Physiology of Pregnancy (Continued)

Progesterone relaxes intestinal smooth muscle and slows peristalsis.

• 1. Enlarging uterus displaces stomach above esophageal sphincter, causes intragastric pressure
• 2. Progesterone causes a relative relaxation of esophageal sphincter
• 3. May also be reflux of bile into stomach due to pyloric incompetence

• General enlargement of heart and left ventricle. Heart is displaced anterolaterally secondary to rise in level of diaphragm, which leads to altered ECG and possible changes that mimic ischemia.
• On auscultation: at end of T1, both components of S1 become louder with exaggerated splitting. After midpregnancy 90% of women demostrate S3 gallop. Systolic ejection murmurs occur along left sternal border in 96% of pts.

There is increased turnover from lipoproteins, creating an increased supply to most tissues, and increased supply for steroid production. Total cholesterol is raised post-partum in all mothers.

At 26-28 weeks GA.

It increases soon after conception. It reaches 60% above non-pregnant level by 16 weeks and remains elevated for remainder of pregnancy.

• Pyelonephritis
• bacteriuria+urinary stasis predispose patients

It falls by 22% due to hemodilution, despite the increase in synthetic rate.

Increased distensibility and pressure of veins.

Urinary stasis-decreased ureteral peristalsis and mechanical compression of ureter

• Hepatic funciton increases
• Plasma globulin and fibrinogen concentrations increase
• Synthetic rate of albumin increases
• Velocity of blood flow in hepatic veins decreases
• Serum alk phos increases largely due to placental production

• 1. Increases in size
• 2. Empties more slowly
• 3. Cholestasis, probably due to a hormonal effect.

• The gland increases in weight and sensitivity.
• Prolactin: plasma levels rise a few days postconception. At term levels are 10-20 fold higher than nonprego

FSH: blunted response to GnRH. Progressive decreased response at 3 wks after ovulation

Luteinizing Hormone: Response to GnRH diminishes and finally disappears.

human chorionic gonadotropin (hCG)- coregulates and stimulates adrenal and placental steroidogenesis. Stimulates fetal testes to secrete testosterone.Thyrotrophic activity

human placental lactogen (hPL)- anti-insulin and growth hormone-like effects lead to impaired maternal glucose and free fatty acid release.

Increase! Pregnancy is a hypercoagulable state and a disorder may become apparent during pregnancy.

Reactivity increases in T2 and T3 and returns to normal at 12 wks post partum.

• Neutrophil count increases in T1 and continues until 30 weeks, also metabolic activity and phagocytic function increase.
• Lymphocytes counts remain unchanged but function is suppressed.

• It rises early in pregnancy
• An ESR=100mm/hr is not uncommon in normal preg.

• Circulating RBC mass increases by 18% if no Fe supplement and by 30% with Fe.
• Retic count increases by >2%
• MCV usually increases

• By 50% due to increase in RBCs and plasma.
• This increase is greater in multi compared to primigravidas.

• 1.GFR increase
• 2.Quantity of glucose filtered in urine greater than nonpregnant
• 3.Tubular threshold for glucose is variable
• 50% of pregos

Progesterone increases Na+ excretion, but its increase is balanced by effects of increased aldosterone, mineralocorticoids, and prostaglandins. Renal retention of Na+ results in water retention.

• They lose some resorptive capacity.
• Results in protein loss up to 300mg/24hr

produces maternal steroids and synthesizes proteins that are related to the maintenance and protection of the pregnancy from immunologic rejection.

decidua

The precursor cells for the placenta and membranes

On day 5-6 of development, the blastocyst adheres to the endometrium.

24 hrs after ovulation in the third of the fallopian tube adjacent to the ovary (ampulla)

Cervical effacement.

accumulation of glycosaminoglycans and increase in water content and vascularity.

• They contract spontaneously or in response to uterine movement (can be the source of pelvic/inguinal pain)
• In labor, contractions of the ligaments pull the uterus forward.

• nonpregnant: uterine artery most important
• pregnant: ovarian arteries-20-30% (in 70% of women)

Pruritis gravidarum: generalized severely pruritic excoriations.(Tx with antipruritics and cholestyramine)

Impetigo herpetiformis(pustular psoriasis of pregnancy)- pustules with minimal itching on genitalia, medial thighs, umbilicus, breasts and axillae. Can cause maternal sepsis. (Tx: systemic corticosteroids and ABX for secondary infxn)

Herpes gestationis: severely pruritic erythematous papules, vesicles, bullae on abdomen and extremities. Causes growth restriction and prematurity. (Tx mild case with topical steroids+antihistamines, More severe- tx with systemic corticosteroids.

PTH-concentration falls. But PTH is greater in mother while calcitonin is greater in fetus at term leading to fetal bone deposition.

Cause striae on abdomen, breasts etc.

Can cause spider nevi and palmar erythema

• Increase in melanocyte stimulating hormone.
• *Suntans acquired in pregnancy last longer than usual.

• 1. serum levels rise during 2nd half, but insulin resistance increases
• 2. Insulin resistance swithces carbohydrate to fat utilization

• 1. Size of islets of langerhans increase during pregnancy
• 2. Number of beta cells increase
• 3. Number of insulin receptor sites increase

They fall markedly by 20 weeks. This reduces colloid osmotic pressure in plasma->edema.

• Total thyroxine levels and throxine binding globulin increase. The result is that free thyroxine remains normal and mother remains euthyroid.
• *All goiter should be investigated

• Plasma cortisol and other corticosteroids increase progressively from 12 weeks to term to reach 3-5 times nonpregnant levels
• 1/2 life of plasma cortisol is increased and clearance reduced.

• Source: yolk sac, fetal gastrointestinal tract, fetal liver
• Function: regulates fetal intravascular volume (osmoregulator)
• -AFP peaks b/w 10-13 weeks gestational age, then declines thereafter
• -Detectable as early as 7 weeks gestation

• Source: decidualized endometrium
• Function: regulates fluid and electrolyte flux through the fetal membranes

• Source: placental tissue, decidua, hypothalamus (maternal)
• Function: stimulates placental ACTH release and participates in the surge of fetal glucocorticoids associated with late T3 fetal maturation
• Cortisol has feedback with placental CRH production

• Source: trophoblasts
• Function: antagonizes insulin->maternal glucose intolerance, lipolysis, and proteolysis

• Source: trophoblasts
• Function: stimulates an increase in circulating maternal free cortisol

• Source: placenta
• Function: maintains corpus luteum. Stimulates adrenal and placental steroidogenesis.

• Postcnception day Tissue/Organ formation
• 4-Blastula
• 7-12-implantation
• 13-primitive streak
• 16-neural plate
• 19-21-first somite
• 23-25-closure of anterior neuropore
• 25-27-arms bud, closure of posterior neuropore
• 28-legs bud
• 44-sexul differentiation.