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Phase 3a > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

Define pneumonia?

A

Any inflammatory condition affecting the alveoli of the lungs, but in the vast majority of patients this is secondary to a bacterial infection.

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2
Q

List some symptoms of pneumonia?

A

Cough
Sputum
Dyspnoea
Chest pain: may be pleuritic
Fever

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3
Q

List some signs of pneumonia?

A

Inflammation - fever and tachycardia
Reduced O2 sats
Reduced breath sounds
Bronchial breathing

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4
Q

What investigations are used for pneumonia?

A

X-ray

Bloods - FBC, ESR, CRP, U&Es

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5
Q

What is the most likely causative organism of bacterial pneumonia in children?

A

Streptococcus pneumoniae

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6
Q

What are some causes of typical bacterial pneumonia?

A

Streptococcus pneumoniae
Haemophilus influenzae
Staphylococcus aureus: commonly after influenza infection

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7
Q

What is a cause of atypical baterial pneumonia?

A

Mycoplasma pneumoniae

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8
Q

What type of pneumonia is commonly seen in alcoholics?

A

Klebsiella pneumoniae

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9
Q

What is the first line management for childhood pneumonia?

A

Amoxicillin is first-line for all children with pneumonia

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10
Q

What is the second line management for childhood pneumonia, if first line fails?

A

Macrolides may be added if there is no response to first line therapy

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11
Q

What is the management for childhood pneumonia if there is suspected mycoplasma or chlamydia?

A

Macrolides should be used if mycoplasma or chlamydia is suspected

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12
Q

If childhood pneumonia is associated with influenza, what is the alternative first line management?

A

In pneumonia associated with influenza, co-amoxiclav is recommended

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13
Q

What is the difference between acute bronchitis and pneumonia?

A

No other focal chest signs in acute bronchitis other than wheeze.
No systemic symptoms

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14
Q

A cough which is barking and seal-like, with symptoms worse at night would indicate what?

A

Croup

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15
Q

What are the classical features of croup?

A

Cough which is barking and seal-like, with symptoms worse at night.

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16
Q

What is the management for croup?

A

Single dose of oral dexamethasone regardless of severity.
Second line - Prednisolone

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17
Q

What is the emergency management for croup?

A

High-flow oxygen and nebulised adrenaline

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18
Q

Why would you never perform a throat examination on a child with suspected croup?

A

Never perform a throat examination on a patient with croup due to risk of airway obstruction

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19
Q

What sign would be seen on a posterior-anterior chest X-ray of a child with croup?

A

Subglottic narrowing, commonly called the ‘steeple sign’

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20
Q

What sign would be seen on a lateral chest X-ray of a child with croup?

A

Swelling of the epiglottis - the ‘thumb sign’

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21
Q

What is the main organism that causes croup?

A

Parainfluenza virus accounts for the majority of cases of croup

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22
Q

When is croup more common in the year?

A

Autumn

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23
Q

Define asthma? What type of sensitivity reaction is asthma?

A

A chronic inflammatory disorder of the airways secondary to type 1 hypersensitivity

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24
Q

Why is diagnosis of asthma in children difficult?

A

It is common for young children to wheeze when they develop a virus (‘viral-induced wheeze’)

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25
Q

Patient with asthma may also suffer from what conditions?

A

Other IgE-mediated atopic conditions such as:

Atopic dermatitis (eczema)
Allergic rhinitis (hay fever)

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26
Q

What are asthma patients most likely allergic to? What else will they have?

A

Aspirin
Will most likely have nasal polyps if this is the case

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27
Q

What are the features of asthma?

A

Cough - worse at night
Dyspnoea
Expiratory wheeze
Reduced peak expiratory flow rate

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28
Q

What is FEV1?

A

Forced expiratory volume - volume that has been exhaled at the end of the first second of forced expiration

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29
Q

What is FVC?

A

Forced vital capacity - volume that has been exhaled after a maximal expiration following a full inspiration

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30
Q

What are the typical spirometry results in asthma?

A

FEV1 - significantly reduced
FVC - normal
FEV1% (FEV1/FVC) < 70%

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31
Q

What are the first-line investigations for asthma?

A

Fractional exhaled Nitric Oxide OR
Eosinophil count

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32
Q

What is the second-line investigation for asthma?

A

Bronchodilator reversibility (BDR) with spirometry

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33
Q

What is the first line management for asthma?

A

Salbutamol

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34
Q

What is a side effect of salbutamol?

A

Tremor

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35
Q

What type of drug is salbutamol?

A

Short-acting-beta agonist (SABA)

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36
Q

What is the mechanism of action of salbutamol?

A

Relaxation of the smooth muscles of the airways

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37
Q

What is the additional second line management for asthma?

A

Inhaled corticosteroids

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38
Q

What are the side effects of inhaled corticosteroids?

A

Oral candidiasis
Stunted growth in children

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39
Q

Give some examples of inhaled corticosteroids in asthma? What are the side effects?

A

Beclometasone dipropionate
Fluticasone propionate

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40
Q

What is the additional third line management for asthma?

A

Leukotriene receptor antagonist (LTRA) - Montelukast

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41
Q

What is the fourth-line management for asthma?

A

Salmetrol

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42
Q

What type of drug is salmetrol?

A

Long-acting beta-agonist

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43
Q

What is the mechanism of action of salmetrol?

A

They work by relaxing the smooth muscle of airways

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44
Q

What would the assessment of a moderate asthma attack show in children?

A

SpO2 > 92%
No clinical features of severe asthma

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45
Q

What would the assessment of a severe asthma attack show in children?

A

SpO2 < 92%
PEF - 33-50%
Too breathless to talk or feed
Use of accessory neck muscles

HR - >125 (>5 years), >140 (1-5 years)
RR - >30 (>5 years), >40 (1/5 years)

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46
Q

What would the assessment of a life-threatening asthma attack show in a child?

A

SpO2 <92%
PEF - PEF <33% best or predicted
Silent chest
Poor respiratory effort
Agitation
Altered consciousness
Cyanosis

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47
Q

What is the management for mild-moderate acute asthma in children?

A

Beta-2-agonist via a spacer (>3 years use close fitting mask)
1 puff every 30-60 seconds. Max 10 puffs
If no symptom control refer to hospital

Steroid therapy for 3-5 days
2-5 years - 20mg prednisolone OD
>5 years - 30-40mg prednisolone OD

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48
Q

What would the assessment of a moderate asthma attack show in adults?

A

PEFR 50-75% best or predicted
Speech normal
RR < 25 / min
Pulse < 110 bpm

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49
Q

What would the assessment of a severe asthma attack show in adults?

A

PEFR 33 - 50% best or predicted
Can’t complete sentences
RR > 25/min
Pulse > 110 bpm

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50
Q

What would the assessment of a life-threatening asthma attack show in adults?

A

PEFR < 33% best or predicted
Oxygen sats < 92%
‘Normal’ pC02 (4.6-6.0 kPa)
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma

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51
Q

What would the assessment of a
near-fatal asthma attack show in adults?

A

Raised pC02 and/or requiring mechanical ventilation with raised inflation pressures.

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52
Q

What is the management for a life-threatening acute asthma attack in adults?

A

Admission to hospital
15L oxygen in non-rebreathe mask if 02 sats low (until spO2 94-98)
Nebulised SABA (salbutamol)
40-50mg prednisolone PO - 5 days

Ipratropium bromide in all life-threatening or whom have not responded to SABA / Steroids

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53
Q

What is the criteria for discharge in patients who have had an acute asthma attack?

A

Stable on their discharge medication (i.e. no nebulisers or oxygen) for 12-24 hours
Inhaler technique checked and recorded
PEF >75% of best or predicted

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54
Q

Define bronchiolitis?

A

Bronchiolitis is a condition characterised by acute bronchiolar inflammation

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55
Q

What is the pathogen which causes bronchiolitis?

A

Respiratory syncytial virus (80%)
Rhinovirus (20%)

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56
Q

What is the investigation of choice for bronchiolitis?

A

Immunofluorescence of nasopharyngeal secretions may show RSV

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57
Q

What is the management for bronchiolitis?

A

If SpO2 persistently >92% - humidified oxygen

Accessory:
NG feeding
Suction of secretions

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58
Q

What would classify a patient as high-risk in bronchiolitis?

A

Bronchopulmonary dysplasia (e.g. Premature)
Congenital heart disease
Cystic fibrosis

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59
Q

Define cystic fibrosis?

A

A genetic disorder which causes increased viscosity of secretions (e.g. lungs and pancreas)

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60
Q

What is the inheritance pattern of cystic fibrosis? What gene is involved?

A

Autosomal recessive

Cystic fibrosis transmembrane conductance regulator gene (CFTR), which codes a cAMP-regulated chloride channel

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61
Q

What organisms may colonise cystic fibrosis patients?

A

Staphylococcus aureus
Pseudomonas aeruginosa
Burkholderia cepacia
Aspergillus

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62
Q

What are the presenting features of cystic fibrosis?

A

Neonatal - Meconium illness, jaundice (20%)
Recurrent chest infection (40%)
Steatorrhoea, failure to thrive (30%)
Liver disease (10%)

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63
Q

What are some other features of cystic fibrosis?

A

Short stature
Diabetes mellitus
Delayed puberty
Rectal prolapse (due to bulky stools)
Nasal polyps
Male infertility, female subfertility

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64
Q

What is the diagnostic test for cystic fibrosis?

A

Guthrie test (‘heel prick) for screening
Sweat test - sweat chloride > 60 mEq/l (normal < 40 mEq/l)

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65
Q

What is the most common cause of a false negative sweat test?

