Child Health Flashcards

1
Q

Why should you not examine the upper airway in suspected airway obstruction?

A

As it can lead to increased distress and breathlessness

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2
Q

In which respiratory infections should you not examine the upper airway and why?

A

Croup
Epiglottitis

As it can cause further obstruction

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3
Q

In what age group is croup most common?

A

6 months - 3 years

Peaks at age of 2

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4
Q

What is the main cause of croup?

A

Viral respiratory infection - typically parainfluenza

Causes infection of the upper airways

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5
Q

What are the differentials for upper airway obstruction in children?

A
Epiglottitis 
Foreign body aspiration 
Croup 
Allergic reaction 
Tonsillar abscess
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6
Q

How can you tell the difference between mild, moderate and severe croup?

A

Mild - just seal like barking cough
Moderate - plus stridor and sternal recession
Severe - plus agitation, lethargy, decreased level of consciousness. Signs of respiratory failure

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7
Q

What is the management of croup?

A

Mild - oral dexamethasone
Moderate - plus nebulised adrenaline
Severe - hospital admission, oxygen, nebulised adrenaline and dexamethasone

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8
Q

What is epiglottitis?

A

Inflammation and swelling of epiglottis

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9
Q

What are the symptoms of epiglottitis

A
Dyspnoea 
Dysphonia (difficulty speaking)
Dysphagia (difficulty swallowing)
Fever
Irritability 
Pooling of oral secretions and saliva
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10
Q

How is epiglottitis managed?

A

Hospital admission
Intubation
IV antibiotics
Corticosteroids

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11
Q

Which bronchus are foreign body aspiration more likely to go down and why?

A

Right main bronchus

As the left one has a more acute angle

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12
Q

Why is inhalation of a circuit battery dangerous?

A

Can set up an electrical circuit in moist environment

This can cause oesophageal perforation

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13
Q

What is laryngomalacia?

A

Congenital abnormality of the larynx cartilage

This predisposes a child to dynamic supraglottic collapse during inspiratory phase of respiration

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14
Q

When does laryngomalacia present?

A

In first few weeks of life

Usually spontaneous resolution by 2 years

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15
Q

Why is the presentation of epiglottitis in children becoming more uncommon?

A

Due to the HiB vaccination

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16
Q

What are the actions of histamine?

A

Vasodilation
Bronchoconstriction
Localised irritation
Endothelial cell separation

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17
Q

When would you prescribe someone an adrenaline pen?

A

If they have a history of anaphylaxis - with previous cardiovascular and respiratory involvement
Evidence of previous airway obstruction
Poorly controlled asthma
If they react to small amounts of allergen
If they cannot easily avoid an allergen

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18
Q

What is the feeding requirements for neonates?

A

150ml/kg/day - up to 1 month

100ml/kg/day - after 1 month

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19
Q

In which congenital heart conditions would the lung fields appear brighter on a chest X-ray?

Why is this?

A

Ventricular septal defect
Patent ductus arteriosis
Cardiac failure

This is because too much blood is going to the lungs

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20
Q

In which congenital heart conditions would the lung fields appear darker on a chest X-ray?

Why is this?

A

Fallouts tetralogy
Pulmonary stenosis

Too little blood going to the lungs

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21
Q

What are the risk factors for a neonate having congenital heart disease?

A

Rubella during pregnancy
Diabetes during pregnancy
Using ACEi, statins, lithium during pregnancy
Smoking/drinking during pregnancy
Consanguinity - where parents are blood relatives

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22
Q

What are the different aycanotic congenital heart defects?

A
Ventricular septal defect
Arterial septal defect 
Patent ductus arteriosis (PDA)
Coarction of the aorta 
Aortic valve stenosis
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23
Q

What are the different cyanotic congenital heart defects?

A

Tetralogy of fallout (TOF)
Transposition of the great arteries (TGA)
Ebsteins anomaly

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24
Q

At what oxygen saturations would cyanosis start to occur?

A

Between 80-85% of oxygen

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25
Q

What is the most common congenital heart disease?

A

Ventricular septal defect (VSD)

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26
Q

What kind of murmur is heard in VSD?

A

Pan systolic murmur

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27
Q

How does VSD present in neonates?

A

Usually asymptomatic in first few weeks of life

After that they present with poor feeding, often becoming breathless when feeding, and poor weight gain

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28
Q

How is VSD diagnosed?

A

Echocardiogram

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29
Q

What causes the PDA close after birth

A

High circulating oxygen

Fall in prostaglandin

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30
Q

Why might a PDA stay open after birth?

A

Preterms - as lungs are less mature so less sensitive to oxygen
Sensitivity to low levels of prostaglandin - so stays open
Rubella infection

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31
Q

What are the signs of a PDA?

A

Continuous machinery murmur - left scapula
Large volume, bounding, collapsing pulse
Wide pulse pressure
Left subclavicular thrill

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32
Q

How is a PDA managed?

A

Indomethacin (NSAID) - which inhibits prostaglandin synthesis and causes PDA to close

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33
Q

What conditions are screened for at the neonatal heel prick test?

A

Sickle cell disease
Cystic fibrosis
Congenital hypothyroidism
Inherited metabolic diseases (x6)

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34
Q

Why might you not give high flow oxygen to a baby with heart failure?

A

If you were relying on the PDA to maintain a viable circulation

High oxygen concentrations can cause duct failure and lead to worsening of condition

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35
Q

What is the pathophysiology of cystic fibrosis?

A

Mutation in chloride transporter
Chloride cannot be pumped out of cells, which is usually responsible for dragging water out with it
This results in not enough water being dragged into the airways
This results in the mucus being thick and sticky, blocking the airway
Mucus is usually responsible for trapping bacteria and being wafted out by cilia
If Mucus is thick it is unable to be cleared, which can result in difficulty breathing and increase risk of respiratory infections

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36
Q

How might cystic fibrosis be diagnosed?

A

Neonatal heel prick test
Sweat test - check for chloride levels
Genetic test
X ray - may show signs of bronchiectasis
Stool analysis - as high levels of nutrients may suggest poor absorption

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37
Q

What chemical is used during the sweat test?

A

Pilocarpine - applied to skin which causes sweating

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38
Q

How does cystic fibrosis in children commonly present?

A

Neonatally - can present with meconium ileus, prolonged jaundice
In childhood - may present as recurrent chest infections, steatorrhoea, or failure to thrive

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39
Q

How is cystic fibrosis managed?

A

Physiotherapy - to clear airways
Antibiotics - to treat recurrent chest infection
Medicines to make mucus in lungs thinner - e/g, mannitol dry powder
Bronchodilators - to widen airways and make breathing easier
Pancreatic enzyme supplements

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40
Q

What are the main causes of bronchiectasis in children?

A
Cystic fibrosis 
Primary ciliary dyskinesia 
Severe respiratory tract infection 
Immune deficiency 
Poor lung development 
Blockage due to nut
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41
Q

What is appropriate diet for a child with cystic fibrosis?

A

High calorie
High fat
Pancreatic enzyme supplementation for every meal

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42
Q

What is the stepwise management for a child aged 5-16 with asthma?

