Neonatology Flashcards

1
Q

what are the three shunts in the foetal circulation?

A
  1. ductus venosus
  2. foramen ovale
  3. ductus arteriosus
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2
Q

role of ductus venosus

A

passes bloods from placenta via the umbilical vein through the liver to the IVC

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3
Q

role of the foramen ovale

A

passage of blood from right to left atria

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4
Q

role of ductus arteriosus

A

passes blood from the right ventricle to the aorta using the pulmonary artery

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5
Q

what blood does the umbilical vein carry?

A

oxygenated

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6
Q

what blood do the umbilical arteries carry?

A

deoxygenated

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7
Q

what preparations for birth are made in the 3rd trimester?

A

surfactant production (type II pneumocytes)
accumulation of glycogen
accumulation of brown fat
accumulation of subcutaneous fat
swallowing of amniotic fluid to grow lungs

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8
Q

preparations during labour/delivery

A

catecholamines/ cortisol increases
crying absorbs lung fluid into lymphatics
vaginal delivery squeezes lungs

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9
Q

what happens to the circulation when birthed

A

pulmonary vascular resistance drops
lungs expand
systemic vascular resistance drops
prostaglandins close ducts

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10
Q

what does the ductus venosus become?

A

ligamentum teres

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11
Q

fate of foramen ovale

A

closes

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12
Q

fate of ductus arteriosus

A

becomes ligamentum arteriosus

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13
Q

respiratory complications in the new-born?

A
PPHN
meconium aspiration
TTPN
RDS
Potter's syndrome
pneumothorax
pneumonia
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14
Q

other complications in the new-born

A
diaphragmatic hernia
HIE
fistula
PDA
intraventricular haemorrhage
NEC
ROP
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15
Q

what is PPHN?

A

patent PDA and PFO so pulmonary vascular resistance fails to drop

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16
Q

diagnosis of PPHN

A

pre and post-ductal saturation as artery that supplies upper right limb leaves aorta before PDA (high oxygenation)

positive result if more than 3% difference

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17
Q

what can cause TTPN

A

C-section has no squeezing of lungs so fluid is not absorbed

18
Q

presentation of TTPN

A

tachypnoea and grunting within first 6 hours

19
Q

management of TTPN

A

screen for infection

self-limiting and transient

20
Q

what causes RDS

A

lack of surfactant

pre-terms usually

21
Q

management of RDS

A

maternal steroids

surfactant

22
Q

what is Potter’s syndrome?

A

renal agenesis

23
Q

why is Potter’s syndrome involved with the lungs?

A

no urine is produced so no amniotic fluid is swallowed leading to pulmonary hypoplasia

24
Q

what is NEC (necrotising enterocolitis)?

A

inability to handle milk and bacteria enters the blood

25
Q

what is ROP (retinopathy of prematurity)?

A

abnormal blood vessel growth in the eye

26
Q

what adaptations are made in the first few hours of life?

A

thermoregulation

glucose homeostasis

27
Q

how is heat lost?

A

radiation
convection
conduction
evaporation

28
Q

why do newborns lose heat rapidly?

A

large SA to volume ratio

29
Q

can babies shiver?

A

no so they breakdown stored fat for heat

30
Q

what do babies use as brain fuel?

A

ketones

31
Q

what happens to glucose homeostasis at birth?

A

changes from a continuous infusion to intermittent bolus

32
Q

causes of hypoglycaemia in the new-born

A
increased demand (unwell)
low stores (small/ premature)
inappropriate endocrinology e.g. GDM or hyperinsulinaemia (mother on beta blockers)
33
Q

what causes physiological jaundice?

A

foetal Hb is broken down but the conjugating pathway is immature so there is an increase in unconjugated bilirubin

34
Q

when does physiological jaundice occur?

A

2-5 days

35
Q

reasons for pathological jaundice?

A

kernicterus

biliary atresia

36
Q

what is term?

A

37 weeks gestation

37
Q

what is post-term?

A

beyond 41 weeks

38
Q

when is pre-term?

A

under 37 weeks

39
Q

what scale is used to assess progression?

A

APGAR score

40
Q

what is a normal APGAR score?

A

above 8

41
Q

resuscitation in children?

A

airway is more neutral (not head tilt, chin lift)

therapeutic cooling in cerebral palsy

42
Q

types of cerebral palsy

A
ataxic
paraplegic
diplegic
hemiplegic
dyskinetic 
quadriplegic