Placental&fetal physiology Flashcards

1
Q

Describe when plugging of the spiral arteries takes place.

A
  • During early pregnancy the volume of endovascular trophoblast is such that it plugs the mouths of the spiral arteries, preventing maternal blood flow into the placenta
  • The plugging coincides with the period of histiotrophic nutrition
  • up to 10-12 weeks, the trophoblast cells stop maternal blood coming in through the maternal circulation& surrounding the placenta
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2
Q

Which hormone is the basis of the pregnancy test

A

hCG

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3
Q

What do elevated levels of oxidative stress in the peripheral regions of normal pregnancies cause?

A

villous regression and formation of the smooth chorion laeve

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4
Q

What are the functions of the placenta?

A
  • respiratory organ
  • nutrient transfer
  • excretion of fetal waste products
  • hormone synthesis
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5
Q

Is the fetal umbilical vein deoxygenated?

A

no. It is the only venous circulation in man that is oxygenated

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6
Q

How are amino acids transported across the placenta

A
  • System A: sodium dependent; transports small non-essential AAs e.g alanine, glycine and serine; 3 isoforms= SNAT1,SNAT2 &SNAT4. SNAT1 is a major contributor to system A activity; regulated by cytokines and hormones (insulin, IL-6, leptin & TNF alpha)
  • System L: sodium independent, non-essential AAs exchanged for essential AAs e.g leucine, phenylalanine-enabling transport against conc. gradient.Regulated by mTOR nutrient sensing pathway
  • Taurine transporter- transport taurine against conc., gradient- co transport with sodium& chloride.
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7
Q

Outline FA transport in the placenta

A
  • Lipoprotein lipase releases NEFAs from the triglycerides in lipoproteins
  • NEFAs are then transported across the trophoblast cells by fatty acids transport proteins( FATP)
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8
Q

When does the fetus start swallowing amniotic fluid?

A

-From 12 weeks gestation

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9
Q

Outline the development of the fetal alimentary track

A
  • Intestinal villi formed by 16 weeks & well developed by 19weeks gestation
  • Gut development important for amniotic fluid homeostatis
  • Gastrin, motilin& somatostatin regulate growth and development- present in gut by 13 weeks, maturity by 24weeks
  • Digestive enzymes e.g disaccharides present by 9-10 weeks, maturity at term
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10
Q

Describe glucose homeostasis in the fetus

A
  • Fetus is dependent on placental transfer of glucose from mother; fetus has little capacity for gluconeogenesis; necessary enzymes do not function at ambient low pO2
  • Fetus syntesises insulin from 9-11 weeks. Not derived from mother. Fetal insulin determines glucose metabolism. Excess glucose leads to excess growth & fat deposition. Inadequate glucose leads to emaciation
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11
Q

Describe macrosomia & the complications associated with it

A
  • Macrosomnia is being overweight at birth
  • associated with maternal obesity& diabetes
  • Increased risk of still
  • C-section often needed
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12
Q

Describe fetal fluid homeostasis

A
  • Fluid& electrolyte balance maintained primarily by placenta, but also fetal membranes
  • Fetal urine important component of amniotic fluid (0.5l/day)
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13
Q

Outline Fetal urine production

A
  • 3% CO goes to the kidney
  • Fetal GFR is 50% of that of an adult
  • Urine: fetal bladder fills & empties every 20-30 mins
  • 10-15ml/kg/h
  • 500-700ml/day at term
  • hypotonic due to immature ADH
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14
Q

How much amniotic fluid exchange occurs in the fetus within 24hours

A

500ml, most swallow membranes

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15
Q

Define oligohydramnios

A

too little amniotic fluid

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16
Q

Define polyhydramnios

A

Too much amniotic fluid

17
Q

What are the contents of the amniotic fluid?

