8. Pregnancy Flashcards

1
Q

What does implantation involve?

A

Interaction between trophoblast cells and epithelium of the uterus. Embedding of the blastocyst into the endometrium depending on invasive property of trophoblasts with outer layer synctiotrophoblast and underlying cytotrophoblast.

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2
Q

What is meant by implantation being interstitial?

A

Uterine epithelium is breached and conceptus implants within the stroma.

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3
Q

What happens to the placental membrane through pregnancy?

A

It gets thinner as the needs of the foetus increase.

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4
Q

What is meant by the placenta being haemomonochorial?

A

One layer of trophoblast separates maternal blood from foetal capillary wall.

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5
Q

What are the aims of implantation?

A

Establish the basic unit of exchange, anchor the placenta, establish maternal blood flow within the placenta.

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6
Q

What makes up the basic unit of exchange in implantation?

A

Primary villi - early, finger-like projections of trophoblast.
Secondary villi - invasion of mesenchyme into core.
Tertiary villi - invasion of mesenchyme core by foetal vessels.

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7
Q

How is the placenta anchored in implantation?

A

Establishment of outermost cytotrophoblast shell.

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8
Q

What are the two key features of the histology of the endometrium in preparation for implantation?

A

Decidualisation and remodelling or spiral arteries.

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9
Q

What is decidualisation in implantation preparation?

A

Pre-decidual cells, decidual reaction provides balancing force for invasive force of trophoblast, stimulated by progesterone.

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10
Q

What is remodelling of spiral arteries in implantation preparation?

A

Creation of low resistance vascular bed, maintains high flow required needed to meet foetal demand, particularly in late gestation.

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11
Q

What are the possible implantation defects?

A

Ectopic pregnancy - implantation at site other than uterine body, usually fallopian tube although it can be peritoneal or ovarian.
Placenta praevia - implantation in lower uterine segment.
Incomplete invasion - placental insufficiency -> pre-eclampsia.

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12
Q

What is the structure of the placenta by the beginning of the fourth month?

A

Foetal portion - formed by chorion frondsum and bordered by chorionic plate.
Maternal portion - formed by decidua basalis.
Space between (intervillous spaces) - filled with maternal blood.

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13
Q

What happens in the fourth and fifth months to the decidua?

A

It forms a number of decidual septa which project into intervillous space but don’t reach chorionic plate. They divide the placenta into cotyledons.

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14
Q

What is the first trimester placenta like?

A

Placenta is established, it’s a barrier to diffusion as still relatively thick, complete cytotrophoblast layer beneath the synctiotrophoblast.

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15
Q

What is the full term placenta like?

A

Surface area for exchange dramatically increased, barrier is now thin - cytotrophoblast layer beneath synctiotrophobalst lost.

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16
Q

What are the foetal blood vessels within the placenta?

A

Two umbilical arteries (deoxygenated blood from foetus to placenta) and one umbilical vein (oxygenated blood from placenta to foetus).

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17
Q

Where do the cotyledons receive blood from?

A

Through 80-100 spiral arteries that pierce the decidual plate.

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18
Q

What is the role of spiral arteries?

A

Pressure forces oxygenated blood deep into intervillous spaces and bathe numerous small villi in the villous tree in oxygenated blood. Pressure decreases so blood flows back from chorionic plate to decidua to enter endometrial veins.

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19
Q

What are the factors that influence passive diffusion of substance across the placenta?

A

Concentration gradient - steeper gradients means more diffusion.
Barrier to diffusion - placental membrane gradually thins throughout pregnancy as demands of foetus increases.
Diffusion distance - haemomonochorial.

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20
Q

Which substances can transport across the placenta by simple diffusion?

A

Water, electrolytes, urea and uric acid, gases.

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21
Q

Which substance can transport across the placenta by simple diffusion?

A

Glucose.

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22
Q

Which substances can transport across the placenta by active transport?

A

Amino acids, iron, vitamins by specific transporters expressed by syncytiotrophoblast.

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23
Q

In what dangerous way is the placenta not a true barrier?

A

Teratogens can cross it and damage the foetus.

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24
Q

What are some teratogens?

A

Thalidomide, alcohol, therapeutic drugs, drugs of abuse, maternal smoking.

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25
Q

What pathogens can cross the placenta and which diseases do they cause?

A

Varicella zoster -> shingles, cytomegalovirus -> herpes, treponema pallidum -> syphilis, toxoplasma gondii -> toxoplasmosis, rubella -> German measles.

26
Q

What are the protein hormones produced by the placenta?

A

Human chorionic gonadotrophin, human chorionic somatommotrophin, human chorionic thyrotrophin, human chorionic corticotrophin.

27
Q

What is the role of hCG?

A

Supports secretory function of corpus luteum.

28
Q

Why can hCG be measured to indicate pregnancy?

A

It’s made in the first two months of pregnancy by the syncytiotrophoblast which is specific to pregnancy. It is secreted in maternal urine so easily measured.

29
Q

What is the role of hCG?

A

Influences maternal metabolism so there is more glucose available for the foetus.

30
Q

What are the steroid hormones produced by the placenta?

A

Progesterone and oestrogen.

31
Q

What are the roles of steroid hormones from the placenta in pregnancy?

A

Maintain pregnancy state. Progesterone influences maternal metabolism by increasing appetite.

32
Q

Apart from protein and steroid hormones, what does the placenta synthesise?

A

Glycogen, cholesterol, and fatty acids.

33
Q

When does immunological competence begin to develop?

A

In the first trimester, the foetus makes all the components of complement.

34
Q

When is maternal immunoglobulin transported to the foetus?

A

At around 14 weeks.

35
Q

How is IgG transported to the foetus in pregnancy?

A

Via receptor mediated pinocytosis.

