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y4 paediatrics > Intro Week Lectures 2 > Flashcards

Intro Week Lectures 2 Flashcards

1
Q

When during pregnancy is fetal growth the fastest?

A

Peaks in 2nd trimester

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2
Q

How fast should children grow normally?

A

Growth velocity 5-7cm/yr

Falls slowly to <5cm/yr pre-pubertally

mid-childhood spurt at 6-8 yrs

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3
Q

First sign of puberty in girls v boys?

A

Breast change in girls/testicular growth in boys (4 mls size)

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4
Q

Sign of completion of puberty in girls v boys?

A

menarche in girls/ 10 mls size testes in boys

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5
Q

What tools can you use to assess growth?

A

Leicester height measure (stadiometer), weighing scales, head circumference
Growth charts
Bone age
Prader orchidometer

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6
Q

Short stature with normal growth velocity suggests what?

A

constitutional delay

Often associated with medical conditions e.g. asthma
Delayed bone age
Later onset of puberty
Often familial, will eventually achieve genetic height potential

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7
Q

Causes of short stature with slow velocity?

A

Chronic disease - e.g. Coeliac
GH deficiency
Skeletal dysplasia
Syndromes e.g Turner, Down, Prader-Willi,
Endocrine e.g hypothyroidism, hypopituitarism, Cushings
Child abuse

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8
Q

How may isolated growth hormone deficiency present?

A

midline defects e.g. cleft lip and cleft palate
undescended testes

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9
Q

Questions to ask patient / parents with suspected Turner’s?

A

Lymphoedema of hands/feet in neonates
Congenital Heart Disease
Recurrent ear infections
Learning difficulties– coordination, numerical
Delayed puberty – primary amenorrhoea

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10
Q

How can Turner’s syndrome be managed?

A

Growth Hormone – supraphysiological doses
Pubertal hormones
Educational help
Hearing aid/grommets
Cardiac monitoring
Osteoporosis prevention

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11
Q

What conditions are screened for in newborn screening?

A

Phenylketonuria (PKU)

Congenital Hypothyroidism

Sickle Cell Disease (SCD)

Cystic fibrosis (CF)

Medium chain Acyl- CoA-dehydrogenase deficiency (MCADD)

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12
Q

Causes of tall stature in children?

A

Familial
Early / precocious puberty
Hyperthyroidism, GH secreting adenomas
Marfan’s, Klinefelters

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13
Q

How does Marfan’s syndrome present?

A

tall stature with arm span to height ratio > 1.05
high-arched palate
pes planus
arachnodactyly
pectus excavatum
lungs: repeated pneumothoraces
eyes: upwards lens dislocation

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14
Q

Define hypersensitivity

A

Objectively reproducible symptoms or signs following exposure to a defined stimulus (e.g. food, drug, pollen) at a dose which is tolerated by normal people

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15
Q

Define allergy

A

A hypersensitivity reaction initiated by specific immunological mechanisms, leading to disease. This can be IgE mediated or non-IgE mediated.

Allergy is not a disease, but a mechanism leading to a disease

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16
Q

Define atopy

A

A personal and/or familial tendency to produce IgE antibodies in response to ordinary exposures to potential allergens, usually proteins.

Strongly associated with asthma, rhinitis and conjunctivitis, eczema and food allergy.

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17
Q

Define anaphylaxis

A

Severe, potentially life-threatening generalised or systemic hypersensitivity reaction which is characterised by being rapid in onset, effecting airway, breathing or circulatory problems, and is usually associated with skin and mucosal changes.

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18
Q

How may anaphylaxis present in children?

A

Signs that are difficult to interpret: behavioural changes, fussing, irritable
hoarseness (after crying), drooling
regurgitation (common after feeds)
drowsiness, somnolence (after feeds)

Signs obvious but non-specific: rapid onset coughing, choking, stridor
sudden, profuse vomiting
rapid onset unresponsiveness

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19
Q

How do allergies develop?

A

Allergic diseases occur when individuals make an abnormal immune response to harmless environmental stimuli, usually proteins

The developing immune system must be ‘sensitised’ to an allergen before an allergic immune response develops.

Sensitisation may be ‘occult’ e.g. sensitisation to egg in from exposure to trace quantities in maternal breast milk.

