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Notes: Female Reproductive Pathophysiology – Ovaries

Acknowledgements and Preamble

  • Acknowledgement of Country: RMIT University acknowledges the people of the Woi wurrung and Boon wurrung language groups of the eastern Kulin Nation on whose unceded lands we conduct the business of the University. RMIT respectfully acknowledges their Ancestors and Elders, past and present, and Traditional Custodians across Australia where we conduct our business.

  • Preamble to Reproductive Lectures:- Acknowledge that some people are born with intersex variations (physical sex characteristics that don’t fit traditional female or male norms).

    • Acknowledge that transgender individuals may have reproductive organs that differ from traditional male/female descriptions; these variations are not covered in these lectures.

    • Not all trans and gender-diverse people affirm gender via surgery.

    • Goal to challenge heteronormativity by identifying heteronormative and cisnormative language and practices within the context of the reproductive system.

Learning Objectives

  • Identify and describe the common pathological conditions of the ovaries:- Ovarian Cysts

    • Polycystic Ovarian Syndrome (PCOS)

    • Ovarian Cancer

Ovarian Cysts

  • Ovarian cysts often develop due to normal hormonal changes in puberty, during menopause, or during pregnancy.

  • Prevalence: about 1/10 of women have ovarian cysts (≈ 10%).

  • Characteristics:- Cysts may be noted on periodic examination and can increase or decrease in size with the menstrual cycle.

    • Most are benign and rarely cause problems.

    • Treatment: Surgery is rarely needed – laparoscopy is uncommon.

    • Most ovarian cysts go away on their own.

  • Simple cysts vs Functional cysts:- Simple cysts: a fluid-filled sac on the ovary.

    • Functional cysts: a type of simple cyst arising as part of the normal menstrual cycle and related to ovulation.

  • Ovarian Cysts – Causes (functional cysts dominate):- Follicular cysts: each oocyte is surrounded by a capsule or follicle. If the follicle fails to rupture and release the oocyte, the follicle becomes filled with fluid → cyst.

    • Corpus luteum cysts: occurs when a corpus luteum fills with blood. The corpus luteum develops from the follicle after ovulation and secretes progesterone and estrogen.

    • Theca lutein cysts: mainly occurs after infertility treatment with hormones. Hormone stimulation drives follicle growth; cysts may develop as a side effect.

  • Follicular cysts: benign, fluid-filled mass; thin-walled; lined by 1–4 layers of granulosa cells; filled with follicular fluid.

  • Ovarian Cysts – Signs and Symptoms:- Usually asymptomatic.

    • If large or ruptured: intraperitoneal haemorrhage and abdominal pain.

    • Hormone production by cysts can affect the endometrium and the menstrual cycle.

    • Signs/symptoms include:

    • Heavy or irregular periods;

    • Abnormal vaginal bleeding between periods (spotting);

    • Very large cysts: pressure on bowel or bladder, abdominal swelling, fullness, and pressure;

    • Pain with urination or constipation.

Polycystic Ovarian Syndrome (PCOS)

  • PCOS is characterized as Hyperandrogenic anovulation and is the most common endocrinopathy in women.

  • Prevalence and demographic data:- Affects 8% - 13% of women of reproductive age.

    • Affects 21% of Indigenous women.

    • 70% of anovulatory women have PCOS.

    • >80% of hyperandrogenic women have PCOS.

    • Familial tendency: 20 - 40% of affected individuals have affected sisters.

  • PCOS is one of the most common endocrine and metabolic disorders in premenopausal women.

  • PCOS Definition (endocrine imbalance):- High levels of estrogen, testosterone, and LH.

    • Decreased secretion of FSH.

  • Clinical picture (extremely variable):- Androgen excess is a relatively uniform characteristic.

    • Typical triad: oligomenorrhoea/amenorrhoea, hirsutism, obesity.

    • May see infertility, acne, alopecia, increased androgens, insulin resistance.

