Laboratory evaluation of illness Flashcards
Physiological jaundice
serum-bilirubin peaks within 1-7 days remains high for 2 weeks (4 weeks if prem)
contributing factors
- increased RBC breakdown due polycythaemia, ineffective erythropoiesis
- impaired conjugation by immature UDP-glucoronyl transferase
- increased absorption of bilirubin deconjugated by glucoronidase in meconium
- BM jaundice
Pathological jaundice
early rapidly rising or persistent unconjugated hyperbilirubinaemia - haemolytic disease of newborn - ABO or Rhesus incomapatibility - inherited RBC defects - prenatal infection - syphillis - hypothyroidism - IEOM conjugated hyperbilirubinaemia - infection - CMV/ hepatitis - metabolic disorders - galactosaemia, a1-antitrypsin deficiency, tyrosinaemia - biliary atresia
Management of unconjugated jaundice
1st line - phototherapy - converts bilirubin to soluble form
inadequate response or excessive rise in bilirubin - consider exchange transfusion
infants given phototherapy must be adequately hydrated
Calcium and phosphate
actively transported across placenta - foetal values higer than maternal
large amount acquired third trimester - prem infants at risk
s-ca falls after birth lowest day 1-2 rises plateau at day 5
neonatal hypercalcaemia uncommon
hypophosphataemia - low dietary intake
neonatal hyperparathyroidism
Hypocalcaemia
common in NEONATES (1-4 days) LBW or prem perinatal asphyxia, stress, trauma IDM, hyperparathyroidism, PE tranfusion large volumes citrated blood LATE NEONATAL PERIOD excessive phosphate intake - cow's milk renal failure hypoparathyroidism OLDER INFANTS critical illness hypoparathyroidism hypomagnesaemia Vit D/mineral deficiency
Childhood rickets
tetany/convulsions, bone deformities
causes
- Nutritional vit D deficiency
- Hypophosphataemia rickets - inherited or renal tubular disease
- Vit D dependant rickets type 1 or type 2 ( 1 a-hydroxylase deficiency or vit D receptor deficits)
