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Paediatrics > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What are the phases of normal growth

A

Fetal Phase
Infantile Phase
Childhood phase
Pubertal growth spurt

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2
Q

What drives Fetal growth, height velocity

A

Uterine environment
E.g. maternal diet, placental insufficiency, Size of mother

Fastest phase of growth

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3
Q

What drives infantile phase of growth, height velocity

A

Growth hormone - IGF axis

Slow, prolonged

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4
Q

What drives childhood phase of growth, height velocity

A

Nutrition

Rapid rate, decelerating

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5
Q

What drives pubertal growth spurt

A

Testosterone and oestrogen

Growth hormone

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6
Q

What do you measure for growth?

A 
Weight 
Height
Head circumference
BMI 
Bone age
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7
Q

How to measure height

A

> 2: standing height
<2: lying length
Sitting height

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8
Q

What are signs of significant abnormalities of height

A

Measurements below 0.4th of above 99.6th centiles, or outside midparental height range
Markedly discrepancy from weight
Serial measurements which cross growth centile lines after 1st year of life

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9
Q

How to calculate mid-parental height and target height

A

Mid parental height = parents height/2 + 7 for boys, - 7 for girls
Target height = MPH +-8.5 cm

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10
Q

How to plot growth parameters

A

UK WHO chart
Different charts for age and gender
They are constructed to ethnicity, socioeconomic status, overall standards of health and nutrition, changes over time

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11
Q

Define growth deceleration

A

Growth velocity below 5th percentile

Height drops across two or more percentiles on growth chart

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12
Q

How can you identify growth failure

A
  1. Height centile
  2. Parental height
  3. Height velocity - subjective to phases of growth
  4. Height trajectory - height falling across centile lines, detect abnormal growth before height centile falls below second centile
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13
Q

Define short stature

A

Height below second centile (2SDs below mean)

Height below 0.4th centile - extreme short statue

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14
Q

How to measure height velocity?

A

Two accurate measurements at least 6 months apart

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15
Q

Causes of short stature

A 
Normal variant
Idiopathic
Endocrine 
Genetic 
Chronic illness
MSK
Psychosocial
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16
Q

What are normal variant causes of short stature

A

Familial short stature
Constitutional delay of growth and development: short stature in adolescence due to delay in onset of puberty, but final height reaches target height. There is delayed bone age and delayed pubertal development

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17
Q

What are idiopathic causes of short stature

A

Idiopathic short stature
Small for gestational age without catch-up: patients who are born SGA but have not caught up in height by 4 years, requires GH treatment

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18
Q

What are endocrine causes of short stature

A 
Hypothyroidism
Hypopituitarism 
Cushing’s syndrome 
Untreated CAH - accelerated bone growth 
Hyperthyroidism - accelerated bone growth
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19
Q

What are genetic causes of short stature

A 
Turners Syndrome 
Noonan Syndrome 
Down’s syndrome 
Prader-Willi syndrome  
DiGeorge Syndrome (CATCH-22)
Russel-silver Syndrome
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20
Q

What are common chronic illnesses that cause short stature

A 
Present with faltering growth (underweight) 
Coeliac disease - first 2 years
Crohn’s disease
CKD
Cystic fibrosis 
TB - measles, vitamin D infection 
Bronchiectasis 
CHD 
Malnutrition
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21
Q

Causes of disproportionate short stature

A 
Skeletal dysplasia (abnormal bone formation): 
achondroplasia - autosomal dominant
hypochondoplasia, 
osteogenesis imperfecta - Group of disorders of collagen metabolism leading to bone fragility, bowing and fractures; T1 present with #s, blue scleral hearing loss; T2 more severe, stillborn

Rickets
Spinal disorders: scoliosis, irradiation

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22
Q

What are psychosocial causes of short stature

A

Psychosocial deprivation: physical/emotional abuse, neglect; resumes normal growth once removed from adverse enviro
Eating disorders
Fetal alcohol syndrome

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23
Q

Growth chart for familial short stature

A

Following growth centile within predicted range for parental height

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24
Q

Growth chart for SGA without catch up

A

Short stature from birth

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25
Q

Growth chart for constitutional delay of growth and puberty

A

Short stature in adolescence due to delayed puberty

Delayed bone age

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26
Q

Growth chart for endocrine cause of short stature

A

Falling off height centiles
Weight centile > height centile
Delayed bone age

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27
Q

Growth chart for short stature caused by psychosocial/chronic illness

A

Falling off height centiles
Weight centile > height centile
Delayed bone age

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28
Q

How do you measure bone age?

