Growth Flashcards

1
Q

Why are children regularly measured

A
  1. As normal growth and development is a sign of a healthy child, abnormal growth can indicate that there is an underlying condition
  2. Measuring children allows an opportunity for health promotion with families
  3. Regular measurement reassures parents
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2
Q

What do regular measurements include?

A

Regular measurements include weight, height (<2 lying, >2 standing), and occipito-frontal head circumference.

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3
Q

How do UK growth charts work?

A

Standard UK growth charts exist for height and weight, and are separate for girls and boys. These were plotted by measurement of cross-sectional data of thousands of children at different ages at one point in time
- Growth charts are matched for age, gender, health, nutrition, and (from >4 years) ethnicity
- Allowances are made for prematurity (<37 weeks’ gestation) for the first 2 years by plotting actual age and then drawing an arrow to adjust to gestational age
o The adjustment is from weeks born before 40 weeks

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4
Q

Interpreting growth charts

A

Children tend to grow following a centile or parallel to a centile, therefore crossing centiles implies excess growth or growth failure (including early and late puberty)

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5
Q

How is failure to thrive defined?

A
  • Failure to thrive is defined as growth that crosses two centile lines on a growth chart. This is an indication of ill health and should be investigated
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6
Q

What are height velocity charts?

A

Height velocity charts also exist, ideally heights are measured at least 6 months apart, and these again follow a normal distribution. A child needs to grow with a height velocity above the 25th centile to maintain their position on a linear growth chart
- Growth failure is therefore defined as a height velocity below the 25th centile over at least 18 months. This should be investigated

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7
Q

How is mid parental height calculated?

A

If the mid-parental height ((mother’s height + father’s height)/2 + 7cm for boys, - 7cm for girls) is also >2.6 standard deviations from normal, there is likely to be no pathology

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8
Q

When else should you investigate growth further

A

A marked discrepancy between height and weight centiles is also an indication to investigate further

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9
Q

How is BMI calculated?

A

BMI is calculated as weight (KG)/ height (m)2

  • Children are overweight if their BMI is >91st centile and very overweight if their BMI is >98th centile
  • Children are underweight if their BMI is <2nd centile
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10
Q

Foetal Growth

A

Foetal growth is determined by the size of the mother and by placental nutrient supply. Hormones involved include IGF-2, HPL, and insulin

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11
Q

Infant Growth

A

The infancy component involves rapid decelerating growth in the first 2 – 3 years. This growth is determined by nutrition and is the fastest period of growth (other than foetal)
• The rate is around 18cm per year

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12
Q

Childhood Growth

A

The childhood component is the slowest phase of growth, from 2/3 years to puberty. This growth is initially determined by nutrition, but later determined by hormones e.g. GH
• The rate is around 6cm per year

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13
Q

Pubertal Growth

A

The pubertal growth spurt occurs from puberty to ~14/15 for girls and ~16/17 for boys, stopping with the fusion of the epiphyses due to oestrogen. This is determined by both GH and sex hormones
• The rate is around 10cm per year at its peak, this is typically at tanner stage III breasts in girls and 12cc testicular volumes in boys

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14
Q

Final Height

A
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15
Q

Growth Hormone Axis

A

Growth hormone release is regulated by a hypothalamo-pituitary axis. The hypothalamus initiates the axis by releasing somatostatin release inhibiting factor (SRIF) and growth hormone releasing
factor (GHRF) in response to neurotransmitters, hypothalamic hormones, and other factors e.g. food, sleep, stress, exercise

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16
Q

What effect does SRIF and GHRF have?

A
  • SRIF inhibits release of GH from somatotrophs in the anterior pituitary, whereas GHRF promotes release of GH from somatotrophs
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17
Q

What effect does GH have?

A

GH has a direct effect on promotion of growth on bone, and stimulates IGF-1 production in the liver
o IGF-1 is the main effector hormone for growth, and stimulates proliferation of the epiphyseal growth plate
- SRIF, GH, and GHRF have negative feedback on the hypothalamus. GH and IGF-1 have negative feedback on the pituitary

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18
Q

What is considered short stature

A

Short stature is height >2 standard deviations from the mean (below the second centile).

