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Semester 4 Revision > Growth > Flashcards

Growth Flashcards

1
Q

What does the foetus use as fuel when it is near term?

A
  • uses ~5g glucose/kg/d
  • substrates are principally glucose and amino acids
  • insulin is the dominant hormone
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2
Q

What are the actions of insulin?

A
  • increased glucose uptake in muscle, fat and liver
  • decreased lipolysis
  • decreased amino acid release from muscle
  • decreased gluconeogenesis in liver
  • decreased ketogenesis in liver
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3
Q

What are the energy stores by weight in a baby?

A

about 1% glycogen

about 16% fat

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4
Q

How are stores converted to fuels?

A

Anabolic actions of insulin are opposed by the counter-regulatory (catabolic) hormones:

  • glucagon
  • adrenaline
  • (cortisol)
  • (growth hormone)
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5
Q

What is the glucagon surge?

A
  • as plasma glucose levels fall at birth, plasma glutton levels rise rapidly
  • this activates gluconeogenesis, opposing insulin
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6
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 (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
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7
Q

What happens in the oxidation of fat?

A
  • terminal two carbon group removed from fatty acid and bound to coenzyme a, ax acetyl CoA (beta oxidation)
  • acetyl groups can then be utilised to form ketone bodies (acetone and beta hydroxybutyrate)
  • acetyl groups can also enter the kerb’s cycle as an energy source
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8
Q

How care ketone bodies formed?

A
  • beta oxidation removes 2-carbon units

- these are used to make ketone bodies

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9
Q

What happens in the fasting (post-absorptive) state?

A
  • substrates are mobilised peripherally through action of counter-regulatory hormones
  • insulin is opposed
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10
Q

What happens in the fed (post-prandial) state?

A
  • infant diet is 50% fat and 40% carbohydrate
  • CHO is mainly lactose
  • breast milk contains a lipase
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11
Q

What happens as a result to babies who have problems in terms of switching fuel supply?

A
  • demand exceeds supply
  • hyperinsulinism
  • counter-regulatory hormone deficiency
  • inborn errors of metabolism
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12
Q

What does the extremely small preterm baby require?

A
  • high demand
  • small nutrient stores
  • immature intermediary metabolism
  • establishment of enteral feeding delayed
  • poor fat absorption
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13
Q

What does the IUGR baby have?

A
  • high demands (especially brain)
  • low stores (liver, muscle, fat)
  • immature gluconeogenic pathways
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14
Q

What are the results on an infant of a diabetic mother?

A
  • high maternal glucose
  • therefore high fatal glucose
  • fetal and neonatal hyperinsulinism
  • neonatal macrosomia and hypoglycaemia
  • look chubby in the face like the michelin man
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15
Q

What are other causes of hyperinsulinism (other than diabetic mother)?

A
  • beckwith wiedermann

- islet cell dysregulation: nesiodioblastoma

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16
Q

What are symptoms of beckwith wiedermann?

A
  • macroglossia (large tongue)
  • macrosomia
  • midline abdominal wall defects (exomphalos, umbilical hernia, diastasic recti)
  • ear creases or ear pits
  • hypoglycaemia
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17
Q

What are other deficiencies of counter regulatory hormones?

A
  • hypothalamic-pituitary-adrenal insufficiency: septo-optic dysplasia
  • waterhouse-friderichsen: severe adrenal haemorrhage with adrenal gland dysfunction secondary to sepsis or hypoxia
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18
Q

What are causes of neonatal hypoglycaemia?

A
  • glycogen storage disease (usually type I)
  • galactosaemia
  • MCCAD (medium chain acyl-CoA dehydrogenase deficiency)
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19
Q

What is glycogen storage disease (type I)?

A
  • deficiency of glucose-6-phosphatase
  • hypoglycaemia and lactic acidosis in newborn
  • hepatomegaly in older child
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20
Q

What is 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 (Gal-1-put) which is missing in Galactosaemia, leading to toxic levels of galactose-1-phosphate
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21
Q

What does galactosaemia present with?

A
  • hypoglycaemia
  • jaundice and liver disease
  • poor feeding and vomiting
  • cataracts and brain damage
  • E Coli sepsis
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22
Q

What is the basic anatomy of the breast?

A
  • about 20 radially arranged lobes with duct system draining down to nipple
  • more recent evidence suggests about 9 lobes (4-18) are functional, the rest are vestigial
  • each lobe can be considered a separate functional unit
  • non-lactating breast about 50% fat, lactating breast about 30% fat
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23
Q

What is the mammary gland drainage system?

A
  • ductal sytem drains into ‘lactiferous sinuses’ beneath areola of the breast
  • sub cutaneous, intraglandular and retromammary fat deposits
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24
Q

What is the in vivo anatomy of the lactating breast?

A
  • ‘lactiferous sinuses’ not found
  • about 9 ducts emerge at the nipple
  • the ducts are tortuous and branch near the nipple
  • about 70% of glandular tissue within 8cm of the nipple
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25
Q

What is the structure of the mammary glands?

A
  • mid-trimester view
  • basic secretory unit is the alveoli set within connective tissue structure
  • lined by mammary epithelial cells (cuboidal or low columnar)
  • myoepithelial cells surround the alveoli
  • these are contractile and responsible for milk ejection
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26
Q

What preparation for breast feeding is done during pregnancy?

