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3a Paediatrics > Paeds growth, puberty and endocrine (ILA2) > Flashcards

Paeds growth, puberty and endocrine (ILA2) Flashcards

1
Q

What are the 4 phases of normal human growth?

A
  1. fetal
  2. infantile phase (infancy ->18 months)
  3. childhood phase
  4. pubertal growth spurt
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2
Q

What are the determinants of the fetal growth phase?

A

dependent on the uterine environment so determined by…

  • size of mother and father
  • placental nutrition
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3
Q

What are the determinants of the infantile growth phase?

A
  • nutrition
  • good health
  • good function and happiness
  • thyroid hormones
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4
Q

What are the determinants of the childhood growth phase?

A
  • genetics
  • good health
  • happiness
  • good nutrition
  • growth hormone
  • thyroid hormones - cause cartilage cell division and bone formation
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5
Q

What are the determinants of the pubertal growth phase?

A
  • testosterone and oestrogen - fusion of epiphyseal growth plates, cessation of growth
  • growth hormone
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6
Q

How should measurements be recorded?

A

measurements should be plotted on a growth gentile chart

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7
Q

Which measurements are recorded for growth?

A
  1. weight
    electronic scales, naked
  2. height
    <2 y/o = lying down height
  3. head circumference
    occipitofrontal circumference
  4. body mass index
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8
Q

What are significant abnormalities of height?

A

measurements below 0.4th or above 99.7th gentile

markedly discrepant from weight

serial measurements which cross growth gentile lines after 1st year of life

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9
Q

What is the first sign of puberty in females?

A

breast development

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10
Q

What is the first sign of puberty in males?

A

testicular enlargement

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11
Q

List the features of puberty in a female

A

breast development - 8.5-12.5 y/o

menarche- occurs 2.5 years after puberty, signals growth coming to end

pubic hair growth - after breast development

rapid height growth

acne

body odour

mood changes

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12
Q

List the features of puberty in a male

A

testicular enlargement = >4ml volume using orchidometer

pubic hair growth - between 10-14 y/o

rapid height growth - later than females

acne

body odour

mood changes

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13
Q

Define short stature

A

height below the 2nd centile

2 standard deviations below the mean

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14
Q

If it is disproportionate short stature, what else should you measure?

A

sitting height
subischial leg length
limited radiographic skeletal surgery to identify skeletal abnormality

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15
Q

List the possible causes for short stature

A
  1. familial
  2. constitutional delay in puberty and growth
  3. small for gestational age / preterm
  4. chromosomal disorders
  5. malnutrition/ chronic illness e.g. coeliac, crohns, CKD, CF, CHD
  6. psychological deprivation
  7. endocrine e.g. hypothyroidism, growth hormone deficiency, bushings
  8. idiopathic
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16
Q

How is a child with short stature assessed?

A

Examination of the growth chart - height, weight, head circumference

determine the mid parental height

history - preterm, birth weight, feeding history, developmental milestones, chronic illness, medications (corticosteroids)

examination - dysmorphic features, chronic illness, evidence of endocrine illness, pubertal stage

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17
Q

Which investigations can you do for short stature?

A

x-ray of hand/ wrist - can show bone age

FBC- anaemia

creatinine

calcium, phosphates, alkaline phosphatase

TSH

karyotype

growth hormone tests

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18
Q

What are the possible causes for tall stature?

A
  1. familial
  2. obesity
  3. secondary - hyperthyroidism, excess sex steroids, congenital adrenal hyperplasia, true gigantism
  4. syndromes e.g. klinefelters, marfarn syndrome, sotos syndrome
  5. excessive growth at birth - maternal diabetes, primary hyperinsulinism,
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19
Q

What is classed as delayed puberty?

A

absence of pubertal development by…
14 y/o in females
15 y/o in males

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20
Q

List the possible causes of delayed puberty?

A
  1. constitutional delay
    familial, most common
  2. Low gonadotropin secretion
    systemic disease e.g. CF, crohns, asthma, hypothyroidism
    Hypothalamic pituitary disorders e.g. anorexia, starvation, growth hormone deficiency
    Kallmann syndrome
  3. High gonadotropin secretion
    chromosomal abnormalities e.g. Klinefelters, Turners
    steroid hormone enzyme deficiency
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21
Q

How is delayed puberty managed?

