Growth Flashcards
Which trimester is insulin most important in? (4)
3rd trimester where you get hyperplasia of β cells of pancreas
Produces increased amount of insulin
Allows fat stores to be laid down
Anabolic hormone is essential in foetal state in order to grow your body
What are the actions of insulin? (6)
Removes glucose from circulation into tissues
INCREASED glucose uptake into muscle, fat + liver
DECREASED lipolysis
DECREASED a.a. release from muscle
DECREASED gluconeogenesis in liver
DECREASED ketogenesis in liver
Establishing breastfeeding
Little milk is available at first - average intake of colostrum + 7mls/feed in first 24hrs
A newborn initially has to meet demand from stores
The energy requirement for a newborn = 4-6g glucose/kg/day
Later, milk is available as high fat food
What is CMR? (1)
Cerebral metabolic rate
What percentage of an adult’s CMRglucose does a baby have at birth? (1)
30%
What accounts for the highest proportion of the baby’s resting energy expenditure? (1)
Its brain (energy partitioning)
What proportion (by weight) of the newborn’s body do glycogen + fat make up? (2)
1% glycogen (stored in liver)
16% fat
How are the anabolic actions of insulin opposed? (4)
By counter-regulatory catabolic hormones
Glucagon, adrenaline, (cortisol, GH)
Switched on during labour + delivery
Surge of adrenaline = first step in driving catabolism
What happens during the glucagon surge? (2)
Plasma glucose levels fall at birth causing plasma glucagon to rise rapidly Activates gluconeogenesis (opposing insulin)
What happens during a postnatal fast? (2)
Baby needs to utilise stores to provide glucose as an energy source for tissues
Gluconeogenesis + ketogenesis occur
What happens in gluconeogenes? (3)
Process of providing glucose from stores = muscle (a.a.s + glycogen) + fat
Via substrates e.g. lactate, pyruvate, alanine + glycerol
What happens in ketogenesis? (2)
Process of providing ketone bodies (which act as fuel)
From breakdown of fat
What happens in the oxidation of fat? (4)
Terminal 2 carbon groups removed from fatty acid + bound to coenzyme A, as acetyl CoA
β oxidation
Acetyl group can then be utilised to form ketone bodies (acetone + β hydroxybutyrate)
Acetyl groups can also enter the Krebs cycle as an energy source
What happens to newborn in fasting (post-absorptive) state? (3)
When baby is born it goes from continuous nutrition across the placenta to periods of time where baby receive nothing b/w feeds
Substrates are mobilised peripherally through action of catabolic hormones
Insulin is opposed
What happens to newborn in fed (post-prandial) state? (3)
Infant diet is 50% fat + 40% carb (milk)
Carb is mainly lactose
Breast milk contains a lipase
What are potential metabolic problems of babies? (4)
Demand exceeds supply
Hyperinsulinsim
Counter-reg hormone deficiency
Inborn errors of metabolism
What happens with an extremely small preterm baby with demands exceeding supply? (6)
Small nutrient stores
Immature intermediary metabolism = enzyme/hormone pathways not working properly
Establishment of enteral feeding delayed
Can’t feed babies in large amount as would vomit + aspirate
So feed in v small amounts + support with IV nutrition
Poor fat absorption
What is IUGR? (6)
Intrauterine growth restriction Indicates path process has occurred High demands (especially brain) Low stores (liver, fat) Immature gluconeogenic pathways Small for gestational age (SGA) = fall below 10th percentile for gest age
What happens to the infant of a diabetic mother? (5)
High maternal glucose = high foetal glucose
Foetal + neonatal hyperinsulism
Neonatal macrosomia = excessive birth weight
Hypoglycaemia (hypoketotic hypoglycaemia)
Abnormally large fat stores
What are other causes of hyperinsulism? (7)
