Maternal Physiology Flashcards

1
Q

What happens to the levels of B-HCG, oestrogen, and progesterone throughout pregnancy in each trimester?

A

1st trimester- B-HCG, oestrogen and progesterone increase (B-HCG produced by placenta to keep corpus luteum alive –> corpus luteum produces oestrogen and progesterone)

2nd trimester- B-HCG decreases (after peak at 7 weeks), oestrogen and progesterone still increase (produced by ovaries and placenta)

3rd trimester- B-HCG, oestrogen, progesterone decrease to signal parturition!

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2
Q

What does prolactin do?

A

Stimulates production of breast milk

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3
Q

What do placental lactogens do?

A

Modify metabolic state of mother to increase energy supply to foetus

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4
Q

What do corticotropins-releasing hormones (CRH) do?

A

Increase production of cortisol in mother

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5
Q

What effect does cortisol have in pregnancy?

A

Stimulate uterine contraction

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6
Q

Increases in which hormones can increase the risk of pre-term labour?

A

Increased CRH stimulates increased production of cortisol, which stimulate uterine contraction. Increased CRH increases the risk of premature uterine contraction.

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7
Q

Describe the hormonal involvement in kicking of parturition

A

. Foetal stress causes anterior pituitary to release ACTH, which stimulates adrenal gland to release cortisol
. Cortisol causes decrease in oestrogen and progesterone (B-HCG already decreased), increase in prostaglandins from placenta
. Increased prostaglandins stimulates uterine contraction

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8
Q

What is the positive feedback mechanism during labour? How does it arise?

A

. Baby stretches cervix as it exits, causing hypothalamus to release oxytocin
. Oxytocin stimulates production of more prostaglandins, resulting in more uterine contraction

(More prostaglandins= more uterine contraction= means baby stretches cervix more as it comes out, more oxytocin released, more uterine contraction etc.)

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9
Q

Describe the main anatomical changes to the mother during pregnancy

A

Uterus- expands, heavier, hypertrophy, displaces diaphragm upwards
Heart- pushed up and to the left by displaced diaphragm, apex shifts laterally, left ventricular hypertrophy
General- weight gain, decreased calcium in bones, endometrial changes, development of mammary gland to form lactating breast

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10
Q

What happens to blood (plasma) volume, haematocrit, and haemoglobin levels during pregnancy?

A

Blood volume increases (due to RAAS activation)
Haematocrit decreases (blood volume increases more than EPO)
Haemoglobin increases

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11
Q

Why is it important that blood volume increases/haematocrit decrease during pregnancy?

A

Lower haematocrit means the blood is less viscous (less RBCs in given volume), so there’s better placental perfusion

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12
Q

Why is it important that haemoglobin increases during pregnancy?

A

So if there’s blood loss during parturition there will still be sufficient oxygen for the mother and foetus

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13
Q

How can a pregnant lady increase their haemoglobin levels?

A

Take iron and folic acid supplements

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14
Q

What happens to total peripheral resistance during pregnancy? Which molecules are responsible for this?

A

VEGF, PLGF, NO, and progesterone decrease total peripheral resistance by stimulating vasodilation, formation of new vascular beds, and lower blood pressure

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15
Q

How do the changes in blood volume and peripheral resistance affect cardiac output during pregnancy? Why is this effect important?

A

Increased blood volume and decreased peripheral resistance means increased cardiac output (increased stroke volume x HR)
Important to meet increased oxygen demand during pregnancy

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16
Q

How does increased cardiac output and increased peripheral resistance during pregnancy affect blood pressure? How about systolic and diastolic BPs?

A

Causes increase in blood pressure because BP = CO x TPR (total peripheral resistance)

Systolic BP is stable throughout
Diastolic decreases until 20 weeks (due to decreased TPR), then increases to normal by term

17
Q

What is aortocaval compression? When does it occur and what negative effects can it have?

A

. In mid-pregnancy onwards
. When supine, enlarged uterus of pregnant woman compresses the inferior vena cava and abdominal aorta
. Compressed IVC = decreased venous return, preload, CO, and thus decreased BP –> mother can lose consciousness
. Compressed abdominal aorta = decreased uteroplacental and renal blood flow –> reduced kidney function and perfusion to foetus

18
Q

How can aortocaval compression be avoided?

