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Reproduction > Physiology of Pregnancy and Lactation > Flashcards

Physiology of Pregnancy and Lactation Flashcards

1
Q

summarise the stages of fertilisation from ovulation to implantation

A

fimbrae sweep ovum into oviduct, carried by smooth muscle contraction and cilia
fertilisation occurs in ampulla of fallopian tube (day 1)
cleavage, division and differentiation
morula
blastocyst containing inner cell mass (becomes fetus) and trophoblast (accomplishes implantation and develops into fetal portions of placenta)
blastocysts reaches uterus day 4-5 and implants days 5-7

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2
Q

how does implantation occur

A

cords of trophoblastic cells invade the endometrium
as they carve deeper into endometrium make hole for the blastocyst and the boundaries between the cells in the advancing trophoblastic tissue disintergrate
when implantation is finished the blastocyst is completely buried in the endometrium (day 12)

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3
Q

what happens to the different parts of the blastocyst

A 
inner cells become embyro 
outer cells (trophoblastic cells) burrow into endometrium and become the placenta
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4
Q

do maternal and foetal circualtions mix

A

no

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5
Q

what tissue is the placenta derived from

A

both trophoblast and decidual tissue (endometrium during pregnancy)

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6
Q

how is the placenta formed

A

trophoblast cells (chorion) differentiate into mulinucleate cells (syncytiotrophoblasts) which invade decidua and break down capillaries to form cavities filled with maternal blood

developing embryo send capillaries into syncytiotrophoblast projections to form placental villi

each villus contains foetal capillaries separated from maternal blood by a thin layer of tissue (no direct contact between bloods)

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7
Q

what gestation is the placenta functional

A

week 5

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8
Q

what exchange occurs at placenta

A

2 way exchange of resp gases, nutrients, metabolites

largely down diffusion gradient

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9
Q

what does hCG do to the corpus luteum

A

signals it to continue secreting progesterone

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10
Q

what does progesterone do to decidual cells

A

stimulates them to concentrate glycogen, proteins and lipids

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11
Q

as the placenta develops it extends villi into the uterine wall, what does this do

A

increases contact area between uterus and placenta meaning more nutrients and waste materials can be exchanged

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12
Q

what provides the early nutrition for the embryo

A

corpus luteum

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13
Q

what is the intervillous space and what is its function

A

within villi mothers blood is in intervillous soace along with blood vessels from the embryo. these re separated by a thin membrane

circulation within the intervillous space acts as an arteriovenous shunt (passage between artery and vein)

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14
Q

what structure acts as the fetal lungs

A

the placenta

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15
Q

what is the respiratory function of the placenta

A

supplies O2

removes CO2

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16
Q

how does the placental exchange of gas happen

A

maternal O2 rich blood
umbilical blood is a mix of arterial and venous blood, O2 poor
O2 diffuses from maternal into foetal circulation system (PO2 maternal> PO2 fetal)

CO2 partial pressure is elevated in fetal blood, follows a reversed gradient

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17
Q

what happens to the blood after placental gas exchange

A

O2 rich fetal blood returns to fetus via umbilical vein

maternal O2 low blood flows back into the uterine veins

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18
Q

how does the fetus receive sufficient oxygenation

A

fetal Hb has increased ability to carry O2
higher Hb concentration in fetal blood (50% more than in adults)
bohr effect (fetal Hb can carry more O2 in low pCO2 than in high pCO2)

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19
Q

how does water cross placenta

A

along its osmotic gradient (exchange increases during pregnancy up to 35th week)

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20
Q

how do electrolytes cross placenta

A

follow H20

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21
Q

which electrolytes can only go from mother to fetus and not back

A

iron and Ca2+ - why anaemia common in pregnancy

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22
Q

how does glucose cross placenta

A

(fetus’ main source of energy)
passes the placenta via simplified transport
(high glucose need in 3rd trimester)

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23
Q

how do fatty acids cross placenta

A

free diffusion

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24
Q

what is diffusion of waste products across placenta based on

A

concentration gradient

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25
Q

what teratogenic drugs can cross the placenta

A 
thalidomide 
carbamazepine
coumarins 
tetracycline
alcohol, nicotine, heroin, cocaine, caffeine

drugs (exclusing alcohol) cause 3% of all congenital malformations

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26
Q

what effect does hCG have

A

prevents involution of the corpus luteum

affect on the testes of the male fetus (development of sex organs)

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27
Q

when does hCG peak

A

8-12 weeks

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28
Q

what is the role of human placental lactogen

A

produced from week 5 of pregnancy
growth hormone like effects - protein tissue formation
decreases insulin sensitivity in mother- more glucose for the fetus
involved in breast development