Beckwith Wiedemann: - macroglossia (large tongue) - macrosomia (excessive birth weight) - midline abdominal wall defects (exomphalos, umbilical hernia, diastasis recti) - ear creases/pits - hypoglycaemia Islet cell dyregulation
What happens in congenital adrenal hyperplasia (CAH)? (3)
Enzyme defect = usually due to 21-hydroxylase deficiency
Girl has undergone virilisation in the womb (too much testosterone)
Important as can present with salt wasting crisis due to lack of aldosterone
Other deficiencies of counter-regulatory hormones (4)
H-P-A insufficiency = septo-optic dysplasia
Waterhouse-Friderichsen = severe adrenal haemorrhage with adrenal gland dysfunction secondary to sepsis or hypoxia
Name some inborn errors of metabolism (4)
Glycogen storage disease (type 1)
Galactosaemia
MCAD (medium chain acyl-coA dehydrogenase deficiency)
(Causes of neonatal hypoglycaemia)
What is glycogen storage disease (type 1)? (3)
Deficiency of glucose-6-phosphatase
Hypoglycaemia (during periods of fasting or stress) + lactic acidosis in newborns
Hepatomegaly in older child
What is galactosaemia? (7)
Deficiency of galactose-1-phosphate uridyl transferase (Ga-1-put) Leads to toxic levels of galactose-1-phosphate Presents with: - hypoglycaemia - jaundice + liver disease - poor feeding + vomiting - cataracts + brain damage - E coli sepsis
What happens to galactose in the absence of galactosaemia? (1)
Galactose (from lactose = galactose + glucose) is broken down by to glucose by galactose-1-phosphate uridyl transferase
Which hormone dominates in the foetal state? (1)
Insulin (anabolic)
What hormones are vital in post-natal metabolic adaption? (1)
Catabolic counter regulatory hormones (especially glucagon)
What can metabolic adaption to extra-uterine life be compromised by? (3)
IUGR
Premature birth
Inborn errors of metabolism
Describe the anatomy of the breast (3)
~20 radially arranged lobes
~9/10 functional, rest are vestigial
Each lobe = separate functional unit
What percentage fat does the lactating + non-lactating breast consist of? (2)
Non-lactating = ~50% Lactating = ~30%
Describe mammary gland drainage (2)
Ductal system drains into lactiferous sinuses beneath areola of breast
Subcutaneous, intra-glandular, retro-mammary fat deposits
Describe ‘in vivo’ anatomy of the lactating breast (3)
Lactiferous sinuses not found
~9 ducts emerge at the nipple
Ducts are tortuous + branch near nipple
~70% of glandular tissue within 8cm of nipple
Mammary gland structure (3)
Basic secretory unit is the alveoli set within connective tissue structure
Linked by mammary epithelial cells (cuboidal or low columnar)
Myo-epithelial cells surround the alveoli -> contractile + responsible for milk ejection
What is lactogenesis I? (3)
Preparation in pregnancy
Placental lactogen + prolactin promote dev. of breast (surge of these hormones when pregnant)
Prog. + oest. inhibit milk secretion
What is lactogenesis II? (4)
Post-partum
Abrupt fall in prog. + oest. reduces inhibition
Suckling stimulus release prolactin which drives milk synthesis
Suckling (+ higher centres) release oxytocin driving milk ejection
Autocrine inhibition from duct cells? (2)
As alveoli fill up with milk, further milk production is inhibited
If milk is not removed from breast, no more is produced
How is milk synthesis controlled? (3)
Prolactin released from ant. pit. in response to suckling
Milk synthesis is lead by infant demand
Peak in prolactin ~20mins after suckling begins causing synthesis of milk for next feed
What is the ‘let down’ reflex? (3)
Oxytocin release from post. pit. causes milk ejection
Cause myoepithelial cells around alveoli to contract releasing milk into milk ducts in nipple
Reflex may become conditions i.e. might still get let-down reflex when you think about baby/hear another baby crying etc.
What are the myoepithelial cells responsible for? (2)
Contraction + ejection of milk into milk ducts
In response to release of oxytocin