A
  1. find the cause and treat
  2. if reassured puberty will occur, no treatment needed

oral oxandrolone in young males or oral testosterone in older males

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22
Q

How is premature sexual development defined?

A

development of secondary sexual characteristics before 8 y/o in females or 9 y/o in males

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23
Q

What are the 4 patterns of premature sexual development?

A
  1. precocious puberty
  2. premature breast development = thelarche
  3. premature pubic hair development
  4. isolate premature menarche
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24
Q

how is precocious puberty classified?

A

categorised by levels of pituitary gonadotropics, FSH and LH…

  1. Gonadotropic dependent “true precocious puberty”
  2. gonadotropin independent “false precocious puberty”
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25
Q

Describe “true” precocious puberty (gonadotropin dependent)

A

when there is premature activation of the hypothalamic pituitary gonadal axis

the sequence of pubertal development is normal

common in females - ovaries are sensitive to gonadotropins but uncommon in males as testes insensitive to gonadotropins from pituitary

Cause: idiopathic, hypothyroid, infection

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26
Q

Describe “false” precocious puberty

A

when there is excess sex steroids outside the pituitary gland

sequence of pubertal development abnormal

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27
Q

In a male with precocious puberty, how would examining the testes help with excluding pathological causes?

A

BILATERAL ENLARGEMENT OF TESTES >4ml vol
gonadotropin dependent
causes: intracranial tumour, liver tumour

PREPUBERTAL ENLARGED TESTES
gonadotropin independent
cause: adrenal pathology

UNILATERAL ENLARGE TESTES
cause: gonadal tumour

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28
Q

List the causes of gonadotropin dependent precocious puberty

A

idiopathic
familial
CNS abnormalities e.g. infection, brain injury, neurofibromatosis, hydrocephalus
hypothyroidism

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29
Q

List the causes of gonadotropin independent precocious puberty

A

adrenal disorders e.g. tumours, congenital adrenal hyperplasia
ovarian tumour e.g. granulosa cell
testicular tumour e.g. leydig cell
exogenous sex steroids

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30
Q

How is undescended testes assessed?

A

diagnosis should be made at routine examination of the newborn

can be palpable - felt in groin but cannot be manipulated into the scrotum - or impalpable

if bilateral (25%) then need to karyotype

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31
Q

What are the possible complications of undescended testes?

A

infertility
torsion
psychological
testicular cancer

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32
Q

How common is congenital hypothyroidism?

A

1 in 4000 births

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33
Q

What are the causes of congenital hypothyroidism?

A
  1. maldescent of the thyroid** - linguinal mass diagnosed on USS (most common in UK)
  2. dyshormonogenesis
    error of thyroid hormone synthesis, most common in consanguineous families
  3. iodine deficiency **
    most common cause in developing world
  4. TSH deficiecny
    associated with pituitary dysfunction
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34
Q

How is congenital hypothyroidism detected?

A

detected in neonatal screening by the Heel Prick test (Guthrie test) which shows raised TSH

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35
Q

What is the importance of detecting congenital hypothyroidism?

A

needs to be detected within the first 4 weeks as can cause irreversible cognitive impairment

it is a preventable cause of severe learning difficulties

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36
Q

How might a baby present if they are born with congenital hypothyroidism?

A 
prolonged jaundice !
faltering growth 
macroglossia, puffy face
hypotonia 
feeding problems 
constipated 
pale, mottled, dry skin
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37
Q

How is congenital hypothyroidism treated?

A

life long thyroxine treatment

15mcg / Kg/ day

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38
Q

What is the most common cause of hypothyroidism in children?

A

autoimmune thyroiditis

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39
Q

How is your risk of autoimmune thyroiditis increased?

A

if have other autoimmune disease/ family history e.g. SLE, vitiligo, rheumatoid arthritis, type 1 diabetes, addissons

Downs syndrome

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40
Q

List the features of hypothyroidism

A 
lethargy, tiredness
constipation
brittle hair
dry skin 
cold intolerance / cold peripheries 
short stature / delayed puberty 
pale, puffy eyes 
obesity 
slipped upper femoral epiphysis 
bradycardia
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41
Q

How is hypothyroidism managed?

A

thyroxine

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42
Q

How does hyperthyroidism present?

A 
anxiety
sweating
weight loss
diarrhoea 
rapid growth in height
increased appetite 
tremor
tachycardia 
goitre 
eye signs
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43
Q

Which eye signs are seen with hyperthyroidism?

