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Reproduction, Development and Aging > Pregnancy and Birth > Flashcards

Pregnancy and Birth Flashcards

1
Q

Gestational trophoblastic disease

A

Hydatidiform mole

Placental trophoblast proliferation, can be benign or malignant

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2
Q

Negative pregnancy hCG levels

A

below 5 mIU/mL

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3
Q

Anembryonic pregnancy

A

Blighted ovum/afetal sac

Gestational sac where fetus hasn’t developed

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4
Q

Fetal demise

A

Fetus hasn’t survived

Not an emergency

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5
Q

Normal fetal heart rate

A

120–140 bpm

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6
Q

Threatened miscarriage

A

Incidence of around 25-30%
Bleeding in first trimester
Subchorionic bleeding –not always bad, bleed can seal on its own
If bleed occurs on opposite side to the fetus it’s less of a worry, but if it occurs on the sam side it can obstruct placental formation

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7
Q

Abnormal gestation sac

A

Lack of yolk sac and double decidual reaction, therefore lack of embryo

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8
Q

Preeclampsia

A

Hypertension specific to second half of human pregnancy
3–8% of all pregnancies
Proteinuria

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9
Q

Recurrent miscarriage

A

3+ miscarriages with the same partner
Usually in a row and usually early in the pregnancies
Often due to issues with placenta formation

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10
Q

Spontaneous miscarriage

A

Nature’s way of dealing with a non-viable embryo

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11
Q

Essential functions of the placenta

A

1) Self maintenance/renewal
2) Exchange/transport/transfer
3) Separation of foetus from mother
4) Protection of foetus from maternal functions
5) Protection of foetus from maternal immune system

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12
Q

Placental burrowing

A

1) Adhesion
2) Lacunar phase starts at day 8
3) Lacunar phase ends at day 12
In the human placenta, the trophoectoderm implants into endometrium (ICM first)
Primitive syncytium digests decidua and eats its way into the endometrium
At day 12 the embryo is fully enclosed in the uterine wall

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13
Q

Real placenta

A

After day 12, when the placenta is fully enclosed in the uterine wall

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14
Q

Villous period

A

Real placenta development after day 12
Cytotrophoblasts proliferate and invade the trabeculae which become primary villi
The lacunar system is now called the intervillous space, which is where maternal blood eventually ends up
At about day 14, cells of the extraembryonic mesenchyme invade the primary villi, forming secondary villi

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15
Q

Tertiary villi

A

18–20 days in, capillaries form in the villi, forming tertiary villi
The vessels in the villi connect to the umbilical vessels carrying blood to and from the foetus

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16
Q

Floating villi

A

Villi that are suspended in the intervillous space, not in contact with the maternal tissues
Responsible for the exchange and barrier functions of the placenta

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17
Q

Chorion laeve

A

Placental membrane

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18
Q

Chorion frondosum

A

Placenta itself

At six weeks, completely surrounds embryo

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19
Q

Villous regression

A

At the beginning, the placenta is round. To become oval and flat, the more lateral villi and those near the uterine lumen regress to form the chorion leave. The villi at the base of the implantation site form the chorion frondosum.

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20
Q

Anchoring villi

A

Crucial to placenta function
In a few villi, cytotrophoblasts break through the syncytiotrophoblast. The cytotrophoblasts spread laterally around the implantation site, forming a cytotrophoblast shell which remains in contact with maternal tissue. Columns of cytotrophoblasts continue to stream out of the anchoring villi to invade the decidua and spiral arteries during the first and second trimesters.

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21
Q

Role of placenta formation in regards to spiral arteries

A

Spiral arteries usually have a layer of smooth muscle in the walls that is tonically active. Invading cytotrophoblasts move down the spiral arteries, replacing the smooth muscle and becoming endovascular trophoblasts. This inhibits muscular activity and is thought to be key in preventing preeclampsia, as this process is not completed in preeclamptic patients.

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22
Q

Endovascular trophoblast plugs

A

Important to establish placental physical presence so the fetus can tolerate the blood flow
Embryos are designed to live in low oxygen environments so the trophoblast plugs prevent premature perfusion to avoid mechanical and oxidative injury
Breaks down around 10 weeks, full perfusion of placenta should resume by 13 weeks
Not solid –red blood cells can’t pass through but plasma can

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23
Q

Villous

A

Branch of the placenta

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24
Q

Villous cytotrophoblast

A

Trophoblast progenitor cell type found mainly in the first trimester underlying the syncytiotrophoblast

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25
Q

Syncytiotrophoblast

A

Cell that covers entire surface of placenta
Formed by fusion of villous cytotrophoblasts –does not replicate but additional fusion of villous cytotrophoblasts can replace parts

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26
Q

Extravillous cytotrophoblast

A

Differentiated cells that have migrated out of the villous placenta towards the maternal tissues

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27
Q

Structural changes of the placenta with gestational age

A

During early pregnancy, stroma of the villi become cellular and vascularised. During the 2nd trimester, villous cytotrophoblast thins down. During the 3rd trimester, villous cytotrophoblast is sparse.
Branching of the villi increases and the size of the placenta increases.

