Endometriosis is an inflammatory, estrogen-dependent disease characterized by the presence of ectopic endometrial tissue (glands and stroma) outside the uterus, typically in the pelvis but rarely at distant sites (lung, vagina, bowel, bladder, ureter).

Because it is estrogen-dependent, it resolves after menopause or when inducing a pseudomenopause state. Pathogenesis theories include:

• Retrograde Menstruation: Occurs in 90% of women, but only a minority develop the disease. Defective clearance may lead to implantation. Explains why women with vaginal outflow obstruction or short menstrual cycles have higher risk.
• Coelomic Epithelium Transformation: Metaplasia of Mullerian duct lining due to hormonal stimuli.
• Genetic & Immunologic Factors: Altered humoral immunity (B-cell function) failing to clear endometrial cells. Higher incidence (6-9 times more) in first-degree relatives.
• Vascular & Lymphatic Spread: Embolization explains distant sites (e.g., lungs, joints, kidney, skin).

Severity of symptoms does NOT correlate with the extent of disease seen on laparoscopy. Key symptoms include:

• Reproductive tract: Secondary dysmenorrhea (starts few days before menses), chronic pelvic pain, deep dyspareunia, and subfertility (due to anatomical distortion of fallopian tubes and periadnexal adhesions).
• Gastrointestinal Tract (GIT): Dyschezia (painful defecation) and cyclical rectal bleeding are key indicators of Pouch of Douglas (Rectovaginal) Endometriosis.
• Urinary tract: Cyclical haematuria, dysuria.
• Lung: Cyclical haemoptysis & haemopneumothorax.

Signs on examination: Thickening/nodules at uterosacral ligament, tenderness at Pouch of Douglas, fixed retroverted uterus, and blue/red spots on vagina.

Laparoscopy is the Gold Standard for diagnosis (diagnostic and therapeutic). Finding dense adhesions strongly suggests endometriosis. Lesions appear as powder burn, gunshot, or burned match stick spots.

Transvaginal Ultrasound (TVUS) diagnoses Endometriomas (Chocolate Cysts) and "kissing ovaries", but negative TVUS does not exclude peritoneal lesions. CA-125 may be elevated but alone is not of diagnostic value.

Revised American Society for Reproductive Medicine (r-ASRM) Classification:

• Stage 1 (Minimal): Isolated implants, no adhesions.
• Stage 2 (Mild): Superficial implants scattered, no significant adhesions.
• Stage 3 (Moderate): Multiple deep/superficial implants, adhesions present on tubes/ovaries.
• Stage 4 (Severe): Deep implants, large endometriomas, dense adhesions.

Medical treatment suppresses ovarian function (induces amenorrhea) but does not remove local disease permanently (symptoms recur after stoppage):

• NSAIDs: For analgesia (potentiated with paracetamol/codeine).
• Combined Oral Contraceptive Pills (COCP): Continuous use (3-6 packs) to induce pseudopregnancy.
• Progestins: High dose Medroxyprogesterone Acetate (MPA) or Depot form causes endometrial atrophy. Levonorgestrel Intrauterine System (LNG-IUS) is also effective for pain.
• Danazol/Gestrinone: Androgenic effects, induce atrophy. Limited by side effects (weight gain, acne, voice deepening).
• GnRH Agonists: Induces pseudomenopause. Long-term use (>6 months) causes osteoporosis, hence "Add-back" therapy (low dose HRT) is used.

Surgical treatment includes conservative (Laparoscopic ablation/cystectomy) and definitive (Total Abdominal Hysterectomy with Bilateral Salpingo-Oophorectomy (TAH-BSO)). Endometriomas do not resolve with medical therapy; surgical excision is the treatment of choice.

Adenomyosis is the presence of endometrial glands and stroma within the myometrium associated with adjacent smooth muscle hyperplasia.

Epidemiologically distinct from endometriosis: more common in parous, middle-aged women (late 30s-40s).

Classic presentation: Heavy painful menstruation (Menorrhagia & secondary dysmenorrhea) with a bulky, tender uterus.

Diagnosis: Magnetic Resonance Imaging (MRI) is the investigation of choice. TVUS shows asymmetrical myometrial thickening or subendometrial cysts/linear striations.

Treatment: Levonorgestrel Intrauterine System (LNG-IUS) preferred medically over endometrial ablation (which fails due to deep lesions). Hysterectomy is the definitive surgical treatment (does not always require oophorectomy).

Pregnancy is confirmed via Human Chorionic Gonadotropin (hCG). In normal early pregnancy, serum hCG doubles every 48 hours (rises by >63%).

