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15 Cards in this Set
- Front
- Back
These embryonic cells produce hormones during pregnancy.
IS THIS FC NECESSARY? |
Cytrotrophoblast and
Syncitiotrophoblast: Direct contact w/maternal blood in intervillous space; preferentially secreted into mother Makes protein hormones (hCG) |
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hCG subunits and homology.
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HCG:
Alpha subunit: homologous to FSH, LH, TSH Beta subunit: specific to HCG, but similar to LH Detectable at 6 days post implantation (before missed menses) |
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hCG function
Diagnostic Utility (Syndrome Specific) |
Critical for maintenance of corpus luteum (PG production to maintain endometrium)
Later stimulates T secretion by fetal testes Weak thyrotrophic activity Higher in Trisomy 13/21, and lower in trisomy 18 |
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Human Placental Lactogen:
AKA When is it produced? Produced by? |
Human Chorionic Somatomammotropin (HCS)
Produced day 18 of pregnancy (not essential for normal pregnancy!) Produced by syncytriotrophoblast |
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HPL Function
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Increases insulin levels (diabetogenic)
Stimulates IGF-1 production, induces insulin resistance Enhances lipolysis (critical in fasting state) |
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hCG levels vs hPL levels
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hCG rises very rapidly, peaking at 10 weeks from LMP
hPL begins to rise around 6 weeks, and increases exponentially, peaking at birth |
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Effect of food intake on hPL.
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Food intake will increase glucose levels and cause a decrease in hPL; thus, decreased lipolysis/FFA's
Note: glucose passes readily from maternal compartment to placental compartment to fetal compartment |
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Effect of fasting state (sleep) on hPL.
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Inc'd hPL-->inc'd lipolysis and FFA
Ketones increase and readily pass into fetus |
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Describe sources of progesterone production throughout pregnancy.
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For first 7-10 weeks from LMP, corpus luteum produces PG to maintain endometrium
Marked increase in placental PG from 6 weeks to term 17OH PG rises early (ovarian origin), but returns to baseline by 10 weeks (only need corpus luteum for first 10 weeks!) |
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Progesterone function.
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Uterine relaxation
Prepared endometrium for implantation Breast glandular dev't Suppresses maternal immune response Substrate for production of fetal steroids (GC's, MC's)--fetus can't make PG! |
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Describe progesterone synthesis and transfer in the maternal, placental, and fetal compartments.
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Maternal: LDL Cholesterol and Pregneneolone both enter Placental Compartment
Placental: LDL-->Pregnelenon-->Progesterone (PG can then go to mom or baby); can't go any further bc lacks 17-alpha hydroxylase CYP17 Fetal: LDL Cholesterol-->Prenenolone; can't go any further bc lacks 2-beta OH dehydrogenase Pregnenolone can re-enter placenta |
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Estrogens:
Precursors Sources |
Androgen is estrogen precursor
Ovary and extra ovarian sites: E1, E2 Placenta produces E3 (E1 and E2 to a lesser extent) |
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Describe progesterone synthesis and transfer in the maternal, placental, and fetal compartments.
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Estrogen function
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Physiologic changes of pregnancy
Breast preparation for lactation Cervical ripening--preparation for labor |
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Placental sulfatase:
Function Result of Deficiency |
Enzyme required to produce estrogen in placenta
Deficiency results in failure to have cervical ripening; failure to go into labor (post dates pregnancy)--x-linked recessive dz seen in males, assocd postnatally with ichthyosis (severe cracked skin ) |