menstrual cycle , amenorrhoea and dysmenorrhea.pdf.pptx

Menstrual cycle, amenorrhoea and dysmenorrhea for nursing students.
Created for academic presentation purposes.
It is intended for nursing and allied health students and can also be used as a final review for medical students.

1. 📚. Normal Menstrual Cycle & HPO Axis 👉 Hypothalamus Produces GnRH ( decapeptide ) in the arcuate nucleus. GnRH release is pulsatile : Early follicular: every ~90 min Pre-ovulatory: every ~60–70 min Luteal: lower frequency but higher amplitude Controlled by stress, nutrition, emotions, physical activity. GnRH travels via the hypophyseal venous plexus to act on pituitary gonadotrophs

2. 👉 Pituitary Gland 📚. Normal Menstrual Cycle & HPO Axis Gonadotrophs release FSH & LH in response to pulsatile GnRH . α-subunit of FSH, LH, TSH, hCG is identical; β-subunit is unique. Continuous GnRH → receptor downregulation → used therapeutically for fibroids, endometriosis. FSH: Recruits follicles at cycle start. Stimulates granulosa cells → aromatase → estrogen. LH: Stimulates theca cells → testosterone → estrogen in granulosa cells. LH surge → follicle rupture → ovulation. Luteinizes granulosa cells → progesterone in luteal phase

3. 📚. Normal Menstrual Cycle & HPO Axis 👉 Ovary Finite follicle pool present at birth. Fetal life: 8–10 weeks: primordial follicles. 20–24 weeks: primary follicles. Secondary follicles: zona pellucida → dormant until puberty.

4. At puberty: o FSH recruits follicle cohort each cycle. o Follicles produce estrogen & inhibin → negative feedback on FSH. o Dominant follicle: more FSH/LH receptors, aromatase, estrogen → persists; rest undergo atresia (unless rescued by gonadotropins in ART). o Other factors: insulin, IGF-1, EGF. o Dominant follicle develops: cumulus oophorus , antrum , corona radiata → released at ovulation. • Post-ovulation: o Ruptured follicle → corpus luteum → progesterone & estrogen. o If no pregnancy: corpus luteum → corpus albicans in ~9–10 days. 👉 Ovary 📚. Normal Menstrual Cycle & HPO Axis

5. 📚. Phases of the Menstrual Cycle 👉 Menstrual Phase (Day 1–5) Regression of corpus luteum → drop in estrogen/progesterone. Functionalis layer sloughs, basalis layer retained. Histology: disintegrating glands/ stroma , leukocyte infiltration, RBC extravasation. 👉 Proliferative Phase (up to ovulation) Estrogen → endometrial proliferation. Basal arteries form spiral arteries in new functionalis . Glands: straight, narrow lumens.

6. 📚. Phases of the Menstrual Cycle 👉 Secretory Phase (after ovulation) Corpus luteum progesterone: glands secrete glycogen, mucus. Glands tortuous, lumens dilated; stroma edematous. Spiral arteries become convoluted. If no implantation: corpus luteum regresses → ischemia → menstruation. 👉 Normal Cycle Features Length: 21–35 days (average ~28). Menses: 3–7 days; blood loss 20–80 mL (difficult to measure). Normal: heaviest in first 1–3 days; ≤4 pads/day, no flooding/clots. Spotting mid-cycle can be normal (post-ovulatory estrogen drop). Mild cramps normal; shouldn’t limit daily activities.

7. 📚. Amenorrhea & Oligomenorrhea 👉 Definitions Amenorrhea: Absence of menstruation. Primary: No menarche by 16, OR no thelarche by 14, OR no menarche within 2 yrs of thelarche . Secondary: Cessation of menses for ≥6 months. Oligomenorrhea : Cycles >35 days 👉 Primary Amenorrhea – Causes Hypothalamic: Constitutional delay (familial). Stress, anorexia, over-exercise, chronic illness. Kallmann syndrome ( GnRH deficiency + anosmia). Destructive lesions ( tumours , encephalitis).