A

skin oedema, often due to hypoalbuminaemia/ hypoproteinaemia secondary to pancreatic exocrine insufficiency

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66
Q

What is the management for cystic fibrosis?

A

Lung physiotherapy
High calorie, high fat diet
Vitamin supplementation
Pancreatic enzyme supplements taken with meals
Lung transplant

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67
Q

In what patients is a lung transplant contraindicated for cystic fibrosis?

A

Chronic infection with Burkholderia cepacia

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68
Q

Define acute epiglotitis?

A

Acute epiglottitis is rare but serious infection caused by Haemophilus influenzae type B

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69
Q

What are the features of acute epiglotitis?

A

Rapid onset
High temperature, generally unwell
Stridor
Drooling of saliva

‘Tripod’ position: the patient finds it easier to breathe if they are leaning forward and extending their neck in a seated position

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70
Q

What would you see on a posterior-anterior view X-ray for acute epiglottis?

A

Subglottic narrowing - ‘steeple’ sign

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71
Q

What would you see on a lateral view X-ray for acute epiglottis?

A

Swelling of epiglottis - ‘thumb’ sign

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72
Q

What should you not do in acute epiglottitis?

A

Do NOT examine throat due to risk of acute airway obstruction

Diagnosis is made by direct visualisation but this should only be done by senior staff who are able to intubate if necessary

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73
Q

What is the management for acute epiglottitis?

A

Immediate senior involvement, including those able to provide emergency airway - endotracheal intubation may be necessary

Oxygen
IV antibiotics - Ceftriaxone

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74
Q

Why are children more likely to get otitis media?

A

Shorter Eustachian tube

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75
Q

What are most otitis media infections caused by?

A

URTI precedes otitis media.

Streptococcus pneumonaie
Haemophilus influenzae
Moraxella catarrhalis

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76
Q

What otoscopy findings would be observed for otitis media?

A

Bulging tympanic membrane → loss of light reflex
Opacification or erythema of the tympanic membrane
Perforation with purulent otorrhoea

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77
Q

What is the management of otitis media?

A

Analgesia - NSAIDs and Paracetamol

Antibiotics not routinely offered

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78
Q

What are the exceptions for not giving antibiotics for otitis media?

A

43210

4: >4days
3: NEWS>3 (systemically unwell)
2: less than 2 + bi(2)laterally
1: (I)mmunocompromised
0 : it looks like a hole (perfOration)

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79
Q

What antibiotic is used for otitis media when indicated?

A

5-7 days amoxicillin

erythromycin or clarithromycin if allergy

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80
Q

Define glue ear?

A

Glue ear describes otitis media with an effusion (other terms include serous otitis media)

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81
Q

What is the most common cause of conductive hearing loss?

A

Glue ear

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82
Q

What is the management for glue ear?

A

First presentation - watchful waiting for 3 month

Grommets

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83
Q

What are grommets?

A

Grommets are tiny tubes inserted into thetympanic membraneby an ENT surgeon.

This allows fluid from the middle ear to drain through the tympanic membrane to the ear canal.

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84
Q

Define periorbital cellulitis?

A

Peri-orbital (also known as pre-septal) cellulitis is inflammation and infection of the superficial eyelid

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85
Q

What organisms cause peri-orbital cellulitis?

A

Staphylococcus aureus
Staphylococcus epidermidis
Streptococcusspecies

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86
Q

Define squint (strabismus)?

A

Squint (strabismus) is characterised by misalignment of the visual axes. Squints may be divided into concomitant (common) and paralytic (rare).

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87
Q

What is concominant squint?

A

Misalignment of the visual axis due to imbalance in extraocular muscles
Convergent is more common than divergent

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88
Q

What is paralytic squint?

A

Misalignment of the visual axis due to paralysis of extraocular muscles

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89
Q

What is the management for squint (strabismus)?

A

Referral to secondary care - eye patches may help prevent amblyopia

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90
Q

What is amblyopia?

A

The brain fails to fully process inputs from one eye and over time favours the other eye

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91
Q

What is atrial flutter?

A

Atrial flutter is a form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves

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92
Q

What would ECG changes be for atrial flutter?

A

Sawtooth appearance (flutter waves / f wave)

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93
Q

What is the immediate management for atrial flutter?

A

Synchronised cardioversion with anticoagulant

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94
Q

Define AF?

A

Atrial fibrillation is the most common sustained cardiac arrhythmia in which there is an increased risk of stroke

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95
Q

What are the different types of AF?

A

First detected episode
Recurrent episodes
Permanent AF

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96
Q

What are the types of recurrent AF?

A

Paroxysmal AF - Terminates spontaneously
Persistent AF - Non-self terminating (>7 days)

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97
Q

What are the features of AF?

A

Palpitations
Dyspnoea
Chest pain
Irregularly irregular pulse

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98
Q

What are the two types of control used in the management of AF?

A

Rhythm control (preferred under certain criteria)
Rate control

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99
Q

What is the role of rhythm control in AF management?

A

Try to get the patient back into, and maintain, normal sinus rhythm. This is termed cardioversion.

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100
Q

What is the first-line criteria for rhythm control in haemodynamically unstable patients?

A

Haemodynamically unstable - electrical cardioversion

E.g. hypotension, heart failure

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101
Q

What is the criteria to use rhythm control first in AF management in haemodynamically stable patients?

A

Short duration of symptoms (less than 48 hours) OR
Be anticoagulated for a period of time prior to attempting cardioversion - 3 weeks.

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102
Q

What pharmacological agents are used for cardioversion in AF?

A

Amiodarone
Flecainide (if no structural heart disease)

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103
Q

What is the role of rate control on AF management?

A

Accept that the pulse will be irregular, but slow the rate down to avoid negative effects on cardiac function

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104
Q

What pharmacological management is used for rate control in AF?

A

A beta-blocker or a rate-limiting calcium channel blocker (e.g. diltiazem) is used first-line

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105
Q

What happens if one drug does not control rate adequately in AF?

A

Combination therapy with any 2 of the following:
Betablocker
Diltiazem
Digoxin

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106
Q

What is a common contraindication for beta-blockers for rate control in patients with AF?

A

Asthma

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107
Q

When is there the highest risk of embolism leading to stroke in AF?

A

The moment a patient switches from AF to sinus rhythm

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108
Q

What is the CHA2DS2-VSAc score used for?

A

Calculates stroke risk for patients with atrial fibrillation

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109
Q

What score calculates stroke risk for patients with atrial fibrillation?

A

CHA2DS2-VSAc

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110
Q

What are the individual scores in the CHA2DS2-VSAc scoring system?

A

C - congestive heart failure - 1
H - hypertension - 1
A2 - Age - Age >= 75 - 2, Age 65-74 - 1
D - diabetes - 1
S2 - Prior Stroke, TIA or thromboembolism - 2
V - Vascular disease (IHD, PAD) - 1
S - sex (female) - 1

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111
Q

What is the anticoagulation strategy based on CHA2DS2-VSAc score?

A

0 - No treatment
1 - Male - consider coagulation, Female - no treatment
2 or more - Offer anticoagulation

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112
Q

What should be performed if CHA2DS2-VSAc score = 0 and why?

A

ECHO to exclude valvular heart disease

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113
Q

What pharmacological agents are used first-line for anticoagulation in AF?

A

DOACs:

Apixaban
Dabigatran
Edoxaban
Rivaroxaban

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114
Q

What pharmacological agent is used second-line for anticoagulation in AF?

A

Warfarin due to requiring regular blood tests to check the INR

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115
Q

What score is to assess the patient’s bleeding risk before anticoagulation is commenced?

A

ORBIT score

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116
Q

What is an ORBIT score used for?

A

To assess the patient’s bleeding risk before anticoagulation is commenced

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117
Q

List three types of supra-ventricular tachycardia?

A

Atrioventricular nodal re-entrant tachycardia (AVNRT)
Atrioventricular reentrant tachycardia (AVRT) e.g. Wolf-Parkinson White syndrome

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118
Q

What is the most common type of supra-ventricular tachycardia?

A

Atrioventricular nodal reentrant tachycardia (AVNRT)

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119
Q

What is the first line acute management for supra-ventricular tachycardia?

A

Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe
Carotid sinus massage

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120
Q

What is the definitive management for supra-ventricular tachycardias?

A

Radio-frequency ablation of the accessory pathway

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121
Q

What pharmacological management may be given for supra-ventricular tachycardias?

A

Intravenous adenosine:

Rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg

Verapamil if asthmatic

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122
Q

Define Wolff-Parkinson White syndrome?

A

A congenital accessory conducting pathway between the atria and ventricles leading to atrioventricular re-entry tachycardia (AVRT)

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123
Q

What would an ECG show for right-sided accessory pathway Wolff-Parkinson-White syndrome?

A

Short PR interval
Wide QRS complex with slurred upstroke - Delta wave
Left axis deviation - majority of cases

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124
Q

What would an ECG show for left-sided accessory pathway Wolff-Parkinson-White syndrome?

A

Short PR interval
Wide QRS complex with slurred upstroke - Delta wave
Right axis deviation
Dominant R wave in V1

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125
Q

What is would ventricular fibrillation show on an ECG?

A

No QRS complex can be identified, ECG completely disorganised

Patient is likely to be unconscious

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126
Q

What is the management for ventricular fibrillation?

A

Immediate Dc cardioversion

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127
Q

What are the two types of ventricular tachycardia?

A

Monomorphic VT: most commonly caused by myocardial infarction

Polymorphic VT: A subtype of polymorphic VT is torsades de pointes

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128
Q

What is the management for ventricular tachycardia?

