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Y2 Child Health > Week 1 > Flashcards

Week 1 Flashcards

1
Q

What is the normal weight of a newborn

A

2.5 - 4.0 kg

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2
Q

What is the environment like for babies during contractions

A

Hypoxic

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3
Q

How do babies resist the hypoxic environment during contractions

A

Foetal Hb releases O2

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4
Q

Why is prolonged labour dangerous

A

Because the baby is under hypoxic conditions and prolonged labour will cause O2 reserves to run out

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5
Q

What hormones are involved in helping babies to adapt to environment after birth

A

Cortisol
Adrenaline

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6
Q

What happens to baby’s lungs after birth

A

Baby’s lungs would normally be filled with lung fluid when they are still in the uterus. The fluid becomes absorbed when the baby becomes ready to be delivered

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7
Q

Why may preterm babies still have fluid in their lungs

A

Because the baby is taken out too early so the lung fluid is not fully absorbed yet

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8
Q

What are the perinatal adaptations right after a baby is born

A

Alveolar expansion
Change from foetal to newborn circulation
Decreased pulmonary arterial pressure

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9
Q

How do unborn babies have high pulmonary pressure

A

Hypoxic environment
Vasoconstricors

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10
Q

What effect does hypoxia have on pulmonary arteries and why

A

Vasoconstriction; to divert blood to better oxygenated areas, optimizing ventilation/perfusion matching and systemic oxygen delivery.

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11
Q

What effect does hypoxia have on systemic arteries

A

Vasodilation

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12
Q

What causes the decrease in pulmonary pressure after the baby is born

A

Oxygen

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13
Q

What happens if the pulmonary pressure does not decrease after the baby is born

A

Persistent Pulmonary Hypertension

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14
Q

What are the 2 shunts in foetal circulation

A

Foramen ovale
Ductus Arteriosus

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15
Q

Where is the foramen ovale found

A

At the septum between the 2 atria

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16
Q

Where is the ductus arteriosus found

A

It is a shunt that forms a passageway between the aorta with pulmonary artery

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17
Q

When is foramen ovale formed

A

4th week of gestation

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18
Q

Describe how the foramen ovale is formed

A
  1. Septum primum forms between the primitive atria and extends downwards towards dorsal endocardial cushion
  2. Before complete fusion, ostium primum forms
  3. Ostium primum eventually narrows and closes as septum primum grows
  4. apoptosis occurs in septum primum and forms ostium secundum
  5. ostium secundum provides communication between the atria after the ostium primum closes completely
  6. septum second then extends towards dorsal endocardial cushion and forms over the ostium secundum but does not fuse completely
  7. the result is a passageway between the septum secundum and ostium secundum = foramen ovale
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19
Q

Function of foramen ovale

A

Allows blood from right atrium to flow into the left atrium

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20
Q

Describe foetal circulation, start with how deoxygenated blood exits

A
  1. Deoxygenated blood exits the babies into the placenta via umbilical arteries
  2. Deoxygenated blood that goes through the placenta picks up oxygen
  3. Oxygenated blood from placenta enters the baby via umbilical vein
  4. Blood bypasses through the liver via ductus venous then goes into the right atrium through vena cava
  5. foramen ovale allows oxygenated blood to enter the left atria -> left ventricle -> aorta -> pumped to the brain
  6. Deoxygenated blood from the foetus body enters the right atrium as well -> right ventricle -> pulmonary artery
  7. deoxygenated blood bypasses the lungs via ductus arteriosus, entering the aortic arch
  8. this allows less oxygenated blood to then enter the descending aorta to supply lower organs
  9. also allows it to enter the umbilical arteries -> placenta to be oxygenated again
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21
Q

Which vessel allows oxygenated blood to bypass the foetal liver

A

Ductus venosus

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22
Q

Which vessel carries oxygenated blood from the placenta to ductus venosus

A

umbilical vein

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23
Q

How many umbilical arteries are there

A

2

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24
Q

What is the remnant of ductus venosus called

A

Ligamentum venosum

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25
Q

Why is it important for foetus to have high pulmonary pressure

A

So that the blood can bypass the lungs and flow to the placenta which has lower pressure