A

Left wrist x Ray - skeletal maturity

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29
Q

What factors affect growth

A

Genetics
General health - nutrition, thyroid function
Timing of pubertal growth spurt
Psychosocial environment

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30
Q

Assessment of short stature

A

Pathological short stature —>
Dysmorphic features present
—> proportionate = genetic
—> disproportionate = MSK

Dysmorphic features absent
—> increased weight for height = endocrine
—> decreased weight for height = chronic illness, nutritional, emotional

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31
Q

Investigations for short stature

A 
Growth chart
Target height 
Height velocity 
Bone age - left wrist and hand x Ray 
FBC 
Metabolic profile: U+E, calcium, glucose, LFT 
Urinalysis
TFT
Karyotyping
IGF-1
Anti-tissue transglutaminase 
ESR
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32
Q

Further investigations for short stature

A

GH stimulation test
Diurnal cortisol Levels, urinalysis cortisol Levels, dexamethasone suppression test
Skeletal survey

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33
Q

Indications for growth hormone treatment

A 
GH deficiency
Turner syndrome
Prader-Willi syndrome 
CKD
SHOX deficiency 
IUGR/SGA with failure of catch-up growth
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34
Q

Prevalence of diabetes mellitus in children

A

2 in 1000

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35
Q

Classification of diabetes in children

A

Type 1 - 98% cases
Type 2 - older children w obesity, FHx
Maturity onset diabetes of the young - strong FHx, group of autosomal dominant genetic disorders that cause non-insulin dependent diabetes of <25 year old
Drugs
Pancreatic insufficiency - CF, iron overload in thalassaemia
Endocrine - Cushing’s
Genetic - Turners, Down’s
Neonatal Diabetes - due to defective B cell function
Gestational Diabetes

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36
Q

Aetiology of T1 DM

A

Genetic predisposition
Environmental precipitants - viral infection, diet, cows milk proteins
Autoimmune destruction of pancreatic Beta islet cells

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37
Q

Clinical features of diabetes

A 
Presentation peaks at spring and autumn 
Early: 
Polyuria, polydipsia, weight loss
Secondary enuresis
Intercurrent illness: Skin sepsis, Candida, other infections 
Late - diabetic ketoacidosis: 
Smell of acetone on breath
Vomiting
Dehydration
Abdominal pain 
Hyperventilation (Kussmaul breathing from acidosis) 
Hypovoaemic shock
Drowsiness
Coma
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38
Q

Diagnosis of T1 DM in children

A

In symptomatic child:
Raised random blood glucose >11.1 mmol/L
Glycosuria
Ketosis

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39
Q

what are the components of Initial management of T1DM

A 
Parent and child education 
Insulin
Diet
Blood glucose monitoring
Management of acute complications - acute hypoglycaemia, DKA
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40
Q

What is covered in educational programme for child and family

A 
Understanding of diabetes
Injection of insulin
Blood glucose monitoring
Diet
Exercise
Sick day rules
Recognition and treatment of hypoglycaemia
Voluntary groups
Psychological impact of life long condition
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41
Q

Types of insulin used in T1DM in children

A

Human insulin in concentrations of 100 units:

Rapid acting insulin analogues: insulin lispro (Humalog), insulin aspart (Novorapid)
Very long acting insulin analogues: insulin detemir (Levemir), glargine (Lantus)
Short-acting human insulin: Actrapid, Humulin S
Intermediate acting insulin: Insulatard, Humulin I

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42
Q

How should insulin be administered

A

Subcutaneous injection

Method - at anterolateral thighs, abdomen, buttocks; rotation of injection sites, skin pinched and injected at 45 degrees

Complications - lipohypertrophy, lipoatrophy, intramuscular injection (painful)

