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Semester 4 > Growth > Flashcards

Growth Flashcards

1
Q

What are the actions of insulin?

A
  • Increased glucose uptake in the muscle, fat, and liver
  • Fall in the following and you will also feel faint + hungry and dizzy when there is a shortage
    • Gluconeogenesis in the liver
    • Amino acid release from the muscle
    • Lipolysis
    • Ketogenesis in the liver
  • Removes glucose from the circulation and into the tissues where it is stored.
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2
Q

How to establishing breastfeeding

A
  • @ first not much milk is available.
  • Average intake of colostrum + 7mls feed in the first 24 hours. New born has to initially meet demands from stores
  • Later, milk is available as a high fat food.
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3
Q

What is the energy need for newborn

A
  • The energy need for new born is 4-6g glucose/kg/day
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4
Q

What happens during a postnatal fast

A
  • The baby has to utilise stores to provide glucose as energy source for the tissues
  • Gluconeogenesis = process of providing glucose from stores - muscle, amino acids and glycogen, + fat via substrates such as lactate, pyruvate, alanine and glycerol
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5
Q

What is ketogenesis

A
  • Is process of providing ketone bodies - act as fuel, from fat breakdown.
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6
Q

Fat structures + metabolism of fat

A
  • Glycerol backbones have fatty acids attached. Can Knock off fatty acids from the glycerol back bone. Binding to AcoA = beta oxidation –>

This can also be used to make ketone bodies which babies can use

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7
Q

Describe fat oxidation?

A
  • The terminal 2 carbon group is removed from fatty acid and bound to coenzyme A, as AcoA - (Beta oxidation). Acetyl groups can then be used to form ketone bodies (acetone and beta hydroxybutyrate). Acetyl groups can also go into the Krebs cycle, as an energy source.
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8
Q

how are ketone bodies formed?

A
  • Beta oxidation removes 2 carbon units, which are used to make ketone bodies
  • Anaerobic respiration - this works as a metabolic fuel for the brain
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9
Q

Describe fasting, in the post absorptive state

A
  • Substrates get mobilised peripherally through the action of counter regulatory hormones
  • Insulin gets opposed if you are fasting. When baby is born, go from having uninterrupted nutrition across placenta = to periods of time where you have to wait for food.
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10
Q

Describe the fed, post prandial state

A
  • Infant diet is = 50% fat +40% carbohydrate, CHO is mainly lactose. Breast milk contains lipase.
  • There are deliveries made which make: ketone bodies and blood glucose. Beta oxidation and ketone bodies are present when you have just had a meal
  • Carbs from milk = from lactose. Get lots of blood glucose from the blood stream and then this is stored in the peripheral tissues. Glycogen can be rapidly broken down as an energy source when needed in a fast
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11
Q

What are metabolic needs for adults compared to babie

A
  • 30 kilocalories/g/day for adults, and 4x this amount of energy needed for babies to grow because have to maintain and grow. Fastest rate of growth is mid gestation at 20 weeks.
  • Cannot feed babies like this: when you feed them - they would vomit the milk out. Feed them small amounts and support with IV nutrition. Gastro tract is there from 18-20 weeks onwards. Born at 25 weeks = anatomy is there but nothing is working exactly how it should so you have a limited capacity to digest any milk that is given.
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12
Q

describe the The IUGR baby

Intrauterine growth restriction baby

A
  1. SJ small for gestational age (below a certain percentile level, which can be normal)
  2. IUGR - indicates that a pathological process has occurred to make a baby smaller than they should be.
    - High demands, especially the brain
    - Low stores, liver, muscle and fat - immature gluconeogenic pathways
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13
Q

what are the characteristics of Infant of diabetic mother

A
  • High maternal glucose, high fetal glucose, fetal and neonatal hyperinsulinism
    • Neonatal macrosomia and hypoglycaemia

Cherubic. Big chubby cheeks. Difference between this + a normally big baby =

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14
Q

Other cases of hyperinsulinsim

A
  • Beckwith Wiedemann
  • Macroglossia, large tounge, macrosomnia, midline abdominal wall defects (exomphalos, umbilical hernia, diastasis recti)
  • Ear creases or ear pits
  • Hypoglycaemia
  • Islet cell dysregulation - nesiodioblastosis
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15
Q

What is Nesiodioblastosis

A

Islet cell dysregulation

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16
Q

Other deficiencies of counter regulatory hormones

A
  • Hypothalamic- pituitary adrenal insufficiency = septoptic dysplasia
  • Waterhouse - Friderichsen - severe adrenal haemorrhage with adrenal gland dysfunction secondary to sepsis or hypoxia.
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17
Q

What is Waterhouse Friderichsen

A
  • Severe adrenal haemorrhage
    Ø With adrenal gland dysfunction

Secondary to sepsis or hypoxia

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18
Q

What is septo-optic dysplasia caused by?

