Adaptation at Birth Flashcards

1
Q

what are the functions of the placenta

A
fetal homeostasis
gas exchange 
nutrient transport to fetus 
waste product transport from fetus 
acid base balance 
hormone production 
transport of IgG
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2
Q

what does the fetal liver do

A

produces albumin, clotting factors and RBCs

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3
Q

what does the fetal kidney do

A

excretes urine, contributes to amniotic fluid

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4
Q

describe the fetal circulations

A

The oxygenated blood is carried from the placenta to the fetus via the umbilical vein. About half of this blood passes through the hepatic capillaries and the rest flows through the ductus venosus into the inferior vena cava. Blood from the vena cava is mostly deflected through the foramen ovale into the left atrium, then to the left ventricle, into the ascending and descending aorta to supply to the fetus
goes back to placenta via the pulmonary arteries (branches of descending aorta)
Deoxygenated blood from the superior vena cava flows into the right atrium, right ventricle, and then into the pulmonary artery. Because of high pulmonary vascular resistance, only about 5 to 10 per cent of the blood in the pulmonary artery flows to the lungs, the majority of it being shunted through the patent ductus arteriosus and then down the descending aorta

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5
Q

name the three shunts in the fetal circulation and what they allow

A
ductus venosus (allows umbilical vein to pass through liver)
foramen ovale (right to left shunt in heart, reduced blood going to lungs)
ductus arteriosus (reduces blood going to lungs, mean oxygenated and deoxygenated blood mix in descending aorta)
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6
Q

what does the fetus do in the 3rd trimester to prepare for birth

A

produce surfactant
accumulation of glycogen - liver, muscle, heart (to prepare for starvation state)
accumulation of brown fat- between scapular and around internal organs (insulating fat)
accumulation of subcutaneous fat
swallowing amniotic fluid and ‘practise breathing’

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7
Q

where is surfactant produced

A

type 2 pneumocytes in alveoli

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8
Q

what is the role of surfactant

A

needed for gas exchange

reduces surface tension of alveoli allowing them to expand

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9
Q

what adaptations happen to the fetus during labour

A

increased catecholamine and cortisol at the onset of labour
synthesis of lung fluid stop
during vaginal delivery lung fluid gets squeezed out
first cry helps absorb left over fluid into lymphatic system

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10
Q

what colour do babies come out

A

blue/ pale

gradually goes pink after starts to breath/ cry

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11
Q

why is delayed cord clamping important

A

allows blood volume and immunoglobulin transfer to baby, helps prevent amaemia

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12
Q

what happens to the circulation after birth

A

pulmonary vascular resistance drops (onset of breathing expands and aerates the lungs)
systemic vascular resistance rises (cord clamped, placenta =low resistance vascular bed removed)
oxygen tension rises (pO2 rises from 2-3.5 kPa to 9-13kPa)
duct (venosus and arteriosus) constricts
foramen ovale closes

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13
Q

what is the fetal level of oxygen (pO2)

A

2-3.5 kPa

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14
Q

what causes duct constriction in fetal adaptation

A

increased pO2 (muscle layer is oxygen sensitive)
decreased flow of blood
decreased prostaglandins

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15
Q

when does the ductus close

A

physiological closure within first few hours/ days

anatomical closure within 7-10 days

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16
Q

what happens to the foramen ovale

A

closes or persists as PFO (10%)

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17
Q

what happens to the ductus arteriosus

A

becomes ligamentum arteriosus or persists as duct

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18
Q

what happens to the ductus venosus

A

becomes ligamentum teres

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19
Q

what can cause failure of cardiorespiratory adaptation

A
asphyxia (causing hypoxia/ acidosis) 
prematurity 
sepsis 
hypoxia (meconium aspiration) 
cold stress
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20
Q

what is persistent pulmonary hypertension of the newborn

A

when lung vascular resistance fails to fall meaning the shunts stay open (right to left flow at PFO and PDA)
Any oxygenated blood comes back into La however PFO and PDA means the oxygenated blood mix with deoxygenated meaning majority of circulation will be deoxygenated blood

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21
Q

what direction of flow in the shunts

A

right to left

22
Q

what can cause persistent pulmonary hypertension

A
asphyxia (causing hypoxia/ acidosis) 
prematurity - lack of surfactant 
sepsis 
hypoxia (meconium aspiration) 
cold stress
23
Q

what is a way of diagnosing PPHN

A

compare oxygenation of blood in right upper limb to left lower limb
branches that supply the right upper limb are pre ductal (will receive oxygenated blood) where as branches to other three limbs are post ductal (will be deoxygenated)
anything more than 3% difference = PPHN

