Pregnancy and Placental Physiology Flashcards
Pre-implantation
< 1 week
Hyperplasia but not hypertrophy
Fate of cells not determined, low sensitivity to teratogens and developmental abnormalities → great regenerative capacity
Histiotrophic phase = cells in the trophoblast are digested to become the nutrition for the embryo (not reliant on placenta (hemotrophic) for nutrition yet)
Gastrulation`
Weeks 2-3
Cell migration through primitive streak (hyperplasia)
Formation of ectoderm (CNS + skin), mesoderm, and endoderm
Very susceptible to teratogens
Organogenesis period
Weeks 3-8
Mix of hyperplasia and hypertrophy
structures established, cell prolif, migration, cell-cell interaction, and tissue re-modeling
neural tube must close by day 27 to prevent nerve degeneration
Extremely (maximum) susceptible to teratogens
Fetal/neonatal period
8 weeks and beyond
Tissue differentiation, growth (hypertrophy) and maturation
Toxic exposures effect growth and functional maturation
CNS and reproductive abnormalities, behavior and motor deficits
Effects of nutrient excess teratogenic
Iodide excess: Congenital goiter and mental/physical disabilities
Vitamin D excess: facial and mental abnormalities
Vitamin A excess: CNS abnormalities risk increases above 10,000 IU
Fluoride excess: spina bifida occulta
Effects of nutrient deficiency teratogenic
Protein: microcephaly
Vitamin A: eye abnormality, microcephaly
Vitamin D: fetal rickets
Vitamin E: congenital abnormalities
Vitamin K: coumadin syndrome
Folate: NTDs
Iodine: cretinism (mental/physical retardation)
Copper: connective tissue defects, brain and bone abnormalities genetic inborn errors of Cu metabolism
Zinc: NTD (short periods can cause)
Symptoms of FAS
Characteristics: craniofacial dimorphism, growth retardation, retarded psychomotor and intellectual development
- thin upper lip, smooth philtrum, small palpebral (eyelids) fissures
Alcohol related birth defects: microcephaly and heart, kidney, lung malformations
Alcohol related neurodevelopmental disorder: IQ, attention
Hyperhomocysteinemia
Despite plasma [homocysteine] ↓ during pregnancy 30-60%
Elevated homocysteine can auto-oxidate free radicals and is associated with oxidative damage
Due to low 5-methyl-THF levels (dietary, genetic)
↑ risk preeclampsia, spontaneous abortion, recurrent early miscarriage and NTD
High preconception homocysteine associated with LBW
Neural tube defects
Possibly causes
Anencephaly = head of neural tube fails to close
- results in missing portion of brain/skull/scalp → fetal death shortly after birth
Spina bifida - incomplete closure of neural tube → nerve damage, some level of paralysis
Possibly causes: folate deficiency, extreme heat/fever, severe overweight, diabetes (IDDM), genetics
Hormones secreted by the placenta and what they do
human chorionic gonadotropin - maintains corpus luteum which secretes estrogen and progesterone
human chorionic somatomammotropin (placental lactogen) - produced late gestation
- catabolic phase
progesterone - produced by corpus luteum until week 10, then placenta
- inhibits pituitary release of LH and FSH to prevent ovulation
- suppresses uterine contractility
estrogen - maximal towards end of pregnancy
- stimulates myometrium growth and mammary gland development
- antagonizes myometrial suppression by progesterone
Nutrients transported by facilitated or active diffusion across placenta and why?
Facilitated:
long chain FA - disequilibrium for brain development
sugar - high glucose levels are teratogenic
Active:
amino acids
cations (Ca, Fe, I, PO4)
How does malnutrition lead to IUGR
Malnutrition → low blood volume expansion → low cardiac output → low placental blood → decreased placenta size/nutrient transfer → fetal growth retardation (IUGR)
EFA deficiencies → defects in placental integrity → IUGR and LBW
eicosanoids play roles in vasodilation and nutrient delivery