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26
Q

What is Apgar score

A

Evaluation of the baby’s status right after birth

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27
Q

When is Apgar score done

A

1 minute after birth
5 minutes after birth

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28
Q

What are the components of Apgar score

A

color
heart rate
reflexes
muscle tone
respiration

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29
Q

What is the normal Apgar score

A

7-10

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30
Q

What should be done if the baby’s Apgar score is still below the normal range at 5 minutes

A

Repeat Apgar score every 5 minutes up till 20 minutes and intervene when needed

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31
Q

Why is skin to skin care right after birth important

A

Helps mother produce prolactin and oxytocin to produce breast milk
Helps babies familiarise where to feed
Helps babies adapt to perinatal life better

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32
Q

Why do healthy babies have little calorific intake in the first 24 hours

A

Because healthy babies have enough glycogen reserve to sustain themselves

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33
Q

What vitamin is offered and strongly encouraged to be given to babies and why

A

Vitamin K
Because babies have low vitamin K reserve and giving them vitamin K can prevent hemorrhagic diseases

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34
Q

What is Caput succedaneum

A

Oedema that occurs underneath the scalp shortly after birth

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35
Q

What is cephalhaematoma

A

Build up of blood between the periosteum and the skull bone

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36
Q

Difference between caput succedaneum and cephalhaematoma

A

Caput is oedematous (can indent when pressed) whereas cephalhaematoma cannot
Caput is at its max. size at birth whereas cephalhaematoma max. size is 12-24 hours after birth
Cephalhaematoma has a distinct margin whereas caput does not

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37
Q

What is red reflex

A

When shine a torch onto the babies eyes, it gives a direct visualisation of the baby’s retina which is red

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38
Q

What condition may the baby have if he does not have a red reflex

A

Congenital cataract

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39
Q

What can cause cephalhaematoma

A

Rupture of blood vessels due to pressure being applied during delivery

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40
Q

What delivery methods can cause caput succedaneum and cephalhaematoma

A

Forceps
Ventouse (vacuum)

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41
Q

What are ebsteins pearls and are they alarming?

A

A type of white gingival cysts.
Usually not harmful and will resolve within 2 weeks but seek for help if the cysts are irritating the baby and causing poor feeding

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42
Q

What are the acyanotic heart defects (PACV)

A

Patent ductus arteriosus
Atrial septal defect
Coarctation of the aorta
Ventricular septal defect

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43
Q

Why are PACV acyanotic not cyanotic

A

Because it just mixes deoxygenated blood with oxygenated blood / narrows the aorta so it is less oxygenated but there is still oxygen pumped to tissues

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44
Q

What are the common features in acyanotic heart defects

A
  1. causes left to right shunt
  2. oxygenated blood from the left flows to the right
  3. causes increased blood flow to the lungs = pulmonary hypertension
  4. More blood to lungs = more blood to the left side = left ventricular hypertrophy
  5. Pulmonary hypertension makes it harder to pump blood through = right ventricular failure
  6. eventually congestive heart failure
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45
Q

What syndrome can be caused if acyanotic heart defects are not treated

A

Eisenmenger syndrome

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46
Q

Any lesions above the level of the nipples causes what type of murmur

A

Ejection systolic murmur

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47
Q

Any lesions below the level of the nipples causes what type of murmur

A

Pansystolic murmur

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48
Q

Any symptoms in mild VSD?