A

Immediate cardioversion
IV amioderone

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129
Q

Define ventricular ectopic?

A

Ventricular ectopics are premature ventricular beats

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130
Q

What is the management for ventricular ectopic?

A

Reassurance in otherwise healthy people
Beta blockers and Ca channel blockers for palpitations

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131
Q

What is the management for Torsades de Pointes?

A

IV magnesium sulphate

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132
Q

What are the acyanotic congenital heart defects?

A

Ventricular septal defect
Atrial septal defect
Patient ductus arteriosus
Coarctation of the aorta
Aortic valve stenosis

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133
Q

What are the cyanotic congenital heart defects?

A

Tetralogy of Fallot
Transposition of the great arteries (TGA)
Tricuspid atresia

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134
Q

What is the most common congenital heart disease?

A

Ventricular septal defects (VSD) - close spontaneously in around 50% of cases

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135
Q

What are the risk factors for VSD?

A

Trisomys
Congenital infections

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136
Q

What are the features of VSD?

A

Failure to thrive
Pan-systolic murder
Features of heart failure:
Tachypnoea
Hepetomegaly
Pallor
Tachycardia

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137
Q

Define transposition of the great arteries?

A

A cyanotic congenital heart disease caused by the failure of the aorticopulmonary septum to spiral during septation

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138
Q

What is a risk factor for transposition of the great arteries?

A

Diabetic mothers

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139
Q

Describe the anatomical changes seen in transposition of the great arteries?

A

Aorta leaves the right ventricle
Pulmonary trunk leaves the left ventricle

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140
Q

What are the features of transposition of the great arteries?

A

Cyanosis
Tachypnoea
Loud single S2 sound and prominent right ventricular impulse

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141
Q

What is the management for transposition of the great arteries?

A

Prostaglandins e.g. alprostadil to maintain ductus arteriosus
Surgical correction is definite treatment

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142
Q

What is the most common cause of congenital heart disease to be found in adulthood?

A

Atrial septal defect

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143
Q

What are the features of atrial septal defects?

A

Ejection systolic murmur, fixed splitting of S2
Embolism may pass from venous to left side causing stroke
RBBB with RAD - osmium secundum (70%)
RBBB with LAD - ostium primium

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144
Q

What is an atrioventricular septal defect?

A

Deficiency of the atrioventricular septum of the heart that creates connections between all four of its chambers

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145
Q

What is the most common cause of cyanotic congenital heart disease?

A

Tetralogy of Fallot by actual incidence
Transposition of the great arteries presents more

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146
Q

Define Tetralogy of Fallot?

A

Ventricular septal defect (VSD)
Right ventricular hypertrophy
Right ventricular outflow tract obstruction, pulmonary stenosis
Overriding aorta

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147
Q

What determines the degree of cyanosis and clinical severity on Tetralogy of Fallot?

A

The severity of the right ventricular outflow tract obstruction

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148
Q

What are the features of Tetralogy of Fallot?

A

Cyanosis and ‘tet’ spells which may result in loss of consciousness
Ejection systolic murmur - due to pulmonary stenosis

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149
Q

What would a ‘boot’ shaped heart indicate on X-ray?

A

Tetralogy of Fallot

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150
Q

What is the management for Tetralogy of Fallot?

A

Prostaglandin e.g. alprostadil to maintain ductus arteriosus
Surgery

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151
Q

What would be indicative of Tetralogy of Fallot on an X-ray

A

‘boot’ shaped heart

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152
Q

What classification system is used to classify the severity of heart failure?

A

The New York Heart Association (NYHA) classification

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153
Q

What is the The New York Heart Association (NYHA) classification used for?

A

Used to classify the severity of heart failure.

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154
Q

NYHA Class I would indicate what?

A

No symptoms
No limitation

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155
Q

NYHA Class II would indicate what?

A

Mild symptoms
Slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea

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156
Q

NYHA Class III would indicate what?

A

Moderate symptoms
Marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms

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157
Q

NYHA Class IV would indicate what?

A

Severe symptoms
Unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity

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158
Q

What is heart failure?

A

Heart failure may be defined as a clinical syndrome where the heart is unable to pump enough blood to meet the metabolic needs of the body.

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159
Q

What is heart failure with reduced ejection fraction defined as?

A

Left ventricular ejection fraction is typically defined as < 35 to 40%

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160
Q

What type of dysfunction do patients with HF-pEF have?

A

Diastolic dysfunction (impaired ventricular filling during diastole).

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161
Q

Diastolic dysfunction (impaired ventricular filling during diastole) would be what type of heart failure?

A

HF-pEF

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162
Q

What type of dysfunction do patients with HF-rEF have?

A

HF-rEF patients typically have systolic dysfunction (impaired myocardial contraction during systole)

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163
Q

Systolic dysfunction (impaired myocardial contraction during systole) would be what type of heart failure?

A

HF-rEF

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164
Q

What is the most common reason for a heart failure patient to present to the Emergency Department?

A

The most urgent symptoms are often due to left ventricular failure, resulting in pulmonary oedema.

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165
Q

Left ventricular failure would present with what symptoms?

A

Pulmonary oedema:
Dyspnoea
Orthopnoea
Paroxysmal nocturnal dyspnoea
Bibasal fine crackles

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166
Q

Right ventricular failure would present with what symptoms?

A

Peripheral oedema - ankle/sacral oedema
Raised jugular venous pressure
Hepatomegaly
Weight gain due to fluid retention
Anorexia (‘cardiac cachexia’)

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167
Q

What are the first line investigations for heart failure?

A

N-terminal pro-B-type natriuretic peptide (NT-proBNP)
B-type natriuretic peptide (BNP)

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168
Q

What would normal levels of NTproBNP and BNP be?

A

BNP - < 100 pg/m
NTproBNP - < 400 pg/ml

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169
Q

What would raised levels of NTproBNP and BNP be?

A

BNP - 100-400 pg/ml
NTproBNP - 400-2000 pg/ml

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170
Q

What would high levels of NTproBNP and BNP be?

A

BNP - > 400 pg/ml
NTproBNP - > 2000 pg/ml

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171
Q

What would the interpretation be of a raised NTproBNP blood test?

A

Arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks

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172
Q

What would the interpretation be of a high NTproBNP blood test?

A

Arrange specialist assessment (including transthoracic echocardiography) within 2 weeks

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173
Q

What is the first-line pharmacological management of heart failure?

A

ACE-Inhibitor
Beta-blocker

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174
Q

What are some examples of beta-blockers that may be used in treatment of heart failure?

A

Bisoprolol
Carvedilol
Nebivolol

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175
Q

What are the second-line therapies for heart failure?

A

Aldosterone antagonist
SGLT-2 inhibitors

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176
Q

What are some examples of aldosterone antagonists used in heart failure?

A

Spironolactone
Eplerenone

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177
Q

What should you be conscious of when prescribing both ACE inhibitors and aldosterone antagonists in heart failure patients?

A

They both cause hyperkalaemia - therefore potassium should be monitored

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178
Q

What are some examples of SGLT-2 inhibitors?

A

Canagliflozin
Dapagliflozin
Empagliflozin

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179
Q

What is the mechanism of action of SGLT-2 inhibitors?

A

Reduce glucose reabsorption and increase urinary glucose excretion

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180
Q

What class of drugs have not been shown to reduce mortality in heart failure?

A

No long-term reduction in mortality has been demonstrated for loop diuretics such as furosemide

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181
Q

Define rheumatic fever?

A

Rheumatic fever develops following an immunological reaction to a recent (2-4 weeks ago) Streptococcus pyogenes infection

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182
Q

How is a diagnosis of rheumatic fever made?

A

Jones criteria - diagnosis is based on evidence of recent streptococcal infection accompanied by:
2 major criteria
1 major with 2 minor criteria

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183
Q

What is the evidence of recent streptococcus infection for diagnosis if rheumatic fever?

A

Raised or rising streptococci antibodies,
Positive throat swab
Positive rapid group A streptococcal antigen test

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184
Q

What are the major criteria for a diagnosis of rheumatic fever?

A

JONES:

(J)oint - Polyarthritis
(O)rgan involvement - Carditis
Subcutaneous (N)odules
(E)rythema marginatum
(S)ydenham’s chorea - late feature

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185
Q

What are the minor criteria for a diagnosis of rheumatic fever?

A

FEAR:

Fever
ECG changes - Prolonged PR interval
Arthralgia (not if arthritis a major criteria)
Raised ESR or CRP

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186
Q

What is the Jones criteria used for?

A

A diagnosis of rheumatic fever

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187
Q

What is the management for rheumatic fever?

A

Oral penicillin V
NSAIDs

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188
Q

What is infective endocarditis?

A

An infection of the endocardium - typically infects valves of the heart

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189
Q

How is a diagnosis of infective endocarditis made?

A

Using the Modified Duke criteria:

2 x Major criteria
1 x Major criteria and 3 Minor criteria
5 Minor

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190
Q

What valve is most commonly affected in infective endocarditis?

A

Mitral valve

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191
Q

What valve is most likely affected in IV drug users?

A

Tricuspid

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192
Q

What is the most likely causative organism in infective endocarditis?

A

Staphylococcus aureus

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193
Q

What used to be the most common and still is the most common cause of infective endocarditis in developing countries?

A

Streptococcus viridans:
Streptococcus mitis and Streptococcus sanguinis which are both found in the mouth

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194
Q

What is the most common cause of infective endocarditis following prosthetic valve surgery (<2 months)?