A
  • ‘lactogenesis I’
  • placental lactogen and prolactin promote development of the breast
  • progesterone and oestrogen inhibit milk secretion
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27
Q

What is lactogenesis postpartum (lactogenesis II)?

A
  • fall in progesterone ad oestrogen levels reduces inhibition
  • suckling stimulus releases prolactin driving milk synthesis
  • suckling (and higher centres) release oxytocin driving milk ejection
  • some autocrine inhibition from duct cells

if you do not remove milk from the breast you will not make more.

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28
Q

What controls milk synthesis?

A
  • prolactin released in response to sucking
  • milk synthesis is led by infant demand

suckling causes more synthesis of milk for next feed.

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29
Q

What is the ‘let down’ reflex?

A
  • oxytocin release causes milk ejection
  • reflex may become conditioned

sends signal to hypothalamus, to posterior pituitary which will release oxytocin. Control from higher centres, still get let down reflex when baby cries.

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30
Q

How do drugs suppress lactation?

A
  • decrease prolactin secretion
  • dopamine agonists
  • eg bromocriptine, cabergoline
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31
Q

How do drugs augment lactation?

A
  • increase prolactin secretion
  • dopamine antagonists
  • eg domperidone, metoclopramide
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32
Q

What is the secretory pathway?

A

major nutritional component in milk is protein which is packaged in a vesicle to the golgi where calcium and phosphate are added, lactose is synthesised. Lactose can’t travel across so goes in later. The vesicle fuses with the cell membrane and the contents go into the limen

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33
Q

What are the components of breast milk?

A
  • nutrients – macronutrients and trace elements (low “solute load”)
  • immunoglobulin (secretory IgA)
  • cells (macrophages and lymphocytes)
  • non-specific immune components
  • growth factors
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34
Q

What changes occur to the volume and composition of breast milk?

A

Can produce enough milk to fully feed child to 6 months of age. Initially milk has lower levels of lactose which will increase over time. Salt and other ions will drop over time.

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35
Q

What changes in milk composition occur during the feed?

A

Fat concentration increases as the baby feeds. If baby not growing well, can express the milk first then use the hind milk for the baby to help it to grow

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36
Q

What is the nutritional value of breast milk?

A
    • Protein
  • human milk: whey 70%, casein 30%, cows milk: whey 18%, casein 82% (casein low solubility in acid media)
  • lactoferrin, lysozyme and sIgA are whey proteins important in host defence
    • Lipids
  • human milk contains LCPUFA important for brain/retinal development (AA, C20, n-6, DHA, C22, n-3). Cow’s milk contains only C18 LCPUFA, linoleic (n6) and linolenic (n3) precursors
  • bile salt activated lipase
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37
Q

What is the GI benefits of breastmilk?

A
  • human milk improves gastric emptying

- human milk is important in preventing NEC in the preterm infant

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38
Q

What are the immunological benefits of breastmilk?

A

bugs really like iron, so when iron is removed there is less bacterial growth - lactoferrin, trying to stop sepsis. (lactoferrin: inhibits bacterial growth by binding iron)

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39
Q

What effects do the various immune factors have?

A

sIgA: specific immune response, binds bacterial adherence sites

Complement: C1 to C9 present in low concentration milk, with high amounts of C3 (able to opsonise bacteria in conjugation with IgA)

Lactoferrin: inhibits bacterial growth by binding iron

Lysozyme: cleaves peptidoglycans of bacterial walls

Cytokines: anti-inflammatory cytokines predominate in human milk, allows human milk to protect but not injure the gastrointestinal tract

PAF acetylhydrolase: inhibits platelet activating factor

Oligosaccharides: inhibit binding of enteric/respiratory epithelium

Cellular elements: neutrophils and macrophages

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40
Q

What are the short term benefits of breastfeeding?

A

• Improved immunity, less infections and infectious morbidity
- Gastro-intestinal infection: dujits et al, 2010, Dutch study
- Respiratory infections: galton bachrach VR et al (2003). Developed world study
- Urinary tract infections (Marild S et al (2004)). Swedish study
SIDS: the German study of sudden infant death is a case-control study of 333 infants who dies of sudden infant death syndrome. This study shows that breastfeeding reduced the risk of sudden infant death syndrome by about 50% at all ages throughout infancy and for as long as the infant is breastfed

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41
Q

What are the long term infant benefits of breastfeeding?

A

• Type 1 and 2 diabetes
• Obesity: breastfeeding has been found to generally reduce the risk of obesity
• Allergic disease: there is evidence that breastfeeding for at least four months, comparted with feeding infant formula made with intact cow’s milk protein, prevents or delays the occurrence of atopic dermatitis, cow’s milk allergy, and wheezing in early childhood
• Childhood leukaemia: a meta-analysis has concluded that both short term and long term breastfeeding reduce the risk of childhood acute lymphoblastic leukaemia (ALL) and acute myeloblastic leukaemia (AML).
• Cholesterol levels: adolescents have a reduction of 14% in their ratio of LDL to HDL cholesterol if they were fed breastmilk in infancy.
Blood pressure: a review from the USA investigated the effects of breastfeeding in developed countries

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42
Q

What are the benefits of breastfeeding for the mother?

