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GDAN year 2 G&D with some aging > NORMAL AND ABNORMAL GROWTH IN CHILDREN > Flashcards

NORMAL AND ABNORMAL GROWTH IN CHILDREN Flashcards

1
Q

growth

A

A complex biological phenomenon that starts at conception and is regulated by nutritional, hormonal and genetic factors
- reaches its peak in the second trimester of pregnancy

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2
Q

3 phases of somatic growth in children

A

infancy
childhood
puberty

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3
Q

most important determinants in the pahses

A

infancy - nutrition
childhood - growth hormone
puberty - sex steroids and growth hormone

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4
Q

growth patterns in each growth phase

A

infancy - deceleration of rapid foetal growth rate
childhood - slow decoration except mid childhood adrenal spurt
puberty - pubertal growth spurt

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5
Q

measuring growth

A

growth chart

BMI

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6
Q

growth chart

A

heigth
weight
head circumference
- on chart demonstrates percentile

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7
Q

BMI

A
  • BMI = Mass (kg)/Height (m) squared
  • proxy for body fat
  • BMI for children is plotted on chart for gender and age
  • online calculator for children and adults
    BMI applications
  • identification of children above/below a healthy weight is the first step
  • used in schools and hospitals
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8
Q

bone age

A

bone is degree of maturity of a Childs bone

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9
Q

how is bone age calculated

A
  • uses standardised x rays
  • estimate the maturity of each epiphyseal centre of the LH wrist to derive a score
  • The age at which the score is on the 50th centile is the bone age of the individual
  • can be used to predict a childs future height
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10
Q

causes of short stature

A

post natally most common nutrition

  • consittutional
  • intra uterine growth retardation
  • systemic disease
  • iatrogenic
  • inherited
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11
Q

polygenetic disorder

A
  • where there is an integration in the genetic pathway and the environmental defects
  • eg cardiac disease, neural tube defects, chronic cancer
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12
Q

environmental factors

A
  • drugs/chemicals (thalidomide, epanutin, warfarin, alcohol, fluoride)
  • radiation
  • infection
  • metabolic
  • hyperthermia
  • vascular
  • amniotic bands (Where the inner layer of the placenta is damaged during pregnancy, thin strands of bands become tangled around the body restricting blood flow)
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13
Q

birth defect types

A

single/isolated defects

multiple defects

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14
Q

single birth defect

A
  • not the same as single gene defect
  • only one part of the developing fetus has been affected
  • common and mulit factoral
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15
Q

multiple birth defects

A
  • associations
  • sequences
  • field complexes
  • syndromes
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16
Q

association

A 
Combination of at least 3 anomalies which are associated statistically but underlying mechanism not clear 
V           Vertebral anomalies
A            Anal atresia
C	     Cardiac defect
T            Tracheo –
E            Esophageal atresia
R            Radial and Renal anomalies
L	      Limb abnormality
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17
Q

sequences

A

potters sequnce

Pierre robin sequence

18
Q

potters sequence

A
  • oligohydramnios
  • insufficient amniotic fluid in uterus, fetus is squashed
    can lead to
    • squashed facies
    • joint contractures
    • bowed limbs
    • lung hypoplasia
19
Q

Pierre robin sequence

A
  • early mandibular hypoplasia
  • glossoptosis
  • failed palatal closure
    Management implications
  • breathing difficulties
  • feeding difficulties
  • cleft palate
  • speech therapy
  • dental care
  • possible learning difficulties
20
Q

field complexes

A

Insult to a localised part of an embryo resulting in abnormalities in adjacent structures of disparate embryonic origin

21
Q

cause of Hemifacial microsomia

A
  • Disturbance of blood supply to the first and second branchial arches in first 6 weeks of pregnancy leads to hemifacial microsomia
22
Q

result of hemifacial microsomia

A
  • localised underdevelopment of the face

- one side does not grow, affecting cheek lower jaw, muscles, nerevs ect

23
Q

Trisomy 21 cause and effects

A
  • genetic disorder due to 3rd copy of chromosome 21

- associated with growth delay, intellectual intelligence lowers, facial features