Transvaginal Ultrasound (TVUS) can see a gestational sac at 4.3-4.6 weeks (when it is 2-4mm). An intrauterine pregnancy should be visible when hCG is discriminatory zone >1500-2000 IU/L. A Yolk Sac (indicates true gestational sac, ruling out ectopic pseudosac) is seen when the sac reaches 8mm.

Miscarriage is defined as pregnancy loss before 24 weeks gestation or fetal weight <500g (WHO definition uses <20 weeks). More than 80% occur in the first 12 weeks.

Risk Factors: Advanced maternal age (most important!), paternal age, smoking/alcohol, uterine anomalies, obesity, and previous history of miscarriage.

• Chromosomal Abnormalities (50-60%): The most important and common cause. Autosomal trisomy is the most frequent, followed by polyploidy/monosomy. Increased by maternal age. Presents often as Blighted Ovum (anembryonic pregnancy, empty sac >25mm).
• Endocrine Causes: Luteal phase deficiency (insufficient progesterone from corpus luteum <8 weeks), Polycystic Ovary Syndrome (PCOS), poorly controlled Diabetes Mellitus, Hypothyroidism (thyroid autoantibodies).
• Uterine Anomalies: Septate/bicornuate uterus, submucosal fibroids, Asherman’s syndrome (intrauterine adhesions from vigorous curettage). Cervical incompetence causes 2nd-trimester loss.
• Immunological: Antiphospholipid syndrome, thrombophilia.
• Infections: Uncommon cause. Toxoplasmosis, CMV, Chlamydia, Syphilis, Listeriosis, Malaria.

Classic triad of early pregnancy disorders: Amenorrhea, lower abdominal pain, vaginal bleeding.

• Threatened Abortion: Mild bleeding, no/mild pain. Cervix is CLOSED. Fetus is viable on U/S. Treat with rest, reassurance, and Anti-D if Rh-negative (after 12 wks). High risk for later issues (preterm labor, manual removal of placenta) even if bleeding stops.
• Inevitable Abortion: Cramps, heavy bleeding, membrane rupture. Cervix is OPEN. Abortion will certainly follow.
• Incomplete Abortion: Heavy bleeding with passage of clots/tissue. Cervix is OPEN. U/S shows Retained Products of Conception (RPOC). Requires medical (Misoprostol) or surgical evacuation (Suction Curettage) to prevent hypovolemic/cervical shock.
• Complete Abortion: Uterus is empty, pain/bleeding resolves, cervix is closed. Needs hCG follow up to exclude ectopic if previous U/S didn't confirm intrauterine.
• Missed Abortion: Dead embryo retained. No bleeding or light bleeding. Loss of pregnancy symptoms. Cervix is CLOSED. Diagnosed if Crown-Rump Length (CRL) ≥ 7mm with no heart beat, or Mean Gestational Sac ≥ 25mm with no fetal pole (Blighted Ovum). Risk of Disseminated Intravascular Coagulation (DIC) causing hypofibrinogenemia if retained >4 weeks.
• Septic Abortion: Uterine infection (mixed E.coli, Bacteroides, Clostridia) presenting with fever, tachycardia, pelvic tenderness, offensive discharge. Can lead to septic shock, renal failure. Treat with IV Cephalosporin + Metronidazole followed by evacuation.

Recurrent Miscarriage (RM) is defined as 3 or more consecutive pregnancy losses before 24 weeks of gestation. Affects 1-2% of women.

• Immunological (15%): Antiphospholipid Syndrome (APS) is a major treatable cause. Anticardiolipin/lupus anticoagulant antibodies cause placental vascular thrombosis and infarcts. Systemic Lupus Erythematosus (SLE) also causes RM.
• Genetic (2%): Balanced reciprocal translocations in parents. High sperm DNA fragmentation (linked to smoking, alcohol, obesity, advanced paternal age).
• Anatomic: Congenital (septate/bicornuate uterus) or acquired (cervical weakness causes 2nd trimester loss, submucosal fibroids impede implantation, Asherman syndrome). Adenomyosis impedes implantation via macrophages and NK cells.
• Endocrine: Polycystic Ovary Syndrome (PCOS) via insulin resistance and luteal phase insufficiency, poorly controlled Diabetes Mellitus, Thyroid disorders (hypo/hyperthyroidism & autoantibodies).
• Thrombophilias: Inherited (Factor V Leiden mutation, Prothrombin gene mutation) or acquired (Antithrombin III/Protein S deficiency).
• Idiopathic: Up to 50% remain unexplained.

