEN mutation)

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25
Q

what are the investigations for endometrial hyperplasia?

A

USS, hysteroscopy, biopsy

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26
Q

what are the presentations for endometrial hyperplasia?

A

abnormal bleeding - IMB, PCB, PMB

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27
Q

what are the treatments for endometrial hyperplasia?

A

medical - IUS or P4 or surgical TAH

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28
Q

how can endometrial hyperplasia produce cancer?

A

nedometrial hyperplasia to endometriod carcinoma is progression from simple hyperplasia through to complex atypical hyperplasia and invasive carcinoma. Simple is common and carcinoma is less frequent - the chances of progression through the pathway increase the farther down the pathway a woman is

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29
Q

what is the cause of simple hyperplasia and what is seen?

A

it is caused by excess oestrogens from a variety of possible sources and it shows an overgrowth of the whole epithelium therefore a thick endometrium on USS

30
Q

what happens in complex hyperplasia?

A

the glandular epithelium increases and the epithelium can be folded into complex architectural structures

31
Q

what happens in atypical/intraepithelial neoplasia?

A

the cells show architectural changes of neoplasia with increased nuclear cytoplasm ratio - larger nucleus and less cytoplasm and there are irregular shapes, increased number of mitoses and some of these are abnormal

32
Q

what is the malignant progression of hyperplasia?

A

when there is normal to non atypical hyperplasia which resembles normal proliferative endometrium, then atypical hyperplasia/endometrial intraepithelial neoplasia - presence of cytological abnormalitiy and then endometriod adenocarcinoma which shows invasion into the myometrium

33
Q

what is the presentation and investigations for endometrial adenocarcinoma?

A

the presentation is IMB or PMB or pain if late, and the investigations are USS biopsy and hysteroscopy

34
Q

what is the staging and treatment used for endometrial adenocarcinoma?

A

FIGO staging 1-4

medical P4, surgery TAH-BSO or adjuvnant therapy such as chemo or radiotherapy

35
Q

what is the prognosis of endometrial adenomcarcinoma?

A

5YSR for stage 1 is 90%

for stages 2-3 is less than 50%

36
Q

what is the prevalence of endometrial adenocarcinoma?

A

it is the most common cancer of the female genital tract with 9200 cases per year and 2500 deaths in the UK

37
Q

what are the types, incidence of these and age of onset for the endometrial adenocarcinomas?

A

there are two types
type 1 is endometriod and it is around 7% of cases at pre or perimenopausal age
type 2 is serous which is around 25% of cases at postmenopausal age

38
Q

what are the precursors to the types of endometrial adenocarcinoma?

A

type 1 - endometrial hyperplasia

type 2 - endometrial atrophy

39
Q

what are the mutations and E status of endometriod and serious adenocarcinomas?

A

endometrioid - PTEN and KRAS mutations with a positive E2 status
serous - P53 mutation and E2 negative

40
Q

what are the grades for endometrioid and serous adenocarcinomas?

A

grade 1,2,3 for endometrioid and grade 3 only for serous

41
Q

what is polycystic ovary syndome?

A

it is an endocrine disorder with hyperandrogenism, menstrual abnormalities and polycystic ovaries. 6-10% of women have this but 20-30% have polycystic ovaries.

42
Q

what is the diagnosis for POS?

A

rotterdam criteria - 2/3 of the following:

polycystic ovaries, irregular periods of over 35 days and hyperandrogenism resulting in hirsutism or biochemical

43
Q

what are the investigations for POS?

A

USS< fasting biochemical screen with drop is FSH and a rise in LH, testosterone and DHEAS, or OGTT

44
Q

what are the treatments of POS?

A

lifestyle weight loss, medical - metformin, OCP or clomiphene or surgical - ovarian drilling

45
Q

what are the links with POS?

A

inferility, endometrial hyperplasia and adenocarcinoma

46
Q

what are epithelial tumours?

A

they are the most common group of ovarian neoplasms representing 90% and there are three major carcinoma histologic types which are serous - tubal, endometriod - endometrium and mucinous - endocervical. Each type contains benign/borderline/malignant variatns

47
Q

how are benign tumours classified?

