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Semester 4 > Repro Session 8 > Flashcards

Repro Session 8 Flashcards

1
Q

What does the yolk sac become after the primitive gut tube has formed?

A

Proximal umbilical cord

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2
Q

What causes the amniotic sac to increase in size?

A

Foetus and fluid

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3
Q

What is the chorionic sac occupied by?

A

Expanding amniotic sac

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4
Q

What obliterates the chorionic cavity?

A

Amniochorion formation

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5
Q

What are the aims of implantation?

A

Establish basic unit of exchange, anchor placenta and to establish maternal bloodflow

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6
Q

How is the basic unit of exchange established in implantation?

A

Villi development

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7
Q

Describe the different stages of villi in their development.

A

Primary: early finger-like projections of trophoblast
Secondary: invasion of mesenchyme into core
Tertiary: invasion by foetal BV

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8
Q

Why is implantation said to be interstitial?

A

Uterine epithelium is breached and the conceptus implants in the stroma

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9
Q

Why is the placental membrane said to be haemomonochorial during implantation?

A

1 layer of trophoblast between maternal blood and foetal capillaries

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10
Q

Is there usually mixing of maternal and foetal blood?

A

No due to haemomonochorial placental layer

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11
Q

How is the placenta anchored in implantation?

A

Establishment of outermost cytotrophoblast shell

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12
Q

What has happened in embryonic development by the end of the 2nd week?

A

Conceptus has implanted; embryo, amniotic cavity and yolk sac are suspended by the connecting stalk in the chorionic cavity

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13
Q

What are the alternative names of the smooth and villous chorion?

A

Smooth = chorionic sac. Villous = placenta

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14
Q

What can uncontrolled invasion by the blastocyst at an inappropriate site of implantation lead to?

A

Haemoperitoneum

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15
Q

What is placenta praevia?

A

Implantation in lower 1/3 of uterine segment

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16
Q

When is C-section necessary in placenta praevia?

A

If internal os is occluded

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17
Q

What is there a risk of in placenta praevia?

A

Haemorrhage

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18
Q

What is placenta accreta?

A

Excessive invasion of chorionic villi

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19
Q

How do placenta accreta, increta and percreta differ?

A 
Accreta = invasion of myometrium
Increta = into myometrium
Percreta = through myometrium
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20
Q

What is the pathogenesis of pre-eclampsia?

A

Failure of epithelial to endothelial transformation at 20+ wks results in unknown circulating factor causing maternal hypertension and proteinuria

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21
Q

What is the cycle of events in placental insufficiency?

A

Failure of maternal artery remodelling to low resistance; increased vascular resistance in fetoplacental vascular bed; deceased metabolically active placenta

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22
Q

What are prepared in each uterine cycle in anticipation of implantation?

A

Pre-decidual cells

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23
Q

Why can pre-decidual cells be considered “check point” cells?

A

Decidual reaction provides balancing force for invasive trophoblast

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24
Q

How far does the trophoblast invade into the endometrium normally?

A

To spiral arterioles but no further

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25
Q

What happens when the cytotrophoblast from ends of anchoring villi attach to terminal ends of spiral arteries?

A

Undergo epithelial to endothelial transformation

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26
Q

How are the BV of the endometrium altered upon implantation?

A

From small diameter with high resistance to large diameter, low resistance vessels

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27
Q

How do the villi on the surface of the chorion develop?

A

Those on chorionic pole grow to form chorion frondosum. On aembryonic pole they degenerate to form chorion laeve

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28
Q

What decidua layer covers the chorion frondosum?

A

Basalis

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29
Q

What is the decidua basalis?

A

Decidual plate with glycogen that will form placenta

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30
Q

What happens to the decidua capsularis membrane over the chorion laeve?

A

Stretches and degenerates

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31
Q

What does the chorion laeve fuse with?

A

Uterine wall

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32
Q

How can foetal membranes be shared by monozygotic twins?

A

One zygote with separate implantation sites–> 2 amnions and chorions. One morula with 2 intracellular masses and bilaminar discs forms 2 amnions and 1 chorion. One blastocyst and bilaminar disc with 2 primitive streaks forms shared amnion and chorion

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33
Q

What is there a risk of in a shared amnion and chorion between monozygotic twins?