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29
Q

what is the role of progesterone in pregnancy

A

development of decidual cells
decreases uterus contractility- makes uterus relax
preparation for lactation

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30
Q

what are the forms of oestrogen that are secreted in higher volumes as pregnancy progresses

A

estradiol (most secreted)
estriol
estrone

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31
Q

what is the role of estrogens in pregnancy

A

enlargement of uterus
breast development
relaxation of ligaments

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32
Q

what can relaxation of ligaments in pregnancy cause

A

pelvic girdle pain

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33
Q

how do hCG levels increase in a normal pregnancy

A

should double (or increase by >60%) every 48 hours in a singleton early pregnancy

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34
Q

what can hCG levels be used to help diagnose

A 
ongoing viable pregnancy (doubling, or >60% rise) 
ectopic pregnancy (static or slow rising) 
failing pregnancy (falling)
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35
Q

what are the side effects of hCG

A

nausea and vomiting

36
Q

what can cause high levels of hCG

A

multiple pregnancy

molar pregnancy

37
Q

when do hCG levels start to fall

A

from 12-14 weeks

38
Q

what does placental release of CRH (corticotrophin releasing hormone) cause

A 
ACTH release in mother 
increase aldosterone (=hypertension) and cortisol (= oedema and insulin resistance = gestational diabetes)
39
Q

what does HCG (HC thryotropin) released from the placenta cause

A

hyperthyroidism in the mother

40
Q

what does increased Ca2+ demands of the placenta cause

A

hyperparathyroidism in the mother

41
Q

what happens to cardiac output in pregnancy

A

is increased by 30-50% (begins 6wk gestation and peaks at 24 wks) due to demands of the uteroplacental circulation

decreases in last 8 weeks (becomes sensitive to body position, uterus compresses vena cava)

increases 30% more during labour

42
Q

what causes the cardiac output to increase in pregnancy

A

placental circulation
increased metabolism
skin thermoregulation
renal circulation

43
Q

what can the increase CO cause in pregnant mothers

A 
ECG changes 
functional murmurs (usually mild systolic and normal but always investigate)
heart sounds
44
Q

what happens in HR in pregnancy

A

increases with to 90/min to increase cardiac output

45
Q

what happens to BP in pregnancy

A

drops during 2nd trimester (uteroplacental circulation expands and peripheral resistance decreases - vasodilation)

with multiple pregancies cardiac output increases more and BP drops lower

lowest at 17-24 wks, rises after this back to normal (36wks) then can go higher than BP before pregnancy

46
Q

what haematologic changes happen in pregnancy

A

plasma volume increases proportionally with cardiac output (50%)

erythropoesis (RBC) increases (25%)

Hb is decreases by dilution (this decreases blood viscosity)

iron requirements increase significantly (6-7 mg/ day in 2nd trim)- supplements usually needed

47
Q

why lung changes happen in pregnancy

A

increase in progesterone (signals brain to lower CO2 levels)

enlarging uterus interferes with lung function - works to lower CO2

48
Q

how does progesterone lower CO2 levels

A

increases CO2 sensitivity in respiratory centres of brain

49
Q

what happens in O2 consumption in pregnancy

A

increases to meet metabolic needs of fetus, placenta and mother (20% above normal)

50
Q

how is CO2 physically reduced in pregnancy

A

RR increases
tidal and minute volume increases (50%)
pCO2 decreases slightly
vital capacity and PO2 dont change

51
Q

what happens to the urinary system in pregnancy

A

GFR and renal plasma flow increase (up to 30-50%, peaks at 16-24 wks)

increased re-absorption of ions and water (due to placental steroids and aldosterone)

slight increase in urine formation

52
Q

how do postural changes affect renal function

A

when in:
up right position renal function decreased
supine position increased
lateral position during sleep increased significantly

53
Q

what is pre-eclampsia

A

pregnancy induced hypertension and proteinuria

54
Q

what are the features of pre-eclampsia

A

increasing BP since 20th week- hypertension
kidney function declines causing salt and water retention- oedema of face and hands
renal blood flow and GFR decreases

55
Q

what causes pre eclampsia

A

?extensive secretion of placental hormones
?immune response to fetus
insufficient blood supply to placenta- ischaemia

56
Q

who is pre-eclampsia more common in

A

women with pre existing hypertension, diabetes, autoimmune disease (e.g. lupus), renal disease, FHx of pre-eclampsia, obesity, multiple gestations (twins)