A

• Breastfeeding releases oxytocin, which causes the uterus to contract, and reduces the risk of postpartum haemorrhage
Women who breastfeed are at lower risk of:
• Breast cancer: good evidence to suggest that breastfeeding protects against breast cancer
- 47 epidemiological studies including 50,000 controls and 97,000 cases showed a 4.3% decreased risk of breast cancer with duration of lactation (95%Cl: 2.9-5.8, p

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43
Q

What are the primitive reflexes?

A

Rooting and suckling.

rooting: touch cheek and baby turns to the side of the stimulus - this is a reflex

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44
Q

What are the signs of good attachment?

A
  • Mouth wide open
  • Mouth full
  • Chin is close to breast
  • Lower lip everted
  • Suching changes
  • More of the areola is visible above the baby’s mouth than below

Positioning is the relationship between the baby’s body and the mother’s

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45
Q

What are the patterns of sucking?

A

Non-nutritive sucking – short bursts of sucking, 5 seconds?

Nutritive sucking – long periods of sucking

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46
Q

What can happen when latching-on goes wrong?

A
  • Incorrect positioning and attachment
  • Traumatised nipple
  • Ineffective breast drainage
  • Leads to infection of breast tissues or ‘mastitis’
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47
Q

What is required for lung development at birth?

A

Simultaneous growth

  • Vascular elements
  • Tubular airway elements
  • Different cell types

Variety of growth factors required

  • Hepatocyte nuclear factor 3beta – foregut
  • Fibroblast growth factor-10, sonic hedgehog, bone morphogenetic protein 4 (BMP4) – outgrowth of new end buds
  • Gli proteins – branching
  • Vascular endothelial growth factor (VEGF) – angiogenesis
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48
Q

What alveolar development occurs at birth?

A
  • 24 weeks, saccules develop: capillaries develop around each (VEGF)
  • 32 weeks, shallow indentations
  • most development post term: mainly by growth in number, adult numbers by 4 years
  • Pneumocytes: type 1 and 2 presetn at 22 weeks, from 24 weeks lamellar bodies are present
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49
Q

What is the secretion of lung liquid?

A
  • secondary active transport of Cl from interstitium to lumen Na and H2O passive
  • liquid production allows for positive pressure of 1cmH2O
  • lung fluid is required for lung growth but not branching
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50
Q

What is the absorption of lung liquid?

A
  • active sodium transport in apical membranes
  • labour and delivery: adrenaline release reduced secretion and resorption begins
  • thyroid hormone and cortisol required for maturation of the foetal lung response to adrenaline
  • exposure to postnatal oxygen increases sodium transport across the pulmonary epithelium
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51
Q

What are examples of lung liquid pathology?

A

Oligohydramnios

  • early rupture
  • kidney abnormalities

Foetal breathing abnormalities

  • neuromuscular disorders
  • phrenic nerve agenesis
  • CDH
  • Foetal breathing slows lung liquid loss – maintains expansion

Delivery without labour
- Elective caesarean section – TTN (transient tachypnoea newborn)

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52
Q

About surfactant…

A

Produced by type 2 pneumocytes

  • Surfactant phosphatidylcholine (PC) produced in endoplasmic reticulum
  • Stored in lamellar bodies

Degraded in alveoli

  • Absorbed and recycled by alveolar cells
  • > 90% PC is reprocessed
  • turbover time is 10 hours

Negative feedback system to regulate release

  • also stretch receptors
  • B adrenergic receptors on type 2 cells – increases with gestation
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53
Q

Why do we need surfactant?

A
  • Prevents atelectasis – reduces work to breathe
  • Achieved by reduced surface tension solid at body temperature – becomes a solid monolayer, stabilises alveoli
  • Laplace equation internal pressure = 2xsurface tension/radius
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54
Q

What is surfactant?

A

• Mix of phospholipids, neutral lipids and protein
• Lipids most important:
- PC comprises ~80%, PG ~10%
- 60% PC disaturated, predominantly palmitic acid
- therefore dipalmitoyl phosphatidycholine is the major component of surfactant

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55
Q

What is the composition of surfactant?

A

other lipids: neutral lipids such as cholesterol, alters fluidity of membranes

proteins: 4 types, SP-A……D. 5-10% of surfactant by weight

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56
Q

What is SP-A?

A
  • large glycol protein
  • gene on chromosome 10, only expressed in lung
  • increased production after 28 weeks
  • essential in: determining structure or tubular myelin, stability and spreading of phospholipids, negative feedback loop
57
Q

What is SP-B?

A
  • 1-2% of surfactant by weight
  • gene on chromosome 2
  • glucocorticoids increase expression
  • required for: formation of tubular myelin, spreading, combined with lipid mixtures – most of the surface activity in vitro and increases lung compliance in vivo, protects surfactant film from inactivation by serum proteins
58
Q

What are SP-C an d SP-D?

A

SP-C

  • chromosome 8
  • 35 amino acids
  • significantly enhances adsorption and spreading on phospholipids

SP-D

  • molecular weight of 46000
  • increased expression with gestation
  • expression is widely distributed in epithelial cells
  • no significant surfactant activity
  • immune function
59
Q

What causes surfactant maturation?

A
  • glucocorticoids
  • thyroid hormones
  • insuline
60
Q

How do glucocorticoids cause surfactant maturation?

A
  • increased production at the end of gestation
  • increases DPPC
  • dexamethasone enhances beta2-adrenoceptor gene expression – leads to increased surfactant secretion
61
Q

How do thyroid hormones cause surfactant maturation?

