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.
Describe the normal placenta.
- Normal placenta - maternal circulation oozes out → fetal placenta dips into that blood.
- Cross section of villi (fetal structures) - blood vessels lined by trophoblasts. Trophoblasts allow the exchange of nutrients.
- Placental villi lined by trophoblasts surrounded by pool of maternal blood, allowing exchange of nutrients. Normally there is no mixing of fetal and maternal blood (during birth/pathology).
Outline chorioamnionitis.
• Infection and inflammation of (placenta) chorionic membrane and villi.
- 1-4% of normal births.
- 40-70% of premature births.
• More common in premature births.
• Risk factors - early rupture of membranes, nulliparity, prolonged labour, race/ethnicity.
• Local - vaginal flora, genital mycoplasma, Candida.
• Systemic - TB, Syphilis, Toxoplasma, Rubella, CME (TORCH).
• Inflammation, WBC, infarctions.
• Neonatal sepsis, asphyxia, death (of fetus).
Outline ectopic pregnancy.
• Implantation outside uterus.
• 1% pregnancy.
• 90% in fallopian tubes (most common).
• Ovary, abdomen, etc. rare.
• Risk factors - obstruction, PID, stricture, IUD (intrauterine devices), tumours, endometriosis etc. in 50%, rest idiopathic (50%).
• Embryo/placental tissue within dilated tube filled with haemorrhage.
• Complications - abortion, bleeding, chorioamnionitis, choriocarcinoma (rare).
- Ectopic pregnancy once of the common causes of choriocarcinoma.
Outline eclampsia & pre-eclampsia.
AKA toxemia of pregnancy.
• Diagnosis - development of HTN, proteinuria, oedema in 3rd trimester (pre-eclampsia) + seizures, DIC (eclampsia).
- Associated with seizures and DIC - eclampsia - more severe form.
• 5-10% pregnancies.
• Aetiology - unknown/genetic/immune.
• Risk factors - primi/molar pregnancy, later age.
• Pathogenesis - placental ischaemia - abnormal spiral arteries → decreased placental vasodilators and renin angiotensin inhibition → hypertension and glomerulonephritis.
• Placental infarction, haemorrhage, necrosis.
• Chorionic villi underperfusion, cytotrophoblast hyperplasia.
• Complications - DIC, CCF, fatal.
- Seizures.
• Multiple aetiologies leading to abnormal vessels causing narrowing → ischaemia → generalised endothelial cell injury → vasospasm, vascular permeability, activation of coagulation → pre-eclampsisa. When convulsions start second → known as eclampsia.
Outline Hydatidiform Mole.
Tumours of placenta - benign to malignant. Most benign known as partial mole. Highest malignancy - choriocarcinoma.
- Gestational Trophoblastic Disease.
- Spectrum of trophoblast neoplasms.
- Benign to malignant.
- Partial mole - benign, fetal parts seen, ovum + 2 sperms (triploid) - beta-HCG.
• Fetal parts or even fetus can be seen.
• Due to ovum and 2 sperms - triploid tissue producing beta-HCG. - Complete mole - no fetal parts, 2% → choriocarcinoma. 2 sperms (diploid).
• 2% of cases transform to choriocarcinoma.
• Fusion of 2 sperms (diploid) - no ovum. - Invasive mole - aggressive.
• Complete mole, more aggressive.
• When the same molar tissue starts infiltrating into the wall of the uterus - complete mole. On USS, moles appear as snow storm. - Choriocarcinoma - malignant, Asians and Africans more common.
• High grade malignancy of complete mole.
• Can occur as a secondary from complete mole or it can occur as a primary tumour from germ cells.
Increased beta-HCG → high grade → poor prognosis.
Outline complete mole.
- Entire uterine cavity is filled with swollen villi.
- The villi are each 1 to 3 mm in diameter and appear grape-like.
- Individual molar villi, many of which have cavitated central cisterns, exhibit considerable trophoblastic hyperplasia and atypia. No blood vessels within villi.
• Complete mole - when all the villi are hydatid (look like grapes). Not fetal parts. Considerable trophoblastic hyperplasia. Hyperplastic trophoblastic cells make it more aggressive or even malignant.
Differentiate between partial and complete moles.
Partial: • Partially cystic, few BV. • Fetal parts + • Focal hyperplasia of trophoblasts (only in some parts). • Triploid (ovum + 2 sperms). • Rare carcinoma (usually benign). • Relatively less beta-HCG
Complete: • All villi cystic, no BV. • No fetal parts. • Diffuse trophoblastic hyperplasia. • Diploid (2 sperms). • Choriocarcinoma 2%. • High beta-HCG levels.
Outline choriocarcinoma.
Clinical:
• High grade, malignancy of trophoblasts.
- High grade cancer of trophoblastic tissue.
• Bloody, brownish discharge accompanied by a rising titre of hCG.
- Appears as multiple areas of haemorrhage.
Risk factors:
• Extremes of age (<20, >40), 25% after abortion, (abnormal gestation)*
Types:
• Gonadal - poor prognosis.
- Occurs in gonads. High grade.
• Gestational - good prognosis (100% cure with chemotherapy).
- Develop from the mole. Responds well to chemotherapy.
Morphology:
• Haemorrhagic, highly pleomorphic cells (markedly irregular).
- Rapid spread to other organs e.g. lungs with secondary deposits.
Placental site Trophoblastic tumour - no hCG, aggressive, poor prognosis. Rare.
