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Reproductive Physiology > Pregnancy/Placenta/maternal change/ Fetal Growth > Flashcards

Pregnancy/Placenta/maternal change/ Fetal Growth Flashcards

1
Q

What hormones are secreted from the placenta? how do they change throughout pregnancy?

A

CG, Chorionic somatotropin (CS), progesterone, Estrone (E1), Estradiol (E2), Estriol (E3), Prostaglandin F2a and PGE2; all grually increase steadily except hCG which rises drastically peaks, drops a little and plateaus

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2
Q

Where is CG synthesiszed? What are its important properties?

A

syncytiotrophoblast layer of placenta; functionally similar to LH; B subunit more glycosylated so has longer plasma life; B fragment is used diagnostically to monitor onset and progression of pregnancy

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3
Q

What are the functions of CG?

A

stimulates luteal progesterone synthesis via LH receptors, stimulates luteal relaxin and inhibin production, acts via cAMP to stimulate cholesterol uptake, synthesis of steroidgenic enzymes and progesterone synthesis by syncytiotrophoblast by 7th wk, and is responsible for morning sickness-> activates neurons in area postrema-> chemosensitive area for vomiting reflex

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4
Q

What can cause a false CG signal?

A

ectopic pregnancy and hydatidiform mole

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5
Q

What causes the CG signal in ectopic pregnancy?

A

sluggish transport , embryo implants in oviduct wall, rise in CG at beginning, doubling time is slow, CG levels peak at 1IU and drop due to fetal death, must correlate with blood test and ultrasound

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6
Q

What is responsible for the CG signal in a hydatidiform mole?

A

lack of fetus results in unregulated CG secretion past normal time- ultrasound monitoring- levels reach 500K IU= hydatidiform mole

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7
Q

What is the placenta luteal shift?

A

7th week CL of pregnancy non-responsive to CG downregulation of LHR-> progesterone secretion starts to decline; by this time placenta under stimulation of CG starts to secrete enough P to rescue pregnancy

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8
Q

What is different in the placenta synthesis of progesterone and steroid hormones?

A

no StAR protein

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9
Q

The fetal placental unit plays an important role in turning DHEA to what? What synthesizes the DHEA?

A

weakest estrogen (E3) thus controlling gestational increase in E2; fetal adrenal gland

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10
Q

Why cant the fetal zone produce progesterone? what does it use placental progesterone for?

A

lack of 3BHSD; produces small amounts of aldosterone and cortisol from placental progesterone (low level expression of 21-hydroxylase, CYP11B1 (Cortisol) and CYP11B2 (aldosterone)

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11
Q

What role does cortisol play in fetal growth and development?

A

generally interferes with growth, important role in organ maturation in late 2nd and 3rd trimesters; levels kept at minimum

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12
Q

What hormone in the placenta protects the fetus from the mothers cortisol?

A

type II 11BHSD, inactivates cortisol to cortisone, prevents the disruption of androgen production (E3)

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13
Q

At 20weeks trophic action of what hormone is necessary for fetal and definitive zones?

A

ACTH-stimulates production of all adrenal steroids

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14
Q

By the 25th week ACTH has doen what to the Definitive zone?

A

grows and matures more rapidly, contributes to rising level of corticosteroids, particularly cortisol, shift in negative feedback regulation

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15
Q

why is progesterone required throughout pregnancy?

A

reduces myometrial oxytocin receptors, reduces sensitivity to estradiol (1st through mid 3rd trimester) and PGF2a and PGE2 synthesis (prevent uterine contraction when oxytocin secretes in response to uterine stretch

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16
Q

What protects mother from steroid overexposure (progesterone)?

A

most is bound to SHBG produced by liver

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17
Q

What does estradiol stimulate around 20 wks?

A

11BHSD synthesis by syncytiotrophoblast-> increased cortisol to cortisone conversion; increases through term; cortisol negative feedback on ACTH secretion is minimized despite increase in serum cortisol levels; ACTH maintains adrenal DHEA-> placental estradiol production

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18
Q

In 3rd trimester what happens hormonally that is necessary for parturition?

