11.4 Contraception, Cervical Cancer Screening & Gynaecological Malignancies

Contraceptive Methods & WHO Medical Eligibility Criteria (MEC)

The World Health Organization (WHO) and CDC Medical Eligibility Criteria for Contraceptive Use stratify medical conditions into four risk tiers:

• MEC Category 1: A condition for which there is no restriction for the use of the contraceptive method.
• MEC Category 2: A condition where the advantages of using the method generally outweigh the theoretical or proven risks.
• MEC Category 3: A condition where the theoretical or proven risks usually outweigh the advantages (method not recommended unless other methods are unavailable or unacceptable).
• MEC Category 4: A condition that represents an unacceptable health risk; ABSOLUTE CONTRAINDICATION.

Combined Hormonal Contraceptives (COCs, Patch, Vaginal Ring)

Combined methods contain ethinylestradiol paired with a synthetic progestin. Mechanism: suppresses pituitary LH and FSH secretion to inhibit ovulation, thins the endometrium, and thickens cervical mucus.

MEC Category 4 Absolute Contraindications for Estrogen-Containing Contraceptives:

1. Migraine with Aura at Any Age: Ethinylestradiol significantly multiplies the baseline risk of ischemic stroke.
2. Age >= 35 Years Who Smoke >= 15 Cigarettes/Day: Synergistic multiplication of myocardial infarction and arterial thrombosis risk (smoking < 15 cigarettes/day at age >= 35 is MEC 3).
3. History of or Current Venous Thromboembolism (DVT / PE), or known inherited thrombogenic mutations (e.g., Factor V Leiden, Prothrombin G20210A mutation, Antithrombin III deficiency).
4. Severe Hypertension: Systolic blood pressure >= 160 mmHg or diastolic blood pressure >= 100 mmHg, or hypertension with documented vascular disease.
5. Current or Past Breast Cancer: Active hormone-receptor-positive malignancy (MEC 4; past history without recurrence for 5 years is MEC 3).
6. Ischemic Heart Disease, Stroke, or complicated valvular heart disease (pulmonary hypertension, history of subacute bacterial endocarditis, atrial fibrillation).
7. Diabetes with Nephropathy, Retinopathy, Neuropathy, Other Vascular Disease, or Duration >20 Years: CHCs are MEC 3/4 according to severity, rather than uniformly MEC 4.
8. Severe Decompensated Cirrhosis, Hepatocellular Adenoma, or hepatocellular carcinoma.
9. Postpartum < 21 Days: Substantially elevated baseline postpartum thromboembolic risk.

Progestin-Only Contraceptives

Progestin-only methods avoid estrogen-mediated hepatic synthesis of coagulation factors (factors II, VII, VIII, X, and fibrinogen). They are safe (MEC 1 or 2) in women with migraine with aura, controlled hypertension, heavy cigarette smoking, and history of VTE.

• Progestin-Only Pill (POP): Norethisterone (requires strict 3-hour daily dosing window) or Desogestrel (75 mcg daily; suppresses ovulation in 97% of cycles, allowing a 12-hour missed-pill window).
• Depot Medroxyprogesterone Acetate (DMPA / Depo-Provera): 150 mg IM every 12 weeks. High contraceptive efficacy; induces amenorrhea in 50% at 1 year and 70% at 2 years. Key considerations:
  • Bone Mineral Density (BMD): Induces reversible reduction in BMD via suppression of ovarian estradiol production. BMD recovers completely following discontinuation; routine restriction beyond 2 years is unnecessary if no other risk factors for osteoporosis exist.
  • Weight Gain: Average 2 to 4 kg weight gain over 1 to 2 years.
  • Delayed Return of Fertility: Median delay of 9 to 10 months (up to 18 months) following the final injection.
• Subdermal Etonogestrel Implant (Nexplanon): Single 4 cm rod inserted subdermally in the upper arm, licensed for 5 years in the US and UK as of 2026; follow the local product licence elsewhere. The most effective reversible contraceptive method available (Pearl Index < 0.05). Primary side effect: unscheduled, irregular menstrual spotting or amenorrhea.
• Levonorgestrel Intrauterine System (LNG-IUS / Mirena): Highly effective for up to 8 years; local endometrial suppression with negligible systemic levels; reduces menorrhagia and dysmenorrhea.

Copper Intrauterine Device (Cu-IUD / TCu380A)

• High-efficacy, completely non-hormonal contraception lasting 10 to 12 years. Mechanism: sterile foreign-body inflammatory reaction toxic to sperm and blastocysts.
• Adverse Effects: Increases menstrual blood loss by 30-50% and exacerbates dysmenorrhea (avoid in patients with baseline severe menorrhagia).
• MEC 4 Contraindications: Unexplained abnormal vaginal bleeding (prior to diagnostic evaluation), active pelvic inflammatory disease or purulent cervicitis, distorted uterine cavity (large submucosal fibroids), and Wilson disease.