A

based on their components - cystic are cystadenomas, fibrous are adenofibromas and both are cystadenofibromas

48
Q

what are cystadenocarcinomas?

A

they are malignant epithelial tumours

49
Q

what are the origins of ovarian neoplasms?

A

they are surface epithelial tumours, sex cord stromal tumours or germ cell tumours

50
Q

what are serous cystadenocarcinomas?

A

they are characterised by complex, branching, papillae and glands incorporating slit like spaces - there is destructive stromal invasion is identified most conspicuously within the confluent solid growth pattern exhibited within the ovarian cortex

51
Q

what are germ cell tumours?

A

they are 15-20% of all ovarian tumours and are germinatous or non germinatous

52
Q

what is the main germinatous tumour?

A

it is a dysgerminoma which is malignant and chemosensitive

53
Q

what are the main types of non germinatous tumours?

A

teratomas which show differentiation towards multiple germ layers, yolk sac tumours and choriocarcinomas

54
Q

what differentiation is shown in choriocarcinomas and yolk sac tumours?

A

in YS there is differentiation towards extraembryonic yolk sac, malignant and chemosensitive
chorio show differentiation to the placenta, malignant and are often unresponsive

55
Q

what are sex cord stromal tumours?

A

they are rare and arise from ovarian stroma which was derived from sec cord of embyronic gonad - they can generate cells from the opposite sex and can be sertoli leydig cell tumours, granulosa cell tumours or thecomas/fibromas or fibrothecomas

56
Q

what are fibrothecomas etc?

A

they are benign and thecomas and fibrothecomas produce E2 - also rarely androgens - fibromas are hormonally active
comprised of spindle cells - plump spindle cells with lipid droplets gives the thecoma appearance
meigs syndrome - ovarian tumour, right sided hydrothroax and ascites

57
Q

what are sertoli leydig?

A

sex cell stromal tumours that produce androgens and 10-25% are malignant

58
Q

what are granulosa cell tumours?

A

they are low grade malignant and produce E2

59
Q

what is the prevalence of ovarian cancer?

A

it is the second most common gynae cancer with over 7000 women in the UK diagnosed and over 4000 deaths per year. 80% are over 50y/o and 80-90% are epithelial

60
Q

what are the risk factors for ovarian cancer?

A

FH, increased age, PMH opf breast cancer, smoking, E2 only HRT, Lynch II syndrome, obestiy and nulliparity

61
Q

what are protective factors for ovarian cancer?

A

OCP, breast feeding and hysterectomy

62
Q

what are the presentations of ovarian cancer?

A

they are non specific symptoms - urinary frequency, pain, bloating, weight loss, PV bleeding, anorexia

63
Q

what is the staging of ovarian cancer?

A

FIGO 1-4

64
Q

what is the treatment of ovarian cancer?

A

for less than stage 1C is TAH, BSO omentectomy, appendectomy, lymphadenectomy and adjuvant chemo - this is only in sensitive GCTs

65
Q

what is the prognoses for ovarian cancer?

A

43% 5YSR

66
Q

what are the types of ovarian metastatic tumours?

A

mullerian and non mullerian tumours

67
Q

what is a mullerian tumour?

A

it is the most common ovarian metastatic tumour that is in the uterus, fallopian tubes, pelvic peritoneum, contralateral ovary

68
Q

what is a non mullerian tumour?

A

it is spread through lymphatic spread or haematogenous and goes to the GIT, breast - lobular, melanoma and the kidney and lung and directly to the bladder and rectum

69
Q

what is endometriosis and what is endometritis?

A

endometriosis is ectopic endometrial tissue and endometritis is chronic inflammation of the endometrium

70
Q

what is leiyomyomata?

A

it is benign tumour of the smooth muscle of the myometrium

71
Q

what are the features of PCOS?

A

common, multiple follicular cysts, hyperandrogenism and menstrual irregularity

CP (38 decks)

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