Investigations:

• Screening for Anticardiolipin & Antiphospholipid antibodies (Requires 2 positive tests at least 12 weeks apart of IgG/IgM to exclude transient infection positivity).
• Thyroid Function Tests (TFT) & antithyroid autoantibodies.
• Pelvic U/S and/or Hysterosalpingography (HSG) for uterine anatomic anomalies.
• Parental Karyotyping & Cytogenetic analysis of Products of Conception (POC) to detect unbalanced translocations.
• Thrombophilia screening (especially with 2nd-trimester losses).

Treatment:

• Antiphospholipid Syndrome: Treat with Low-dose Aspirin + Unfractionated Low Molecular Weight Heparin (LMWH). Prednisolone & IVIg have limited benefit.
• Genetic: Gamete donation or In Vitro Fertilization (IVF) with Pre-implantation Genetic Diagnosis (PGD).
• Anatomic: Cervical cerclage for incompetence, surgical resection of septa/fibroids.
• Empirical Aspirin for ALL recurrent miscarriages is common but shows NO evidence of improvement unless APS is proven.

Ectopic Pregnancy is implantation outside the normal uterine cavity. It is the most common cause of pregnancy-related death in the first trimester (mainly due to substandard care).

Sites: 95-97% in the Fallopian tube, mostly the Ampullary portion (80%). The Interstitial/Cornual part (2.5%) is highly dangerous and causes 20% of ectopic deaths due to severe rupture hemorrhage (as it traverses the myometrium).

Risk Factors:

• Previous ectopic pregnancy (Increases recurrence risk to 10%).
• Pelvic Inflammatory Disease (PID) & STDs (Chlamydia/Gonorrhea, multiple partners).
• Tubal surgery (ligation, salpingotomy) or previous abdominal surgery (Appendicectomy, CS).
• Contraceptive failure (IUDs, Progesterone-only pills).
• Assisted Reproductive Techniques (IVF).
• Smoking (alters tubal function dose-dependently) and in-utero Diethylstilbestrol (DES) exposure.

Presentation:

Classic Triad: Missed period, vaginal bleeding (old/brown/decidual cast), and unilateral pelvic pain.

• Acute (Ruptured): Severe abdominal pain, shock (hypotension, tachycardia, fainting), shoulder tip pain (diaphragmatic irritation by blood), rigid abdomen.
• Subacute: Most common diagnostic problem. Hemodynamically stable, mild tenderness.

Diagnosis:

Transvaginal Ultrasound (TVUS) is the single best tool. If hCG is above the discriminatory zone (1500-2000 IU/L) and NO intrauterine sac is seen, suspect ectopic. Beware of a pseudogestational sac (fluid collection surrounded by endometrium in uterus) seen in 10-20%.

Serial Serum B-hCG for Pregnancy of Unknown Location (PUL): In normal pregnancy, hCG rises >63% in 48 hrs. In ectopic, it fails to rise normally (rises <35%) or plateaus. Failing pregnancy shows falling hCG (half-time 24-36 hrs).

Serum Progesterone <5 ng/ml suggests failing/ectopic pregnancy; >25 ng/ml nearly excludes ectopic.

Laparoscopy is considered the gold standard for definitive diagnosis (and therapy) when ultrasound is inconclusive.

1. Medical Treatment (Methotrexate):

Folic acid antagonist (inhibits DNA synthesis). Given as a single IM dose (1mg/kg). Accounts for 25-30% of ectopic treatments. Strict Criteria for Methotrexate:

• Hemodynamically stable patient with minimal symptoms.
• No embryonic cardiac activity on U/S.
• Ectopic mass size < 3.5 cm.
• Serum B-hCG < 5000 IU/L.
• No hemoperitoneum on U/S.
• No contraindications (No liver/renal/blood disease, no active infection, not breastfeeding, compliant patient).

Must monitor hCG on Day 4 and Day 7 (must drop >25% between day 4 and 7, otherwise give second dose - needed in 15% of cases). Patient must strictly avoid pregnancy for 3 months (teratogenic).

2. Surgical Treatment:

Required if unstable, ruptured, or failed medical therapy. Done via Laparoscopy (preferred) or Laparotomy (if shocked).