Emergency Contraception (EC)

1. Copper IUD: The most effective form of emergency contraception (> 99% efficacy). Must be inserted within 5 days (120 hours) of unprotected sexual intercourse (UPSI) or within 5 days of the earliest estimated ovulation day. Provides ongoing long-term contraception.
2. Ulipristal Acetate (EllaOne): Selective progesterone receptor modulator (SPRM) administered as a single 30 mg oral dose. Delays or inhibits ovulation even after the LH surge has begun (until the LH peak). Effective up to 120 hours (5 days) after UPSI. Demonstrates superior efficacy compared to levonorgestrel, particularly between 72 and 120 hours and in overweight/obese women. Rule: Hormonal contraception must be withheld for 5 days after ulipristal intake to avoid mutual receptor antagonism.
3. Levonorgestrel (Plan B / Postinor): Synthetic progestin taken as a single 1.5 mg oral dose. Inhibits ovulation only if taken before the luteinizing hormone (LH) surge commences. Approved for use up to 72 hours (3 days) after UPSI (efficacy drops significantly beyond 72 hours). Efficacy is substantially diminished in women with BMI > 26-30 kg/m2 (in whom Cu-IUD or double-dose 3 mg levonorgestrel is advised).

Cervical Cancer: Screening, Cytology & FIGO Staging

Cervical cancer remains a major preventable cause of cancer illness and death among Caribbean women. Vaccination, screening and timely treatment are central regional priorities.

Etiology & Molecular Oncogenesis

Persistent infection with high-risk oncogenic types of Human Papillomavirus (HPV) drives > 99% of cervical cancers:

• HPV Type 16: Causes 50% to 60% of cases (predominantly squamous cell carcinoma).
• HPV Type 18: Causes 10% to 15% of cases (disproportionately responsible for endocervical adenocarcinoma).
• Other high-risk oncogenic types: 31, 33, 45, 52, 58.
• Molecular Oncoproteins:
  • E6 Oncoprotein: Binds and accelerates the ubiquitin-mediated degradation of the p53 tumor suppressor protein, abolishing cell cycle arrest and apoptosis.
  • E7 Oncoprotein: Binds and inactivates the retinoblastoma (pRb) protein, freeing E2F transcription factors to drive uncontrolled progression from the G1 phase into the S phase of the cell cycle.

Screening Modalities & Low-Resource Caribbean Strategies

• Cytology (Pap Smear): Conventional or Liquid-Based Cytology (LBC) performed every 3 years from age 21 to 29.
• High-Risk HPV Co-Testing / Primary HPV Screening: Preferred every 5 years from age 30 to 65.
• Visual Inspection with Acetic Acid (VIA): Widely adopted in resource-constrained Caribbean public healthcare systems. Involves applying 3% to 5% dilute acetic acid to the cervix and examining under bright white light after 1 minute. Precancerous dysplastic cells contain dense nuclear proteins that coagulate, appearing as sharp, well-demarcated opaque acetowhite lesions near the squamocolumnar junction (transformation zone). Single-visit ablation is appropriate only when the entire transformation zone and lesion are visible and coverable, without endocervical extension or suspected invasion, and the patient is not pregnant. Ineligible or suspicious lesions require specialist assessment, biopsy or excision as indicated.

Cytological Triage & Cervical Intraepithelial Neoplasia (CIN)

• ASC-US: Under age 25, repeat cytology at 1 year; a negative reflex HPV test permits 3-year cytology. From age 25, use HPV status and prior screening history: HPV-positive ASC-US with unknown history usually requires colposcopy; a recent negative HPV-based screen may permit 1-year surveillance. HPV-negative ASC-US with unknown history permits 3-year follow-up.
• LSIL: Under 25, repeat cytology at 1 year; perform colposcopy for persistent low-grade abnormalities at 2 years or high-grade cytology sooner. From 25, use HPV status/history to choose colposcopy or surveillance. ASC-H/HSIL require colposcopic assessment; qualifying HSIL in nonpregnant patients>=25 may receive expedited excision. Obtain ECC when indicated, particularly for high-grade cytology or an incompletely visible SCJ; never in pregnancy.
• CIN 1 (Mild Dysplasia): Dysplasia confined to the lower third of the cervical epithelium. Natural history: > 60% to 70% regress spontaneously within 1 to 2 years. Managed conservatively with surveillance (repeat co-testing in 12 months); excisional treatment is contraindicated unless lesion persists > 2 years.
• CIN 2 / CIN 3 (High-Grade Squamous Intraepithelial Lesion - HSIL): Dysplasia involving the lower two-thirds (CIN 2) or full thickness (CIN 3) of the epithelium. High risk of progression to invasive carcinoma (up to 30% in CIN 3 if untreated). CIN 3 requires treatment, usually excision by LEEP/LLETZ or cone biopsy. For CIN 2 under 25, observation with 6-month colposcopy/cytology is preferred when the SCJ/lesion are fully visible and endocervical sampling excludes CIN 2+; persistence for 2 years requires treatment.