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20
Q

Outline the process of mast cell activation in IgE mediated allergy

A

antigen binds to specific IgE

IgE releases mediators such as histamine, tryptase and prostaglandins

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21
Q

Describe onset and resolution of sxs in IgE mediated versus non-IgE mediated allergy

A

IgE : comes on within 2 hours, usually resolves within 12 hours

non-IgE: comes on hours or days post ingestion, may continue for days

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22
Q

Describe sxs in IgE mediated allergy

A

Gastrointestinal such as vomiting, pain and diarrhoea

Cutaneous such as urticaria, angiodema, pruritis

Respiratory such as acute rhinoconjunctivitis, wheezing, coughing, stridor

Cardiovascular such as collapse due to hypotension

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23
Q

Describe sxs in non-IgE mediated allergy

A

Often non-specific symptoms.

These can include diarrhoea, vomiting, colic/pain, blood in the stool, gastrooesophageal reflux and food refusal or aversion.

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24
Q

Give some examples of IgE-mediated clinical phenotypes

A

Acute urticaria and angioedema, anaphylaxis, oral allergy syndrome

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25
Q

Give some examples of non-IgE-mediated clinical phenotypes

A

Food protein induced proctocolitis, food protein induced enteropathy, allergic dysmotility

26
Q

How might an IgE mediated reaction appear in the skin?

A

pruritus
erythema
acute urticaria
acute angioedema

27
Q

How might a non-IgE mediated reaction appear in the skin?

A

pruritus
erythema
atopic eczema

28
Q

What questions could you ask a parent to determine if their child has asthma or a viral wheeze?

A

Does your child have a diagnosis of asthma?
Is your child ever wheezy? When do they become wheezy? What triggers it?
Do they get symptoms with exercise, stress, with colds?
Do they cough at night?
Do they respond to salbutamol? How do you give the salbutamol?

29
Q

What questions would you ask the parent of a child with eczema?

A

When did the eczema start?
What happened around the time of weaning?
Severity? When did the eczema get worse?
How much moisturiser / steroid do you use?

30
Q

What should you ask in the family history component of an allergy history?

A

Does anyone in the family have: Asthma, Hay fever, Eczema, Food allergies

Any pets at home?

31
Q

How can allergies be diagnosed?

A

specific IgE immunoassay
skin prick
Gold standard for food allergy is DBPCFC (Double blind placebo controlled food challenge)

32
Q

How can allergies be managed?

A

allergen avoidance
disease specific tx e.g. non-sedating antihistamines for urticaria, emollients/steroids for eczema

33
Q

How would you explain to a patient how to use their EpiPen?

A

lie down

remove blue safety cap - ‘blue to the sky, orange to the thigh’

hold pen with fist - don’t put thumb over the top as if wrong way round will stab finger

jab the EpiPen firmly into your outer thigh at a right angle until you hear a click. Hold firmly for 3 seconds, before removing and safely discarding

massage the injection site for 10 seconds

elevate your legs

if the first injection does not work, do a second injection after 5-15 minutes

call 999

34
Q

What are the two main brands of adrenaline auto-injector?

A

EpiPen
Jext- good for older children / teenagers as links with an app

35
Q

What online resource can be helpful for education and mx of children with allergy?

A

itchy sneezy wheezy - educational website

36
Q

What is the acute mx of anaphylaxis?

A

Assessment: ABCDE

First-line treatment
IM adrenaline

Second- and third-line treatment
Removal of the trigger and call for help
Posture
Oxygen
Fluids
Other drugs e.g. β2-agonists, glucocorticoids

37
Q

What is involved in the long term risk reduction of anaphylaxis?

A

Risk assessment

Emergency preparedness:
Allergen identification, Emergency Action Plan, Adrenaline Auto-injector prescription

Allergen avoidance

Immunomodulation

38
Q

Dose of adrenaline to give in kids in anaphylaxis?

A

0-6 years or up to 30kg : 0.15 mg
6-12 years or 30-50 kg : 0.30 mg
> 12 years or above 50kg : 0.50 mg

39
Q

What effects risk of anaphylaxis?

A

Age: infants, adolescents, elderly

Concomitant disease: asthma and other respiratory diseases, cardiovascular disease, psychiatric illness

Concomitant medication e.g. beta-blockers, ACE inhibitors

Cofactors that amplify anaphylaxis: stress, infection
exercise

Allergen itself - prevalent?

40
Q

What to ask in a history of a food allergy

A

food and amount eaten, timing of symptoms
nature of symptoms (each system)
details around event (e.g. cold, exercise)
associated allergies (i.e. asthma, eczema)
concomitant diseases

41
Q

What is the underlying pathology in inguinal hernias and hydrocoeles in infants?

A

patent processes vaginalis

fully patent = inguinal hernia

partially patent = hydrocoele ( enough space for peritoneal fluid to escape but not for bowel to pass through)

42
Q

Parents bring in child to ED with sudden appearance of fluctuant testicular swelling that transilluminates following recent viral illness =

A

hydrocoele

during viral illness production of peritoneal fluid increases so may cause hydrocele to become more obvious

43
Q

What is the gubernaculum?