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19
Q

Commonest causes of short stature

A

The commonest causes of short stature are familial short stature and constitutional delay

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20
Q

Primary Growth Disorders

A

where there is an intrinsic growth plate abnormality
o Genetic syndromes e.g. Down’s, Turner’s, Russell-Silver
o IUGR with failure to catch up
o Congenital bone disorders e.g. osteogenesis imperfecta, achrondroplasia

21
Q

Secondary Growth Disorders

A

o Psychosocial deprivation
o Malnutrition e.g. neglect, malabsorptive disease, anorexia
o Chronic disease of any form
▪ Height centile > weight
o Endocrine disorders e.g. GH/IGF-1 deficiency, steroid excess, hypothyroidism
▪ Weight centile > height, or height and weight both affected
o Medication e.g. steroids

22
Q

If child is small but following centile lines

A

consider: familial short stature, low birthweight, constitutional delay, and skeletal dysplasias

23
Q

If there is failure to thrive

A

consider: endocrine causes, chronic illness, nutritional issues, and psychosocial deprivation

24
Q

What should history include?

A

o Obstetric history e.g. prenatal complications, gestation, birthweight
o Feeding history and nutritional history
o Developmental milestones
o Family history of growth patterns
o Systems review for underlying chronic disease

25
Q

What should examination include?

A
  • Examination should look for dysmorphic features (chromosomal disorder), disproportionality of short stature (skeletal dysplasias), signs of chronic disease, signs of endocrine causes, and pubertal stage
26
Q

When to investigate?

A

If there are no features of disease, and the child is following their genetic growth potential, review in 12 months and calculate growth velocity. If this is reduced, investigate

27
Q

What investigations should be carried out?

A
Hand and wrist X ray
FBC, U&amp;Es
Bone Profile
TSH
Karyotype
EMA &amp; TTG Antibodies
CRP/ESR
GH provocation tests
IGF-1 Measurements
Dexamethasone suppression test
MRI Head
Skeletal Survey
28
Q

What does hand and wrist x ray tell you?

A

This can identify bone age, which has a marked delay in hypothyroidism and GH deficiency. There is a moderate delay in constitutional delay, and no delay in familial short stature

29
Q

What does FBC tell you?

A

Anaemia may occur in coeliac/IBD

30
Q

What do U&Es tell you?

A

Renal Disorders

31
Q

What does a bone profile tell you?

A

Renal and bone disorders

32
Q

What does TSH tell you?

A

Hypothyroidism

33
Q

What will karyotyping tell you?

A

Tuner’s syndrome and other chromosomal disorders

34
Q

What will EMA and TTG antibodies tell you?

A

Coeliac

35
Q

What will CRP/ESR tell you about?

A

IBD

36
Q

What GH provocation tests are there and what can they tell you?

A

Insulin Deprivation Test, Glucagon test

Tells you about GH deficiency

37
Q

What does IGF 1 measurement tell you?

A

Disorders of the GH axis

38
Q

what does MRI head tell you

A

Exclude Intracranial Tumours

39
Q

What will dexamethasone suppression test tell you?

A

Cushing’s

40
Q

What will skeletal survey tell you?

A

Scoliosis

41
Q

Constitutional Delay: Who does it occur in

A

Constitutional delay in growth and puberty is familial, and usually has occurred in the parent of the same sex. This is more common in males

42
Q

What is constitutional delay?

A

Rather than an abnormality, it is a variation in the normal timing of puberty and the child will reach normal height. However, it can be psychologically distressing and if this is the case, the onset of puberty can be induced with androgens or oestrogens

43
Q

Features of constitutional delay

A
  • The legs with be proportionately long, relative to the back
  • Growth charts will be low initially, and then cross centile lines at puberty to a normal final height. Familial short stature will be low throughout.
44
Q

GH deficiency

A

Growth hormone deficiency may be an isolated deficit, or it may be secondary to pan-hypopituitarism. It can also be due to Laron syndrome (defective GH receptors), or disorders of the GH-IGF1 axis

45
Q

Causes of pan-hypopituitarism

A

craniopharyngioma, head trauma, meningitis, and cranial irradiation

46
Q

How is GH deficiency treated?

A

treated with subcutaneous injections of GH (also indicated in IUGR with growth failure, Turner’s, and renal failure). This improves muscular strength and body composition as well as vertical height
- Discontinue when the child reaches their final height, or if their growth velocity increases by <50% from baseline in the first year of use

47
Q

Non organic failure to thrive

A
  • Non-organic failure to thrive is associated with a broad spectrum of psychosocial and environmental deprivation, including inadequate availability of food
48
Q

Organic causes of failure to thrive

A

o Inadequate intake due to impaired suck/swallow, cleft palate
o Inadequate retention due to vomiting and GORD
o Increased nutritional requirements due to chronic illness in general
o Failure to utilise nutrients e.g. syndromic disorders
o Impaired nutrient absorption