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Endo Exam 2 > Pregnancy and Parturition > Flashcards

Pregnancy and Parturition Flashcards

1
Q

general timeline of fertilization and implantation

A 
ovulation day 0
fertilization- 1
Blastocyst enters uterine cavity- 4
Implantation- 5
Trophoblast forms and attaches to endometrium- 6
Trophoblast begins to secrete HCG- 8
HCG "rescues" corpus luteum- 10
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2
Q

Major hormones of pregnancy

A

Human chorionic gonadotropin (hCG)

  1. Progesterone
  2. Estrogens
    a. Estrodiol
    b. Estrone
    c. Estriol
  3. Human placental lactogen (hPL)/ Human chorionic somatomammotropin (hCS)
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3
Q

Hormones of pregnancy- first trimester

A

hCG rescues corpus luteum to stimulate luteal estrogen and progesterone production
Placenta takes over hormone synthesis from corpus luteum
- “Luteal-placental shift”
- Progesterone & estrogen levels may decrease during transition

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4
Q

hormones of pregnancy- 2nd and 3rd trimester

A

Maternal progesterone & estrogen levels continue to rise

Maternal-placental-fetal unit takes over production

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5
Q

hCG

A

First Hormone produced by syncytiotrophoblasts
Pregnancy tests detect β-subunit (β-hCG)
Rapidly accumulates in maternal circulation within 24 hrs. of implantation
Half-life ~ 30 hrs.

Considered to be responsible for nausea of “morning sickness”

hCG peaks ~ 10 weeks of gestation
Serum levels double every 2-3 days during first 6 weeks

Structurally related to LH, FSH, TSH
Most similar to LH
Binds LH receptor with high affinity

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6
Q

Actions of hCG

A

1° Action:
Stimulate LH receptors on corpus luteum
Prevents luteolysis
Maintains high luteal-derived progesterone production before the placenta takes over (1st 10 wks.)

Other hCG actions:
Weakly binds TSH receptors
Transient gestational hyperthyroidism
Stimulates fetal Leydig cells  Testosterone
Stimulates fetal adrenal cortex
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7
Q

Progesterone

A

Luteal-Placental shift completed ~ 8-10 weeks
Switch from corpus-luteum-derived to placenta-derived progesterone

↑ maternal progesterone throughout pregnancy

Absolutely required to maintain a pregnant uterus
Quiescent myometrium

Progesterone production is independent of fetus
Can not be used as an indicator of fetal health

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8
Q

Progesterone actions and high levels attributed to…

A

High levels of progesterone production continues with availability of:
CYP11A1, and 3β-hydroxysteroid dehydrogenase (3β-HSD), and maternal cholesterol

Major progesterone actions in pregnancy:
↓ uterine motility/contractions
↑secretory activity necessary for nouishment, growth, and implantation of the embryo
↑ fat deposition early in pregnancy
Stimulates appetite, diverts energy stores from sugar to fat

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9
Q

Estrogens

A

Placenta takes over luteal-production of estrogens
Needs 19-carbon androgen (DHEA-S) from fetal adrenal gland

Feto-placental unit responsible for production of:
Estradiol-17β
Estrone
Estriol (major estrogen of pregnancy)

Estrogen production depends on a healthy fetus
Estriol levels can be used as an indicator of fetal health

Estrogens are required for parturition

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10
Q

Major actions of estrogens in pregnancy

A

Increases:

↑ Uteroplacental blood flow
↑ Uterine smooth muscle hypertrophy (mitogenic effect)
↑ LDL receptor expression on syncytiotrophoblasts
↑ Prostaglandins
↑ Oxytocin receptors
↑ Mammary gland growth
↑ Prolactin secretion (maternal pituitary)

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11
Q

Progesterone and Estrogen levels through pregnancy

A

they both increase

Estrogen:Progesterone ratio shifts later in pregnancy –>
preparing for parturition

↓ estrogens and progesterone after parturition allows for PRL action on the breast and lactation

