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Lifecycle Unit 2 Test > Endocrinology of Pregnancy > Flashcards

Endocrinology of Pregnancy Flashcards

1
Q

Functions of Placental and Maternal Hormones

A

Maintain the corpus luteum during the first 7-10 wks

Adjust maternal metabolism to provide nutrients to the fetus

Stimulate the maternal circulatory system to transport gases and nutrients to and from the growing fetus

Dampen uterine contractility

Prepare the maternal tissues for childbirth

Prepare the breasts for lactation

Hormones are intimately involved in the complex processes that lead to parturition

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2
Q

What are the major Hormonal Changes in Pregnancy- Endocrine System

A

Insulin sensitivity early-resistance later (GDM)

Earlier conversion to fatty acid metabolism due to decreased maternal glycogen stores from fetal-placental glucose demands–fasting ketones

Changes in thyroid hormone levels (hCG)

Increased iodine requirements (goiter, hypothyroid)

Changes in autoimmunity (PPT)

Estrogen induced pit growth (Sheehan’s)

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3
Q

What are the cardiovascular and hematologic changes in pregnancy?

A

30-50% increase in C.O. (decompensation in CAD, CHF, Marfan’s, valvular stenosis)

Decreased SVR leads to decreased BP; no change in pulm vasc resistance in pts with pulm htn

Increase in HR

30-40% increase in blood volume (anemia of pregnancy)

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4
Q

Respiratory/Acid Base Changes from Hormones in pregnancy

A

Increase in tidal volume, minute ventilation leads to resp alkalosis

Compensated metabolic acidosis leads to lower buffering capacity (earlier DKA)

Increase in O2 consumption

Nasal mucosal edema (stuffy nose, sinusitis)

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5
Q

Renal Changes in Pregnancy

A

40-60% increased GFR (clearance of iodine, drugs) leads to decreased BUN and Cr

Increased renal blood flow

Altered tubular function (glucosuria)

Decreased ureteral peristalsis (pyelo)

Lowered osmostat for vasopressin release and thirst (hyponatremia)

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6
Q

GI Changes in Pregnancy

A

Decreased LES (GERD, aspiration pneumonia)

Decreased stomach emptying, peristalsis (gastroparesis, delayed absorption, constipation)

Decreased GB emptying (cholestasis)

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7
Q

What are the polypeptide-releasing hormones from placenta?

A

CRH (20-fold increase at term)
GnRH (stims hCG)
GHRH
TRH

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8
Q

What are the most important polypeptide hormones from placenta?

A

hCG
hPL (hCS)
hPGH (hGH-V)

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9
Q

hCG

A

Maintains corpus luteum (especially progesterone) in early pregancy (PEAKS EARLY at 10 weeks)

Glycoprotein (39 kD)

Secreted by syncytiotrophoblast

Alpha common to LH, FSH, TSH

Regulates differentiation of cytotrophoblast to syncytiotrophoblast; controls trophoblastic invasion

Induces apoptosis of endometrial T-cells to promote immune survival of embryo

TSH activity at high levels

Stimulates fetal Leydig cells to produce fetal testosterone

May cause hyperemesis

Stimulates Relaxin leading to increased GFR/Renal blood flow and decreases SVR in rats; studies ongoing in humans

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10
Q

hPGH

A

Contributes to insulin resistance of pregnancy (peaks later)

Secreted by syncytiotrophoblast

Differs from pit GH by 13 aa

Not regulated by GHRH

Same avidity for receptor

Secreted tonically; replaces pit GH by ~20 wks

Does not cross placenta but regulates IGF-1

Decreased by glucose; increased by hypoglycemia

Potent somatogen

Lost during normal labor and 1 hr after placenta removal

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11
Q

CRH

A

Likely plays a role in partuition (peaks later)

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12
Q

Steroid Hormones from Placenta

A

Progesterone

Estrogen (up to 100-fold increase)

1,25-OH Vit D

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13
Q

Placental Anatomy (when develops)

A

Day 4, embryo differentiated into inner cell mass (fetus) and trophectoderm (placenta)
6-7 days—endometrial attachment of trophoblast

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14
Q

What are the 2 types of trophoblastic cell phenotypes

A

mononuclear Cytotrophoblast (early)

Syncytiotrophoblast (multinuclear layer on surface of villi; predominates later)

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15
Q

Syncytiotrophoblast

A

Major site of protein and steroid production

Hemochorioendothelial placentation

Directly bathed by maternal blood within intervillous space

Separated from fetal blood by several layers of tissue

Net transfer of steroids and polypeptide hormones to maternal blood is&raquo_space;> fetus

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16
Q

What transfers across placenta?

