Week 6 - Ovarian & Gestation Disorders Flashcards
Outline ovary disorders.
Inflammation/infections rare.
• Unlike other organs.
Ovarian cysts - commonest.
• Commonest clinically.
Non-neoplastic (small)
• Follicular, epithelial, Luteal etc.
• Polycystic ovary syndrome.
• Non neoplastic small cysts so common they are considered physiological, seen in many ovaries.
Neoplasms (large)
• Benign (cystadenoma).
• Malignant cystadenocarcinoma.
• Teratoma (benign and malignant).
Ovarian tumours (particularly benign) are very large because they are asymptomatic in the early stage and there is a lot of space for growth before it presents clinically.
Outline gestational disorders.
Disorders of placenta • Eclampsia, pre-eclampsia. • Hydatidiform mole. • Choriocarcinoma. - Hydatidiform mole and choriocarcinoma both tumours.
Outline polycystic ovary syndrome (PCOS).
• Ovarian disorder → anovulation, polycystic ovaries.
- Unknown aetiology. Results in anovulation. Grafian follicles become cystic instead of normal ovulation. Become cystic without rupturing and form multiple cysts.
• Increased androgens and oestrogens by abnormal follicles.
- Abnormal follicles produce excess androgens and oestrogens → results in clinical features.
• DUB and decreased fertility (Stein-Levinthal Syndrome)
- DUB, oligomenorrhoea, decreased fertility/infertility.
- Used to be known as Stein-Levinthal Syndrome.
• 6-10% teens/young adults. Oligomenorrhoea, acne, hirsutism.
- Present with the above due to increased androgens.
• Obesity, infertility, HTN, DM2 (syndrome X).
- Patients have increased obesity, HTN and insulin resistance (giving rise to T2DM).
• Arrested follicle development → cysts.
- Instead of normal ovulation → Grafian follicles become cysts → produce both androgens and oestrogens.
Describe the pathology of PCOS.
• Enlarged ovaries - twice (6-8cm).
• Bilateral subcortical follicular cysts.
• Increased androgens and oestrogens.
• Stromal hyperplasia.
- Due to excess hormones.
• Risk of endometrial hyperplasia and cancer.
- Excess oestrogens cause endometrial hyperplasia and cancer.
Outline the clinical diagnosis of PCOS.
• Patients with irregular bleeding and younger age - if since menarche with hirsutism → ask for 17hydroxyprogesterone levels from lab. If normal → confirms PCOS. If high → confirms congenital adrenal hyperplasia.
Outline menopause.
• Cessation of ovulation/menstrual cycles/(associated with) genital atrophy.
- Age related degenerative change.
• Physiological ~50, >45, <40 is pathological (ovarian failure).
• Characterised by decreased oestrogens, decreased inhibin, increased androgens and increased FSH.
- In case of menopause, gonadotrophs increase, oestrogens decrease.
• Many follicles in ovary but not responding to gonadotrophins.
- Do not become cystic.
• Rapid follicle maturation - short anovulatory cycles.
- Rapid due to increased FSH - results in short anovulatory cycles.
• Gonadotrophin levels of >30 mIU (high) and FSH>LH are diagnostic.
Identify the clinical features of menopause.
• Vasomotor hot flushes: 80%, few minutes, night sweats. Oestrogen withdrawl symptom. >1 year is pathological → HRT.
- Hot flushes commonest - feature of oestrogen withdrawal.
• Labia, Vagina, Uterus, Breast and Endometrial atrophy,
• Boney atrophy - osteoporosis. Post menopausal women have increased incidence of hip fractures 0.3 to 20/1000.
• Cardiovascular - increased IHD, increased cholesterol - HRT prevents.
• Psychological - depression, irritability, sleep deprivation.
- Age related degeneration - genetic factors, environment, lifestyle, systemic diseases - can aggravate this.
- Decreased hypothalamic function - gonadotrophin releasing hormone - resulting in atrophy of ovary → results in oestrogen decline → gives rise to clinical features of hot flushes, bone loss, IHD, psychological abnormalities.