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12
Q

hPL

A

human placental lactogen

Also called: Human chorionic somatomammotropin (hCS)

Produced by syncytiotrophoblasts
Levels rise throughout pregnancy
Directly proportional to placental growth

hPL/hCS is structurally similar to GH and PRL

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13
Q

actions of hPL

A

Antagonizes insulin action → “diabetogenicity of pregnancy”
↑ glucose availability for the fetus
Inhibits maternal glucose uptake
Lypolytic action –> shift maternal energy use to FFAs
Stimulates mammary gland development

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14
Q

Diabetogenicity of Pregnancy

A

State of insulin-resistance and hyperinsulinemia
Second half of pregnancy: shift from anabolic state towards fat utilization and glucose sparing
↑ insulin secretion
↓ responsiveness to insulin

Existing diabetes can be further increased with pregnancy
Diabetes can develop for the first time during pregnancy
“Gestational diabetes” if resolved after pregnancy

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15
Q

Overview: Maternal-Placental-Fetal Unit

A

Mother, placenta, and fetus are distinct units

Fetal health can decline even with a functioning placenta

A non-functioning placenta is always detrimental to the fetus

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16
Q

Endocrine Function of the Placenta

A

Syncytiotrophoblasts produce steroid and peptide hormones

Functions of placenta:
Maintain pregnant state of the uterus
Stimulate lobuloalveolar growth and function of maternal breasts
Adapt aspects of maternal metabolism and physiology to support fetal growth
Regulate aspects of fetal development
Regulate the timing and progression of parturition

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17
Q

Placental limitations

A

Cannot make adequate cholesterol

Lacks enzymes
    required for complete
    biosynthetic pathway
    for estrone, estradiol,
    and estriol production
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18
Q

Maternal endocrine changes: pituitary

A

↑ Prolactin (PRL)
Estrogen promotes PRL release from anterior pituitary
Lactotroph hypertrophy and hyperplasia

↑ Pituitary size x 2
If compressed against optic chiasm, enlarged pituitary can cause dizziness and vision problems
Can be susceptible to vascular insult and necrosis – Sheehan’s syndrome

↓ LH and FSH production
Negative feedback inhibition of estrogens + progesterone

ADH secretion augmented
Threshold altered by progesterone action
ADH released at lower osmolality (lower “set point”)

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19
Q

Maternal Endocrine Changes: Thyroid

A

↑ Thyroid size
Thought to be stimulated by hCG

hCG cross-reacts with TSH receptors
Transient gestational hyperthyroidism
During hyperthyroid period when hCG levels are increased, TSH levels decrease due to negative feedback on TSH production

↑ Total T4 and Total T3 (2x)
Estrogen promotes increased liver production of thyroxine-binding globulin (TGB)
No change in Free T4 and Free T3

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20
Q

Maternal Endocrine Changes: Adrenal

A

↑ Cortisol
↑ Total Cortisol
Estrogens stimulate ↑ liver production of cortisol-binding globulin (CBG)
↑ Free Cortisol levels
Late in pregnancy; ↑ ~ 2x by parturition
Cortisol is inactivated by placental 11β-dehydrogenase type 2 which protects exchange of cortisol between fetus and mother

↑ Aldosterone (~ 8-10 x)
Estrogens stimulate ↑ liver production of angiotensinogen and renal renin production
↑ ANG II (estrogens antagonize vasopressive action) and Aldosterone
Does not result in hypernatremia (ADH and fluid retention), hypokalemia, or hypertension
Progesterone blunts aldosterone action as well (competes for mineralocorticoid receptors)

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21
Q

Maternal Weight Gain

A

For a woman with a normal BMI:
25-35 lb. increase with pregnancy

Example ~30 lbs.
11 lbs. fat
1.5 lb. uterus
4.5 lbs. breasts
1.5 lbs. placenta
2.2 lb. amniotic fluid
2 lb. maternal blood and interstitial fluid
7 lbs. fetus
22
Q