A

Place pregnant lady on lateral tilt to avoid supine position where uterus compresses IVC and ab aorta

19
Q

How does the respiratory system adapt during pregnancy to meet increased oxygen demand?

A

Chest expands, increased vascularisation of upper respiratory tract, hypersensitivity to CO2 to increase RR (mediated by progesterone)
Increased TV and alveolar ventilation = increased pO2, decreased pCO2

Higher pO2 on maternal side of placenta increases oxygen transfer to foetus
Lower pCO2 increases transfer of foetal CO2 to maternal blood to be expired

20
Q

What happens to the kidneys during pregnancy?

A

Kidneys enlarge

  • Increased vasculature, vasodilation, increased interstitial space
  • Enlarged parenchyma, Bowman’s capsule, dilation of calyces, renal pelvis, and ureter due to progesterone
21
Q

What happens to the bladder during pregnancy?

A

Loses tone = urinate more frequently and with more urgency

22
Q

Why is there increased risk of UTI during pregnancy?

A

. Renal calyces (chambers where urine passes) enlarge, so more urinary tract stasis = increased chance of infection
. Glycosuria (due to decreased FF and increased RPF) increases risk of UTI

23
Q

Which hormone is involved in enlargement of the kidneys during pregnancy?

A

Progesterone

24
Q

What are RPF, GFR, and FF?

A

RPF- renal plasma flow
GFR- glomerular filtrate rate
FF- filtration fraction (proportion of fluid filtered into kidney tubules)

25
What happens to RPF, GFR, and FF during pregnancy?
. Renal vascular resistance decreases= increased RPF (decreases in third trimester) . GFR increases . FF decreases (due to decreased filtration pressure caused by decreased renal vascular resistance/TPR), increases in later pregnancy back to normal level
26
How do you calculate FF?
FF= GFR/RPF
27
Why do pregnant women get glycosuria?
. Increased RPF and decreased FF means more glucose in filtrate . High amount of glucose in tubules can't all be reabsorbed in PCT, so more glucose excreted in urine
28
Why may the mother have a glucose deficit during pregnancy?
. Glucose from mother crosses placenta to foetus | . Increased glucose excretion (glycosuria due to increased RPF and decreased FF)
29
What is the evidence supporting maternal glucose deficit/'accelerated starvation'?
. Lower fasting glucose (fasting hypoglycaemia) in first trimester . Ketones in maternal blood
30
What is the evidence against maternal glucose deficit/'accelerated starvation'?
. After initial hypoglycaemia during first trimester, blood glucose goes back to normal in 2nd and 3rd trimesters
31
How do glucose levels revert back to normal mid-pregnancy?
. Increased absorption of glucose from small intestine . Increased gluconeogenesis and glycolysis . Increased lipolysis (more FFA oxidation- mother can use ketones and glucose given to foetus) . Mild insulin resistance and decreased uptake of glucose by mother's tissues
32
How does the placenta help the foetus avoid maternal rejection?
Placenta prevents maternal and foetal blood mixing and prevents maternal immune cells reaching foetus (no MHC/HLA proteins) --> any maternal immune cells that manage to get through placenta are phagocytosed by Hoffbauer cells (foetal macrophages)
33
How does the endometrium help the foetus avoid maternal rejection?
. Decrease in maternal helper T-cells, increase in T-reg cells (fewer helper T-cells means less immune response, more T-reg cells means more immune suppression) . Suppression of uNK cells (by glycoproteins secreted by decidual stroma cells) . Secretion of immunosuppressive placental galectins and anti-inflammatory factors
34
How do EVTs (extra-villous trophoblast cells) help the foetus avoid maternal rejection?
``` . HLA class I antigens on EVTs bind with KIRs on uNK cells . This prevents uNK from producing cytokines that cause foetal lysis ```
35
What are KIRs?
Killer cell immunoglobulin-like receptors
36
How does the foetus gain acquired immunity?
Mother's IgG antibodies cross placenta
37
What happens if anti-foetal antibodies from the mother cross the placenta? What is the exception to this response?
. Usually they are diluted out by circulating antigens in the foetus, except with Rhesus antigen incompatibility (mother Rh -ve but foetus Rh +ve, immune response will be mounted if second child is Rh +ve)