general

Question 1

what is not part of the heelprick?

Answer 1

GSDs
galactossaemia
*CAH just added

Question 2

give examples of what the following findings on antenatal USS might mean:
- dilated cerebral ventricles
- choroid plexus cysts
- nuchal pad thickening
- dilated renal pelvis
- echogenic bowel

Answer 2

• dilated cerebral ventricles: hydrocephalus, corpus callosum agenesis
• choroid plexus cysts: abnormal karyotype
• nuchal pad thickening: cystic hygroma e.g. T13, T18, Turners
• dilated renal pelvis: PUV, VUR
• echogenic bowel: CF, T21, mec

Question 3

example causes of oligohydramnios vs polyhydramnios

Answer 3

polyhydramnios: mutiple gestation, T2DM, GIT obstruction, polyuria causes e.g. Barrters, reduced swallowing e.g. neuromuscular, TTTS

oligohydramnios: DRIPPPC - demise, renal abnormalities, IUGR, PROM, post-dates, placental insufficiency, chromosomal abnormalities

Question 4

genetic tendency for dizygotic vs monozygotic

Answer 4

monozygosity is NOT inherited
4x risk if mum was dizygotic

Question 5

monochorionic must be what zygotic?
dizygotic must be what chorionic?

Answer 5

monochorionic must be monozygotic
dizygotic must be dichorionic

Question 6

DCDA
MCDA
MCMA
biggest causes of late deaths?

Answer 6

DCDA = FGR
MCDA = TTTS
MCMA = cord entanglement

Question 7

TTTS - issues in recipient vs donor

Answer 7

artery-vein shunt
recipient: larger, polyhydramnios, polycythaemia, CV decompensation, hydrops, cardiac hypertrophy
donor: smaller, oligohydramnios, anaemia, hypovolaemia, ‘stuck twin’, microcardia

Question 8

TRAP syndrome in MC twins

Answer 8

artery-artery shunt
pump twin vs acardiac-acephalic twin (lethal for recipient)

Question 9

premmie kidneys vs term kidneys

Answer 9

premmie kidneys:
o ↓ GFR
o ↓ tubular reabsorption of sodium and bicarbonate
o ↓ secretion of potassium and hydrogen
o ↓ capacity to concentrate/dilute urine

Question 10

urine output D1 vs D2 of life

Answer 10

UO D1 1ml/kg/hr, D2 2ml/kg/hr

Question 11

insensible losses - where are they lost? biggest determinant?

Answer 11

2/3 skin, 1/3 respiratory
ELBW (BW <1000 g) infants - thin skin and higher SA:V ratio

Question 12

what gestation lacks the ability to coordinate for breastfeeding?

Answer 12

<34 weeks

Question 13

early PN in VLBW prevents what?

Answer 13

catabolism, and has better neurodevelopmental outcomes

Question 14

what is the only component in breastmilk not present in cow’s milk?

Answer 14

DHA - incorportated into brain and retinal phospholipid membrane

Question 15

DDx for neonatal respiratory distress

Answer 15

PSA CHART
Pneumonia
Surgical - diagphragmatic hernia
Aspiration (mec)

Cardiac
HTN (pul)
Airway e.g. bronchogenic cyst, ENT
RDS
TTN

Question 16

central vs obstructive apnoea

Answer 16

Obstructive apnoea = absence of airflow but persistent chest wall movement; inspiratory efforts persist

Central apnoeas = decreased CNS stimuli to respiratory muscles; inspiratory efforts absent

Question 17

Pharmacotherapy for apnoeas

Answer 17

methylxanthines
1. Caffeine = fewer side effects (less tachycardia + feed intolerance), longer half-life, enteral absorption more reliable, no monitoring required unless signs of toxicity
2. Theophylline = shorter half-life, narrow therapeutic window, requires monitoring, needs to be given more frequently

Question 18

complications of severe neonatal apnoeas

Answer 18

BPD
IVH
ROP

Question 19

apnoea of prematurity - what age does it start?

Answer 19

Attributable to the immaturity of the respiratory centre in the brain. Onset is from days 2-7 of life. Apnoea beginning immediately after birth suggests another cause.

Question 20

premature breathing vs apnoea

Answer 20

Periodic breathing: Three or more periods with no respiratory effort lasting 3 seconds or more in a 20 second period. This is a normal neonatal breathing pattern and does not involve changes in heart rate or colour

Question 21

pathogenesis of RDS/HMD

Answer 21

preterm - reduced surfactant and worse quality (less protein and phosphatidylglycerol)
high surface tension
low lung volume and compliance
hypoxaemia from VQ mismatch, atelectasis and oedema

Question 22

what gestation is mature surfactant present

Answer 22

35 weeks

Question 23

CXR of RDS

Answer 23

ground glass
hyperinflation, bell thorax
+/- bronchograms

Question 24

some risks of surfactant therapy

Answer 24

ETT block
PTX due to sudden change in compliance
pulmonary haemorrhage

Question 25

CPAP vs surfactant for preterm neonate at delivery at risk of RDS

Answer 25

CPAP started at birth is as effective as prophylactic or early surfactant and is the approach of choice for the delivery room management of a preterm neonate at risk for RDS

Question 26

main risk factor for BPD

Answer 26

<1250g - 97% cases

Question 27

main pathology of BPD (now, not pre-surfactant)

Answer 27

disruption of lung development with arrest prior to alveolar phase of development (results in larger lungs with fewer alveoli)

Question 28

when to consider antenatal steroids?

