An infant who was born at 35 weeks gestation is classified as:
A. Early term
B. Full term
C. Preterm
D. Post-term
C. Preterm
- full term = 39 - 40 (+6) weeks of gestation
early = 2 weeks prior
late = 1 week after - preterm = < 37 weeks
- post-term = ≥ 42 weeks
which age group has the highest mortality rate?
A. neonates
B. infants
C. children
D. adolescents
A. neonates
leading cause of death for
< 5 y/o vs 5-9 y/o
(choose from: congenital abnormalities, preterm birth, communicable diseases, injuries)
- < 5 y/o: preterm birth
-> system-wide failure of organ maturity - 5-9 y/o: injuries (e.g. traffic acidents)
core idea of why fetus can be well in womb but so unwell right after birth
body systems are still immature
=> baby cannot maintain HOMEOSTASIS
esp if baby is born preterm
biological differences bet child and adult:
* no of cells
* proportion of stem and progenitor cells
* proliferation rate of cells
* cellular senescence
children have
* lesser number of cells than adults
* higher proportion of stem and progenitor cells
* higher proliferation rate
* less common in children
- cellular senescence ocurs in children as a sculpting tool
-> specific cells are told to stop dividing so that body can take shape
(e.g. regression of Wolffian duct) - while cellular senescence in adults occur as stress response
differences in metabolic activity in children vs adults:
* metabolic rate
* caloric requirement (kcal/kg/day)
* protein requirement (g/kg/day)
* micronutrient requirement per day
core concept:
children are undergoing tissue and bone formation
while adults are only undergoing maintenance
=> ALL are higher in children
- total amount for calories, protein and micronutrient may be lower than adults, just that per kg it’s def higher
- even higher in infants and neonates
what site is most commonly used for bone marrow procedures
POSTERIOR iliac crest
* in children, most skeleton contains red marrow
* red (haematopoietic) -> yellow (fatty) marrow with growth
* in healthy adults, red marrow persists mainly in axial skeleton and proximal humerus/femorus
changes in haemoglobin (Hb) levels with growth
(children -> adults)
- initial decrease
<- fetal Hb (HbF — α2γ2) is being replaced by
adult Hb (HbA — α2β2) - before increasing all the way till adulthood
why is a child’s resting heart rate higher that that of an adult
child’s heart is smaller
→ smaller stroke vol
⇒ heart has to pump more times to maintain adequate cardiac output
how can chronic steroid use (e.g. for asthma)
result in poor growth in a child
- directly inhibit growth plate:
inhibits chondrocyte prolferate, increase apoptosis, reduce cartilage matrix synthesis - decrease release of GH,
decrease production of IGF-1
and decrease sensitivity of growth plate to IGF-1
recall GH pathway:
GHRH (hypothalamus) -> GH (pituitary) -> IGF-1 (liver)
-> growth plate cartilage proliferation => bone lengthening
changes in immune system with growth
(neonate -> child -> adult)
- innate immune system: already relatively well developed at BIRTH
- adaptive immune system: immature,
will develop over time with exposure to pathogens and vaccines
what type of infection has the highest rate of hospitalisation?
bacterial, fungal, parasitic or viral?
bacterial
bcos can cause systemic disease (bacteraemia/septicaemia)
while viral infections usually just cause organ disease and is self-limited
why are newborn NOT given all vaccinations at birth
- immature immune systems
which may result in vaccines not being safe or well-tolerated
or not producing the desired immune response - maternal antibodies may neutralise the vaccine antigens
=> interfere w/ effectiveness of vaccines
why is MMR vaccine given at 12 months of age in some countries (e.g. Singapore)
but at 9 months of age in other countries
- by right shld be 12 months
<- maternal antibodies would have diminished enough not to interfere w/ vaccine’s efficacy - but given earlier (9 months) in high-risk settings
(e.g. measles is common/endemic)
why does serum creatinine increase w/ age
even though GFR also increases w/ age
by right as GFR increases -> better kidney function
-> creatinine more effectvely remove => lower levels in serum
- muscles use creatine phosphate for energy
-> giving creatine as a metabolite - thus since muscle mass increases w/ age
=> creatine also increases w/ age
Is elevated creatine levels in a newborn
within the first 48 hours of birth normal
YES
* at birth and in the first 24–48 hours, a newborn’s serum creatinine reflects the mother’s creatinine
← creatinine cross placenta
* maternal creatinine is cleared over next 3-5 days
⇒ serum creatinine should fall to normal neonatal levels
what type of antibiotic should children be given,
bacteriostatic or bacteriocidal?
bacteriocidal
* bacteriocidal = kill bacteria directly
bacteriostatic = stop growth/propagation of bacteria, wait for WBCs to kill bacteria
* children has immature immune system
=> worse at clearing bacteria
how to differentiate conjugated vs unconjugated hyperbilirubinemia
* physical findings (stools, urine, skin colour)
* % of total bilirubin made up of conjugated bilirubin
physical:
* conjugated: pale stools (<- stercobilin)
and tea-coloured urine (<- urobilin),
greenish-yellow skin colour
* unconjugated: no change in stools or urine,
lemon yellow skin colour
lab: conjugated should be 15-20% of total
there is jaundice in both
(= accumulation of bilirubin — yellow pigment),
but conjugated bilirubin can undergo oxidation inside hepatocytes and bile duct
-> form bilibverdin which is green
when is neonatat jaundice (= hyperbilirubinemia) physiological vs pathological
- physiological: days 2 - 14 of life
- pathological:
1. day 1 of life
2. AFTER day 14 of life
3. if it’s prolonged
complications of neonatal jaundice
- KERNICTERUS
= high levels of UNCONJUGATED bilirubin that cross BBB and deposit in brain tissue - babies are at higher risk than adults
due to:
1. BBB is immature (not fully developed) and thus more permeable to bilirubin
2. other factors (e.g. lower albumin binding capacity to unconjugated bilirubin)
is physiologcal neonatal jaundice (NNJ) conjugated or unconjugated hyperbilirubinemia?
how about pathological NNJ?
- physiological = unconjugated
- pathological = still MAINLY unconjugated,
but can also be conjugated
(conjugated hyperbilirubinemia is ALWAYS pathological)
causes of physiological NNJ
recall! associated w/ unconjugated hyperbilirubinemia
- physiological mechanims (e.g. liver immaturity, destruction of relative excess of RBCs, increased enterohepatic circulation)
- premature birth
<- liver even more immature - breast milk jaundice
<- some enzyme in milk increase enterophepatic circulation
causes of pathological NNJ
recall: mainly unconjugated, but can also be conjugated hyperbilirubinemia
- unconjugated:
basically mainly due to increased bilirubin production due to haemolysis!
1. (most common!) ABO incompatibility
2. inherited conditions like G6PD deficiency
3. variety of factors during delivery
(e.g. bruising during procedure to suck baby out,
reduced bleeding from placenta,
positioning of baby below level of placenta after birth,
increased duration taken to clamp cord)
4. cancers like polycythemia - conjugated: obsturction in GB/bile duct/ampulla of Vater,
e.g. biliary atresia = bile ducts blocked or damaged
physeal fracture
* definition
* complications
- fractures involving physis
(i.e. growth plate or cartilage bet epiphysis and metaphysis) - growth arrest in that bone
<- disruption to stem cells
(which are supposed to differentiate into osteoblasts) - which can then result in limb length discrepancy
- and even scoliosis
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