A

1st line - SABA
2nd line - low dose ICS
3rd line - leukotrine receptor antagonist (LTRA)
4th line - low dose ICS and LABA (stop LTRA)
5th line - maintenance reliever therapy (MART) with ICS

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43
Q

What is Harrison’s sulcus?

A

It is a horrizontal groove on the lower border of the thorax corresponding to the costal insertion of the diaphragm

It is an indicator of chronic asthma in children or obstructive respiratory disease

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44
Q

What is the presentation of asthma in a child?

A
Recurrent viral respiratory infections 
Wheeze 
Dry cough 
Breathlessness 
Symptoms typically worse at night
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45
Q

Any safeguarding concerns should be reported to who?

A

Social services

Also report to the safeguarding lead - this may be a designated doctor or nurse

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46
Q

What is the pathophysiology of shaken baby syndrome?

A

Babies have weak neck muscles
Therefore if an infant is shaken their head will move uncontrollably
This movement causes the baby’s brain to be thrown against side of skull - which can cause bruising, swelling or bleeding

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47
Q

What are the 3 conditions that may indicate shaken baby syndrome?

A

Encephalopathy
Subdural haematoma
Retinal haemorrhage

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48
Q

What imaging would you do if you suspected shaken baby syndrome?

A

MRI/CT scan - look for any bleeding or swelling in brain
Skeletal x ray - may reveal fractures
Ophthalmic exam - looking for retinal haemorrhage

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49
Q

What are the differentials for bruising in a child?

A
Accidental injury 
Non accidental injury 
Clotting disorder - Von willbrands, haemophilia, thrombocytopenia 
Henoch-scholein purpura 
Meningococcal septicaemia 
Leukamia 
Mongolian blue spot
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50
Q

What investigations would you do if a child presented with bruising?

A

Bloods - FBC, U&E, LFTs, clotting screen, bone profile
Blood film
INR and APTT - if appropriate

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51
Q

What are the differentials for Fracture in a child?

A
Non accidental injury 
Accidental injury 
Brittle bone disease (osteogenesis imperfecta)
Copper deficiency 
Vit D deficiency 
Vit C deficiency 
Ehlers Danlos syndrome 
JOBs syndrome
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52
Q

What are the differentials for burns/scalds in a child?

A

Non accidental injury - especially if glove stocking syndrome
Accidental injury
Bulbous impetigo - bacterial infection
Staphylococcal Scalded skin syndrome (SSSS)

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53
Q

What are the signs of a fabricated or induced illness (FII)?

A

Often on background of existing disease
OR bizzare new illness
Strange new symptoms
Parental reportage not keeping with physical findings
Symptoms not witnessed by other (e.g, fits not seen by school)

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54
Q

What is a child protection medical assessment?I

A

Medical assessment requested by social services
Carried out by a consultant
Detailed history and exam taken which is recorded
Any other relevant investigations done
The doctor will then produce a report for social services about the likelihood of an injury being accidental or not

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55
Q

What are the red flags for abuse regarding bruising in children?

A

If on face, back or buttock

If bruise outlines an object e/g, hand, belt

If there is fingertip bruising

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56
Q

What are the toxic trio for child abuse?

A

1) domestic violence
2) parental mental health problem
3) parental substance abuse problem

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57
Q

What is a body map and when is it used?

A

It is used to accurately document visible findings on examination

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58
Q

What are the differentials for chronic abdominal pain in children?

A
Chronic recurrent abdominal pain syndrome 
Constipation 
Peptic ulcer disease 
IBS
IBD
Abdominal migraine
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59
Q

Which type of IBD is more common in children?

A

Crohn’s disease

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60
Q

How is Crohn’s disease managed in children?

A

Diet - liquid protein diet is successful in achieving remission
Then slowly introduce different foods to see what is safe

Medication - steroids, immunosuppressive meds, biologics - these can be used if diet is unsuccessful

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61
Q

When should you diagnose a functional gut disorder in a child with recurrent abdominal pain?

A

When all other disorders have been ruled out

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62
Q

What are the causes for blood in stools in children?

A

Bacterial infection - e.g campylobacter, salmonella
IBD
Tearing from anal vein
Intussusception - note that child would present acutely unwell

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63
Q

What are the differentials for acute abdominal pain in a child?

A
Gastroenteritis 
DKA
Appendicitis 
Intussusception 
UTI
Henoch-sholein purpura 
Testicular torsion
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64
Q

At what age is intussception most common?

A

Between the ages of 3 months - 2 years

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65
Q

What are the causes of intussusception?

A

May have preceding viral illness
Swelling in the bowel wall
Meckels diverticulum (congenital outpouching)

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66
Q

What are the symptoms of intussusception?

A

Severe abdominal pain
Child may get pain when they draw the legs up
Dehydration signs - fewer wet nappies, sunken fontanelle, dry mucous membranes
Fever
Acitis
Blood in stool - red currant jelly stool

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67
Q

How would you diagnose intussusception?

A

Abdominal exam - can sometime palpate it

USS - doughnut sign

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68
Q

How is intussusception managed?

A

Fluids - rehydrate child
Nasogastric tube - to drain stomach and bowel contents
Antibiotic - to reduce infection

Air enema - passed up child bottom and releases air. This has effect of pushing the bowel back

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69
Q

What should you always ask any child that presents with diarrhoea and vomiting?

A

Travel history
Contact history - anybody else ill, any animals?
Vaccination history

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70
Q

Which conditions can cause weight loss in children?

A
Coeliac disease
Type 1 diabetes
Hyperthyroidism 
IBD
Malignancy
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71
Q

Which mental health problems may cause weight loss in children?

A

Anorexia nervosa
Depression
OCD
Autism

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72
Q

What are the risks of rapid weight loss?

How can you check for these?

A

Hypoglycaemia - check BMs
Risk of infection - FBC
Cardiac arrhythmia - ECG

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73
Q

What are the 3 main eating disorders seen in young people?

A

Anorexia Nervosa
Bulimia Nervosa
EDNOS

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74
Q

What are the behavioural features of anorexia nervosa?

A

Feeling fat, unhappy with body shape
Won’t eat in front of others
Hiding food
Compulsive exercise

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75
Q

What are the clinical features seen in someone with anorexia nervosa?

A
Weight loss 
Amenorrhoea 
Headaches - due to dehydration 
Constipation - as gastric motility slows down 
Dry skin and hair loss 
Lethargy 
Dizziness/fainting 
Cool peripheries
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76
Q

What are the features of bulimia nervosa?

A

Binging on food and then vomiting
Can occur alongside self harm
Weight is often normal
Associated with low self worth

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77
Q

Why do people with eat disorders abuse laxatives?

A

They struggle with sensation of food in their bodies

So take laxatives to relieve this feeling

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78
Q

What are the side effects of laxatives?

A

Electrolyte imbalances - can lead to cardiac arrest
Dehydration
Oedema - happens when patients stop taking them, which leads to fluid overload
Loss of bowel motility - in chronic laxative use

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79
Q

What is the cause of anorexia nervosa?

A

Neuro-biological illness - important to explain that it is not the patients fault

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80
Q

What does emancipated mean?

A

When a patient looks abnormally thin

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81
Q

What is Lanugo hair?

A

Hair on face that happens in anorexia nervosa - this is a response to the loss of the insulating effect of fat tissue

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82
Q

Why is weight for height ratio used instead of BMI in children?