A
  • Hypothalamic- pituitary adrenal insufficiency = septo-optic dysplasia
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19
Q

Inborn errors of metabolism: describe neonatal hypoglycaemia

A
  • Causes of neonatal hypoglycaemia, include:
    • Glycogen storage disease (usually type 1)
    • Galactosaemia, MCAD (medium chain acyl-coA dehydrogenase deficiency)
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20
Q

Glycogen storage disease (type 1)

A
  • Deficiency of G-6-Phosphatase, hypoglycaemia and lactic acidosis in new born.

Hepatomegaly in older child.

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21
Q

describe Galactosaemia

A
  • Lactose in milk is broken down to galactose + glucose
    Ø Galactose = then broken down to glucose
    ○ By galactose 1 phosphate
    ○ by Uridyl Transferase (Gal-I-put)
    § Uridyl transferase is missing in Galactosaemia. This leads to toxic levels of galactose 1 phosphate
  • If you do not have the right levels of converting enzyme you will make toxic levels of Galatcose 1 phosphate.
  • Presents with:
    • Hypoglycaemia, jaundice and liver disease, poor feeding and vomiting, cateracts and brain damage, E coli sepsis
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22
Q

describe breast anatomy

A
  • 20 radially arranged lobes. System of ducts draining down to nipple. About 9 lobes (4-18) are functional, the rest vestigial. Each lobe = separate functional unit.
    Ø Non-lactating breast = 50% fat
    Ø Lactating about 30% fat.
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23
Q

describe Drainage of the mammary gland

A
  • This system of ducts drains into “lactiferous sinuses” underneath the breast areola.
  • There are subcutaneous, intraglandular and retromammary fat deposits
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24
Q

Structure of the mammary gland

A
  • Around the alveolar there are myoepithelial cells.
  • The basic secretory unit = alveoli set within connective tissue structure, which are lined by mammary epithelial cells (cuboidal or low columnar cells). Myoepithelial cells surround the alveoli.

Myoepithelial cells are contractile + responsible for milk ejection

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25
Q

Preparations in pregnancy

A
  • “Lactogenesis I”
  • There is placental lactogen + prolactin which promote breast development, prepped for milk production in pregnancy. Will start to cause hyperplasia of glandular tissues within the breast.
  • There is also autokine inhibition from duct cells.
  • If milk is not removed from the breast = no more milk produced.
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26
Q

What inhibits milk secretion?

A
  • Progesterone and oestrogen both inhibit milk secretion
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27
Q

Lactogenesis post partum - lactogenesis

A
  • Fall in progesterone and oestrogen levels reduces inhibition
  • Suckling stimulus will release prolactin; which will drive milk synthesis. Suckling = releases oxytocin driving milk ejection. There is also some autocrine inhibition from duct cells
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28
Q

Describe what suckling will do

A
  • Suckling stimulus will release prolactin. Prolactin drives milk synthesis
  • Sucking + higher centres will release oxytocin which drives the ejection of milk
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29
Q

Control of milk synthesis

A
  • Prolactin released in response to sucking, from the anterior pituitary.
  • Milk synthesis is led by infant demand
  • Suckling > nerve pathways > ant. Pituitary > prolactin in the blood > milk producing alveolus
  • Sucking episode = synthesis for next feed.
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30
Q

Describe the let-down reflex

A
  • Oxytocin release causes milk ejection. The reflex might become conditioned. The surrounding myoepithelial cells that surround contract and let out milk.
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31
Q

Effect of drugs that suppress lactation?

A
  • Fall in prolactin secretion
  • Dopamine agonist
    • Bromocriptinne
    • Cabergolie
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32
Q

Effect of drugs that Augment lactation?

A
  • Increased prolactin secretion
  • Dopamine antagonists
    • Domperidone
    • Metoclopramide
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33
Q

breast secretory pathways?

