Pregnancy Flashcards

1
Q

What is the gestational age

A

Used clinically
Time zero - first day of last menstrual period
Expressed in completely weeks plus days

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2
Q

What is the embryonic age

A

Used in embryology
Time zero = fertilisation
Expressed in days or ongoing weeks

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3
Q

When does implantation occcur

A

Begins day 6/7, complete by day 10 after ovulation

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4
Q

What are the 3 stages of implantation

A

apposition, attachment and penetration

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5
Q

What is the inner layer of the trophoblast

A

composed of mononuclear cells and is known as cytotrophoblast

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6
Q

What is the outer layer of the trophoblast

A

multinucleated cells and is known as syncytiotrophoblast - makes hCG

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7
Q

What is the role of hCG

A

feeds back to corpus luteum which is making progesterone, which then maintains pregnancy (positive feedback loop). Endometrium becomes deciduliased (dilating blood vessel in the presence of NK cells).

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8
Q

What are recurrent miscarriages

A

3 or more sequential miscarriages with the same partner.

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9
Q

What happens at Day 12 after implantation

A

extraembryonic structures develop from extraembryonic endoderm and then cavitates. Embryo getting nutrition by diffusion.

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10
Q

What happens at Day 13 after implantation

A

primitive amniotic cavity forms. Primitive yolk sac is pinched off.

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11
Q

What is the end of the second week of implantation characterised by

A

first appearance of chorionic villi

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12
Q

How is the chorion leavae formed

A

the villi on the decidua capsularis pole degenerate

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13
Q

How is the chorion frondosum formed

A

Villi adjacent to the decidual plate rapidly grow and expand

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14
Q

How is the placenta formed

A

Chorion frondosum and decidual plate

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15
Q

When do spiral arteries open

A

Spiral arteries open (closets to the embryo) during the first trimester. Dilated but plugged by cytotrophoblast. These plugs break down for intervillous flow. 6 weeks post conception to see on USS

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16
Q

What happens if spiral arteries fail to open

A

pre-eclampsia occurs (high blood pressure, systemic condition characterised by proteinuria). Failed adaption to paternal antigens in the placenta.

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17
Q

How can pre eclampsia be picked up on uterine artery doppler screening

A

Should be continuous flow in diastole. Pre-eclampsia, pattern will be same as in non-pregnant women (absent flow at the end of diastole.

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18
Q

When is aspirin given for pre-eclampsia

A

Aspirin given before 16 weeks to reduce risk. Have to be given before gestation

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19
Q

What are the characteristics at the end of the fourth month

A

placenta has attained its definitive form.
Maternal portion formed by the decidual plate and a fetal portion, made by the chorion frondosum
Amniotic membrane and chorionic membrane (closest to the placenta)
Maternal circulation 500ml/minute
Average blood loss at delivery is 300-500 ml

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20
Q

What happens when cleavage occurs before implantation

A

Dichorionic

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21
Q

What happens when cleavage occurs 6-8 days into implantation

A

Monochorionic, diamniotic

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22
Q

What happens when cleavage occurs after day 8

A

Monoamniotic

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23
Q

What is chronionicity

A

Number of gestational sacs

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24
Q

What is gastrulation

A

Formation fo the 3 layers fo the embryo

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25
Q

When is the first sign of polarity notices

A

14 days = formation of primitive streak (bottom) and buccopharyngeal membrane (head

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26
Q

What does the ectoderm comprise

A

epidermis, hair, nails, nervous system, mammary glands (carcinoma)

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27
Q

What does the mesoderm comrpise

A

connective tissue, musculoskeletal system, gonads (cancers are sarcomas)

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28
Q

What does the endoderm comprise

A

epithelial lining GI and resp tracts and bladder, liver, pancreas

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29
Q

What is sacrococcygeal teratoma

A

Tumour in newborns in the coccyx. Causes heart failure

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30
Q

What do ectodermal dysplasias cause

A

inability to sweat, teeth do not form

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31
Q

What is Hirschprung’s disease

A

Neural crest disorder: absence of nerves in the colon. Forms toxic megacolon.