• Salpingectomy (Removal of tube): Done if tube is severely damaged, recurrent ectopic in same tube, uncontrolled bleeding, healthy contralateral tube, or completed family.
• Salpingostomy/Salpingotomy (Conservative): Linear incision to remove gestation, leaving tube to heal. Has higher bleeding risk and a 10-15% risk of persistent trophoblastic tissue (requires strict hCG follow-up). Done ONLY if patient desires fertility AND contralateral tube is damaged.

Always give Anti-D Immunoglobulin (250 IU) to Rh-negative mothers within 72 hours!

GTD arises from conceptus cells and produces extremely high levels of Beta-Human Chorionic Gonadotropin (B-hCG) as an ideal tumor marker.

Risk factors: Extremes of maternal age (>45 years increases risk 300x), Asian ethnicity, previous molar pregnancy (10x risk, mostly complete), low dietary carotene/animal fat.

Genetics & Pathology:

• Complete Hydatidiform Mole: 46,XX (paternal only). Empty anucleated egg fertilized by duplicated sperm (or rarely 46,XY from 2 sperms). Fetus is ABSENT. Diffusely hydropic villi, diffuse trophoblastic hyperplasia.
• Partial Hydatidiform Mole: Triploid (69,XXY/XXX). Normal egg + 2 sperms (dispermy). Fetus is PRESENT (but non-viable by 10-12 wks). Focal hydropic villi, focal hyperplasia. Often misdiagnosed as missed abortion.

Familial recurrent hydatidiform mole syndrome: Rare autosomal recessive condition. DNA is biparental. Requires egg donation to achieve normal pregnancy.

Symptoms: Amenorrhea, heavy bleeding, passage of grape-like vesicles, Uterus larger than dates (doughy consistency). Exaggerated pregnancy symptoms: Hyperemesis gravidarum, early onset pre-eclampsia (< 20 weeks), clinical hyperthyroidism, respiratory distress.

Ultrasound for Complete Mole shows a classic Snow storm appearance (multiple sonolucencies) and bilateral theca-lutein cysts. Partial mole resembles miscarriage.

Malignant Forms (Gestational Trophoblastic Neoplasia - GTN):

• Invasive Mole: Myometrial invasion, causing hemorrhage, hematuria, rectal bleeding, or uterine perforation. Nearly always follows complete mole.
• Choriocarcinoma: Highly malignant. Metastasizes early via blood to Lungs (causing hemoptysis), brain, liver, vagina. Shows sheets of trophoblasts WITHOUT villi. Biopsy is absolutely contraindicated due to massive bleeding risk.
• Placental Site Trophoblastic Tumor (PSTT) & ETT: Rare, occurs slowly on average ~3.4 years post-pregnancy. Presents with abnormal bleeding and lower hCG. Less chemosensitive, primarily requires Hysterectomy + node sampling.

1. Evacuation: Suction curettage is the method of choice for complete mole. Sharp curettage is rejected (perforation/Asherman risk). Strictly avoid oxytocic agents before/during early evacuation to prevent trophoblastic tissue embolization into maternal venous spaces. Medical termination is contraindicated for complete mole.

2. Follow-Up: Serial serum B-hCG (every 2 weeks until normal, then monthly for 6-12 months). Strict contraception for 12 months (or 6m post-normal hCG) to avoid confusing a new pregnancy with disease relapse. IUDs are contraindicated until hCG is zero (perforation risk). COCPs are recommended by USA, but historically UK avoids them until hCG is normal.

3. Chemotherapy for GTN: Indicated if hCG plateaus (3 samples), rises (2 samples), remains >20,000 IU/L after 4 weeks, or if metastasis is present (lungs/brain/liver).

• Low-Risk (FIGO score ≤ 6): Single-agent Methotrexate with folinic acid (causes mucositis, no alopecia).
• High-Risk (FIGO score ≥ 7): Multi-agent EMA-CO (Etoposide, Methotrexate, Actinomycin, Cyclophosphamide, Vincristine). Brain/liver metastases or long interval from pregnancy increase the score significantly.

Hysterectomy: Indicated if excessive bleeding, chemo-resistant, or older patient completing family. (Doesn't prevent metastasis, follow-up still needed).

Leiomyomas (Fibroids) are benign monoclonal tumors of the smooth muscle. They are the most common benign tumors of the female genital tract. They are strictly Estrogen and Progesterone dependent (they grow rapidly in pregnancy, and naturally shrink post-menopause).

Protective factors: Increased parity, smoking, long-term COCP or DMPA use, levonorgestrel IUS.

Risk factors: Nulliparity, obesity (increased BMI), African descent, family history, high red meat consumption.

