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Year 3- Repro > Maternal Changes in Pregnancy > Flashcards

Maternal Changes in Pregnancy Flashcards

1
Q

Fertilisation occurs in the…

A

ampulla of the uterine tube

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2
Q

The uterine tube is not just passive tube from the ovary to the uterus

A

It is the place where the embryo will spend the first week of its life.
Therefore it contains a special protective and signalling environment between the embryo and the walls of the uterine tube.

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3
Q

When does differentiation occur?

A

Around day 4/5

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4
Q

What are the two cell types during differentiation?

A

There is a trophoblast layer around the edge
This forms part of the embryonic part of the placenta. This is the part that implants into the uterus

There is the inner cell mass
This forms the foetus. These are totipotent stem cells that can differentiate into any cell type.

There is the blastocoel (fluid filled cavity)

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5
Q

When do endometrial changes reach their maximum?

A

7 DAYS after ovulation

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6
Q

When is the implantation window?

A

6 – 10 days after the LH spike. At this point, the uterus is receptive

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7
Q

What causes the pre-deciduaization?

A

The corpus luteum (which the egg came out of a week ago) has been producing progesterone. This causes a lot of pre-decidualization
There are more secretions from secretory glands
Spiral arteries become more tortious

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8
Q

Pre-decidualization occurs when?

A

9 to 10 days after ovulation decidual cells cover surface of uterus

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9
Q

what happens after pre-decidualization?

A

Decidualization if pregnancy occurs, decidual cells (modified become filled with lipids and glycogen. Decidua becomes maternal part of the placenta.

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10
Q

Glandular secretions of the endometerium contains?

A

Glandular secretions of endometrium contains growth factors, adhesion molecules (expressed on the surface that trophoblastic cells will attach to), nutrients, vitamins, matrix proteins and hormones.

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11
Q
A

As the embryo approaches the surface of the uterus, the endometrium, the cells attach and invade:

Decidual cells on surface of endometrium become filled with lipids and glycogen- becomes maternal part of the placenta.

All of the cytotrophoblastic cells from the sirface fuse together and become almost like one large cell with many nuclei.

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12
Q

What do the mass cytoptrophoblastic cells release?

A

They will release adhesion molecules, proteases and angiogenesis.
When you get a lot of cells fusing together to form one big cell with a lot of nuclei, it is called a syncytium. So the trophoblasts fused together is called a syncytiotrophoblast:

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13
Q

Syncytiotrophoblast

A

The syncytiotrophoblast results from cell fusion (forms a multi-nucleated cytoplasmic mass) and invades the endometrium.

Chorionic gonadotropin is an autocrine growth factor for the blastocyst.

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14
Q

Invasion in implantation- stage 1

A

There is an invasion
The embryonic part of the placenta is formed with chorionic villi. This increases surface area.
At the same time, in the maternal placenta, there formation of lacuna, which are large blood filled spaces.

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15
Q

Blood supply in implantation- stage 2?

A

Ultimately the villi will project into the blood filled spaces to allow the exchange of gasses etc.

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16
Q

Implanting day 7-8

A

Syncytiotrophoblast erodes the endometrium. Cells of the embryonic disc form epiblast and hypoblast. Epiblast develops fluid filled amniotic cavity.

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17
Q

12 day blastocyst

A

Implantation complete as extraembryonic mesoderm forms discrete layer beneath cytotrophoblast.

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18
Q

16 day embryo

A

Cytotrophoblast and associated mesoderm have become the chorion and chorionic villi are extending. Lacunae filled with maternal blood mingle with villi.

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19
Q

brief outline of implantation

A

Looking at just the embryo:
The first thing that occurs is the differentiation into two cell types
Now the inner cell mass will differentiation into another two cell types, forming a bilayered embryonic disc.
Then there is the yolk sac and the start of formation of an amniotic cavity on top. There are now three layers of the embryo: ectoderm, mesoderm and endoderm.

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20
Q

In the mature maternal-foetal interface (maternal at the top and foetal at the bottom):

A

Chorionic villi project into the lacuna
Mothers supply goes through the lacuna
There is no actual mixing of blood supply, but they are so close together that there is transfer across.