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43
Q

Insulin regimen for children and why is it recommended

A

Basal-bolus regimen:
By Continuous subcutaneous insulin pump or multiple daily injection
Rapid acting insulin + long acting insulin

Allows greater flexibility
Achieves best glycaemic control
Reduce risk of long term complications

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44
Q

What is ‘honeymoon’ period

A

Reduced insulin requirements and good glycaemic control that occurs shortly after presentation/diagnosis
Requirement subsequently increases during puberty

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45
Q

Blood glucose targets in children

A

4 - 7 mmol/L before meals

HbA1C <48 mmol/mol (6.5%)

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46
Q

Methods of blood glucose monitoring

A

Blood glucose diary
Continuous glucose monitoring sensors
Blood ketone testing
HbA1C

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47
Q

Benefits of continuous glucose monitoring sensors

A

Control insulin delivered from pump

Allows detection of asymptomatic episodes of nocturnal hypoglycaemia, times of poor control during the day

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48
Q

when do you need to do blood ketone testing

A

Mandatory during illness or poor control

49
Q

Diet changes in T1DM

A

High complex carbohydrate and modest fat content
High fibre intake - sustained release of glucose
Avoid refined carbohydrates - rapid swings of glucose
Carbohydrate counting - to calculate insulin requirements for meal

50
Q

Clinical features of hypoglycaemia in T1DM

A 
Hunger
Tummy ache
Sweating
Feeling faint, dizzy, wobbling of legs 
Pallor
Irritability 
Seizures 
Coma

Loss of awareness of symptoms with frequent hypoglycaemia

51
Q

Management of hypoglycaemic episode in T1DM

A

Glucose tablets / sugary drink
Oral glucose gels - If uncooperative
Glucagon injection - if severe w reduced level of consciousness

Give carbohydrate rich foods after treatment

52
Q

Investigations for DKA

A 
Blood glucose - >11
Blood ketones - >3
U+E, creatinine - dehydration 
Blood gas - pH <7.3 or bicarbonate <15
Blood and urine culture - precipitating event 
Cardiac monitor - Hypokalaemia 
Weight
53
Q

Management of DKA

A
  1. Fluids:
    - initial resuscitation
    - gradual fluid replacement over 48hrs (risk of cerebral oedema)
    - 0.9% NaCl w 40mmol KCl for first 12hrs + 5% glucose once <14mmol, 0.45% NaCl W 40mmol KCl for next 12hrs
    - monitor blood glucose hourly, blood ketones 2 hrly, U+E and ABG 4 hrly
  2. Insulin:
    - IV infusion 0.1u/kg/Hr
  3. Potassium:
    - falls w insulin treatment and rehydration
    - Start K+ replacement w start of maintenance fluids
    - continuous cardiac monitoring, 4 hrly plasma K+ measurements
  4. Acidosis: avoid bicarbonate replacement, tx w fluid and insulin
  5. Re-establish oral fluids, SC insulin, normal diet
  6. Identify and treat underlying cause
54
Q

Aims of long term management for DM

A

Normal growth and development
Maintaining normal home and school life
Good diabetes control
Encouraging children to become self-reliant with adult supervision until they can take responsibility
Anticipating and minimising hypoglycaemia
Maintain HbA1c <48 mmol

55
Q

Why is it important to monitor HbA1C

A

Levels above 48mmol/L increases risk of long term complications exponentially

56
Q

Assessment of diabetes

A

Episodes of hypoglycaemia, DKA, hospital admission
Is there still Awareness of hypoglycaemia
Absence from school
Interference with normal life
HbA1c
Blood glucose diary
Insulin regimen
Injection sites for lipohypertrophy or lipoatrophy
Diet

57
Q

How to monitor for development of complications in DM

A

Height, weight and BMI - at each visit
BP - HTN
Microalbuminuria - annually from 12 years
Pulses and sensation - circulation
Retinal photography - annually from 12 years
Feet - annually
Coeliac and thyroid disease - screen at diagnosis, screen for thyroid annually and coeliac if symptomatic
Annual flu vaccination

58
Q

What are problems with long term diabetes control

A

Eating too many sugary foods without insulin
Infrequent unreliable glucose testing - ‘perfect’ results
Illnesses - variable required dose of insulin
Exercise
Eating disorders
Family disruption
Inadequate family support, understanding, motivation

