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Stage 2: Human Deveopment > Fetal Physiology > Flashcards

Fetal Physiology Flashcards

1
Q

Describe the fetal alimentary tract development

A
  • Intestinal villi formed by 16 weeks and well developed by 19 weeks
  • Gastrin, motilin and somatostatin regulate growth and development (present in gut by 13 weeks, maturity by 24 weeks)
  • Digestive enzymes e.g. disaccharidases present by 9-10 weeks, maturity at term
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2
Q

Explain how embryonic age is calculated and used

A
  • Time zero = fertilisation (day 14 = ovulation)
  • Expressed in days or ongoing weeks i.e. first week is day 1-7, second week is day 8-14, so 5th week = day 29-36
  • Used in embryology
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3
Q

When is the endometrium receptive?

A

During the narrow implantation window

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4
Q

What does oestrogen do in the pre-receptive phase?

A

Prime the endometrium

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5
Q

What are two endometrium reasons for infertility?

A

1) Unresponsive endometrium - doesn’t respond to good quality embryos and let them implant (may not be an unhealthy embryo)
2) Over-responsive endometrium - receptive to low-quality embryos so lets them implant

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6
Q

When can you see the fetal heart beat?

A

4 weeks into conception (D32) when the embryo is 4mm

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7
Q

Why is it important for gut development to happen early?

A
  • Gut development is important for amniotic fluid homeostasis
  • Fetus swallows amniotic fluid from 12 weeks gestation
  • Therefore the alimentary tract acts as one v early
  • Therefore microvilli need to be established early
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8
Q

Describe glucose homeostasis in the fetus

A
  • Fetus is dependent on placental transfer of glucose from the mother
  • It has little capacity for gluconeogenesis as the necessary enzymes do not function at ambient low pO2
  • Fetus synthesises insulin from 9-11 weeks - this is not derived from the mother, insulin doesn’t get across the placenta
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9
Q

What are the effects of fetal insulin and maternal glucose on the fetus?

A
  • Fetal insulin determines glucose metabolism
  • Excess glucose leads to excess growth and fat deposition
  • Inadequate glucose leads to emaciation
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10
Q

What happens to mothers in terms of glucose homeostasis?

A
  • All mothers get a bit insulin resistant (diabetic) so have a higher blood sugar
  • This stimulates transfer of glucose to the fetus
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11
Q

Why do women get gestational diabetes?

A
  • Pregnant women have a higher blood sugar
  • Therefore a women will develop gestational diabetes if she is already obese and a bit diabetic
  • 5-7x more likely for women with gestational diabetes to then develop T2D
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12
Q

What are the parts of an external fetal monitor?

A

1) Transducer for sensing uterine contractions

2) Transducer for sensing fetal heart rate (FHR)

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13
Q

How is fetal heart rate (FHR) controlled?

A
  • Complex
  • Parasympathetic (vagal) tone is dominant, not sympathetic like adults
  • FHR is subject to modulating influences e.g. catecholamines, chemoreceptors and baroreceptors
  • These influence generally act on FHR via the ANS
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14
Q

What are the two differences in fetal/pre-natal circulation vs post natal circulation?

A

1) The presence of the placental circulation - blood doesn’t need to go to the lungs
2) Lack of circulation to the lungs and diverted away from the liver

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15
Q

What are adaptations that allow the fetal circulation to function as it does?

A

1) Umbilical vein and artery
2) Ductus venosus (prevents liver)
3) Foramen ovale (in heart)
4) Ductus arteriosus (in descending aorta)

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16
Q

Describe the path of fetal circulation

A

1) Blood from placenta doesn’t go through the liver tissue due to the ductus venosus (shunt) bc the liver is not needed e.g. for storing glucose or fats
2) The blood then goes straight from the RH to LH via foramen ovale to the descending aorta
3) Blood from the RH doesn’t go up to the pulmonary arteries due to the ductus arteriosus - instead it goes from the pulmonary artery to the aorta
4) Lungs only get a bit of blood to survive (20% of CO)

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17
Q

When is fetal hypoxia common?

