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Repro 313 > Lecture 17: Physiology of Pregnancy > Flashcards

Lecture 17: Physiology of Pregnancy Flashcards

1
Q

describe the relationship between the foetus and mother;

A

Essentially a parasite (genetically foreign) and wants as many nutrients as possible to grow

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2
Q

What does the placenta produce?

A

Many hormones and growth factors

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3
Q

What may create immunological tolerance e to the foetus?

A

The placenta may induce immunological tolerance

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4
Q

Give an overview of the interelationship between the mother and foetus;

A
  • Without the health of the mother the foetus wont make it.

- Mums CV and immune system adapt to support pregnancy

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5
Q

What are the maternal adaptations to pregnancy?

A

Changes in most systems of the body, including;

  • The maternal cardiovascular system
  • The haematological system
  • The genital system
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6
Q

Does the number of pregnancies influence maternal adaptation?

A

First pregnancies tend to be more prone to complications of mal-adaptation than subsequent adaptations

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7
Q

Describe the length of time the adaptations occur for?

A

“9” months of pregnancy, more like 40 weeks

profound changes take place in the maternal physiology to allow gestation to proceed for nine months

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8
Q

What are the two greatest changes of the maternal CV system?

A

Increased cardiac output

Reduced peripheral resistance

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9
Q

How is increased cardiac output achieved?

A

10% increase in SV and 10-15% increase HR

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10
Q

Describe how peripheral resistance is reduced;

A
  • Increased hormone levels (estrogen, prostaglandins) cause vasodilation, thus decreased vascular resistance
  • Decreased peripheral resistance causes a small decrease in systolic blood pressure and a more marked decrease in diastolic blood pressure.
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11
Q

When do CV changes occur in pregnancy?

A

CV changes begin very early in pregnancy, reach their peak during the second trimester and then remain relatively constant until delivery.

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12
Q

Describe the changes in blood flow to the uterus in pregnancy?

A
  • Uterine vessels become dilated, blood flow increases from 45mL/min to 750mL/min
  • These cells must increase drastically in length and width (radial artery 200% increase in diam) == cellular proliferation
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13
Q

Describe the vasculature of the placenta;

A

The placenta is fed by the uterine arteries -> arcuate -> radial -> spiral arteries

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14
Q

Why do these vascular changes occur?

A

Because of changes in the progesterone and estrogen levels

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15
Q

Describe how progesterone causes vascular changes;

A

Firstly is produced by the corpus luteum and then by the placenta;
- induces vascular relaxation in the uteroplacental circulation but does not appear to have a systemic affect

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16
Q

Describe how estrogens cause vascular changes;

A

Estrogen;

  • Reduces vascular resistance mainly in reproductive tissues
  • Alters the ratio of type 1/3 collagen in the vessel wall
  • Increases angiontensinogen by synthesis in the liver, leading to increased serum levels of ANG 2
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17
Q

If ANG2 is a vasoconstrictor then how come it is released in pregnancy and why does it not cause hypertension?

A

There is an 8 fold increase in ANG2 to increase electrolyte re-absoprtion and blood volume

but

The affects of ANG2 on vasoconstriction appear to be blunted in normal pregnancy.
= increased vasodilator response

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18
Q

What are prostenoids and how do they change in pregnancy?

A

Prostenoids/prostaglandins are derived from arachidonic acid.

  • PGI2 (vasodilator) increases 5 fold by term
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19
Q

Do all prostaglandins cause vasodilation?

A

No some can cause vasoconstriction but in pregnancy this equilibrium favours vasodilation and of note there is no increase in TXA activity.

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20
Q

Whats the vasodilators of pregnancy?

A

Prostaglandins

Nitric Oxide

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21
Q

Describe NO

A

NO is produced by vascular endothelial cells in response to shear stress of blood flowing over the vessel walls

NO acts locally
Has a half life of 6 seconds
Causes arterial wall relaxation and dilation

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22
Q

How does NO change in pregnancy?

A
  • During pregnancy some tissues has enhanced Nitric Oxide Synthase activity
  • NO contributes to maternal systemic vasodilation and reduced vascular reactivity (i.e to SNS) during normal pregnancy
  • NO has localised uterine actions
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23
Q

What are the NO localised uterine actions?