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28
Q

Decidua basalis

A

The decidua underlying the implantation site

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29
Q

Decidua capsularis

A

The decidua overlying the implantation site – the part that heals back behind the embryo

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30
Q

Decidua peritalis

A

The decidua around the remainder of the uterus

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31
Q

Fusion of the decidua capsularis with the decidua peritalis

A

As gestation progresses, the amniotic cavity enlarges, obliterating the uterine cavity, leading to fusion of the two decidua.

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32
Q

The placental membranes

A

Amnion
Chorion
Decidua

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33
Q

Amnion

A

Avascular membrane which covers the cord and the placenta

34
Q

Chorion

A

Placental membrane which carries fetal vessels

35
Q

Vessels of the umbilical cord

A

2 arteries and 1 vein

36
Q

Wharton’s jelly

A

A gelatinous substance in the umbilical cord containing a network of myofibroblasts my spaces filled with mucopolysaccharides

37
Q

Mucopolysaccharides in the umbilical cord

A

Found in Wharton’s jelly
Responsible for providing turgor to the cord so that it can’t be pulled tight which would cause blood supply to be occluded

38
Q

Placental adaptations to increase transport

A

1) Tortuous villous structure, large surface area
2) Syncytiotrophoblast has microvillous surface for increased surface area
3) In 3rd trimester, most villi are tertiary for transport purposes
4) In 3rd trimester, fetal capillaries are closely apposed to syncytiotrophoblast

39
Q

Gas transfer in the placenta

A

Fetal blood has a greater affinity for oxygen due to high concentration of haemoglobin (around 80% as opposed to adults 50%)
As maternal blood picks up fetal metabolites, the pH lowers, decreasing the affinity for oxygen and offloading it in the blood lake, in turn picking up carbon dioxide to go back to mum. The reverse occurs on the fetal side.

40
Q

Amniotic fluid functions

A

1) Buoyant medium without constriction allows symmetric foetal growth
2) Cushions the foetus
3) Prevents adhesions of the foetus with the membranes
4) Allows foetus to move (important for muscle development)
5) Development of GI/resp tract by breathing and swallowing (practice for later)

41
Q

Amniotic fluid origins

A

1) Initially, ultrafiltrate of maternal plasma
2) Major foetal contribution
3) After 20 weeks, foetal urine and surface of placenta and cord

42
Q

Amniotic fluid clearance

A

1) Fetal swallowing
2) Moving across foetal skin before keratinisation occurs (around 24 weeks)
3) Moving across foetal membranes into the maternal circulation or into the foetal vessels of the placenta and umbilical cord

43
Q

Polyhydramnios

A

Excessive amniotic fluid, possibly due to loss of swallowing

Common in diabetic pregnancy

44
Q

Oligohydramnios

A

Lack of amniotic fluid possibly due to foetal kidney problems

45
Q

2 types of diagnostic tests for foetal genetic anomalies

A

Amniocentesis

Chorionic villus sampling

46
Q

Some diseases that the placenta prevents transmission of

A

Hep B (although risk of transmission during birth)
Rabies
Measles
Malaria

47
Q

Some diseases that the placenta permits transmission of

A 
HIV
CMV
Smallpox
Rubella
Toxoplasmosis
48
Q

hCG production in pregnancy

A

By the preimplantation trophectoderm and then the syncytiotrophoblast

49
Q

Which hormones does hCG share its alpha chain with?

A

TSH, LH and FSH

50
Q

Which hormones does hCG share its beta chain with?

A

None – they are unique to the hormones

51
Q

hCG functions

A

Because hCG is so similar to LH, it can bind to the LH/hCG receptor and transmit similar signals as LH, causing luteal support. The corpus luteum doubles in size about a month into pregnancy under hCG influence, causing progesterone and oestrogen release.

52
Q

Luteal support

A

hCG has strong leutotrophic properties and is important in stimulation the production of progesterone and oestrogen by the ovary during the first 6–8 weeks of pregnancy. This stops the regression of the corpus luteum.