Degenerative Changes:

• Red Degeneration: Acute infarction/necrosis due to outgrowing blood supply. Classically occurs in mid-pregnancy (2nd trimester). Presents with sudden severe localized pain, tenderness, mild pyrexia, and leukocytosis. Managed strictly conservatively (analgesia).
• Hyaline Degeneration: Asymptomatic softening and liquefaction as it outgrows blood supply.
• Cystic Degeneration: Follows hyaline degeneration with central necrosis leaving cystic spaces.
• Calcification: Seen in postmenopausal women. Detected incidentally on X-ray.
• Malignant transformation (Leiomyosarcoma): Extremely rare (0.5%). Current genetic opinion is that sarcomas arise de novo in the 7th decade, and fibroids DO NOT undergo neoplastic change.

Most fibroids are asymptomatic. Symptoms depend on location:

• Submucous: Bulge into the cavity. Most likely to cause Heavy Menstrual Bleeding (Menorrhagia) and Subfertility (prevents implantation/recurrent loss).
• Intramural: Centrally within myometrium.
• Subserous: Outer wall. Causes Pressure symptoms (urinary frequency, constipation, hydronephrosis).

Signs: Firm, lobulated abdomino-pelvic mass moving with the cervix.

Diagnosis: Ultrasound (TVUS for submucous/small intramural; Transabdominal for large/hydronephrosis). MRI is the most accurate to map locations precisely, required prior to uterine artery embolization.

Asymptomatic needs conservative observation (repeat U/S in 6-12m).

Medical Treatment (for bleeding):

• Tranexamic Acid / NSAIDs (Less effective if >3cm or submucous).
• Progestins (Mirena IUS): Reduces bleeding but doesn't shrink fibroids. May be expelled if cavity is heavily distorted.
• Ulipristal Acetate (SPRM): Reduces bleeding, induces amenorrhea, and shrinks fibroid volume by 25%.
• GnRH Agonists: Induce pseudomenopause. Used Pre-operatively (for 3-4 months) to shrink fibroid size (by 40%), reduce vascularity, treat anemia, and allow smaller surgical incisions (vaginal vs abdominal). Rapid regrowth after stopping. Long term contraindicated due to osteoporosis.

Surgical/Procedural Treatment:

• Hysterectomy: Definitive cure for women who completed their family.
• Myomectomy: Preserves fertility. Power morcellation risks spreading occult sarcomas.
• Uterine Artery Embolization (UAE): Infarcts and shrinks fibroid. Contraindicated if active PID, asymptomatic, or if patient specifically desires future fertility (impacts ovarian reserve/placenta). Must do MRI first.
• High Intensity Focused Ultrasound (HIFU): MRI-guided thermal necrosis. Time-consuming, risks bowel/nerve burns.

Endometrial Hyperplasia is irregular excessive proliferation of endometrial glands resulting in an increased gland-to-stroma ratio (>2:1). It is the direct precursor to Endometrial Carcinoma.

WHO 2014 Classification:

• Hyperplasia without atypia: Risk of progression to cancer is <5% (1-3%) over 20 years. Often regresses spontaneously. Histologically shows irregular cystic expansion (Swiss cheese appearance).
• Atypical Hyperplasia: Risk of progression to cancer is 25-50% (and 46% of cases already have co-existing frank malignancy upon definitive resection). Characterized by enlarged nuclei, prominent nucleoli, and cellular crowding/budding (back-to-back glands). Treat as cancer!

Presentation: Usually presents as Abnormal Uterine Bleeding (AUB) — heavy menses, intermenstrual, irregular, or crucially, Postmenopausal Bleeding (PMB).

Diagnosis:

• Transvaginal Ultrasound (TVUS): If endometrial thickness is < 3-4mm in a postmenopausal woman, cancer is virtually excluded. In premenopausal women, TVUS is mainly to rule out polyps (since thickness varies with cycle).
• Endometrial Sampling: Mandatory for definitive histological diagnosis.
  • Pipelle (Outpatient): Flexible suction device. No anesthesia needed. Limitations: inadequate sampling, fails if cervix is stenosed (28% of cases), misses focal lesions (0.9% cancer miss rate).
  • Hysteroscopy & D&C: Under anesthesia. Directed biopsy under direct visualization. Used if Pipelle fails, stenosis present, or focal lesions seen on TVUS.

