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Pregnancy complications, fatal morbidity and assisted reproduction EAR7 > Maternal physiological adaptations to pregnancy > Flashcards

Maternal physiological adaptations to pregnancy Flashcards

1
Q

What are the pregnancy hormones

A 
Progesterone 
Oestrogen 
Placental prolactin 
Placental lactogens 
Corticotropin-releasing hormone (CRH)
Aldosterone 
EPO
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2
Q

What produces progesterone in pregnancy

A

Corpus lute and then placenta

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3
Q

What produces oestrogen in pregnancy

A

Placenta and fetes

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4
Q

How does fetus protect itself from secreted hormones

A

Placental polarity/barrier

Fetus can conjugate steroids to sulphates making them biologically inactive

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5
Q

What does placental prolactin do

A

Breast chances, behavioural changes

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6
Q

What do placental lactogens do

A

For maternal insulin and glucose metabolism, lipolysis, EPO

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7
Q

What does cirticotropin releasing hormone do

  • where is it released from
  • What are the risks of increased levels
A

Leads to increased secretion of cortisol from mother- its a stress response

Released from placenta

Increased levels can affect nutrient transfer and the placental clock. Risks can be pre-term labour, early parturition signals

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8
Q

What does aldosterone affect

A

Plasma volume

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9
Q

What does EPO affect

A

Red blood cells

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10
Q

What cytokines are released in pregnancy

A

Pro-inflammatory interleukins, TGF-beta

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11
Q

What vasodilatory mediators are released in pregnancy and use

A

VEGF, NO (for vasodilation and angiogenesis)

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12
Q

how does uterus change in pregnancy

A

Expands and increases in weight

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13
Q

How does uterine musculature change in pregnancy

A

Hypertrophy. Needed for expulsion of fetus at parturition

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14
Q

What happens to heart during pregnancy

A

Apex of heart moved to anterior and to the left (pushed up and rotated forwards)

Left ventricular hypertrophy to cope with increased maternal cardiac output

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15
Q

What happens to calcium concentrations in pregnancy

A

Increased intestinal calcium absorption, maternal bone loss may occur in last trimester and lactation. Reversible

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16
Q

What happens to blood volume in pregnancy and how does this occur

A

Increase (over 40%)

Stimulation of RAAs- aldosterone leads to increased sodium and water retention so increased plasma volume

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17
Q

What happens to red cell mass during pregnancy and why

A

Increases linearly

Increased renal EPO increases red cell mass

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18
Q

What happens to hematocrit and haemoglobin during pregnancy and why

advantage of this

A

Fall. Because plasma volume increases more than cell mass

Advantage- decreased viscosity leads to reduced resistance in flow so better placental perfusion

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19
Q

What happens to haemoglobin during pregnancy and why is this beneficial

A

50% higher. Useful protection against any blood loss at delivery

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20
Q

What will help restore haemoglobin levels in pregnant women

A

Iron and folic acid

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21
Q

What relaxes smooth muscle cells of arteries

A

VEGF
PLGF
NO
Progesterone

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22
Q

What do angiogenic, permeability and vasoactive factors do to vasculature

What is the consequence of this

A

Vascular dilatation and relaxation of peripheral vascular tone

Establishment of the new vascular beds, including the utero-placental circulation

Lowers blood pressure (contributes to increased blood volume)

-Reduction in peripheral vascular resistance which reduces by about 40% in mid pregnancy, rising slowly to term

23
Q

What happens to stroke volume in pregnancy and why

A

Increase

-Because of increase in blood volume which means more blood enters heart (preload) and decrease in peripheral resistance due to vasodilation leads to reduced after load

24
Q

What happens to maternal heart rate in pregnancy

A

Increase

25
Q

What happens to cardiac output during pregnancy and why is this needed

A

Increase

-AN extra 30-50ml of oxygen is consumed per minute during pregnancy

26
Q

What can happen to women with valvular heart disease during pregnancy and why

A

Pulmonary oedema

Have difficulty accommodating raised CO

27
Q

What is systolic and diastolic bp like during pregnancy

A

Systolic- remains stable

Diastolic- early, falls and reaches plateau at around 20 weeks and rises to normal values by term

28
Q

IN mid-pregnancy what can happen if a woman lays supine

A

Enlarging uterus compresses both the inferior vena cava and the abdominal aorta.