36
Q

When are adult levels of IgG attained post birth?

A

Aged 3.

37
Q

Explain the pathophysiology of haemolytic disease of the newborn.

A

Rhesus blood group incompatibility of mother and foetus. The mother has been previously sensitised to rhesus antigen from a previous pregnancy. IgG against rhesus crosses the placenta and attacks the foetal RBCs.

38
Q

Why is haemolytic disease of the newborn uncommon now?

A

Prophylactic treatment given to a rhesus negative mother pregnant with a rhesus positive foetus to prevent sensitisation in the event of exposure to the antigen.

39
Q

What are the physiological cardiovascular system changes in pregnancy?

A

Blood volume increases, cardiac output increases, stroke volume increases, heart rate increases. Systolic BP shouldn’t increase as systemic vascular resistance decreases enough to outweigh other changes.

40
Q

What is hypotension in pregnancy due to?

A

Progesterone effects on systemic vascular resistance.

41
Q

Why does BP return to normal in the third trimester?

A

Aortocaval compression by gravid uterus reduces return to the heart.

42
Q

What are the physiological urinary system changes in pregnancy?

A

Renal plasma flow increases, glomerular filtration rate increases, filtration capacity stays intact, functional renal reserve decreases.

43
Q

Why is urinary stasis potentially a problem in pregnancy?

A

Progesterone relaxes the smooth muscle in walls of the ureters which can causes stasis, hydroureter, UTIs, or pyelonephritis. Pyelonephritis can induce pre-term labour.

44
Q

What are the physiological respiratory system changes in pregnancy?

A

Diaphragm is displaced but the AP and transverse diameters of the thorax increase. So O2 consumption increases by 20%, functional residual capacity decreases, vital capacity is the same, tidal volume increases, respiratory minute volume increases, alveolar ventilation rate increases, respiratory rate is unchanged.

45
Q

What causes physiological hyperventilation in pregnancy?

A

Progesterone drive it causing the mother to blow off the extra CO2 that the foetus produces.

46
Q

How does the mother’s body respond to physiological hyperventilation in pregnancy?

A

Respiratory alkalosis means the kidneys respond by producing and reabsorbing less HCO3-.

47
Q

What are the physiological carbohydrate metabolic changes in pregnancy?

A

Glucose and amino acid metabolism are altered to favour nutritional supply to the foetus. Fat is laid down in the first half of pregnancy to meet the later demands of the foetus. Progesterone stimulates appetite in the first half and changes glucose into fat synthesis. Oestrogen stimulates increase prolactin increase to cause maternal resistance to insulin leading to less glucose usage by the mother and more gluconeogenesis, maximising availability of glucose to foetus. Mother’s energy needs are met later by metabolising peripheral fatty acids.

48
Q

How is glucose transported to the foetus?

A

Across the placenta by facilitated diffusion.

49
Q

What is gestational diabetes?

A

Carbohydrate intolerance first recognised in pregnancy and not persisting after delivery.

50
Q

What are the risks associated with poor control of gestational diabetes?

A

Macrosomic foetus, stillbirth, increased risk of congenital defects.

51
Q

What is the pathophysiology of gestational diabetes?

A

Maternal insulin secretion rate usually increases as pregnancy proceeds. The pancreatic B-cells meet the demand with B-cell hyperplasia and hypertrophy as well as increased rate of insulin synthesis in the B-cell. In some women, the pancreas can’t respond to the increased demand so there isn’t enough insulin -> loss of control of metabolism -> diabetes.

52
Q

What happens to women with gestational diabetes after childbirth?

A

Metabolic demands of pregnancy are removed and hormone levels change so the endocrine pancreas responds adequately and diabetes disappears.

53
Q

What are the physiological changes to lipid metabolism in pregnancy?

A

Increased lipolysis from T2 so increased fatty acid concentration on fasting - substrate for maternal metabolims.

54
Q

What is a risk with increased use of fatty acids in pregnancy?

A

Ketoacidosis, which combined with compensatory respiratory alkalosis.

55
Q

What are the physiological changes to the thyroid in pregnancy?

A

Thyroid binding globulin production increases, T3 and T4 increase but T4 stays within the normal range from increased binding globulin. hCG has an effect on the thyroid meaning T3/4 production is stimulated. TSH is decreased due to negative feedback.

56
Q

What are the physiological changes to the gastrointestinal system in pregnancy?

A

Anatomical changes - alterations in positions of viscera, e.g. appendix moves from RLQ to RUQ as uterus enlarges.
Physiological changes - smooth muscles relaxation by progesterone leads to delayed emptying in GI tract, stasis in biliary tract, and increased risk of pancreatitis.

57
Q

What are the physiological changes to the haematological system in pregnancy?

A

Pregnancy is a pro-thrombotic state - high amount of fibrin at site of implantation (increased fibrinogen and clotting factors, decreased fibrinolysis), stasis and venodilation -> thromboembolic disease in pregnancy.
Anaemia due to increase in plasma volume. RBC mass also increase but not to the same degree => physiological anaemia from mismatch or from iron/folate deficiency.

58
Q

What are the physiological changes to the immune system in pregnancy?

A

Foetus is an allograft so there is non-specific suppression of the local immune response at materno-foetal interface. Also transfer of antibodies (IgG or rhesus, can also stimulate TSH receptors of destroy developing foetal thyroid -> Graves or Hashimoto’s).

59
Q

What is involved in antenatal screening?

A

History and examination, blood test, urinalysis.

60
Q

How is a pre-eclamptic pregnancy different to a normal pregnancy?

A

Vasoconstricted instead of vasodilated, plasma contracted instead of plasma expanded, raised blood pressure vs blood pressure lowered or normal, proteinuria, and pitting oedema.