  • Diagnostic criteria (Dx criteria): two of the following three, after exclusion of other etiologies (e.g., Cushing’s syndrome, androgen-secreting tumour):- Ovulatory dysfunction (oligo- or anovulation);

    • Hyperandrogenism;

    • Polycystic ovarian morphology on ultrasound (PCOM).

  • PCOS – Clinical Features:- Anovulation: oligomenorrhoea/amenorrhoea; infertility/subfertility; early pregnancy loss.

    • Long-term risk of endometrial hyperplasia/cancer due to unopposed oestrogen effects on the endometrium (risk RR approx 2-6 fold).

    • Metabolic consequences: obesity; hyperlipidaemia (up to 70% have high LDL);

    • Insulin resistance/hyperinsulinemia (≈ 30%);

    • Type 2 diabetes mellitus (T2DM) by age 30 in 7-10%;

    • Increased risk of heart disease and hypertension.

  • PCOS – Pathophysiology:- Involves genetic, hormonal, and environmental factors.

    • Androgen excess: elevated androgens (e.g., testosterone) → hirsutism, acne, scalp hair thinning.

    • LH–FSH imbalance: elevated LH relative to FSH disrupts normal ovarian function and contributes to cyst formation.

    • Insulin resistance: higher insulin stimulates ovaries to produce more androgens and drives metabolic disease (obesity, T2DM, cardiovascular disease).

    • Ovarian dysfunction: irregular ovulation or anovulation, menstrual irregularities, infertility, ovarian cyst formation.

    • Chronic inflammation: low-grade inflammation may contribute to insulin resistance and hormonal imbalance.

Ovarian Cancer

  • Ovarian malignancies are among the most lethal gynecological cancers; 5th leading cause of cancer death in women.

  • More common in women over 50 years.

  • Primary lesions arise from normal ovarian structures; secondary lesions can originate from endometrium, breast, colon, stomach, or cervix.

  • Risk factors (more ovulations):- Nulliparity;

    • Early menarche;

    • Late menopause;

    • Estrogen-only hormone replacement therapy (HRT);

    • Smoking;

    • Obesity.

  • Protective factors (fewer ovulations):- Multiparity;

    • Prolonged use of oral contraceptives;

    • Breastfeeding.

Ovarian Cancer – Primary Ovarian Neoplasms

  • Epithelial cell tumours:- Cystadenomas; carcinoma (accounts for 70% of all ovarian malignancies).

  • Stromal cell tumours (sex-cord stromal tumours).

  • Germ cell tumours.

Ovarian Tumours – Primary Features

  • Primary ovarian neoplasms may be:- Solid or cystic or both;

    • Unilateral or bilateral;

    • Histopathology: clearly malignant, clearly benign, or borderline/uncertain malignant potential.

  • Clinical presentation:- Often incidental and asymptomatic;

    • Abdominal bloating and increased abdominal girth;

    • Pelvic/abdominal pain; chronic pain with pressure on bladder/bowel; dyspareunia;

    • Acute pain from bleeding, rupture, or torsion;

    • Vaginal bleeding.

Serous Ovarian Cancers

  • Serous ovarian cancers are the most common type of ovarian tumours.

  • Typical age: 30-40 years.

  • Tumour cells are serous in nature.

  • Usually cystic with thin walls and filled with clear serous fluid.

  • Often bilateral.

  • Subtypes:- Benign: serous cystadenoma (≈ 60%);

    • Borderline: ≈ 15%;

    • Malignant: serous cystadenocarcinoma (≈ 25%).

  • Category: Ovarian epithelial tumours.

Ovarian Non-Epithelial Tumours – Germ Cell Tumours (Teratomas)

  • Teratomas arise from undifferentiated germ cells and can differentiate into multiple tissue types.

  • Possible tissues include hair, bone, cartilage, and thyroid follicles.

You Should Now Be Able To

  • Identify and describe the common pathological conditions of the ovaries:- Ovarian Cysts;

    • Polycystic Ovarian Syndrome (PCOS);

    • Ovarian Cancer.