Maternal Changes In Pregnancy

Question 1

Talk about the journey of the egg from Ovulation - Late blastocyst (6)

Answer 1

1) Ovulation in Uterine tubes
2) Fertilisation in Ampulla of uterin tube
3) Cleavage in Uterine tube
4) Morula entering Uterus
5) Early blastocyst in uterus
6) Late blastocyst implanted in uterine wall

Question 2

Human blastocyst (3)

Answer 2

Inner cell mass - forms the foetus

Trophoblast- forms part of the placenta

Blastocoel- Fluid filled cavity

Question 3

Uterine receptivity- Endo max changes (4)

Answer 3

Endometrial changes reach their maximum about 7 days after ovulation. The implantation window 6 – 10 days after the LH spike.

Pre-decidualizaton 9 to 10 days after ovulation decidual cells cover surface of uterus.

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

Glandular secretions of endometrium contains growth factors, adhesion molecules, nutrients, vitamins, matrix proteins and hormones.

Question 4

Syncytiotrophoblast merging (3)

Answer 4

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

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.

Question 5

Implantation (days 7-16) (3)

Answer 5

Implanting day 7-8: Syncytiotrophoblast erodes the endometrium. Cells of the embryonic disc form epiblast and hypoblast. Epiblast develops fluid filled amniotic cavity.

12 day blastocyst: Implantation complete as extraembryonic mesoderm forms discrete layer beneath cytotrophoblast.

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

Question 6

Maternal-foetal interface summary

Answer 6

bottom half is embryo
top half is mother

Question 7

Maternal recognition of pregnancy (3)

Answer 7

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

hCG prevents the death of the corpus luteum so the endometrium is not shed.

The corupus luteum continues to produce steroids estrogen and progesterone. Rapid change in maternal systems in response to luteal and later placental steroids

Question 8

Serum hCg maximum + monitory benefit (2)

Answer 8

Serum hCG maximal by 9 – 11 weeks.

Useful for monitoring early pregnancy complications e.g. ectopic pregnancy
or miscarriage

Question 9

Placental steroidogenesis (7 – 8 weeks) - Proge. + Estrogens (8)

Answer 9

Progesterone:
* Synthesised directly from cholesterol
* Decidualization (CL)
* Smooth muscle relaxation – uterine quiescence
* Mineralocorticoid effect – cardiovascular changes
* Breast development (glands and stroma)

Estrogens - Estradiol (E2), Estriol (E3):
* Synthesised from steroids derived from foetal and maternal adrenals. Placenta lacks 17α-hydroxylase & 17,20 lyase
* Development of uterine hypertrophy
Metabolic changes (insulin resistance)
* Cardiovascular changes
* Increased clotting factor production (haemostasis)
* Breast development (glands and stroma)

Question 10

Average total weight gain (3)

Answer 10

9-13kg

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

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.

Question 11

Basal metabolic rate (4)

Answer 11

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

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

Question 12

Glucose (3)

Answer 12

First trimester Maternal reserves: Pancreatic cells increase in number raising circulating insulin so more glucose is taken up into tissues. Fasting
serum glucose decreases.

Second trimester Foetal reserves: Placental Lactogen causes insulin resistance, ie less glucose into stores and increase in serum glucose.

Transfer of glucose to foetus: Increased glucose level in blood during 2nd trimester. Glucose is transported across placenta as foetal energy source. Foetus stores some in liver

Question 13

Total water gain + why? (5)

Answer 13

Up to 8.5 litres total water gain

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.