A
  • Uterus has NOS activity, which decreases at the end of gestation
  • Uterine arteries have increased endothelial NOS activity
  • NO is also produced by EVTs - may hep invasion (of spiral art.) or contribute to vasodilatory environment
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24
Q

Describe the heamotological changes of pregnancy;

A
  • Increased BV
  • Increased plasma volume
    (these occur at different rates)
  • Haematocrit declines in pregnancy as plasma volume increases faster than cell mass (but RBC does increase in mass)
  • Plasma volume increases by 1250mL by 30 weeks then becomes stable.
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25
Q

How is there changes in blood and plasma volume in pregnancy?

A
  • Renin and aldosterone progressively increase 8 fold in pregnancy
  • Retain noromotension by vasodilator response
  • Vascular compliance
26
Q

When else do females plasma/BV change?

A

During the regular menstrual cycle

27
Q

Describe plasma volume change over time

A
  • By 8-10 weeks of gestation, plasma volume inc. 10% (similar to mesntural cycle)
  • by 10 weeks of gestation there are significant CV adaptations already, Plasma expansion occurs after this, thus plasma volume doesnt cause the CV changes
28
Q

What are pregnant women at risk of developing in relation to CV changes?

A
  • Pre-eclampsia (hypertension +proturia)

- Anemia (B/C extra iron required by the foetus, placenta and the increased in RBC mass.

29
Q

What is the point of the CV adaptations?

A
  • CV adaptations mean that uterine blood flow increases from 50ml?min to 700-800mL/min = placenta/foetus can exchange more nutrients and gasses with the mother, ensuring healthy foetal growth.
30
Q

How do CV adaptations help during birth?

A

Birth is traumatic! Th Cv adaptations help protect the mother from risks of delivery such as haemorrhage

31
Q

Describe the haemodynamic changes at birth

A
  • 0.5L vaginal singleton borth
  • 1L vaginal twins
  • 1L c section
32
Q

How does the pregnant women respond to blood loss in child birth?

A

Non-pregnant women would vasoconstrict and produce new blood.

Pregnant women are hypervolemic thus modifying the response and they do not respond to this blood loss. (there is continuing blood volume decline by diuresis and a slow loss of red cells with time post partum)

Haematocrit slowly returns to normal post partum

33
Q

How does the foetus pose an immunological risk?

A
  • It is considered foreign by the maternal immune system

- The placenta is in intimate contact with maternal blood and high numbers of immune cells in the decidua

34
Q

Why is the foetus not rejected?

A
  • Placenta hides itself from immune system

- Trophoblasts alter the expression of cytokines from immune cells in order to dampen down the maternal immune response.

35
Q

Describe how the placenta hides itself;

A

Trophoblasts do not express class 1 or 2 MHCs. = hiding it. (HLA-A,B)

Trophoblasts express a combination of HLA-C, G and E MHC molecules which actively help the placenta avoid immune attack

36
Q

Describe HLA-G function;

A

HLA-G can interact with receptors on cytotoxic T lymphocytes and natural killer cells, inhibiting their ability to induce cell lysis.

37
Q

Describe how shedding contributes to maternal tolerance

A

Synctiotrophoblasts are an epithelial layer that constant shed into maternal circulation
- Trophoblast debris interact with endothelial cells and macrophages in maternal circulation

= may play a role in immunological tolerance of the placenta / foetus

38
Q

What happens when maternal CV adaptation goes wrong?

A

Pre-eclampsia ; hypertension + proterurea

39
Q

Describe the affects of pre-eclampsia

A
  • Affects most maternal organs
  • Found only in pregnancy
  • Triggered by something from the placenta
  • An exaggerated inflammatory response leading to vascular dysfunction
  • Failure of the normal vascular adaptation to pregnancy

More common in first pregnancies

40
Q

What can cause pre-eclampsia

A

Pre-eclampsia is the result of defective maternal adaptation of the CV and or immune systems to pregnancy

  • Defective uterine sprial art. remodelling
  • Release of pro-inflam trophoblast debris (instead of adaptive cytokines)
  • Inability of the maternal CV system to cope with the increased inflammatory profile.
  • Multifactorial disease
41
Q

Describe RAAS in pre-eclampsia;

A

Pre-eclamptic women have;

  • Lower RAS components
  • But increased ANG 2 sensitivity in their adrenal cortex and vascular system
42
Q

What happens to vasodilators in pre-eclampsia?

