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SF4 - Test 3 > 2 - Maternal Adaptations to Pregnancy > Flashcards

2 - Maternal Adaptations to Pregnancy Flashcards

1
Q

What hormone is Chorionic Gonadotropin (hCG) similar to?

What receptor does hCG use?

How does it’s half-life compare to LH?

Where is hCG produced?

What is a clinical application of testing for this hormone?

What are the principle actions of hCG?

A
  • hCG is similar to LH, and uses LH receptors
  • hCG has a longer halflife due to glycosylation
  • hCG is produced by cells of the syncytiotrophoblast shortly after implantation; and can be measured as a means of detecting pregnancy
  • Principle Actions: Prevent Luteolysis of Corpus Luteu, Promote Progesterone Production
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2
Q

Where is progesterone synthesized?

By Week 8, what is the primary source of progesterone?

What structure synthesizes progesterone using what maternal sources? What amount of this is released into maternal circulation?

What is the main target of progesterone?

A
  • Progesterone is synthesized by Corpus Luteum and Placenta; by week 8 theplacenta is the primary source of progesterone
  • Progesterone is synthesized by syncytiotrophoblast using maternal LDL / VLDL as primary source of choleterol; 90% released into maternal circulation
  • The main target of progesterone is the female reproduction tract = maintenance of pregnancy
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3
Q

What direct actions does progresterone have on the female reproductive tract to maintain pregnancy?

Affect secretory function? Endometrium/Decidua? Uterine contractions? Cervix?

A
  1. Stimulates endometrial differentiation and enhance secretory function
  2. Corpus Luteum progesterone sustain embryo until formation of functional placenta
  3. Prepares endometrium for implantation/facilitates formation of the decidua
  4. Inhibits uterine contractions
  5. Acts on cervix to produce vicous mucus
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4
Q

What does the synthesis of estrogens during pregnancy require?

A
  • Estradiol 17B
    • Maternal and Fetal Adrenal Cortex
    • Fetal = DHEA-S + Sulfatase = DHEA
      • –>3BHSD = Androstenedione
        • –> Testosterone
          • –>P450Aromatase = Estradiol-17B
  • Estrone
    • Maternal and Fetal Adrenal Cortex
    • Fetal = DHEA-S + Sulfatase = DHEA
      • –>3BHSD = Androstenedione
        • –>P450Aromatase = Estrone
  • Estriol
    • Fetal Adrenal Cortex = DHEA-S
      • Fetal Liver = + OH = OH-DHEA-S
        • Sulfatase: OH-DHEA
          • P450Aromatase = Estriol
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5
Q

What is Chorionic Somatomammotropin (hCS) similar in structure to?

What are its major functions?

What is the principle form of GH in pregnant women?

A
  • Similar to GH and PRL in structure
  • Major Functions:
      1. Stimulates lipolysis and antagonizes action of insulin on maternal glucose utilization (causes glucose to rise)
        * Maintains adequate nutrient (glucose) glow to developing fetus
      1. Has prolactin-line effects
  • The prinicple form of growth horon in pregnant women is Placental Growth Hormone (hGH-V)
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6
Q

What causes most maternal adaptations to pregnancy?

What regulates the cause of these?

A

Hormones released by the placenta

Secretion appears to be autonomous; feedback mechanisms still exist–however setpoints may be altered

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7
Q

How does the cardiovascular system change w/pregnancy?

Total Peripheral Resistance

Cardiac Output

Blood Volume

Uterine Blood Flow

What is Intrauterine Growth Restriction?

A

Decrease in total peripheral resistance

Increase in Cardiac Output, Blood Volume

Major increase in Uterine Blood Flow as pregnancy progresses (maintain max dilation)

IUGR results from sustained reduction in placental perfusion

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8
Q

What controls the changes in uterine flow in the following stages?

Initial Phase

Second Phase

Third Phase

A
  • Initital Phase
    • Estradiol / Progesterone; occurs before implantation and early placentation
  • Second Phase
    • Growth/remodeling of uteroplacental vasculature to support placental development
    • Dilated, Low resistance system
  • Third Phase
    • Progressive uterine artery vasodilation to meet increasing nutritional needs of growing fetus
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9
Q

What factors cause the fall in peripheral resistance (and subsequent increase in cardiac output)?