A

asymptomatic
normal growth

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49
Q

Symptoms in moderate - severe VSD in infants

A

Poor feeding
Failure to thrive (weight is at low percentiles)
Sweating while feeding
SOB
Murmur
Recurrent chest infections
Congestive heart failure

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50
Q

What is thrill

A

Murmur felt on the chest when it is loud enough
Only grade 5 or above murmurs

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51
Q

Does VSD cause thrill

A

Not typically.
The murmur for VSD is usually grade 2-3

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52
Q

What type of murmur is heard in VSD

A

Pansystolic murmur loudest at the lower left sternal border

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53
Q

When are the symptoms of VSD usually presented

A

6-8 weeks after birth
CHF may occur 4-6 weeks after symptoms start

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54
Q

Investigations for VSD

A

Pulse oximetry
Echo
ECG
CXR

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55
Q

What may be seen on ECG for VSD

A

Left ventricular hypertrophy
Right ventricular hypertrophy

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56
Q

What ECG pattern does LVH have

A

increased voltage in V5 and V6 or leads II, III, and aVF

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57
Q

What ECG pattern does RVH have

A

tall R waves or upright T waves in leads V4R and V1

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58
Q

Management for moderate to severe VSD

A

Diuretics - furosemide and spironolactone
High calories feeding
Surgery when there is enough weight gain

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59
Q

Are there any symptoms of atrial septal defect in children?

A

Children are usually asymptomatic.
May get recurrent chest infections

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60
Q

When do symptoms of atrial septal defect develop if it doesn’t close by itself

A

before age of 40

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61
Q

What symptoms of ASD develop later in life

A

Palpitations
fatigue
Dyspnea
Exercise intolerance
Murmur

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62
Q

What murmur is heard in ASD

A

Ejection systolic murmur loudest at upper left sternal edge
Split second heart sound (S2)

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63
Q

What causes the split S2 in ASD

A

Increase in blood flow into right ventricle causing increase in right ventricular ejection time hence delayed opening of pulmonary valve

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64
Q

Investigations for ASD

A

Pulse oximetry
Echo
ECG
CXR

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65
Q

What ECG pattern can be seen in ASD

A

RBBB (right ventricular bundle block) due to delayed depolarisation causing delayed RV ejection

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66
Q

What ECG pattern does RBBB show

A

widened, M shaped QRS in V1-3
Slurred S in I, aVL, V5-V6

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67
Q

Management for ASD

A

Mostly closes by itself so does not require treatment

In serious cases -> percutaneous surgical closure

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68
Q

What is coarctation of the aorta

A

A birth defect that causes narrowing of the aorta

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69
Q

What CHD are associated with coarctation of the aorta (usually occurs with it)

A

bicuspid aortic valve
Ventricular septal defect

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70
Q

Which syndrome is associated with coarctation of the aorta

A

Turner’s syndrome

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71
Q

What is Turner’s syndrome

A

A condition that only occurs in females when one of the X chromosomes is missing / partially (XO)

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72
Q

Where does the narrowing usually occur in coarctation of the aorta

A

Near the origin of left subclavian artery

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73
Q

If severe, what can coarctation of the aorta cause

A

Hypertension of the upper body
Hypoperfusion of lower body
Left ventricular hypertrophy
Congestive heart failure

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74
Q

Why may babies not show signs of coarctation of the aorta for the first few days of life

A

Due to patent ductus arteriosus
They may deteriorate after the ductus arteriosus closes due to worse narrowing

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75
Q

Signs and symptoms of coarctation of the aorta

A

Delayed/weak pulses in lower limbs
BP higher in upper body than lower limbs
Lower limbs appear cyanotic
Murmurs
Lower limb weakness

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76
Q

Where can the murmur of coarctation of the aorta usually be heard

A

Underneath the Left clavicle and left scapula

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77
Q

Management of coarctation of the aorta (if severe)

A

Prostalglandin E2
Surgery
Hypertension treatment
Treat Congestive Heart failure if presented

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78
Q

Why is prostaglandin E2 a management for coarctation of the aorta

A

Because it keeps the ductus arteriosus patent which reduces the symptoms of coarctation of the aorta

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79
Q

Treatment of hypertension in patients under 55 years old and not of African / African Caribbean descent

A
  1. ACEi
  2. ACEi + CCB / thiazide diuretics
  3. ACEi + CCB + thiazide diuretics
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80
Q

Treatment of hypertension in patients over 55 years old or of Black African or African Caribbean descent

