SEARCH RESULTS FOR: Oligomenorrhea

Polycystic Ovarian Syndrome

Polycystic Ovarian Syndrome (PCOS): Pathogenesis and clinical findings Genetic Susceptibility: ↑ Expression of LH receptors in granulosa cells, and anterior pituitary ↑ production of luteinizing hormone (LH) ↑ Serum LH compared to FSHà higher levels of LH increasingly activate thecal cells Excess nutrients (from overeating and sedentary behavior) is stored as visceral fat ↑ Central adiposity (accumulation of fat around abdominal area) Adipose tissue ↑ secretion of estrogen, inflammatory mediators, adipokines, free fatty acids ̄ Hepatic synthesis of sex hormone-binding globulin Acne Hair loss on scalp, and less commonly eyebrows and eyelashes (alopecia) Excessive hair growth around mouth, chin, chest, abdomen, upper arms, thighs, and upper & lower back (hirsutism) Metabolic syndrome develops, including ↑ insulin resistance, obesity, dyslipidemia, liver disease, & cardiovascular disease Theca cells in ovaries ↑ androgen secretion ↑ Serum androgens State of hyperandrogenism Androgen and estrogen levels are elevated too early in menstrual cycle (estrogen has negative feedback inhibition on anterior pituitary hormone production) Early suppression of FSH Limited proliferation of follicles Relative reduction in secretion of progesterone Imbalance between progesterone and estrogen Unpredictable ovulation ↑ Circulating insulin- like growth factor Growth factor promote keratinocyte and dermal fibroblast proliferation Velvety, darkening of the skin fold areas such as back of neck, armpit area, groin (acanthosis nigricans) ↑ Risk of type 2 diabetes mellitus Since granulosa cells normally convert testosterone to estrogen, ̄ granulosa cell function means more testosterone exists Since follicle stimulating hormone (FSH) activates granulosa cells, ̄ FSH means ̄ granulosa cell function. Follicles arrested in development accumulate fluid, becoming cysts Polycystic ovaries visible on ultrasound Infertility Unpredictable uterine bleeding ↑ Risk of endometrial hyperplasia & endometrial cancer Irregular menstruation (amenorrhea/oligomenorrhea) Authors: Lauren Standerwick Claire Song Reviewers: Mackenzie Grisdale Amy Fowler Christina Schweitzer Michelle J. Chen Dr. Yan Yu* Dr. Bernard Corenblum* Dr. Sylvie Bowden* * MD at time of publication Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Nov 20, 2017; updated Dec 15, 2024 on www.thecalgaryguide.com

Oligomenorrhea

Oligomenorrhea: Pathogenesis and clinical findings Polyendocrine Metabolic Ovarian Syndrome (PMOS) Adipose tissue inflammation & metabolic signalling defects trigger insulin resistance Hyperinsulinemia ↓ Insulin-like growth factor- binding protein-1 (IGFBP-1) → ↑ free IGF activity ↑ Anterior pituitary sensitivity to gonadotropin-releasing hormone (GnRH) ↑ Luteinizing hormone (LH) & ↓ sex hormone binding globulin (SHBG) from liver Stimulates ovarian theca cells to ↑ androgen production ↑ Free testosterone, total testosterone, androstenedione, dehydroepiandrosterone sulfate & 11-oxygenated androgens Hyperandrogenism Lifestyle & behavioural factors (eating disorders, extreme exercise, excessive stress, extreme weight changes) ↑ Cortisol ↑ Leptin (regulates long term energy balance & weight) Authors: Sonika Khurana Reviewers: Catherine R Jarvis Clara Letef Sandra Peacock* *MD at time of publication Chronic hypoestrogenism ↓ Estrogen → ↓ osteoclast apoptosis (cell death) → ↑ bone resorption (destruction) ↓ Bone density Chronic hyperestrogenism Unopposed estrogen Endometrial hyperplasia/cancer Hormonal imbalances Perimenopause (natural decline in ovarian function leading up to menopause) Prolactinoma, antipsychotic medications & structural (trauma) pituitary stalk damage Hypothyroidism Hyperthyroidism ↓ Thyroid hormones ↑ Thyroid hormones ↓ Ovarian follicles ↑ SHBG from liver ↑ Thyroid Releasing Hormone (TRH) release from hypothalamus ↑ Sex hormone binding → ↓ free circulating sex hormones ↓ Inhibin B production from ovarian granulosa cells ↑ Peripheral conversion of androgens into estrogen ↓ Negative feedback on pituitary ↑ Thyroid stimulating hormone (TSH) ↑ Estrogen Stimulates lactotroph cells in pituitary ↑ Follicle Stimulating Hormone (FSH) & ↑ LH to stimulate immature follicles ↑ Prolactin ↓ GnRH → ↓ LH & FSH Immature follicles fail to respond to FSH Inadequate follicle maturation causes anovulation & no corpus luteum is formed → no progesterone released Lack of progesterone to stabilize endometrium leads to endometrium proliferation & unstable shedding Oligomenorrhea Irregular menstrual cycles (>35 days apart) Hypothalamic-pituitary-ovarian axis is disrupted Chronic anovulation Chronic hyperandrogenism Insulin resistance ↑ Hair follicle stimulation ↑ Sebaceous glands’ oil production Metabolic dysfunction & ↑ inflammation damages vascular function ↑ Insulin production triggers cholesterol accumulation in vessel walls & promotes atherosclerosis Infertility & reproductive issues Hirsutism (excessive growth of dark coarse hair) Acne ↑ Cardiovascular disease risk Diabetes Legend: Pathophysiology Mechanism Sign/Symptoms/Lab Finding Complications Published Jul 7, 2026 on www.thecalgaryguide.com Creative Commons License