A
  • Low resistance uteroplacental circulation caused by spiral artery remodeling
  • Generalized decrease in systemic vascular tone
    • Humoral Factors:
      • Estrogens (Prostacyclins - PGI2 , NO)
      • Progesterone (smooth muscle relaxation)
      • Relaxin (NO from corpus luteum)
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10
Q

What changes are observed to cardiac performance with pregancy?

Stroke Volume?

Heart Rate?

Cardiac Output?

Preload?

Afterload?

A
  • Decreased SVR
  • Increase Stroke Volume + Increase HR = Increase Cardiac Output
    • Estrogen/Progesterone increase compliance of heart, increases Preload (diastolic volume)
    • Increased central venous volume
    • Aortic Pressure (afterload) is decreased
  • Heart rate INCREASES during pregnancy
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11
Q

How does posture effect cardiac output during pregnancy? Clinical presentation?

A

Weight of fetus in supine position compresses the Inferior Vena Cava, decreasing venous return, can result in Supine Hypotensive Syndrome

When standing, venous pressure increased in legs and may cause peripheral edema

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12
Q

How does blood volume change with pregnancy?

How does plasma volume compare to red blood cell mass?

A

Maternal blood volume increases

Plasma Volume Increase > Red Blood Cell Mass Increase; thus there is a decrease in hematocrit leading to “physiological anemia of pregnancy”

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13
Q

How does systolic blood pressure, diastolic blood pressure, and mean arterial pressure change during pregnancy?

Why is there a difference in the DBP/MAP change?

How do they change in late-pregnancy?

A
  • SBP, DBP, MAP decline through the middle of the 2nd trimester
    • ​Due to decrease in peripheral vascular resistance
  • DBP/MAP fall more than SBP due to reduced vascular resistance
    • Thus, Pulse Pressure Increases
  • During late pregnancy, BP may return to normal or exceed regular values
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14
Q

How do plasma protein levels change during pregnancy?

Albumin

Clotting Factors

Serum Binding Globulins

A
  • Albumin Levels Decrease
    • Decrease oncotic pressure
    • Decrease viscosity
  • Plasma fibrinogen/clotting factors Increase
    • ​Induces hypercoaguable state (prevent post-partum hemorrhage); thrombosis risk
  • Serum binding globulins Increase
    • ​E2 stimulates synthesis of TBG, CBG, SHBG
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15
Q

How do the kidneys change during a normal pregnancy?

A
  • Increased renal vasodilation increases renal blood flow, increase in Glomerular Filtration Rate (GFR)
  • Kidneys increase in size
  • Increased GFR causes decrease in serum cretinine, urea, uric acid
  • Increased protein excretion
  • Increased glucose excretion (glycosuria)
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16
Q

How does the sodium balance change during pregancy?

A
  • Na+ is retained during pregnancy (increased plasma volume)
    • [Na+] is lower vs non-pregnant woman, due to increase in plasma volume
  • Plasma Renin, Angiotensinogen, Aldosterone all increase
    • ​Due to decrease in BP
    • Estrogen/Progesterone Stimulate renin synthesis
    • Hepatic angiotensinogen synthesis
  • Vasoconstrictor receptors relaced for Angiotensin II
17
Q

How does osmoregulation and thirst change in pregnancy?

A
  • Plasma osmolality is decreased
    • ​Increased plasma volume > Increased Na+
  • Plasma ADH mostly unchanged; thus during pregnancy, regulation shifted leftward
  • “Thirst” is increased
  • Ability to respond to change via ADH system is unchanged
18
Q

How does the maternal respiratory system adapt to pregnancy?

Lung volumes and resistance

A
  • Residual Volume is decreased
  • Functional Residual Capacity is decreased
  • Total pulmonary volume is decreased
  • Vital Capacity is unchanged
  • Pulmonary Resistance is decreased
19
Q

How does alveolar ventilation change with pregnancy?

How does progesterone change alveolar ventilation?

What facilitates the transfer of CO2 from fetal to maternal blood?

What compensates for this alkalosis?

A

Alveolar ventilation is increased

Tidal Volume is increased

Alveolar PCO2 is decreased (alveolar ventilation > metabolic rate)

Respiration Rate is Unchanged

- - -

Progesterone increases alveolar ventilation by increasing sensitivity of central chemoreceptors to CO2

Facilitates transfer of CO2 from fetal blood to maternal blood!