A
  1. CCB
  2. CCB + ACEi
  3. CCB + ACEi + thiazide diuretics
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81
Q

Examples of an ACE inhibitor

A

Lisinopril
Ramipril
Benazepril

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82
Q

Examples of CCB

A

Amlodipine
Verapamil
Dilitiazem

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83
Q

Examples of a thiazide diuretic

A

Hydrochlorothiazide
Indapamide

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84
Q

Which drug is used if ACE inhibitor is not tolerated

A

ARB (angiotensin II receptor blocker)

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85
Q

Which drug is preferred to be used when the patient has hypertension + heart failure

A

Thiazide diuretics

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86
Q

Risk factors of patent ductus arteriosus

A

Premature birth
Maternal Rubella infection
Genetics

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87
Q

What happens to blood in the heart of a child with patent ductus arteriosus

A

Blood from aorta enters the pulmonary artery and mixes with the deoxygenated blood
More blood flow into the lungs

88
Q

How does patent ductus arteriosus lead to right and left ventricular hypertrophy

A
  1. Blood from the aorta flows into pulmonary artery and mixes with the blood in it
  2. This increases pressure in the pulmonary artery and pulmonary vessels = pulmonary hypertension
  3. The increase in pulmonary pressure makes it harder for the right ventricle to pump blood into the pulmonary artery -> right ventricular hypertrophy
  4. Increased blood flow to pulmonary vessels also means more blood is flowing into the left side
  5. so it also causes left ventricular hypertrophy
  6. may eventually cause congestive heart failure
89
Q

Neonatal presentation of patent ductus arteriosus (if severe)

A

Shortness of breath
poor feeding
Murmur
failure to thrive

90
Q

What type of murmur is heard in patent ductus arteriosus

A

Pansystolic crescendo decresendo machinery murmur

91
Q

What is a crescendo decrescendo murmur

A

a murmur that initially increases in intensity, peaks, and then decreases in intensity

92
Q

Management of patent ductus arteriosus

A

Ibuprofen / indomethacin to induce closure
If drug therapy does not work -> trans catheter or surgical closure

93
Q

How does ibuprofen and indomethacin induce closure of ductus arteriosus

A

Reduces prostaglandin E2 synthesis
Stimulate ductus arteriosus smooth muscle contraction

94
Q

What is considered as a preterm baby

A

A birth that occurs before 37 completed weeks of gestation

95
Q

What is considered as a term baby

A

A birth that occurs between 37-42 completed weeks of gestation

96
Q

What is considered as a post term baby

A

A birth that occurs after 42 completed weeks of gestation

97
Q

What is considered as extremely preterm

A

< 28 completed weeks of gestation

98
Q

When should you induce birth

A

at 41 weeks

99
Q

What physical factors increases risk of having preterm babies

A

Cervical incompetence
Uterine malformation
Multiple pregnancy (triplets / twins)
Antepartum haemorrhage
Intrauterine growth restriction
Preterm Prelabour rupture of membranes

100
Q

Environmental risk factors for preterm babies

A

Smoking
Drinking
Drugs (illicit / prescribed)
Poor nutrition
Chronic conditions (hypertension)
Back to back pregnancy
Previous preterm deliveries
High maternal age

101
Q

What is antepartum haemorrhage

A

bleeding from the genital tract that occurred between 24 weeks and prior to birth

102
Q

Common problems in preterm babies

A

Poor temperature control
Sepsis
Nutritional compromise
Respiratory distress syndrome
Patent ductus arteriosus
Necrotising enterocolitis
Intraventricular haemorrhage
Hypoglycaemia
Hyponatraemia

103
Q

Why may delayed cord clamping be done for premature babies

A

Shown to improve changing circulation, lowers incidence of NEC and intraventricualr haemorrhage

104
Q

Why do most preterm babies require oxygen

A

Due to premature lungs / fluid still in lungs

105
Q

Why are preterm babies at risk of hypothermia

A

Large surface area to volume ratio
Low BMR
Low fat so less fat insulatino
Minimal muscular activity