A
  • T4 increases surfactant production
  • T3 crosses placenta
  • TRH increases phospholipid independent of T3,4
62
Q

How does insulin cause surfactant maturation?

A
  • Delays maturation of type 2 cells, decreases % saturated PC
  • Delayed PG
  • Increased sugar levels delay lung maturation
63
Q

What can cause surfactant pathology?

A

Prematurity

  • PC relatively unsaturated – unstable monolayer which buckles on expiration
  • PG replaces PI with increased gestation
  • Leaky capillary membranes – fibrin deposition – inhibits reduction off surface tension – hyaline membranes

SP deficiencies

  • SP-B: absence leads to markedly reduced PG no secretion of normal surfactant, lethal. Lung transplant possible for some
  • SP-C: interstitiallung disease
64
Q

What happens to the lungs at birth?

A
  • Lung liquid production ceases during labour
  • Fetal breathing ceases
  • Cooling stimulates breath along with other senses
  • Central chemoreceptor detection of hypoxia
  • First breath median time 10 seconds
  • High inspiratory pressure
  • Active expiration with high pressure
  • Air replaces fluid within minutes
  • Some squeezed out
  • Most absorbed into lymphatics )1 hour) and capillaries (6-24 hours)
  • Rapid fall in airway resistance, increased FRC
  • Slower increase in compliance over 24 hours
65
Q

How is breathing regulated?

A

Normal Rhythm

  • Inspiration – inspiratory muscle contraction
  • Passive expiration
  • Active expiration

Generated in respiratory centre
- Ventrolateral brainstem

66
Q

How is breathing controlled?

A

Induced by breathing hypoxic gases for 5 minutes (solid lines). The dashed line indicates that apnoea may occur in preterm infants, resembling a foetal response.

Prematurity
• Respiratory centre less well developed
• Very immature neonate responds like a foetus – apnoea
• Cold babies don’t have initial hyperventilation
• Sometimes, premies just stop breathing

67
Q

How are we built to withstand labour?

A

Neurological adaptation…

  • ? Fewer synapses and reduced oxygen requirement
  • newborn brains utilise non-oxidative glycolysis
  • utilise ketone bodies as energy source

Hypoxia leads to redirection of blood flow in the foetus

68
Q

About haemoglobin…

A
  • Adult haemoglobin
  • 2 alpha chains
  • 2 beta chains

oxygen is carried in the blood in two forms: (1) dissolved in plasma and RBC water (about 2% of the total) and (2) reversibly bound to haemoglobin (about 98% of the total).

Different globin chains form at different times through development. One alpha equivalent chain and 2 beta equivalent chains.

Red blood cells are formed by different organs at different times.

Blue: xi
Red: epsilon

  • foetal haemoglobin
  • 2 alpha chains
  • 2 gamma chains
69
Q

About foetal haemoglobin…

A
  • HbF binds oxygen with greater affinity than HbA
  • Allows oxygen to be transferred from mother to baby across placenta

At a lower level of oxygen the HbF is better saturated than adult Hb.
In a mixture ofgases, each gas has apartial pressurewhich is the hypotheticalpressureof that gas if it alone occupied thevolumeof the mixture at the sametemperature.[1]The total pressure of anideal gasmixture is the sum of the partial pressures of each individual gas in the mixture

70
Q

About 2,3 Diphosphoglycerate…

A
  • 2,3 Diphosphoglycerate binds to deoxygenated Hb with greater affinity than oxygenated Hb
  • promotes release of oxygen

In adults and older children.
By selectively binding to deoxyhemoglobin, 2,3-BPG stabilizes the T state conformation, making it harder for oxygen to bind hemoglobin and more likely to be released to adjacent tissues. 2,3-BPG is part of afeedback loopthat can help prevent tissuehypoxiain conditions where it is most likely to occur.
In pregnant women, there is a 30% increase in intracellular 2,3-BPG. This lowers the maternal hemoglobin affinity for oxygen, and therefore allows more oxygen to be offloaded to the fetus in the maternal uterine arteries. The foetus has a low sensitivity to 2,3-BPG, so its hemoglobin has a higher affinity for oxygen. Therefore although the pO2 in the uterine arteries is low, the foetal umbilical arteries (which are deoxygenated) can still get oxygenated from them.
23dpg biproduct of glycolysis

71
Q

About HbF and 2,3 DPG…

A
  • 2,3 DPG does not bind to HbF as effectively as it binds to HbA
  • so HbF binds oxygen with greater affinity than to HbA

The foetus has less 2,3 DPG. Foetal Hb binds to oxygen much better than adult Hb

72
Q

About the liver’s blood supply…

A

The liver needs a high oxygen supply as it is very metabolically active. The blood flows through the ductus spinosus which is a foetal connection and doesn’t exist in adults. The blood then flows into the IVC and into the atrium.

The blood that flows into the IVC is joined by blood from the legs. Therefore, the blood in the IVC has a slightly lower saturation than the blood going to the liver

73
Q

What does the Eustachian valve do?

A

In foetal life, the Eustachian valve helps direct the flow of oxygen-rich blood through the right atrium into the left atrium and away from the right ventricle. The Eustachian valve directs blood through the foramen ovale.

