Switching on a fuel supply Flashcards

1
Q

What are the actions of insulin?

A
  • Increased glucose uptake in muscle, fat and liver
  • Decreased lipolysis
  • Decreased AA release from muscle
  • Decreased gluconeogenesis in liver
  • Decreased ketogenesis in liver
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2
Q

Why is it good to establish breastfeeding quickly?

A
  • little milk available at first
  • newborn has to meet demands from stores
  • Requirement = 4-6g glucose /kg/day
  • Later milk is available as a high fat food - 50% of calories in it is fats
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3
Q

How are stores converted to fuels?

A
  • Anabolic actions of insulin are opposed by counter-regulatory (catabolic) hormones: glucagon, adrenaline, cortisol, GH
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4
Q

What is the glucagon surge?

A
  • As plasma glucose levels fall at birth, plasma glucagon levels rise rapidly
  • This activates gluconeogenesis, opposing insulin
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5
Q

What happens during a postnatal fast?

A
  • The baby will need to utilise stores to provide glucose as an energy source for the tissues
  • Gluconeogenesis is the process of providing glucose from stores - muscle (AAs and glycogen) and fat via substrates such as lactate, pyruvate, alanine and glycerol
  • Ketogenesis is the process of providing ketone bodies (which ac as a fuel) from the breakdown of fat
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6
Q

What are the 3 rate limiting steps in the gluconeogenesis process?

A
  • PEPCK, F1,6-BPase and G6pase
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7
Q

How is fat oxidised?

A
  • Terminal two carbon group is removed from FA and bound to coenzyme A, as acetyl CoA (beta oxidation)
  • Acetyl groups can then be utilised to form ketone bodies (acetone and beta-hydroxybutyrate)
  • Acetyl groups can also enter the Kreb’s cycle as an energy source
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8
Q

What is the fasting (post-absorptive) state?

A
  • Straight after eating
  • Substrates are mobilised peripherally through action of counter-regulatory hormones (catecholamines, cortisol and glucagon)
  • Insulin is opposed
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9
Q

What sort of problems can babies have with metabolism?

A
  • Demand exceeds supply
  • Hyperinsulinism
  • Counter-regulatory hormone deficiency
  • IEM
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10
Q

What problems will an extremely small preterm baby have?

A
  • High demands, small nutrient stores
  • Immature intermediary metabolism
  • Establishment of enteral feeding delayed
  • Poor fat absorption - GIT wont work well, can put milk in, but wont be absorbed properly
  • Extremely little fat stores to maintain blood glucose levels - they will go down and stay down
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11
Q

What problems will an IUGR (inuterine growth restriction) baby have?

A
  • High demands (especially brain)
  • Low stores (liver, muscle, fat)
  • Immature gluconeogenic pathways
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12
Q

What problems may arise if the mother is diabetic?

A
  • High maternal glucose and so high foetal glucose
  • Foetal and neonatal hyperinsulinism
  • Neonatal macrosomia and hypoglycaemia
  • At risk of very problemati hypoglycaemia - wont have made ketones so one of the defence mechanisms has gone
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13
Q

What are other causes of hyperinsulinism?

A
  • Beckwith Wiedemann

- Islet cell dysregulation - Nesiodioblastosis

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14
Q

What are symptoms of Beckwith Wiedemann?

A
  • Macroglossia
  • macrosomia (big baby)
  • Midline abdominal wall defects (exomphalos, umbilical hernia, diastasis recti)
  • Ear creases or ear pits
  • Hypoglycaemia
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15
Q

What causes CAH?

A

21 hydroxylase deficiency

- Build up of androgens - cannot make aldosterone or cortisol

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16
Q

What IEMs can cause neonatal hyPOglycaemia?

A
  • Glycogen storage disease (usually type 1)
  • Galactosaemia
  • Medium chain acyl-CoA dehydrogenase deficiency (MCAD)
17
Q

What is glycogen storage disease (type 1)?

A
  • Deficiency of G-6-phosphatase
  • Hypoglycaemia and lactic acidosis in newborn
  • hepatomegaly in older child
18
Q

What causes galactosaemia?

A
  • lactose in milk is broken down to galactose and glucose
  • Galactose is then broken down to glucose by galactose-1-phosphate uridyl transferase
  • This enzyme is missing in galactosaemia, leading to toxic levels of galactos-1-phosphate
19
Q

What are the symptoms of galactosaemia?

A
  • Hypoglycaemia
  • Jaundice and liver disease
  • Poor feeding and vomiting
  • Cataracts and brain damage
  • E coli sepsis
20
Q

SUMMARY

A
  • insulin dominates in the foetal state
  • Counter-regulatory hormones (esp glucagon) have vital role in postnatal metabolic adaptation
  • Tissue stores, particularly fat laid down in 3rd trimester are important energy stores in the first few days
  • metabolic adaptation to extrauterine life is compromised by IUGR, preterm birth or IEM