A

embryological structure that guides the descent of the testes - becomes the tunica vaginalis (double layer that surrounds the testes)

44
Q

What type of inguinal hernia is more common in kids?

A

indirect - passes through the deep and then superficial inguinal ring

can cause obstruction!!! - look for hernia in young child with bowel obstruction of unknown cause

45
Q

What should be done if a paediatrician assesses that a child’s testicle is not situated within the scrotum after 3 months?

A

straight to examination under anaesthetic and diagnostic laparoscopy

USS is unhelpful as the testicle will be very small and difficult to see

46
Q

Why is it important that testes are surgically returned to the scrotum if undescended ?

A

reduced risk of testicular cancer

allows to self examine for testicular tumour as risk is still higher than general population

ideal temperature for hormone production and maintaining fertility

reduced risk of trauma

47
Q

What does the blue dot sign on an infant’s testis suggest?

A

torted hyatid of morgagni (Mullerian remnant)

48
Q

Give some causes of bilious vomiting in neonates

A

duodenal atresia
jejunal atresia
malrotation with volvulus
meconium ileus
necrotising enterocolitis

NOT pyloric stenosis - in PS obstruction is above the 2nd segment of the duodenum where bile enters the GI tract so vomitus will not be bilious

49
Q

What is the definition of diabetes?

A

Fasting plasma glucose > 7.0 mmol/l

2 hour post prandial plasma glucose > 11.0 mmol/l during an OGTT

50
Q

How should you investigate a child who presents to the GP with suspected T1DM?

A

Children and young people with suspected T1DM
should be offered immediate (same day) referral to multidisciplinary paediatric diabetes team - risk of deterioration to DKA

51
Q

Ix in paediatric diabetes?

A

BMI
HbA1c
OGTT
Fasting Insulin
Fasting C peptide
Autoantibodies

52
Q

What is DKA?

A

diabetic ketoacidosis - caused by uncontrolled lipolysis which results in an excess of free fatty acids that are converted to ketone bodies

hyperglycaemia (plasma glucose more than 11 mmol/litre) and

acidosis (indicated by blood pH below 7.3 or plasma bicarbonate below 15 mmol/litre) and

ketonaemia (indicated by blood ketones > 3 mmol/litre) or ketonuria (++ and above on the standard strip marking scale)

53
Q

Suspect DKA even if the blood glucose is normal in a child or young person with known diabetes and any of the following:

A

nausea or vomiting

abdominal pain

hyperventilation

dehydration

reduced level of consciousness

54
Q

When a child or young person with suspected or known DKA arrives at hospital, measure their:

A

capillary blood glucose

capillary blood ketones (beta‑hydroxybutyrate) or urine ketones

capillary or venous pH and bicarbonate

55
Q

Give some of the main differences between T1DM and T2DM

A

Deficiency of insulin v insulin resistance
Absent C peptide v detectable C peptide
Markers of autoimmunity v none
Sudden v gradual onset
Ketoacidosis common v rare
Not obese v obese

56
Q

How do you calculate fluid requirements in children?

A

for 24 hours:

First 10 kg - 100 ml/kg
Second 10 kg - 50 ml/kg
Subsequent 10 kg – 20 ml/kg

57
Q

What are the fluid requirements of neonates born at term?

A

Day 1 – 50 ml/kg/day
Day 2 – 75 ml/kg/day
Day 3 – 100 ml/kg/day
Day 4 – 120 ml/kg/day
Day 5 onwards - 150 ml/kg/day

58
Q

Why do preterm babies have a high fluid requirement ?

A

very fragile skin = large fluid losses

require more fluid replacement than term babies and incubators often contain humidified air

59
Q

What fractures should raise suspicion of physical abuse?

A

Metaphyseal fractures - bucket handle or
corner fractures
Rib fractures - commonly posterior
Skull fracture - usually non parietal and
associated with subdural haemorrhage
Scapular fractures
Sternal fractures

60
Q

Give some differentials for unexplained bruising

A

NAI
Congenital melanocytic naevi
Thrombocytopenia
Haemophilia
Henoch-Schonlein purpura (HSP)

61
Q

What is a skeletal survey used for?

A

Children under 2 with suspected physical abuse
Used to detect occult bone injury

Ideally within 72 hours, provides imaging of the whole skeleton

62
Q

Why do babies have a large amount of brown fat?

A

carries a high water volume to prevent them from becoming dehydrated

colostrum is calorie rich but does not contain enough fluids

significant WL in babies suggests dehydration

y4 paediatrics (17 decks)

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