Hyperplasia WITHOUT Atypia:

• Eliminate reversible factors (e.g., stop unopposed HRT, encourage weight loss).
• Progestin Therapy: First-line treatment. The Levonorgestrel Intrauterine System (LNG-IUS / Mirena) is preferred (fewer side effects). Alternatively, continuous oral progestins (Medroxyprogesterone or Norethisterone) for at least 6 months.
• Follow-up: Repeat endometrial biopsy every 6 months until 2 consecutive negative biopsies.
• Hysterectomy is NOT first-line. Indicated ONLY IF: progresses to atypia, fails to regress after 12 months of therapy, relapse occurs, bleeding persists, or patient refuses medical follow-up.

Atypical Hyperplasia:

• Total Hysterectomy (preferably Laparoscopic) is the treatment of choice immediately due to the 46% risk of co-existing frank cancer.
• Fertility-sparing option (only for highly selected young patients or completely unfit for surgery): High-dose progestins (Mirena) with strict biopsy follow-up. Relapse rate is very high.

Endometrial Carcinoma is the most common gynecological malignancy in Western countries. It typically presents early, providing a good prognosis.

Risk Factors (Mainly for Type 1):

• Unopposed Estrogen Exposure (HRT without progesterone).
• Obesity: Adipose tissue converts androgens to estrone via aromatase. Major driver of the epidemic in developed nations.
• Nulliparity, Early menarche, Late menopause (>52 yrs).
• Polycystic Ovary Syndrome (PCOS): Chronic anovulation leads to continuous estrogen without progesterone withdrawal. (Must give artificial withdrawal bleeds).
• Tamoxifen Therapy: Anti-estrogen in breast, but has pro-estrogenic effects on the endometrium. Associated with polyps, hyperplasia, and rare carcinosarcomas.
• Lynch Syndrome II (Hereditary Non-Polyposis Colorectal Cancer - HNPCC): DNA Mismatch Repair (MMR) gene defect. High risk of colon and endometrial cancer.

Protective Factors: Combined Oral Contraceptives (COCPs reduce risk by 50%), Multiparity, Progestin IUDs, Physical exercise, and Smoking (has a paradoxical anti-estrogenic effect).

Dualistic Classification:

• Type 1 (Endometrioid, 80%): Estrogen-dependent. Arises from a background of atypical hyperplasia. Usually Grade 1-2. Favorable prognosis. Seen in perimenopausal/obese women. PTEN mutations common.
• Type 2 (Non-Endometrioid, Serous/Clear Cell, 10-20%): Not estrogen-dependent. Arises from atrophic endometrium. High grade by definition. Poor prognosis, aggressive, early spread. P53 mutations.

Molecular Classification (TCGA - The Cancer Genome Atlas):

• POLE-mutant: Very good clinical outcome, low recurrence.
• MMR-deficient: Intermediate prognosis (10% linked to Lynch Syndrome).
• No specific molecular profile (NSMP): Diagnosis of exclusion, intermediate/excellent outcome.
• p53-abnormal: Serous-like, very poor prognosis.

Presentation: Presents EARLY. Postmenopausal Bleeding (PMB) is the hallmark symptom (accounts for 90% of cases, though only 10% of PMB is cancer). Advanced disease presents with pelvic pain, bowel/bladder dysfunction, or bony metastases.

Diagnosis:

• TVUS: Endometrial thickness >4mm requires biopsy in PMB.
• Endometrial Biopsy (Pipelle/Hysteroscopy): Yields histological type and grade (1, 2, or 3).
• MRI of Pelvis: Best imaging for preoperative clinical staging. Assesses depth of myometrial invasion and cervical/lymph node involvement.
• CT Chest/Abdomen/Pelvis: Done for high-grade (Type 2) tumors to exclude distant metastases (lungs, vagina are common sites).

Staging: It is strictly Surgico-Pathological. Key factors determining recurrence risk and the need for post-operative radiotherapy are: Depth of myometrial invasion, tumor grade, and Lymphovascular Space Invasion (LVSI).

• Standard Surgical Treatment: Total Abdominal Hysterectomy and Bilateral Salpingo-Oophorectomy (TAH-BSO) is the core treatment. Laparoscopic approach is highly preferred if feasible.
• High-Grade (Type 2) or High-Risk Type 1: Requires complete surgical staging which adds Omental biopsy, Peritoneal washings, and Pelvic/Para-aortic lymph node dissection.
• Adjuvant Therapy: Radiotherapy (Vaginal vault brachytherapy or external beam) prevents recurrence in intermediate/high risk. Chemotherapy is for advanced/metastatic stages.
• Fertility Sparing (Hormonal Therapy): High-dose progestins (Mirena) ONLY for young women strictly wishing to preserve fertility with Grade 1, Stage 1A disease, or for patients totally unfit for surgery. Relapse rate is very high.