Bulk of the blood going from IVC through into IVC into right atrium, through foramen ovale and into left atrium
The heart has various developmental stages and get the septa formed as a result between atria

74
Q

About the blood supply from the umbilical arteries downwards…

A

The umbilical arteries course downward to the internal iliac arteries before entering the aorta. They supply the buttocks and the lower extremities via the latter part of the internal iliac arteries
The umbilical vein courses upward along the falciform ligament to the underside of the liver. Here it divides into two vessels, the portal vein and the ductus venosus. The ductus venosus joins with the inferior vena cava.
Xray of preterm baby
Umbilical venous catheter – mechanism that can be used to deliver fluids to the baby
Left tube is within the aorta

75
Q

About foetal circulation…

A 
¥	Gas exchange occurs in Placenta
	Receives deoxygenated blood
	Delivers oxygenated blood
	Umbilical Vein (80-90% saturated, 4.7kPa)
¥	Preferential streaming of Oxygenated blood
	Myocardium and brain
¥	Intracardiac and extracardiac shunts
           3 shunts
76
Q

About foetal pulmonary vessels…

A

High pulmonary vascular resistance

  • Large muscle mass
  • High resting tone

Ductus Arteriosus

  • Muscular wall
  • Kept open by low Oxygen tension
77
Q

What happens to the circulation at birth?

A

¥ Placental circulation ceases
Umbilical vessels constrict: stretch and rise in oxygen tension
¥ Shunts close
Flow through ductus venosus falls
Fall in venous return through IVC
Closes over 3 – 10 days

78
Q

About pulmonary vascular resistance…

A
  • Lung expansion
  • Pulmonary stretch receptors
  • Increased oxygen tension
  • 8-10x rise in blood flow
79
Q

What causes the shunt closure?

A
  • fall in PVR leads to massive rise in venous return to left atrium
  • RA and LA pressures equalize
  • Flap of foramen ovale pushed against atrial septum
  • Fall in PVR leads to bidirectional flow in DA
  • Mechanism of DA closure: oxygen rise

¥ Foramen Ovale
Fall in PVR leads to massive rise in venous return to left atrium
RA and LA pressures equalise
Flap of foramen ovale pushed against atrial septum
¥ Ductus Arteriosus
Fall in PVR leads to bidirectional flow in DA
Mechanism of DA closure: Oxygen rise
Foramen Ovale closes within minutes to hours of birth
PGE2 production from Placenta stops
DA functional closure in 96 hours

80
Q

What can happen as a result of abnormal circulation?

A
  • Transition may not be permanent
  • Pulmonary arterioles very reactive and constrict to certain stimuli: hypoxia, hypercarbia, acidosis, cold
  • Rise in PVR and right to left shunting: foetal circulation
81
Q

What is patent ductus arteriosus?

A

If the baby is sick then the duct doesn’t close as it should. Normally it just narrows gradually, but in preterm babies it can stay open for a very long time

Asymptomatic
Continuous machinery murmur

Heart failure

  • Fast breathing
  • Increased work of breathing
  • Sweating during feeding
  • Poor feeding
  • Poor growth
  • Rapid pulse
  • Bounding pulse

if the shunt stays open then the heart has to work harder as it has to pump a lot more blood. this has knock on effects.

82
Q

What can patent ductus arteriosus be caused by?

A
  • Premature babies
  • Babies with respiratory distress
  • Down syndrome
  • Rubella
  • Congenital heart disease
83
Q

What is the treatment for patent ductus arteriosus?

A
  • indomethacin, ibuprofen

- surgery

84
Q

What is atrial septal defect?

A

Most common congenital cardiac malformation in adults.

Atrial septal defect causes left to right shunt due to the high compliance of the right atrium and the difference inpressure between the two atria. Secondary to this mechanism, the pressure in the pulmonary circulation is increased.

A person with no other heart defect, or a small defect (less than 5 millimeters) may not have symptoms, or the symptoms may not occur until middle age or later

85
Q

What are the symptoms of an atrial septal defect?

A
  • Difficulty breathing (dyspnea)
  • Frequent respiratory infections in children
  • Feeling the heart beat (palpitations) in adults
  • Shortness of breathwith activity

In infants, small ASDs (less than 5 mm) will often not cause problems, or will close without treatment. Larger ASDs (8 to 10 mm), often do not close and may need a procedure.
Important factors include the size of the defect, the amount of extra blood flowing through the opening, and whether the person has any symptoms.
Some people with ASD may have other congenital heart conditions. These may include a leaky valve or a hole in another area of the heart.

86
Q

What is auscultation?

A

Because the pressure in the left atria initially exceeds that in the right, the blood flows in a left to right shunt. This high volume of blood next passes into the right ventricle, and the ejection of the excess blood through a normal pulmonary valve produces the prominent mid-systolic flow murmur as heard in this sample. This murmur is best heard over the “pulmonic area” of the chest, and may radiate into the back as with the murmur of pulmonary stenosis. The most characteristic feature of an atrial septal defect is the fixed split S2. As mentioned in the murmur overview, a split S2 is caused physiologically during inspiration because the increase in venous return overloads the right ventricle and delays the closure of the pulmonary valve. With an atrial septal defect, the right ventricle can be thought of as continuously overloaded because of the left to right shunt, producing a widely split S2. Because the atria are linked via the defect, inspiration produces no net pressure change between them, and has no effect on the splitting of S2. Thus, S2 is split to the same degree during inspiration as expiration, and is said to be “fixed.”

87
Q

What as the possible complications of an atrial septal defect?

