pregnancy

when does the highest rate of pregnancy loss occur?

often occur in early stages due to early embryonic death

what are some causes of early embryonic death?

• embryo: polyspermy, aneuploidy, abnormal development

• maternal factors: infections, hormonal diseases (imbalances), uterine diseases/defects

non-invasive placenta

• implant later

• large surface area

• relatively loose attachment to uterus

invasive placenta

• implant early

• small surface area

• invade deep into uterus

chorionic villi

functional unit for nutrient exchange in chorion surface

diffuse placenta

• uniform distribution of chorionic villi

• horse, pig

cotyledonary placenta

• numerous discrete “buttons” (cotyledons) of chorionic villi

• ruminants (sheep, cows, goats)

zonary placenta

• band-like zone of chorionic villi

• canids, felids

discoidal placenta

• regional disc of chorionic villi

• primates, rodents

epitheliochorial placenta

• uterine epithelial + endothelial cells separate fetal/maternal blood

• horses, pigs, ruminants (cows, sheep, goats)

endotheliochorial placenta

• uterine endothelial cells separate fetal/maternal blood

• canids, felids

hemochorial placenta

• neither uterine epithelial nor endothelial cells separate fetal/maternal blood

• more efficient nutrient exchange

• primates, rodents

functions of the trophoblast

1. maternal recognition of pregnancy signaling

   • hormone production

2. implantation

3. fetal part of placenta

allantois functions

• collect liquid waste from the embryo

• gas exchange

• present early on before fetus is functional

how does the placenta create an immunological barrier?

• camouflage by trophoblasts

• reduced immunological activity in the uterus: immune reactions are inhibited by products of the uterus and trophoblast

• antibodies cannot cross the placenta in any species until the end of pregnancy, and they never cross in species with non-invasive placentas

how are antibodies delivered to the offspring?

• in species with invasive (hemochorial) placentas, antibodies are actively transported across the placenta in late gestation

• in species with non-invasive placentas, antibodies are passed via colostrum (antibodies do NOT cross the placenta)

what hormones does the placenta produce to modulate maternal physiology?

• steroid hormones

  • estrogens, progesterone

• protein hormones (more species differences)

  • chorionic gonadotropins (CG): hCG, eCG, rodent placental lactogens

  • placental lactogens (prolactin and GH activity)

  • many others

estrogen metabolism in the placenta

• trophoblast has high levels of aromatase but primary products are generally less active estrogens

• fetus inactivates estrogens by fetal liver sulfation → trophoblast reactivates and sends weak estrogens to maternal circulation

• “environmental” estrogens are frequently not susceptible to inactivation by these pathways

sources of progesterone during pregnancy

• corpus luteum (luteal progesterone)

  • prolonged life after maternal recognition of pregnancy

  • secondary CL in equids

• trophoblasts (placental progesterone)

  • constitutive

  • does not require LH

endometrial cup

• unique structure in equids for eCG production

• chorionic trophoblast cells invade endometrial stroma and detach from fetal membrane, forming endometrial cup → produce eCG

  • due to the non-invasive placenta, trophoblast cells must invade stroma to get eCG into maternal circulation

what is the function of eCG from the endometrial cup?

• results in luteinization/ovulation of a secondary follicle, forming a secondary CL

• eCG mainly has LH activity in the mare → maturation and ovulation of secondary follicle → secondary corpus luteum → luteal progesterone production

• synthesizes eCG from ~ day 40-120

placental lactogens

• group of hormones evolutionarily related to growth hormone and prolactin (pituitary hormones)

• ex. rodent placental lactogen (PRL activity), human placental lactogen (mainly PRL activity and some GH activity)

what effects do placental hormones exert?

• most hormones exert effects on mother for successful pregnancy and lactation

  • repro tract: low muscle excitability in uterus, histotroph secretion, local immune suppression, increased blood supply, closed cervix

  • suppress HPG axis

  • metabolism: store energy during early pregnancy; during late pregnancy, make nutrients available to fetus

  • calcium turnover: increase maternal dietary absorption and bone resorption (especially during fetal bone ossification)

  • increase cardiac output to uterus (20% vs 2%)

  • preparations for postnatal life: develop mammary gland; maternal behavior

what are the three main stages in prenatal development?

• early pregnancy: organogenesis

• mid-pregnancy: system development, including specializations to survive in the uterus (cardiovascular system, oxygen exchange)

• late pregnancy: GROWTH, preparations for independence, final touches

late pregnancy fetal GI function

• fetus swallows amniotic fluid

• undigested material accumulates as meconium (first poop)

  • meconium retention is one of the most common causes of colic

why is fetal respiration important during late pregnancy?

the fetus “breathes” amniotic fluid, strengthening the diaphragm

fetal kidney function in late pregnancy

begins to urinate into the allantoic sac

fetal endocrine function during late pregnancy

• thyroid: thyroid hormone axis critical for fetal growth and neural development

• pancreatic islets: develop ability to store and mobilize glucose

• adrenal gland: ACTH-regulated cortisol production critical for initiation of labor. glucocorticoids increase surfactant in the lungs

how is fetal growth controlled?

fetal growth is influenced by:

• fetal insulin, thyroid hormone, local growth factors, (maybe) placental lactogens

• genetics

• available nutrients: number of developing fetuses, efficiency of placental exchange, size of mother

**note: fetal growth is NOT influenced by growth hormone