53
Q

Other than in pregnancy, what would cause high hCG levels?

A

Choriocarcinoma
Hydatidiform mole
Some testicular tumours

54
Q

Why is hCG important in pregnancies with male foetuses?

A

It has an LH-like activity that stimulates testosterone synthesis by Leydig cells of the testis in male foetuses

55
Q

How do trophoblasts synthesise progesterone?

A

Syncytiotrophoblast expresses various receptors to assist LDL uptake and use LDL cholesterol derived from the maternal circulation

56
Q

Functions of progesterone in pregnancy

A

Maintains uterine quiescence and converts the uterine environment to one conducive to pregnancy
Induces formation of the decidua, but this is not essential for implantation

57
Q

Where are progesterone receptors expressed?

A

Glands and stromal cells in the endometrium/decidua

58
Q

Oestrogen production by the placenta

A

Progesterone produced by placenta and converted to androgen in the fetal adrenals. The androgen goes back to the placenta where it is aromatised to oestrogen. Therefore, oestrogen, unlike progesterone, requires a live foetus as well as a functioning placenta.

59
Q

Anencephalic pregnancy

A

The foetus possesses atrophic adrenals, therefore usually have low levels of oestrogen

60
Q

Cardiovascular changes in pregnant mother

A

Increased CO due to 10% increase in SV and 10%–15% increase in HR
Reduced peripheral vascular resistance to avoid hypertension
Effects of angiotensin II seem to be blunted in normal pregnancy, possibly due to receptor changes, preventing vasoconstriction

61
Q

What causes the CV changes in a pregnant mother?

A

Oestrogen is a vascular permeabilising agent which can reduce vascular resistance, mainly in reproductive tissues
Can alter the ratio of type I/type III collagen in the vessel wall

62
Q

Haematological changes in pregnant mother

A

Increased blood volume and plasma volume (but at different rates)
Haematocrit declines due to fast rate of plasma increase

63
Q

How does haematocrit return to normal after birth?

A

During delivery, there is substantial blood loss, but this is not compensated for. Excess hypervolaemia after this is lost through postpartum diuresis and loss of RBCs, allowing the haematocrit to slowly return to normal

64
Q

Immune cells of the decidua

A

Almost no B cells therefore no antibody production
About 10% leukocytes are T cells
70% of leukocytes are specialised NK cells

65
Q

Skin changes in pregnant mother

A 
Pigmentation changes in nipples and areola
Linea nigra
Chloasma in neck and face
Striae gravidarum
Hair retention
66
Q

Birth weights

A

<2.5 kg = low BW
<1.5 kg = very low BW
<1 kg = extremely low BW
>4.5 kg = macrosomia

67
Q

SGA

A

Small for gestational age

<10th %ile

68
Q

LGA

A

Large for gestational age

>90th %ile

69
Q

Postmenstrual age

A

IVF + 2 weeks (from date of last menstrual period)

70
Q

Fetal insulin

A 
Key for:
Glucose uptake
Fat deposition
Protein anabolism
May promote fetal growth via tissue accretion and fat storage
71
Q

FGR due to undernutrition

A

Placental insufficiency

Maternal undernutrition

72
Q

FGR due to pathology

A

Congenital

Aneuploidy

73
Q

Fetal growth

A

Growth normally constrained by maternal environment
Provided minimal endocrine requirements are met, growth is regulated by substrate supply
About 16 g/kgbw/day

74
Q

Postnatal growth

A

Growth is normally limited to genetic potential

Provided minimal nutritional requirements are met, growth is regulated by endocrine status

75
Q

Common examples of maternal constraint of fetal growth

A

Adolescent mother
Multiple pregnancies
Maternal body habitus
First born child

76
Q

Glucocorticoids in fetal growth

A

Causes slowing of growth and induces expression of GH receptors in the liver
Prepares baby for birth

77
Q

Fetal growth restriction

A

Growth potential limited by pathological process, often due to poor placentation

78
Q

Gestational diabetes

A

Glucose intolerance developing in pregnancy

If the baby gets excess nutrition then they produce excess insulin and have excessive growth

79
Q

Maternal causes of poor foetal growth

A 
Maternal disease
Smoking
Substance use
Uterine malformations
Obesity
Social deprivation
80
Q

Placental/foetal causes of poor foetal growth

A 
Placental insufficiency
Multiple pregnancy
Intrauterine infection
Congenital malformation
Chromosomal and genetic disoders

Reproduction, Development and Aging (5 decks)

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