A

During delivery - most babies survive it well

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18
Q

Describe the fetal circulatory response to hypoxia

A

1) HR falls
2) Resistance in the umbilical artery increases so blood gets diverted to where it’s required
3) Resistance in the middle cerebral artery decreases thus protecting flow to the fetal brain
4) Blood flow increases to the heart and adrenal glands
5) Blood flow is reduced to skeletal muscle and kidneys producing oligohydramnios

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19
Q

Why might the fetus be constantly hypoxic during pregnancy and what does this lead to?

A
  • The fetus may be constantly hypoxic due to poor placental blood flow
  • This leads to oligohydramnios due to reduced blood flow to kidneys
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20
Q

What changes in the fetal circulation at delivery?

A

1) Cord occlusion (cord clamped) decrease RA pressure so foramen ovale closes
2) Inspiration causes vasodilation of pulmonary artery and decreases resistance in pulmonary circulation reducing flow through the foramen ovale and ductus arteriosus
- Pulmonary arterial pressure decreases over the hours after birth
- Pulmonary circulation opens up, closing shunts
3) Increased arterial pO2 leads to closure of ductus arteriosus
4) Reduction in formation prostaglandin E2 and prostacyclin as these delay duct closure

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21
Q

What medication may be used therapeutically after birth to accelerate duct closure?

A

NSAIDs

22
Q

What are the key components of a mature lung?

A

1) Structural development - ready for birth and normal breathing
2) Lung liquid production and reabsorption - in the uterus, fluid production keeps lungs open, but at birth this liquid needs to be removed, stimulation of fluid out of lungs at birth
3) Pulmonary surfactant
4) Pulmonary blood flow to the lungs

23
Q

What must the lung have to establish effective gas exchange?

A

1) Structural maturity - large SA:vol ratio, small blood/gas barrier
2) Differentiated epithelial cells - type 1 (surface area) and type 2 (secrete surfactant) alveolar epithelial cells
3) Large vascular network

24
Q

How is the fetus normally secreting fluid in the lungs?

A

Normally, the fetus is producing fluid into the potential airspace of the lungs/bronchi

25
Q

What is fetal lung liquid controlled by?

A

1) Rate of lung liquid secretion
2) Rate of lung liquid efflux
- Resistance to efflux (e.g. in larynx) during pregnancy is very high and greatly reduced at birth

26
Q

What measures of fetal lung and heart function can be measured on US?

A

1) FHR

2) Practice breathing movements on chest wall - to strengthen the muscles

27
Q

What is pulmonary surfactant made up of?

A

70-80% phospholipids, 10% protein, 10% cholesterol

28
Q

What is the action of pulmonary surfactant?

A
  • Forms a lattice like structure
  • Decreases surface tension = the collapsing pressure exerted upon the alveoli
  • Stabilises the lung
  • Prevents alveoli from collapsing in
  • Increases compliance
29
Q

What law explains the action of surfactant?

A

LaPlaces’s Law P=2T/r, where P is the collapsing pressure, T is the surface tension and r is the radius of the alveolus

30
Q

From when is surfactant secreted?

A

30 weeks

31
Q

Describe surfactant deficiency in premature infants

A
  • Premature infants may be born with surfactant deficient lungs
  • Neonatal respiratory distress syndrome
  • Increasing work of breathing, decreased lung compliance, alveolar collapse (would cause death)
32
Q

How is surfactant deficiency in premature infants managed?

A

1) Exogenous surfactant i.e. synthetic or modified natural surfactant (bovine e or porcine) is given to babies after they are born
2) A mother going into preterm labour e.g. 28 weeks is given a course of 3 shots of glucocorticoid (steroid/cortisol) which goes across the placenta and to the lungs, inducing production of surfactant so that babies can breathe when they are born

33
Q

What problems can premature babies have although they might be fine?