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21
Q

When is the morula formed?

A

Day 4 = Morula, a solid ball of cells formed as the zygote undergoes cleavage

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22
Q

When is the early blastocycst formed?

A

Day 6 = Early blastocyst, a hollow ball of cells with a fluid-filled cavity
Have two cell types Inner cell mass, trophoblast and blastocyst cavity

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23
Q

When is the late blastocyst formed?

A

Day 10 = Late blastocyst, pre-embryo with the embryonic disk, two layers of cells that become the embryo proper.
Inner cell mass, differentiates into two, each with a fluid filled space: amniotic cavity and yolk sac

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24
Q

When is the gastrula formed?

A

Day 16 = Gastrula, embryo with three primary germ layers (ectoderm, Mesoderm and endoderm.
In-between the yolk sac and the amniotic cavity there is a third layer.

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25
Q

briefly summarise the maternal foetal interface

A

Embryo, becomes a morula, and then forms a blastula.
The primitive endoderm develops into the amniotic sac
The epiblast gives rise to the three germ layers of the developing embryo during gastrulation (endoderm, mesoderm, and ectoderm).

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26
Q

Ectoderm

A

skin (epidermis), brain spinal cord (CNS) sensory organs

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27
Q

mesoderm

A

heart, skeletal muscle, kidneys, urogenital, connective tissue

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28
Q

endoderm

A

lining of gastro-intestinal, respiratory and urogenital tract

29
Q

what is the basis of the pregnancy test and where is it made?

A

Human chorionic gonadotrophin (hCG) secreted by the syncytiotrophoblast increases rapidly and is basis of pregnancy test.

30
Q

function of the corpus luteum

A

hCG prevents the death of the corpus luteum so the endometrium is not shed.
Is similar to LH, has the same alpha subunit. So binds to the LH receptor

31
Q

What goes on in the corpus luteum?

A

The corupus luteum continues to produce steroids estrogen and progesterone. Rapid change in maternal systems in response to luteal and later placental steroids
The progesterone will supress the pituitary and hypothalamus so there is no production of FSH or LH. This stops the cycle. The progesterone keeps the endometrium intact and you start to develop the placenta.

32
Q

what would happen if there was no hCG?

A

If there was no hCG, then the CL will die and stop producing progesterone. The lack in progesterone induces the endometrium to be shed.
The level of progesterone will drop so low that the negative feedback is removed from the pituitary and hypothalamus so they will begin to produce FSH and LH, leading to the recruitment of follicles into a new menstrual cycle.

33
Q

What happens to the progesterone production after weeks 8-9??

A

At around 8/9 weeks, the placenta takes over the progesterone production.
hCG is maximal by 9-11 weeks, it is produced by the trophoblastic cells of the embryo.

34
Q

What hormones control maternal changes in pregnancy?

A

Most of the maternal changes in pregnancy are down to progesterone and estrogens:
They are both steroids and therefore bind to directly to transcription factors causing direct effects by turning on genes, having widespread effects throughout the body.

35
Q

Role of progesterone in maternal changes?

A

Decidualization (CL)
Smooth muscle relaxation – uterine quiescence
Mineralocorticoid effect – cardiovascular changes
Breast development (glands and stroma)

36
Q

Role of estrogens in maternal changes?

A

Estradiol (E2), Estriol (E3)
Rely on steroids from foetus and maternal adrenals
Development of uterine hypertrophy
Metabolic changes (insulin resistance)
Cardiovascular changes
Increased clotting factor production (haemostasis)
Breast development (glands and stroma)

37
Q

Average weight gain?

A

9-13kg

About 2.0 kg in total in the first 20 weeks
Then approximately 0.5 kg per week until full term at 40 weeks
A total of 9 -13 kg during the pregnancy.

38
Q

Where does weight gain go to?

A

Foetus and placenta 5 kg
Fat and protein 4.5 kg
Body Water (excluding that in other listed structures)
1.5 kg intravascular
interstitial
intracellular
Breasts 1 kg
Uterus 0.5 - 1kg

39
Q

Why is failure to gain weight during pregnancy alarming?

