Pregnancy Development

Sperm capacitate (mature) in the female reproductive tract over 6+ hours, gaining ability to fertilize. They navigate cervical mucus, uterus, and fallopian tube via chemotaxis (progesterone gradient) and rheotaxis. At the egg, sperm undergo acrosome reaction releasing enzymes that penetrate the zona pellucida. Sperm-egg fusion triggers cortical reaction blocking polyspermy. The zygote completes meiosis II. After 24 hours, the first cleavage division begins. Implantation occurs on day 7-9 after ovulation.

Human chorionic gonadotropin is secreted by syncytiotrophoblast starting at implantation. Its main role is to maintain the corpus luteum (which produces progesterone) until placental progesterone takes over at 8-10 weeks (luteal-placental shift). Levels double every 48-72 hours in early pregnancy, peak at 8-11 weeks, then decline. Slow rise suggests ectopic or failing pregnancy; very high levels — molar pregnancy or multiples. Beta-hCG is the basis of pregnancy tests; quantitative levels guide management of ectopic pregnancy and miscarriage.

Weeks 3-8 after fertilization (gestational weeks 5-10) is the critical period when most organs form. Highest teratogenic risk. Drugs and infections cause specific birth defects depending on timing. Examples: thalidomide caused phocomelia; isotretinoin causes craniofacial and CNS defects; rubella in 1st trimester causes deafness, cataracts, cardiac defects; alcohol causes fetal alcohol syndrome. Avoid all unnecessary medications and live vaccines. Folic acid 400-800 μg daily before conception prevents neural tube defects (closure complete by week 6).

Hypertensive disorder of pregnancy after 20 weeks: BP ≥ 140/90 on two occasions plus proteinuria (≥ 300 mg/24h) or end-organ dysfunction. Severe features: BP ≥ 160/110, thrombocytopenia, transaminitis, renal insufficiency, pulmonary edema, neurologic symptoms. Pathophysiology: defective trophoblast invasion of spiral arteries, placental ischemia, anti-angiogenic factor release (sFlt-1, soluble endoglin), endothelial dysfunction. Treatment: BP control (labetalol, nifedipine, hydralazine), magnesium sulfate (seizure prophylaxis), and definitive treatment is delivery.

Cardiac output increases 30-50% by 24 weeks (increased SV and HR). Plasma volume expands 50%, RBC mass 25% — physiologic anemia. Tidal volume rises 40% (progesterone drives respiratory alkalosis). GFR rises 50% (creatinine should be lower, ~0.5 mg/dL). Insulin resistance increases (placental hPL and cortisol) — gestational diabetes screen at 24-28 weeks. Hypercoagulable state (factors I, VII, VIII, IX, X up; protein S down) — VTE risk 5-10x. Uterine size: 12 weeks at pubic symphysis, 20 weeks at umbilicus, term at xiphoid.

Multifactorial. Fetal CRH from placenta rises through pregnancy. Late-pregnancy increase in estrogen/progesterone ratio increases uterine excitability. Oxytocin receptors upregulate. Prostaglandins (PGE2, PGF2α) soften the cervix and stimulate contractions. Stretching of the cervix triggers oxytocin release (Ferguson reflex) — positive feedback. Three stages: 1st (cervical dilation to 10 cm), 2nd (full dilation to delivery), 3rd (placental delivery). Average duration: 12-18 hours nullipara, 6-8 multipara. Augmentation: oxytocin (Pitocin); induction: prostaglandins, oxytocin, mechanical methods.

Hyperglycemia first recognized in pregnancy. Affects 7-9% of US pregnancies. Caused by placental hormones (hPL, progesterone, cortisol, GH) inducing insulin resistance — usually compensated by increased β-cell insulin output, but inadequate response causes GDM. Screening: 50-g glucose challenge at 24-28 weeks; if abnormal, 3-hour 100-g OGTT confirms. Risks: macrosomia, shoulder dystocia, neonatal hypoglycemia, preeclampsia, cesarean delivery. Treatment: diet, exercise, insulin or metformin if needed. 50% develop type 2 diabetes within 10-20 years.