A

BMI is less reliable in children

Can assess the height to their age

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83
Q

At what ratio would the weight to height ratio concern you?

A

If less than 75%

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84
Q

How would you manage a patient with anorexia nervosa?

A

Hospital admission for stabilisation
Encourage to eat - aim for 0.5-1kg weight gain per week
Commence on vitamins (thiamine, vit B, multivitamins)
When stable can discharge and support with multiple teams in community - child psychiatrist, dietician, family therapist, paediatrician

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85
Q

What bloods do you have to monitor when treating a patient with anorexia nervosa and why?

A

Must monitor phosphate
Drop in phosphate is a marker of re feeding syndrome
This may precipitate respiratory arrest

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86
Q

What are the differentials for vomiting in a child?

A
Feeding issues 
Gastroesophageal reflux disease 
Gastroenteritis 
Pyloric stenosis 
Meningitis 
Urinary tract infection 
Coeliac disease 
Intussusception
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87
Q

What are the signs of dehydration in a child?

A
Sunken anterior fontanelle 
Dry mucous membranes
Tachycardia 
Oliguria (lack of urination)
Reduced capillary refill time (>3 seconds)
Reduced skin turgor
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88
Q

Which children are at an increased risk of dehydration?

A

Low birth weight
Age <1 year
More than 2 vomiting episodes and more than 5 diarrhoea episodes in last 24 hours

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89
Q

How would you manage dehydration associated with vomiting/diarrhoea in children?

A

Rehydration with oral rehydration solution
Give by nasogastric tube if child is unable to drink or there is persistent vomiting
Give fluids in severe dehydration

Also remember to monitor urine output, as well as the number of vomit and stool

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90
Q

How do oral rehydration solutions (ORS) work?

A

They provide a mix of glucose, electrolytes and salts, which help with the absorption of sodium in the intestines

As the sodium is absorbed, then water is able to follow - helping the body to rehydrate

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91
Q

What are the signs of hypernatraemia?

A
Jittery movements 
Increased muscle tone
Hyperreflexia 
Convulsions 
Drowsiness or coma
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92
Q

What are the main causes of gastroenteritis in children?

A

Rotavirus - especially in children under the age of 2
Adenovirus - more common in young children
Norovirus - more common in adults
Campylobacter
C.diff
Salmonella
Shigella
E.Coli 0157 - less common in children but should always be considered

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93
Q

When would you want to do further investigations in a child presenting with gastroenteritis?

A
Recent travel abroad
If diarrhoea isn't improving by day 7 
In suspected septicaemia 
If there is blood or mucus in stool 
In an Immunocompromised child
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94
Q

What is the usual time course of gastroenteritis?

A

Vomiting should settle in 2-3 days
Diarrhoea should settle by day 5-7

Most children should recover completely within 2 weeks

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95
Q

How does haemolytic uraemic syndrome present?

A

Bloody diarrhoea
Abdominal pain
Nausea and vomiting

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96
Q

What is the pathophysiology of HUS?

A

E.coli 0157 produces shiga toxin
This binds to cells causing microvascular thrombosis, fragmentation of erthrocytes and destruction of platelets
This results in renal insufficiency
Also effects the hear, intestines, pancreas and CNS

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97
Q

How is HUS managed?

A

DO NOT USE ANTIBIOTICS - these can cause further renal damage
Mainly supportive treatment
Make sure patient is adequately hydrated - but take care to avoid fluid overload
Treat any anaemia with transfusion or dialysis

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98
Q

What fluids would you give in fluid resuscitation in a child?

A

20ml/kg 0.9% sodium chloride by rapid IV infusion

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99
Q

What fluids do you give in fluid maintenance for a child?

A
0.9% NaCl and 5% dextrose 
A: 100ml/kg for first 0-10kg
B: 50ml/kg for 10-20kg
C: 20ml/kg for >20kg
(A+B+C=D)
To get the amount in ml/hour, do D divided by 24 hours
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100
Q

What are the main differentials for fever in child?

A
URTI
Meningitis 
UTI
Bronchiolitis - if in 1st year of live 
Kawasakis disease - if lasting longer than 5 days 
Tonsillitis 
Otitis media 
Epiglottitis 
Septic arthritis
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101
Q

How does Kawasaki’s disease present?

A
Fever lasting more than 5 days 
Cervical lymphadenopathy 
Conjunctival infection (red eyes)
Cracked lips, strawberry tongue 
Polymorphous rash - rash due to sensitively to sun
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102
Q

What group of patients would you be more likely to see kawasakis disease in?

A

Children under 5 years

Children from northeast Asia, especially japan and Korea

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103
Q

How would you manage a patient with suspected kawasakis disease?

A

IV immunoglobulin and aspirin - these reduce risk of coronary artery aneurysm
Steroids
ECHO - to check for coronary artery aneurysm

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104
Q

What are the differentials for a non-blanching rash in a child?

A

Meningitis
Henoch-scholein purpura
Idiopathic thrombocytopenia Purpura
Measles - rash can become non-blanching after 3-4 days

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105
Q

What is henoch-schonlein purpura?

A

Type of vasculitis that commonly occurs in children
Typically seen in children following an infection
Degree of overlap with IgA nephropathy (Berger’s disease)

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106
Q

How does henoch-schonlein purpura present?

A

Palpable purpuric rash over buttocks and extensor surfaces and arms and legs
Abdominal pain
Polyarthritis (joint pain)
Features of IgA nephropathy e.g, haematuria, renal failure

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107
Q

How is HSP usually managed?

A

Supportive care as generally self limiting condition
Pain relief for analgesia

Check U&Es and PCR for kidney function

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108
Q

What are the non-specific symptoms that children can present with when they have meningitis?

A
Fever
Vomiting/nausea 
Lethargy 
Irritability 
Refusing food/drink 
URTI symptoms
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109
Q

What are the specific meningitis symptoms?

A
Stiff neck 
Headache 
Altered mental stat
Bulging fontanelle (in children <2)
Photophobia 
Seizures
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110
Q

What are the kernigs and brudzinski’s signs?

A

Signs that might suggest meningitis
Kernigs - pain in neck when hips are flexed to 90 degrees and knees extended
Brudzinski’s sign - when neck is flexed this causes hips and knees to flex

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111
Q

What are the contraindications for doing a lumbar puncture?

A
Evidence of raised ICP 
Focal neurological signs 
Signs of shock 
Signs of meningococcal septicaemia (Purpuric rash)
Coagulation abnormalities 
Infection at puncture site
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112
Q

How can you tell the difference between viral, bacterial and TB meningitis from the CSF interpretation?

A

Bacterial: high neutrophils, high protein, low glucose
Viral: high lymphocytes, normal protein, normal glucose
TB: high lymphocytes, high protein, low glucose

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113
Q

How would you manage meningitis or meningococcal septicaemia?

A

Primary care - IM benzylpenicillin

Secondary care - IV cefatriaxone (plus amoxicillin if <3 months old)

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114
Q

When would you use steroids to treat meningitis?

A

If there is suspected or confirmed bacterial meningitis
Give first steroid dose within 4 hours of starting antibiotics

NOTE: do not use steroids in children <3 months

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115
Q

What are the most common causes for meningitis in neonates?

