Pregnancy Flashcards
Lactogens
GH
- hGH
- PRL
By placenta
- hGH-V
- hPL
All bind @ PRL R
regulate nutrient mobilization & utilization during pregnancy
Growth Hormone
hGH & hGH-V
hGH-V replaces hGH during 2nd trimester

Reduced hCG-V
impaired placental f
low maternal IGFs
red nutrient delivery
IUGR (intra uterine growth restriction) &/ SGA (small for gestational age)
hCG-V continuous manner
I GHRH & pit GH
PRL
Rise during pregnancy
Reg nutrient mobilization & growth & dev

Hormonal suppression of lactogenesis during pregnancy
Progesterone blocks lactogenesis
- acts on breast
- suppress up reg of PRL R
- blocks true lactogenesis
- PRL is elevated by can’t stimulate lactogensis
- Estrogen stim alveoli & duct dev
- estrogen stim colostrum
Clostrum- rich in Y, protein, mild laxative, low in lipid, carbs & H2O
hPL
4-5 wk of gestation
homology w/ GH & PRL
Interacts w/ PRL & GH R
elevated associated w/ maternal insulin R
Normal glucose transport
glucose primary substrate for fetal metabolism
GLUT on both sides of trophoblast
Via facilitated diffusion
Placenta consumes 50-75%
4-8 mg/kg/min
Gestational Diabetes
weight reduction
hazy eyesight
incontinency
increased thirst & hunger
exasperation & irritation
Hyperglycemia & GDM
Prevalence in cultures (high w/ american indians, asians, hispanic & black women)
Hihger risk of developing DM2
Insulin R
can increase by 3x in pregnancy
2nd & 3rd trimesters
- increase hPL, hGH-V, IGF-1, PRL, CRH & progesterone
- decreased pit hGH
- lower pancreatic B cell compensation
- increased calories
elevated hPL correlates w/ hyperglycemia/insulin R/GDM
Insulin R
Mother–> hyperglycemic–> preeclampsia & hyperT–> can cause preTerm delivery
placenta & fetus–>hyperglycemia–>increased fetal growth–> can cause LGA infant
BV Changes
anemia is normal during pregnancy (slight)
Plasma vol increases disproportionate to RBC cell mass
Uterine Blood Flow

CV Changes

Renal & GFR

GFR increases to handle increase in PV & CO
Decrease in 3rd trimester so increase vasoconstriction of renal BVs w/ preeclampsia
Incrased release of vasoactive cmpds
renal vascular endothelium exhibits lesions
symport across renal endothelium is dysregulated
Leads to proteinuria
Preeclampsia
Hemolysis
ELevated liver enz
Low Platelet count
Preeclampsia
vascular change & proteinuria
decrease in RPF
Increase endothelins
Increase ROS
Vasoconstriction & swelling
Reduced endotehlial fenestrae
Dysregulated symport across renal endothelium
Maternal Fetal O2 exchange
maternal & fetal blood travel in same direction
for most nutrients fetal levels equilbrate w/ mom venous levels

O2
adequate blood flow supplies embryo/fetus w/ nutrients & O2
FHB has higher O2 binding affinity than maternal Hb
This allows for highly efficient transfer of low sat maternal blood in intervillous space to yeild highly ox blood in umbilical v.
fetal EPO from fetal liver that cant cross placenta

O2 transport
O2 transport across placenta is by diffusion & highly efficient
- diffuse through RBC mem
- into syncytiotrophoblast
- into BM & across villous stroma
- across vascular endoth lining fetal BV
- into fetal RBC
- quickly binds to FHb
Placenta consumes 30% of O2