+-----------------------------------------------------------------------------------------+
|                        CERVICAL CANCER: FIGO STAGING & MANAGEMENT                       |
+-----------------------------------------------------------------------------------------+
                                             |
                   +-------------------------+-------------------------+
                   |                                                   |
                   v                                                   v
         [ EARLY STAGE DISEASE ]                             [ LOCALLY ADVANCED DISEASE ]
  - Stage IA: Microscopic invasion <= 5 mm             - Stage IB3: > 4 cm confined to cervix
    * IA1 (<= 3 mm): Cone biopsy or Simple Hysterectomy - Stage IIA2: > 4 cm, upper 2/3 vagina
    * IA2 (> 3 to <= 5 mm): Simple/Modified Radical      - Stage IIB: Parametrial invasion
  - Stage IB1 (<= 2 cm) & IB2 (> 2 to <= 4 cm):           - Stage III: Lower 1/3 vagina or pelvic sidewall
    * Radical Hysterectomy (Wertheim Procedure)       - Stage IVA: Bladder or rectal mucosal invasion
      with Bilateral Pelvic Lymphadenectomy                                    |
                   |                                                           v
                   v                                         DEFINITIVE CONCURRENT CHEMORADIATION
          PRIMARY SURGERY                                    - External Beam Radiotherapy (EBRT)
          (Curative Intent)                                  - Intracavitary Brachytherapy
                                                             - Weekly Intravenous Cisplatin
                                                             (CCRT IS THE STANDARD PRIMARY TREATMENT)

FIGO Staging and Therapeutic Management

Cervical cancer is staged clinically and pathologically:

• Stage I: Confined strictly to the cervix uteri.
  • Stage IA: Microscopic invasion<=5 mm: IA1<=3 mm, IA2>3–<=5 mm. IA1 without LVSI and with clear margins can be treated by conization or simple hysterectomy. IA2 usually requires nodal assessment with modified radical surgery; selected low-risk cases may receive less radical or fertility-sparing treatment.
  • Stage IB: Invasion>5 mm, confined to the cervix: IB1<=2 cm, IB2>2–<=4 cm, IB3>4 cm. IB1/IB2 commonly receive radical hysterectomy with pelvic nodal assessment; the operation removes uterus, cervix, parametria and upper vagina. Selected low-risk cases may receive less radical surgery after specialist assessment.
• Locally Advanced Cervical Cancer (Stage IB3, IIA2, IIB to IVA):
  • Stage IIB: Extension into the parametrial tissue (does not reach pelvic sidewall).
  • Stage III: Involves lower third of vagina (IIIA), extends to pelvic sidewall and/or causes hydronephrosis/non-functioning kidney (IIIB), or involves pelvic/para-aortic lymph nodes (IIIC).
  • Stage IVA: Direct extension into mucosa of bladder or rectum.
  • Management: Primary surgery is generally avoided because many patients would also require radiotherapy, increasing morbidity. Standard definitive therapy is Concurrent Chemoradiation (CCRT): External Beam Radiotherapy (EBRT) to the pelvis plus intracavitary Brachytherapy combined with weekly intravenous Cisplatin (which functions as a radiosensitizer).

Endometrial Carcinoma: Risk Factors & Diagnostic Evaluation

Clinical Presentation & Cardinal Rule

Postmenopausal Bleeding (PMB) is endometrial cancer until proven otherwise. While atrophic endometritis and atrophic vaginitis are the most common overall etiologies of PMB (60-80%), endometrial adenocarcinoma is diagnosed in approximately 10% of women presenting with postmenopausal bleeding.

Risk Factors & Pathophysiological Types

Endometrial cancer is driven primarily by chronic, unopposed estrogen exposure:

• Obesity (adipose tissue aromatase converts circulating adrenal androstenedione into estrone).
• Nulliparity, early menarche, late menopause (> 55 years).
• Polycystic Ovary Syndrome (PCOS) / chronic anovulation.
• Estrogen-only hormone replacement therapy without progestins.
• Tamoxifen Therapy: Exerts antagonistic effects on breast tissue but paradoxical pro-estrogenic agonist effects on the postmenopausal endometrium, increasing endometrial cancer risk 2- to 3-fold.
• Lynch Syndrome (HNPCC): Germline mutation in DNA mismatch repair genes (MLH1, MSH2, MSH6, PMS2); carries a 40% to 60% lifetime risk of endometrial cancer.