A

Group B strep
E.Coli
Listeria Monocytogenes - this is sensitive to amoxicillin which is why you give it to children <3

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116
Q

What is the most common cause for meningitis in children aged 3 months - 5 years

A

Niessria meningitis
Streptococcus pneumoniae
Haemophilis influenza B

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117
Q

What is the most common causes for meningitis for children over the age of 5?

A

Niesseria Meningitis

Streptococcus Pneumoniae

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118
Q

Which vaccinations are given to children to help prevent against meningitis?

A

Men B - protects against group B strep (given at 8, 16 weeks and 1 year)
Hib/MenC - protects against haemophilis influenza and meningitis C (given at 8, 12 and 16 weeks, and 1 year)
Prevenar 13 - protects against step pneumonia (given at 8 weeks, 16 weeks, and 1 year)

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119
Q

What should all children have after having meningitis?

Why?

A

An audiology assessment
This is done at 4 weeks after discharge

The risk of hearing impairment is high - bilateral hearing loss can occur in up to 4% of patients

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120
Q

What are the main gross motor developmental milestones?

A
6 months - good head control 
9 months - can sit unsupported, can crawl 
12 months - can stand and cruise
18 months - can walk unsupported 
2 years - can jump, kick, throw 
3 years - can pedal tricycle
121
Q

What are the main vision and fine motor milestones?

A

6 weeks - can fix and follow
6 months - can transfer objects from hand to hand
1 year - effective grip
18 months - can stack 2-3 cubes
2 years - can stack 6 cubes, can draw a circle
3 years - can stack 10 cubes, can use knife and fork

122
Q

What are the main hearing, speech and language milestones?

A
3 months - turn to sounds, coos 
6 months - vocalises 
9 months - babbles e.g, mama
12 months - imitates sounds (1 or 2 words)
18 months - >5 words
2 years - can say 2 word phrases 
3 years - can say short sentences
123
Q

What are the main social, emotional and behavioural milestones?

A
6 weeks - smiles 
6 months - enjoys facial expressions 
9 months - waves bye bye 
12 months - plays peekaboo
18 months - can mimic actions 
2 years  - can use objects to play 
3 years - can peer interact and role play
124
Q

What is Lyme disease?

A

Bacterial infection cause by a tick bite - where the tick is a carrier for the bacteria borrelia burgodoferi (Not all ticks carry this bacteria)

125
Q

What are the 3 stages of Lyme disease?

A

Early disease - fever, arthralgia, malaise, rash
Several weeks after - meningitis, facial palsy, arthritis
Years/months later - neuropsychiatric manifestations

126
Q

What is the name of the rash which is commonly seen in Lyme disease?

A

Erythema Migrans

It is an expanding circular rash - can occur up to month after a tick bite and last for several weeks

Looks like a bulls eye

127
Q

What is the treatment for Lyme disease?

A

Amoxicillin and cefuroxime

128
Q

What are the common symptoms of UTI in children?

A
Fever 
Vomiting 
Irritability 
Poor feeding 
Failure to thrive 
Loin tenderness (pyelonephritis)
129
Q

What is the most common pathogen responsible for UTI in children?

A

E.Coli

130
Q

If you suspect a UTI in a children under the age of 3 months, what should you do?

A

Urgent referral to paediatric specialist unit
Parenteral antibiotics
Urine sample sent for urgent microscopy and culture

131
Q

How can you get a urine sample from a child?

A

Clean catch sample is recommended
If unobtainable can use urine collection pads
When not possible to use non invasive methods then you could use suprapubic aspiration guided by USS

132
Q

Deepest on the microscopy results, when would you treat as a UTI and when would you not?

A

Both Nitrate and Leukocyte positive - UTI
Nitrate positive but leukocyte negative - UTI
Nitrate negative but leukocyte positive - only start antibiotic if clinical signs of UTI
Nitrate negative and leukocyte negative - No UTI

133
Q

At what age would an upper UTI be more common?

A

In a child less than 3 months old

134
Q

What is the antibiotic of choice for lower UTI in children?

A

1st line - Trimethoprim

2nd line - nitrofurantoin

135
Q

What is the antibiotic of choice for upper UTI in children?

A

1st line - cefalexin

2nd line - co-amoxiclav

136
Q

Regarding UTIs in children, when would you want to investigate further?

A

In children <6 months old with UTI
In children with recurrent UTIs
If any features of an atypical UTI are present

137
Q

What defines an atypical UTI?

A

If the child is seriously ill
If there is poor urine flow
If there is an abdominal or bladder mass
If there is raised creatinine
In septicaemia
Failure to respond to treatment within 48 hours
Non E.Coli infection

138
Q

What defines a recurrent UTI in children?

A

2 or more upper UTI
1 upper and 1 or more lower UTI
3 or more lower UTI

139
Q

When would you want to do a renal USS in a child with a UTI?

Why?

A

If they are <6 months
If they have atypical UTI

To check for any hydronephrosis due to obstruction or vesicoureteric reflex

140
Q

What is an MCUG?

What is the use in it?

A

Micturating cystogram
Where you fill bladder with contrast and take x ray as child voids urine
Helps to identify any vesicoureteric reflex (VUR), OR posterior urethral valves

141
Q

What is DMSA?

A

Dimercaptocuccinic acid scintigraphy

Radionucliotide scan of kidneys - isotope is given and healthy kidneys takes up isotope whereas unhealthy tissue does not

142
Q

When would you do a DMSA and why?

A

If a child had recurrent UTI or atypical UTI <3 years

Carried out 4-6 months after infection to look for any renal scaring and damage which followed after infection

143
Q

If DMSA shows scaring of kidney after infection, what are the protocols?

A

There is a 10% risk of developing hypertension in long term

Child will need annual assessment of BP

144
Q

If MCUG shows VUR on x-ray, what is the follow Up protocol in children?

A

Usually prophylactic antibiotic given to prevent UTI
If low grade VUR - then will resolve by age 3-4
If high grade VUR - then children are at risk of recurrent UTIs

145
Q

What are posterior urethral valves?

A

Condition in boys where there is a blockage in the urethra which occurs during development

Results in one or both kidneys not forming properly

146
Q

How may posterior urethral valves present?

A

May present with dribbling of urine in baby boys

May present in utero with a lack of amniotic fluid - as the majority of fluid is made up of urine

147
Q

What is nocturnal enuresis?

What age group is it most common in?

A

Bedwetting
The most common type of urinary incontinence in children

5-10 year olds (tends to resolve after then)

148
Q

How many times must a child wet their bed for a diagnosis of nocturnal enuresis to be made?

A

Minimum episode of once a month for at least 3 months

149
Q

How can nocturnal enuresis be managed conservatively?

A

Avoid caffeine based drinks
Encourage adequate fluid intake - as fluid restriction may make it work
Treat constipation - if this is causing it
Ensure correct voiding posture
Encourage children to void every 2-3 hours during the day

150
Q

What are the other non conservative management options for nocturnal enuresis?

A

Alarm training - small alarm attached to bed, if it gets wet then it sets the alarm off and wakes the child up so they can go to the toilet

Desmopressin - acts to reduce production of urine by increasing water resporption (this is a last resort)

151
Q

Why is an early morning urine sample best for identifying kidney and bladder disease?