Advantages over open surgery (laparotomy): Shorter hospital stay, less pain, quicker recovery, less postoperative adhesions (vital for maintaining fertility), less wound infection.

Laparotomy is still necessary for: Very large/malignant masses, severe adhesions, or extreme emergencies requiring rapid access.

Preoperative Evaluation: Evaluate risk of adhesions (PID, Endometriosis history), previous surgical scars, and abdominal wall hernias.

Entry Techniques:

• Closed Technique (Veress Needle): Spring-loaded obturator prevents organ injury. Inserted umbilically. Sensation of "2 pops" (fascia then peritoneum). Angle is 45 degrees in thin women (up to 60 in obese). Disadvantage: Higher risk of major vascular injury (aorta is <4 cm from umbilicus).
• Open Technique (Hasson): Direct visualization, safer vascularly but longer.
• Palmer’s Point: Alternate entry site (3 cm below left costal margin in midclavicular line). Used if periumbilical adhesions (previous surgery), umbilical hernias, or massive pelvic mass. Contraindications: Splenomegaly, previous gastric surgery, portal hypertension. Stomach must be emptied via NG tube prior.

Complications: Port-site hernia (fascia must be sutured if port >10mm), bowel damage.

Visualization of the uterine cavity. Can be diagnostic (outpatient, no anesthesia) or operative (anesthesia/paracervical block needed). Used for AUB, polyps, submucous fibroids, lost IUD, Asherman's.

Distension Media: Required to expand cavity (pressure ~70-80 mmHg).

• Electrolyte-containing (Normal Saline, Ringer's): Used for diagnostic or bipolar surgery.
• Electrolyte-poor (1.5% Glycine, 5% Dextrose, Mannitol, Sorbitol): Used for monopolar operative hysteroscopy.

Complications:

• Uterine Perforation: Most common complication. Carries risk of bowel or vascular injury.
• Fluid Absorption (Overload) Syndrome: Systemic absorption of electrolyte-poor media causes Hyponatremia and Hypo-osmolarity. Leads to nausea, vomiting, cerebral edema, seizures, coma, and death. Risk massively increases if intrauterine pressure exceeds mean arterial pressure (>100 mmHg) or prolonged surgery. Strict fluid balance monitoring is mandatory.

Normal ovary size is 3x2x1 cm. Covered by single layer of flat epithelial cells. Shrinks post-menopause.

Differential diagnosis for pelvic mass: Gynecological (pregnancy, ectopic, fibroid, cyst), GI (appendicular mass, diverticular abscess), Urological (pelvic kidney, distended bladder).

Functional (Physiological) Cysts: Most common in young women. Incidence is decreased by COCP use.

• Follicular Cysts: Most common. Due to non-rupture of dominant follicle or failed atresia. Must be >3cm (normal follicle <2.5cm). Lined by granulosa cells. Unilocular, simple. Treatment: Observation; usually resolve in 8-16 weeks.
• Corpus Luteum Cysts: Occur after ovulation. Persist without pregnancy. Can reach 5cm before regressing. Resolves spontaneously.
• Theca Lutein Cysts: Associated with massive hCG (e.g., Molar pregnancy, choriocarcinoma, multiple gestation, ovulation induction). Usually bilateral. Resolve when hCG drops.

Most common tumors overall (60-65%), and 90% of all malignant ovarian tumors are epithelial. Peak in older/postmenopausal women (mean 64 yrs).

• Serous Tumors: Lined by ciliated columnar epithelium (tube-like). Benign (Serous cystadenoma), borderline, or malignant. 30% are bilateral. Malignant forms have solid/cystic parts and show psammoma bodies (calcospherules).
• Mucinous Tumors: Lined by mucus-secreting columnar cells (cervical-like). Typically Multilocular and HUGE (can weigh >14kg). Complication of borderline/malignant rupture: Pseudomyxoma Peritonei (jelly belly), causing bowel matting and obstruction.
• Endometrioid Tumors: Hard to distinguish from endometriosis. Can be malignant.
• Clear Cell Tumors: Aggressive subtype if malignant.
• Brenner Tumors: Transitional cell tumor (bladder-like epithelium). Mostly benign. Solid.

Most common ovarian tumors in young women (early 20s). 30% of all tumors.