A

Staphylococcus epidermidis due to colonisation of indwelling lines

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195
Q

What are some poor prognostic markers for infective endocarditis?

A

Staphylococcus aureus infection
prosthetic valve (especially ‘early’, acquired during surgery)
Culture negative endocarditis
Low complement levels

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196
Q

What is the initial blind therapy for infective endocarditis with a native valve?

A

Amoxicillin, consider adding low-dose gentamicin

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197
Q

What is the initial blind therapy for infective endocarditis with a prosthetic valve?

A

Vancomycin + rifampicin + low-dose gentamicin

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198
Q

What is the initial blind therapy for infective endocarditis with a native valve and penicillin allergy?

A

Vancomycin + low-dose gentamicin

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199
Q

What is the therapy for staphylococci infective endocarditis with a native valve?

A

Flucloxacillin

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200
Q

What is the therapy for staphylococci infective endocarditis with a native valve and penicillin allergy?

A

Vancomycin + rifampicin

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201
Q

What is the therapy for staphylococci infective endocarditis with a prosthetic valve?

A

Flucloxacillin + rifampicin + low-dose gentamicin

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202
Q

What is the therapy for staphylococci infective endocarditis with a prosthetic valve and penicillin allergy?

A

Vancomycin + rifampicin + low-dose gentamicin

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203
Q

What is the therapy for streptococci infective endocarditis?

A

Benzylpenicillin

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204
Q

What is the therapy for streptococci infective endocarditis with penicillin allergy?

A

Vancomycin + low-dose gentamicin

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205
Q

What is the Modified Duke criteria used for?

A

A diagnosis of infective endocarditis

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206
Q

What are the major criteria used in the Modified Duke critieria?

A

Two positive blood cultures
Endocardial involvement on ECHO

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207
Q

What are the minor criteria used in the Modified Duke critieria?

A

Predisposing heart condition or IVDU
Fever >38ºC
Immunological - Osler’s nodes, Roth spots
Vascular - Janeway lesions, clubbing, splinter haemorrhages
Positive blood cultures

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208
Q

What is the most common cause of vomiting in infancy?

A

Gastro-oesopageal reflux disease

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209
Q

What are the features of GORD in children?

A

Typically develops before 8 weeks
Vomiting - after feeds or being laid flat
Excessive crying, especially while feeding

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210
Q

What is the management of GORD in children?

A

30 degree head up during feeds
Sleep on their backs
Not being overfed - smaller more frequent feeds
Thickened formula trial
Alginate therapy trial
Metoclopramide with specialist input

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211
Q

Define pyloric stenosis?

A

Pyloric stenosis typically presents in the second to fourth weeks of life with vomiting

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212
Q

What is pyloric stenosis caused by?

A

It is caused by hypertrophy is the circular muscles of the pylorus

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213
Q

What are the risk factors for pyloric stenosis?

A

Male 4x more likely
Family history
First-born children

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214
Q

What are the classical features of pyloric stenosis?

A

Projectile vomiting following a feed
Constipation and dehydration
Palpable mass on upper abdomen
Hypochloraemic, hypokalaemic alkalosis

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215
Q

How is a diagnosis of pyloric stenosis made?

A

Ultrasound

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216
Q

What is the management of pyloric stenosis?

A

Ramstedt pyloromyotomy

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217
Q

When should an IBS diagnosis be considered?

A

The following for 6 months:
(A)bdominal pain
(B)loating
(C)hange in bowel habit

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218
Q

When should an IBS diagnosis definitely be made?

A

Patient has abdominal pain relieved by defecation or associated with altered bowel frequency stool form, in addition to 2 of the following 4 symptoms:
Altered stool passage
Abdominal bloating
Symptoms made worse by eating
Passage of mucus

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219
Q

What are some red flag queries of IBS?

A

Rectal bleeding
Unexplained weight loss
Family history of bowel cancer
Onset after 60 years old

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220
Q

What are the IBS investigations in primary care?

A

FBC
ESR / CRP
Coeliac disease screen (TTG)

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221
Q

What are the first-line pharmacological agents used in IBS?

A

Pain: antispasmodic agents hyoscine butylbromide(Buscopan)
Constipation: laxatives but avoid lactulose
Diarrhoea: loperamide is first-line

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222
Q

What is the general dietary advice for IBS?

A

Regular meal times
Avoid missing meals / long gaps
8 cups of fluid per day
Restrict tea and coffee
Restrict alcohol and fizzy drinks
Limiting high fibre foods
Limit fresh fruit
Increasing intake of oats and linseeds for wind and bloating

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223
Q

What is the most common cause of traveller’s diarrhoea?

A

Escherichia coli

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224
Q

What antispasmodic agent is used for IBS?

A

Hyoscine butylbromide(Buscopan)

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225
Q

What laxative should be avoided in IBS?

A

Lactulose

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226
Q

What pharmacological agent is used for constipation in IBS?

A

Loperamide

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227
Q

What is the second line pharmacological agent used in IBS?

A

Tricyclic antidepressant - Amitriptyline 5-10mg at night

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228
Q

Describe the typical presentation seen in Escherichia coli diarrhoea?

A

Watery stools
Abdominal cramps and nausea
12-48 hour incubation period

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229
Q

Describe the typical presentation seen in Giardiadis diarrhoea?

A

Prolonged, non-bloody diarrhoea
> 7 days incubation period

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230
Q

Describe the typical presentation seen in Shigella diarrhoea?

A

Bloody diarrhoea
Vomiting and abdominal pain
48-72 hours incubation period

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231
Q

Describe the typical presentation seen in Cholera diarrhoea?

A

Profuse, watery diarrhoea
Severe dehydration resulting in weight loss

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232
Q

Describe the typical presentation seen in Staphylococcus aureus diarrhoea?

A

Severe vomiting
1-6 hours incubation period

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233
Q

Describe the typical presentation seen in Campylobacter diarrhoea?

A

A flu-like prodrome is usually followed by crampy abdominal pains, fever and diarrhoea which may be bloody
May mimic appendicitis
Complications include Guillain-Barre syndrome
48-72 hours incubation period

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234
Q

Describe the typical presentation seen in Bacillus cereus diarrhoea?

A

Vomiting within 6 hours, stereotypically due to rice OR
Diarrhoeal illness occurring after 6 hours

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235
Q

Describe the typical presentation seen in ameobiasis diarrhoea?

A

Gradual onset bloody diarrhoea, abdominal pain, and tenderness which may last for several weeks
> 7 days incubation period

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236
Q

What is the management for constipation in children?

A

Movicol
Lactulose is second line

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237
Q

What is the classical feature of appendicitis?

A

Peri-umbilical abdominal pain which radiates to the right iliac fossa
Anorexia (not hungry) and vomiting

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238
Q

How is appendicitis diagnosed?

A

Neutrophil dominant leucocytosis
Urine analysis - pregnancy exclusion
Thin, male patients diagnosed without imaging
Female - US for pelvic organ pathology

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239
Q

What is the management for appendicitis?

A

Laparoscopic appendicectomy
Prophylactic IV antibiotics

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240
Q

What are the two hernias seen in children?

A

Congenital inguinal hernia
Infantile umbilical hernia

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241
Q

What is the management for congenital inguinal hernias?

A

Surgically repaired soon after diagnosis as at risk of incarceration - contents of the hernial sac are stuck inside by adhesions

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242
Q

What is the management for infantile umbilical hernias?

A

The vast majority resolve without intervention before the age of 4-5 years

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243
Q

Define failure to thrive?

A

Failure to thrive refers to poorphysicalgrowth and development in a child

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244
Q

What viral pathogens are most likely to cause viral gastroenteritis?

A

Rotavirus
Norovirus

Adenovirus is a less common cause and presents with a more subacute diarrhoea

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245
Q

Define Crohn’s disease?

A

Crohn’s disease is a form of inflammatory bowel disease.

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246
Q

Where along the bowel does Crohn’s disease affect?

A

It commonly affects the terminal ileum and colon but may be seen anywhere from the mouth to anus

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247
Q

What histological layers of the bowel does Crohn’s disease affect?

A

Inflammation occurs in all layers, down to the serosa, this is why patients with Crohn’s are prone to strictures, fistulas and adhesions

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248
Q

What are the features of Crohn’s disease?

A

Non-specific - weight loss and lethargy
Diarrhoea (may be bloody) - adults
Abdominal pain - most prominent in children
Perianal disease - tags or ulcers

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249
Q

What are the most common extra-intestinal features of Crohn’s disease and ulcerative colitis that are related to disease activity?

A

Arthritis
Erythema nodosum
Episcleritis - more common in CD
Osteoporosis

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250
Q

What is the most common extra-intestinal feature of Crohn’s disease and ulcerative colitis?

A

Arthritis

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251
Q

What are the most common extra-intestinal features of Crohn’s disease and ulcerative colitis that are NOT related to disease activity?

A

Uveitis
Pyoderma gangrenosum
Clubbing
Primary sclerosing cholangitis - more common in UC

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252
Q

What blood sample is a good indicator of disease activity in Crohn’s disease?

A

CRP

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253
Q

What is the investigation of choice for Crohn’s disease and what would it show?

A

Colonoscopy - deep ulcers and skip lesions

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254
Q

What would histological sampling of Crohn’s disease show?

A

Inflammation of all three layers of the serosa
Goblet cells are increased
Granulomas

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255
Q

What would the result be of a small bowel enema for Crohn’s disease?

A

Strictures - ‘Kantor’s string sign’
Proximal bowel dilation
‘Rose thorn’ ulcers
Fistulae

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256
Q

What are the main complications of Crohn’s disease?