Cardiovascular Changes

A

↑ Blood volume
↓ hematocrit

  1. ↑ Cardiac Output
    CO = HR x SV
    ↑ HR
    ↑ SV
  2. ↓ TPR
    ↓ hematocrit
    ↑ vasodilation
    ↑ vascularity (addition of low-resistance placental circuit)
  3. ↓ MAP (or remains close to normal)
    MAP = CO x TPR
    ↑ CO
    ↓ TPR
23
Q

Increased Blood Volume

A

↑ blood volume ~45% near end of pregnancy (75-100% for twins, triplets)

Facilitates adequate fetal perfusion & exchange of nutrients/wastes

Protects mother from blood loss during delivery

24
Q

Increased Plasma Volume

A

↑ plasma volume (~ 50%)

↑ NaCl retention
↑ Aldosterone (some action blunted by progesterone)
Estrogen stimulates ↑ angiotensinogen (liver) & renin (renal) production  angiotensin II & aldosterone
↑ H2O retention and intake
Lower threshold for ADH/AVP release and thirst during pregnancy (overall ↓ osmolality)
Increased sensitivity of osmoreceptors

25
Q

Decreased Hematocrit

A

↓ Hematocrit during pregnancy (“physiological anemia”)
~ 36% vs. 38%
↑ RBC production rate doesn’t match ↑ plasma expansion

↓ Viscosity: ↓ TPR
Helps minimizes maternal cardiac work as CO increases

26
Q

Increased Cardiac Output

A

↑ 30 – 50% by end of pregnancy (~ 35% ↑ in 1st trimester)

CO = HR x SV
↑ HR (15-20 bpm)
↑ SV

27
Q

SV Plateau or Decrease Late in Pregnancy

A

Very late stages of pregnancy:
SV may periodically decrease due to compression of the IVC
↓ VR leads to ↓ EDV leads to ↓ SV

Positional changes

28
Q

Distribution of Increased CO

A 
Increased distribution of blood flow:
Uterus: 15% of CO (~ 1% normally)
Renal: ↑ by 40% 
Elimination of additional wastes
Skin: temperature regulation
Heart: support increased CO
Breasts: mammary development

No change: brain, gut, skeleton

29
Q

Decreased TPR/SVR

A

Low-resistance circuit added in parallel: utero/placental circulation
Vasculogenesis and angiogenesis

Vasodilation
Estrogen & progesterone: proposed antagonists to vasopressive action (ANGII)
Progesterone may promote vasodilation as a smooth m. relaxant

30
Q

Decreased or Same Mean Arterial Pressure

A

MAP = CO x TPR
↑ CO and ↓ TPR
Result: MAP is same or lower vs. pre-pregnancy MAP
Benefit: ↓ afterload and cardiac work

31
Q

Pregnancy and Edema: Starling Forces

A

↑ capillary hydrostatic pressure
↑ venous pressure in L.E. due to:
Compression of IVC by growing uterus
Increased venodilation under hormonal influence

  1. ↓ capillary colloid osmotic pressure
    Maternal synthesis of plasma proteins does not keep pace with increase in plasma volume
32
Q

Factors Contributing to Respiratory Changes

A

Mechanical & hormonal changes lead to Increased alveolar ventilation

  1. Elevation of diaphragm
    Increased intra-abdominal pressure with fetal growth
    Progesterone effect: relaxing m. and fascia
    ↓ RV and ↓ FRC
  2. ↑ O2 demand and CO2 production
    Support of fetal metabolism and pregnancy
    ↑ O2 consumption (~20%)
3.	↑ Sensitivity to CO2 
Progesterone effect (estrogen)
↓ Medullary respiratory center set-point for respiratory                              response to central chemoreceptor detection of CO2
↑ TV and Alveolar Ventilation
↓ Pco2 (From ~ 40 to 32 mmHg)
33
Q