Pathological Subtypes:

• Type I Endometrioid Adenocarcinoma (80%): Estrogen-dependent, arising from atypical endometrial hyperplasia / EIN. Associated with PTEN mutations and microsatellite instability. Well differentiated, indolent, favorable prognosis.
• Type II Serous & Clear Cell Carcinoma (15-20%): Estrogen-independent, arising in atrophic endometrium. Associated with TP53 mutations. Poorly differentiated, aggressive, early intraperitoneal and lymphatic spread, poor prognosis.

Diagnostic Evaluation

1. Transvaginal Ultrasound (TVS): Measures double-wall endometrial thickness (ET) in the sagittal plane. In postmenopausal women with bleeding, an ET <= 4 mm carries a negative predictive value > 96% for excluding endometrial cancer.
2. Endometrial Biopsy: An ET > 4 to 5 mm, a heterogeneous endometrial stripe, or recurrent bleeding mandates histological sampling via outpatient Pipelle biopsy or hysteroscopy with dilatation and curettage (D&C).
3. Surgical Management: Hysterectomy with bilateral salpingo-oophorectomy is standard. Nodal assessment is tailored to tumour risk/stage, commonly using sentinel-node mapping; systematic pelvic/para-aortic dissection is reserved for selected indications. Adjuvant radiotherapy and chemotherapy depend on stage, histology and molecular risk.

Ovarian Neoplasms: Classification & Clinical Management

Ovarian cancer causes substantial mortality because many cases present at an advanced stage (Stage III or IV), with subtle, insidious symptoms that delay diagnosis.

Histopathological Subtypes

• Epithelial Ovarian Carcinoma (90%): High-Grade Serous Carcinoma (HGSC, 70%; predominantly originates from the fimbriated ends of the fallopian tubes as Serous Tubal Intraepithelial Carcinomas [STIC]), endometrioid, clear cell, and mucinous carcinomas. Strongly associated with germline BRCA1 mutations (39-44% lifetime risk) and BRCA2 mutations (11-17% lifetime risk), as well as Lynch syndrome.
• Germ Cell Tumors (5%): Arise from primitive germ cells, most common in young women aged 10 to 30. Includes mature cystic teratoma (dermoid cyst; benign, carries teeth/hair), dysgerminoma (associated with elevated LDH), and yolk sac tumor (endodermal sinus tumor; produces alpha-fetoprotein [AFP], displays characteristic Schiller-Duval bodies).
• Sex Cord-Stromal Tumors (5%): Granulosa cell tumors (produce estradiol, causing precocious puberty, abnormal bleeding, or endometrial hyperplasia; monitored with serum inhibin B; displays Call-Exner bodies) and Sertoli-Leydig cell tumors (produce testosterone, causing virilization and hirsutism).

Clinical Presentation & Risk of Malignancy Index (RMI)

Classic symptoms are persistent and progressive: abdominal bloating, early satiety, pelvic fullness, urinary urgency, and unexplained weight loss with increasing abdominal girth (ascites). Physical exam discloses a fixed, solid, irregular, nodular adnexal mass with ascites.

Risk of Malignancy Index (RMI): A validated triage tool that stratifies pelvic masses to determine the need for referral to a gynecologic oncologist: RMI = Ultrasound Score (U) x Menopausal Score (M) x Serum CA-125 (in U/mL).

• Ultrasound Score (U): Points assigned for multilocular cysts, solid areas, bilateral lesions, ascites, and intra-abdominal metastases (0 features = U score 0; 1 feature = U score 1; >= 2 features = U score 3).
• Menopausal Score (M): Premenopausal = 1; Postmenopausal = 3.
• CA-125: Absolute serum concentration in U/mL (CA-125 is elevated in > 80% of epithelial ovarian cancers, but is non-specific in premenopausal women due to endometriosis, fibroids, and PID).
• RMI Score > 200 carries high sensitivity and specificity for ovarian malignancy and mandates immediate surgical oncological referral.

Surgical & Medical Management

• Primary Cytoreductive Surgery: Specialist surgery usually includes TAH-BSO, omentectomy and removal of visible peritoneal disease, aiming for zero visible residual tumour. Early-stage nodal staging depends on histology and whether results change treatment. In advanced disease, remove suspicious/enlarged nodes; routine systematic dissection of clinically normal pelvic/para-aortic nodes is not indicated.
• Systemic Chemotherapy: First-line adjuvant chemotherapy when indicated for high-risk early-stage or advanced disease is intravenous Carboplatin plus Paclitaxel administered every 3 weeks for 6 cycles. Maintenance therapy with PARP inhibitors (e.g., Olaparib) is standard of care for patients with BRCA1/2 mutations or homologous recombination deficiency (HRD).