A

People with a larger or more complicated ASD are at an increased risk for developingother problems, including:

  • Arrhythmias, particularly atrial fibrillation
  • Heart failure
  • Heart infections (endocarditis)
  • High blood pressure in the arteries of the lungs (pulmonary hypertension)
  • Stroke

Chest X-ray showing an enlarged cardiac silhouette due to the right atrium and left ventricle. The mid-arch is bulged, and the pulmonary vascularity is increased

88
Q

Why are neonates at increase risk of heat loss, and what can this cause?

A

Babies have a 2.5 to 3 times higher surface area to volume ratio so more heat is lost.

Less insulation as subcutaneous fat less
Reduced ability to generate heat
-	Respiratory distress
-	Acidosis
-	Hypoglycaemia
-	Hyperbilirubinaemia
89
Q

How do babies create heat for themselves?

A
  • Non-shivering thermogenesis
  • Highly vascular
  • Sympathetic innervation
  • Increased mitochondrial content
  • Can double heat production
  • Move about more
  • The term infant also can generate some heat by shivering thermogenesis, which is an increase in non-purposeful skeletal muscle activity signaled by cutaneous nerve endings via central motor neurons. Shivering thermogenesis seems to be of secondary importance to the newborn human.
  • Heat production occurs at the cost of Oxygen consumption
  • Uncoupling protein-1
  • Brown fat
90
Q

What is thermal stress?

A
  • Energy needed to maintain a normal temperature

- Environment which minimizes energy requires to maintain core temperature (36.5-37.5^C)

91
Q

What are the various mechanisms of heat loss?

A
  • radiation
  • convection
  • conduction
  • evaporation
92
Q

What are routes of fluid loss?

A
  • Stool 5ml/kg/day
  • Kidneys
  • Respiratory tract – depends on temperature and humidity of inspired gas
  • Respiratory rate, tidal volume, dead space
  • Skin
93
Q

How do the kidneys function in fluid balance?

A
  • Full complement of 1 million nephrons by 34 weeks
  • Functionally immature at birth
  • Reduced GFR
  • Limited concentrating ability
94
Q

What are the ways of adaptation to extrauterine life?

A
  • Foetal circulation
  • Transition circulation
  • Temperature control
  • Fluid balance
95
Q

What is Kerlberg’s ICP model?

A
  • Infancy, childhood and puberty (the ICP-model) breaks down growth mathematically
  • The components of the human growth curve from birth to adulthood strongly reflect the different hormonal phases of the growth process
  • The model provides an improved instrument for detecting and understanding growth failure
96
Q

What happens up to week 10 in foetal growth?

A
  • From the 10th week of gestation the developing organism is called a foetus
  • All major structures are already formed in the foetus and continue to grow and develop
97
Q

What happens between week 10-12 in foetal growth?

A
  • The eyelids close and will not reopen until about the 28th weeks
  • Tooth buds, which will form the baby teeth, appear
  • The limbs are long and thin
  • The foetus can make a fist with its fingers
  • Genitals appear well differentiated
  • Red blood cells are produced in the liver
  • Heartbeat can be detected by ultrasound
98
Q

What happens between weeks 13-16 in foetal growth?

A

At week 15, main development of external genitalia is completed

99
Q

What happens at week 22 in foetal growth?

A
  • The foetus reaches a length of 28cm, and weighs about 500g
  • Eyebrows and eyelashes are well formed
  • All of the eye components are developed
  • The foetus has startle reflex
  • Footprints are fingerprints continues forming
  • Alveoli are forming in lungs
100
Q

What happens at week 24 in foetal growth?

A
  • The foetus reaches a length of 38cm and weighs about 1.2kg
  • The nervous system develops enough to control some body functions
  • The eyelids open and close
  • The cochlea are now developed, though the myelin sheaths in neural portion of the auditory system will continue to develop until 18 months after birth
  • The respiratory system, while immature, has developed to the point where gas exchange is possible
101
Q

What happens at week 30 in foetal growth?

A
  • The foetus reaches a length of about 38-43cm and weighs about 1.5kg
  • The amount of body fat rapidly increases
  • Rhythmic breathing movements occur, but lungs are not fully mature
  • Thalamic brain connections, which mediate sensory input, form
  • Bones are fully developed, but are still soft and pliable
102
Q

What happens at week 34 in foetal growth?

A
  • The foetus reaches a length of about 40-48cm, weighs about 2.5-3kg
  • Lanugo begins to disappear
  • Body fat increases
103
Q

What happens between week 35 +0 until week 39 +6 in foetal growth?

A
  • The foetus is considered full-term at the end of the 39th week of GA
  • Length – 48 to 53cm
  • No lanugo except on the upper arms and shoulders
  • Small breast buds are present on both sexes
104
Q

What are the growth factors that play a role in foetal life?

A
  • Insulin like growth factors (IGF2,1)
  • Foetal insulin – modulates the expression of the foetal IGF
  • Foetal glucocorticoid – tissue differentiation and prenatal development of the organs such as, for example, lungs (maturation of the surfactant), liver (control of glycaemia)
  • Thyroid hormone
105
Q

About foetal GH…

A
  • ?? effect on prenatal growth

- near normal growth in congenital hypopituitarism

106
Q

What is normal linear growth in infancy?

A
  • Rapid growth 25cm in first year with marker deceleration of growth rate
  • Depends a lot on nutrition
107
Q

What is normal linear growth in childhood?