Respiratory alkalosis is compensated by increased renal excretion of bicarbonate

20
Q

Hormon changes with pregnancy:

Anterior Pituitary

Lactrotropes? (–>PRL)

ACTH

GH

Thyroid (+ TSH), PTHrP, T3/T3, TBG

FSH / LH

A
  • Ant. Pituitary - Increase Size
  • Lactotropes = Hyperplasia (due to high estrogens)
    • ​PRL = Increase
  • ACTH = Increase (decrease before delivery, increase during delivery)
  • GH = No Change (source changes)
  • Thyroid - Increase Size; Increase T3/T4/TBG
    • TSH = Lower in 1st trimester
    • Thyrotropic effect of hCG
    • PTHrP Increase
  • FSH / LH = Decreased (very low)
21
Q

How do beta cells change during pregnancy?

A

Hypertrophy and hyperplasia of beta cells occurs

Increase in peripheral resistance to metabolic effects of insulin due to elevated levels of maternal hPL and cortisol

*Pregnancy hormons antagonize insulin action*

22
Q

How does the adrenal cortex change with pregnancy?

What protects the fetus from maternal cortisol?

A

Increase in total cortisol levels; due to increased ACTH / estrogen-induced CBG synthesis

Placentgal HSD 2 protects fetus from cortisol (converts to cortisone)

23
Q

How does the GI System usually change during pregnancy?

GI motility, food absorption, lower esophageal sphincter tone?

Gall bladder function and emptying?

A
  • GI motility, food absorption, lower esophageal sphincter decrease
    • ​Constipation, heartburn, indegestion..
  • Intragastric Pressure increase
    • Heartburn
  • Gall bladder functioning/emptying are impaired
24
Q

What triggers development of breasts in puberty?

What triggers further branching?

What is size increase due to?

(non-pregnancy associated growth)

A

Breast development begins in response to rise in estrogen production at puberty; also requires GH (IFG-1)

Estradiol/Progesterone triggers increased branching

Size increase due to increase in stromal/adipose tissue

25
Q

What triggers breast development during pregnancy?

What permissive effects occur?

A

Extensive lobuloalveolar development

Triggered by high Prolactin, Human Placental Lactogen (hPL), estrogen, progesterone

Permissive effects from GH, IGF-1, Insulin, Cortisol

26
Q

What receptor does dopamine inhibit prolactin secretion?

What causes reversal of this (secretion)?

What is most important stimulus for PRL release?

How does PRL change during pregnancy and after birth?

A
  • Dopamine acts through G protein to inhibit adenylyl cyclase and activate K+ channels to hyperpolarize membrane (shut down PRL secretion)
  • High estrogen promotes lactotropes and prolactin synthesis
  • Suckling is most potent postpartum stimulus for PRL release
  • Steadily increaes during gestation, drops off following birth, suckling increases production
27
Q

What is the mechanism of PRL Action?

A
  • PRL is tyrosine kinase receptor, acts through JAK/STAT pathway
28
Q

How is lactation inhibited during pregnancy?

What causes initiation of lactation?

How does PRL act on epithelial cells?

What is the principle signaling pathway of PRL?

A
  • Lactation is inhibited by high progesterone/estrogens
  • Lactation is initiated by drop in progesterone/estrogen, lactation inducing effects of prolactin
  • PRL acts on epithelial cells to promote milk synthesis and secretion
  • PRL signaling pathways involves JAK/STAT proteins
29
Q

What stimulates milk ejection?

What causes cessation of lactation?

A
  • Oxytocin actions on myoepthelial cells to promote milk ejection
    • ​Suckling is principle stimulus (blocks dopamine)
    • Crying, etc. other stimulus trigger release
  • No suckling = No PRL release = loss of hormone synthesis/secretion
  • No suckling = No Oxytocin, negative feedback from engorged breasts
30
Q

What are three important reflexes mediated by suckling?

Milk Secretion

Milk Ejection, Pathway?

Supression of GnRH

A
  • Milk Secretion - PRL
  • Milk Ejection - Oxytocin
    • ​G protein, IP3/diacylglycerol pathway
  • Supression of GnRH - Lactational Amenorrhea
31
Q

How does oxytocin affect uterine contractions? What inhibits this in first two trimesters?

Does oxytocin initiate labor? How do levels change with cervix?

What are clinical applications of oxytocin?

A
  • Oxytocin stimulates uterine contractions; blocked first two trimesters by oxytocinases in uterus
  • Oxytocin does NOT initiate labor
  • Cervix increase is positive feedback loop on Oxytocin release
  • Oxytocin used to induce labor, enhance contractions, reduce postpartum bleeding
32
Q
A

SF4 - Test 3 (12 decks)

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