A
  • Produce protein which is packaged in the vesiclce and goes to the golgi apparatus.
  • Vesicle then fused.
  • Lipids make in the ER. Fat globules are surrounded by membrane and then pinch off into the lumen. Water, ions etc move across by osmosis and then other elements like sectory IgA binds with a binding protein on the inside of the cell membrane.
    Paracellular pathways + Transcellular Pathways
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34
Q

What are the components of breast milk?

A
  • Nutrients = macronutrients and trace elements (low solute load)
  • Ig, Secretory IgA, Cells
  • Non-specific immune components
  • Growth factors
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35
Q

what are the components of human breast milk? [lipids]

A
  • Human milk has LCPUFA.
    Ø Important for brain and retinal development
  • Cows milk only contains C18 LCPUFA, linoleic, n6 and linolenic n3 precursors
  • As adults = can make DHA + acids from these precursors. Harder for babies to do so.
  • Populations of those who have long chain PUFA acids = have lower rate of CVS, metabolic, and dementia syndromes in old age + omega 3 from fish gives these effects.
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36
Q

what are the components of human breast milk? [proteins]

A
  • Human milk =
    • Whey 70%, casein 30%
    Casein makes curds which sit in the stomach and satisfy baby
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37
Q

What special component does human milk contain

A

LCPUFA. Which is important for brain + neuronal development

- Long chain PUFA acids = lower rates of CVS + metabolic + dementia issues

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38
Q

What component does cow milk contain

A
  • C18 LPUFA only
    • Linoleic, n6, linolnic n3 precursors
    • As adults we can make DHA + acids that we need from these precursors
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39
Q

Effect of breast feeding on GI

A
  • Human milk = improves gastric emptying.
  • Human milk is important in preventing NEC in preterm infant. Looks like a string of beads.
  • If you give premie formula milk = much higher chance of getting this condition, or inflammation which can cause brain injury.
  • Higher morbidity associated with formula.
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40
Q

Immunity in breast milk : things that included in breast milk

A 
Immune factor
sIgA
complement
lactoferrin
Lysozyme
Cytokines
PAF acetyl hydrolase
Oligosaccharides 
Epidermal growth factors 
Cellular elements
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41
Q

Describe the immune effect of sIgA in breast milk

A
  • Specific immune resp. binds bacterial adherence sites
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42
Q

Describe the immune effect of complement in breast milk

A
  • C1 to C9 present in low conc in human milk.

- Higher amounts of C3 (can opsonise bacteria in conjctation with IgA)

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43
Q

Describe the immune effect of lactoferrin in breast milk

A
  • Inhibits bacterial growth by binding iron
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44
Q

Describe the immune effect of cytokines in breast milk

A
  • Anti inflammatory cytokines predominate in human milk

- Allows human milk to protect but not injure the gastro tract

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45
Q

Describe the immune effect of PAF acetyl in breast milk

A

Inhibits platelet activating factor

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46
Q

Describe the immune effect of oligosaccharides in breast milk

A
  • Inhibits the binding of enteric / resp pathogens epithelial cells
    • Probiotics and prebiotics. = non digestible oligos which go through to the colon and act for food for normal baterial flora.
    • Not like the bacterial flora of formula milk that infants have. (pre)
    • Probiotics are the actual bugs.
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47
Q

Describe the immune effect of epidermal growth factor in breast milk

A

Enhance the development of GI epithelium

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48
Q

Describe the immune effect of cellular elements in breast milk

A

Neutrophils and macrophages

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49
Q

Describe the immune effect of lysozyme in breast milk

A
  • Cleaves peptidoglycans of bacterial walls
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50
Q

what is the enteromammary axis?

A
  • Gut lumen of mother contains Peyers patches.

Antigens stimulate lymphocytes, to go to circulation = secretion of IgA into breast milk.

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51
Q

Secretory IgA roles in breastfeeding?

A
  • Secretory IgA is fine tuned to meet the bugs that are in the environment.
52
Q

Short term benefits of breast milk?