A
  • 4-8cm per year, mild deceleration towards puberty

- hormones play an important role (growth hormone, thyroid hormone)

108
Q

What is normal linear growth in puberty?

A
  • Increased sex hormones (oestrogen and androgens), big increase in growth hormone
  • Females: starts average 2 years earlier than boys, beginning/max growth spurt: breast development, end point: menarche (slows down and stop)
  • Male: beginning: 4 mls testes, growth spurt starts: mid/late puberty with 6-10ml testes, peak height velocity: 10-12 mls testes (average 14 years)
    • Male average 12.5-14cm taller than female due to additional 2 years pre-pubertal growth, greater growth spurt
109
Q

What is canalisation?

A

According to the concept of canalisation, infants and children stay within one or two growth centiles, and therefore, any crossing on height centiles always warrants further evaluation.

Crossing of centiles a normal event in child development, though in a clinical setting crossing centiles should still be taken seriously

110
Q

What is catch up growth?

A
  • Catch-up growth is characterised by height velocity above the limits of normal for age for at least 1 year after a transient period of growth inhibition; it can be complete or incomplete
  • The increased growth rate following IUGR is usually called catch-up growth
  • Complete – results in a mean final height close to the mean target height
  • Hypotheses – the neuroendocrine and growth plate hypothesis
111
Q

What is catch down growth?

A
  • Seen in children who start off at high percentile in early infancy
  • Between 6 and 18 months of age these children show a fall on their percentile growth chart
  • Over time they match their genetic programming and then they grow at this lower percentile, but along their genetic potential
  • They have normal physical, psychological and behavioural development
  • However, a fall of more than2 major percentiles warrants investigations
112
Q

About pubertal growth…

A
  • Begins with the activation of the hypothalamic-pituitary-gonadal axis
  • Ends with the attainment of reproductive capability and the acquisition of adult body composition
  • Typically, growth consists of a phase of acceleration, followed by a phase of deceleration, and the eventual cessation of growth with the closure of epiphyses
113
Q

What is the physiology of puberty?

A

Fetal:

  • GnRH neurones arise from the olfactory placode and migrate to the hypothalamus along the olfactory tract
  • Under the control of genes eg KAL, FGF8

At Birth:
- Hypothalamic-pituitary-gonadal axis (HPG) “active”

3-6 month and rest of childhood:
- Quiescent, very low gonadotrophin levels

Puberty – reactivation of HPG axis
• Neurotrnsmitters (eg Kisspeptin (+), neurokinin B(+), MKRB3(-)) signalling on its receptors in hypothalamus
• Increased amplitude of GnRH pulses (initially nocturnal, later day time as well)
• Activate gonadotropic axis for FSH, LH synthesis
• Feedback to hypothalamus to amplify GnRH release

114
Q

About skeletal growth…

A
  • Skeletal growth – environmental and genetic influences
  • Subperiosteal apposition
  • Endosteal resorption
  • Remodelling
115
Q

What factors effect skeletal growth?

A
  • Growth Hormone: increases the rate of mitosis of chondrocytes and osteoblasts, and increases the rate of protein synthesis (collagen, cartilage matrix, and enzymes for cartilage and bone formation)
  • Parathyroid hormone: increases the resorption of calcium from bones to the blood, thereby raising blood calcium levels and increases the absorption of calcium by the small intestine and kidneys
  • Calcitonin: decreases the reabsorption of calcium from bones thereby lowering blood calcium levels
  • Oestrogen/testosterone: promotes closure of epiphyses of long bones, thereby stopping growth, and helps retain calcium in bones, thereby making a strong bone matrix
116
Q

What is skeletal dysplasia?

A
  • Disproportionate short stature
  • Heterogeneous: short limb, short trunk
  • Abnormalities of cartilage and bone growth
117
Q

What is the social influence on growth?

A
  • Growth patterns respond to environmental pressures
  • If environment supports the genetic template that regulates development, the resulting interaction is positive
  • A systemic force that interferes with the achievement of their human genetic potential
118
Q

Why do we monitor growth?

A

Public health:

  • Screening
  • Surveillance

Clinical Practice:

  • Assessment of health and nutrition
  • Diagnosis of disease
  • Monitoring of disease

Monitoring growth of whole populations gives us info on general health, nutrition and wellbeing – recognised as being an indicator of public health, poor growth due to malnutrition leads to increased risk of infections and death, plus worse school performance

As clinicians, also monitor growth of individual patients.
Helps us assess their overall health and nutrition, diagnose some diseases that present primarily as poor growth, plus monitor disease and response to treatments

119
Q

When do we monitor growth?

A
  • In the UK, no longer a universal child growth screening programme
  • Babies weighed at birth then in the first few weeks of life. Might be weighed more in the first year. Then usually not weighed routinely again.
  • Used to weigh and height at school entry.
  • Now only tends to be if there is a ‘problem’ eg go to the doctors or a hospital
120
Q

How do we monitor growth?

A
  • Weight
  • Height
  • Head circumference

There is a huge importance of correct measurements. Infants and pre-mobile children are weighed on cradle scales, electronic. Length is not very accurate below two when they can stand still. Height measurement is important. OFC is also important to assess brain growth.