59
Q

Influence of puberty on diabetes

A

Biological - In pubertal growth spurt, oestrogen, testosterone, growth hormone and insulin-like growth factors cause insulin resistance
Thus increase in insulin requirement

Psychological - concrete and abstract thinking about long term effects of diabetic control —> focus on immediate effects of good diabetes control

60
Q

Influence of diabetes on adolescents

A

Biological - grow and pubertal delay, obesity if insulin not reduced towards end of puberty
Psychological - reduced self esteem
Social - increased risk from smoking, alcohol, drugs

61
Q

Measures to manage diabetes in adolescents

A

Focus on immediate benefits of good diabetes control - short term goals suggested by themselves
Communicate enthusiastically their efforts to improve diabetes control
United team approach
Peer group support

62
Q

What are causes of SGA without catch up

A 
First trimester: 
TORCH infections
Maternal PKU
Fetal alcohol syndrome
Recreational drug abuse

Second trimester:
Pre eclampsia
Diabetes Mellitus

Neonatal:
Cows milk allergy
GORD

63
Q

Causes of tall stature

A

Familial - most common

Secondary endocrine:
Congenital adrenal hyperplasia - excess steroids
Precocious puberty - excess sex hormones
Hyperthyroidism
True gigantism - excess GH

Syndromes:
Long legged - Klinefelter, Marfan, Homocystinuria
Sotos Syndrome

Excessive growth at birth:
Maternal diabetes
Primary hyperinsulinism
Beckwith Syndrome

64
Q

What age do fontanelles close

A

Posterior - 8 weeks

Anterior - 12-18 months

65
Q

When do most head growth occur

A

First two years

80% head growth by 5 years

66
Q

What does increase in head circumference across centile lines mean

A

Normal in first few months

Rise in ICP

67
Q

Define microcephaly

A

Head circumference below 2nd centile

68
Q

Causes of microcephaly

A

Familial
Congenital infection
Autosomal recessive condition
Acquired after insult to developing brain - perinatal hypoxia, hypoglycaemia, meningitis

69
Q

Define microcephaly

A

Head circumference above 98th centile

70
Q

Define macrocephaly

A

Head circumference above 98th centile

71
Q

Causes of macrocephaly

A

Tall stature
Familial
Raised ICP - subdural haematoma, tumour, neurofibromatosis
Sotos Syndrome (cerebral gigantism)
CNS storage disorders - Mucopolysaccharidosis

72
Q

Investigations for increase in head circumference across centile lines

A

Cranial uss - If anterior fontanelle open

CT/MRI

73
Q

Causes of skull asymmetry

A

Plagiocephaly - positional moulding

Craniosyntosis

74
Q

What causes plagiocephaly

A

Infants lying on their back
Hypotonia
Preterm infants

75
Q

How to differentiate plagiocephaly from craniosyntosis

A

Both: paralellogram shaped head, frontal protuberance
Plagiocephaly: all sutures open, ear displaced anteriorly, flattening at back of skull
Craniosyntosis: fusion of cranial sutures, ear displaced posteriorlyn

76
Q

What is craniosyntosis

A

Premature fusion of cranial sutures, leading to distortion of head shape

77
Q

Types of craniosyntosis

A

Localised:
Sagittal - long narrow skull
Coronal - asymmetrical skull
Lambdoid - flattening of skull

Generalised - microcephaly

78
Q

Causes of generalised craniosyntosis

A

Genetic syndromes:
Crouzon Syndrome - exophtalmos
Apert Syndrome - syndactyly

79
Q

Investigations for asymmetrical head

A

Palpable ridge
Skull x Ray
Cranial ct
(For fused sutures)

80
Q

What are female stages of puberty

A

Breast development - starts bw 8.5-12.5
Pubic hair growth, Rapid height growth - occurs after breast development
Menarche - occurs 2.5 years after start of puberty, signals growth coming to an end with 5cm height gain remaining

81
Q

What are Male stages of puberty

A

Testicular enlargement - measured using orchidometer, first sign of puberty
Pubic hair growth - follows testicular enlargement, 10-14 years
Rapid height growth - 18 months after first sign of puberty, occurs much later and greater magnitude than females