• Mature Cystic Teratoma (Dermoid Cyst): Most common germ cell tumor. Benign. Derived from 2-3 germ layers (mostly ectoderm). Contains hair, teeth, bone, sebum. Diagnosed via X-ray (teeth) or U/S. High risk of Torsion (15%) due to heavy, fatty composition causing acute severe pain.
• Immature Teratoma: Solid, Malignant. Contains immature embryonic tissue (often neuroectoderm).
• Dysgerminoma: Malignant. Female equivalent of seminoma. High incidence in abnormal gonads (Androgen Insensitivity Syndrome, gonadal dysgenesis). Secretes LDH, sometimes B-hCG.
• Yolk Sac Tumor (Endodermal Sinus Tumor): Malignant. Highly aggressive. Marker: Alpha-Fetoprotein (AFP) elevated. Schiller-Duval bodies histologically.
• Embryonal Carcinoma: Rare, secretes B-hCG and AFP.
• Choriocarcinoma (Non-gestational): Malignant. Secretes extremely high B-hCG.

Derived from ovarian stroma.

• Fibroma: Most common sex cord tumor. Solid, hard, white, fibrous. Presents in older women (50s). Prone to torsion due to heaviness. Associated with Meigs Syndrome: Triad of Ovarian Fibroma + Ascites + Pleural Effusion. Resolves completely upon removal of the tumor.
• Thecoma: Solid, yellow (lipid-rich). Usually Estrogen-producing, leading to endometrial hyperplasia/PMB.
• Granulosa Cell Tumor: Most common malignant sex-cord tumor (low malignant potential). Secretes massive amounts of Estrogen and Inhibin. Causes precocious puberty in girls, or PMB/hyperplasia in postmenopausal women. Call-Exner bodies histologically. Late recurrences can occur. Treated with Unilateral Salpingo-Oophorectomy in young, TAH-BSO in old. No effective chemo.

Benign Mass Presentation: Often asymptomatic, or vague pressure, abdominal swelling, menstrual disturbance (hormonal tumors), torsion (acute pain).

EOC is the deadliest gynecological cancer due to late vague presentation (66% present at Stage 3 or 4). Chronic ovulation/inflammation is the main pathophysiologic theory.

Risk Factors: Nulliparity, early menarche/late menopause, Endometriosis & PID (chronic inflammation), BRCA1 & BRCA2 mutations, Lynch Syndrome II.

Protective Factors: Multiparity, COCP use (>5 years reduces risk 50%), breastfeeding, Tubal ligation, Hysterectomy with ovarian preservation.

Presentation: Often vague. Pelvic/abdominal pain, persistent bloating, early satiety, increased abdominal girth (ascites), unexplained weight loss, urinary frequency.

Investigations:

• CA-125: Tumor marker (>35 IU/L is abnormal). Elevated in 80% of serous EOC. Not specific (rises in endometriosis, fibroids, PID). A rapidly rising level indicates malignancy. CA 19-9 elevated in Mucinous EOC. AFP/hCG in young women for germ cell tumors.
• TVUS Features of Malignancy: Multilocular cyst, thick septations, Solid areas/papillary projections, bilateral lesions, Ascites, metastasis.
• Risk of Malignancy Index (RMI) = U/S Score (0, 1, 3) × Menopausal Status (1 if pre, 3 if post) × CA-125 level.
• CT Scan: Chest/Abdomen/Pelvis for high-grade staging/metastasis detection.

Management heavily depends on the RMI:

• Low Risk (RMI < 25): <3% cancer risk. If cyst <5cm, manage conservatively; observe with TVUS/CA-125 every 4 months for 1 year. If surgery requested, laparoscopy is acceptable.
• Moderate Risk (RMI 25-250): 20% risk. Laparoscopic oophorectomy. Full staging if malignant.
• High Risk (RMI > 250): >75% risk. Manage in cancer center. Laparotomy with full staging. (CA-125 >200 alone refers to oncologist).

Surgical Staging (Surgico-Pathological):

• Stage 1: Confined to ovaries. (1a: one ovary intact, 1b: both ovaries intact, 1c: ruptured/ascites/washings positive).
• Stage 2: Extension to pelvis (uterus, tubes).
• Stage 3: Extension to abdominal peritoneum/nodes. 3a: Microscopic seeding. 3b: Implants <2cm. 3c: Implants >2cm or positive nodes.
• Stage 4: Distant metastases (Liver parenchyma, Pleural effusion).

Treatment: Cytoreductive Surgery (Debulking) is the supreme goal (TAH-BSO + Complete Omentectomy + Resection of metastases, sometimes appendicectomy/bowel resection) to leave no macroscopic disease, followed by Platinum-based Chemotherapy.