A

Twin-to-twin transfusion

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34
Q

What layers are present in the first trimester placenta?

A

Complete syncytiotrophoblast and cytotrophoblast layer

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35
Q

What forms the foetal component of the first trimester placenta?

A

Trophoblast with secondary and tertiary villi and extramebryonic mesoderm (chorionic plate)

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36
Q

What forms the maternal component of the first trimester placenta?

A

Uterine endometrium

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37
Q

What are stem villi?

A

Extensions of mesoderm from chorionic plate to cytotrophoblast shell to give extraembryonic vasculature

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38
Q

What happens in endovascular invasion of the first trimester placenta?

A

Maternal vessels are eroded so that blood flows into intevillous spaces

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39
Q

How do the stem villi in the first trimester placenta?

A

Free villi extend from them

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40
Q

What happens to the syncytium in the first trimester placenta?

A

Becomes thin and breaks off as syncytial knots in maternal circulation

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41
Q

How does the foetal aspect of the placenta appear?

A

Umbilical vessels radiate to chorionic vessels under transparent amnion

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42
Q

How does the maternal aspect of the placenta appear?

A

Surrounding amniochorion ruptured, cotyledons separated by decidual septa and covered by thin layer of decidua basalis

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43
Q

What changes have occurred from the first trimester to term placenta?

A

SA for exchange dramatically increased, placental barrier thin, cytotrophoblast layer lost, discoid with 15-25 cm diameter

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44
Q

Why is a small population of cytotrophoblast cells retained in the term placenta?

A

For repair

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45
Q

What blood vessels are present in the umbilical cord?

A

2 umbilical arteries carrying deoxygenated blood from foetus to mother and 1 umbilical vein carrying oxygenated blood from placenta to foetus

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46
Q

Which blood vessels in the umbilical cord are oxygen rich and poor?

A

Umbilical arteries are oxygen poor, veins oxygen rich

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47
Q

What are the metabolic functions of the placenta?

A

Synthesis of glycogen, cholesterol and fatty acids

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48
Q

Why does the latent a synthesis cholesterol?

A

For steroid hormone synthesis

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49
Q

What are the endocrine functions of the placenta?

A

Produce protein and steroid hormones

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50
Q

What protein hormones does the placenta produce?

A

hCG, hCsommatomammotrophin (placental lactogen), hCthyrotrophin, hCcorticotrophin

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51
Q

What is hCG and analogue of?

A

LH

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52
Q

What is the function of placental lactogen?

A

Diabetogenic mother and breast development

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53
Q

What steroid hormones does the placenta synthesise?

A

Progesterone and oestrogen

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54
Q

What effect does progesterone have on appetite in the pregnant female?

A

Increases

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55
Q

Why do trophoblast disease and choriocarcinoma cause very raised hCG?

A

Endocrine function of placenta is in syncytiotrophoblast

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56
Q

What does the placenta take over steroid hormone production from in the 11th week?

A

Corpus luteum

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57
Q

What happens to hCG levels when the placenta takes over steroid hormone production?

A

Decrease

58
Q

What is a molar pregnancy?

A

When the outer cell mass only develops

59
Q

What is choriocarcinoma?

A

Malignant trophoblast if cancer

60
Q

How is exchange of water, electrolytes, urea and uric acid achieved by the placenta?

A

Simple diffusion

61
Q

How is AT of a.a. And iron achieved by the placenta?

A

Specific transporters in syncytiotrophoblast

62
Q

How is glucose transported across the placenta?

A

Facilitated diffusion

63
Q

Describe gas exchange across the placenta.

A

O2, CO2 and CO via simple diffusion limited by flow

64
Q

Why does gas exchange across the placenta need careful monitoring, especially in childbirth?

A

Cord compression can be rapidly fatal as foetal oxygen stores are small

65
Q

What makes complement components in the first trimester?

A

Foetus

66
Q

What happens at 14wks that causes development of passive immunity for the foetus?

A

Maternal IgG transported via receptor-mediated process so foetal [IgG] exceeds those in maternal circulation

67
Q

What does development of passive immunity depend on?

A

Mother’s exposure to pathogens

68
Q

Is the placenta a protective or true barrier and why?

A

Protective because some substances readily access foetus via placenta

69
Q

Give some examples of known teratogens.