A

exophthalmos
ophthalmoplegia
lid retraction
lid lag

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44
Q

Which tests are performed in hyperthyroidism and what would expect to find?

A

THYROID FUNCTION TESTS

low TSH 
high T4 (thyroxine)
high T3 (triiodothyronine)
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45
Q

How is hyperthyroidism treated?

A

carbimazole or propylthiouracil
SE= neutropenia

beta blockers
symptomatic relief

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46
Q

Are strawberry marks self limiting?

A

yes, appear in first month of life

increase in size until 3-15 months old

self limiting and shrink as get older

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47
Q

What can be used to shrink larger strawberry marks?

A

propanolol

48
Q

How does a port wine stain manifest?

A

vascular malformation of capillaries in the dermis

49
Q

Which conditions are associated with a port wine stain?

A

sturge weber syndrome

Klippel Trenaunay syndrome

50
Q

Describe the appearance of a mongolian blue spot?

A

blue purple birthmark on lower back/ limbs/ buttocks

51
Q

Who are mongolian blue spots more common in?

A

also called congenital dermal melanocytosis

non caucasian ancestry e.g. south indian

52
Q

What would you suspect if a child had >5 cafe au lait patches (light brown oval shaped)?

A

neurofibromatosis type 1

53
Q

List the infectious causes of nappy rashes

A

contact dermatitis

infantile seborrhoeic dermatitis

candida infection

atopic eczema

54
Q

How are nappy rashes managed?

A
  1. use disposable nappies
  2. protective emollient used sparingly
  3. hydrocortisone cream if severe
55
Q

What are the possible complications of chicken pox?

A
  1. secondary bacterial infection* - with staphylococcus or group A strep, can lead to toxic shock syndrome
  2. encephalitis
  3. purpura fulminans
56
Q

Which virus is responsible for hands, foot and mouth disease?

A

coxsackie (enterovirus)

57
Q

How does hand foot and mouth disease present?

A

painful vesicular lumps on hands, dorsum of feet and mouth (oral ulcers) and tongue

fever

58
Q

Which organisms are responsible for impetigo?

A

staph. aureus

group A strep.

59
Q

Describe the appearance of an impetigo infection

A

lesions on face, neck and hands
erythematous macule that becomes vesicular/ pustular
rupture of vesicles with exudate of fluid
causes honey crusted lesions

60
Q

How is impetigo infection treated?

A

topical antibiotic e.g. mupirocin
OR
systemic antibiotics if severe e.g. flucloxacillin

61
Q

What is staphylococcal scalded skin syndrome?

A

exfoliative staphylococcal toxin causing separation of epidermal skin through granular cell layers

62
Q

How does staphylococcal scalded skin syndrome present?

A 
fever
malaise
purulent, crusting and localised infection around eyes, nose and mouth
widespread erythema 
dry skin
63
Q

How is staphylococcal toxin syndrome treated?

A

IV flucoloxacillin and analgesia

64
Q

Which immunisations are given when you are a newborn

A

BCG - if high risk

Hep B - if positive mother

65
Q

What is the “5 in 1” vaccine and when is this given?

A

give at 2, 3 and 4 months of age

  1. diphtheria
  2. tetanus
  3. pertussis
  4. H. influenzae type B
  5. polio
66
Q

When is the meningococcal B vaccine given?

A

2, 4 and 12 months

67
Q

When is the pneumococcal conjugate vaccine given?

A

2, 4 and 12 months

68
Q

When is the oral rotavirus vaccine given?

A

2 and 3 months

69
Q

When is the MMR vaccine given?

A

at 12-13 months and then 3 years 4 months

70
Q

When is the booster of h. influenzae type b given?

A

12-13 months

71
Q

When is meningococcal C vaccine given?

A

12-13 months

72
Q

At what age is the HPV vaccine given to girls?

A

12-13 years old

73
Q

Which vaccine is given to new students at university or at 14 years old?

A

meningococcal ACWY conjugate vaccine

74
Q

What is the difference between primary and secondary immunodeficiency disorders?

A

primary = genetically determined deficit in immunse system e.g. X linked, autosomal recessive

secondary = caused by another disease/ treatment e.g. malignancy, HIV, splenectomy

75
Q

How does someone with an immunodeficiency disorder present?

A 
children with infections that are...
S- severe e.g. meningitis, pneumonia 
P- prolonged
U- unusual - present atypical, unusual pathogen
R- recurrent
76
Q

How are children with immunodeficiency disorders managed?