A

Urine is more concentrated in morning

So contains higher amounts of elements and proteins

152
Q

At what level of proteinuria would you be concerned?

A

> 20mg/mmol - this may indicate tubular disease
200mg/mmol - this is nephrotic ranges

ACR: >30mg/mmol

153
Q

What is the diagnostic triad for nephrotic syndrome?

A

Proteinuria >35g/L in 24 hours
Hypoalbuminaemia - circulating albumin <25g/L
Odema - due to less protein in circulation so cannot keep hold of water in intracellular spaces, therefore more water leaks out into the extracellular spaces

154
Q

What is the more common form of nephrotic syndrome in children?

A

Minimal change disease

155
Q

What are the known causes of minimal change disease?

A

Idiopathic
NSAID use
Paraneoplastic - associated with Hodgkin’s lymphoma

156
Q

How is minimal change disease managed in children?

A

8 week course of oral prednisolone

157
Q

What are the main complications of nephrotic syndrome?

A

Thromboembolism - due to loss of antithrombin III
Hyperlipidemia - due to loss of albumin, the liver increases more albumin and has a side effect of lipid production
Infections - due to loss of Ig from kidneys, this is more recognised in children

158
Q

Why are children with nephrotic syndrome more at risk of sepsis?

A

Due to loss of antibody proteins

159
Q

Which bacterial is most responsible for sepsis related to nephrotic syndrome in children?

A

Streptococci infection

160
Q

What is the prognosis for children with nephrotic syndrome after steroid treatment?

A

1/3rd - no relapse
1/3rd - infrequent relapse
1/3rd - frequent relapse

161
Q

What is renal Agenesis?

A

Where one kidney is either absent or underdeveloped due to hereditary renal adysplasia

162
Q

What is renal hypoplasia?

A

Where one kidney is smaller than the other

163
Q

What is a horseshoe kidney?

A

Where both kidneys are fused at the lower pole

164
Q

What is the most common cause of AKI in children?

A

Pre renal cause

Due to intravascular fluid depletion and poor renal perfusion - where children are dehydrated or have fluid loss

165
Q

What are the differentials for seizures in children?

A
Vasovagal syncope 
Breath holding attack 
Reflex asytolic syncope
Febrile convulsions 
Epilepsy 
Meningitis
166
Q

How does vasovagal syncope present in children?

A

Normally occurs when a child faints in a hot and stuffy environment
Or can occur after standing too long
Think of 3 P’s (Position, prodrome, provoking factors)
Clinic movements only last a few seconds

167
Q

How would a breath holding attack present?

A

Precipitated by anger or crying
Toddler cannot catch their breath because of this
They may go blue, pale and stiff and limp
LOC may occur but quick recovery

168
Q

How would reflex asytolic syncope present?

A

Triggered by fear, anxiety or pain (common triggers are head trauma or cold food)
Typically child becomes pale and limp, losing consciousness briefly
Followed by involuntary tonic/clinic movements
Urinary continuance may happen but NO tongue biting
Episodes last <1 minute and child makes rapid recovery

169
Q

How do febrile convulsions present?

A

High temperature triggers seizure (>38) - usually following viral illness
Tonic/clonic seizure lasting <5 mins usually

170
Q

At what age group do febrile seizures effect?

A

Between 6 months and 6 years of age

171
Q

What is the difference between a simple febrile seizure and a complex febrile seizure?

A

Simple - <15 mins, does not reccur within 24 hours

Complex - >15 mins, recurs more than once in 24 hours, asscoatied with post neurological abnormalities

172
Q

How would you counsel a parent whose child had a febrile seizure?

A

Common - effect 3% of children
Explain why it happens
30-40% may have another one - if this happens then ensure child is led down and stabilise head and wait for it to pass
If lasting >5 mins then should seek medical attention
If it recurs within 24 hours then will need hospital admission
Slight increase in risk of developing epilepsy when older

173
Q

What is the prevalence of epilepsy in children?

A

0.5%

174
Q

What are the common risk factors for developing epilepsy?

A
Birth asphyxia 
Meningitis when young 
Cerebral palsy 
Trauma 
Febrile seizures in childhood 
Genetic link
175
Q

What are the known triggers for epilepsy?

A

Watching TV
Flashing lights
Lack of sleep

176
Q

What is status epilepticus?

A

Where a seizure lasts for longer than 5 minutes

177
Q

How is status epilepticus managed?

A

Oxygen, check glucose
Step up after every 5 mins:
1st line - buccal midazolam or rectal diazepam
2nd line - IV lorazapam
3rd line - IV phenytoin (to be delivered by glass syringe)

178
Q

What would indicate further investigation via CT/MRI when a child has a seizure?

A

Suspected raised ICP
Progressive neuroglocial deficit
In any child under the age of 2
If there is focal epilepsy
If there is associated learning difficulties
If epilepsy is resistant to full doses of 2 appropriate drugs

179
Q

What is the inheritance pattern of the majority of inborn errors of metabolism?

A

Autosomal recessive

180
Q

What is the difference between organelle disease and small molecule diseases in regards to inborn errors of metabolism?

A

Organelle disease - inheritance of metabolism in an organelle of the cell e.g mitochondria, lysosomes
These typically result in chronic neurodegnereation

Small molecule disease - inheritance of metabolism of a process in the cytoplasm. These are typically manageable by diet

181
Q

What is phenylketonuria (PKU)?

A

Inborn error of metabolism (small molecule disease)
Screened for at newborn heel check
Lack of enzyme that converts phenylalanine to tyrosine
Leads to build up of phenylalanine (amino acid)
This can be toxic to the brain at high concentrations - can cause seizures

182
Q

How do you manage phenylketonuria (PKU)?

A

Body doesn’t produce this amino acid - so the only way you can get it is through diet
Therefore can manage PKU with low protein diet
To avoid being protein deficient - child can take protein supplements of all amino acids (apart from phenylalanine)

183
Q

What is medium-chain acyl CoA dehydrogenase deficiency (MCADD)?

A

Lack of acyl-CoA dehydrogenase enzyme
This is responsible for breaking down fats in the body
Means that when the body is using lots of energy e.g, when they are ill, or when they are exercising, they may need this pathway
And as fats are unable to be broken down fully then it can lead to a build up of toxic metabolites

184
Q

How is MCADD managed?

A

Manage catabolic episodes - ensure to take sugary drinks when ill (vomiting, diarrhoea, fever)

When vomiting replace with 10% dextrose solutions

Avoid long periods without eating during newborn period

185
Q

How might a baby with an inborn error of metabolism present?

A
Poor feeding 
Drowsiness
Sleepiness
Vomiting 
Low energy 
Seizures
186
Q

What are the important investigations to consider in a newborn who appears drowsy after a period of good health?

A
Sugar levels 
ABG
Ammonia levels 
Chloride 
U&amp;Es
187
Q

What are the normal ranges for ammonia in neonates and children?

A

Neonates <100micromols/L

Children <50micromols/L

188
Q

How would you work out an anion gap?

A

(Na+K) - (Cl+bicarbonate)

189
Q

What is a normal anion gap?

A

<11

190
Q

What are the pathological causes of hyperammonia in children?

A

Severe sepsis
Liver failure
Severe cardiac disease
Inborn error of metabolism

191
Q

Where does ammonia come from?