A
  • Better immunity –> Less infections + infectious morbidity
  • GI infection, respiratory infection, UTIs.
  • SIDS risk reduced during breast feeding.
53
Q

Long term benefits of breast milk

A
  • T1/T2 diabetes. Reduce risk of obesity. Allergic diseases = reduced risk (like atopic dermatitis)
  • Reduced risk of childhood leukaemia. Fall in cholesterol levels (14% fall in LDL:HDL ratio)
  • Blood pressure = positive effects.
  • Infancy breast feeding = long standing benefits.
  • It makes children smarter = the smaller and the more preterm that you are (matters less for term infants) - 1990 study.
  • Major determinant of whether or not someone breast feeds = education and social class is higher, makes you more likely to breastfeed.
54
Q

Patterns of sucking in breastfeeding

A
  • Non nutritive (short) - makes milk get let down
  • Nutritive sucking - longer and more drawn out
  • Tummy to tummy positioning.
  • Poor latch = trauma and therefore infection to the nipple.
55
Q

describe lung development @ `16-17 weeks

A

all airway branches are formed + no additional branching happening.

56
Q

describe lung development @ `16-24 onwards

A

saccules. & @ 12 weeks = established alveoli along the lungs.
Ø Majority of alveolar development happens half term. Can get structural pathology inside the lung that stops them working properly.

57
Q

describe secretion of the lung liquid

A
  • Secondary active transport of Cl from interstitium to the lumen
    • Na and H20 : passive
  • Liquid production allows for positive pressure of 1cmH20
  • Lung fluid is needed for lung growth, but not branching
    Lung fluid = made by active transport of chloride. More chloride = more flow of water and sodium along a diffusion gradient. Distending pressure allows the lungs to stay open. Other components the lung structure rather than a whole part of it.
58
Q

Lung liquid - absorption [in cardiorespiratory development]

A
  1. Active sodium transport in apical membranes
  2. Labour + delivery: adrenaline release leads to reduced secretion and resorption begins
  3. Thyroid hormone and cortisol needed for maturation of the fetal lung response to adrenaline
  4. Exposure to post natal oxygen increases the sodium transport across the pulmonary epithelium
59
Q

Oligohydramnios - lung liquid pathology

A
  • Early rupture
  • Kidney abnormalities = obstructions to their renal outflow etc where amniotic fluid is lower in volume

Pushing more fluid out of the lungs

60
Q

Fetal breathing abnormalities - lung liquid pathology

A
  • Neuromuscular disorders
  • Phrenic nerve agenesis
    • Prevents baby having normal fetal breathing movements.
  • CDH
  • Fetal breathing slows lung liquid loss

Maintains expansion

61
Q

Surfactant characteristics?

A 
- This is produced by type 2 pneumocytes 
• Surfactant phosphatidylcholine PC
• Produced in the endoplasmic reticulum
• Stored in the lamellar bodies 
- Degraded in alveoli 
• Absorbed + recycled by alveolar cells 
• More than 90% PC is reprocessed 
• Turnover time 10 hours 
- Negative feedback system to regulate release 
• Also stretch receptors 
• B adrenergic receptor on type 2 cells 
○ This increases with gestation
62
Q

what is the action of surfactant?

A
  • Reduces surface tension of the lungs and prevents the alevoli from falling down. Secretions into alveolar pace.
  • Prevents atelectasis - reduces the work to breathe
  • Achieved by reduced surface tension
    • Solid @ body temperature
    • Become a solid monolayer
    ○ Stabilises alveoli
  • Laplace equation
    • Internal pressure
    • 2 x surface tension / radius
63
Q

What is surfactant + what is it mainly made up of?

A
  • A mixture of phospholipids
  • Neutral lipids
  • Protein
  • Lipids are the most important
    • PC comprises = 80%
    • PG = 10%
    • 60% PC disaturated, predominantly palmitic acid
    • Therefore dipalmitoyl phosphatidycholine = major component of surfactant

Function = phospholipids are the most important component.

64
Q

What is the major component of surfactant?

A

Dipalmitoyl phosphatidycholine (50%)

65
Q

Composition of surfactant

A
  • 50% = Dipalmoitoylphosphatidylcholine
  • 7% Phosphatidylglyercol
  • 8% Serum Proteins
66
Q

SP-A characteristics

A
  • Large glycoprotein
  • Gene on chromosome 10
  • Only expressed in the lung
  • There is a rise in production after 28 weeks onwards
  • Allows for the stability and spreading of phospholipids. iG born before 28 = less surfactant and altered composition which affects function.
67
Q

What is SP-A essential in

A
  1. Determining the structure of tubular myelin
  2. Stability and spreading of phospholipids
  3. Negative feedback loops
68
Q

SP-B characteristics

A
  • 1-2% surfactant by weight
  • Gene on chromosome 2
  • Glucocortids increase expression
69
Q