A

anti- microbial prophylaxis e.g. azithromycin prophylax and cotrimoxazole to prevent PCP

screening for end organ damage

immunoglobulin replacement therapy

bone marrow transplant

77
Q

Define hypersensitivity

A

objectively reproducible symptoms or signs following exposure to a defined stimulus at a dose that is usually tolerated by most people

78
Q

Define allergy

A

a hypersensitivity reaction initiated by specific immunological mechanisms - IgE mediated or non IgE mediated

79
Q

Define anaphylaxis

A

a serious allergic reaction with bronchial, laryngeal or cardiovascular involvement that is rapid in onset and may cause death

80
Q

What is the hygiene hypothesis?

A

that increased prevalence of allergies is due to altered microbial exposure associated with modern living conditions

81
Q

Name some common stimuli causing allergic disease

A

INHALANT ALLERGENS
e.g. house dust mite, plant pollens, pet dander, mould

INGESTANT ALLERGENS
e.g. cows milk, nuts, soya

INSECT BITES/ STINGS
e.g. drugs, natural rubber latex

82
Q

Describe the clinical course of IgE mediated reactions

A
  1. EARLY PHASE (within minutes of exposure to allergen)
    caused by release of histamine and mast cells
    sneezing, vomiting, angiooedema, bronchospasm , CV shock
  2. LATE PHASE (4-6 hours after)
    nasal congestion in upper airways, cough, bronchospasm
83
Q

What measures can be taken to prevent allergic disease?

A

avoid using formula milk from cows milk

use probiotics during late pregnancy (prevent eczema)

early introduction of peanut and egg to infants diet

nutritional supplements e.g. omega 3 fatty acids, vitamin D, antioxidants

84
Q

What is the difference between a primary and secondary reaction for a food allergy?

A

primary reaction = childs first exposure of the food and react e.g. peanut, egg, milk

secondary reaction= due to cross reactivity between portions in fresh fruit/veg/nuts and those present in pollen

85
Q

Describe the symptoms of an IgE mediated food allergy?

A 
10-15 minutes after ingestion of food
urticaria
facila swelling 
anaphylaxis
wheeze, stridor
shock, collapse
86
Q

describe the symptoms of a non IgE mediated food allergy

A 
diarrhoea
vomiting
abdominal pain 
faltering growth
colic
87
Q

What is the gold standard investigation to diagnose a food allergy?

A
  1. exclusion of relevant food under dieticians supervision followed by a double blinded placebo controlled food challenge
88
Q

How is an food allergy attack managed?

A

adrenaline IM by EpiPen

89
Q

Describe the symptoms of allergic rhinitis (hay fever)

A

coryza
conjunctivitis
cough
associated with eczema, sinusitis, adenoidal hypertrophy, asthma

90
Q

How does atopic eczema present?

A

rashes - itchy, scratching, erythematous and weeping
dry skin
flare ups

91
Q

List some of the causes that exacerbate eczema

A 
bacterial infection 
viral infection
ingestion of allergen e.g. egg
contact with irritant 
environment e.g. heat, humidity 
psychological stress
92
Q

How is atopic eczema managed?

A
  1. AVOID IRRITANTS - avoid soap and biological detergent, wear pure cotton clothing
  2. EMOLLIENTS - applied liberally 2/3 time a day an after bath
  3. TOPICAL CORTICOSTEROIDS - e.g. 1% hydrocortisone effective for flare ups
93
Q

What are the increased risk factors for type 1 diabetes?

A

genetic

associated with other autoimmune disorders e.g. hypothyroidism, SLE, vitiligo, addissons, coeliac, rheumatoid arthritis

94
Q

What is the pathology behind type 1 diabetes?

A

destruction of the pancreatic beta cells by an autoimmune process causing insulin deficiency

95
Q

Describe the cells of the pancreas and what they each produce

A

alpha cells - produce glucagon - increase blood sugar by breakdown of glycogen

beta cells - produce insulin - decrease blood sugar

delta cells - produce somatostatin - inhibit alpha and beta cells

96
Q

Outline the classic triad of symptoms of type 1 diabetes

A
  1. polyuria
  2. polydipsia
  3. weight loss
97
Q

How is diagnosis of type 1 diabetes confirmed?

A
  1. raised random blood glucose >11.1 mmol/L
  2. glycosuria
  3. ketosis
98
Q

What is the normal range for a fasting plasma glucose and then after eating?