82
Q

Age for premature sexual development

A

Girls - 8

Males - 9

83
Q

Types of premature sexual development

A

Precocious puberty
Premature breast development
Premature pubic hair development
Isolated premature menarche

84
Q

Types of precocious puberty

A

Gonadotrophin dependent - central/true; due to premature activation of HPG axis, with normal sequence of pubertal development and high LH/FSH Levels

Gonadotrophin independent - pseudo/false; due to excess sex steroids, with abnormal sequence of pubertal development and low LH/FSH Levels

85
Q

Causes of precocious puberty in females

A

Gonadotrophin dependent:
Idiopathic/familial - most common
Pituitary adenoma

Gonadotrophin independent:
Congenital adrenal hyperplasia
Adrenal tumours
—> pubic hair/adult body odour/acne/virilization of genitalia before breast development

86
Q

Why is gonadotrophin dependent PP commonly familial/idiopathic in females but likely pathological in males

A

Ovaries sensitive to secretions of gonadotrophins from pituitary gland

87
Q

How can you distinguish clinically bw different causes of precocious puberty in males

A

Bilateral enlargement of testes - gonadotrophin dependent (volume >4ml)
Prepubertal testes - gonadotrophin independent
Unilateral enlarged testes - gonadal tumour

88
Q

Causes of precocious puberty

A

Gonadotrophin dependent:
Idiopathic/familial
CNS abnormalities - congenital (hydrocephalus), acquired (infection, post irradiation, brain injury), tumours
Hypothyroidism

gonadotrophin independent: 
Adrenal - tumour, congenital adrenal hyperplasia
Ovarian tumour (granulosa cell) 
Testicular tumour (Leydig cell) 
Exogenous steroids
89
Q

Management of precocious puberty

A

Gonadotrophin-releasing hormone analogue - to delay onset of menarche
Medroxyprogesterone acetate, ketoconazole - for gonadotrophin independent pp to inhibit sex steroids

90
Q

Clinical features of premature breast development (thelarche)

A

6 month - 2 year old
Asymmetrical, not beyond stage 3 (juvenile smooth contour)
Absence of pubic hair and significant growth spurt
Self-limiting

91
Q

What is premature pubarche

A

Development of pubic hair before <8 in female and <9 with no other signs of sexual development

92
Q

Pathophysiology of premature pubarche

A

Accentuation of normal maturation of androgen production by adrenal gland

93
Q

Clinical features of premature pubarche and pathological pubarche

A

In Asian/black
Slight increase in growth rate and bone age
Self limiting

Pathological - aggressive virilisation

94
Q

Investigations for premature pubarche

A

Urinalysis steroid profile
Androgens in blood
X Ray left hand and wrist - Bone age

95
Q

Define delayed puberty

A

Absence of pubertal development by 14 in girls and 15 in boys

96
Q

Causes of delayed puberty

A

Constitutional delay of growth and puberty/familial
Hypogonadotrophic hypogonadism:
Systemic disease - CF, severe asthma, Crohn’s, organ failure, starvation, excess physical training, anorexia nervosa
HP distorder - pituitary dysfunction, isolated gonadotrophin deficiency, intracranial tumour, Kallmann Syndrome (LH deficiency)
Acquired hypothyroidism

Hypergonadotrophic hypogonadism:
Chromosomal abnormalities - Klinefelter, Turner
Steroid hormone enzyme deficiencies
Acquired gonadal damage - surgery, chemotherapy, trauma, torsion, autoimmune

97
Q

Why is delayed puberty more common in boys

A

Relative insensitivity of testes to gonadotrophin
Thus more common in boys
But more likely pathological in girls

98
Q

Management of delayed puberty in boys

A

Assessment - Pubertal staging (testicular volume)
Reassurance
Oxandrolone - androgenic steroid
IM testosterone

99
Q

Investigations for delayed puberty in girls

A

Karyotyping
TFT
Sex steroid hormones

100
Q

Clinical value of hypoglycaemia

A

Plasma glucose <2.6mmol/L

101
Q

Why is hypoglycaemia common in infants

A

High energy requirements and poor glucose reserves (from gluconeogenesis + glycogenolysis)