A

A failure to gain weight or sudden change requires investigation.
Constant weight monitoring can cause anxiety.

40
Q

Metabolic Rate?

A

Rises by:
350 kcal/day mid gestation
250 kcal/day late gestation
(75% foetus and uterus; 25% respiration)
9 calories = 1g fat, therefore 40g fat for 350kcal

41
Q

What happens to glucose levels?

A

Glucose increases in the maternal circulation in order to cross the placenta.

42
Q

Glucose in the First trimester - maternal reserves

A

The pancreatic cells increase in number raising circulating insulin so more glucose is taken up into tissues. Fasting serum glucose decreases
So the pancreas releasing more insulin results in hyperinsulinemia, this means that any sugar in the mothers circulation is rapidly taken up and stored as glycogen in the liver. So if you measure fasting blood glucose levels they will be low.

43
Q

Glucose in the Second trimester - Foetal reserves

A

Placental Lactogen causes insulin resistance, ie less glucose into stores and increase in serum glucose.
So at this point the placenta is developed and starts producing lactogen, lactogen causes insulin resistance.
So as there is insulin resistance, when there is sugar in the blood stream and levels will rise higher than normal.

44
Q

Transfer of glucose to foetus

A

Increased glucose level in blood during 2nd trimester. Glucose is transported across placenta as foetal energy source. Foetus stores some in liver. Increased concentration gradient.

45
Q

Why do baby girls have a larger than normal uterus when born>

A

Uterus grows in response to raised maternal oestrogen levels

46
Q

Why does insulin resistance develop in pregnancy?

A

n the first trimester, the embryo is small therefore its metabolic demands are very low, the mother wants to store as much glycogen, fat and energy as possible therefore there is an increase in insulin.
In the second trimester, the embryo is much bigger therefore its metabolic demands are much higher. So now the mother is no longer storing and instead wants a high level of glucose in the blood so that there is a larger concentration gradient across the placenta. So with insulin resistance in the 2nd trimester you get high blood sugar levels in the mother which increases the concentration across the placenta and drives sugar towards the growing foetus.

47
Q

Water gain?

A

Water increases in (up to 8.5l):
Foetus
Placenta
Plasma volume
Breasts
Uterine muscle
Amniotic fluid
Oedema – lungs, connective tissue, leakage, swollen ankles.

48
Q

Water gain is caused by

A

Estrogen and progesterone
are so high that they act like mineralocorticoid….retain more sodium from kidneys thereby increasing blood volume.

RAAS –
placental renin production. Estrogen upregulates angiotensinogen synthesis by liver leading to increased angiotensin II and aldosterone. Despite higher ANGII women resistant to AT2 receptor mediated vasoconstriction because progesterone decreases vasosensitivity.
So get fluid retention but NOT high blood pressure/vasoconstriction

Connective tissue
and ligaments take on water and become a bit softer.

Resetting osmostat,
Steroids affect the osmostat so there is a decreased thirst threshold. Decrease in oncotic pressure (albumin).

49
Q

IOxygen consumption increases- how?

A

The respiratory centre in the brain becomes more sensitive to carbon dioxide.
Hypercapnic drive – it is the levels of CO2 that stimulates the respiratory centre to breathe. So as CO2 rises = breathe more
So will breathe more deeply and a little quicker

The thoracic anatomy changes
The ribcage is displaced upwards and ribs flare outwards.
This partly creates space for the baby, but it also increases breathing.

Overall the minute volume (amount of air breathed in a minute) increases by 40%
This results in an increase in Arterial oxygen concentration (pO2) by 10%
The arterial CO2 concentration decreases by 15-20%

This is beneficial as at the maternal: foetal interface, there is a large concentration gradient of oxygen favouring transfer of oxygen across the placenta from the mother to the foetus. There is also a very low concentration of CO2 on the mothers side, this facilitates transfer of CO2 from the foetus to the mother
Also the foetus will express foetal haemoglobin which has a higher affinity for oxygen

This is mainly caused by estradiol and progesterone

50
Q

Maternal blood changes- plasma volume?

A

Increases (45% )

51
Q

Red cell mass change

A

Increases (18%) so oxygen capacity increases by nearly 20%

52
Q

Although some changes occur, why might the mother seem anaemic?