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32
Q

What happens in the fourth emboryonic week

A

neurulation
Cranial neuropore closes D25 (non-closure is anencephaly, lethal), caudal neuropore closes D27 (non-closure is spina bifida)

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33
Q

What is holoprosencephaly

A

failure of forebrain to divide and develop. Associated with other midline and facial defects, Tri 13. Severity varies

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34
Q

What is cardiogenesis

A

canalisation of cardiogenic clusters in the mesoderm results in the formation of the paired heart tubes.

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35
Q

How does the GI system develop

A

Primitive gut tube differentiates to foregut (temporally closed by the oropharyngeal membrane until 4th week. Blood supply for celiac artery), midgut (connected to yolk sac until 5th week), and hindgut (temporally closed by cloacal membrane, which ruptures in the 7th week)

Midgut rotates 90 degrees counter clockwise around the axis of the SMA and the umbilical cord. 10th week, midgut retracts back into the abdomen and rotates a further 180 degrees

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36
Q

What is omphalocoele

A

often coexists with T18. Intestine are outside body, covered by a thin layer of tissue.

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37
Q

What is gastroschisis

A

gut is outside and parallel. Isolated defect. More common in young women.

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38
Q

What does VEGF do

A

Cause proliferaiton of blood vessels

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39
Q

When is the brain most susceptible

A

10 weeks onwards

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40
Q

How does the placenta develop

A

develops over the entire surface of the chorion and then regresses to form the discoid placenta

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41
Q

When do arterial plugs disappear and what happens

A

12 weeks of pregnancy. As plugs disappear, oxidative stress and therefore apoptosis increases. Plugging coincides with period of histotrophic nutrition.

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42
Q

What are the functions of the placenta

A

Respiratory organ
Nutrient transfer
Excretion of fetal waste products
Hormone synthesis

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43
Q

What causes foetal growth restrictin

A

can be caused by inability to trophoblasts to erode arterial plugs
Once placenta is abnormal, reversal is not possible
Early delivery will be needed

44
Q

What is placenta abruption

A

Placenta coming away from uterine wall

45
Q

Describe the nutrient transport system i nthe syncytiotrophoblast

A

GLUTs - predominately GLUT-1 active transporter
FATPs
Lipases cleaving NEFAs from TAGs, which are then transported across the trophoblast cells by FATP
AA transporters: system A, system L and taurine transporter

46
Q

Describe the placental gas exchange

A

Foetus umbilical arteries: higher pCO2 than foetal umbilical vein as excess CO2 is taken by maternal circulation. pO2 is foetus is low (1/3 of mother) - creates concentration gradient

47
Q

How is CO2 transported

A

facilitated by carbonic anhydrase enzyme

48
Q

What is the foetal alimentary tract

A

intestinal villi formed by 16 weeks and well developed by 19 weeks. Gut development important for amniotic fluid homeostasis. Gastrin, motilin and somatostatin regulate growth and development - present in gut by 13 weeks. Digestive enzymes e.g. disaccharides present by 9-10 weeks

49
Q

When does the foetus synthesise inuslin

A

9-11 weeks - Determines glucose metabolism. Excess glucose leads to excess growth and fat deposition. Inadequate glucose leads to emaciation

50
Q

Why is the foetus dependent on mother for glucose

A

little capacity for gluconeogenesis as enzymes do not function at ambient low pO2

51
Q

What are smaller babies susceptible to

A

fewer nephrons in the kidneys. Higher chance of hypertension. ACE inhibitors contraindicated for pregnant women

52
Q

What is polyhydramnios

A

Too much amniotic fluid

53
Q

What is oligohydramnios

A

Too little amniotic fluid

54
Q

Describe fluid homeostasis in the foetus

A

maintained by placenta and foetal membranes. Urine important component of amniotic fluid (0.5L/day). 3% cardiac output to kidney (25% in adult). GFR 50% of adult. Foetal bladder fills and empties every 20-30 minutes.

55
Q

Why is foetal urine hypotonic

A

Hypotonic due to immature ADH.