A

estradiol gradually overrides inhibitory effects of progesterone and starts inducing oxytocin receptors and synthesis of PGF2a and PGE2 in myometrium

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19
Q

What are the three components of the fetal placenta unit?

A

fetal adrenal gland and liver and the syncytiotrophoblast (placenta)

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20
Q

What stimulates the fetal adrenal gland? What are its products?

A

ACTH; takes progesterone and synthesizes aldosterone, cortisol, DHEA and DHEAS; also cholesterol from maternal blood to DHEA and DHEAS

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21
Q

What function does the liver play in the fetal placenta unit?

A

takes in DHEA and DHEAS from fetal adrenal gland; 16ahydroxylase makes 16aOHDHEA and 16aOHDHEAS which goes to the placenta

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22
Q

What does the placenta do in the fetal placenta unit? What stimulates its activity?

A

takes in cholesterol from mom and synthesizes progesterone which goes to mom and baby; takes in DHEA, DHEAS from fetal adrenal and makes E1 and E2, takes in 16aOHDHEA and 16aOHDHEAS from fetal liver and makes E3

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23
Q

What enzymes are involved in placenta synthesis of progesterone?

A

SCC and 3BHSD1

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24
Q

What enzymes are involved in placental synthesis of E1? E2?

A

sulfatase if from DHEAS; the 3bHSD1 (andrestenedione) then aromatase (E1) then release or 17BHSD (E2)

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25
Q

What enzymes are involved in placental synthesis of E3?

A

sulfatase if from 16aOHDHEAS; 3BHSD1 (16aOHA) then aromatase (E3)

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26
Q

What is the placenta permeable to ?

A

glucose (main energy source), O2, AA, FA, Na, K, Cl, ketone bodies, vitamins, many viruses and lipid soluble narcotics, IgG

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27
Q

What is the placenta impermeable to?

A

immunoglobins (except IgG) and many embryotoxic chemicals, protein hormones

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28
Q

What has minor permeability in the placenta but is inactivated en route? What enzymes are involved?

A

cortisol, epinephrine and T3/T4; cortisol to sortisone by 11BHSD2, epinephrine to metanephrine by COMT, and T3/T4 inactivated by iodothyronine-inner-ring deiodinase

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29
Q

What methods of transport does the placenta utilize? examples?

A

simple diffusion (gas, Na K, CL, and steroids), active transport (glucose, AA, Ca, PO4, I, and Fe), facilitated diffusion (FFA), pinocytosis ( gamma globin, transferrin, and albumin), and bulk flow (H2O)

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30
Q

Why and how does the respiration rate increase during pregnancy?

A

to deliver additional O2 and remove excess CO2 from fetal metabolism; progesterone stimulates maternal respiratory center

31
Q

Why does BV increase during pregnancy?

A

30%; cope with extrablood supply to placenta and compensate for blood loss during delivery(approx. 25% of increase)

32
Q

Why and by how much does RBC mass increase? is it sufficient?

A

20-30% carry more O2 and ; increased plasma volume results in physiological anemia

33
Q

How does CO change and why during pregnancy?

A

by 40% due to incremental increase in SV and HR

34
Q

What happens to renin levels during pregnancy?

A

increase; Na retention

35
Q

What happens to plasma levels of aldosterone and Angiotensin II during pregnancy?

A

increase resulting in net increase in renal electrolytes and fluid uptake

36
Q

What happens to peripheral resistance and BP during pregnancy?

A

remains unaltered; BP w/in normal

37
Q

How does toxemia happen?

A

if prostacyclin synthase or thromboxane synthase don’t work; PGG2 cant go to PGI2 (potent vasodilator and inhibitor of platlet aggregation) or TXA2 (potent vasoconstrictor and platelet aggregator); PGG2 become PGE2, PGF2a and PGD2

38
Q

How does progesterone effect the enzymes involved in toxemia?

