Maternal changes in pregnancy Flashcards

1
Q

During pregnancy there are changes in nearly every bodily system. What is the cause of this?
When does the body return to normal

A
  • In pregnancy, sex steroids rise immensely which affects bodily systems
  • Mechanical displacement: uterus growth displaces many internal organs.
  • Foetal requirements: mum provides for foetus, as well as meeting own needs

changes within body systems due to pregnancy return to normal within ~6 weeks. Uterine muscle loses oedema fast, but may still take some time to return to its pre-pregnancy size

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2
Q

Describe a blastocyst

A

The cells of the ICM become everything so they are totipotent cells
This is usually around week 6

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3
Q

What is the implantation window?
What happens 9-10 days after ovulation
What happens to endometrium if implantation and pregnancy occurs?

A

The implantation window 6 – 10 days after the LH spike.
Pre-decidualizaton: 9-10 days post-ovulation decidual cells cover uterus surface
Decidualization: if pregnancy occurs, decidual cells fill w lipids + glycogen. Decidua becomes maternal placenta.

Cells fuse to form a multi-nucleated syncytiotrophoblast & invades the endometrium.
Chorionic gonadotropin (hCG) is an autocrine growth factor for blastocyst, produced at this point.

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4
Q

How do hormones fluctuate throughout pregnancy?

A

Human chorionic gonadotrophin (hCG) secreted by the syncytiotrophoblast increases rapidly
hCG prevents CL death so the endometrium is not shed.

The CL produces E2 and P4, but later on the placenta takes over to produce these hormones at 10-12 weeks of gestation

Maximal hCG by 9 – 11 weeks
Serum βHCG (quantitative) useful for monitoring early pregnancy complications e.g. ectopic pregnancy, miscarriage

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5
Q

Which hormones does the placenta produce and what are their actions on the pregnant mother?
what do both hormones do?

A

Progesterone= synthesised directly from cholesterol
- Luteal P4 causes decidualization (CL)
- Placental P4 causes sm relaxation – uterine quiescence
- Mineralocorticoid effect – cardiovascular changes
- Breast development (glands and stroma)

Estradiol (E2), Estriol (E3)
Placenta primarily makes estriol. BUT this lacks 17α-hydroxylase & 17,20 lyase needed for cortisol & testosterone synthesis. Hence relies on fetal & maternal adrenals for this
- Uterine hypertrophy
- Insulin resistance
- CVS changes inc clotting factor production
- Breast development (glands and stroma)

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6
Q

How much weight gain happens in pregnancy?

foetus & placenta VS fat & protein VS Body Water Vs Breasts VS Uterus

how much weight gain in first 20 weeks - then how much kg per week until full term

A
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7
Q

What happens to BMR during pregnancy? How can you meet these increased energy demands?

A

Rises by:
350 kcal/day mid gestation
250 kcal/day late gestation
(75% foetus & uterus; 25% respiration)

To meet these inc. energy demands: 40g extra fat for 350kcal

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8
Q

What happens to glucose levels in 1st vs 2nd trimester?

A

First trimester: Pancreatic cells increase, raising circulating insulin- more glucose is taken up, fasting serum glucose decreases.

Second trimester: placental Lactogen causes insulin resistance-serum glucose increases
Increased glucose level in blood in 2nd trimester. Glucose is transported across placenta as foetal energy source. Foetus stores some in liver.

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9
Q

Pregnant women gain up to 8.5 litres of water. What causes water gain during pregnancy?
estrogen & progesterone, placenal renin - but what doesn’t occur?, what retains water, 2 things which decrease

A

Estrogen & progesterone act like mineralocorticoid; retain more Na–> increasing blood vol
Placental renin production stimulates RAAS. Estrogen upregulates AT–> increased ang II & aldosterone.
But AT2 receptor mediated vasoconstriction doesn’t occur despite higher Ang II bc progesterone decreases vasosensitivity

Connective tissue & ligaments retain water + soften
Resetting osmostat and decreased thirst threshold
Decreased oncotic pa due to decreased albumin - can lead to tissue fluid accumulation + edema

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10
Q

What happens to oxygen consumption during pregnancy?

use diagram for rest of info

A

O2 consumption is driven by oestradiol and progesterone.
Consumption increases due to:
Increased sensitivity to CO2 (increased hypercapnic drive) + thoracic anatomy changes displace the ribcage

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11
Q

4 ways maternal blood is different?
Maternal plasma VS red cell mass, circulating volume & what this leads to, wbcs, clotting factors, fibrinogen

A

plasma volume increase & red cell mass increases due to increased iron absorption from gut
Circulating volume increases from 4.5 to 6.0L - this leads to apparent anaemia as Hb conc. also falls (Haemodilution effect)

Inc. wbcs, clotting factors and hypercoagulability (bc u can tear during birth)
Inc. fibrinogen to prep for placental separation, but inc thrombosis risk :(

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12
Q

4 effects of pregnancy on CVS?
what expands, what does oestradiol upregulate, 2 things which increase VS 1 which decreases + why?
what may occur in 3rd trimester?