Thus should not be fasted for >4 hours

102
Q

What are the neurological consequences of hypoglycaemia in childhood

A

Epilepsy
Severe learning difficulties
Microcephaly
- period of most rapid brain growth

103
Q

Causes of hypoglycaemia in childhood

A

Fasting:

  1. Insulin excess
    - insulin therapy in DM
    - persistent hypoglycaemic hyperinsulinism If infancy
    - autoimmune
  2. Without insulin excess
    - ketotic hypoglycaemia of childhood
    - hormonal deficiency: GH, ACTH, Addisons
    - liver disease

Non fasting

  • maternal diabetes
  • fructose intolerance
  • galactosaemia
104
Q

What is ketotic hypoglycaemia

A

When children readily become hypoglycaemic after short period of starvation due to limited reserves for gluconeogenesis

105
Q

What is persistent hypoglycaemic hyperinsulinism of infancy

A

Genetic mutations leading to dysregulation of insulin release by beta islet cells
Causes persistent neonatal hypoglycaemia

107
Q

Investigations for hypoglycaemia

A

If cause unknown, collect blood + first available urine

Laboratory blood glucose
GH, IGF1, cortisol, insulin, C-peptide, fatty acids, ketones, glycerol, lactate, amino acids

First urine after hypoglycaemia - organic acids

108
Q

Physiological changes in thyroid hormone levels after birth

A

Fetal period: synthesis of reverse T3 - inactive

After birth: surge in TSH, rise in T3 + T4

109
Q

Causes of congenital hypothyroidism

A

Thyroid aplasia
Ectopic thyroid gland
Dysmorphogenesis

110
Q

What is the screening test for congenital hypothyroidism and why is it needed

A

Day 5 Serum TSH (Guthrie test)

Common
Preventable cause of severe learning difficulties

111
Q

Clinical features of congenital hypothyroidism

A

Prolonged jaundice - thyroxine for bilirubin metabolism
Neonatal hypoglycaemia
Signs of hypothyroidism - Constipation, Cold intolerance, dry skin, Delayed development, Coarse facies, Large tongue, Hoarse cry, Goitre

112
Q

Management of congenital hypothyroidism

A

Thyroxine

Started before 2 weeks of life - prevent cretinism

116
Q

When should you check blood glucose in children

A

Becomes septic/seriously ill - ABC DEFG
Prolonged seizure
Altered state of consciousness

117
Q

Cause of acquired hypothyroidism

A

Autoimmune thyroiditis

  • presence of antithyroid peroxidase antibodies (TPO)
  • Hashimoto’s disease
  • initial transient hyperthyroid phase: lymphocytic destruction and release of preformed hormones
118
Q

Clinical features of acquired hypothyroidism

A 
Females
Short stature 
Delayed puberty/amenorrhoea
Learning difficulties
Deterioration in school work 
Initial thyrotoxic phase - tremulous
Hypothyroidism - cold intolerance, dry skin, constipation, obesity, bradycardia, thin dry hair, slow reflexes, poor concentration
119
Q

Investigations for autoimmune hypothyroidism

A

TSH
Serum free T3 t4
TPO - positive (confirm autoimmunity)
TRAb - negative (TSH receptor antibodies, rule out Graves’ disease)

120
Q

Causes of hypopituitarism

A

Congenital:
pituitary hypoplasia, aplasia
midline defects

Acquired:
Tumours - craniopharyngioma
Irradiation
Infection - meningitis

121
Q

Clinical features of congenital hypopituitarism

A

Short stature
Prolonged neonatal jaundice - hypothyroidism
Neonatal hypoglycaemia - hypothyroidism
Undervirilisation of boys - micropenis

122
Q

Why do you get undervirilisation in boys from hypopituitarism

A

Virilisation of external genitalia requires hormones thus functioning pituitary

123
Q

Indications for growth hormone therapy

A 
Growth hormone deficiency
Turner syndrome
Prader Willi Syndrome
Chronic renal insufficiency 
SGA without catch up at 4 years old
Short stature homebox-containing gene (SHOX) deficiency

Paediatrics (15 decks)

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