57
Q

what is eclampsia

A

extreme pre-eclampsia (lethal without Tx)

vascular spasms, extreme hypertension, chronic seizures and coma

58
Q

what is the treatment for eclampsia

A

vasodilation and cesarean section

59
Q

what is the average maternal weight gain (and what causes it )

A

11 kg

  • fetus (3.5 kg)
  • extra-embryonic fluid/ tissues (2 kg)
  • uterus (1 kg)
  • breasts (1 kg)
  • body fluid (2.5 kg)
  • fat accumulation (1 kg)
60
Q

how much extra food is needed in pregnancy

A

200 extra calories/ day
30g/ day or protein
end of pregnancy fetus needs 5mg/kg/min of glucose= 2.5mg/kg/min for mother

61
Q

what causes the increased metabolic demand in pregnancy

A

85% fetal metabolism

15% stored as maternal fat

62
Q

what are the 2 metabolic phases of pregnancy

A

1st-20th week= mothers’ anabolic phase:

  • anabolic metabolism of mother
  • small nutritional demands of the conceptus

21st-40th week (esp last trim) catabolic stage

  • high metabolic demands of fetus
  • accelerated starvation of mother
63
Q

why should starvation of mother be avoided in pregnancy

A

as circulating ketones bad for babies brain

64
Q

what happens physiologically in the anabolic phase of pregnancy

A
  • normal/ increased sensitivity to insulin
  • lower plasmatic glucose level
  • lipogenesis, glycogen stores increase
  • growth of breasts, uterus, weight gain
65
Q

what happens physiologically in the catabolic phase of pregnancy (accelerated starvation)

A
  • maternal insulin resistance
  • increased transport of nutrients through placental membrane
  • lipolysis
66
Q

what causes insulin resistance in pregnancy

A

HPL, cortisol and growth hormone

67
Q

what are the special nutritional needs in pregnancy

A

folic acid- reduces risk of neural tube defects, ideally taken before conception
vit D supplements (esp if mother overweight)
high protein diet (higher energy intake)
iron supplements may be required
B vitamins for erythropoesis

68
Q

towards the end of pregnancy the uterus progressively becomes more excitable- what does this mean

A

it becomes more contractile

progesterone inhibits contractility of uterus while oestrogen increases it

69
Q

how does the uterus become more excitable during end of pregnancy

A

estrogen: progesterone ratio changes
progesterone inhibits contractility of uterus while oestrogen increases it
oxytocin (from maternal posterior pituitary gland) increases contractions and excitability
mechanical stretch of uterine muscles and cervix by fetal head increases contractility

70
Q

where is oxytocin release from

A

fetus

mothers posterior pituitary

71
Q

what controls the timing of labour

A

oxytocin
adrenal glands
prostaglandins

72
Q

what are braton hicks contractions

A

infrequent, irregular contractions that involve only mild cramping- preparing for birth, false labour
become more frequent and stronger then labour pains begin

73
Q

what does cervical stretching cause the release of

A

oxytocin

74
Q

what do strong uterine contractions and pain from the birth canal cause

A

neurogenic reflexes from spinal cord that induce intense abdominal muscle contractions

75
Q

what is parturition

A

initiation of labour

76
Q

what hormone induces oxytocin receptors on uterus

A

estrogen

77
Q

what does oxytocin cause

A

uterine contractions

stimulates placenta to make prostaglandins

78
Q

what do prostaglandins cause

A

more vigorous contractions of uterus

79
Q

what is full dilation

A

10 cm

80
Q

what can induce labour

A

vaginal prostaglandins and oxytocin injection

intracervical ballon/ sweep- mechanical stretch

81
Q

what are contractions like in late labour

A

strong, 3-4 every 10 minutes

82
Q

what are the stages of labour

A

1st- cervical dilation (8-24 hours)
2nd- passage through birth canal (few mins to 120 mins)
3rd- expulsion of placenta

83
Q

how does estrogen affect production and release of milk

A

stimulates growth of ductile system

inhibit milk production

84
Q

how does progesterone affect production and release of milk

A

development of lobule-alveolar system

inhibit milk production

85
Q

how does prolactin affect production and release of milk

A

stimulates milk production steady rise in weeks 5-birth)
1-7 days after birth prolactin induces high milk production
stimulates colostrum (low volume, not fat- high in protein and immunoglobulins for fetal immunity)

86
Q

what is the milk let down reflex

A

suckling stimulus (mechanoreceptors in nipple) or the sound of a childs cry causes release of prolactin (makes more milk) and oxytocin (causes breast to push out milk via smooth muscle contraction)

Reproduction (51 decks)

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