What is is normally converted to?

A

It comes from amino acids as the side chain amine group

When proteins are broken down in the blood then circulating ammonia is converted into urea (less toxic form)

192
Q

Why would you get a build up of ammonia if there was a problem with the urea cycle?

A

Ammonia cannot be converted to urea

193
Q

What are the 2 inborn errors of metabolism groups which lead to hyperammonaemia?

A

Urea cycle disorders - ammonia cannot be converted to urea
Organic acidaemias - where there is an abnormal upstream of enzyme blockage, leading to metabolic acidosis and hyperammonemia

194
Q

What is galactosemia?

A

An inborn error of metabolism that presents in the first few weeks of life
Due to lack of the enzyme galactose-1-phosphate urydial transferase (GAL-1-PUT)
Baby’s cannot break down galactose

195
Q

How is galactosemia managed?

A

Treat with special galactose free diet
Galactose is present in most dairy products and baby formulas
So you have to give substitutes like soy milk

196
Q

What is the normal feeding for a newborn?

A

Should be feeding 150mg/kg/day

Should be feeding every 3-4 hours at least

197
Q

How would you check with a mum if the baby is feeding okay?

A

Ask how long baby is feeding for - should be 5-10 mins
Does baby feel sleepy afterwards - this is normal
Ask about stool colour - stool should be passed after every feed (stool is usually dark black for first few days of life then changes to chicken korma colour)

198
Q

What is the normal amount of weight loss for neonates?

A

Normal for neonates to lose up to 10% of weight in first week of life - this is because they are adjusting to breast feeding

Weight loss will stop by 3-4 days and should have regained weight by end of 2nd week

199
Q

What are the differentials for weight loss in neonates?

A
Poor feeding e.g poor techniques
Neglect 
Cystic fibrosis 
Cows milk protein allergy 
Congenital heart disease 
Pyloric stenosis
200
Q

How does cows milk protein allergy present?

A
Constipation or diarrhoea 
Blood in stool 
Vomiting 
Weight loss
Irritability 
Papular macular rash (Hives like)
Skin reactions - swelling of lips, and face around eyes
Eczema
201
Q

How is cows milk protein allergy managed>

A

Advised to remove all cows milk from child’s diet for period of time - either use special formula OR if breast feeding mum should cut out all cows milk from diet
Every 6-12 months assess to see if intolerance is gone - slowly try to introduce cows milk
Child normally grows out of it by 5 years

202
Q

What are the common features of autism in a child?

A

Difficulties in communication and social interaction
Social isolation
Not knowing how to take turns
At a younger age may present with tantrums, frustration and being a difficult child
Repetitive behaviours

203
Q

Which medical disorders are associated with autism?

A

Fragile X syndrome
Tuberous sclerosis
Williams syndrome
Rubella

204
Q

How do you diagnose ADHD?

A

Inattention, hyperactivity and impulsivity

Must be present for at least 6 months
Must have started to show symptoms before the age of 12
Must be present in 2 or more setting (e.g, at home and at school)

205
Q

What are the risk factors for ADHD?

A
Family history 
Substance use 
Psychiatric illness
Maternal smoking 
Low birth weight
206
Q

How is ADHD managed?

A

Environmental modifications is the main management
Psychoeducation - parents and child attend ADHD focus group to understand ADHD and how it presents in order to make environmental modifications
School accommodations - work to create individual education plan
(Contact SENCO - special educational needs coordinator)
Stimulant medications - e.g, Ritalin (methylphenidate) - if symptoms are still an issue after environment modifications have been made

207
Q

What is the stepwise medical management for ADHD?

A

1st line - methylphenidate (Ritalin)

2nd line - lisdexamefetamine, dexamfetamine

208
Q

What is cerebral palsy?

A

Disorder of tone, posture and movement

Cause by a non progressive brain lesion in a developing brain

This brain damage can occur before, during or soon after birth

209
Q

When do the symptoms of cerebral palsy usually present?

A

In the first 2-3 years of life

210
Q

What are the symptoms of cerebral palsy?

A

Delay in reaching motor milestones - e.g, not sitting by 8 months, or not walking by 18 months
Seeming too stiff or too floppy
Weak arms or legs
Fixity, jerky or clumsy movements
Walking on tip toes
Early hand preference (in first year of life)
Asymmetrical movement or posture

211
Q

What does hemeplegic cerebral palsy mean?

A

Where the brain lesion only effects one hemisphere - so only the opposite side of the body is effected

This is the most common form of cerebral palsy

212
Q

What are the causes of cerebral palsy?

A

Any damage to the brain before, during or after birth. These can include:

  • premature birth
  • infection during pregnancy
  • birth hypoxia
  • any pregnancy complication
  • head trauma soon after birth
  • meningitis in neonate
213
Q

What is HIE?

A

Hypoxia ischemic encephalopathy

Where there is reduction in the supply of oxygen to the brain, due to a low blood flow to the brain. This occurs just before or after birth when an infants brain doesn’t receive enough oxygen or blood

214
Q

What is perventricular leukomalacia?

A

A type of brain injury that affects premature infants
Involves the death of small areas of white matter in the brain around the ventricles
Due to hypoxic/ischemic insult
Is a high risk factor for cerebral palsy

215
Q

What are the 3 types of cerebral palsy?

A

Spastic (70-80%) - stiff movements, motor cortex damage
Ataxic (6%) - shaky movements, cerebellum damage
Dyskinetic (choreo-athetoid) - involuntary movements, basal ganglia damage

216
Q

How is cerebral palsy managed?

A

No cure - mainly conservative management
Physiotherapy - to help with movement
Speech therapy - to help with communication and swallowing
Medications to reduce muscle tone
Surgery - to treat movement or growth problems

217
Q

What medications are available for patients with cerebral palsy to help reduce muscle tone?

A

Baclofen - treats muscle spasticity
Diazepam - muscle relaxants
Botulinum toxin - muscle relaxant

218
Q

What is muscular dystrophy?

A

A group of disorders where there is degeneration of the muscles leading to muscle weakness

They are a group of inherited genetic conditions

MD is a progressive condition which means it gets worse over time

219
Q

What are dystrophinopathies?

A

They are the most common type muscular dystrophy
Due to a mutation in the dystrophin gene - this is an important protein link in muscles (in the absence of the gene muscle cells destabilise and die)

220
Q

What are the 2 dystrophinopathies?

What is there genetic inheritance?

A

Duchenne muscular dystrophy (DMD)
Becker muscular dystrophy (BMD)

X-linked recessive - so most commonly present in males

221
Q

What is the difference between DMD and BMD?

A

DMD - mutation in dystrophin so there is no protein production. This is much more severe and symptoms occur by the age of 5

BMD - mutation in dystrophin so there is protein production but it is misformed. This is a milder form of DMD. Symptoms present later between the age of 10-20

222
Q

What are the signs and symptoms of muscular dystrophy?

A

Late motor development
Tie toeing gait
Calf pseudohypertrophy - large calves (due to fat and firboids)
Gowers sign

223
Q

What is gowers sign?

A

When a child has to use there hands to help them up from a squatting to standing position due to lack of thigh muscle strength

224
Q

How is muscular dystrophy diagnosed?