106
Q

Why is important to prevent hypothermia in babies

A

Because hypothermia increases severity of all other preterm morbidities
Once you correct hypothermia, other issues such as hypoxia and hypoglycaemia tend to resolve more easily too

107
Q

How may hypothermia lead to hypoglycaemia

A
  1. Increases metabolism to try release more heat
  2. = increase glucose uptake
  3. uses more glycogen store
  4. since newborns do not have much reserves, glycogen store may be depleted leading to hypoglycaemia
108
Q

How to prevent hypothermia in babies

A

Wrap in plastic bags
Transformer mattress
Skin to Skin
Prewarmed Incubator
Hats, gloves, socks

109
Q

Why are preterm babies at increased risk of nutritional compromise

A

limited reserves
Gut immaturity
immature metabolic pathways

110
Q

Why is donor milk the second best option after breast milk to supply nutrients

A

Because a lot of the nutrients are lost when the donor milk is frozen and defrosted

111
Q

Signs and symptoms of sepsis in newborn

A

Quiet
Poor feeding
Poor muscle tone
Tachypnea
Tachycardia
Jaundice
Temperature instability
These are very non-specific signs

112
Q

Early onset of neonatal sepsis indicates that the bacteria is acquired

A

before or during delivery

113
Q

Late onset of neonatal sepsis indicates that the bacteria is acquired

A

After delivery (nosocomial or community sources)

114
Q

What is considered as early onset of sepsis

A

in the first 72 hours of life

115
Q

What are the bacteria causing early onset neonatal sepsis

A

Group B Strep
Gram negatives (E. coli)

116
Q

What are the bacteria causing late onset neonatal sepsis

A

Coagulase negative Staph
Gram negatives (E. coli)
Staph Aureus

117
Q

What factors could have contributed to increased risk of sepsis in premature babies

A

Immature immune system
Intensive care environment
Tubes and lines to support the child (foreign substances)

118
Q

How does intensive care environment increase risk of sepsis

A

The environment allows bacteria to stay in the body for a longer period of time

119
Q

Risk factors for respiratory distress syndrome in neonates

A

Prematurity (incidence is inversely proportional to the amount of gestation weeks)
Maternal diabetes
Multiple pregnancies (twins / triplets)

120
Q

Why is RDS uncommon after 36 weeks of gestation

A

Due to development of pneumocyte surfactant production at 35 weeks

121
Q

Cause of RDS in neonates

A
  1. Immature type II pneumocyte cannot produce surfactant
  2. leads to increase in surface tension in alveoli
  3. causes alveoli to collapse
  4. lung collapses (atelectasis)
122
Q

Signs and symptoms of RDS

A

Tachypnea
Grunting
Cyanosis
Nasal flaring
Intercostal retraction

123
Q

Investigations for RDS

A

Chest Xray - check for atelactasis
Arterial blood gas - hypoxia +/- hypercapnia

124
Q

Management of RDS

A

Antenatal corticosteroid - if at risk of having a preterm baby
Surfactant
Ventilation

125
Q

What is intraventricular haemorrhage (IVH)

A

Bleeding in the ventricles around the brain due to damage of the new fragile blood vessels

126
Q

Risk factors for IVH

A

Prematurity
Early onset of neonatal sepsis
RDS
Low birth weight
Hypoxia

127
Q

Symptoms of IVH

A

Diminished moro reflex
Low muscle tone
Sleepiness
Apnoea

128
Q

Complications of IVH

A

Metabolic Acidosis
Developmental delay
Seizures
Cerebral palsy

129
Q

How may IVH lead to metabolic acidosis

A

Blood loss -> decreased cardiac output -> inadequate perfusion to organs -> rely on anaerobic respiration -> increased lactic acid production -> acidosis

130
Q

What is Moro reflex

A

Aka Startle reflex
Normal reflex in response to sound / movement: Babies will throw back his head and extend his limbs and cries