What is SP-B essential in

A
  1. Forming tubular myelin
  2. Spreading
  3. Combined with lipid mixtures - most of the surface activity in vitro + increases lung compliance in vivo
  4. Protection of surfactant film from inactivation by serum proteins
70
Q

SP-C characteristics

A
  • Chromosome 8
  • 35 amino acids (q. small)
  • Significantly enhances adsorption and spreading on phospholipids
71
Q

SP-D characteristics

A
  • Different function in the lung = not to do with the alveolar hyperface, but to do with immune function and protecting the organisms.
  • Molecular weight of 46000
  • Increased expression with gestation
  • Expression = widely distributed in epithelial cells
  • No significant surfactant activity, & has immune function
72
Q

explain the importance of glucorticoids in the maturation of surfactant?

A

Exposure of the fetus & lungs increases amount of DPPC present

  • Increased production @ the end of gestation
  • Increases DPPC
  • Dexamethasone, enhances Beta 2 adrenoreceptors gene expression
  • This leads to an increased surfactant secretion
73
Q

explain the importance of thyroid hormones in the maturation of surfactant?

A

positive

  • T4 increases surfactant production
  • T3 crosses placenta
  • TRH increases phospholipid independent of T3, T4
74
Q

explain the importance of insulin in the maturation of surfactant?

A
  • Delays maturation of type 2 cells
  • Decreases % saturated PC
  • Delayed PG

Increased sugar levels delay lung maturation

75
Q

How does pathology of surfactant arise?

A
  1. Prematurity 2. SP deficiencies
    - Pathology of surfactant in prematurity
    • SP-B
    • Absence leads to markedly reduced PG
    • No secretion of normal surfactant
    • Lethal - lung transplant possible for some
    - Pathology of surfactant in SP deficiencies
    • SP C

Interstitial lung disease

76
Q

birth/labour and lung liquid production - what happens?

A
  • Lung liquid production stops during labour
  • Fetal breathing ceases along with the other senses
  • Central chemoreceptor detection of hypoxia
  • First breath median time 10 seconds
  • High inspiratory pressure
  • Active expiration with high pressure
  • Air will replace fluid within minutes
  • Some is squeezed out
  • Most is absorbed into the lymphatics (1hr)
  • And into the capillaries (6 to 24 hrs)
  • There is a rapid fall in airway resistance - increase FRC
  • Slower increased in compliance over 24 hours
    Liquid = grey. Air = whiter.
  • Reduced airway resistance.
  • Baby takes longer amount of time to get the same compliance.
77
Q

Regulation of breathing

A
  • Normal rhythm = baby needs to regulate its breathing. Comes from
    • Inspiration = inspiratory muscle contraction
    • Passive expiration
    • Active expiration
  • Generated in respiratory centre
    • Ventrolateral brainstem
  • These areas tell us about the co2 content in our blood. Measure how rhythmic our breathing is.
78
Q

Control of breathing in new borns - how?

A
  • Normal rhythm = baby needs to regulate its breathing. Comes from
    • Inspiration = inspiratory muscle contraction
    • Passive expiration
    • Active expiration
  • Generated in respiratory centre
    • Ventrolateral brainstem
  • These areas tell us about the co2 content in our blood. Measure how rhythmic our breathing is.
79
Q

Control of breathing - in prematurity

A
  • The respiration centre is less well developed
  • Very immature neonates responds like fetus = apnoea
  • Cold babies do not have initial hyperventilation
  • Sometimes, premies just stop breathing
  • Because the response to hypoxia = blunted. Can lead themselves to hypoxic situations & start breathing less.
  • Hyporegulation
  • Can stop this happening by giving them caffeine. Improves neurological outcomes.
  • Hypoxic fetus = start redirecting blood flow to the vital organs and not to the stomach etc. If babies are born because of obstructive labour
80
Q

Neurological adaptation of breathing

A
  • The respiration centre is less well developed
  • Very immature neonates responds like fetus = apnoea
  • Cold babies do not have initial hyperventilation
  • Sometimes, premies just stop breathing
  • Because the response to hypoxia = blunted. Can lead themselves to hypoxic situations & start breathing less.
  • Hyporegulation
  • Can stop this happening by giving them caffeine. Improves neurological outcomes.

Hypoxic fetus = start redirecting blood flow to the vital organs and not to the stomach etc. If babies are born because of obstructive labour.