A

More permeable to lipid soluble molecules

Hormones > 1200 Daltons have minimal access

Hormones actively metabolized by placenta:

  1. T4 to rT3 by Type III Monodeiodinase (protects baby to some degree from hyperthyroidism)
  2. Cortisol to Cortisone by 11-B hydroxysteroid dehydrogenase (why it’s relatively safe to give some steroids in pregnancy)
17
Q

What are the similarities in structure among hCG and TSH, FSH, and LH

A

Same alpha subunit

In high levels, can stimulate TSH hormone receptors

18
Q

hCG–Endocrine Clinical Correlates

A

hCG has TSH activity first trimester

hCG-induced hyperthyroidism with HG

Lack of hCG doubling 1st trim—missed Abortion

No gestational sac; hCG >1500 U/L-ectopic

No cardiac activity; hCG>9000-missed Abortion

Altered in placental insuff and trisomies: increased hCG in Down’s–decreased Trisomy 18

19
Q

Human Placental Lactogen (hPL) or Human Chorionic Somatomamotropin hCS)

A

Participates in the metabolic adjustments that deliver nutrients tot he developing fetus (peaks later)

Secreted by syncytiotrophoblast

Secretion rate parallels placental weight

Detected at 5-10 days-peaks ~32 wks

Made in massive quantities

Originally thought to be insulin resistance hormone of pregnancy

Facilitates mobilization and utilization of FFAs for energy by increased lipolysis

Both insulin and anti-insulin effects

Stimulates insulin secretion

Weak GH activity and mainly a lactogen—Promotes growth of mammary tissue and stims prolactin

20
Q

What is the major insulin resistance hormone of pregnancy? And why do we need that?

A

hPGH

Maternal insulin resistance necessary to shunt glucose and amino acids to fetus to ensure adequate growth

hPGH decreased in growth restricted fetuses

Women with pre-existing insulin resistance develop GDM due to further insulin resistance from placental hormones and inadequate insulin secretion

21
Q

Progesterone

A

Steroid hormone

Critical to maintain pregnancy

Corpus luteum produces it prior to 8-11 wks

Biosynthesis dependent on number of LDL receptors on trophoblast plasma membrane

~85% enters maternal circulation

22
Q

Functions of Progesterone

A

Promotes decidua formation

Substrate for synthesis of cortisol and aldosterone in the definitive zone of the fetal adrenal cortex

Inhibits uterine contractions

Modulates immune system (promotes Th2 ab and suppresses Th1 cell mediated response)

Stimulates minute ventilation

Smooth muscle relaxant (GI, uterus; GU)

Promotes lobular development in the breast; inhibits milk secretion

May contribute to decreased SVR

23
Q

When do we give progesterone to pregnant women?

A

Given for luteal phase defects

Given to prevent preterm labor

24
Q

Misoprostone

A

Progesterone antagonist

Abortifactant

25
Q

How does progesterone affect the health of the mother?

A

Autoimmune ds may improve; worsens post-partum (MS, PPT, Grave’s)

Gastroparesis worsens; GERD, aspiration pneumonia

Ureteral relaxation results in urinary reflux, high risk of pyelonephritis

26
Q

Estrogen in pregnancy (where does it come from and what are the effects it exerts)

A

Levels may increase ~100-fold

High levels of placental aromatase

DHEAS converted to estrogens by placenta

90% estradiol secreted into maternal circ

Stimulates growth of myometrium

Induces hypercoagulable state (increases clotting factors, fibrinogen)

Induces protein synthesis (increased SHBG, TBG, CBG)

Induces lactotrophs; Inhs Dopa leads to increased PRL but antagonizes PRL at level of breast

Peripheral vasodilation (decrease SVR, BP)

Increases C.O.

Inc mucosal edema (sinusitis, epistaxis)

Increased uterine blood flow and decreased resistance

Inc blood volume (anemia)

Inc renal perfusion and GFR (increased proteinuria)

Inc TG synthesis

Increases Pit size and vasculature

27
Q

What is primarily responsible for the hypercoagulable state of pregnancy? What is the increased risk for thrombosis?

A

5-10 X risk of thrombosis in pregnancy

Estrogen causes:

Stasis (venous flow decreases by 50% by 3rd trim)

Vascular Damage (vaginal del or C-section)

Hypercoagulability:
 increased factors V, VIII, vWF, fibrinogen
 increased resistance APC (40%)
 increased PAI-1 and PAI-2
 decreased Prot S
 Increase in D-dimers and TAT complexes

Risk back to baseline by 6 wks PP

28
Q

What is the effect of estrogen-containing OCPs on lactation?

A

May inhibit it!

29
Q

Pancreatitis in pregnancy

A

Estrogen induced hypertriglyceridemia can cause pancreatitis

30
Q

What is the leading cause of maternal mortality in US and UK?

A

Thromboembolism

PE’s account for 15-20% of pregnancy-related deaths in US

Relative risk of VTE 10X non-pregnant state–1/1,000 vs 1/10,000

31
Q

Sheehan’s syndrome

A

Estrogen causes pit size to increase;

prolactin macroadenomas may enlarge

pit at risk for ischemia

Lifecycle Unit 2 Test (19 decks)

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