24
Q

what is the management for PPHN

A

ventilation
oxygen
nitric oxide (given through ventilator, dilates pulmonary arteries to decreased vascular resistance)
sedation (so dont breath against ventilator)
inotropes (cardiac contractility will be impaired)
ECLS- membranous oxygenation, very invasive, only done in glasgow

25
Q

what is the presentation of transient tachypnoea

A

usually healthy babies born by c section
tachypnoeic
can grunt
is transient
a diagnosis of exclusion, will have fluid in horizontal fissure on x ray

26
Q

what causes transient tachypnoea

A

baby taking longer to absorb fluid in lungs - eg not squeezed out when birth via c section

27
Q

why do babies loose so much heat

A
large surface area 
wet and naked when born 
big head 
if premature will have very thin epithelial layer - more evaporation 
have no shivering mechanism
28
Q

what are the 4 ways babies loos heat

A

convection
evaporation
conduction
radiation

29
Q

how do babies thermoregulate

A

non shivering thermogenesis:
-heat produced by breakdown of stored brown adipose tissue in response to catecholamines
-not efficient in first 12 hours of life
=peripheral vasoconstriction

30
Q

what temperature should you aim for babies to be

A

36-5 to 37.5

31
Q

what is acrocynosis

A

when hands a feet of baby stay blue for a couple days- is normal, heat is important to fix it though

32
Q

what are small for dates/ preterm babies at higher risk of hypothermia

A

low stores of brown and subcutaneous fat
larger surface area to volume ratio
thin epithelial layer

33
Q

how do you prevent hypothemia in babies

A
dry 
hat 
skin to skin 
blanket/ clothes 
heated mattress 
incubator
34
Q

how do neonates maintain glucose homeostasis

A

interruption of glucose from placenta + little oral intake of milk= drop in insulin and increase in glycogen
mobilisation of hepatic glycogen stores for gluconeogenesis
ability to use ketones as brain fuel

35
Q

what can cause hypoglycaemia in a neonate

A

increased energy demands:

  • unwell
  • hypothermia

low glycogen stores:

  • small/ premature
  • high circulating maternal glucose

inappropriate insulin/ glucagon ration:

  • maternal diabetes
  • hyperinsulinism

some drugs

36
Q

how do you avoid/ treat hypoglycaemia

A

identify those at risk
feed effectively
keep warm
monitor

37
Q

what is the difference between foremilk and hindmilk

A

foremilk has more glucose, water and antibodies

hindmilk has more protein, fat and calories

38
Q

what does the suckling stimulus cause in breastfeeding mothers

A

posterior pituitary releases oxytocin = milk ejection

anterior pituitary releases prolactin= milk production

39
Q

what does colostrum contain

A

IgA, cellular immunity, growth factors

40
Q

is weight loss normal after birth

A

up to 10% normal - due to fluid loss

41
Q

what is the risk of dehydration in babies

A

hypernatraemia

usually due to delayed lactation

42
Q

how is fetal haemoglobin different from adult

A

higher affinity

lower oxygen delivery power

43
Q

what does increased 2,3 BPG do to Hb oxygen curve

A

shifts it to the tight

44
Q

what causes physiological anaemia

A

adult Hb synthesised more slowly than fetal Hb is broken down
causes a physiological anaemia - lowest level at 8-10 weels

45
Q

what does good recticulocyte (immature red blood cells) levels in babies mean

A

bone marrow working (haematopoiesis)

46
Q

what causes physiological jaundice

A

breakdown of fetal haemoglobin
Conjugating (liver enzymes) pathways immature
Rise in circulating unconjugated bilirubin
not harmful unless very high levels

47
Q

what suggests jaundice is pathological

A

if early (<24 hrs) or prolonged

48
Q

what is the treatment for jaundice

A

phototherapy (blue light converts unconjugated bilirubin into excrete-able form and is peed out)
if severe exchange transfusion

49
Q

what might very high levels pf unconjugated bilirubin cause

A

cross BBB, goes to basal ganglia and can cause significant cerebral changes leading to cerebral palsy

50
Q

what babies are most at risk of adaptation problems

A
Hypoxia / asphyxia during delivery
Particularly small or large babies
Premature babies
Some maternal illnesses and medications
Ill babies – sepsis, congenital anomalies