paediatric clinical chemistry Flashcards

1
Q

what are some common causes of problems in neonates with Low birth weight ?

A

Respiratory distress syndrome (RDS) ((Retinopathy of prematurity (ROP))

Intraventricular hemorrhage (IVH)

Patent ductus arteriosus (PDA)

Necrotizing enterocolitis (NEC)

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2
Q

how does necrotising enterocolitis present?

A

Inflammation of the bowel wall progressing to necrosis and perforation

Bloody stools

Abdominal distension

Xray will show Intramural air

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3
Q

when does full maturity of glomerular and tubular function occur?

A

glomerular - 2 years old

tubular - even longer

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4
Q

how does renal structure and function differ in neonates?

A

Low GFR for surface area

Short proximal tubule means there is a lower reabsorptive capability than in the adult although:

Loops of Henle/distal collecting ducts are short and juxtaglomerular - less ability to concentrate urine

Distal tubule is relatively unresponsive to aldosterone: -> more Na loss, less K+ loss.

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5
Q

what is the total body water in prem neonates, term neonate, adult?

A

prem neonate - 80%

term neonate - 75% so all babiees lose weight in their first week after birth. they should regain after day 7

adult - 60%

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6
Q

what is a neonates requireement for sodium, water and potassium?

A

they need:
6x more water
3.5x more sodium
2x more potassium

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7
Q

why is a preemature neonate <30wks not to be given potassium supplement immediately?

when to be given it?

A

can cause hypernatraemia

wait till they produce a urine output of > 1 ml/kg/hr first.

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8
Q

which drugs are not to be given to a premature neonate <30wks and why?

A

§ Bicarbonate for acidosis - contains high Na+
§ Antibiotics (usually sodium salts)

§ Caffeine/theophylline (for apnoea) - increases renal sodium losses

§ Indomethacin (for PDA) - causes oliguria

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9
Q

what is a likeely cause of hyponatraemia in neonates?

A

Congenital adrenal hyperplasia (CAH):
Most commonly caused by deficiency of 21-hydroxylase

This leads to reduced cortisol and aldosterone which leads to salt loss

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10
Q

what are the clinical features of Congenital adrenal hyperplasia (CAH)

A

§ Hyponatraemia/hyperkalaemia with volume depletion

§ Hypoglycaemia (due to lack of cortisol)
§ Ambiguous genitalia in female neonates

□ This is not an obvious feature in male neonates (they may present with a salt-losing crisis)

§ Growth acceleration

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11
Q

what are the Reasons for and aetiology of Neonatal Hyperbilirubinaemia?

A

Aetiology:
Haemolytic disease (ABO, rhesus etc)
 G-6-PD deficiency
 Crigler-Najjar syndrome

Reasons:
○ High level of bilirubin synthesis
○ Low rate of transport into the liver
○ Enhanced enterohepatic circulation

• IMPORTANT: the bilirubin is unconjugated

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12
Q

why is hyperbilirubinaemia an issue?

A

free bilirubin causes Kernicterus (bilirubin encephalotpathy) - after crossing blood brain barrier

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13
Q

how is hyperbilirubinaemia treated?

A

Depends on albumin levels - used to set thresholds
becuase albumin binds to bilirubin

threshold lower in preterm babies due to less albumin

options:
○ No treatment
○ Phototherapy
○ Exchange transfusion

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14
Q

what are the causes of prolonged jaundice in neonates?

A

§ Prenatal infection/sepsis/hepatitis
§ Hypothyroidism
§ Breast milk jaundice

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15
Q

in conjugated Hyperbilirubinaemia, what counts as a pathological Conjugated bilirubin?

A

> 20 µmol/L is ALWAYS pathological

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16
Q

what is the aetiology of Conjugated Hyperbilirubinaemia?

A

§ Biliary atresia (MOST COMMON)
□ 20% are associated cardiac malformations,
polysplenia, situs inversus
□ Early surgery is essential (< 6 months)

§ Choledochal cyst

§ Ascending cholangitis in TPN*
□ The lipids in the TPN seem to cause an ascending
cholangitis

§ Inherited metabolic diseases:
- galactoseamia, peroxismal disorder etc

  • total parenteral nutrition
17
Q

what are calcium and potassium levels like in neonates?

A
  • After birth, all babies’ calcium will fall

* Phosphate is higher in babies (they are good at reabsorbing phosphate)

18
Q

what conditions presents as:

fraying, splaying and cupping of long bones

A

osteopaenia of prematurity

19
Q

what does the biochemistry look like in osteopaenia of prematurity ?

A

Calcium within reference range

Phosphate <1mmol/L

Alk phos >1200 U/l ( 10 x adult ULN)

1,25 vit d deficiency

20
Q

treatment of osteopaenia of prematurity ?

A

Phosphate / calcium supplements

1 alpha calcidol

21
Q

what is an alternative preesentation of rickets?

A

Tetany / hypocalcaemic seizure

Hypocalcaemic cardiomyopathy

22
Q

list 3 genetic causes of rickets?

A

Pseudo vitamin D deficiency I
- Defective renal hydroxylation

Pseudo vitamin D deficiency II
- Receptor defect

Familial Hypophosphataemia
- Raised urine phosphoethanolamine