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REI Written Boards SKORY > Pregnancy > Flashcards

Pregnancy Flashcards

1
Q

Maternal GH in pregnancy

A

[decreases] placental GH replaces pituitary GH in maternal circulation, not detectable at term

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2
Q

Maternal TSH in pregnancy

A
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3
Q

Maternal T3/T4 in pregnancy

A
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4
Q

Maternal CRH in pregnancy

A

Not suppressed by glucocorticoids (may be increased)

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5
Q

Maternal cortisol in pregnancy

A

- Cortisol binding protein increases in pregnancy -> total circulating cortisol increases more than free cortisol

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6
Q

Maternal prolactin in pregnancy

A
  • Gradual increase across pregnancy

- At term PRL levels 10X (>200 ng/mL)

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7
Q

Maternal estrogens in pregnancy

A

[increases]
Early pregnancy: Aromatization of maternal androgens
After 20 weeks: Conversion of fetal androgens
- Maternal contribution of DHEA-S is very low
(maternal estrogen very low if fetus lacks adrenal gland)
- Fetus secretes >200 mg DHEA-S daily; >10x of mother

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8
Q

Maternal ACTH in pregnancy

A

Maternal pituitary ACTH also increased under effect of CRH produce in the cytotrophoblast
Not suppressed by glucocorticoids (may be increased)

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9
Q

Maternal ACTH and cortisol peak in pregnancy

A

Delivery (increase throughout pregnancy)

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10
Q

CBG in pregnancy

A
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11
Q

CRH regulators (6)

A

Vasopressin, NE, AGII, PGs, neuropeptide Y, oxytocin

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12
Q

Protects fetus from maternal increases in cortisol

A

Placental 11B HSD (converts cortisol to cortisone)

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13
Q

Tx symptomatic prolactinoma (visual disturbance) in pregnancy

A
  • Bromocriptine -> reduce maternal and fetal circulating levels to baseline levels
  • Amniotic fluid PRL is unaffected by bromocriptine
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14
Q

Main estrogen of pregnancy

A

Estriol (E3)

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15
Q

Estriol (E3) in pregnancy

A

Increases 1000x

16 precursors derived from fetal liver

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16
Q

High estriol implications in pregnancy

A
  • Acute fetal hypoxia
  • Multiple gestation
  • Risk for preterm labor
  • 21-OH CAH
17
Q

Low estriol implications in pregnancy

A
  • Impending or present fetal demise
  • Adrenal hypofunction
  • Placental sulfatase deficiency
  • Placental aromatase deficiency
  • Drug-related effects
18
Q

Placental sulfatase deficiency inheritance, genetics

A
  • X- linked (essentially all are male); 1 per 2-3000 newborn males
  • Complete deletion on the gene within the X (p-region)
19
Q

Placental sulfatase deficiency diagnosis

A

Diagnosis: low estriol in pregnancy (not used anymore), high intra-amniotic DHEA-S, normal DHEA, normal androstenedione (differentiate from CAH)

20
Q

Placental sulfatase deficiency clinical presentation of fetus

A

Clinically: hyperkeratosis, increased scaling, corneal opacities, pyloric stenosis, cryptorchidism

21
Q

Placental aromatase deficiency inheritance, genetics

A

Autosomal recessive; 2 mutations, aromatase gene on chromosome 15

22
Q

Placental aromatase deficiency clinical implications for mother and fetus (M vs F)

A
  • Maternal hirsutism occurs (still has some peripheral maternal aromatization if mom is not affected by aromatase mutation) – usually in second half of pregnancy, regresses after delivery
  • Female fetus is virilized (ambiguous genitalia)
  • Female child: hyperandrogenism, multi-cystic ovaries, hypergonadotrophic hypogonadism, absent breast development
  • Male child: normal puberty, infertile (estrogen essential for spermatogenesis), no pubertal growth spurt, osteoporosis develops early
23
Q

From where are Estrone (E1) and Estradiol (E2) derived in pregnancy?

A

Equally from maternal and fetal precursors

24
Q

From where is Estetrol (E4) derived in pregnancy?

A
  • Synthesized in the fetal liver from E2 and E3 by the two enzymes 15α- and 16α-hydroxylase
  • Alternatively synthesized with 15α-hydroxylation of 16α-hydroxy-DHEA sulfate as an intermediate step
25
Q

Which estrogen in pregnancy is only detectable during pregnancy?

A

Estetrol (E4)

26
Q

Ddx of maternal hirsutism/virilization in pregnancy

A
  • Drug/progestin exposure
  • Pregnancy luteomas
  • Theca-lutein cysts
  • Sertoli-Leydig tumors
27
Q

Pregnancy luteoma clinical presentation

A
  • Usually discovered incidentally (in third trimester), produce little androgen
  • 1/3 reported cases have maternal hirsutism or virilization
  • Fetal virilization related to maternal virilization (80% of virilized mothers will deliver virilized female fetuses
28
Q

Theca-lutein cysts clinical presentation and risk factors

A
  • Associated with elevated HCG
  • risk factors – multiples, isoimmunization, molar pregnancy/GTD, gestational diabetes
  • 30% of women with theca-lutein cysts will become virilized, no cases of fetal virilization of female fetus
29
Q

Sertoli-Leydig tumors clinical presentation and association

A
  • Very rare, associated with anovulatory infertility

* Highest risk of maternal and fetal virilization – but low overall

30
Q

Why fetus escapes virilization

A

o Aromatase (P450c19/P450arom)
o Increased in SHBG produced by placenta
o Virilization in the Fetus may occur in luteomas due to DHT production

31
Q

Enzymatic blocks by compartment

A
  • Fetus lacks 3B HSD (conversion of delta 5 androgens to delta 4 androgens)
  • Placenta lacks c17 – 17-hydroxylase and 17,20 desmolase
  • [Remember: P450 c17 (17alpha hydroxylase) only in theca and P450arom (aromatase) only in granulosa]
32
Q

Placental progesterone

A
  • Progesterone synthesis independent of quantity of precursor available from fetus (fetus contributes no precursor)
  • Progesterone synthesis is derives from MATERNAL cholesterol [Remember: placenta has c17 block, including 17,20 lyase, so placenta CAN make progestins independent of fetal androgens (DHEA)]
  • LDL is taken in via endocytosis (mediated by estrogen)
33
Q

Fetal TSH

A

Peaks at 28 wks, remains high; T3 low, rT3 high

34
Q

Fetal FSH/LH

A

o GNRH neurons develop and migrate week 6 to week 9 (fetal pituitary LH determines fetal T at 12 weeks)
o HPO vascular system complete by 20 weeks
o LH/FSH increase dramatically, reaching a peak between week 20 and week 24
o Decline after midgestation due to negative feedback from placental steroids
o After birth, acute increase in LH and FSH
o Gonadal steroids peak in 3-6 months of age (boys) and 12-18 months of age (girls)

35
Q

Fetal PRL

A

Increases throughout

36
Q

Fetal CRH

A

Initially secreted at 16 weeks, increase with gestational age, capacity to regulate pituitary ACTH by 2nd tri

37
Q

Fetal ACTH

A

Fetal adrenal levels decrease after midgestation

38
Q

Peptides that do NOT cross the placenta

A

TSH, insulin, and heparin

REI Written Boards SKORY (20 decks)

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