131
Q

How to assess a baby’s Moro reflex

A
  1. Hold the baby face up with both hands
  2. Lift the baby’s head above their body
  3. let the head gently fall onto your hand
  4. Baby will feel like they are falling so they will extend their arms and drawback rapidly
132
Q

Management of IVH

A

Packed RBC / Frozen plasma
Sodium bicarbonate infusion
Anticonvulsants
Acetazolamide (decreases intracranial pressure)
Surgery

133
Q

Why may acetazolamide be used for IVH

A

to decrease CSF production to prevent hydrocephalus

134
Q

Why may sodium bicarbonate be used in IVH

A

to correct metabolic acidosis

135
Q

What are anticonvulsants for in IVH

A

Seizures

136
Q

Prevention of IVH

A

Antenatal steroids
Indometacin
Vitamin K given to babies

137
Q

What is the main reason for a term baby being small for its gestational age and why

A

Mother was smoking during pregnancy.
Because smoking reduces oxygen transfer across the placenta

138
Q

If the mother has hepatitis C, what is required to determine the risk of vertical transmission to the baby

A

HCV RNA viral load - the higher the viral load, the higher the risk

139
Q

If the mother has hepatitis C, what other condition increases the risk of vertical transmission

A

HIV

140
Q

If the mother has hepatitis C, is breastfeeding still encouraged

A

Yes, because hepatitis C is not transmitted through breastmilk, it is bloodbourne transmission

141
Q

What infections contraindicate breastfeeding

A

HIV
CMV
TB if not yet started treatment

142
Q

What is the normal temperature range for newborns

A

36.5 -37.5

143
Q

Risk factors for hypoglycaemia in neonates

A

Maternal diabetes
Small for gestational age
Hypothermia

144
Q

Signs and symptoms of hypoglycaemia

A

Jitteriness
Excessive sleepiness
Hypotonia
Seizures (if severe hypoglycaemia)

145
Q

What condition must be listed into differential diagnosis in neonates and why

A

Sepsis because it presents non-specifically

146
Q

What is NAS (Neonatal Abstinence Syndrome)

A

Symptoms of withdrawal that occurs when a baby withdraws from certain drugs (illicit / prescribed) he was exposed to in the womb

147
Q

Which type of drug is the most likely to cause NAS

A

Opioid drugs

148
Q

Symptoms of NAS

A

Diarrhea
Poor feeding
Seizures
Sweating
Trembling

149
Q

Management of NAS

A

Skin to skin
Breastfeeding
Keeping them warm
Oral morphine therapy

150
Q

Indication of usage of oral morphine in NAS

A

Took 3 NAS scores, each taken 4 hours apart and each of them are above 8 points

151
Q

Why do preterm babies have more mild symptoms of NAS

A

Because they are less exposed to the drug than full term babies

152
Q

What is jaundice

A

It is a clinical sign that causes yellow discolouration of the skin or sclera

153
Q

What causes neonatal jaundice

A

Hyperbilirubinaemia that can be unconjugated / conjugated bilirubin

154
Q

What type of progression of jaundice do infants have

A

Caudal progression - face first then extends downwards

155
Q

Describe bilirubin metabolism (from haem break down to formation of unconjugated bilirubin)

A
  1. At the end of RBC lifespan, they are destroyed by macrophages in the spleen and liver
  2. Causes release of haemoglobin
  3. Haemoglobin is split into 2 parts: haem and globin components
  4. Haem component is converted to iron and biliverdin
  5. Bilverdin is then converted to unconjugated bilirubin by biliverdin reductase
156
Q

Describe bilirubin metabolism (from unconjugated bilirubin to enterohepatic metabolism)

A
  1. Unconjugated bilirubin is transported to the liver by albumin (bc it is not water soluble)
  2. In the liver, unconjugated bilirubin is converted into conjugated bilirubin by UDPGT adding glucuronic acid
  3. Conjugated bilirubin is transported into the biliary ducts then secreted into duodenum
  4. Reaches the colon where it is converted into urobilinogen and stercobilinogen
  5. 10-15% of those are reabsorbed back into the bloodstream and returns back to the liver = enterohepatic circulation
157
Q

Why can conjugated bilirubin be reabsorbed by the gut but not unconjugated bilirubin

A

Because it is water soluble. Unconjugated bilirubin is not water soluble

158
Q

Which disease causes a mutation in UGT1A1 which can worsen jaundice and why

A

Gilberts disease
Because it reduces the amount of UDPGT

159
Q

Some bilirubin can travel across BBB. Why is this concerning ?