• Growth chart displays the ‘normal’ range of measurements for children of all ages
• What is ‘normal’?
- Representative of a group ie reference?
- Optimal for a group ie standard?
• Does ‘normal’ depends on ethnicity/social class etc?

Once we have the measurements we plot them on a chart.

Growth charts a way of displaying data and patterns. Collect cross sectional data on growth of children at all ages. Plot out the patterns. Growth expressed in centiles, lines based on SDs from the mean. Each line represents 2/3 SD and lines are evenly spaced. Go from 0.4th centile to 99.6th centile.

Normal healthy children follow a line.
Do you think they are representative or standard? And are they affected by eg ethnicity?
New charts are optimal ie describe what growth should look like, older charts were reference

Ethnicity does affect growth, know that black babies are often heavier and have more muscle mass, South Asian origin babies are often smaller
Social class effects likely to be nutritional – dispute over whether poverty causes poor growth or in fact obesity!  Growth is not the same as nutrition.  Can weigh a lot but be malnourished
121
Q

How do we plot growth charts?

A
  • All have a 0-4 chart copy as a handout
  • Read off age
  • Read up to measurement
  • Single dot in black ink – no crosses or lines

Babies born 37-42 weeks plot at 0 on main chart
Before 37 completed weeks use preterm section on the left and transfer over at corrected age 2 weeks
To track growth we plot chronological age and corrected age ie if baby born at 34 weeks they are born 6 weeks early, so plot on prem bit until they are 8 weeks of age, then start plotting on main bit. When they are 8 weeks of age, they are 2 weeks corrected age. So dot at 8 weeks, then dotted line back and arrow head at 2 week

122
Q

What factors affect growth?

A
  • Nutrition – main influence perinatally
  • Genetics – increasingly important as get older
  • Hormones – increasingly important as get older
  • Timing of puberty – can cause feviations from your line
  • Disease
123
Q

What is the classic pattern of rate of growth’?

A
  • Rate of growth highest in fist year of life
  • Lowest around primary school age
  • Rises again at puberty
  • Falls right down when puberty ends (different ages for girls and boys)
124
Q

What are some possible problems with growth?

A
  • Faltering growth: term used in young children, weight that is crossing down the centiles
  • Short stature: term used to describe a short child who is not meeting their height potential
  • Underweight: term used for a thin older child who has a BMI less than the 2nd centile for age and gender
  • Overweight: term used to describe the child who has a BMO=I above the 91st centile for age and gender
  • Obesity: term used to describe a child who has a BMI above the 98th centile for age and gender
125
Q

About body mass index (BMI)…

A
  • Weight for height measure
  • NOT a measure of adiposity
  • Affected by other factors eg muscle mass
  • Need to adjust for age so use a centile chart
126
Q

What is anencephaly?

A

Anencephaly is the absence of a major portion of the brain, skull, and scalp that occurs during embryonic development. It is a cephalic disorder that results from a neural tube defect that occurs when the rostral (head) end of the neural tube fails to close, usually between the 23rd and 26th day following conception

127
Q

What is myelomeningocele?

A

A myelomeningocele is a defect of the backbone (spine) and spinal cord. Before birth, the baby’s backbone, spinal cord and the structure they float in (spinal canal) do not form or close normally. A myelomeningocele is the most serious form of spina bifida

128
Q

What is holoprosecephaly?

A

Holoprosencephaly is a disorder caused by the failure of the prosencephalon (the embryonic forebrain) to sufficiently divide into the double lobes of the cerebral hemispheres. The result is a single-lobed brain structure and severe skull and facial defects

129
Q

What is neurodevelopment?

A

Synapses achieve maximum density at 6-12 months after birth.

At birth: cerebral cortex primitive, neurons poorly connected.

Physical growth of nervous system: myelination of nerves and an increase in the number of connections between cells.

Myelination progresses: nervous control of various functions improve. Continues throughout childhood

130
Q

What factors influence development?

A 
Biological Influences
•	Inherited characteristics eg cognitive potential and temperament
•	Antenatal and perinatal history
•	General health
•	Vision and hearing

Developmental Progress

Environmental Influences
• Opportunities such as sensitive and supportive parenting and education
• Threats such as social and economic deprivation
• Experience and encouragement

131
Q

What developmental scales are there?

A
  • Gross motor
  • Fine motor
  • Vision
  • Speech
  • Hearing
  • Social
132
Q

What are developmental milestones?

A

The age at which major skills that are crucial to a child’s progress in each of the 4 spheres of development are achieved

133
Q

Why are scales independent?

A
  • Fine motor on gross motor
  • Gross motor on vision
  • Social on vision
  • Hearing on gross motor
134
Q

What is developmental delay?

A

Failure to acquire a particular developmental skill at an age when 95% of peers have done so.

135
Q

What are patterns of developmental delay?

A
  • global delay

- specific delay

136
Q

What is global delay?

A

Delay in 2 or more areas of development.

Widespread problem of

  • Brain structure: genetic, asphyxia, infective, trauma
  • Sensory input: severe neglect
137
Q

What are examples of specific delays?

A

Specific Part of Brain

  • Speech delay
  • Some blindness

Defect of effector units

  • Myopathies
  • Neuropathies

Defect of sensory organ

  • Blindness
  • Deafness
138
Q

What diagnostic approach is taken to developmental delays?

A
  • screening
  • evaluation of development
  • looking for causes
  • correcting the correctable
  • promoting development

Semester 4 Revision (8 decks)

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