Reproductive Health Issues PDF

Primary Amenorrhoea Primary: Failure to menstruate by age 16 (but normal secondary sexual characteristics) or by age 14 (with no signs of sexual maturation) Causes can be sorted by location: 1. Hypothalamic level: Low body weight, stress, severe diet restriction (anorexia)/heavy exercise, Kall...

Primary Amenorrhoea Primary: Failure to menstruate by age 16 (but normal secondary sexual characteristics) or by age 14 (with no signs of sexual maturation) Causes can be sorted by location: 1. Hypothalamic level: Low body weight, stress, severe diet restriction (anorexia)/heavy exercise, Kallmann’s syndrome 2. Pituitary level: Tumour 3. Ovarian level: PCOS (normal LH/FSH levels), Turner’s syndrome 4. Uterine level: Gonadal Dysgenesis (Imperforate hymen, Mullerian agenesis, Inter-vaginal septum) Androgen insensitivity 5. Systemic: Constitutional delay (i.e. late bloomer), hyper or hypothyroidism Secondary Amenorrhoea Secondary: Absence of three menstrual cycles (if normally regular) or 6 months (if normally oligomenorrhea) Causes can be sorted by location: 1. Hypothalamic level: Low body weight, stress, severe diet restriction/heavy exercise 2. Pituitary level: Tumour or infarction (usually during labour) 3. Ovarian level: PCOS (normal LH/FSH levels) or early menopause (high FSH/LH) 4. Uterine level: Pregnancy, physical obstruction, iatrogenic 5. Systemic: Breastfeeding, hyperthyroidism, Cushing’s Polycystic Ovarian Syndrome (PCOS) Diagnostic Criteria: 2 of the following 1. Features of hyperandrogenism 2. Oligo or Anovulation 3. Polycystic ovaries on ultrasound Pathophysiology is not fully understood but we do know PCOS is associated with: 1. Insulin resistance → hyperglycemia → increased storage of glucose as adipose tissue → truncal obesity 2. High LH → Hyperandrogenism → hirsutism, oily skin, acne 3. Low FSH → oligo or anovulation → infertility Management: Diet and lifestyle (weight loss improves cycle regularity and decreases diabetes) COCP to control menstrual cycle and hyperandrogenism Menorrhagia Uterine Systemic Infection Iatrogenic Polyps Coagulopathy Adenomyosis (endometrial tissue growing Endocrine (hypothyroidism) in the uterine wall) Leiomyoma/Fibroid (benign growths) Malignancy Pelvic Pain in Females Ovarian Tubal Uterine Other Cyst Pelvic inflammatory Fibroid Appendicitis Malignancy disease Malignancy Diverticulitis Torsion (BAD) (inflammation of the Endometriosis IBD upper genital tract, (cyclical pain) Renal stones usually caused by Adenomyosis UTI/Pyelonephritis STIs) Ectopic pregnancy Ectopic Pregnancy Implantation and maturation of a fertilised embryo outside of the uterine cavity Occurs in 1% of pregnancies 97% arise in the fallopian tube These can rupture and cause massive internal haemorrhage - EMERGENCY Patient will usually present with the classic triad of: 1. Constant abdominal pain 2. Known pregnancy (but not always) or features of pregnancy ○ Amenorrhoea ○ Breast tenderness ○ Nausea and vomiting 3. Bleeding (but not always) If the ectopic has ruptured: Shock (pale, cold, lightheaded from blood loss) Urge to defecate (blood pools in the pouch of Douglas and puts pressure on the rectum) ANY FEMALE OF REPRODUCTIVE AGE WITH ABDO PAIN SHOULD GET A PREGNANCY TEST Menopause Menopause: The final menstrual period (FMP) in a woman who has not had a hysterectomy (average age is 51.5 years) Perimenopause: From the onset of cycle irregularity through until 12 months after the FMP Menopause transition: From onset of cycle irregularity to FMP More anovulatory cycles Irregular menses Lighter/heavier menses Symptoms of oestrogen insufficiency/excess (if more follicles are being recruited) Premature Ovarian Insufficiency Defined as the cessation of ovarian function before 40 years of age Idiopathic (most common) Physical insults: ○ Ionising radiation ○ Chemotherapy ○ Viral infection ○ Smoking ○ Surgery Genetic: Fragile X or Turner’s ○ Fragile X (found in 10% of POI) Hyperactivity, autism-like behaviour, attention deficit Elongated face, prominent jaw, large ears Expansion of an unstable CGG repeat on the X chromosome (>200 when normal is 7-44) ○ Turner’s (45X) Short stature, gonadal failure Enzyme/gonadotropin defects Immune disturbances Consequences of Menopause Loss of cyclical oestrogen production