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2022 REI Written Boards > 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 - & what is different about it’s feedback?

A

Not suppressed by glucocorticoids (may be increased)

Detected after 15 weeks increase until term; huge increase in 3rd trimester

Likely involved in labor

  • Different feedback/stimulation than hypothalamic
    • Cortisol from placenta drives CRH, CRH drives mat/fet pit
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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)

preg is state of relative hypercortisolism

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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 (9 stimulatory, 3 inhibitory)

A

increased by: glucocorticoids, activin, interleukins, Vasopressin, NE, AGII, PGs, neuropeptide Y, oxytocin

decreased by: progesterone, inhibin, nitric oxide

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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
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17
Q

Low estriol implications in pregnancy

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

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20
Q

Placental sulfatase deficiency clinical presentation of fetus

A

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

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21
Q

Placental aromatase deficiency inheritance, genetics

A

Autosomal recessive; 2 mutations, aromatase gene on chromosome 15

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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
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23
Q

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

A

Equally from maternal and fetal precursors

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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
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25
Q

Which estrogen in pregnancy is only detectable during pregnancy?

A

Estetrol (E4)

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26
Q

Ddx of maternal hirsutism/virilization in pregnancy

A
  • Drug/progestin exposure
  • Pregnancy luteomas
  • Theca-lutein cysts
  • Sertoli-Leydig tumors
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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…so 21-C cannot become 19-C
  • [Remember: P450 c17 (17alpha hydroxylase) only in theca and P450arom (aromatase) only in granulosa]

Placenta also missing 16α -hydroxylase to convert 16aOH DHEAS (fetal adrenals must do it)

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

When secreted? When can it regulate ACTH by?

A

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

37
Q

Fetal ACTH

Increase or decrease? by when?

A

Fetal adrenal levels decrease after midgestation

38
Q

Peptides that do NOT cross the placenta

A

TSH, insulin, and heparin

39
Q

Which ER & PR’s more important in initial pregnancy success?

A

ER-alpha & PR-alpha

40
Q

Maternal physiology in early & late pregnancy:

Early:
Increased deposition of… (3)
Increased _ production & sensitivity (1)

Late:
Switch from __ to ___
Baby utilizes ___ & ___, Mom utilizes ___, ___ & ___

A

o Early – increased deposition of fat, protein, water/volume; increased insulin production & sensitivity

o Late – switch from carbs to fat utilization
 Glucose & AA’s to baby
 Free FA, ketones & glycerol to mom

41
Q

Which part of brain enlarged in pregnancy? and why?

A

Anterior lobe enlarges up to 3-fold due to hyperplasia/hypertrophy of lactotrophs to produce more prolactin

42
Q

Maternal gonadotropins in pregnancy

A

declines (high E/P4; inhibin A & B from placenta)

43
Q

Maternal MSH in pregnancy

A

increased (intermed lobe) (hyperpigmentation)

44
Q

Posterior pituitary in pregnancy (ADH & Oxytocin)

A
  • Resetting of ADH osmoreceptors; sodium falls (hCG mediated)
  • Increased ADH clearance; sometimes transient diabetes insipidus
  • Oxytocin rises, parturition and let down
45
Q

Maternal TBG in pregnancy

A

Increased (E increased production and sialylation, which reduces clearance; and hCG)

46
Q

Maternal PRL in pregnancy

A

Increased throughout, driven by Estrogen

47
Q

Maternal adrenals in pregnancy (RAAS system & aldo)

A
  • P4 increase vasodilation → decrease in BP → cardiac output and angiotensin II go up → stimulates RAAS system
  • Aldosterone – large increase throughout; maintains sodium balance
48
Q

Decidual proteins

A
  • Cortisol
  • Prolactin (no dopamine control here – regulated fetal fluid balance @ amnion)
  • IGFBP-1 – inhibits IGF binding in decidua
  • Progesterone-Associated Endometrial Protein (PAEP/PP-14) – immunosuppressant effects; low in ectopics
49
Q

Glycogen synthesis/storage in pregnancy:

Rate-limiting step?

A

Glucose uptake from mom is rate limiting step; which is why we have diabetic -like state – to push glucose to placenta

50
Q

hCG:

Size?

types, and what is special about the types?

A
  • 36-40 kDa glycoprotein
  • Regular hCG, hyperglycosylated hCG (1.5-2x more sugar residues – the type we give, stimulates corpus luteum longer than regular hCG, leading to OHSS risk)
51
Q

When is:

WOI? (related to cycle (28d), LH surge, ovulation)

when does hCG start by?

A
  • WOI - day 16-22 of 28d cycle or 5-10d after the LH surge or 5-6d after ovulation
  • hCG starts 9-11d after LH peak, 8th day after ovulation or 1st day after implantation

Must start by 10th day of ovulation

52
Q

thyrotropic activity of hCG

A

1/4000 of TSH

53
Q

What to do to test if it’s pituitary hCG?

A

often low; ocp test – short course to see if it drops the production

54
Q

What produces hPL?

A

cytotrophoblast then syncytiotrophoblasts

55
Q

Actions of hPL (2) - & why?

A

Stimulates insulin and IGF-1 release

Stimulates lipolysis to FFA; reduced glucose uptake

  • Preferentially use fat for fuel (mother)
  • Preserve glucose and amino acids for fetus
  • Minimize protein catabolism
56
Q

Where does the DHEAS needed by the placenta come from?

A

Primarily fetal adrenal (some maternal - 10%)

57
Q

Fetal cortisol

A
  • Placenta does NOT synthesize cortisol de novo but regulates exposure of fetus by 11βHSD 1 or 2
  • 11βHSD-2 converts cortisol → inactive cortisone
  • Excess fetal exposure = problems (IUGR, etc.)
58
Q

Timeline of androgens needed to make estriol

A

Before 20wks: Androgens come from mother

After 20wks: Fetal androgens

59
Q

What is the best test to diagnose Addison’s in pregnancy?

A

ACTH stim test

(if cortisol rises appropriately, no adrenal insufficiency)

59
Q

What is the effect of bromocriptine in the placenta?

A

Decreased fetal serum prolactin (decreased cord blood levels) with normal amniotic fluid levels

60
Q

Fetal prolactin

A
  • Pituitary prolactin is the only fetal pituitary hormone to increase during pregnancy
  • Amniotic fluid: Parallel maternal serum concentration until week 10, rise markedly until 20th, then decrease until delivery
61
Q

Placental sulfatase deficiency - clinical issues

A

patients go way beyond term, require C/S- cervix fails to soften and dilate

62
Q

What is the effect of flutamide during pregnancy? What if taken in mid-second trimester?

A

Non-steroidal androgen receptor antagonist

Hepatotoxic

1st trimester – feminization of male external genitalia

2nd trimester – decrease penis length

63
Q

anti-androgens in pregnancy

A

should all be discontinued

64
Q

Patient with Sheehans syndrome is most likely to have issues with which hormones?

A
  • All patients have GH, prolactin, and gonadotropin deficiency
  • Majority have TSH and ACTH deficiency
65
Q

Danazol in pregnancy - effect on female fetus

A

since binds androgen receptors (displaces testosterone, increases free testosterone levels) & decreases estradiol levels → masculinization of female fetus

2022 REI Written Boards (21 decks)

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