A

if you look and measure blood you would think she was anaemic due to the dilution effect. Plasma volume has increased by 40% but RBC only by 20%. So there is fewer rbc per ml.

There is increased efficiency of iron absorption from gut.
Haemodilution apparent anaemia as concentration of Hb falls

Non-pregnant range Hb 12 - 16g/dl
Pregnant range Hb 10.5 - 13g/dl
But will have 20% more RBC

Circulating volume increases from 4.5l to 6l

Increase in white cells and clotting factors, blood becomes hypercoagulable. Increased fibrinogen for placental separation, but increased risk of thrombosis DVT.

53
Q

CVS changes- uterus

A

Expanding uterus
pushes heart causes changes to ECG and heart sounds

54
Q

CVS changes- Peripheral vasodilation

A

(CO = BP/TPR)

Mediated by endothelium dependent factors such as nitric oxide synthesis upregulated by E2 20-30% fall in TPR so CO increases…
Estrogen upregulates NO synthesis this promotes relaxation of smooth muscle and vasodilation. So there is a fall in total peripheral resistance.

55
Q

CVS changes- cardiac output

A

INCREASED (CO = HR x SV)
increased heart rate (8-10bpm) but primarily stroke volume (force of contraction)
begins as early as 3 weeks to max 40% at 28 weeks
BP decreases in 1st 2 trimesters

SO… The heart is working harder, but the total peripheral resistance is going down, and there is an increased number of RBCs. So it is a low pressure high volume system.

Extra work exacerbates pre-existing conditions, eg aortic valve defects, pulmonary hypertension.

56
Q

Changes to vessels

A

There is increased cardiac output and vasodilation by steroids.
There is reduced peripheral resistance and increased flow to:
Uterus
Placenta
Muscle
Kidney
Skin

Neoangiogenesis, including extra capillaries in skin (spider naevi) to assist heat loss.
Pregnancy characterised by low pressure and high blood volume.

57
Q

GI tract changes

A

The GI tract is also affected by steroids such as progesterone and estrogen
They increase appetite and thirst
There is a reduction in GI motility
there is less peristalsis and more relaxation of smooth muscle.
This can lead to constipation
There is a relaxed lower oesophageal sphincter
This can lead to acid reflux
There is a large uterus
This presses on the stomach and can also cause the acid reflux
Usually have small frequent meals.

58
Q

Folic Acid in pregnancy

A

Folic acid is an important cofactor in DNA synthesis, in purine synthesis.
So supplementation advised up to 400µg/day until week 12
Ideally 3 months before pregnancy.
Deficiency can lead to birth defects eg spina bifida (neural tube defects).
The uterus, placenta and foetus are all incredibly dynamic – there is a mass amount of growth in these few week

59
Q

Urinary system

A

There is a steroid mediated smooth muscle relaxation so there is relaxation of the urinary tract (dilates and relaxes).
BUT this can lead to an increase in UTIs
In the kidney there is increased blood flow (due to vasodilation) this will lead to an increased GFR (filtration)
This will increase clearance of creatinine, urea, uric acid.
Glucose re-absorption is less effective.
Relaxin from corpus luteum/placenta stimulates formation of endothelin which mediates dilation of renal arteries by nitric oxide synthesis.

Progesterone and VEGF cause resistance to angiotensin II mediated vasoconstriction leading to further vasodilation and increased renal blood flow and increased GFR.

Urinary frequency will increase as the baby is pressing on the bladder

60
Q

Placental cortisol & CRH

A

Corticotrophin releasing hormone (CRH)
Is released into maternal and foetal circulation by placenta.
This causes the babys hypothalamus pituitary adrenal axis to be activated.
The adrenal glands will produce cortisol.
Possibly involved in labour initiation (placental biological clock).