leads to: Vasomotor symptoms (hot flushes, night sweats) ○ 1-5 minute sensation of heat/sweating +/- chills/clamminess/anxiety provoked by warming, stress, food ○ Due to a reduced thermoneutral zone ○ Mechanism is unclear (not just oestrogen withdrawal) but clonidine reduces hot flush frequency Formication (crawling sensation on skin) Muscle/joint pains Anxiety/depression/irritability (1 in 3 experience severe psychological symptoms at menopause) Fatigue, Sleep disturbance (insomnia, poor sleep quality) Lessened memory/concentration (probably related to normal aging) Low libido (decreased testosterone) Vaginal dryness and urogenital symptoms (late) ○ Dryness due to decreased production of vaginal lubricating fluid, loss of elasticity and atrophy of the epithelium ○ Can contribute to painful intercourse, vaginitis, vulval itching and burning ○ Treated with topical estradiol (E2) creams ○ Urological symptoms include increased frequency, recurrent cystitis, dysuria and incontinence = Overall diminished wellbeing Long Term Consequences of Menopause Osteoporosis because of: Ageing → Reduced physical activity → Loss of stimulation of osteocytes → Decreased bone formation Vitamin D deficiency/Reduced calcium absorption → Secondary hyperparathyroidism → Increased bone resorption Menopausal oestrogen decline → Increased RANKL, decreased OPG → Increased osteoclast activity → Increased bone resorption = Low bone mass and loss of bone architecture resulting in: Pathologic (low-trauma) fractures Spinal compression fractures (back pain, loss of height, postural deformities) Risk of CVD/Metabolic syndrome Weight change is related to ageing not menopause but during menopause weight distribution changes Altered energy metabolism → Increased abdominal and intra-abdominal adiposity → Atherosclerosis “Menopausal Metabolic Syndrome” → Atherosclerosis ○ Dyslipidemia: Increased TGLs and LDL, decreased HDL ○ Insulin resistance ○ Increased blood pressure ○ Chronic inflammation Delayed or Absent Puberty Defined as the absence of secondary sexual characteristics at age 13 in girls and 16 in boys. 3 causes: 1. Nonpathologic/Transient (“late bloomer”) 2. Hypogonadotropic hypogonadism/Secondary failure = Low LH and FSH ○ Deficiency in pulsatile GnRH, FSH or LH secretion ○ Due to issues with the hypothalamus or pituitary stalk Congenital: Kallmann syndrome (congenital HH, anosmic hypogonadism) Acquired: CNS tumours or congenital malformations Functional: Anorexia nervosa, intense exercise, IBD, coeliac 3. Hypergonadotropic hypogonadism/Primary failure = High LH and FSH, direct gonadal dysfunction(usually due to dysgenesis) Klinefelter syndrome (47XXY) = small testes, zero sperm count, low testosterone, very high LH and FSH Turner’s syndrome (45X) = short stature, no functional gonads Kallmann’s Syndrome Congenital GnRH deficiency due to failure of GnRH neurons to migrate into the hypothalamus Triad of: ○ GnRH deficiency → absent puberty → small testes ○ Hyposmia/Anosmia (disruption of olfactory nerves) ○ Hypoplasia of the olfactory lobes 4x more common in males than females Treatment: ○ Gonadotropin therapy (to establish fertility, stimulate testicular growth) HCG (similar to LH) FSH ○ Testosterone after 5 years for virilisation (need to mimic normal puberty) Androgen Deficiency in Men Androgens are responsible for establishing and maintaining virilisation Symptoms of deficiency: General: ○ Decreased sense of wellbeing ○ Tiredness, poor stamina, poor concentration ○ Depression, irritability Sexual: Decreased libido, decreased ejaculate volume, erectile failure Organ specific (kinda like menopause actually) ○ Decreased muscle mass and strength ○ Osteoporosis and fracture ○ Increased fat mass ○ CVD and metabolic Treatment: Testosterone Male Infertility Infertility is defined as the absence of conception after 1yr of regular, unprotected intercourse around the time of ovulation. About 1:20 men are subfertile, 60% with no identifiable cause Spermatogenesis issues (60%) ○ Idiopathic/Genetic (majority) ○ Acquired (drugs/toxins/infection) Obstruction (30%) ○ Congenital BCAV (bilateral congenital absence of the vas) ○ Vasectomy ○ STI Intercourse (7%) ○ Erectile and ejaculatory dysfunction ○ Anatomical abnormalities ○ Psychosexual issues Sperm antibodies (2%) Endocrine (