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
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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
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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
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CV Changes
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Renal & GFR
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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