Lecture 35 - Uterine and ovarian pathology Flashcards

1
Q

Endometriosis

A

Ectopic endometrium

number of theories behind it - regurgitation theory, metaplasia theory, stem cell theory, metastasis theory

causes bleeding into tissues and then fibrosis

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2
Q

Symptoms of endometriosis

A

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

History - 25% asymptomatic, dysmenorrhea, dyspareunia, pelvic pain, subfertility, pain on passing stool, dysuria

Lx : Laparoscopy

Rx : Medical (COCP, GnRH agonists/antagonists, progesterone antagonists) or surgical (ablation/ TAH-BSO)

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3
Q

Links to endometriosis

A

Ectopic pregnancy, ovarian cancer, IBD

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4
Q

What is endometritis

A

Inflammation of the endometrium

Pelvic inflammatory disease, retained gestational tissue, endometrial TB, IUCD infection

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5
Q

Histology of endometritis

A

lymphocytes/plasma cells

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6
Q

History of endometritis

A

Abdominal/pelvic pain, pryrexia, discharge, dysuria, abnormal vaginal bleeding

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7
Q

examination/testing for endometritis

A

Biochemistry/microbiology, Ultrasound scan

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8
Q

Treatment/medication for endometritis

A

Analgesia, antibiotics, remove cause

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9
Q

Endometrial polyps

A

Sensile/polypoid E2- dependent uterine overgrowths

< 10% women (40-50’s)

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10
Q

History for endometriall polyps

A

often asymptomatic, Intermenstrual/post menopausal bleeding, menorrhagia, dysmenorrhoea

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11
Q

Investigations for endometriall polyps

A

USS, Hysteroscopy

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12
Q

Treatment for endometriall polyps

A

Expectant, medical, (P4/GnRH agonists), surgical (curettage

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13
Q

Prognosis for endometriall polyps

A

less than 1% are malignant

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14
Q

Leiomyoma (uterine fibroids)

A

Benign myometrial tumours with E2/P4 dependent growth

  • 20% women 30-50’s
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15
Q

Risk factors for Leiomyoma

A

Genetics, nulliparity, obesity, PCOS, Hypertension

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16
Q

History for Leiomyoma

A

Often asymptomatic, menometorrhagia, subfertility, pregnancy problems, pressure sx

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17
Q

investigations for Leiomyoma

A

Bimanusal examination, USS

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18
Q

Treatment for Leiomyoma

A

Medical (IUS,NSAIDs/OCP/P4/FE2+; non-medical (artery embolixation, ablation, TAH

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19
Q

Prognosis for Leiomyoma

A

Menopausal regression, malignancy risk 0.01%

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20
Q

Endometrial hyperplasia

A

excessive endometrial proliferation ( inrease E2, less P4)

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21
Q

risk factors for Endometrial hyperplasia

A

obesity, exogenous E2, PCOS, E2 -producing tumours,tamoxifen, HNPCC ( PTEN mutations)

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22
Q

Types of Endometrial hyperplasia

A

Simple non-atypical, simple atypical

Complex non-atypical, complex atypical

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23
Q

History of Endometrial hyperplasia

A

Abnormal bleeding - IMB/PCB/PMB

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24
Q

Investigations of Endometrial hyperplasia

A

USS, hysteroscopy +/- biopsy

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25
Q

Treatment for Endometrial hyperplasia

A

Medical (IUS, P4), surgical (TOTAL ABDOMINAL HYSTERECTOMY)

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26
Q

Prognosis for Endometrial hyperplasia

A

endometrial adenocarcinoma, regression

27
Q

Malignant progression of hyperplasia

A

Normal - Non-atypical hyperplasia (Resembles normal proliferative endometrium) - Atypical hyperplasia (Presence of cytological abnormality) (EIN - Endometrial Intraepithelial Neoplasia) - Endometroid adenocarcinoma (Invasion into myometrium)

28
Q

Endometrial adenocarcinoma

A

Most common cancer of female genital tract; 9,200 new cases/ 2.500 deaths/yr UK

29
Q

History of Endometrial adenocarcinoma

A

Post menopausal bleeding, Intermenstrual bleeding, pain if late

30
Q

Investigations

A

uss, biopsy, hysteroscopy

31
Q

Staging of Endometrial adenocarcinoma

A

FIGO (1-4)

32
Q

Treatment of Endometrial adenocarcinoma

A
Medical (progesterone), surgery (TAH - BSO), 
adjuvant therapy (chemo-radiotherapy)
33
Q

Prognosis of Endometrial adenocarcinoma

A

Stage 1 = 90% 5 year survival

Stage 2-3 = <50%

34
Q

Difference between Type 1 and Type 2 Endometrial adenocarcinoma

A

Type 1 (endometroid) Type 2 (serous)

Incidence -75% of cases 25% of cases
Age Pre or perimenopausal Post menopausal

Pre-existing state endometrial hyperp Endometrial atrophy
Mutations PTEN, Kras p53
e2 state E2, +ve E2 -ve
Grades 1,2,3 3

35
Q

PCOS

A

Endocrine disorder hyperandrogenism, menstrual abnormalities, polycystic ovaries

6-10% women (20-30% have polycystic ovaries)

