Micturition Reflex
The bladder stores urine (filling phase) and empties via the micturition reflex (voiding phase). Normal adult bladder capacity: 400-600 mL; urge to void at ~150-300 mL.
| Phase | ANS | Receptor | Effect |
|---|---|---|---|
| Filling (storage) | Sympathetic (T10-L2) | Beta-3 (detrusor relaxation), alpha-1 (internal sphincter contraction) | Bladder relaxes; internal sphincter closes |
| Voiding | Parasympathetic (S2-S4) | M2/M3 muscarinic (detrusor contraction) | Detrusor contracts; internal sphincter relaxes |
| External sphincter | Somatic (pudendal nerve) | Nicotinic | Voluntary control; relaxes during voiding |
⭐ Overactive Bladder TreatmentMuscarinic antagonists (oxybutynin, tolterodine, solifenacin) relax detrusor → reduce urge incontinence. Beta-3 agonist (mirabegron) also used. Alpha-1 blockers (tamsulosin) relax internal sphincter → BPH and urinary retention. 5-alpha reductase inhibitors (finasteride) reduce prostate size long-term.
Menstrual Cycle
| Phase | Days | Key Hormones | Events |
|---|---|---|---|
| Menstruation | 1-5 | Low estrogen and progesterone | Functional endometrium sheds; prostaglandins cause cramps |
| Follicular / Proliferative | 1-14 | FSH (dominant); rising estrogen from granulosa cells | Follicle development; endometrial proliferation; cervical mucus thins; basal body temp drops |
| Ovulation | Day 14 | LH surge (triggered by high estrogen — positive feedback) | Dominant follicle ruptures; oocyte released; Mittelschmerz (mid-cycle pain) |
| Luteal / Secretory | 15-28 | LH → corpus luteum → progesterone and estrogen | Endometrium becomes secretory (glands, glycogen); progesterone raises basal body temp by 0.5°C |
| Late luteal | 25-28 | Corpus luteum degenerates; progesterone falls | Endometrium sheds → menstruation begins (unless pregnant) |
🧐 Cervical Mucus ChangesEstrogen (follicular): thin, watery, elastic (Spinnbarkeit) mucus → allows sperm entry. Progesterone (luteal): thick, hostile mucus → blocks sperm (contraceptive mechanism of progestin-only pills). Fern pattern on microscopy = estrogen dominance.
Pregnancy Physiology
| System | Change in Pregnancy | Significance |
|---|---|---|
| Cardiovascular | CO increases 30-50%; SVR decreases; BP decreases (1st and 2nd trimester); HR increases | Physiologic anemia (dilutional); avoid supine position in late pregnancy (IVC compression) |
| Renal | GFR increases 50%; creatinine and BUN decrease; physiologic glycosuria and proteinuria | Normal creatinine in pregnancy is ~0.5-0.8; "normal" creatinine of 1.0 may indicate renal disease |
| Respiratory | Tidal volume increases; RV and FRC decrease; respiratory alkalosis (PaCO2 ~28-32) | Progesterone stimulates breathing; compensated by renal HCO3- excretion |
| Hematologic | Hypercoagulable (factors I, VII, VIII, X, XII increase; Protein S decreases) | DVT/PE risk 5x increased; thromboprophylaxis in high-risk patients |
| Endocrine | hCG maintains corpus luteum in 1st trimester; placenta takes over progesterone/estrogen by week 10 | hCG peaks at 8-10 weeks; basis of pregnancy test |
Spermatogenesis and Male Physiology
- Spermatogenesis takes ~72 days; occurs in seminiferous tubules at ~34°C (below body temp — hence scrotal location)
- FSH stimulates Sertoli cells → inhibin B production (negative feedback on FSH)
- LH stimulates Leydig cells → testosterone production → supports spermatogenesis
- Testosterone: spermatogenesis, libido, muscle mass, bone density, secondary sex characteristics, erythropoiesis
- Testosterone → DHT (5-alpha reductase) in prostate, skin, hair follicles → more potent androgen; responsible for prostate growth and male pattern baldness
⭐ Testosterone and DHT5-alpha reductase inhibitors (finasteride, dutasteride) block testosterone → DHT conversion → used for BPH and male pattern baldness. DHT is responsible for prostate hyperplasia and androgenetic alopecia. Testosterone itself is responsible for central effects (libido, muscle, bone).
Clinical Pearls
🩹 Menopause PhysiologyOvarian follicles depleted → no estrogen/progesterone → FSH and LH markedly elevated (no negative feedback). Symptoms: hot flashes (vasomotor instability), vaginal atrophy, osteoporosis, cardiovascular risk increase. FSH greater than 40 mIU/mL after 12 months of amenorrhea = menopause diagnosis.
⭐ Contraceptive MechanismsCombined OCP (estrogen + progestin): inhibits LH surge → prevents ovulation; thickens cervical mucus; alters endometrium. Progestin-only: primarily cervical mucus thickening. Copper IUD: spermicidal, toxic to fertilization. Hormonal IUD (levonorgestrel): local progestin → endometrial atrophy + cervical mucus thickening.