24
Q

what is trisomy 21

A

down syndrome

25
Q

facial features and intraorally of down sydrnome trisomy 21

A 
Facial eatures
-	small neck
-	small ears
-	eyes slanted upwards
Intraorally 
-	class 3 mallocclusion
-	Large, fissured tongue
-	Periodontal disease
-	Hypodontia
-	Microdontia 
-	Enamel defects
-	Class 3 malocclusion due to maxillary retrognathia
26
Q

disorders of growth and dvleopemnt

A
  • Osteogenesis imperfecta
  • Down’s syndrome
  • X-linked Vitamin D resistant rickets
  • Cleidocranial dysostosis
  • Achondroplasia
  • Gigantism
  • Acromegaly
27
Q

dentinogenetic imperfecta

A
  • Autosomal dominant condition
  • disorder of dentine
  • hypo mineralisation
  • can be associated with OI?
  • affects 1:8000
28
Q

what can cause dentinogenetic imperfect

A

Mutations of dentine sialophosphoprotien

29
Q

classifications of dentine disroders

A

dentinogenetis imperfecta
radicular dentine dysplasia
DI with osteogenesis imperfecta

30
Q

pathology of the dentine disorders

A

dentinogenetis imperfecta (DSPP mutation affecting non collagenous protiens)
radicular dentine dysplasia (radicular pathology)
DI with osteogenesis imperfecta (collagenous proteins affected)

31
Q

dental features of DI

A

1) Teeth have an amber, grey to purple discoloration
2) pulpal obliteration
3) relatively bulbous crowns
4) short narrow roots
5) enamel may be lost following tooth eruption, exposing dentine which wears rapidly
6) normal mantel dentine
7) rest of the dentine has non ordered dentinal tubules
8) affects primary >permanent

32
Q

osteogenetic imperfecta symtoms

A

1) Bone fragility
- multiple fractures
- unstable vertebral column
2) Connective tissue disease with thin blood vessels (bruise easily)
3) poor muscle
4) loose joints
5) hearing loss
6) blue schelra
7) progressive hearing loss
8) dentinal changes
9) Bisphosphonates – risk of osteonecrosis

33
Q

Hypophosphatemic rickets and

cuase

A

AKA X linked vitamin D resisitat rickets

- failure of distal tubular phosphate reabsorption resulting in lower serum phosphate, increase in alkaline phosphatase

34
Q

symptoms of hypophosphatemic rickets

A
  • skeletal deformities
  • short stature
  • bowing of legs
  • frontal bossing
  • large pulp chambers and elongated pulp horns
  • abcesses in the abceses of caries
35
Q

achondroplasia

A

dwarfism is a consequence
sporadic mutation
defect in FGFR gene

36
Q

achrnodplasa symtoms

A
  • shortened arms and legs(upper arms and thigs larger than forarms and lower legS)
  • large head size and frontal bossing
  • flattened nasal bridge
  • crowding due to small jaws especially maxilla
37
Q

cleidocranal dysostkosis and symtoms

A 
Autosomal dominant pathway 
•	Defective development of intramembranous ossification
•	Short in stature
•	Absent clavicles
•	Delayed closure of sutures 
Frontal and parietal bossing
-	hypoplastic maxilla and zygoma 
-	delayed exfoliation of primary teeth
-	multiple supernumeraries
-	multiple unerupted teeth and associated cysts
38
Q

gigantism

A

overproduction of pituriaty growth hormoen

usually due to ademona

39
Q

gigantism after fusion of epiphyses

A

acromegaly

40
Q

gigantism before fusion of epiphyses

A

gigantism of whole skeleton

41
Q

acromegaly

A

continued froth at md condyle- gross prognathism

  • macroglossia
  • spacing of dentition
  • thickened facial soft tissue
  • growth of hands and points
  • joint pain
  • headaches
  • problems with vision

GDAN year 2 G&D with some aging (27 decks)

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