A

induces placental prostacyclin synthase resulting in higher PGI2- makes vacular smooth muscles refractory to hypertensive action of AngII and prevents platelet aggregation

39
Q

How does renal function change during pregnancy?

A

renal plasma flow increases (increased BV, CO and reduction of RVR), GFR increase(40%)-> ^flow of solutes-> ^ Cbicarb and Cwaste, mild glycosuria, maintain positive Na balance and plasma tonicity due to increase aldosterone and renin-angiotensin levels

40
Q

how do the maternal hormones adjust for supplying energy to fetus?

A

8th wk placental CS appear in maternal plasma-> CS suppresses maternal pituitary GH secretion by negative feedback, high CS causes hyperglycemia and peripheral resistance to maternal tissues resulting in increased blood glucose, ketone bodies and FFA; PR to insulin ensures temporal uninterrupted supply of glucose AA and FFa to fetus

41
Q

Why is it important fetus gets plenty supply of nutrients from mom? (esp glucose)

A

fetal liver lacks key enzymes of gluconeogenesis

42
Q

What is GDM?

A

late 2nd and 3rd trimester demands higher insulin secretion; if B cell cant meet demand blood glucose levels increase beyond threshold and high amounts of glucose appear in the urine

43
Q

What causes the increased need for insulin that can lead to GDM?

A

reduced insulin sensitivity from CS compensated by increased insulin secretion, new threshold of glucose homeostasis is set, postprandial glucose returns to preandrial level within 2-3hrs due to higher level of insulin

44
Q

How does the fetus respond to increased blood glucose in GDM?

A

hypersecretion of fetal insulin which intensifies upregulation of IGF-I and downregulation of IGFIBP1 and 2 resulting in excess fat deposition and fetal overgrowth,

45
Q

What can result from unmanaged glycemic control in pre-gestational diabetes?

A

intrauterine growth retardation by inducing placental vascular insufficiency

46
Q

how does maternal TBG change during pregnancy?

A

increased blood estrogen induces ~2x serum [TBG]

47
Q

How does TBG change in pregnancy effect maternal T4 and TSH?

A

lowered free T4-> elevated TSH->enhanced production and secretion of thyroid hormones->new equilibrium btwn free an TBG bound TH (increased demand up to 20wks and persists to term)

48
Q

What happens to the need for iodine during pregnancy?

A

increased; almost double normal intake due to increased GFR and siphoning by fetus, and increase thyroid hormone demand

49
Q

How does CG affect the thyroid?

A

CG (structurally similar to TSH) stimulates the thyroid follicular cells via TSHR; end of 1st trimester CG at its highest, most stimulating of thyroid due to CG so TSH will be suppressed via - feedback; causes some women transient hyperthyroidism

50
Q

What happens to secretion of PTH, Calcitonin and Vit D?

A

all increased to deliver 25-30g of net calcium for fetal bone development; intestinal Ca increases also; calcitonin secreted in response to decreased bone mineralization in mom not serum Ca levels

51
Q

How does ACTH secretion change during pregnancy? What results from this?

A

increased; increase in cortisol production, plasma SHBG levels increase due to estrogen action on liver and most of steroids remain bound to binding protein

52
Q

How does prolactin change in the mother during pregnancy?

A

begin to rise in 1st tri, increase linearly to reach very high levels at term; because lactotrope proliferation stimulated by estrogen, secretion is pulsatile in pregnant women but is not affected by stress as in non-pregnant women

53
Q

When does the fetal GI system develop?

A

2-3 months before term

54
Q

Fetal growth in later 1/3 of gestation is due to what? What are the energy sources?

A

fat deposition, muscle development and bone growth; 60% glucose- large portion converted to fat, lactate oxidation 40%

55
Q

How is iron absorption by the fetus?

A

exceeds Ca and Po4; (fetal hemoglobin)

56
Q

What things affect fetal growth?

A

maternal genotype, health, age and parity, fetal genotype and sex

57
Q

Early to mid-gestation what is occurring in respiratory development?