81
Q

Structural maturation in newborn respiratory system?

A

there is branching and increased alveoli

82
Q

what is the fetal circulation

A
  • Interface between mother and baby = placenta. Baby picks up o2, nutrients + gets rid of waste across the placeenta. This is controlled by diffusion and active transport
83
Q

describe adult Hb

A
  • 2 alpha chains, 2 beta chains

- Iron molecule attached to the porphyrin ring that is in the middle.

84
Q

describe fetal Hb

A
  • 2 alpha chains, 2 gamma chains

- Primary Hb in the fetus is fetal Hb.

85
Q

how does Fetal haemoglobin behave?

A
  • HbF binds oxygen with greater affinity than HbA - allows oxygen to be transferred from mother to baby across the placenta.
  • Adult Hb at a higher o2 level is better saturated. Baby Hb = lower o2 is better to get more o2.
86
Q

2,3 Diphosphoglycerate actions

A
  • Binds to deoxygenated Hb with greater affinity than oxygenated Hb, + promotes the release of oxygen

Venous side
Ø Hb has to be able to discharge o2.
Ø Higher temp, pH, Co2 & 2,3 diphosphoglycerate (which is a biproduct of glycolysis.)
Ø Once the oxygen starts to come off the Hb promotes further release
Ø Then can be carried to the lung
Ø Fetus = less 2,3 DPG.
• Fetal Hb binds oxygen much better than Adult Hb. Transfer of O2 from the mother to the baby.

87
Q

HbF and 2,3 DPG actions?

A
  • 2,3 DPG does not bind to HbF as effectively as it can bind to HbA

So HbF binds o2 with more affinity than to HbA

88
Q

describe umbilical vein flow and hepatic circulation via ductus venosus goes to IVC

A

Ø Comes back to baby throughout umbilical vein.
Ø Venous side = higher circulation than the arterial circulation.
Ø About 50% of oxygenated blood goes to the liver because it is so metabolically active & needs a higher oxygen supply.
500/60% circulation goes to the heart and goes to the ductus arteriosus which is a fetal connection that we do not have.
Ø Blood from the placenta coming into the IVC –> RA –> ustation valve which directs blood through a hole in the 2 atria (foramen ovale).
Ø Get most oxygenated blood going through the foramen ovale into the LA.

Bulk of the blood goes from IVC –> RA –> hole through the R/L atrium –> LA

89
Q

describe Transition circulation for a newborn?

A
  1. Placental circulation will stop, umbilical vessels will constrict and stretch + rise in o2 tension
  2. Shunts close - flow via ductus venosus falls, fall in venous return through IVC
    • IVC and SVC flow = all coming through the LA, rather than half of the cardiac output
    • Hole between the right and left atrium (foramen ovale) starts to close.
  3. Pulmonary vascular resistance falls - lung expansion, pulmonary stretch receptors, increased oxygen tension, and an 8-10x rise in blood flow.
90
Q

what happens when there is Shunt closure in the newborn?

A
  • Foramen ovale: fall in PVR, leads to a rise in venous return to the left atrium, RA and LA pressures equalise, flap of foramen ovale is pushed against atrial septum
  • Ductus arteriosus: fall in PVR leads to bidirectional flow in DA, mechanism of DA closure, oxygen rise
91
Q

what is Thermoregulation

A
  • Finding a balance
  • Babies lose heat more easily than adults. Surface area : volume ratio decreases with age = makes it harder to get so cold.

Percentage body fat also increases with age.

92
Q

why are Neonates at high risk of heat loss and hypothermia

A
  • Cold babies could have a poor outcome, and are 2.5 - 3x higher surface area to body weight ratio
  • Less insulation as subcutaneous fat

Reduced ability to generate heat

93
Q

explain Reduced Thermogenesis in babies

A
  • Movement - babies will start to do more movements.
  • Brown fat burning
    • Rather than producing ATP there is uncoupling of this process and you get heat production instead.
  • Non shivering, thermogenesis (babies are not very good at shivering)
  • Highly vascular
  • Sympathetic innervation - when baby gets stressed, starts to switch to the method of heat production that burns fat.
  • Increased mitochondria content

Can double heat production

94
Q

describe Thermal stress in the Thermo neutral environment

A
  • Energy needed to maintain normothermia
    • Can occur with normal core temperature
    • Baby uses energy to maintain a normal temperature,
      (overheated or cold)

There is a zone, called the thermoneutral zone which uses the minimum amount of energy

95
Q

what is the Thermo neutral environment

A
  • Minimises energy use to maintain core temperature, 36.5-37.5 degrees Celsius
  • Thermoneutral range varies with age and dress
  • Naked 32-35degrees Celsius, dressed 24-27 degrees Celsius
  • Critical temperature
96
Q

what are the mechanisms of heat loss?