A

Small bowel cancer
Colorectal cancer
Osteoporosis

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257
Q

What general points should be made to an individual with Crohn’s disease?

A

Strongly advised to stop smoking
Wary of NSAIDs and COCP - evidence patchy

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258
Q

What is the first-line pharmacological agent used to induce remission in patients with Crohn’s disease?

A

Glucocorticoids - Prednisolone

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259
Q

What is the second-line pharmacological agent used to induce remission in patients with Crohn’s disease?

A

5-ASA drugs - mesalazine

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260
Q

What add-on medications can be given to induce remission for Crohn’s disease patients?

A

Azathioprine or mercaptopurine - assess thiopurine methyltransferase (TPMT) first

Methotrexate is alternative to azathioprine

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261
Q

What pharmacological agents can be used for maintenance therapy in Crohn’s disease?

A

Azathioprine or mercaptopurine - assess thiopurine methyltransferase (TPMT) first

Methotrexate is alternative to azathioprine

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262
Q

What is the management for perianal disease in Crohn’s disease?

A

Oral metronidazole

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263
Q

Define ulcerative colitis?

A

Ulcerative colitis (UC) is a form of inflammatory bowel disease. Inflammation always starts at rectum never spreading beyond ileocaecal valve and is continuous.

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264
Q

Where is the most common site of inflammation in UC?

A

Inflammation always starts at rectum (hence it is the most common site for UC)

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265
Q

What are the features of UC?

A

Bloody diarrhoea
Urgency
Tenesmus - constant feeling of needing to go
Abdominal pain, particularly in the left lower quadrant

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266
Q

What is the investigation of choice for UC?

A

Colonoscopy + biopsy

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267
Q

What is the investigation for severe UC?

A

Colonoscopy should be avoided due to the risk of perforation - a flexible sigmoidoscopy is preferred

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268
Q

What would the findings on endoscopy be for UC?

A

Red, raw mucosa, bleeds easily
Widespread ulceration
Crypt abscesses

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269
Q

What would histological examination of UC show?

A

No inflammation beyond submucosa (unless fulminant disease)
Depletion of goblet cells and mucin from gland epithelium
Granulomas are infrequent

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270
Q

What would a barium enema in a patient with UC show?

A

Loss of haustrations
Superficial ulceration - ‘pseudopolyps’
Long standing disease - ‘drainpipe colon’

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271
Q

What is mild UC?

A

< 4 stools/day, only a small amount of blood

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272
Q

What is moderate UC?

A

4-6 stools/day, varying amounts of blood, no systemic upset

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273
Q

What is severe UC?

A

> 6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)

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274
Q

What is the management agent used in mild-to-moderate UC to induce remission?

A

Topical (rectal) aminosalicyclate
If no response + oral aminosalicyclate
If no response + oral corticosteroid

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275
Q

What aminosalicyclates are used in treatment of UC?

A

Mesalazine and sulfasalazine

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276
Q

What is the management agent used in severe UC to induce remission?

A

Should be performed in hospital
IV steroids are first line

72 hours no improvement -> IV ciclosporin (may also be used if steroids are contraindicated)

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277
Q

What is the management for UC to maintain remission?

A

An oral aminosalicylate
Topical (rectal) aminosalicylate

Can be used together or alone

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278
Q

What would the management be for a UC patient who has had more than 2 exacerbations in the past year?

A

Oral azathioprine or oral mercaptopurine

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279
Q

What may trigger an UC flare?

A

Stress
NSAIDs and antibiotics
Cessation of smoking

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280
Q

Define Coeliac disease?

A

Coeliac disease is an autoimmune condition caused by sensitivity to the protein gluten.

Repeated exposure leads to villous atrophy which in turn causes malabsorption.

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281
Q

What conditions are associated with Coeliac disease?

A

Dermatitis herpetiformis (a vesicular, pruritic skin eruption)
Type 1 diabetes mellitus
Autoimmune hepatitis
Irritable bowel syndrome
Autoimmune thyroid disease

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282
Q

What genes are associated with Coeliac disease?

A

HLA-DQ2 (95%)
HLA-DQ8 (80%)

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283
Q

In what conditions would a patient be screened for Coeliac disease?

A

Autoimmune thyroid disease
Type 1 diabetes mellitus

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284
Q

What are the features of Coeliac disease?

A

Diarrhoea
Failure to thrive - children
Unexplained gastrointestinal symptoms
Prolonged fatigue
Recurrent abdominal pain, cramping and distention
Unexplained weight loss
Unexplained iron-deficiency anaemia, or other anaemia

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285
Q

What are the complications of coeliac disease?

A

Iron, folate, and vitamin B12 deficiency
Hyposplenism
Osteoporosis, osteomalacia
Lactose intolerance
Subfertility

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286
Q

How long should a patient be eating gluten for, before investigations can occur. for coeliac disease?

A

6 weeks

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287
Q

What are the investigations for coeliac disease?

A

Tissue transglutaminase (TTG) antibodies (IgA) are first line
Endomyseal antibodies (IgA)

Endoscopic intestinal biopsy - gold standard

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288
Q

What would a endoscopic intestinal biopsy for coeliac disease show?

A

Villous atrophy
Crypt hyperplasia
Increase in intraepithelial lymphocytes
Lamina propria infiltration with lymphocytes

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289
Q

What is the management for coeliac disease?

A

Avoid gluten
Tissue transglutaminase can be used to check adherence to this

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290
Q

What should all patients with coeliac disease be offered?

A

Pneumococcal vaccine every 5 years due to hyposplenism

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291
Q

Define kwashiorkor?

A

Kwashiorkor, or oedematous malnutrition, is defined as the presence of bilateral pitting oedema, in the absence of another medical cause of oedema

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292
Q

Define marasmus?

A

Marasmus issevere undernutrition— a deficiency in all the macronutrients that the body requires to function

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293
Q

Define Hirschprung’s disease?

A

Hirschsprung’s disease is caused by an aganglionic segment of bowel due to a developmental failure of the parasympathetic Auerbach and Meissner plexuses

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294
Q

What is the pathophysiology behind Hirschprung’s disease?

A

Parasympathetic neuroblasts fail to migrate from the neural crest to the distal colon, meaning there is developmental failure of the parasympathetic Auerbach and Meissner plexuses, leading to uncoordinated peristalsis and therefore a functional obstruction in the bowel

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295
Q

What are the risk factor for Hirchsprung’s disease?

A

3x more common in males
Down syndrome

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296
Q

What are the possible presentations for Hirchsprung’s disease?

A

Neonates - Failure of delay to pass meconium
Older children - constipation, abdominal distention

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297
Q

What are the investigations for Hirchsprung’s disease?

A

Abdominal X-ray
Gold standard - rectal biopsy for diagnosis

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298
Q

What is the management for Hirchsprung’s disease?

A

Bowel irrigation
Definitive - surgery

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299
Q

Define intussusception?

A

Intussusception describes the invagination of one portion of the bowel into the lumen of the adjacent bowel

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300
Q

In what part of the bowel is intussusception most likely to occur?

A

Most commonly around the ileo-caecal region

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301
Q

What age and gender is most likely to be affected by intussusception?

A

Usually affects infants between 6-18 months old.
Boys are affected twice as often as girls

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302
Q

What are the classical features of intussusception?

A

Intermittent, severe, crampy, progressive abdominal pain
Inconsolable crying
During paroxysm the infant will characteristically draw their knees up and turn pale
Vomiting

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303
Q

What other features may be present in intussusception?

A

Sausage-shaped mass in RUQ
Bloodstained stool - red currant jelly is a late sign

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304
Q

What is the investigation for intussusception?

A

Ultrasound

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305
Q

What is the management for intussusception?

A

Reduction by air insufflation under radiological control
If the child has signs of peritonitis then surgery should be performed

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306
Q

Define Meckel’s diverticulum?

A

Meckel’s diverticulum is a congenital diverticulum of the small intestine

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307
Q

What is the most common cause of massive GI bleeding in children between the ages of 1 and 2?

A

Meckel’s diverticulum

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308
Q

What is the investigation for Meckel’s diverticulum if they are haemodynamically stable with less severe or intermittent bleeding?

A

Meckel’s scan - 99m technetium pertechnetate, which has an affinity for gastric mucosa

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309
Q

What is the investigation for Meckel’s diverticulum if they are haemodynamically unstable?

A

Mesenteric arteriography

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310
Q

What is the management for Meckel’s diverticulum?

A

Wedge excision or formal small bowel resection and anastomosis

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311
Q

Define infantile colic?

A

Characterised by bouts of excessive crying and pulling-up of the legs, often worse in the evening

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312
Q

When does infantile colic usually occur?

A

In infants less than 3 months old

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313
Q

What is the management for infantile colic?

A

Appropriate feeding
Upright position while feeding
Adequate burping post-feed
Parental reassurance

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314
Q

What is the difference between cow’s milk protein allergy and cow’s milk protein intolerance?

A

The term CMPA is usually used for immediate reactions and CMPI for mild-moderate delayed reactions

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315
Q

What type of reactions are seen in cow’s milk protein allergy / intolerance?

A

Both immediate (IgE mediated) and delayed (non-IgE mediated) reactions are seen

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316
Q

When does cow’s milk protein allergy / intolerance present?

A

Presents in the first 3 months of life in formula-fed infants, although rarely it is seen in exclusively breastfed infants

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317
Q

What are the features of cow’s milk protein allergy / intolerance?

