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
What drugs suppress lactation? (3)
Less common
Decrease prolactin secretion
Dopamine agonists
Bromocriptine, cabergoline
What drugs augment lactation? (3)
More common
Increase prolactin secretion
Dopamine antagonists
Domperidone, metoclopramide
Why might you prescribe domperidone/metoclopramide? (3)
Augment lactation
Mother’s of pre-term infants may lack normal stimuli to produce breast milk
E.g. no natural suckling, no skin-to-skin contact, interrupted bonding
How are proteins, calcium + phosphates excreted into milk? (4)
Protein produced by rER, packaged into vesicle, transported to GA
C + P added = lactose synthesised
Lactose cannot travel across Golgi so it draws in water causing vesicle to fuse with membrane
Contents discharged into lumen by exocytosis
How are lipids excreted into milk? (3)
Produced on sER + in cytoplasm
Packaged into milk-fat globules surrounded by thin layer of membrane
Pinch off into lumen
How are water/ions excreted into milk? (1)
Move across by osmosis
How is secretory IgA excreted into milk? (3)
Binds to binding protein on inside of cell membrane + has sits own transporter
Excreted across on other side
What can go wrong with paracellular pathways? (4)
Not open during lactation
May be open in pregnancy
Can be open in pathological conditions e.g. mastitis
Premature delivery can mean they’re still open allowing extra components e.g. Na+ to be excreted into breast milk
What are the components of breast milk? (5)
Nutrients (macronutirents + trace elements -> low 'solute load' = good for immature neonatal kidneys) Secretory IgA Cells (macrophages + lymphocytes) Non-specific immune components Growth factors
Comparison of nutrition info between colostrum + mature milk (4)
Colostrum has less kcal
Colostrum has less lactose
Colostrum has more protein
Colostrum has less fat
Comparison of term breast milk + formula milk (2)
Term formula milk is essentially modified cow’s milk containing cow’s protein
Nutritionally term breast milk is equivalent to formula milk (70kcal/100ml compared to 74kcal/100ml)
What changes occur in volume of breast milk? (3)
In first few days postpartum you do not produce much milk
~day 3 you produce much greater volumes of milk which keep up with infant demand
Can exclusively breastfeed child until ~6 months
What changes occur in composition of breast milk? (2)
Initially milk has lower levels of lactose. This increases over time
Initially higher amounts of salt/other ions, decreases over time
What changes occur in composition of breast milk during a feed? (2)
Fat conc. increases as baby feeds
For small/premature babies who are not growing well, mothers are asked to particularly express their fat-rich hindmilk + store their foremilk for later uses
Broadly, what are benefits of breastfeeding? (3)
Baby (nutritional, GI function, immunity)
Mother
Society
Nutritional benefits of breast feeding baby - protein (6)
Human milk = 70% whey, 30% casein
Cow milk = 18% whey, 82% casein
Whey proteins remain in sol. in acid media, more easily digested + promote gastric emtyping
Casien = low solubility in acid media, less digestible
Lactoferrin, lysozyme + sIgA important whey proteins
- resist digestion, line GI tract + form first line of defence
Nutritional benefits of breast feeding baby - lipid (6)
Human milk contains LCPUFA (long-chain polyunsaturated fatty acids) = important for brain/retinal development - arachidonic acid + docosahexaenoic acid
Cow’s milk contains shorter-chained versions - linoleic acid + alpha-linolenic acid (LNA + ALA)
Benefits of high omega 3 intake (DHA) (3)
Lower rate of cardiovascular illnesses
+ dementing illnesses in old age
(High fish inake)
What effect does human milk have on GI tract? (3)
Improves gastric emptying
Important in prevent necrotising enterocolitis (NEC) in preterm infant - high morbidity/mortality
What is NEC? (4)
Necrotising enterocolitis Transmural necrosis of bowel wall Gas bubbles within gut wall Multifactorial in cause Huge inflamm insult leads to higher incidence of brain injury
Why do we give pre-term infant breast milk to prevent NEC? (1)
7-10x higher incidence in pre-term infants if fed using formula milk
If you deliver pre-term what will the neonatal unit ask you to do + why? (2)
To produce breast milk
High morbidity associated with not giving breast milk
Why might pre-term baby not have built-in immunity and why is breast milk important? (2)
IgA is passed across during last trimester
If baby misses last trimester then immunity from breast is even more important
Immune factors of breast milk + their effect (9)
sIgA - specific immune response, binds bacterial adherence sites
Complement
Lactoferrin - inhibits bacterial growth by binding iron
Lysozyme - cleaves peptidoglycans of bacterial walls
Anti-inflamm. cytokines - allows human milk to protect but not injure GI tract
PAF acetylhydrolase - inhibits platelet activating factor
Oligosaccharides - inhibit binding of enteric/resp pathogen to epithelial cells
Epidermal growth factors - enhance development of GI epithelium
Neutrophils + macrophages
Why is sIgA different for each baby? (3)
The gut lumen of lactating mother contains Peyer’s patches
When exposed to bacteria - Ag-stimulated lymphocytes travel in circulation
Secretion of IgA into breast milk specifically in response to bacteria you meet in environment
What are the ST benefits of breastfeeding? (2)
Improved immunity, less infection e.g. GI, resp + UTIs Reduces SIDS (sudden infant death syndrome) by ~50% throughout infancy
What are the LT benefits of breastfeeding? ()
Lowers diabetes risk
Generally reduces obesity risk
Prevents/delays occurrence of atopic dermatitis (cow’s milk allergy) + wheezing in early childhood
Lowers risk of chuldhood leukaemia (ALL + AML)
Adolescents have reduction LDL:HDL cholesterol if fed breast milk in infancy
Does breastfeeding make you smarter? (4)
Feeding study on premature infants
Infants of mothers who chose to breastfeed but were unable were randomised to receive either donor or formula milk
Cognitive outcome at 18 months was better for human milk fed infants
But growth was poorer
What are the benefits of breastfeeding for mothers? (4)
Breastfeeding releasing oxytocin which causes uterus to contract + reduces risk of postpartum haemorrhage
Lower risk of breast cancer
Suggestive evidence that lactation protects against ovarian cancer
Calories equivalent to swimming 30 laps in pool
What primitive reflexes are involved in a ‘‘good latch on’? (2)
Rooting + suckling
What are signs of good attachment? ()
Mouth wide open Mouth full Chin is close to breast Lower lip everted Sucking changes More of the aerola is visible above baby's mouth than below
What is the pattern of non-nutritive sucking? (1)
Stimulates nipples to begin milk production
What is the pattern of nutritive sucking? (1)
More drawn out sucking, helps transfer of milk
Positioning of breastfeeding (1)
Baby’s stomach in contact with mother’s
What happens when ‘latching on’ goes wrong? (4)
Incorrect positioning + attachment
Traumatised nipple
Ineffective breast drainage
- infection of breast tissues or mastitis
How do the lungs develop? (7)
Lung buds come off foregut, divide into L + R lung buds
8wks - branches forming bronchi + bronchioles
16-17wks - finish pseudoglandular stage, no longer branching but further dev.