A

Genetic testing - look for mutations in dystrophin
Creatine kinase (CPK) - this may be raised due to muscle breakdown
Muscle biopsy - to stain for dystrophin protein

225
Q

How is muscular dystrophy managed?

A

No cure
Steroids - can sometimes slow degeneration (but be aware of side effects of long term steroids)
Physiotherapy - to help with symptom management

226
Q

What is global development delay?

A

When a child has significant delay in the milestones of two or more core areas?

227
Q

Which disease are associated with global developmental delay?

A

Down’s syndrome

Tuberous sclerosis

228
Q

What is tuberous sclerosis?

A

Rare genetic conditions
Causes benign tumours to develop in different parts the body
Presents with developmental delays, seizures, disability

Can also present with non cancerous growth on brain, skin, kidneys, heart, eyes and lungs

229
Q

What is the glucose sugar levels needed to diagnose type 1 diabetes?

A

fasting glucose >7

2 hour plasma glucose >11

230
Q

When would you consider type II diabetes in children?

A

If they have strong family history
In obese children
Black or asian descent
Acanthosis nigricans

231
Q

What are acanthosis nigricans?

What are the causes?

A

Black hyperpigmentation found in the skin folds

Type II diabetes
Cushings, PCOS, hypothyroidism
Steroid treatment
Stomach cancer

232
Q

What is C-Peptide?

A

Involved in the production of insulin
When pancreas cells make insulin they release C-peptide as a by product

Therefore it will only be present in type II diabetes as in type I diabetes no insulin is produced

233
Q

What are GAD antibodies?

A

Antibodies present with instruct the immune system to destroy pancreatic insulin producing cells

They are only present in type I diabetes

234
Q

How is type I diabetes managed?

A

Insulin therapy
Can either have multiple injections - one daily long acting insulin, as well as short acting insulin before meals

Or can have insulin pump therapy - continuous device that infuses insulin

235
Q

What are the blood glucose targets for type I diabetics?

A

On waking - 4-7
Before meals - 4-7
After meals 5-9
While driving >5

236
Q

When should type I diabetics monitor their blood glucose levels?

A

Should perform at least 5 capillary blood tests per day

Should monitor more frequently during intercurrent illness

237
Q

What are the diabetic sick day rules?

A

Keep taking insulin even if you are not eating
Check blood sugar every 4 hours - even during the night time
Stay hydrated and drink plenty of unsweetened drinks

238
Q

How many times should HbA1c be measured in type I diabetes?

A

4 times a year

239
Q

How is mild hypoglycaemia managed?

A

Encourage fast acting glucose solution (liquid carbohydrate form)
Recheck BMs in 15 mins
Repeat fast acting glucose if it persists
As symptoms improve, give oral complex long acting carbohydrate to maintain glucose levels

240
Q

How is severe hypoglycaemia managed?

A

IV 10% glucose - if IV available
IM glucagon - if IV not available
Oral glucose solution (glucogel) - if they are fairly conscious

241
Q

What are the different IM glucagon doses for the different ages and weights?

A

> 8 years (or >25kg) - 1mg glucagon

< 8 years (or <25kg) - 500micrograms glucagon

242
Q

Why do type 1 diabetes have to be careful when drinking alcohol?

A

Can cause hypoglycaemia
Diabetics must eat carbohydrate rich foods before and after drinking alcohol
Diabetics must monitor blood glucose regularly when drinking alcohol

243
Q

How does hypoglycaemia caused by alcohol need to be managed and why?

A

IV glucose

As IM glucagon may be ineffective in alcohol induced hypoglycaemia

244
Q

What are the long term complications of type 1 diabetes and how are these monitored?

A

Thyroid disease - check for at diagnosis and annually
Diabetic retinopathy - check annually from 12 years with eye screen
Kidney disease - check ACR annually from 12 years
Hypertension - check annually from 12 years

245
Q

What is diabetic ketoacidosis (DKA)?

A

When there is a severe lack of insulin so the body cannot use intracellular glucose
Therefore it uses fats as an alternative energy source - the breakdown product of fats is ketones
Ketones are poisonous chemicals which when built up can cause acidosis in the body

246
Q

When is a DKA most likely to occur in children?

A

At diagnosis - many type 1 diabetes present with this
When child is ill - as they have poor controlled insulin levels
During growth spurt
If they stop taking insulin for some reason
In patients with insulin pumps if the cannula dislodges

247
Q

How does a DKA present?

A
Nausea or vomiting 
Abdominal pain 
Hyperventilation - respiratory compensation for acidosis 
Dehydration 
Reduced consciousness level
248
Q

What is kussmaul breathing?

A

Deep and laboured breathing associated with severe metabolic acidosis
The body is trying to compensate for the acidosis by blowing off CO2
It is often associated with DKA and kidney failure

249
Q

Is hyperglycaemia always present in DKA?

A

NO

You should always suspect DKA in a symptomatic patient even if their BMs are not elevated

250
Q

How would you investigate someone with suspected DKA?

A

Capillary blood glucose - >11 then this is suggestive
Capillary blood ketones (beta-hydroxybutyrate) - if >3 then this is suggestive
ABG - to check for metabolic acidosis
U&ES - to check for sodium, potassium, urea and creatine plasma bicarbonate

251
Q

When would you diagnose someone with DKA?

A

If any of the following are present:
Ph <7.3
Bicarbonate <18
Beta-hydroxybutyrate (ketones) >3

252
Q

At what ph level would you diagnose severe DKA?

A

Ph <7.1

253
Q

What is the immediate management for a person with suspected DKA?

A

Transfer to a recognised paediatric high dependancy unit

Insulin
Fluids

254
Q

Why would you not give an intravenous fluid bolus to a child with a DKA?

A

As faster rehydration of associated with an increased risk of cerebral oedema

Therefore you must aim to replace the fluid deficit evenly over the first 48 hours

255
Q

How do you decide whether to give subcutaneous insulin and oral fluids as opposed to IV insulin and IV fluids?

A

If the child is alert, and not vomiting or dehydrated - can go for subcutaneous insulin and oral fluids

If the child has decreased consciousness, is vomiting and is clinically dehydrated - then you give IV insulin and IV fluids

256
Q

What IV fluids do you give to someone with DKA?

A

0.9% Sodium chloride with 40mmol potassium chloride (WITHOUT glucose) - use until plasma glucose is below 14

Once glucose falls below 14 - then you can change to 0.9% sodium chloride with 5% glucose and 40mmol potassium chloride

257
Q

How much insulin would you give IV to someone with DKA?

When would you start insulin infusion

A

IV infusion of 0.05-0.1 units/kg/hour

Start insulin within 1-2 hours after beginning IV fluids

258
Q

What must you remember when switching IV insulin to subcutaneous or pump insulin?

A

To start subcutaneous insulin at least 30 mins before stopping IV insulin

To restart insulin pump at least 60 mins before stopping IV insulin

259
Q

If someone with DKA presents with reduced consciousness, what would you consider?

A

Nasogastric tube - to reduce risk of aspiration due to vomiting
Intubation - if they cannot protect airway
Inotropes (e.g, adrenaline) - if they are in hypertensive shock

260
Q

What are the symptoms of cerebral oedema?