A

Thalidomide, alcohol, therapeutic drugs, drugs of abuse

70
Q

What effect does maternal smoking have on pregnancy via an unknown mechanism?

A

Causes embryon and placental disruption

71
Q

How do infectious agents lead to birth defects?

A

Cross placenta to cause foetal infection and subsequent cell death

72
Q

Give some examples of infectious agents that can lead to birth defects.

A

Varicella zoster, CMV, treponema pallidum, toxoplasma gondii, rubella

73
Q

What is rubella syndrome?

A

Microcephaly, PDA and cataracts

74
Q

What is the affect of alcohol crossing the placental barrier?

A

Inhibits bronchial apparatus and CNS development

75
Q

How does haemolytic disease of the newborn arise?

A

Exposure of maternal blood to foetal circulation mounts maternal antibodies against foetal rhesus group which in a following pregnancy cross placenta and ellicit haemolysis

76
Q

Why is haemolytic disease of the newborn now uncommon?

A

Mother and father rhesus groups are tested and prophylaxis offered if necessary

77
Q

How is routine antenatal screening conducted?

A

History and examination for risk factors and FHx, blood tests and urinalysis

78
Q

What is assessed in antenatal blood tests?

A

Blood group for comparison with father’s, Hb levels for anaemia and any infection

79
Q

Why is UTI a potential problem pregnancy?

A

Can lead to pre-term labour

80
Q

What change is seen in cardiac output during pregnancy?

A

Increase of 40% from T1

81
Q

What change is seen in stroke volume during pregnancy?

A

Increase of 35% from T1

82
Q

Why does cardiac output increase in pregnancy?

A

To account for potential significant haemorrhage at birth

83
Q

Why does stroke volume increase in pregnancy?

A

Blood volume has significantly increased

84
Q

What changes are seen in TPR during pregnancy?

A

Decreases 25-30% from T1

85
Q

Why does TPR change during pregnancy?

A

Foetal gas exchange depends on flow

86
Q

How does blood pressure change during pregnancy?

A

Decreases during T1 and T2 but returns to normal in T3

87
Q

What causes blood pressure changes during pregnancy?

A

Decreased vascular resistance due to progesterone

88
Q

Why should women in T3 not lie on their back?

A

Causes aortocaval compression by gravid uterus leading to hypotension

89
Q

What is the treatment for pre-eclampsia?

A

Deliver baby

90
Q

How is pre-eclampsia identified?

A

Maternal hypertension and proteinuria

91
Q

What changes in renal perfusion are seen during pregnancy?

A

Increases by 60-80%

92
Q

Why does RPF change in pregnancy?

A

Cardiac output increases

93
Q

What change is seen in GFR during pregnancy?

A

Increases of 55%

94
Q

Why does GFR change in pregnancy?

A

Progesterone causing afferent and efferent dilation

95
Q

What complications can progesterone action on GFR cause?

A

Hydroureter and urinary stasis

96
Q

What change is seen in creatinine clearance in pregnancy?

A

Increases by 40-50%

97
Q

What happens in protein excretion during pregnancy?

A

Increases

98
Q

What happens to urea levels during pregnancy?

A

Decreases by 50%

99
Q

What accounts for the changes in creatinine clearance, protein excretion and urea levels in pregnancy?

A

Filtration capacity of kidneys

100
Q

What change is seen in bicarbonate levels during pregnancy?

A

Decreased

101
Q

What change is seen in creatinine levels during pregnancy?

A

Decreases

102
Q

Why does the bicarbonate level change during pregnancy?

A

Functional renal reserve decreases as GFR increases

103
Q

What do normal non-pregnant ranges of urea, bicarbonate and creatinine indicate in pregnancy?

A

Renal dysfunction

104
Q

What respiratory changes are seen during pregnancy?

A

Oxygen consumption increases, resting minute ventilation increases, tidal volume increases, RR VC and FEV1 remain constant

105
Q

What causes physiological dyspnoea during pregnancy?

A

Increased respiratory drive due to progesterone

106
Q

Why does tidal volume increase during pregnancy?

A

AP and transverse diameters of thorax increase

107
Q

Why does FRC decrease in T3?

A

Diaphragm is displaced by gravid uterus

108
Q

Why are vital capacity and FEV1 constant in pregnancy?