A

Expanding uterus pushes heart, changes ECG + heart sounds

E2 upregulates NO-> peripheral vasodilation, fall in TPR.
TPR drop causes an increase in CO to meet inc pregnancy demands- done by HR + SV inc from 3 weeks
BP decreases in 1st & 2nd trimester due to decreased TPR. Pre-eclampsia may occur in 3rd trimester

Extra work worsens pre-existing Hx eg aortic valve defects & pulmonary HTN
There is also neoangiogenesis (spider naevi or telangiectasia) to assist w heat loss

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13
Q

3 effects of pregnancy on the GIT?

A
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14
Q

2 reasons why folic acid important in pregnancy? + therefore what is advised

A
  • Folic acid needed for DNA prod. of red cells, therefore folate deficiency leads to macrocytic (megalob) anaemia
  • Folate deficiency can also lead to neural tube folding defects - eg spina bifida
  • Folate supplementation advised. 400mcg daily from 3 months pre-conception to week 12 of pregnancy
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15
Q

4 effects of pregnancy on urinary system?

renal arteries, urinary tract, GFR, urinary frequency

A

CL & placenta -> Relaxin -> endothelin -> vasodilates renal arteries
Urinary tract sm relaxes and dilates, so UTI may persist due to static urine
Progesterone & VEGF resist ang II mediated vasoconstriction -> further afferent vasodilation–> increased renal BF and GFR
Increased GFR increases creatinine, urea & uric acid clearance, however glucose reabsorption is less effective!
Inc. frequency in 1st & 3rd trimesters as expanding uterus presses on bladder

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16
Q

4 things placental cortisol stimulates?

A
  • insulin resistance
  • Foetal lung maturity by way of surfactant development
  • Na retention due to mineralocorticoid action
  • Inc. PGE2 & Oxytocin prod. by placenta
17
Q

Describe the HPA axis to produce cortisol and DHEA
3 effects of Prostaglandins?
how does progesterone play a role?

A

DHEA aromatized into estrogen by placenta -> Increasing E:P ratio & stimulating prostaglandins

PGs inc. BF, uterine contractions & cervical ripening.

Note progesterone inhibits these effects until parturition, when pg levels decrease

18
Q

Draw the foetal HPA axis

A
19
Q

What is the effect of pregnancy on the thyroid?
what can thyroid tests indicate in pregnancy?
what thyroid problem can happen in pregnancy? + what condition can this be related to?

A

Thyroid hormone production rises to meet inc. metabolic pregnancy demands (hCG act on TSHr?) - BUT inc. risk of gestational thyrotoxicosis

Tests may show hyperthyroidism, when pt is acc normal (euthyroid)
Suppressed TSH & high serum T4 may = gestational thyrotoxicosis due to neg feedback along HPT axis
Thyroid dysfunction here also related to hyperemesis gravidarum

20
Q

What drugs are given to patients with gestational thyrotoxicosis
+ what is prefer

A

If pt has Hx of hyperthyroidism eg Grave’s, they may need endo management to maintain normal function

Thionamides carbimazole, methimazole, propylthiouracil inhibit thyroxine synthesis

Propylthiouracil is preferred drug in pregnancy as carbimazole and methimazole (rarely) linked w teratogenic effects.

21
Q

When can uterine fundus be palpated?
what week is uterus fully developed by?
what happens to upper uterus segment vs lower muscle segment? - therefore what do we do?

A

At 12w, the uterine fundus can be palpated just above the symphysis pubis
The uterus begins as small pear + ends up as a large watermelon at 36 weeks, with much more BF too
The upper uterus segment is the part that hypertrophies, the lower muscle segment is much thinner – hence why we do lower segment c-sections

22
Q

Primary function of the cervix is to retain the pregnancy
Cervical changes needed to be able to stretch and dilate during labor and delivery

Describe the changes to cervix during pregnancy
Stretching of uterus & cervix in birth releases what?

A

Changes include: increase in vascularity, softening of tissue from 8 weeks, and gland proliferation
Connective tissue changes prepare for gradual expansion.
Mucus production rises a lot=barrier to infection.

Stretching of uterus & cervix in birth + nipple stimulation during breastfeeding release oxytocin from posterior pit. This helps w parturition, bonding + lactation

23
Q

What is the function of prolactin?
What happens after birth?

A

Prolactin is produced by pit, myometrium & placenta during pregnancy in response to high steroids. However, estrogen and progesterone inhibit PL on milk production.

Sharp drop in estrogen & progesterone levels after placental delivery allows high PL levels to induce lactation.
Sucking activates nipple mechanoreceptors signaling the hypothalamus–> PL secretion from ant. pit.