A

Regurgitation and vomiting
Diarrhoea
Urticaria, atopic eczema
‘Colic’ symptoms: irritability, crying
Wheeze, chronic cough

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318
Q

What are the investigations for cow’s milk protein allergy / intolerance?

A

Skin prick/patch testing
Total IgE and specific IgE (RAST) for cow’s milk protein

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319
Q

What is the management for cow’s milk protein allergy / intolerance if formula fed?

A

First line - Extensive hydrolysed formula (eHF) milk
Amino-acid based formula (AAF)

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320
Q

What is the management for cow’s milk protein allergy / intolerance if breastfed?

A

Continue breastfeeding
Eliminate cow’s milk protein from maternal diet - prescribe calcium supplements

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321
Q

What is the prognosis for cow’s milk protein allergy / intolerance if IgE mediated?

A

55% will be milk tolerant by the age of 5 years

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322
Q

What is the prognosis for cow’s milk protein allergy / intolerance if non-IgE mediated?

A

Most children will be milk tolerant by the age of 3 years

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323
Q

What are the classical features of biliary atresia?

A

Jaundice extending beyond the physiological two weeks
Dark urine and pale stools
Appetite growth and disturbance - may be normal

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324
Q

Define biliary atresia?

A

A paediatric condition involving either obliteration or discontinuity within the extra-hepatic biliary system, which results in an obstruction in the flow of bile.

This results in a neonatal presentation of cholestasis in the first few weeks of life.

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325
Q

What are the signs of biliary atresia?

A

Jaundice
Hepatomegaly with splenomegaly
Abnormal growth

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326
Q

What are the investigations for biliary atresia?

A

Total bilirubin may be normal, whereas conjugated bilirubin is abnormally high.
LFTs - serum bile acids and aminotransferases may be high
Serum alpha 1-antitrypsin
Sweat chloride test for cystic fibrosis
US of the biliary tree and liver

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327
Q

What is the management for biliary atresia?

A

Surgical management is definitive - dissection of the abnormalities into distinct ducts and anastomosis creation
Antibiotic coverage and bile acid enhancers following surgery

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328
Q

Define neonatal hepatitis?

A

Inflammation of the liver that occurs in early infancy between 1-2 months of birth

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329
Q

What are some causes of neonatal hepatitis?

A

20%:
CMV
Rubella
Measles
Hep A, B, or C
80% due to non-specific viruses

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330
Q

What are the features of neonatal hepatitis?

A

Jaundice
Abnormal growth - cannot absorb vitamins
Hepatosplenomegaly

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331
Q

What is the investigation and management for neonatal hepatitis?

A

Liver biopsy using fine needle
Vitamin supplements

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332
Q

Define acute liver failure?

A

Acute liver failure describes the rapid onset of hepatocellular dysfunction leading to a variety of systemic complications

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333
Q

What are some causes of acute liver failure?

A

Paracetamol overdose
Alcohol
Viral hepatitis (usually A or B)
Acute fatty liver of pregnancy

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334
Q

Is a UTI more common in boys or girls?

A

Urinary tract infections (UTI) are more common in boys until 3 months of age (due to more congenital abnormalities) after which the incidence is substantially higher in girls

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335
Q

When should a child with UTI be referred?

A

Infants less than 3 months old should be referred immediately to a paediatrician.
Children aged more than 3 months old with an upper UTI should be considered for admission to hospital.

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336
Q

What is the management for children with UTIs in the community?

A

Oral antibiotics such as cephalosporin or co-amoxiclav should be given for 7-10 days

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337
Q

What should be prompted if a child has a UTI?

A

Urinary tract infection (UTI) in childhood should prompt an investigation for possible underlying causes and damage to the kidneys

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338
Q

What are the causative organisms for UTIs in children?

A

E. coli (responsible for around 80% of cases)
Proteus
Pseudomonas

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339
Q

What factors may predispose children to developing UTIs?

A

Incomplete bladder emptying
Vesicoureteric reflux
Poor hygiene

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340
Q

What is pyelonephritis?

A

Upper urinary tract infection - inflammation of the renal pelvis (join between kidney and ureter) and parenchyma.

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341
Q

What is the most common causative agent of pyelonephritis?

A

E. coli

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342
Q

What are the features of pyelonephritis?

A

Fever, rigors
Loin pain
Nausea
Vomiting
Cystitis - dysuria and urinary frequency

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343
Q

What is the investigation for pyelonephritis?

A

Mid stream urine (MSU) before management commenced

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344
Q

What is the management for pyelonephritis?

A

Local antibiotic guidelines
BNF - broad-spectrum cephalosporin or a quinolone (for non-pregnant women) for 7-10 days

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345
Q

Define nocturnal enuresis?

A

Enuresis may be defined as the ‘involuntary discharge of urine by day or night or both, in a child aged 5 years or older, in the absence of congenital or acquired defects of the nervous system or urinary tract’

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346
Q

What are the two types of nocturnal enuresis?

A

Either primary (the child has never achieved continence) or secondary (the child has been dry for at least 6 months before)

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347
Q

What is the management for nocturnal enuresis?

A

General advice - fluid intake, toileting patterns, lifting and waking
Enuresis alarm - first line when above fails
Desmopressin for short term control e.g. sleepovers or an alarm is ineffective

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348
Q

Define hypospadias?

A

Hypospadias is a common birth defect where the urethra is located in an abnormal position on the ventral surface of the penis

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349
Q

What may hypospadias additionally present with?

A

Cryptorchidism (10%)
Inguinal hernia

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350
Q

What is the management for hypospadias?

A

Corrective surgery at 12 months old
Essential child is NOT circumsised prior to surgery

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351
Q

Define phimosis?

A

Phimosis is the inability to retract the foreskin (distal prepuce) proximally over the glans penis

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352
Q

What is the management for phimosis?

A

Reassurance and hygiene
Topical corticosteroids
Preputial surgery e.g, circumcision or preputioplasty

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353
Q

Define vesicoureteric reflux?

A

Vesicoureteric reflux (VUR) is the abnormal backflow of urine from the bladder into the ureter and kidney

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354
Q

What does vesicoureteric reflux predispose children to?

A

UTI - found in 30% of patients that present with UTI

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355
Q

What are the investigations for vesicoureteric reflux?

A

Urinalysis - first line
Micturating cystourethrogram - Gold standard

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356
Q

What is the management for vesicoureteric reflux?

A

Active surveillance
Prophylactic antibiotics
Surgical management

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357
Q

What is grade I vesicoureteric reflux?

A

Reflux into the ureter only, no dilatation

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358
Q

What is grade II vesicoureteric reflux?

A

Reflux into the renal pelvis on micturition, no dilatation

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359
Q

What is grade III vesicoureteric reflux?

A

Mild/moderate dilatation of the ureter, renal pelvis and calyces

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360
Q

What is grade IV vesicoureteric reflux?

A

Dilation of the renal pelvis and calyces with moderate ureteral tortuosity

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361
Q

What is grade V vesicoureteric reflux?

A

Gross dilatation of the ureter, pelvis and calyces with ureteral tortuosity

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362
Q

What is the classic triad seen in haemolytic ureamic syndrome?

A

Acute kidney injury
Microangiopathic haemolytic anaemia
Thrombocytopenia

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363
Q

What are most cases of HUS secondary to?

A

Classically Shiga toxin-producing Escherichia coli (STEC) 0157:H7 (90% of cases)
Pneumococcal infection
HIV

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364
Q

What are the investigations for HUS?

A

FBC - normocytic anaemia, thrombocytopaenia, schistocytes and helmet cells
Coomb’s test negative
U&Es
Stool culture

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365
Q

What is the management for HUS?

A

Supportive - fluids, blood transfusion, dialysis
No need for antibiotics

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366
Q

What is the classic triad seen in nephrotic syndrome?

A

Proteinuria (> 3g/24hr) causing
Hypoalbuminaemia (< 30g/L) and
Oedema

Hypertension can also be seen

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367
Q

What are the different nephrotic syndromes?

A

Diabetic nephropathy (most common in adults)
Amyloidosis
Minimal change disease
Focal segmental glomerulosclerosis
Membranous neuropathy
Membranoproliferative neuropathy

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368
Q

Define amyloidosis?

A

Amyloidosis refers to the disease state caused by abnormal amyloid protein deposits in organs

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369
Q

Define minimal change disesae?

A

Condition in which the kidneys leak large amounts of protein. It is called “minimal change” because the damage to the kidneys cannot be seen under a microscope.

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370
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal change disease

371
Q

What is the management for minimal change disease?

A

Prednisolone - 80% of cases respond
Cyclophosphamide if not

372
Q

What are the causes of focal segmental glomerulosclerosis?

A

Idiopathic
Secondary to other renal pathology e.g. IgA Nephropathy, reflux nephropathy
HIV
Heroin
Alport’s syndrome
Sickle-cell disease

373
Q

What are the investigations for focal segmental glomerulosclerosis?

A

Renal biopsy:
Focal and segmental sclerosis and hyalinosis on light microscopy
Effacement of foot processes on electron microscopy

374
Q

Which nephrotic syndrome has a high recurrence when renal transplant is performed?

A

Focal segmental glomerulosclerosis

375
Q

What is the management for focal segmental glomerulosclerosis?

A

Steroids +/- immunosuppressants - there is an inconstant response

376
Q

Define membranoproliferative glomerulonephritis?

A

A nephroticand nephritic syndrome in which there is proliferation of mesangial and endothelial cells in the glomerulus

377
Q

What is the management for membranoproliferative glomerulonephritis?

A

Steroids

378
Q

What are the overall complications of nephrotic syndrome?