A
  • Radiation, convection, evaporation, conduction
  • Skin to skin contact = effective at keeping the baby warm and is especially effective for term babies
  • Preterm babies = radiant heater (but every ml of fluid that the baby loses causes a fall in temperature) - but them in a plastic bag and create a greenhouse effect.
97
Q

describe fluid balance with age?

A
  • Total body water falls with age.
  • Distribution of body water in a term newborn infant changes with time. From birth to adulthood = total body water falls and ICM rises, with ECF falls.
  • In the first week the baby has big fluid shifts therefore it is normal for them to lose weight in the first week of life.
98
Q

describe some of our Fluid loss mechanisms

A
  • Via stools = 5mls/kg/day
  • Respiratory tract depends on temperature + humidity of inspired gas
  • Respiratory rate, tidal volume, dead space
  • Skin changes = fluid loss in a baby at the edges of viability can be high.
  • Also via the kidneys
99
Q

WHAT IS KARLBERGS ICP MODEL?

A
  • ICP = Infancy, Childhood + Puberty Model, mathematical method of breaking down growth
  • Components of the human growth curve from birth to adulthood = strongly reflect the different hormonal phases of the growth process

Model = improved instrument for detecting + understanding growth failure

100
Q

The hormone influence of the hypothalamo pituitary axis on the growth plate

A
  • Pituitary gland responds by release of GH.

Has GH receptors

101
Q

What is Puberty?

A
  • Transition from childhood, to achievement of adult stature
  • Through development of secondary sexual characteristics
  • Influenced by
    • Genetic, Nutritional, Environmental, Socioeconomic factors
  • Average age of onset
    • Female = 11 years
    • Male = 12 years
102
Q

What is a fetus

A

From the 10th gestation week developing organism = foetus. All major structures are already formed in the foetus and continue to grow + develop

103
Q

explain + list the Growth factors in fetal life?

A
  • IGF1 + IGF2
  • Fetal insulin = Modulates the expression of fetal IGF
  • Fetal glucocorticoin = Tissue differentiation and prenatal development of the organs such as: lungs (surfactant maturation)
  • TH
104
Q

describe the Physiology of the hypothalmic-pituitary- gonadal axis, in puberty.

A

Ø The neuropeptins act on the hypothalamus.
Ø LH and FSH is released.
Ø Estrogen and testosterone influence growth in puberty
Ø Once Estrogen + testosterone is the cause of the fusion of the growth plates.

105
Q

describe the physiology of puberty

A 
- During puberty there is reactivation of the HPG axis 
	• NT 
		○ Kisspeptin + 
		○ Neurokinin B + 
		○ MKRN3 -
		○ Signalling on its receptors in the hypothalamus 
- Increased amplitude of GnRH pulses 
- Initially nocturnal 
- Later day time as well 
- Activate the gonadotropic axis for FSH, LH synthesis 
- Feedback to the hypothalamus
	• To amplify GnRH release
106
Q

explain Canalisation

A
  • Infants and children stay within 1-2 growth centiles. Therefore any crossing of height centiles warrants further evaluation
  • Crossing centiles = normal event in child development. In clinical setting crossing centiles should be taken seriously.
107
Q

What does Pubertal growth begin with

A
  • Begins with the activation of the hypothalmic-pituitary-gonadal axis
108
Q

What does Pubertal growth end with

A
  • Ends with attainment of reproductive capability + acquisition to adult body composition
  • Growth consists of acceleration, then deceleration, and then the eventual cessation of growth, with closure of epiphyses.
109
Q

describe Skeletal growth process

A
  • This is not just bone elongation + enlargement - depends on the nutritional environment.
  • Starts growth on outside. Bone width increases, as layers are put on the outside (SUB PERIOSTEAL APPOSITION) = putting layers on the outside
  • There are environmental + genetic influences
  • Subperiosteal apposition, endosteal resorption - bone inside is resorbed
  • Remodelling of the growth plate which gives it structure on the outside
110
Q

What are the factors effecting skeletal growth?