24wks onwards - little saccules dev.
By the time the foetus gets to term is has established alveoli
25-26wks - surfactant prodn increase in quantity as foetus develops in womb
Alveolar development continues until 5-6yrs
What growth factors are required for lung development? (4)
Hepatocyte nuclear factor 3β - foregut
FGF-10, sonic hedgehog, bone morphogenetic protein 4 (BMP4) - outgrowth of new end bunds
Gli proteins - branching
Vascular endothelial growth factor (VEGF) - angiogenesis
Timeline of alveolar development? (4)
24wks - saccules develop + capillaries develop around them under VEGF influence
32wks - shallow indentations
Most developmental post term (mainly by growth in numbers, adult numbers by 4yrs)
Pneumocytes:
- type I+II pneumocytes present at 22wks
- lamellar bodies present for 24wks
Structural pathology of lungs before 16wks ()1
Problems are predominantly related to alveolar numbers
Why do we monitor growth? (5)
PUBLIC HEALTH - screening, surveillance, info on general health/wellbeing/nutrition
CLINICAL PRACTICE
- assessment of health + nutrition
- diagnosis of disease that presents primarily as poor growth
- monitoring of disease/response to treatments
When do we monitor growth? (2)
Baby weighed at birth + then in first few weeks
Might be weighed more in 1st year but not routinely again
How do we monitor growth? (3)
Weight
Height/length
Head circumference/optical frontal circumference
(also important to asses brain growth)
How do we measure weight? (3)
No clothes/nappy (baby)
2yrs+ can be weighed in vest pants (no footwear)
Cradle scales for babies/non-mobile infants
How do we measure length? (2)
Below age of 2
Use length board/mat
Measured without nappy/footwear
How do we measure height? (2)
2yrs+
Rigid rule with T piece
How do we measure head circumference? (2)
Narrow plastic/disposable tape
Measurement taken at widest point
How do we monitor growth with growth charts? ()
Plot measurements on growth chart
Shows ‘normal’ range of measurements for children of all ages - optimal for group, not representative of group
How does ethnicity affect growth? (2)
Black babies often heavier, more muscle mass
South Asian origin babies are often smaller
How does social class effect growth? (3)
Nutritional
Does poverty causes poor growth or obesity?
Can be malnourished but weight a lot
What factors affect growth? (5)
Nutrition (perinatal + postnatal)
Genetics (height of parents, genetic disorders)
Hormones (GH, thyroid hormones, sex steroids)
Timing of puberty (girls enter earlier than boys)
Disease (intake, metabolism, output)
Normal growth pattern (4)
Rate of growth highest in first year of life
Lowest around primary school age
Rises again at puberty
Falls again
What is faltering growth? (3)
Weight is crossing down centiles
Start to notice if child has crossed 2 or more lines
Can be suggestive of malnutrition
What is short stature? (2)
Short child who is not meeting their height potential (based on his previous size + parental height)
Can be due to GH deficiency (treat with GH)
What is underweight? (3)
Thin older child with a BMI less than 2nd centile for age + gender
Could be due to anorexia nervosa
(Signs = skipping meals, severe weight loss whilst maintaining height)
What is overweight? (1)
Child with BMI above 91st centile for age + gender
What is obesity? (1)
Child with BMI above 98th centile for age + gender
What is psychomotor development? (1)
Progressive attainment of skill of mental + physical ability
Outline formation of the neural tube (5)
Neuralation
Begins in week 3 gestation
Neural plate (formed by thickening of ectoderm) folds inwards forming neural groove
Neural folds increase in height + meet to form neural tube
Neural crest = mass of tissues b/w neural tube + skin ectoderm
What 3 layers of cells differentiate from neural tube wall? (3)
Outer/marginal layer forms white matter
Middle/mantle layer forms grey matter
Inner layer forms lining of central canal + ventricles of brain
What does the cranial end of neural tube differentiate into in week 4 of gestation? ()
Prosencephalon (forebrain)
Mesencephalon (midbrain)
Rhombencephalon (hindbrain)