A

lungs formed by 4wks; active Cl and concurrent fluid secretion across alveolar and tracheal surfaces, accumulated fluid (isotonic), expands lungs and protects airways from amniotic debris

58
Q

In late gestation what is occurring in respiratory development?

A

Pulm. B-adrenergic stimulation by epi results in loss of alveolar fluid volume and secretion; alveoli gradually close keeping thin film of surfactant from type II alveolar cells (appear 24th wk and secrete 26th)->allows collapse of sacs when secretions decrease

59
Q

What are fetal breathing movements?

A

diaphragm and intercostal muscles contract rhythmically

60
Q

What is hyaline membrane disease?

A

alveolar cells do no produce surfactant, fail to open fully after birth and collapse after each breath leading to damage of alveolar epithelium

61
Q

At birth what causes the onset of breathing?

A

increased [CO2] in blood stimulates respiratory center (cut off umbilical vein) causing diaphragm decent->reduces intrapleural pressure-> forcibly opens alveoli and allows flow of air in

62
Q

What causes the close of the foramen ovale?

A

RAP falls, LAP increases

63
Q

What causes DA to close?

A

hi PO2, low PGE2 and fall in DA pressure due to opened pulmonary capillaries leads to constriction and closure of DA

64
Q

What causes closure of ductus venosus?

A

pressure fall in DV, results in rise in portal blood pressure; initiates hepatic portal circulation too

65
Q

What happens when amniotic fluid is swallowed by the fetus?

A

electrolytes absorbed by GI into fetal circulation, intestinal glucose and AA absorption is limited; small amount of solids (meconium) is accumulated in lower segment of intestine

66
Q

What does sever hypoxia to the fetus induce?

A

fetal defecation resulting in meconium entry into the lungs-> obstruction of airways at brith and damages the lungs due to tissue reactions

67
Q

What causes Neonatal jaundice?

A

fetal liver lacks UDP-glucuronate transferase-> plasma bilirubin levels rise-> days after birth glucuronate conjugation system matures and bilirubin is cleared

68
Q

When are all pituitary hormones first detectable in fetus? How does IGF and PRL levels effect developing fetus?

A

10th-17th week; IGF-I steady increase 20-40wks then drop- fetal fat deposition, muscle and bone development; IGFII higher levels but steady 20-30wks steep increase 30-40wks helps IGF-I; PRL rise from 30-40 wks and then drops

69
Q

What happens to fetal levels of cortisone, cortisol and ACTH? how does this effect the fetus?

A

cortisone high and peaks at term then drastically drops-breakdown of fetal and maternal cortisol; cortisol levels increase from 20wks with rapid increase just before term then drop down- organ maturation; ACTH steady slow decrease then drops down at term- stimulation of adrenal gland to make DHEA and DHEAS for placental synthesis of progesterone (DHEA is high and drops after birth because of the above)

70
Q

What does cortisol do for fetal development?

A

increase B1 adrenergic receptors in lungs and surfactant synthesis; promotes ductus closure, increased glycogen stores in liver, increased T4 and T3, promotes islet cell maturation, increases NE to E conversion in adrenals

71
Q

How is epinephrine important in organ development in the fetus?

A

increased surfactant release, decrease lung water, increased CO, BP and PR; increased glycogenolysis in liver, increased glucagon and decreased insulin

72
Q

Does the mother effect fetal thyroid development?

A

no, independent of maternal TSH (doesn’t corss placental barrier; minimal amount of T4 and T3 crosses and majority inactivated by placental monodeiodinase, free iodine crosses placenta and fetal thyroid is sensitive to its inhibitory effects

73
Q

how and when is fetal PTH calcitonin system developed? how does it function?

A

PT glands fully formed 5-12wk; PTH stimulates placental Ca transport; high Ca stimulates synthesis and release of calcitonin

74
Q

When is insulin-glucagon system developed in the fetus?

A

a and b cells formed by 8-10wks, immature, uncontrolled glucose, AA and FFA delivery to fetus causes fetal B cell hyperactivity and hyperinsulinemia

Reproductive Physiology (8 decks)

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