A

1) Lower IQ

2) Problems with infection

34
Q

Explain the role of cortisol in in late pregnancy

A
  • There is evidence that cortisol plays a role in maturation - there is a sudden surge in cortisol before birth
  • Cortisol stimulates:
    1) Surfactant synthesis and secretion
    2) Epithelial cell differentiation
    3) Lung liquid reabsorption
    4) Increases activity of anti-oxidants
35
Q

Describe the role of fetal haemoglobin

A

1) Predominantly HbF
2) HbF has a higher affinity for oxygen that adult Hb due to a lower sensitivity to 2,3-DPG
3) pO2 in fetal circulation is low (30 mmHg) but this is compensated for by a high Hb concentration and greater oxygen affinity
4) Gradual switch to HbA starts from 28 weeks with HbF:HbA 80:20 at birth

36
Q

Why is pO2 low in the fetus?

A

To reduce oxidative stress

37
Q

Describe fetal fluid homeostasis/fetal kidneys

A
  • Fluid and electrolyte balance maintained primarily by placenta, but also fetal membranes
  • Fetal urine important component of amniotic fluid (0.5L/day)
  • 3% of CO to kidney (25% in adult)
  • GFR 50% of adult
38
Q

Describe fetal urine production

A
  • Fetal bladder fills and empties every 20-30mins
  • The baby is constantly swallowing and weeing out amniotic fluid
  • 10-15 ml/kg/h
  • 500-700 ml/day at term
  • The urine is hypotonic due to immature ADH
39
Q

Describes the changes in volume of amniotic fluid in pregnancy

A
  • 12 weeks = 50ml
  • 16 weeks = 150ml
  • Early third trimester = 900-1000ml
  • Term = 800-900ml
  • 500ml exchanged per 24h, most swallowed ? fetal membranes
40
Q

What is oligohydramnios?

A

Too little amniotic fluid

41
Q

What is polyhydramnios?

A

Too much amniotic fluid

  • Can see this on US
  • Often in obese mothers
42
Q

What are the contents of amniotic fluid?

A

1) Urine
2) Amniotic membrane secretions
3) Fetal lung secretions
4) Salivary secretions
5) Fetal epithelial cells, amniotic cells, dermal fibroblasts

43
Q

Describe exchange of amniotic fluid with the fetus

A
  • Fetal swallowing and reabsorption by the intestine
  • Exchange with respiratory tract via lungs
  • Exchange across fetal skin possible only for small lipid soluble gases
  • Net water movement between mother and fetus across chorion frondosum
44
Q

What changes in fetal physiology occur at delivery?

A

1) Pulmonary vascular resistance drops 8-fold partly due to increased arterial pO2 - foramen ovale closes, when cord is clamped blood flow to pulmonary circulation greatly increases
2) Gas exchange commences
3) Liquid secretion stops and liquid cleared
4) Surfactant secretion continues

45
Q

How does lung liquid clearance occur at birth?

A

1) The physical force during labour physically forces liquid from the lungs
2) Activation of epithelial sodium channels (ENaC) - reversal of osmotic gradient, adrenaline and ADH
3) Transpulmonary hydrostatic pressure gradient - pressure difference between the lung interstitial tissue and alveoli

46
Q

When might babies need help with stimulation of their first breath?

A

If they’ve had a tough delivery or born via C section (don’t have physical manipulation and compression, often need another stimulus)

47
Q

What causes stimulation of the the first breath?

A

1) Asphyxia of normal birth (hypoxia)
2) Physical manipulation and compression
3) Cold shock
4) Visual stimulus
5) Gravity

48
Q

How is the baby’s pH at birth measured to determine how acidotic the baby is?

A

Lactate is measured at the scalp of the baby to determine how acidotic the baby is

49
Q

What do we have to monitor in the baby during delivery?

A

Baby’s pO2 and pH

50
Q

What is the consequence of anoxia/prolonged asphyxia during delivery?

A

Severe cerebral damage and complications

Stage 2: Human Deveopment (34 decks)

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