A

Because it can cause encephalopathy which can lead to kernicterus

160
Q

What is kernicterus

A

Cerebral palsy caused by jaundice

161
Q

Risk factors for encephalopathy caused by jaundice

A

Prematurity
Asphyxia
Acidosis
Hypoxia
Hypothermia
meningitis
Sepsis

162
Q

Types of neonatal jaundice

A

Physiological (normal)
Too early
Prolonged

163
Q

What causes physiological jaundice in neonates

A

Bruising during delivery
Immature liver -> immature metabolism of bilirubin
Increased enterohepatic circulation
Shorter RBC life span (so more breakdown of haem)

164
Q

What condition can increase enterohepatic circulation and cause jaundice

A

Intestinal obstruction

165
Q

Which type of bilirubin causes physiological jaundice

A

Unconjugated bilirubin

166
Q

Which type of jaundice is always pathological

A

Jaundice <24 hrs of birth “too earlY”

167
Q

What is “too early” jaundice

A

Pathological jaundice that occurs in <24 hours of life

168
Q

What are the causes of jaundice in <24 hrs of life

A

Haemolytic disorders
Congenital infections
Sepsis

169
Q

What causes haemolysis in neonates

A

Blood group incompatibility
Rhesus incompatibility
Spherocytosis

170
Q

How does rhesus immunisation cause haemolysis

A

If the mother is Rh -ve and the foetus is Rh +ve and the mother has been sensitised to Rh +ve, the mother will start producing antibodies and transfer these across the placenta and cause haemolysis

171
Q

What infections are indicated by early neonatal jaundice

A

TORCH infection
Toxoplasmosis,
Others (syphilis, hepatitis B)
Rubella
Cytomegalovirus
Herpes simplex

172
Q

When is breastmilk jaundice usually presented

A

By first or second week of life

173
Q

Investigations for early pathological jaundice

A

SBR (total bilirubin conc.)
Maternal and baby’s blood group
Direct agglutination test
FBC
CRP (if suspect sepsis)

174
Q

What should you look for when looking at FBC in neonatal jaundice

A

Evidence of haemolysis
Evidence of infection
Unusually shaped RBC

175
Q

What is the direct agglutination test for

A

To detect antibodies on the baby’s RBC

176
Q

What can direct agglutination test rule out as a possible diagnosis for jaundice

A

Sepsis; sepsis is DAT negative

177
Q

What causes jaundice occurring >24 hrs - 14 days

A

Physiological jaundice
breast milk jaundice
Dehydration
Sepsis
Haemolysis
Bruising
Polycythaemia

178
Q

What is polycythaemia

A

high RBC count

179
Q

What is considered as prolonged jaundice

A

lasts longer than would be expected in physiological jaundice
>14 days for term babies
>21 days for preterm babies

180
Q

Causes of persistent unconjugated bilirubinaemia (prolonged jaundice)

A

Physiological jaundice
Breastmilk jaundice
Infection
Biliary obstruction (biliary atresia)
Hypothyroidism
Neonatal hepatitis

181
Q

What type of infection is the main cause of persistent unconjugated hyperbilirubinaemia

A

UTI

182
Q

What are the signs of biliary atresia in babies

A

Pale stool
Dark urine

183
Q

Should you stop breastfeeding if the baby has breastmilk jaundice

A

No, reassure the parents and continue breastfeeding unless the baby becomes unwell