36
Q

investigations for PCOS

A

USS, fasting biochemical screen (dropin FSH, increase in LH, increase in testosteron, Increase in Dehydroepiandosterone), oral glucose tolerance test

37
Q

Dx: Diagnosis of PCOS

A

Rotterdam criteria 2/3 of polycystic ovaries, hyperandrogenism (hirsuitsim/biochemical), irregular periods (over 35 days)

38
Q

treatment for PCOS

A

Lifestyle - weight loss, medical (metformin, OCP, clomiphene (infertility), surgical (ovarian drilling)

39
Q

Links to PCOS

A

infertility, endometrial hyperplasia/ adenocarcinoma

40
Q

Gonadal failure

A

Hypergonadotrophic hypogonadism (primary failure of gonads)

41
Q

Congenital causes of Gonadal failure

A

Turner’s syndrome (XO), Klinefelter’s syndrome (XXY)

42
Q

Acquired causes of Gonadal failure

A

Infection, surgeru, chemo-radiotherapy, toxins/drugs

43
Q

What does secondary failure of gonads result in

A

Hypogonadotrophic hypogonadism (hypothalamic/pituitary failure) resulting in Sheehan syndrome, pituitary tumours, brain injury PCOS

44
Q

Presentation of gonadal failure

A

amenorrhoea/absent menarche; delayed puberty. decreased sex hormones, increase LH and FSH levels

45
Q

Investigations for gonadal failure

A

Hormone profiling, karyotyping

46
Q

Treatment for gonadal failure

A

Difficult - address cause

Hormone replacement therapy

47
Q

Origin of ovarian neoplasms

A

Sex cord stromal tumours - granulosa cells, thecomas, fibrothecomas, Sertoli- Leydig cell tumours

Germ cell tumours - teratomas, yolk sac tumours, embryonal carcinoma dysgerminomas)

Surface epithelial tumours (serous, mucinous, endometroid, transitional cell, clear cell

48
Q

Epithelial tumours

A

Most common group of ovarian neoplasms (90%)

3 major carcinoma histologic types:

Serous (tubal)
Mucinous (endocervical)
Endometrioid (endometrium)

Each type contains benign/ borderline/ malignant variants
Benign tumours subclassified based on components; cystic (cystadenomas), fibrous (adenofibromas), cystic and fibrous (cystadenofibromas)
Malignant epithelial tumours  cystadenocarcinomas

49
Q

Germ cell tumours

A

15-20% all ovarian tumours

Germinamatous and non -germinamatous

50
Q

Germinamatous tumours

A

Dysgerminomas (differentiation - oogonia, malignant, chemosensitive)

51
Q

Non- germinamatous tumours

A
Teratomas (differentiation towards multiple germ layers)
Most mature (benign; 1% malignant transformation) 

Yolk sac tumours (differentiation towards extraembryonic yolk
sac, malignant, chemosensitive)

Choriocarcinomas (differentiation - placenta, malignant,
often unresponsive)

52
Q

Treatment for germ cell tumours

A

surgery with or without chemotherapy

53
Q

Sex cord stromal tumours

A

Rare; arise from ovarian stroma, which was derived from sex cord embryonic gonad

Can generate cells from the opposite sex;

Thecoma/ fibrothecoma/ fibroma

Benign, thecomas and fibrothecomas produce E2 (also rarely androgens), fibromas hormonally inactive
Comprised of spindle cells (plump spindle cells with lipid droplets = thecoma appearance)
Meig’s syndrome = ovarian tumour, right sided hydrothorax, ascites

Granulosa cell tumours

Low grade malignant, produces E2

Sertoli-Leydig cell tumours
Produces androgens; 10-25% malignant

54
Q

ovarian cancer

A

2nd commonest cancer

; >7,100 women >4,300 deaths/yr UK; 80% >50’s; 80-90% epithelial

55
Q

Risk factors for ovarian cancer

A

FH, ↑age, PMH breast cancer, smoking,

E2-only HRT, Lynch II syndrome, obesity, nulliparity

56
Q

Protective factors for ovarian cancer

A

OCP, breastfeeding, hysterectomy

57
Q

History of ovarian cancer

A

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

58
Q

staging of ovarian cancer

A

FIGO 1-4

59
Q

treatment for ovarian cancer

A

Stage <1C epithelial tumours  TAH/BSO, omentectomy, appendectomy, lymphadenectomy & adjuvant chemo - chemo only in sensitive GCTs

60
Q

prognosis for ovarian cancer

A

overall 5 years 43% survival

61
Q

Ovarian metastatic tumours

A

Mullerian tumours ( most common) and Non-Mullerian tumours

62
Q

Mullerian tumours

A

uterus, fallopian tube, pelvic peritoneum, contralateral ovary

63
Q

Non-Müllerian tumours

A

Lymphatic/ haematogenous spread:
GI tract: Large bowel, stomach
(Krukenberg tumour), pancreatobiliary

Breast
Melanoma 
Less commonly, kidney and lung
Direct extension: bladder, rectal
Metastatic tumours are confirmed histologically; prognosis is typically poor