A
Headache 
Agitation 
Irritability 
Unexpected fall in HR
Increased BP
Falls in respiration
261
Q

What is the management of cerebral odema?

A

Mannitol - 20% 0.5-1g/kg over 10-15 minutes

262
Q

What are the risks of insulin in DKA management?

A

Can cause hypokalaemia

If potassium is <3 then think about temporarily stopping insulin infusion

263
Q

Why is important to measure U&Es during DKA management?

A

To measure potassium levels - as insulin can cause hypokalaemia

264
Q

How would you counsel a parent on the MMR vaccine?

A

Given at 12 months and 3-4 years
Protects against Measles, mumps and rubella viruses
These can have serious complications such as meningitis, encephalitis
Vaccine contains weakened versions of the viruses that trigger immune system to produce antibodies
Link to autism - one study in 1998 - has been discredited - and there is no known link
Side effects - developing mild form of measles or mumps (lasting a few days maximum) (not infective)
In rare cases may develop rash - see GP if this occurs
You cannot infect someone else with MMR vaccine

265
Q

What is testicular torsion?

A

Twisting of the spermatic cord within the scrotum
This cord contains vessels which supply blood to the scrotum
Twisting leads to reduced blood flow and can cause sudden pain and swelling

266
Q

What are the symptoms of testicular torsion?

A
Sudden sever pain in scrotum 
Swelling of scrotum 
Abdominal pain 
Nausea and vomiting 
Frequent urination 
Fever
267
Q

At what age is testicular torsion most common?

A

Between the ages of 12 and 18

268
Q

How is testicular torsion managed?

A

Emergency surgery - to save testicle

269
Q

What is henoch-schonlein purpura (HSP)

A

Vasculitis commonly occurring in children
Causes a rash on lower limbs
Not usually serious
But sometimes can lead to kidney problems

270
Q

What are the symptoms of henoch-schonlein purpura (HSP)?

A
Purpuric rash on legs or bottom 
Abdominal pain 
Diffuse joint pain - in knees or ankles 
Scrotal pain - may occur in 13% of boys 
Haematuria
271
Q

What are the risk factors for HSP?

A

Male sex
Aged 3-15 years
Previous URTI

272
Q

How is HSP managed?

A

Most cases of HSP resolve spontaneously within 4 weeks so management is purely symptomatic:
Analgesia - for abdominal pain
Oral prednisolone - for scrotal involvement or severe oedema or abdominal pain
IV corticosteroids - if pain is accompanied by nausea and vomiting

273
Q

If a child with HSP is clinically stable, how would you advise the parents to manage at home?

A

Pain relief for symptoms

Educate on urine dip - contact if there is +++ protein or blood

274
Q

What investigations should you do in a child with HSP and why?

A

U&Es
ACR

As HSP can cause renal damage

275
Q

When should children with HSP be followed up until?

A

Followed up for 6 months with urinalysis and BP monitoring

276
Q

If a child with HSP had abnormal urinalysis then what would you want to do?

A

PCR - check creatinine to assess renal function

277
Q

If a child with HSP had persistent proteinuria or renal insufficiency what would you do?

A

Referral to nephrologist

278
Q

What is immune thrombocytopenic purpura?

A

Disorder of low platelets
Where the blood doesn’t clot due to low platelets
The immune system produces antibodies against platelets

279
Q

When does ITP occur in children?

A

Usually occurs acutely following an illness

280
Q

What are the symptoms of ITP?

A

Bruising easily
Petechiae rash
Spontaneous bleeding - nosebleeds, bleeding from gums
Blood in urine or stool

281
Q

How is ITP managed?

A

In children it usually self resolves in 6 months
However if medication is required you can give:
Prednisolone - which helps to increase platelet count by decreasing the activity of the immune system
Intravenous immunoglobulin - given when you need to increase platelet count quickly e.g, in Cristal bleeding
Rituximab - antibody therapy that targets the immune cells responsible for producing the proteins that attack platelets

282
Q

What should you suspect in anaemic children?

A

Nutrition deficiencies - this is common in children

283
Q

At what age does sickle cell disease present and why?

A

After 6 months

This is because there is a loss of fetal haemoglobin and production of sickle cell haemoglobin

284
Q

What is the pathophysiology in sickle cell disease

A

Genetic disease
RBCs become sickle shaped so are more likely to get stuck in small blood vessels
This can cause pain
Also increases risk of infection - as cells are unable to travel in blood

285
Q

What is the biggest risk to children with sickle cell anaemia?

How is this managed?

A

Risk of infection

Vaccinations
Antibiotic prophylaxis - in children under 5 years

286
Q

How is sickle cell disease managed long term?

A
Pain management (Acute and chronic)
Prompt treatment of investinos 
Management of acute chest syndrome 
Prevention of stroke 
Prevention of chronic organ damage (kidney, renal, pulmonary)
287
Q

Can sickle cell disease be cured?

A

Yes

By bone marrow transplantation

288
Q

What are some treatments used in sickle cell disease?

A

Hydroxycarbamide - to increase the amount of fetal haemoglobin

Blood transfusion - in order to keep HbS below 30%

289
Q

What bacteria are those with sickle cell disease most at risk of getting?

A

Pneumococcal bacteria

290
Q

What is the most common type of childhood cancer?

A

Acute lymphoblastic leukaemia (ALL)

291
Q

How does ALL present

A
Bone/joint pain 
Loss of appetite 
Bruising, nosebleeds, bleeding gums, petechiae 
Lymphadenopathy 
Recurrent infections 
Anaemia
292
Q

What is Ewigs Sarcoma?

A

Rare childhood cancer what develops in the bone

Occurs mainly in teenage years and is more prevelent in boys

293
Q

What is neuroblastoma?

At what age does it present?

A

Cancer of the neural crest cells

Cancer most commonly occurs in the adrenal glands

Generally presents in early childhood before the age of 5

294
Q

At what age does retinoblastoma usually present?

A

In children under the age of 5

295
Q

What are the symptoms of retinoblastoma?

A

White pupil - white colour behind pupil that does not reflect light (known as white reflex)
Crossed eyes - squint or abnormal eye movement
Red eye - due to painful irritation that may persist if tumour is large

296
Q

What is wilms tumour?

What age does it commonly occur?

A

Cancer of the kidney in children

Occurs between the age of 3-4 years

297
Q

What are the causes for neonatal jaundice?

A

Premature birth - as babies cannot process bilirubin
Significant bruising during birth - breakdown of RBCs
Breast feeding - breast fed babies higher risk of jaundice
Haemolysis - due to internal bleeding or infection
Liver malfunction
Enzyme deficiency

298
Q

What is the risk of having a high bilirubin in a baby?

A

Encephalopathy
As high levels of bilirubin are toxic to the brain

Kericternus can occur if bilirubin encephalopathy causes percent damage to the brain

299
Q

How would you counsel a parent whose child has been born with Down’s syndrome?

A

Explain - extra chromosome because of change in the sperm or the egg before birth. This happens by chance
Risk - increasing age
Prognosis - level of learning disability, everyone is different. People from downs are not ill. Life expectancy 50 years
Risk of heart defects - these can be fixed at birth
Long term health problems risk - hypothyroidism, celiac disease, problems with vision or hearing, sleep apnea
More information: Down’s syndrome association