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

Resetting osmostat, decreased thirst threshold. Decrease in oncotic pressure (albumin

Question 14

Oxygen consumption increased(4)

Answer 14

O2- haemoglobin dissociation curve

-prog. + oest. inc. sensitivity to CO2 = increased urge to breathe
breathe more deeply + quicker (inc. by 40)%
= inc. pO2, dec pCO2
= facilitates gas transfer for fetus

Question 15

Maternal blood-iron (5)

Answer 15

Increased efficiency of iron absorption from gut

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

Maternal plasma volume 45% increase
Red cell mass 18% increase
Circulating volume increases from 4.5l to 6

Question 16

Cardiovascular system changes (4)

Answer 16

Expanding uterus : pushes heart = changes ECG and heart sounds

Peripheral vasodilation: mediated by endothelium dependent factors such
as nitric oxide synthesis upregulated by E2 = 20-30% fall in TPR so CO increases…

Increased cardiac output: increased heart rate (8-10bpm) but primarily stroke volume begins as early as 3 weeks to max 40% at 28 weeks
BP decreases in 1st 2 trimesters

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

Question 17

Cardiovascular system- vessels (5)

Answer 17

Increased cardiac output and vasodilation by steroids.

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.

Question 18

Cardiac Output equations (2)

Answer 18

CO = BP/ TPR
CO = HR x SV

Question 19

Gastrointestinal tract (6)

Answer 19

Steroids =
- Appetite + thirst
- Reduced GI Motility = constipation
- Relaxed lower oesophageal sphincter = acid reflux

large uterus = acid reflux = small infrequent meals

Question 20

Dietary supplementation – Folic acid (4)

Answer 20

Folic acid = DNA Production growth blood cells = uterus, placenta + foetus

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).

Question 21

Urinary system (2)

Answer 21

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.

Question 22

Urinary frequency (2)

Answer 22

w/ inc. perfusion of kidneys , filtration rate, thirster than normal, blood vol = high, relaxing urethra + baby pressing on bladder

= increase freq.

Question 23

Cortisol (2)

Answer 23

Cortisol:
Metabolic changes (insulin resistance).
Foetal lung maturity
Mineralocorticoid
action (aldosterone).
Increase prostaglandin
E2 & Oxytocin
production by placenta

hypo = CRH
pituitary = ACTH
adrenal gland - DHEA

Question 24

Placental CRH (2)

Answer 24

CRH released into maternal and foetal circulation by placenta. Increases cortisol (positive feedback) and stimulates adrenocorticotrophic hormone (ACTH) & so DHEA in foetal HPA axis.

DHEA is aromatized into estrogen by the placenta. Increasing E:P ratio
and stimulating prostaglandins which activate blood flow, uterine contractions & cervical ripening.

Question 25

Thyroid gland (5)

Answer 25

Increased production of thyroid hormone to meet increased metabolic demand of pregnancy leads to a risk of gestational thyrotoxicosis hCG may act on TSH receptor.

If patient has a history of hyperthyroidism such as Graves disease they may require endocrine management to maintain normal function.

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

Symptoms can include anxiety, tremor, heat intolerance, palpitations, weight loss or lack of weight gain, goiter, tachycardia, and hyperreflexia but usually associated with persistent vomiting of hyperemesis gravidarum.

Suppressed TSH and high serum T4 may indicate gestational thyrotoxicosis

Question 26

Uterine hypertrophy (3)

Answer 26

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

Question 27

Changes in cervix (4)

Answer 27

Primary function is to retain the pregnancy

Increase in vascularity

Tissue softens 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

Question 28

Prolactin (6)

Answer 28

High circulating concentrations of estrogen and progesterone increase prolactin levels during pregnancy.

Part of a family with human placental lactogen and growth hormone – all have widespread metabolic effects.

During pregnancy prolactin is produced by myometrium and placenta, in addition to the pituitary.

Estrogen and progesterone inhibit the stimulatory effects of prolactin on milk production.

The abrupt drop in estrogen and progesterone levels following delivery allow prolactin to induce lactation.

After birth, sucking activates nipple mechanoreceptors signaling the hypothalamus and causing anterior pituitary prolactin secretion

Question 29

Oxytocin (3)

Answer 29

Stretching of uterus and cervix during childbirth causes release of oxytocin which helps with the birth and emotional bonding with the baby.

Suckling stimulus triggers the release of oxytocin from the posterior pituitary gland, which triggers milk ejection.

Prolactin controls milk production (lactogenesis) but the milk-ejection reflex is due to oxytocin

Question 30

Return to normal (4)

Answer 30

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