8. 📚. Amenorrhea & Oligomenorrhea Pituitary: Hyperprolactinemia (adenoma, hypothyroidism, drugs). Destructive lesions ( tumours , space-occupying). Ovarian: Gonadal dysgenesis (46XX/46XY). Enzymatic defects (e.g., 17-hydroxylase deficiency → hypertension, hypokalemia). Androgen insensitivity. Turner syndrome, mosaicism . Anatomical: Imperforate hymen, transverse septum, cervical agenesis. Müllerian agenesis ( Rokitansky - Küster -Hauser). 👉 Primary Amenorrhea – Causes

9. 📚. Amenorrhea & Oligomenorrhea 👉 Primary Amenorrhea – Approach History: Pubertal milestones: thelarche , pubarche . Family history, stress, smell, headaches, vision. Cyclical pelvic pain (obstructive anomaly). Exam: Tanner staging, BMI, dysmorphism . Smell, visual fields, thyroid, breast, pelvic exam; rectal if needed for uterus. Investigations: FSH, LH, estradiol, testosterone, prolactin, ± TSH. Karyotype, genetic tests. Pelvic US, IVP for Müllerian agenesis. MRI brain for pituitary/hypothalamic lesions

10. Management: Hypothalamic: reassure, lifestyle, estrogen for breast dev., surgery for tumours . Pituitary: dopamine agonists, thyroxine , surgery. Ovarian: HRT, gonadectomy if dysgenetic . Anatomical: surgery for obstruction, neovagina . 📚. Amenorrhea & Oligomenorrhea 👉 Primary Amenorrhea – Causes

11. 📚. Amenorrhea & Oligomenorrhea 👉 Secondary Amenorrhea & Oligomenorrhea – Causes Always rule out pregnancy! Hypothalamic (~35%): stress, weight loss, exercise, chronic illness. Pituitary (~20%): hyperprolactinemia (adenoma, drugs, hypothyroid, renal failure), Sheehan’s, tumours . Ovarian (~40%): premature ovarian failure, PCOS, virilizing tumours , late-onset CAH, Cushing’s. Anatomical (~5%): Asherman’s (uterine synechiae ).

12. 👉 Secondary Amenorrhea – Approach 📚. Amenorrhea & Oligomenorrhea History: Stress, illness, exercise, galactorrhea , virilization , thyroid symptoms, prior uterine surgery. Exam: BMI, hirsutism , acne, acanthosis nigricans , Tanner staging. Investigations: Pregnancy test! LH, FSH, prolactin, E2, testosterone, TSH. DHEA-S, 17-OHP if hyperandrogenism . Withdrawal test. Pelvic US, MRI brain, CT adrenals if needed.

13. Management: Hypothalamic: lifestyle, COCPs. Pituitary: dopamine agonists, thyroxine , surgery. Ovarian: HRT for POF, gonadectomy if dysgenetic . Hyperandrogenism : anti-androgens (spironolactone, CPA), COCPs, surgery if tumour . Anatomical: hysteroscopic adhesiolysis for Asherman’s . 📚. Amenorrhea & Oligomenorrhea 👉 Secondary Amenorrhea – Approach

14. 📚. Dysmenorrhea 👉 Definition Painful menstruation. Primary: No pelvic pathology. Secondary: Due to pelvic disease 👉 Primary Dysmenorrhea Pathophysiology: Ovulatory cycles; prostaglandin-mediated contractions → ischemia. Evidence: Higher prostaglandins in menstrual fluid; NSAIDs effective; anovulatory cycles painless. Features: Cramping lower abdomen, radiates to thighs/back, starts before menses, lasts 48–72 hrs. Nausea, vomiting, headache, diarrhea. Exam: Normal. Management: Reassurance, NSAIDs, COCPs, progestins , antispasmodics ( alverine , hyoscine ). TENS, acupuncture, psychotherapy. If persistent: US, laparoscopy, hysteroscopy.

15. 📚. Dysmenorrhea 👉 Secondary Dysmenorrhea Causes: Endometriosis: Pain before/after menses, dyspareunia, nodularity, endometrioma . Adenomyosis /Fibroids: Menorrhagia, bulky uterus. PID: Discharge, dyspareunia, adnexal mass (abscess/ hydrosalpinx ). Ovarian cysts: Luteal or endometriotic . Pelvic congestion: Dull ache premenstrually , relieved by menses; sexual dysfunction. Key Point: If pain persists despite standard Rx → evaluate for secondary causes.