61
Q

effects of cortisol

A

here are metabolic changes (insulin resistance) in the 2nd half of pregnancy.
Foetal lung maturity – in order for the baby to breathe properly it needs cortisol to produce surfactant to line the alveoli of the lungs which acts to reduce the surface tension of the liquid in the alveoli.
So the surface tension of a small amount of water in the alveoli forces the water to form a drop. If this happens in the alveoli, when the baby is born it will not have the strength to breathe enough to open its alveoli, it will be held together by the surface tension of the water. So, surfactant is produced in the foetal lung to reduce the surface tension of the water so that the baby can breathe, so if there is an immature baby they struggle to breathe.
Mineralocorticoid action (aldosterone).
Increases prostaglandin E2 and Oxytocin production by the placenta
It also increases placental CRH – so acts as a positive feedback

62
Q

ACTH effects

A

Causes the adrenal gland to produce DHEA which is an androgen.
DHEA is aromatized into estrogen by the placenta. By aromatase
The placenta cannot make androgens de novo, (it does not have the enzymes for cholesterol->androgen)
This Increases the E:P ratio (estrogen to progesterone ratio) and stimulating prostaglandins which activate blood flow, uterine contractions & cervical ripening. Which leads to labor.

63
Q

Effects of hPL

A

Human placental lactogen (hPL)
Present only during pregnancy, maternal serum levels rising in relation to the growth of the foetus and placenta. Maximum levels reached near term.
Similar activities to growth hormone.
Metabolic changes – insulin resistance, decrease glucose utilisation, increase lipolysis.
Possibly some role in lactation – cross reactivity with prolactin receptors.

64
Q

Effects of prolactin

A

Increases throughout pregnancy.
Suckling triggers a reflex increasing prolactin production – inhibited by progesterone.
Does not happen before birth. So as baby is born and the placenta is lost, progesterone levels falls removing inhibition -> suckling and milk.
Has inhibitory action on ovaries post partum causing anovulation (stopping cycle) and reduces chances of pregnancy again for the first 3-6 months - not totally effective.

65
Q

Thyroid gland becomes more active during pregnancy… why?

A

The thyroid becomes more active during pregnancy. The metabolic rate increases, energy demands increase.
Increased production of thyroid hormone to meet increased metabolic demand of pregnancy leads to a risk of gestational thyrotoxicosis -too much thyroid hormone
hCG may act on TSH receptor – as they have the same alpha subunit

If patient has a history of hyperthyroidism such as Graves disease they may require endocrine management to maintain normal function.
This is where an antibody is produced against your own TSH receptor, it binds to it and stimulates it resulting in hyperthyroidism.

Biochemical tests may indicate hyperthyroidism in pregnancy where in fact the patient is normal (euthyroid).

Suppressed TSH may indicate gestational thyrotoxicosis.
caused by excessive stimulation of thyroid gland by hCG

66
Q

Uterine hypertrophy- reasons?

A

At 12 weeks gestation the uterine fundus may be palpated through the abdomen above the symphysis pubis.
Large increase in muscle mass during first 20 weeks (50g – 1000g).
After this stretching & increases in blood flow; size reaching a peak at 36 weeks.
After pregnancy it does not go back to its normal size

67
Q

How does the cervix change?

A

Its primary function is to retain the pregnancy
The first thing it wants to do is to make a seal to stop any bacteria from getting in, makes a plug of cervical mucus. BUT it has to be able to let a baby out.
Increase in vascularity

So… From 8 weeks there is preparation for expansion during childbirth
Tissue softens and turns bluer from 8 weeks
changes in connective tissue
begins gradual preparation for expansion
Proliferation of glands
mucosal layer becomes half of mass
great increase in mucus production
protective…ie anti-infective

Stretching of uterus and cervix during childbirth and stimulation of nipples during breastfeeding cause release of oxytocin from the posterior pituitary.
This helps with birth, bonding with the baby, and milk production

68
Q

Returning back to normal

A

Dramatic and rapid fall in steroids on delivery of the placenta.
Most endocrine-driven changes return to normal rapidly.
Uterine muscle rapidly loses oedema but contracts slowly: never returns to pre-pregnancy size.
Removal of steroids permits action of raised prolactin on breast.

69
Q

Why is there an increased risk of DVT?

A

Increase in white cells and clotting factors, blood becomes hypercoagulable. Increased
fibrinogen for placental separation, but increased risk of thrombosis.

Year 3- Repro (34 decks)

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