A
  • GH : influences bone growth. Produces IGF1 which has receptors on the bone and helps with mineralisation

There is calcium retention and mineralisation.

111
Q

Definition of Growth Hormone + characteristics

A
  • Acts on GH receptor and IGF1 receptor
  • Increases mitosis rate of chondrocytes + osteoblasts
  • Increases rate of protein synthesis (collagen, cartilage matrix + the enzymes for cartilage + bone formation)
  • Cartilage is laid down and the bone is formed under the influence of growth hormone. Estrogen and testosterone complete the growth by acting on the growth plate and retain the calcium in form.
112
Q

Parathyroid hormone characteristics

A
  • Increases resorption rate of calcium from the bones, to the blood
  • Therefore raises blood calcium levels + increases the absorption of calcium, by the small intestine and the kidneys
113
Q

What does calcitonin do?

A
  • Decreases the reabsorption of calcium from the bones

- Therefore lowers levels of blood calcium

114
Q

What are the roles of oestrogen + testosterone

A
  • Promotes the closure of the epiphyses of the long bones
  • Therefore stops growth. Helps retain calcium in the bones
  • Thereby maintains a strong bone matrix
115
Q

What is skeletal dysplasia?

A
  • Affects linear growth. Can have influence in foetal life. Child with these has:
  • Disproportionate short stature
  • Heterogenous - short limb + short trunk
  • Abnormalities of cartilage + bone growth
116
Q

what is Psychomotor development?

A
  • Progressive attainment of skills that involve both mental and muscular activity

Ability to turn over, sit, crawl @ will and toddler to walk, talk and control their bladder and bowel functions + solve cognitive problems

117
Q

Formation of the CNS1 - embryogenesis

A

Formation of the neural tube 2. Development of Prosencephalon

118
Q

what is Anencephaly?

A
  • An = without
  • Cephl = brain
  • Failure of the anterior neural tube to close
  • More common in girls. Lack of the telencephalon, (largest part of the brain) that is mostly the:

Cerebral hemispheres like the neocortex etc

119
Q

what is Myelomeningoceoele ?

A
  • Worst type of spina bifida you can get
  • Lumbar region because there is incomplete closing of the back bone and the membranes around the spinal cord
  • Spinal cord protrudes through this opening
  • Lesion high up = hydrocephalus
  • Lower down = kyphoid scolosis
120
Q

what is Holoprosecephaly?

A
  • Brain does not have any hemispheres - failure to split
  • Defects occur in brain structure and function
  • There is a range of severities
  • Milder types = horrible facial defects that can affect face and lips
  • Can get one single eye + missing nose

No cure :(

121
Q

Development of the CNS2 - steps involved in neuronal development

A
  1. Proliferation of the neurones
    - Total complement proliferation
  2. Migration
    - Neurones go where they need to ==> CNS
  3. Organisation
    - Events.. = all circuits are linked up around the brain
    Then myelination
    - Neurospecfic membrane
    - Brain grows rapidly in thee first few months of life and there is development of the dendritic branches
    - Early adult hood = brain mass falls.
    - Decreased brain mass = less able to process information + less reflex ability etc
122
Q

Biological influences on development

A
  • Inherited characteristics like cognitive potential and temperament
  • Antenatal and perinatal history
  • Vision and hearing

This is the potential that the child will have

123
Q

Environmental influences on development

A
  • Opportunities. Support, Parenting, education
  • Threats like socioeconomic development
  • Experience and encouragement
124
Q

give examples of some Primitive reflex pathways

A
  • MORO = hold baby up w one hand and then drop the baby and let their head go from one side to the other
  • Rooting
  • Grasp = hold onto fingers

Placing = hold baby up vertically and put the feet up to hard surface then they will start “walking” and putting one foot up and down

125
Q

what is Global delay - delay in all 4 areas?

A
  • This is delay in 2+ areas of development, widespread problem of brain structure, genetic disorder, asphyxial (o2 starvation that has caused issues w brain development), infective (meningitis), trauma if have been dropped
    • Sensory input, severe neglect
126
Q

what is Specific delay - delayed in just one of the area?

A
  • Severe neglect
  • Specific part of the brain = speech delay, some blindness: birth hypoglycaemia.
  • Defect of effector units, myopathies and neuropathies
  • Defects of sensory organs = blindness and deafness

Semester 4 (10 decks)

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