Answer 28

23 to 34 weeks gestation at high risk for pre-term delivery within the next seven days OR for women having LUSCS 34+0 to 36+6

Question 29

main risk factors for TTN

Answer 29

1. diabetic mother 2. maternal asthma 3. prem 4. caesarean

Question 30

what is TTN caused by?

Answer 30

pulmonary oedema from delayed resorption and clearance of alveolar fluid

Question 31

suctioning in MAS - thoughts?

Answer 31

no evidence to suction a vigorous infant

Question 32

triad for PPHN diagnosis

Answer 32

i. Severe hypoxia in FiO2 100% ii. Evidence of R to L shunt iii. TTE confirmation structurally normal heart

Question 33

3 pathophysiology for PPHN, and which is worst

Answer 33

1. pul VC, vessels normal: pneumonia, hypoglycaemia, polycythaemia 2. pul vessel hypertrophy: maternal PG inhib use, asphyxia 3. reduced pul vascular bed SA: CDH, PPH - almost impossible to reverse

Question 34

biggest risk factor for PPHN

Answer 34

MAS

Question 35

explain the finding of pre-post ductal sats in PPHN

Answer 35

often large diff >10% - R to L shunting

Question 36

PPHN - what Rx? how does it work?

Answer 36

inhaled NO vasodilates, selectively targets pulmonary vessels

Question 37

Subcutaneous emphysema in neonate pathognomonic of what?

Answer 37

pneumomediastinum

Question 38

risk factors for extra-pulmonary air leak

Answer 38

- underlying lung disease - prem - assisted ventilation - oligohydramnios

Question 39

what is the only severe complication in the neonatal period which is worsened by surfactant treatment?

Answer 39

pulmonary haemorrhage

Question 40

most common cause of diaphragmatic paralysis in the neonatal period

Answer 40

birth injury - extreme lateral traction on shoulder > phrenic +/- brachial plexus injury

Question 41

adverse effects and contraindications of inhaled nitric oxide

Answer 41

AE: - Methaemaglobinaemia - Nitrogen dioxide -> pulmonary oedema CI: - theoretical: IVH - toxic compound ?increases bleeding risk - coagulopathies

Question 42

three key features of neonatal encephalopathy

Answer 42

i. Reduced level of consciousness ii. Difficulty with initiating + maintaining respiration iii. Depression of tone and reflexes

Question 43

strongest risk factor of neonatal encephalopathy

Answer 43

IUGR

Question 44

pathophysiology of HIE

Answer 44

primary neuronal death - cellular hypoxia secondary phase - latent phase of neuronal death caused by oedema, toxin accumulation

Question 45

what is the only neuroprotective therapy for HIE

Answer 45

therapeutic hypothermia - must be >35weeks, <6h old - 33-35deg, 72h cooling

Question 46

first line anticonvulsant for HIE

Answer 46

phenobarbitone

Question 47

areas of brain injury with HIE and their clinical correlates

Answer 47

periventricular = motor esp lower = spastic diplegia focal white matter / vascular = unilateral findings, seizures parasagittal injuries = more prox limb weakness, spastic quad

Question 48

clinical presentation of IVH

Answer 48

50% silent stuttering most common = over hours/days catastrophic is least common, mins/hours

Question 49

when does PVL present

Answer 49

usually asymptomatic until the neurological sequelae of white matter damage become apparent in later infancy as spastic motor deficits

Question 50

complications of IVH

Answer 50

post-haemorrhagic hydrocephalus (40% will stop by themselves) PVD PVHI from venous compression in grade IV PVL

Question 51

PVL vs IVH

Answer 51

IVH: venous injury - bleed into ventricles asymmetrical unilateral therefore hemiparesis 90% present within 3rd day of life PVL: arterial - watershed infarct symm legs > arms later

Question 52

what kind of PVL more associated with cognitive deficits

Answer 52

Cystic – most powerful predictor of CP and cognitive defects

Question 53

what causes most hemiparetic CPs

Answer 53

perinatal stroke

Question 54

most arterial perinatal strokes occur in which artery distribution

Answer 54

MCA

Question 55

MCA distribution for humunculus

Answer 55

arm and face > leg (as MCA distribution)

Question 56

PPHN what direction shunt

Answer 56

R>L through PDA/PFO