A

Diaphragm and changes in thorax diameters balance each other out

109
Q

Why is PaCO2 reduced in pregnancy?

A

Increased metabolic CO2 is blown off by physiological hyperventilation

110
Q

Why does physiological hyperventilation not lead to respiratory alkalosis?

A

Renal bicarbonate excretion increases

111
Q

Why are pregnant women predisposed to metabolic acidosis?

A

Renal bicarbonate excretion is increased

112
Q

What changes to carbohydrate metabolism are seen on pregnancy?

A

Increased maternal peripheral insulin resistance, switch to gluconeogenesis

113
Q

What stimulates changes to carbohydrate metabolism in pregnancy?

A

Human placental lactogen mainly but prolactin, oestrogen, progesterone and cortisol also contribute

114
Q

What happens to fasting blood glucose pregnancy?

A

Decreases

115
Q

What happens to post-prandial blood glucose in pregnancy?

A

Increases

116
Q

What is gestational diabetes?

A

Carbohydrate intolerance first recognised in pregnancy that does not persist after delivery

117
Q

What are risk factors for developing gestational diabetes?

A

PCOS, FHx, high maternal age, T2DM, ethnicity, obesity

118
Q

What are the possible consequences of gestational diabetes?

A

Macrosomic foetus, stillbirth, congenital defects

119
Q

What builds fat stores in early pregnancy for lipolysis in T2?

A

Progesterone

120
Q

What is the benefit of lipolysis in T2?

A

Increases plasma free FA that cannot cross placenta therefore increasing glucose available for foetal metabolism

121
Q

Which fatty acids are able to cross the placenta?

A

Essential

122
Q

Why are pregnant women at a higher risk of ketoacidosis?

A

Increased FA synthesis combined with physiological increase in renal bicarbonate excretion

123
Q

Why might TSH be low in normal pregnancies?

A

hCG minimises its function

124
Q

Why does hCG and TSH not lead to high free T4?

A

Very active liver produces thyroid binding globulins

125
Q

What happens to the appendix during pregnancy?

A

Moved to RUQ

126
Q

What are the effects of progesterone on the smooth muscle of the GI tract?

A

Delayed emptying and stasis in biliary tract

127
Q

Why are pregnancy women at an increased risk of pancreatitis?

A

Progesterone on smooth muscle of biliary racy causes stasis and stone formation

128
Q

Why is pregnancy a pro-thrombotic state?

A

Need for fibrin deposition at the implantation site and risk of haemorrhage at birth

129
Q

What are the effects of progesterone on the blood during pregnancy?

A

Increased fibrinogen and clotting factors, decreased fibrinolysis, stasis and venodilation

130
Q

Why can thromboembolic disease in pregnancy not be treated with warfarin?

A

It is a teratogen

131
Q

How does a physiological aneamia arise during pregnancy?

A

Due to dilution as red cell mass increases but does not match the plasma volume increase

132
Q

When does iron and folate deficiency anaemia arise in pregnancy?

A

If increased demands during pregnancy are not met

133
Q

What are the complications of sickle cell disease in pregnant homozygotes?

A

More frequent crises, pre-eclampsia, thrombosis and infections

134
Q

What are the consequences of sickle cell disease in pregnancy heterozygotes?

A

May develop crises

135
Q

What are the implications for pregnancy for homozygous beta-thalassaemia pts?

A

Anaemia in pregnancy is unusual due to iron overload

136
Q

What is the treatment for pregnant homozygous beta-thalassaemia pts with anaemia?

A

Folic acid without iron

137
Q

What are the consequences for heterozygous beta-thalassameia pts during pregnancy?

A

Worsening of chronic anaemia

138
Q

Why is non-specific local immune system suppression needed at the materno-foetal interface?

A

Foetus is an allograft

139
Q

How is the immune system suppression at the materno-foetal interface identified histologically?

A

Different lymphocytes are found at the trophoblast-endometrial boundary

140
Q

How can a foetus develop an abnormal thyroid state?

A

Exchange of maternal autoantibodies e.g. In Graves or Hashimoto’s disease

141
Q

What is the treatment for haemolytic disease of the newborn?

A

IM anti-RH antibodies

142
Q

How does the treatment for haemolytic disease of the newborn act?

A

Foetal rhesus D+ve destroyed before mother mounts response

Semester 4 (33 decks)

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