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Med 3: Pregnancy Complications > Maternal Physiology > Flashcards

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
Q

What happens to RPF, GFR, and FF during pregnancy?

A

. 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
Q

How do you calculate FF?

A

FF= GFR/RPF

27
Q

Why do pregnant women get glycosuria?

A

. 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
Q

Why may the mother have a glucose deficit during pregnancy?

A

. Glucose from mother crosses placenta to foetus

. Increased glucose excretion (glycosuria due to increased RPF and decreased FF)

29
Q

What is the evidence supporting maternal glucose deficit/’accelerated starvation’?

A

. Lower fasting glucose (fasting hypoglycaemia) in first trimester
. Ketones in maternal blood

30
Q

What is the evidence against maternal glucose deficit/’accelerated starvation’?

A

. After initial hypoglycaemia during first trimester, blood glucose goes back to normal in 2nd and 3rd trimesters

31
Q

How do glucose levels revert back to normal mid-pregnancy?

A

. 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
Q

How does the placenta help the foetus avoid maternal rejection?

A

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
Q

How does the endometrium help the foetus avoid maternal rejection?

A

. 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
Q

How do EVTs (extra-villous trophoblast cells) help the foetus avoid maternal rejection?

A 
. HLA class I antigens on EVTs bind with KIRs on uNK cells
. This prevents uNK from producing cytokines that cause foetal lysis
35
Q

What are KIRs?

A

Killer cell immunoglobulin-like receptors

36
Q

How does the foetus gain acquired immunity?

A

Mother’s IgG antibodies cross placenta

37
Q

What happens if anti-foetal antibodies from the mother cross the placenta? What is the exception to this response?

A

. 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)

Med 3: Pregnancy Complications (1 decks)

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