Lecture 35 - Uterine and ovarian pathology Flashcards
Endometriosis
Ectopic endometrium
number of theories behind it - regurgitation theory, metaplasia theory, stem cell theory, metastasis theory
causes bleeding into tissues and then fibrosis
Symptoms of endometriosis
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)
Links to endometriosis
Ectopic pregnancy, ovarian cancer, IBD
What is endometritis
Inflammation of the endometrium
Pelvic inflammatory disease, retained gestational tissue, endometrial TB, IUCD infection
Histology of endometritis
lymphocytes/plasma cells
History of endometritis
Abdominal/pelvic pain, pryrexia, discharge, dysuria, abnormal vaginal bleeding
examination/testing for endometritis
Biochemistry/microbiology, Ultrasound scan
Treatment/medication for endometritis
Analgesia, antibiotics, remove cause
Endometrial polyps
Sensile/polypoid E2- dependent uterine overgrowths
< 10% women (40-50’s)
History for endometriall polyps
often asymptomatic, Intermenstrual/post menopausal bleeding, menorrhagia, dysmenorrhoea
Investigations for endometriall polyps
USS, Hysteroscopy
Treatment for endometriall polyps
Expectant, medical, (P4/GnRH agonists), surgical (curettage
Prognosis for endometriall polyps
less than 1% are malignant
Leiomyoma (uterine fibroids)
Benign myometrial tumours with E2/P4 dependent growth
- 20% women 30-50’s
Risk factors for Leiomyoma
Genetics, nulliparity, obesity, PCOS, Hypertension
History for Leiomyoma
Often asymptomatic, menometorrhagia, subfertility, pregnancy problems, pressure sx
investigations for Leiomyoma
Bimanusal examination, USS
Treatment for Leiomyoma
Medical (IUS,NSAIDs/OCP/P4/FE2+; non-medical (artery embolixation, ablation, TAH
Prognosis for Leiomyoma
Menopausal regression, malignancy risk 0.01%
Endometrial hyperplasia
excessive endometrial proliferation ( inrease E2, less P4)
risk factors for Endometrial hyperplasia
obesity, exogenous E2, PCOS, E2 -producing tumours,tamoxifen, HNPCC ( PTEN mutations)
Types of Endometrial hyperplasia
Simple non-atypical, simple atypical
Complex non-atypical, complex atypical
History of Endometrial hyperplasia
Abnormal bleeding - IMB/PCB/PMB
Investigations of Endometrial hyperplasia
USS, hysteroscopy +/- biopsy
Treatment for Endometrial hyperplasia
Medical (IUS, P4), surgical (TOTAL ABDOMINAL HYSTERECTOMY)
Prognosis for Endometrial hyperplasia
endometrial adenocarcinoma, regression
Malignant progression of hyperplasia
Normal - Non-atypical hyperplasia (Resembles normal proliferative endometrium) - Atypical hyperplasia (Presence of cytological abnormality) (EIN - Endometrial Intraepithelial Neoplasia) - Endometroid adenocarcinoma (Invasion into myometrium)
Endometrial adenocarcinoma
Most common cancer of female genital tract; 9,200 new cases/ 2.500 deaths/yr UK
History of Endometrial adenocarcinoma
Post menopausal bleeding, Intermenstrual bleeding, pain if late
Investigations
uss, biopsy, hysteroscopy
Staging of Endometrial adenocarcinoma
FIGO (1-4)
Treatment of Endometrial adenocarcinoma
Medical (progesterone), surgery (TAH - BSO), adjuvant therapy (chemo-radiotherapy)
Prognosis of Endometrial adenocarcinoma
Stage 1 = 90% 5 year survival
Stage 2-3 = <50%
Difference between Type 1 and Type 2 Endometrial adenocarcinoma
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
PCOS
Endocrine disorder hyperandrogenism, menstrual abnormalities, polycystic ovaries
6-10% women (20-30% have polycystic ovaries)
investigations for PCOS
USS, fasting biochemical screen (dropin FSH, increase in LH, increase in testosteron, Increase in Dehydroepiandosterone), oral glucose tolerance test
Dx: Diagnosis of PCOS
Rotterdam criteria 2/3 of polycystic ovaries, hyperandrogenism (hirsuitsim/biochemical), irregular periods (over 35 days)
treatment for PCOS
Lifestyle - weight loss, medical (metformin, OCP, clomiphene (infertility), surgical (ovarian drilling)
Links to PCOS
infertility, endometrial hyperplasia/ adenocarcinoma
Gonadal failure
Hypergonadotrophic hypogonadism (primary failure of gonads)
Congenital causes of Gonadal failure
Turner’s syndrome (XO), Klinefelter’s syndrome (XXY)
Acquired causes of Gonadal failure
Infection, surgeru, chemo-radiotherapy, toxins/drugs
What does secondary failure of gonads result in
Hypogonadotrophic hypogonadism (hypothalamic/pituitary failure) resulting in Sheehan syndrome, pituitary tumours, brain injury PCOS
Presentation of gonadal failure
amenorrhoea/absent menarche; delayed puberty. decreased sex hormones, increase LH and FSH levels
Investigations for gonadal failure
Hormone profiling, karyotyping
Treatment for gonadal failure
Difficult - address cause
Hormone replacement therapy
Origin of ovarian neoplasms
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
Epithelial tumours
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
Germ cell tumours
15-20% all ovarian tumours
Germinamatous and non -germinamatous
Germinamatous tumours
Dysgerminomas (differentiation - oogonia, malignant, chemosensitive)
Non- germinamatous tumours
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)
Treatment for germ cell tumours
surgery with or without chemotherapy
Sex cord stromal tumours
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
ovarian cancer
2nd commonest cancer
; >7,100 women >4,300 deaths/yr UK; 80% >50’s; 80-90% epithelial
Risk factors for ovarian cancer
FH, ↑age, PMH breast cancer, smoking,
E2-only HRT, Lynch II syndrome, obesity, nulliparity
Protective factors for ovarian cancer
OCP, breastfeeding, hysterectomy
History of ovarian cancer
non-specific symptoms; pain, bloating, weight loss, PV bleeding, urinary frequency, anorexia
staging of ovarian cancer
FIGO 1-4
treatment for ovarian cancer
Stage <1C epithelial tumours TAH/BSO, omentectomy, appendectomy, lymphadenectomy & adjuvant chemo - chemo only in sensitive GCTs
prognosis for ovarian cancer
overall 5 years 43% survival
Ovarian metastatic tumours
Mullerian tumours ( most common) and Non-Mullerian tumours
Mullerian tumours
uterus, fallopian tube, pelvic peritoneum, contralateral ovary
Non-Müllerian tumours
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
