Nutrition Flashcards
Fuel Supply in Foetus
- In the womb, it is an anabolic process so the foetus has a continuous supply of food and grows the most it will ever grow which is around 20 weeks gestation
- Glucose crosses the placenta via facilitated diffusion according to diffusion gradient so more glucose in mother more goes across to the baby and we use approximately 5g/glucose/kg/day
- Substrates are principally glucose and amino acids
Action of Insulin
- In foetus insulin acts as an anabolic hormone with less direct control of blood glucose
- Takes baby from a foetal, anabolic metabolic state into a neonatal state where the baby must rely on body stores (catabolism) between feeds
- Catabolic enzyme systems (not needed in utero) must be switched on in order for this
Establishing Breastfeeding
•Little milk is available at
first
•A new born initially has to meet demands from stores
•The energy requirement for a new born is about 4-6 g glucose/kg/day
Conversion of Stores
• Have a huge surge of stress hormones and adrenaline which switches on the counter regulatory metabolism and that allows you to switch on enzymes that help you break down the stores that you need after you’re born
Which hormones oppose the counter-regulatory hormones?
– glucagon
– adrenaline
– (cortisol)
– (growth hormone)
What happens to blood hormone levels
- Get a sharp fall in plasma glucose after you’re born
- Even if you don’t feed babies the glucose will come up to normal levels
- Baby manage hypoglycemia better than older
- As plasma glucose levels fall at birth, plasma glucagon levels rise rapidly.
- This activates gluconeogenesis, opposing insulin
Postnatal Fast
- 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 (amino acids and glycogen) and fat via substrates such as lactate, pyruvate, alanine and glycerol.
- Ketogenesis is the process of providing ketone bodies (which act as a fuel) from the breakdown of fat
- New borns able to use ketones which you can produce from your fat stores
How do babies manage to not become hypoglycaemic
While the brain accounts for higher proportion of resting energy expenditure, you also have a far lower cerebral metabolic rate in the new born period than at any other time in your life
Describe the fed state
- Infant diet is 50% fat and 40% carbohydrate
- CHO is mainly lactose
- Breast milk contains a lipase
- Blood glucose will be high after a meal and will be mostly lactose broken down into glucose
- Insulin will act on glucose to lay down glucose as body stores
- Converted into fat and is utilized in muscles as glycogen and building block for amino acids
What types of babies have problems with metabolism?
- Demand exceeds supply
- Hyperinsulinism
- Counter-regulatory hormone deficiency
- Inborn errors of metabolism
Managing Extremely Small Preterm Baby
- High demands & Small nutrient stores
- Immature intermediary metabolism
- Establishment of enteral feeding delayed
- Poor fat absorption
- Start with very small amount of breast milk then gradually increase
- Support baby with iv glucose and amino acids and vitamins an fats
- Aim to be on full feed by day 7 of life
Infant of Diabetic Mother
- High maternal glucose high foetal glucose
- Foetal and neonatal hyperinsulinism
- Neonatal macrosomia and hypoglycaemia.
- Small head and big trunk
- High circulating levels of insulin that doesn’t drop in the way it is supposed to
- Can get really low levels of glucose and hypoglycemia
- Insulin also means won’t get any ketone bodies being made so brain isn’t protected from hypoglycemia
Other causes of hyperinsulinism
- Islet cell dysregulation: Nesiodioblastosis
* Beckwith Wiedemann:
Features of Beckwith Wiedemann
–macroglossia (large tongue), –macrosomia –midline abdominal wall defects (exomphalos, umbilical hernia, diastasis recti), –ear creases or ear pits –hypoglycaemia
Inborn Errors of Metabolism
•Causes of neonatal hypoglycaemia include:
– Glycogen storage disease (usually Type 1)
– Galactosaemia
– MCAD (medium chain acyl-coA dehydrogenase deficiency)
Glycogen Storage Disease (Type 1)
- Deficiency of glucose-6-phosphatase
- Hypoglycaemia and lactic acidosis in newborn
- Hepatomegaly in older child