56
Q

What controls foetal heart rate

A

Subject to catecholamine, chemoreceptors, barorepctors. Influences act via ANS. PNS tone dominates

57
Q

What are foetal CV adaptations

A

umbilical vein and artery, ductus venosus (shunt to bypass liver), foramen ovale (blood to enter left atrium from right atrium), ductus arteriosus (shunt for blood from right ventricle to bypass lungs straight to descending aorta)

58
Q

What are the changes at delivery

A

cord occlusion decrease right atrial pressure so foramen ovale closes
Inspiration causes vasodilation (due to NO) of pulmonary artery and decreased resistance in pulmonary circulation reducing flow through foramen ovale and ductus arteriosus

59
Q

What do NSAIDS do

A

Accelerate duct closure

60
Q

What do PGE2 and prostacylcin do

A

Delay duct closure

61
Q

What does increased arterial pO2 do

A

Closure of ductus arteriosus

62
Q

What do T1 alveolar cells do

A

Surface area

63
Q

What do T2 alveolar cells do

A

Secrete surfactant - decrease surface tension and stabilise the lung. Secreted from 30 weeks

64
Q

What happens in surfactant deficiency

A

neonatal resp distress syndrome. Increased work of breathing, decreased lung compliance, alveolar collapse

65
Q

What happens in late pregnancy rise in cortisol

A

stimulates surfactant synthesis and secretion. Epithelial cell differentiation. Lung liquid reabsorption. Increases activity of anti-oxidants

66
Q

Describe foetal Hb change

A

gradual switch to HbA from 28 week. 80:20 ratio at birth. HbF has higher affinity for O2 due to lower sensitivity to DPG.

67
Q

What are the stimuli for first breath

A
Asphyxia of normal birth
Physical manipulation and compression
Cold shock
Visual stimulus
Gravity
68
Q

What is the mean weight gain in pregnancy

A

12kg

69
Q

What are the changes to maternal RBCs

A

Erythropoietin stimulates increased synthesis
Number increases but apparent anaemia due to dilution
Haematocrit falls from 40% to 32%
Approx 30% increase in DPG facilitating offloading of O2 release

70
Q

What increases in pregnancy

A

Anything lipid or lipid soluble increases in pregnancy

71
Q

What decreases in pregnancy

A

Anything water soluble

72
Q

What occurs with folate deficiency and why

A

deficiency causes spina bifida. Folate is required for DNA synthesis for bases (purines and pyrimidines). Also important for DNA methylation.

73
Q

What do oestrogens do

A

Stimulate synthesis of FA and cholesterol
CV adaptation to pregnancy (peripheral vasodilatation)
Growth of uterus (myometrial cells)
Priming of uterus for labour
Weak anti-insulin activity (via enhanced cortisol)
Cervical ripening
Stimulate RAAS (increases renal sodium reabsorption and thus water retention)

74
Q

What does progesterone do

A

Prepared and maintains endometrium to allow implantation
Produced initially by corpus luteum then placenta
May have a role in suppressing the maternal immunological response to foetal antigens thereby preventing maternal rejection of the trophoblast (by decidual NK cells recognising antigens as self)
Plays a role in parturition
Serves as a substrate for foetal adrenal gland production of glucocorticoid and mineralocorticoids
Growth of mammary glands
Maintenance of pregnancy (inhibition of uterine contractility, prevention of ripening of cervix)
Induces over breathing and lowering of maternal CO2

75
Q

What does hCG do

A

Rescue and maintenance of function of corpus luteum. About the 8th day after ovulation or 1 day after implantation - hCG takes over for corpus luteum
Survival of the pregnancy is dependent on corpus luteum progesterone until 7th week of prengncy

76
Q

When does hCG fail to become a good test

A

10 weeks

77
Q

What does hCG bind to

A

TSH receptors of thyroid cells, stimulating thyroid function

78
Q

What does hPL do

A

Increase in maternal plasma free NEFAs
Anti-insulin - increase in maternal insulin, favouring provision of mobilisable AA an fetal protein synthesis as well as glucose for transport to the foetus
Potent angiogenic hormone

79
Q

What does placental growth factor test for

A

Pre-eclampsia

80
Q

What is leptin

A

produced by adipose tissue - inhibits hunger
Secreted by cytotrophoblast and syncytiotrophoblast; maternal levels are significantly higher than in non-pregnant women
Stimulates placental AA/FA transport
Foetal leptin levels correlates positively with foetal birthweight