A

Increased risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine
Hyperlipidaemia
CKD
Infection
Hypocalcaemia

379
Q

What is the classic triad classically seen in nephritis syndrome?

A

Haematuria
Hypertension
Oedema

380
Q

Define post-streptococcal glomerulonephritis?

A

A type of nephritic syndrome which typically occurs 7-14 days following a group A beta-haemolytic Streptococcus infection.

Caused by immune complex (IgG, IgM and C3) deposition in the glomeruli

381
Q

List some different types of nephritis syndrome?

A

Post-streptococcal glomerulonephritis
IgA nephropathy
Goodpasture’s syndrome
SLE
Diffuse proliferative glomerulonephritis
Rapidly progressive glomerulonephritis
Alport syndrome

382
Q

What organism usually causes post-streptococcal glomerulonephritis?

A

Streptococcus pyogenes

383
Q

What are the investigations for post-streptococcal glomerulonephritis?

A

Bloods - Raised anti-streptolysin O titre and low C3

384
Q

What is the management for post-streptococcal glomerulonephritis?

A

Furosemide for hypertension

385
Q

Define IgA nephropathy?

A

Also known as Berger’s disease
Thought to be caused by mesangial deposition of IgA immune complexes

386
Q

What are the classical features of IgA nephropathy?

A

Young male, recurrent episodes of macroscopic haematuria
Typically associated with a recent URTI

387
Q

How may you distinguish between post-streptococcal glomerulonephritis and IgA nephropathy?

A

IgA will occur 1-2 days following sore throat rather than 1-2 weeks in post-streptococcal glomerulonephritis

388
Q

What is the management for IgA nephropathy with isolated haematuria and no / minimal proteinuria?

A

No treatment needed, other than follow-up to check renal function

389
Q

What is the management for IgA nephropathy with haemoaturia, proteinuria, and normal / slightly reduced GFR?

A

Initial treatment is with ACE inhibitors

390
Q

What is the management for IgA nephropathy with haemoaturia, proteinuria, and falling GFR?

A

Immunosuppression with corticosteroids

391
Q

Define Alport syndrome?

A

A genetic disease in which there’s a mutation in the gene COL4A5 that codes for type IV collagen

392
Q

What is the inheritance pattern of Alport syndrome?

A

most commonly X-linked therefore more common in males, Female disease is more severe

393
Q

What is the management for Alport syndrome?

A

ACEi is renoprotective
Renal replacement therapy - dialysis and transplant

394
Q

What are the features of eczema younger children?

A

Itchy, erythematous rash on the extensor surfaces
The face and the trunk are most affected

395
Q

What are the features of eczema in older children?

A

Itchy, erythematous rash on the flexor surfaces and the creases of the neck and face

396
Q

When is the typical presentation of eczema and when does it usually clear?

A

It typically presents before 2 years old.

Clears in around 50% of children by 5 years of age.

Clears in around 75% of children by 10 years of age.

397
Q

What is the general management for eczema?

A

Avoid irritants
Steroid creams and emollients - increased in stepwise manner from weakest to strongest
Wet wrapping

398
Q

What is the mild topical steroid used in eczema?

A

Hydrocortisone 0.5-2.5%

399
Q

What is the moderate topical steroid used in eczema?

A

Betamethasone valerate 0.025% (Betnovate RD)
Clobetasone butyrate 0.05% (Eumovate)

400
Q

What is the potent topical steroid used in eczema?

A

Fluticasone propionate 0.05% (Cutivate)
Betamethasone valerate 0.1% (Betnovate)

401
Q

What is the very potent tropical steroid used in eczema?

A

Clobetasol propionate 0.05% (Dermovate)

402
Q

What is the mnemonic used for stepwise management of topical steroids in eczema?

A

Help Every Budding Dermatologist
Hydrocortisone (mild)
Eumovate (moderate)
Betnovate 0.1 (potent)
Dermovate (very potent)

403
Q

What are the features of TEN?

A

Systemically unwell e.g. pyrexia, tachycardic
Positive Nikolsky’s sign: the epidermis separates with mild lateral pressure

Surface area >30% = TEN
Surface area <10% = SJS

404
Q

What drugs can induce TEN?

A

PePSi CAN

(Pe)nicillins
P()henytoin
(S)ulphonamides
(C)arbamazepine
(A)llopurinol
(N)SAIDs

405
Q

What is the management of TEN?

A

Stop precipitating factor
Supportive care - ICU, volume loss and electrolyte derangement are potential complications
IV imunoglobulin

406
Q

What is allergic rhinitis?

A

Allergic rhinitis (AR) is an immunoglobulin E (IgE)-mediated type 1 hypersensitivity inflammatory nasal condition resulting from allergen exposure in a sensitised individual.

407
Q

What are the three types of allergic rhinitis?

A

Seasonal - same time every year
Perennial - throughout the year
Occupational - within work place

408
Q

What are the features of allergic rhinitis?

A

Sneezing
Bilateral nasal obstruction
Clear nasal discharge
Post-nasal drip
Nasal pruritus

409
Q

What is the management for allergic rhinitis?

A

Allergen avoidance
Oral or intranasal antihistamines
Severe - intranasal corticosteroids

410
Q

What is urticaria?

A

Urticaria describes a local or generalised superficial swelling of the skin. Most common cause is allergy.

411
Q

What are the features of urticaria?

A

Pale, pink raised skin.
Variously described as ‘hives’, ‘wheals’, ‘nettle rash’
Pruritic

412
Q

What is the management for urticaria?

A

Non-sedating antihistamines - continued for up to 6 weeks are first line
Sedating may be considered for night time use

413
Q

What is the management for severe urticaria?

A

Prednisolone

414
Q

Give some examples of sedating and non-sedating antihistamines?

A

Non-sedating antihistamines (e.g. loratadine or cetirizine)
Sedating antihistamines (e.g. chlorophenamine)

415
Q

What drugs can commonly cause urticaria?

A

All People Need Oxygen:

Aspirin
Penicillins
NSAIDs
Opiates

416
Q

Define analphylaxis?

A

Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic hypersensitivity reaction

417
Q

What are some examples of causes of anaphylaxis?

A

Food (e.g. nuts) most common in children
Drugs
Insect venom (e.e. wasp sting)

418
Q

What are the features of anaphylaxis?

A

Airway and/or Breathing and/or Circulation problems

Airway - Swelling of throat and tongue
Breathing - Wheeze and dyspnoea
Circulation - Hypotension and tachycardia

419
Q

What is the immediate management of anaphylaxis for the specific age ranges?

A

<6 months - 100-150 μg adrenaline
6 months - 6 years - 150 μg adrenaline
6-12 years - 300 μg adrenaline
>12 years - 500μg adrenaline

Can be repeated every 5 minutes if necessary

420
Q

Where should adrenaline injection be given for anaphylaxis?

A

Anterolateral aspect of the middle third of the thigh

421
Q

Give an overview of measles?

A

RNA paramyxovirus
Spread via aerosol transmission
Infective from prodromal phase until 4 days after rash starts

422
Q

What is the incubation period of measles?

A

10-14 days

423
Q

What features does the prodromal phase of measles have?

A

Irritable
Conjunctivitis
Fever

424
Q

What are the classic features of measles?

A

Koplik spots before the rash develops (white spots)
Rash - behind ears then whole body
Diarrhoea

425
Q

Describe the rash seen in measles?

A

Discrete maculopapular rash becoming blotchy & confluent desquamation that typically spares the palms and soles may occur after a week

426
Q

What are the investigations for measles?

A

IgM antibodies detected within a few days of rash onset

427
Q

What is the management for measles?

A

Supportive mainly
Admission if immunocompromised or pregnant

Notifiable disease so inform public health

428
Q

What is the most common complication of measles?

A

Otitis media

429
Q

What is the most common form of death in measles?

A

Pneumonia

430
Q

What is the management for individuals who have come into contact with measles?

A

Offer MMR vaccine
Should be given within 72 hours

431
Q

What is the causative pathogen of chickenpox?

A

Primary infection with varicella zoster virus

432
Q

What is the causative pathogen of shingles?

A

Reactivation of varicella zoster virus from dorsal root ganglion

433
Q

Give an overview of chickenpox?

A

Spread via the respiratory route
Can be caught by someone with shingles
infective from 4 days before rash until 5 days after rash appeared

434
Q

What is the incubation period for chickenpox?

A

10-21 days

435
Q

What are the clinical features of chickenpox?

A

Prodromal phase - fever initially
Itchy, rash starting on head/trunk before spreading.
Systemic upset is usually mild

436
Q

Describe the rash seen in chickenpox?

A

Initially macular then papular then vesicular

437
Q

What is the management for chickenpox?

A

Keep cool
Trim nails
School exclusion until all lesions are dry and have crusted over

438
Q

What demographic of patients should receive varicella zoster immunoglobulin (VZIG)?

A

Immunocompromised patients
Newborns with peripartum exposure

If chickenpox develops = IV aciclovir

439
Q

What is a common complication of chickenpox? What may increase the risk of this?

A

Secondary bacterial infection particularly invasive group A streptococcal soft tissue infections may occur resulting in necrotising fasciitis

NSAIDs

440
Q

Give an overview of rubella?

A

aka German measles
Togavirus
Outbreaks are more common in winter and spring
Individuals are infectious from 7 days before symptoms to 4 days after rash onset

441
Q

What are the features of rubella?

A

Prodromal phase - low-grade fever
Rash on the face then whole body - fades by day 3-5
Lymphadenopathy

442
Q

Describe the rash seen in rubella?

A

Maculopapular

443
Q

What are some complications of rubella?