A
  • Urine
  • Amniotic membrane secretions
  • Salivary secretions
  • Fetal epithelial cells,amniotic cells, dermal fibroblasts
18
Q

Outline control of fetal HR

A
  • complex
  • subject to modulating influences such as catecholamines, chemoreceptors& baroreceptors
  • These influences generally act on FHR via the autonomic nervous system
  • Parasympathetic tone dominates (vagal)
19
Q

Describe the fetal circulatory response to hypoxia

A
  • HR falls
  • Resistance in the umbilical artery increases
  • Resistance in the middle cerebral artery decreases thus protecting flow to the fetal brain
  • Blood flow increased to heart and adrenals
  • Blood flow reduced to kidneys producing oligohydramnios
20
Q

What is responsible for the differences between the pre- and postnatal circulations?

A

-Presence of the placental circulation
-Lack of circulation to the lungs
Adaptations which allow this are:
-Umbilical vein & artery
-Ductus venosus
-Foramen ovale
-Ducturs arteriosus

21
Q

Describe the changes that occur at delivery

A
  • Cord occlusion decreases right atrial pressure so foramen ovale closes
  • Inspiration causes vasodilation of pulmonary artery & decreased resistance in pulmonary circulation reducing flow through foramen ovale & ductus arteriosus
  • Increased arterial po2, leads to closure of ductus arteriosus
  • Prostaglandin E2, and prostacyclin delay duct closure
  • NSAIDs accelerate duct closure; may be used therapeutically after birth
  • Pulmonary vascular resistance drops 8-fold partly due to increased arterial po2
  • Gas exchange commences
  • Liquid secretion stops& liquid cleared
  • surfactant secretion continues
22
Q

Which cells secrete surfactant?

A

Type-II alveolar epithelial cells

23
Q

What is the composition of pulmonary surfactant?

A
  • 70-80% phospholipids
  • 10% protein
  • 10% cholesterol
24
Q

What is the function of pulmonary surfactant?

A
  • Form a lattice-like structure
  • Decrease surface tension
  • Stabilise the lung
  • Secreted from 30 weeks
25
Q

Outline the link between surfactant and surface tension

A

Surface tension:
-is the collapsing pressure exerted upon the alveoli
-LaPlace’s law P=2T/r, where P is the collapsing pressure, T is the surface tension and r is the radius of the alveolus
Surfactant:
-decreases surface tension
-Prevents alveoli from collapsing in
-Increases compliance

26
Q

Explain surfactant deficiency& the complications it may bring

A
  • Premature infants may be born with surfactant deficient lungs may cause e.g:
    1. ) Neonatal respiratory distress syndrome
    2. ) Increased work of breathing, decreased lung compliance, alveolar collapse
27
Q

How can surfactant deficiency be overcome?

A

Exogenous surfactant:

  • synthetic
  • Modified natural surfactant( bovine or porcine)
28
Q

What is the role of cortisol in pregnancy

A

-Evidence that cortisol plays a role in maturation
-There’s a LATE pregnancy rise in cortisol
Cortisol:
-stimulates surfactant synthesis& secretion
-Epithelial cell differentiation
-Lung liquid reabsorption
-Increases activity of anti-oxidants

29
Q

Outline fetal haemoglobin

A
  • Predominantly HbF
  • Gradual switch to HbA starts from 28weeks with HbF: HbA 80:20 at birth
  • HbF has higher sensitivity to DPG( 2,3 diphosphoglyceric acid)
  • Partial pressure of o2 in fetal circulation is low (30mmHg) but this is compensated for by high Hb conc. and a greater o2 affinity
30
Q

What is the role of lung liquid clearance at delivery

A

-The physical force during labour; physically forces liquid from the lungs- so there is a faster clearance of lung fluid with those vaginally delivered
-Activation by ENaCs:
reversal of osmotic gradient
adrenaline and vasopressin
-Transpulmonary hydrostatic pressure gradient:
pressure difference between the lung interstitial tissue& alveoli

31
Q

What stimuli can be used for the first breath?

A
  • Asphyxia of normal breath
  • Physical manipulation& compression
  • Cold shock
  • Visual stimulus
  • Gravity