Perinatal Adaptation Flashcards

1
Q

What are the functions of the placenta?

A

Foetal homeostasis, gas exchange, nutrient transport, acid-base balance, hormone production, transport of IgG

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2
Q

What are the three shunts of the foetal circulation?

A

Ductus arteriosus, ductus venosus, foramen ovale

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3
Q

How much of the output from the heart goes to the lungs in the foetal circulation?

A

7% of output goes via lungs

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4
Q

How does the foetus prepare itself for birth in the third trimester?

A

Surfactant production and swallowing of amniotic fluid

Accumulation of glycogen, brown fat and subcutaneous fat

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5
Q

What foetal changes occur during labour and delivery?

A

Increased catecholamines/cortisol at onset of labour

Synthesis of lung fluid stops

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6
Q

What does a vaginal delivery achieve?

A

Squeezes lungs to get rid of fluid

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7
Q

What occurs during the circulatory transition after birth?

A

Pulmonary vascular resistance drops and systemic vascular resistance rises
Oxygen tension rises and circulating prostaglandins drop
Duct constricts and foramen ovale closes

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8
Q

What are the fates of the foetal shunts?

A

Foramen ovale = closes or persists as PFO (10%)
Ductus arteriosus = becomes ligamentum arteriosus, may persist as PDA
Ductus venosus = becomes ligamentum teres

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9
Q

What is the underlying pathophysiology of persistent pulmonary hypertension of the newborn?

A

Failure of the foetal circulatory system to adapt = more common in term infants

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10
Q

What causes hypoxaemia in persistent pulmonary hypertension of the newborn?

A

Secondary to extrapulmonary shunting of blood from right to left via patent ductus arteriosus and foramen ovale

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11
Q

What are the risk factors for persistent pulmonary hypertension of the newborn?

A

Meconium aspiration, pneumonia, congenital diaphragmatic hernia

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12
Q

What are the symptoms of persistent pulmonary hypertension of the newborn?

A

Grunting, cyanosis, low oxygen saturation and BP, tachycardia and tachypnoea

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13
Q

How is persistent pulmonary hypertension of the newborn diagnosed?

A

CXR, echo, pulse oximetry, ABG

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14
Q

How is persistent pulmonary hypertension of the newborn treated?

A

Ventilation, oxygen, nitric oxide, sedation, inotropes, extracorporeal life support (ECLS)

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15
Q

What are the issues with thermoregulation in newborns?

A

Large surface areas, wet when born, no shivering, peripheral vasoconstriction

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16
Q

What is the main source of heat for newborns?

A

Non-shivering thermogenesis

17
Q

How do newborns perform non-shivering thermogenesis?

A

Heat produced by breakdown of stored brown adipose tissue in response to catecholamines = not effective in first 12hrs of life

18
Q

Why are small for date and preterm babies more likely to struggle with thermoregulation?

A

Low stores of brown fat, little subcutaneous fat, larger surface area to volume ratio

19
Q

How can hypothermia be prevented in a newborn?

A

Dry baby, hat, skin-to-skin contact, blanket/clothes, heated mattress, incubator

20
Q

Why do newborns struggle with glucose homeostasis?

A

Interruption of glucose supply from placenta

Very little oral intake of milk

21
Q

What happens to newborns after birth in relation to glucose homeostasis?

A

Drop in insulin and increase in glycogen

Mobilisation of hepatic glycogen stores for gluconeogenesis

22
Q

What can newborns use as brain fuel in place of glucose?

A

Have ability to use ketones as brain fuel

23
Q

What are the risk factors for hypoglycaemia?

A

Increased energy demand = illness, hypothermia
Low glycogen stores = small for date, premature
Inappropriate insulin to glycogen ratio = maternal diabetes, hyperinsulinaemia

24
Q

What reflex is triggered when a baby starts to suckle?

A

Rooting and Suck reflex = feedback loop causes increase in supply

25
Q

How does the composition of breastmilk change over time?

A

changes from colostrum to foremilk and hindmilk

26
Q

Why does foetal haemoglobin become disadvantageous?

A

Increase in 2,3 BPG shifts curve to right

27
Q

Where does haematopoiesis move to after birth?

A

Bone marrow

28
Q

Why does physiological anaemia occur in newborns?

A

Adult haemoglobin synthesised more slowly than foetal haemoglobin is broken down = lowest at 8-10 weeks

29
Q

Are liver enzyme pathways present in newborns?

A

Yes, but they are immature

30
Q

What occurs in physiological jaundice?

A

Breakdown of foetal haemoglobin = conjugating pathways immature, rise in circulating unconjugated bilirubin, not harmful unless very high levels

31
Q

When may jaundice in a newborn be pathological?

A

If it occurs early or is prolonged

32
Q

What are the risk factors for adaptation problems?

A

Hypoxia or asphyxia during delivery
Particularly small or large babies, and premature babies
Ill babies = sepsis, congenital anomalies