A

fasting = 3.4 - 5.6 mmol/L

after eating= <7.8 mmol/L

99
Q

How are type 1 diabetics managed?

A
  1. intensive educational programme - blood glucose finger prick monitoring (aim 4-7), exercise, recognition of DKA/ hypoglycaemia
  2. Insulin
  3. diet - high complex carbohydrates, modest fat content, high fibre, carb counting
100
Q

What are the types of insulin available?

A
  1. rapid acting insulin analogues
    faster onset and shorter duration
  2. short acting soluble human regular insulin
    onset in 30-60 min, peak 2-4 hours
  3. intermediate acting insulin
101
Q

Which factors cause poor diabetes control?

A

eating too many sugary foods

infrequency of blood glucose testing

illness

exercise

eating disorders

inadequate family support and motivation

102
Q

what are the microvascular and macrovascular long term complications of type 1 diabetes?

A

Microvascular - retinopathy, nephropathy, neuropathy

Macrovascular- hypertension, coronary artery disease, cerebrovascular disease

103
Q

What causes diabetic ketoacidosis?

A

lack of insulin has 2 effects..

  1. causes increase in glucagon production which leads to increased secretion of glucose
  2. causes fat to breakdown into fatty acids -> ketones -> ketones are acidic and cause necrosis of cells
104
Q

What are the symptoms of diabetic ketoacidosis?

A 
smell of acetone on breath 
vomiting 
dehydration
abdominal pain 
kussmall breathing 
drowsiness
105
Q

How is diabetic ketoacidosis diagnosed?

A
  1. blood glucose >11.1 mmol/l
  2. blood ketones >3.0 mmol/L
  3. blood gas- metabolic acidosis
106
Q

How is diabetic ketoacidosis managed?

A
  1. FLUIDS - initial resuscitation with 0.9% saline then add 5% glucose when blood glucose <14 mmol/L
  2. IV insulin
    monitor blood glucose hourly
  3. potassium
    need cardiac monitoring and 2-4 hourly potassium measurements
  4. reestablish diet
107
Q

What is Kussmal breathing?

A

increased respiratory take if acidotic

108
Q

What is congenital adrenal hyperplasia?

A

group of autosomal recessive disorders of adrenal steroid biosynthesis

109
Q

describe how congenital adrenal hyperplasia causes its symptoms

A
  1. deficiency of 21 hydroxylase enzyme
  2. results in low cortisol levels
  3. causes increased production of ACTH from anterior pituitary gland
  4. stimulates production of adrenal androgens and testosterone

ALSO unable to produce aldosterone causing salt loss

110
Q

how might a female or male present with 21 hydroxylase deficiency in congenital adrenal hyperplasia?

A

FEMALES
virtilisation of female genitalia e.g. clitoral hypertrophy, fusion of the labia

MALES
precocious puberty
tall stature
salt losing crisis

111
Q

Describe the symptoms of salt losing crisis in congenital adrenal hyperplasia and why does this occur?

A

presents at 1-3 weeks of age in boys
vomiting, weight loss, floppy, circulatory collapse

occurs because of a lack of aldosterone production causing salt loss (low sodium)

112
Q

What are the 3 causes of congenital adrenal hyperplasia?

A
  1. 21 hydroxylase deficiency ** (90%)
  2. 11 beta hydroxylase deficiency (5%)
  3. 17- hydroxylase deficiency (rare)
113
Q

How is congenital adrenal hyperplasia diagnosed?

A

markedly raised levels of metabolic 17-hydroxyprogesterone in blood

114
Q

Outline the biochemical abnormalities in salt loss in congenital adrenal hyperplasia

A

low plasma sodium
high plasma potassium
metabolic acidosis
hypoglycaemia

115
Q

Describe the lifelong management of patients with congenital adrenal hyperplasia

A
  1. glucocorticoids - hydrocortisone
  2. mineralocorticoids for salt loss - fludrocortisone
  3. monitoring growth, skeletal maturity, plasma androgens, 17-hydroxyprogesterone
  4. additional hormone replacement during illness/ surgery
116
Q

How are males in salt crisis managed?

A
  1. saline
  2. dextrose
  3. hydrocortisone IV
117
Q

What is given to mothers who have already had a previous baby with CAH when they have another baby?

A

dexamethasone at conception

3a Paediatrics (9 decks)

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