A
  • Reduced PGI2 by 13-14 weeks
  • TXA rises from 21 weeks leading to hypertensive imbalance
  • Associated with AMDA dysregulation (It inhibits NOS)
  • Blockade of NO synthesis induces pre-eclampsia.
43
Q

Describe hCG structure;

A

2 Chain

Shares its alpha chain with FSH and LH

The hormones all have a unique beta chain

44
Q

What produces hCG?

A

hCG is exclusively produced by the trophectoderm on the preimplantation blastocyst and syncytriotrophoblast of the placenta

Women with multiple pregnancies will experiences even higher levels of hCG, as the amount of syncytiotrophoblast is increased

45
Q

When is hCG detectable?

A

hCG is detectable within the blood/urine within days of implantation

bhCG is used for detecting (as alpha chain is shared)

46
Q

Describe hCG levels on a timescale basis

A

bhCG secretion increases rapidly in the first weeks of pregnancy until 10 weeks of gestation whereafter it drops off.

47
Q

How does hCG influence the corpus luteum?

A
  • hCG plays a critical role in the development of pregnancy by preventing regression of the corpus luteum
  • Thus progesterone secretion by the corpus luteum maintains the endometrium’s receptivity for implantation
48
Q

Describe the action of hCG on the corpus luteum;

A

hCG binds to the LH receptor and thus transmits similar signals to LH =

  • Corpus luteum doubles in size by 4 weeks
  • Also causes ovarian release of estrogen and progesterone during first 6-8 weeks
  • At this point placenta takes over as major source of progesterone
49
Q

Describe hCG and decidua interplay

A

hCG is basically responsible for preventing the uterus returning to its normal cyclic pattern by causing the corpus luteum to continue secreting progesterone and estrogen

Thus these hormones prevent menstruation and maintain the endometrium in a decidualised form

50
Q

How may hCG influence uterine vascular remodelling?

A

hCG may play an important role in uterine remodelling right from the time of implantation

  • angiogenic factor
  • stimulates vasodilation and vascular permeability
51
Q

Where else are high levels of hCG found?

A

Trophoblastic tumors

  • choriocarcinoma
  • testicular tumor
52
Q

How can hCG be used as a contraceptive target?

A

The importance of hCG in maintaining pregnancy can be seen in the use of this hormone as a target for contraceptive vaccines.

Phase 1 and 2 clinical trials indicated safe, efficacy and reversibility for a beta hCG vaccine

53
Q

What are the limitations of the bhCG vaccine?

A
  • The vaccine did not produce antibodies in all women
  • Antibodies were short lasting
  • 3 months to produce antibodies
  • unknown long term effects
54
Q

Describe the uterus

A

non-pregnant = almost solid
70g
10mls

Pregnant uterus is thin walled and muscular with a 5L cavity (can go up to 20L) and weighs 1100g

55
Q

Describe uterine growth;

A

The initial growth of the uterus is at least partially under the control of estrogen

  • Growth is largely due to stretching of existing cells rather than proliferation of cells
  • 5cm in length when non-pregnant, 40-60cm at term
56
Q

Describe the cervix and pregnancy;

A

Cervix softens and glands proliferate to occupy approximately 50% of the mass of the cervix.

Cervix is blocked by mucous plug during pregnancy (prevents infection)

57
Q

How does cervical composition change with pregnancy?

A

80% collagen when non-pregnant

Towards term collagen content of the cervix decreases while its elastin is unchanged but glycosaminoglycans and water increase

Incompetent cervix is associated with repeated miscarriage

58
Q

How does the abdominal wall /skin change in pregnancy?

A

increased blood flow to skin
Flow to hands increases 6-7 fold
Flow to feet also increases

59
Q

How does the abdomen change and skin pigment?

A

Skin,nipple and areola change pigment with pregnancy, (increased malanocyte sitmulating hormone) easier to tan.

Development of linear nigra

Facial pigmentation (regress post preg)

60
Q

What can happen to womens abdomens in pregnancy?

A

IN later pregnancy 50% of women develop striae Gravidarum (reddish streaks formed on the skin, abdomen and thighs, breasts)

Due to overstretching of the skin, elastic fibres may rupture together with small blood vessels

Repro 313 (20 decks)

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