81
Q

How does blood pressure change during pregnancy

A

Total peripheral vascular resistance: decreases (increased NO, prostacyclin, and compliance of vessels due to structural changes)
CO increases
HR increases
Dissecting aortic aneurysm : inner layer of the aorta tears

82
Q

How does skin blood flow change in pregnancy

A

Predominately increases in hands and feed

Leads to increase in skin temp, nail growth etc

83
Q

What are the changes in kidneys in pregnancy

A

Increase in GFR
Plasma conc of renal function i.e. urea and creatinine decrease
Glycosuria
Calciuria
Urinary frequency increases
Urinary stasis due to dilatation of collecting system

84
Q

What are the changes in pulmonary function

A

Tidal volume increases but respiratory reserve volume decrease
pCO2 decreased, pO2 increased, pH unchanged as HCO3 falls
Costal margin and diaphragm altered

85
Q

What are the changes in coagulation and fibrinolysis

A

Changes occur to induce low grade increase in coagulability
Factors VII, VIII and X
Increased fibrinogen leads to increased ESR
Decreased fibrinolytic activity

86
Q

What are the changes in GI

A

Reduced smooth muscle tone: decrease cardiac sphincter tone, decreased motility and mobility
Associated with biliary stasis, increased gastric reflux

87
Q

What is the anaemia threshold for pregnant women

A

Under 110 (commonly due to iron deficiency)

88
Q

What are the risk factors for gestational diabetes

A
BMI above 30 
Previous macrosomic baby weighing 4.5kg or above
Previous GDM
Family history of diabetes
Minority ethnic family origin
89
Q

What is the test for gestational diabetes

A

75g 2 hour oral glucose tolerance test at 24-28 weeks

90
Q

What is the 3 delay mdle

A

recognition by women to seek care, assessing care, receiving appropriate care

91
Q

What is alpha-fetoprotein

A

marker of liver cancer

92
Q

What does relaxin do

A

hormone secreted by the placenta that causes the cervix to dilate and prepares the uterus for the action of oxytocin during labour

93
Q

When can alkaline phosphatase be raised

A

raised due to liver problem or due to placenta

94
Q

Why can pregnancy cause dyspnoea

A

FRC decreased

95
Q

What do to if pregnant women is suspected of PE

A

LMWH safe in pregnancy. Thrombolysis safe in pregnancy CTPA or V/Q scan. Can also use D-dimers (not useful in pregnancy)

96
Q

What are the endocrine changes in pregnancy

A

Overactive thyroid: symptoms should predate pregnancy
Cortisol: cortisol binding globulin changes. Cortisol lowest at night.
Absorption of calcium increase, increase PTH

97
Q

What is Bayes theorem

A

pre-test probability->screening test->post-test probability

98
Q

What to do if maternal HIV is suspected

A

maternal treatment, high risk antenatal care, prevent transmission to neonate

99
Q

What to do if maternal hep b is suspected

A

changes antenatal care prevent transmission, neonate receives vaccine

100
Q

What to do if maternal syphillis is suspected

A

maternal treatment to prevent congenital syphilis

101
Q

What is seen in T21

A

increase nuchal, increased beta, increased PAPP-A

102
Q

What is seen in T18

A

increase nuchal, low beta, really low PAPP-A

103
Q

What is seen in T13

A

lower increase in nuchal, low beta, really low PAPP-A

104
Q

When are chromosomal abnormalities detected

A

Happens between 11+0 to 13+6 gestation by USS
Combined test: foetal nuchal translucency (measures back of foetal neck), maternal serum PAPP-A (lower has increased chance) and maternal serum bhCG (higher has increased chance)

105
Q

When are foetal abnormalities detected

A

Between 18-22 weeks. Earlier detection becoming more common. USS: structure review of organ systems.
Baseline rate of major congenital abnormality: 1-2%
Depends on: exact disease and gestation, skills and training, quality of USS, maternal BMI

106
Q

What can be detected in four chamber view

A

AV septal defect, hypoplastic left heart syndrome, ventricular septal defect, Ebstein’s anomaly

107
Q

What can be detected in great vessels view

A

transposition of the great arteries, tetralogy of fallot, common arterial trunk, coarctation of the aorta