184
Q

Treatment of jaundice

A

Phototherapy
Ensure adequate feeding
Resolve underlying cause

185
Q

What are the treatments for haemolytic jaundice if severe

A

Exchange transfusion
IV immunoglobulin

186
Q

What is required in phototherapy

A

Eye protection

187
Q

Colour of bilious vomit

A

Green

188
Q

What are the most common respiratory tract infections

A

Bronchiolitis
Croup
URTI
Pneumonia

189
Q

Risk factors for stillbirth

A

Increasing maternal age
Previous stillbirth
Multiple Pregnancies
Maternal infections (untreated)
Placental causes
Intrauterine growth restriction
Congenital abnormalities
Obesity / smoking

190
Q

What are the maternal infections that increase risk for stillbirth

A

Cytomegalovirus
Syphilis
Parvo
Herpes
Malaria

191
Q

What is Transient tachypnoea of the newborn

A

When the fluid in lungs do not clear away, causing respiratory distress

192
Q

Transient tachypnoea is most commonly seen in

A

Term babies delivered by C section

193
Q

Which hormone activates the absorption of lung fluid

A

Adrenaline

194
Q

What would CXR show if the baby has transient tachypnoea

A

Fluid (opacity) in the horizontal tissure

195
Q

Causes of pneumothorax in newborn

A

Spontaneous
Resuscitation
Surfactant deficirncy
Meconium aspiration (inactivates surfactant and causes inflammation)

196
Q

How may meconium aspiration occur

A

During stressful stimulus such as long, hard delivery / stress while it is still in the womb
Stress causes the baby to gasp and inhale amniotic fluid which has meconium in it

197
Q

Effects of meconium aspiration

A

Airway obstruction
Inflammation
Surfactant dysfunction
Pneumothorax

198
Q

What can meconium aspiration lead to if severe

A

Asphyxia
Persistent pulmonary hypertension

199
Q

What are the congenital respiratory diseases

A
  • Tracheo-oesophageal fistula
  • Diaphragmatic hernia
200
Q

Investigations for trcheo-oesophageal fistula

A

NG tube and CXR
- NG tube is passed down until it cannot go down further then take a Xray

201
Q

What is tracheo-oesophageal fistula

A

Abnormal connection between the trachea and oesophagus

202
Q

What is diaphragmatic hernia

A

Abnormal hole in the diaphragm causing organs in the abdomen to move up into chest cavity

203
Q

What is hydrops foetalis

A

Build up of fluid in organs

204
Q

What can cause hydrops foetalis

A

Rhesus disease
Chromosomal

205
Q

How does rhesus disease lead to hydrops

A

If severe, it can cause severe anaemia and cause the heart to fail then fluid starts to build up in organs and tissues

206
Q

What is the most common CHD

A

Ventricular septal defect

207
Q

How does VSD affect the heart

A
  1. Can cause blood to flow from left to right side of heart, increasing blood flow to the lungs
  2. Causes pulmonary hypertension
  3. Increase in resistance makes it harder for the right side to pump hence right ventricular hypertrophy
  4. may lead to heart failure if severe
208
Q

Murmur heard in mild ventricular septal defect

A

Loud pan systolic murmur

209
Q

Murmur heard in severe ventricular septal defect

A

Soft, less harsh pan systolic murmur

210
Q

Where can the murmur for VSD be heard

A

left lower sternal border

211
Q

What CHD are critical

A

ToF
TAPVD
hypoplastic heart
Coarctation of the aorta
Transposition of the great arteries

212
Q

What is spina bifida

A

When the spine and spinal cord does not form properly in the womb causing a gap in the spine

213
Q

What is potters syndrome

A

Symptoms due to lack of amniotic fluid and kidney failure

214
Q

Types of abnormal development

A

Globally
Specific
Deviation
Regression

215
Q

What are the areas of development

A

Gross motor skills
Fine motor skills
Hearing and language
Social and Play

216
Q

A child with only speech and language developmental delay may indicate

A

Hearing problems
Verbal dyspraxia
Simple delay - associated with previous late talkers in the family

217
Q

What is verbal dyspraxia

A

Speech difficulty due to difficulty in placing the muscles to talk

Y2 Child Health (3 decks)

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