Respiratory Changes

A 
↓ Functional residual capacity (FRC)
↓ Residual volume (RV) 
↑ Tidal volume (TV)
Respiratory rate ~ unchanged (RR)
↑ minute ventilation, ↑ Alveolar ventilation (VA)
↓ Pco2

Net Result: ↑ ventilation leads to ↓ Pco2
Respiratory alkalosis*
Renal compensation: ↑ HCO3- excretion

34
Q

Maternal-Fetal oxygen exchange

A

↑ Fetal O2 – carrying capacity with ↑ [Hb] late in pregnancy (50% > adult level)

↑ Fetal Hb O2 binding affinity (> maternal)

↓ CO2 affinity, favoring pick-up by maternal blood

35
Q

Renal changes

A

↑ RBF and ↑ GFR (~ 50%+)
Due to ↑ blood volume and CO

  1. ↑ Plasma renin, angiotensin II, and aldosterone
    Estrogens stimulate increased production
  2. ↑ Na+ retention
    ↑ Aldosterone
  3. ↑ H2O retention and intake
    ↓ threshold for ADH/AVP & thirst during pregnancy
    Increased sensitivity of osmoreceptors (Net: ↓ osmolality despite ↑ Na+ retention)
  4. ↓ Serum Na+ (~ 5 mEq/L decrease)
    Change in set-point for ADH/AVP and osmoreceptor sensitivity
36
Q

GI changes

A 
Factors causing reflux:
↓ Gastric emptying rate 	(progesterone) 
↓ LES tone      
	(progesterone)
↑ Intra-abdominal pressure

decreased intestinal motility causing constipation

37
Q

Maternal nutrition

A

↑ protein, iron, and folic acid demand

Protein
Supports fetus, placenta, uterus, breasts, blood volume
Additional 30 g protein/day

Iron
Supports increased maternal Hb, placenta, fetus
7 mg/day absorbed iron requirement (vs. 1.5 mg/day nonpregnant)
60 mg/day supplement recommended

Folate
Supports increased RBC production; protects against neural tube defects
400-800 mg/day folic acid supplementation recommended

38
Q

Parturition

A

Myometrial quiescence during pregnancy
Progesterone
Relaxin

Onset of Labor
38 wks. following fertilization (fetal age)
40 wks. after last menstrual period (gestational age)
Initiated by hormonal (endocrine, paracrine) and mechanical factors
Process not completely understood
Additional proposed involvement of inflammatory signals
Positive feedback mechanisms sustain

39
Q

Beginning of Labor

A

Braxton Hicks Contractions
Periodic episodes of weak, slow rhythmic contractions during pregnancy
Become very strong during the last hours of pregnancy
Eventually become labor contractions
Stretching the cervix
Push baby through the birth canal

False Labor: contractions initially become stronger but then fade away
Failure to re-excite uterus with subsequent positive-feedback mechanism
Afferent pain signals from uterine contractions reflexively result in abdominal m. contraction

40
Q

Labor: Stage 1

A

Cervical Dilation and Effacement
Initiation of labor
Contractions go from ~ 30 min to

41
Q

Labor Stage 2

A

Descent and Expulsion
Active Labor
Cervix fully dilated (10 cm)
Contractions push fetus downward; delivery
Average 20-50 min. (Longer for 1st pregnancy vs. after many)

42
Q

Labor Stage 3

A

Expulsion of the Placenta
Uterus contracts reducing area of attachment
Separation of placenta results in bleeding and clotting
Bleeding limited by uterine contractions that compress vessels supplying placenta
Average 15 min. (Range 10 - 45 mins.)

