Modern classification (used in current textbooks)

• Primary dysmenorrhoea - painful periods with no underlying pelvic pathology; caused by excess prostaglandin (PGF2α) release from the endometrium driving uterine hypercontractility and ischemia. Onset shortly after menarche, typically once ovulatory cycles establish.
• Secondary dysmenorrhoea - pain due to an identifiable pelvic pathology (endometriosis, adenomyosis, fibroids, pelvic inflammatory disease, cervical stenosis, adhesions). Tends to start later in life and may worsen progressively (Berek & Novak's Gynecology, p. 1401-1422).

The traditional "three types" (spasmodic / congestive / membranous)

1. Spasmodic dysmenorrhoea - cramping, colicky lower abdominal pain caused by strong uterine muscle contractions/spasm, usually starting just before or with the onset of bleeding. This corresponds most closely to what is now called primary dysmenorrhoea and responds well to NSAIDs and antispasmodics.
2. Congestive dysmenorrhoea - a dull, dragging pelvic ache and heaviness/bloating that builds in the days before the period starts (pelvic vascular congestion), often accompanied by breast tenderness, irritability, and fluid retention - overlapping with premenstrual syndrome.
3. Membranous dysmenorrhoea - a rare form where large casts of endometrial tissue are shed nearly intact (a "membranous cast" of the uterine lining), causing severe cramping as the cervix dilates to pass the tissue. This is uncommon and can occur with hormonal fluctuations or after certain treatments.

Choriocarcinoma - Short Notes

Definition

Origin / Antecedent Pregnancy

• ~50% follow a complete hydatidiform mole
• ~25% follow a spontaneous abortion
• ~22% follow a normal term pregnancy
• Remainder follow ectopic pregnancy

Epidemiology

Pathogenesis

Morphology

• Gross: soft, hemorrhagic, necrotic uterine mass; viable tumor may be scanty and found only at metastatic sites.
• Microscopy: no chorionic villi (key distinguishing feature from hydatidiform/invasive mole) - instead sheets of anaplastic cuboidal cytotrophoblast intermixed with multinucleate syncytiotrophoblast, numerous (sometimes abnormal) mitoses.
• The tumor invades myometrium, penetrates blood vessels freely, and can extend to serosa/adjacent structures.

Choriocarcinoma - neoplastic cytotrophoblast and syncytiotrophoblast (Robbins & Kumar Basic Pathology, Fig. 17.22)

Clinical Features

• Classic presentation: irregular bloody/brownish vaginal discharge with a persistently rising hCG titer, often without significant uterine enlargement.
• By the time of diagnosis, hematogenous metastases are usually already present:
  • Lungs ~50%
  • Vagina ~30-40%
  • Also brain, liver, kidneys
  • Lymphatic spread is uncommon.

Investigations

• Serial serum β-hCG (markedly elevated, rises faster than in normal/multiple pregnancy)
• Imaging (CT chest/brain, pelvic ultrasound) to stage metastatic disease
• Histology confirms diagnosis when tissue is available

Treatment and Prognosis

• Gestational choriocarcinoma is exquisitely chemosensitive (methotrexate-based regimens, EMA-CO for high-risk disease) - nearly 100% cure rate, even with distant metastases.
• In sharp contrast, choriocarcinoma arising in the gonads (testis/ovary, non-gestational) responds poorly to chemotherapy - an important exam distinction.
• Patients are followed with serial hCG for 6-12 months post-treatment to detect persistence/recurrence.

Key exam differentiators

Recent evidence (surfaced per literature check)

• A 2025 meta-analysis on the burden and histopathological patterns of gestational trophoblastic disease in Africa (PMID: 41120163)
• A 2024 systematic review on contraceptive use after gestational trophoblastic disease, relevant to post-treatment hCG surveillance and pregnancy timing (PMID: 38763274)
• A 2024 meta-analysis on how lung metastasis affects treatment and prognosis in gestational trophoblastic neoplasia, refining the "lungs ~50%" figure above with outcome data (PMID: 38282348)