Vena Cana: This reduces venous return to the heart so fall in pre-load and cardiac output. Resultant fall in BP may be severe enough for the mother to lose consciousness

Aorta: reduction in uteroplacental and renal blood flow. During last trimester, maternal kidney function is markedly lower in the supine than in the lateral position

29
Q

What is maternal oxygen consumption like to all tissues throughout pregnancy

A

Increased

30
Q

What are the structural changes in the respiratory system to accommodate for increased o2 consumption

A

Increased chest expansion, displaced diaphragm, increased vascularisation of upper respiratory tract

31
Q

What are the ventilatory changes in the respiratory system to accommodate for increased o2 consumption

A

Progesterone-mediated hypersensitivity to CO2 increases the respiratory rate

Tidal volume increases

Alveolar ventilation is higher

Therefore there is a fall in arterial and alveolar CO2 tensions. PaO2 increases

32
Q

What is the consequence of a fall in arterial and alveolar CO2 tensions and an increase in PaO2 to the baby

A

The higher PaO2 on the maternal side of the placenta facilitates oxygen transfer to fetus, whilst the lower PaCO2 facilitates transfer of CO2 in the reverse side

33
Q

Anatomical changes to maternal kidneys

A

Kidneys enlarge due to increased vasculature, vascular dilatation and interstitial space increases

Renal parenchymal volumes increase in pregnancy, glomerular diameters are greater

Dilatation of the calyces, renal pelvis and ureter. Increased chances of urinary tract infection

Bladder loses tone: increased urinary frequency, urgency

34
Q

Physiological changes to renal function

A

Increase in renal plasma flow, decrease in renal vascular resistance

Changes in GFR and glomerular filtration fraction

Changes in tubular re-absorption

35
Q

What happens to filtration fraction in early pregnancy

A

Declines in early pregnancy

36
Q

Formula for amount of glucose in urine

A

Amount of glucose filtered through the glomerulus minus the amount reabsorbed by the proximal tubules

37
Q

What may be present in a pregnant woman’s urine

What is a consequence of this

A

Glucose (glycosuria) because filtered load of glucose rises in pregnancy and exceeds maximal rate of reabsorption.

Increases chances of UTI

38
Q

Where does fetus get its glucose from

A

Mother

39
Q

What happens to glucose levels in mother during pregnancy

A

Fasting hypoglycaemia in first trimester, the decrease in glucose levels reach their plateau about 12 weeks gestation. Then it reverts to normal in second and third trimester

40
Q

What do progesterone and insulin do

A

Progesterone increases maternal appetite and stimulates deposition of glucose in fat stores

Increase in insulin secretion favours lipogenesis and storage of fat

41
Q

What is absorption like mid pregnancy onwards

A

Increased absorption

42
Q

What is gluconeogeneis like mid pregnancy onwards

A

Increased

43
Q

What happens to free fatty acids and lipolysis from mid pregnancy onwards

A

Mobilised

44
Q

What does enhanced lipolysis mean

A

Increases free fatty acid oxidation and ketones. It is an alternative fuel and can be used by mother so reduces her need for glucose which can be spared for fetus

45
Q

After 20 weeks of pregnancy, what happens to plasma glucose levels

A

Revert to normal

46
Q

What is the duration of postprandial hyperglycaemia in pregnancy

A

Prolonged

47
Q

What is postprandial hyperinsulinimea

A

During last trimester:

  • Higher glucose peak leads to higher insulin secretion
  • Insulin reaches its peak after 1h
  • Declines slowly but not back to basal levels in pregnancy
48
Q

When is insulin resistance higher

A

Gestational diabetes and maternal obesity

49
Q

How does fetus avoid maternal rejection

A

Placenta is a structural barrier stopping direct contact of maternal blood with fetus

Syncytial structure of the syncytiotrophoblast means maternal immune cells cannot cross to the fetus without going through the cytoplasm and being degraded. If they do manage to transcytose to the placental storm, fetal macrophages will phagocytose maternal immune cells

50
Q

Which immune cells present in endometrium

A

Dendritic cells (APC)
Helper T cells
T regulatory cells
Uterine natural killer cells

51
Q

What happens to T helper cells under the influence of pregnancy hormones

A

Decline relative to the suppressor cells or T regulatory cells in the endometrium (these decrease immune function so maintain materno-fetal tolerance)

52
Q

What can be used to suppress immune reactions

A

Extra- villous trophoblast cells

53
Q

What may soluble factors provide

A

Local immunoprotection of the fetus

Pregnancy complications, fatal morbidity and assisted reproduction EAR7 (8 decks)

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