43
Q

Prostaglandins

A

PGF2 alpha and PGE2
Believed to initiate labor
↑ before onset of labor
Uterus, placenta, & fetal membranes synthesize
↑ uterine smooth m. contractility
Uterine responsiveness to prostaglandins can occur throughout pregnancy

↑ synthesis is stimulated by:
Estrogens (promote conversion of arachidonic acid)
Oxytocin in uterine cells
Uterine stretch

44
Q

prostaglandin actions (3)

A

3 prostaglandin actions:
1. Stimulate myometrial smooth m. contraction
2. Promotes gap junction formation between uterine smooth m. cells
Estradiol also promotes gap junctions
3. Softening, dilatation, and thinning (effacement) of the cervix

Can be used to induce labor in large doses

Aspirin: inhibits labor and prolongs gestation
Reduces PGF2α and PGE2 formation

45
Q

Estrogens

A

Required for parturition
↑ placental secretion throughout pregnancy
Ratio of estrogen:progesterone shifts during the last several months of pregnancy and there is a functional withdrawal of progesterone effects

Estrogen actions to promote increased uterine contractility for parturition:
↑ Gap junctions
↑ Oxytocin receptor expression
↑ Myometrial sensitivity to oxytocin
↑ Prostaglandin production
46
Q

Oxytocin

A

Considered to maintain labor (vs. initiate)
Uterine sensitivity to oxytocin only at end of pregnancy

1° stimulus for oxytocin release: Distention of cervix
Released from posterior pituitary
Neurogenic reflex (Ferguson)
Response to stretching of the cervix
Bursts of oxytocin are released during Labor Stage 1; frequency increases with progression of labor

Estrogen increases number of oxytocin receptors
↑ 80x receptor expression by 36 wks.
↑ 200x receptor expression during early labor

47
Q

Oxytocin actions

A

Receptor activation promotes uterine smooth m. contraction
PLC –> IP3 –> ↑ [Ca2+ ]i –> activate calmodulin –> MLC kinase –> phosphorylation of regulatory light chain –> smooth m. contraction
Stage 3 Labor: uterine contractions important for constricting blood vessels after placental delivery
Promotes hemostasis
Stimulates uterine PGF2α production

48
Q

Placental Corticotropin-Releasing Hormone (CRH)

A

Production and maternal serum levels rise quickly late in pregnancy/labor
↓↓ CRH-binding protein
↑ Free bioactive CRH

CRH promotes myometrial contractions
Sensitizes uterus to prostaglandin & oxytocin

Placental CRH stimulates fetal ACTH
↑ fetal adrenal cortisol (positive feedback for CRH)
Cortisol stimulates placental CRH production (in contrast to inhibitory effect of cortisol on hypothalamic CRH production)
↑ fetoplacental estrogens

49
Q

Relaxin

A

Produced by corpus luteum and placenta

Thought to promote myometrial quiescence during pregnancy

Production increases during labor
May soften cervix during labor

50
Q

Fetal Endocrine Contribution

A

Fetal Hypothalamic-Pituitary-Adrenal Axis

Fetal & placental signals preparing for/initiating labor:
CRH production by the placenta
↑ fetal pituitary production of ACTH
↑ fetal adrenal production of cortisol, DHEA, DHEA-S
↑ fetoplacental estrogen production
Cortisol: positive feedback to ↑ placental CRH production

CRH promotes contractions by sensitizing uterus to prostaglandins and oxytocin
Estrogens also stimulate contractions

51
Q

Fetal Hormones and Pituitary

A

Fetal pituitary : Oxytocin
Fetal placental membranes : Prostaglandins
Fetal adrenals: Cortisol (+ placental CRH)
-Fetal cortisol induces surfactant production in the lungs at about 32 weeks (range 24-35 weeks)

52
Q

Mechanical Factors Increase Uterine Contractility

A

Stretch of smooth m. –> Increases smooth m. contraction
Fetal movement can elicit smooth muscle contraction
Twins are typically born earlier than a single child (~ 19 days)
Indicates significance of mechanical stretch in promoting uterine contractions

Contractions stimulate uterine prostaglandin production
Positive feedback

Ferguson Reflex: Uterine contractions push baby against cervix –> stretching cervix –> stimulating more oxytocin
Positive feedback

Endo Exam 2 (14 decks)

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