Outline neoplasms of the ovary.
• Common, produce oestrogens.
• 80% benign, cystic, young (<50).
- Benign cystadenoma (most common).
• 20% malignant, solid - older (>50).
• Huge benign tumours* - characteristic of ovarian neoplasms.
• 6% of all cancers in women but high mortality (50%) due to silent growth and late detection.
• The rule: cysts are benign, solid are malignant.
Risk factors:
• Not known in majority.
• Nulliparity*, gonadal dysgenesis, family history, BRCA1 (17q12) and BRCA2 (13q12).
Describe the classification of ovary tumours.
• Surface epithelial tumours (commonest ~70%) - Serous tumours - Mucinous tumours • Germ cell tumours (~20%) - Teratoma - Choriocarcinoma • Sex cord stroma tumours • Metastasis
Outline cystadenoma.
• Surface epithelial tumours. - Commonest type. • Serous more common than Mucinous. - Serous - clear fluid. - Mucinous - mucous • 75% benign, 25% malignant. • Frequently bilateral (30-66%). • Multi-loculated cystic tumour. • Benign cystic, malignant solid. • Borderline tumours are partly solid/cystic.
- Multiple cystic cavities.
- Usually lined by simple single layered columnar epithelium.
- Serous cyst adenoma - when it is benign, it has very little solid tissue in the wall of the cyst.
- Borderline tumours - have extensive papillary growth but limited within cyst.
• Serous cystadenocarcinoma - malignant - large papillary growth extending outside of cyst.
- When they come out of the cyst → malignant.
- Tumour extending outside is malignant. Completely solid or partly solid/cystic.
Outline teratoma (germ cell tumour).
• Tumour made up of many different tissues.
- Made up of many different tissues from different embryonic origin - teratoma.
• Benign teratoma → mature tissues, cystic. Commonest is Dermoid cyst - skin lining (cyst has a skin lining with all the ectodermal structures including hair, teeth, many different tissues including internal organs, thyroid).
• Malignant/immature teratoma - many different immature and malignant tissues. Not common.
- Multiple immature and malignant tissues mixed together.
Dermoid cyst microscopy:
• Lined by stratified squamous epithelium, plenty of lymphoid tissue, sebaceous glands. There is also some thyroid tissue (follicles). Any different tissue can be seen.
• Second example - epidermis with hair follicle and sebaceous glands. Usually the cyst contains keratin and sebaceous secretions.
• Microscopy contains many different cancers. Very immature/pleomorphic.
Outline other ovarian tumours.
- Fibroma - stromal tumour - benign.
- Dysgerminoma - same as seminoma of testes, occurring in testes.
- Endometrioid carcinoma - looks like endometrial tissue.
- Brenner tumour - benign, rarely can be malignant.
- Granulosa cell tumour - usually just benign tumour.
Outline Kruckenberg tumour.
- Special type of metastases to ovary, usually from GIT (adenocarcinoma).
- Metastases to the ovary from an adenocarcinoma usually of a GIT origin (either stomach or colon).
- Cancer cells spread to the ovaries in a peculiar manner without producing any haemorrhage or necrosis.
- Solid, greyish white, bilateral.
Identify the complications of ovarian cysts.
• Large mass - nutrition.
- Take up a lot of nutrition due to large mass.
• Torsion, infarction, rupture, hemoperitoneum.
• Autoamputation.
• Perforation - acute → acute abdomen.
- Perforation giving rise to acute abdomen or chronic granulomatous peritonitis.
• Slow → granulomatous peritonitis.
• Haemolytic anaemia - clears after removal of the tumour.
- Tumour induced haemolytic anaemia.
• Progress to malignancy.
Outline ovarian cancer staging.
• Poor prognosis. • Late detection. • CA-125 tumour marker. Measurements are of greatest value in monitoring response to therapy. - Epithelial tumour marker. - When +ve - helpful in monitoring response to therapy. • Stage 1 - within ovary. • Stage 2 - in the adnexal structures. • Stage 3 - peritoneal cavity. • Stage 4 - distant.