A

Arthritis
Thrombocytopenia
Encephalitis
Myocarditis

444
Q

What is the incubation period for rubella?

A

14-21 days

445
Q

What is the rule surrounding the MMR vaccine and pregnancy?

A

MMR vaccines should not be administered to women known to be pregnant or attempting to become pregnant

446
Q

What is the management of rubella?

A

Supportive care - NSAIDs
Notification to public health
Children kept off school for 5 days after rash appears

447
Q

What are the features of poliovirus?

A

Usually asymptomatic.
When symptomatic, the most common presentation is a minor gastrointestinal illness.

448
Q

Give an overview of poliovirus?

A

Enterovirus
Spread through faeco-oral transmission

449
Q

What is the management for poliovirus?

A

Supportive care

450
Q

What pathogen causes slapped cheek syndrome?

A

Parovirus B19

451
Q

What pathogen causes erythema infectiosum?

A

Parovirus B19

452
Q

Give an overview of slapped cheek syndrome?

A

DNA virus
Respiratory route spread
Infectious 3-5 days before rash - therefore no need for school exclusion

453
Q

What is the most likely infective cause of an aplastic crisis in sickle-cell disease?

A

Parovirus B19

454
Q

What is the investigation for a pregnant mother that has been exposed to parovirus B19?

A

Maternal IgM and IgG

455
Q

What are the features of slapped cheek syndrome?

A

Rose red rash on cheeks which may spread to the rest of the body

456
Q

What is the incubation period of roseola?

A

5-15 days

457
Q

Define roseola? What is the causative pathogen?

A

Roseola infantum is a common disease of infancy caused by the human herpes virus 6 (HHV6)

458
Q

What are the features of roseola?

A

High fever: lasting a few days, followed later by a
maculopapular rash
Nagayama spots: papular enanthem on the uvula and soft palate
Febrile convulsions occur in around 10-15%
Diarrhoea and cough

459
Q

Is school exclusion necessary for roseola?

A

School exclusion is not needed

460
Q

Define impetigo?

A

Impetigo is a superficial bacterial skin infection

461
Q

What organisms can cause impetigo?

A

Staphylcoccus aureus
Streptococcus pyogenes

462
Q

Where does impetigo tend to occur on the body?

A

Areas not covered by clothes:
Face
Flexures
Limbs

463
Q

What is the incubation period for impetgo?

A

4 to 10 days

464
Q

What are the features of impetigo?

A

Golden crust to the skin
Very contagious

465
Q

What is the management for non-bullous impetigo?

A

First line - hydrogen peroxide 1% cream
Topical fusidic acid

466
Q

What is the management for extensive impetigo?

A

Oral flucloxacillin
Oral erythromycin if allergy

467
Q

What is the rule about schooling and impetigo?

A

Children should be excluded from school until the lesions are crusted and healed

OR

48 hours after commencing antibiotic treatment

468
Q

What pathogens can cause hand, foot and mouth disease?

A

Coxsackie virus A16
Enterovirus 71

469
Q

What are the features of hand, foot and mouth disease?

A

Mild systemic upset: sore throat, fever
Oral ulcers
Followed later by vesicles on the palms and soles of the feet

470
Q

What is the management for hand, foot and mouth disease?

A

Symptomatic treatment only

Children to not need to be excluded from school

471
Q

What does ART for HIV entail?

A

A combination of at least three drugs, typically two nucleoside reverse transcriptase inhibitors (NRTI) and either a protease inhibitor (PI) or a non-nucleoside reverse transcriptase inhibitor (NNRTI).

472
Q

When should ART be commenced for patients with HIV?

A

Following the 2015 BHIVA guidelines it is now recommended that patients start ART as soon as they have been diagnosed with HIV, rather than waiting until a particular CD4 count, as was previously advocated.

473
Q

Give some examples of entry inhibitors used in ART? How do they work?

A

Maraviroc
Enfuvirtide

Prevent HIV-1 from entering and infecting cells.

474
Q

What is the mechanism of action of the entry inhibitor Maraviroc?

A

Binds to CCR5, preventing an interaction with gp41

475
Q

What is the mechanism of action of the entry inhibitor Enfuvirtide?

A

Binds to gp41, also known as a ‘fusion inhibitor’

476
Q

Give some examples of NRTIs used in ART?

A

‘vu’ in the middle or ‘vir’ at the end

Zidovudine (AZT)
Abacavir
Emtricitabine
Didanosine
Lamivudine
Stavudine
Zalcitabine
Tenofovir

477
Q

What are the general side effects of NRTIs?

A

Peripheral neuropathy

478
Q

What are the side effects of the NRTI tenofovir?

A

Renal impairment
Ostesoporosis

479
Q

What are the side effects of the NRTI zidovudine?

A

Anaemia
Myopathy
Black nails

480
Q

What are the side effects of the NRTI didanosine?

A

Pancreatitis

481
Q

What are some examples of NNRTIs used in ART?

A

‘vir’ in the middle

Nevirapine
Efavirenz

482
Q

What are the side effects of the NNRTI nevirapine?

A

P450 enzyme interaction and rashes

483
Q

What is the side effect of efavirenz?

A

Rashes

484
Q

What are some examples of protease inhibitors used in ART?

A

All end in ‘navir’

Indinavir
Nelfinavir
Ritonavir
Saquinavir

485
Q

What are the side effects of protease inhibitors used in ART?

A

Diabetes
Hyperlipidaemia
Buffalo hump
Central obesity
P450 enzyme inhibition

486
Q

What are the side effects of the protease inhibitor indinavir?

A

Renal stones
Asymptomatic hyperbilirubinaemia

487
Q

What are the side effects of the protease inhibitor ritonavir?

A

A potent inhibitor of the P450 system

488
Q

What is the mechanism of action of integrase inhibitors for ART?

A

Block the action of integrase, a viral enzyme that inserts the viral genome into the DNA of the host cell

489
Q

What are some examples of integrase inhibitors used in ART?

A

‘tegra’ in the middle

Raltegravir
Elvitegravir
Dolutegravir

490
Q

What is the investigation for HIV infection?

A

Combination tests (HIV p24 antigen and HIV antibody)
If the combined test is positive it should be repeated to confirm the diagnosis

491
Q

When should a HIV test be performed after possible exposure?

A

4 weeks and a repeat test at 12 weeks if negative.

492
Q

What is the most common cause of oesophagitis in patients with HIV?

A

Oesophageal candidiasis

493
Q

What are the features of HIV seroconversion?

A

Sore throat
Lymphadenopathy
Malaise, myalgia, arthralgia
Diarrhoea
Maculopapular rash
Mouth ulcers

494
Q

What should happen if a patient with HIV has a CD4 count of < 200/mm³?

A

All patients with a CD4 count < 200/mm³ should receive PCP prophylaxis

495
Q

What is the management of pneumocystis jiroveci?

A

Co-trimoxazole (trimethoprim and sulfamethoxazole)
IV pentamidine in severe cases

496
Q

What should happen if a patient with HIV has a CD4 count of < 50/mm³?

A

All patients with a CD4 count < 50/mm³ should receive mycobacterium avium complex prophylaxis

497
Q

What is the pharmacological prophylaxis management for mycobacterium avian complex?

A

Azithromycin

498
Q

What pathogen causes diptheria?

A

Corynebacterium diphtheriae via endotoxins

499
Q

Corynebacterium diphtheriae causes which disease?

A

Diptheria

500
Q

What is the management for diptheria?

A

Diptheria antitoxin
Azithromycin and clarithromycin

501
Q

What is scalded skin syndrome?

A

A superficial blistering of the skin caused by a type ofstaphylococcus aureusbacteria that producesepidermolytic toxins

502
Q

What is pertussis? What is the causative pathogen?

A

Whooping cough (pertussis) is an infectious disease caused by the Gram-negative bacterium Bordetella pertussis

503
Q

What are the features of pertussis in the catarrhal phase?

A

URTI symptoms

504
Q

What are the features of pertussis in the paroxysmal phase?

A

Cough increases in severity
Worse at night or after feeding
Inspiratory whoop
Infants may have spells of apnoea

505
Q

What are the features of the convalescent phase in pertussis infection?

A

Cough will subside over weeks to months

506
Q

What is the diagnostic criteria for whooping cough?

A

Acute cough >14 days

AND one of following:

Paroxysmal cough
Inspiratory whoop
Post-tussive vomiting
undiagnosed apnoeic attacks in children

507
Q

What is the management for pertussis?

A

An oral macrolide (e.g. clarithromycin, azithromycin or erythromycin)

Notify public health

508
Q

Define tuberculosis?

A

Tuberculosis (TB) is an infection caused by Mycobacterium tuberculosis that most commonly affects the lungs

509
Q

What is primary tuberculosis?

A

A primary infection of the lungs.
A small lung lesion known as a Ghon focus develops. The Ghon focus is composed of tubercle-laden macrophages.
Ghon focus + hilar lymph nodes = Ghon complex

510
Q

What is secondary tuberculosis?

A

If the host becomes immunocompromised the initial infection may become reactivated.

Reactivation generally occurs in the apex of the lungs and may spread locally or to more distant sites

511
Q

What is latent tuberculosis?

A

Patients with latent tuberculosis are asymptomatic and non-infectious.

512
Q

What are the investigations for latent tuberculosis?

A

Tuberculin skin test - positive
Interferon-Gamma Release Assay (IGRA) or Mantoux test combined with a normal chest X-ray - rules out active tuberculosis

513
Q

What is the management for latent tuberculosis?

A

3 months of isoniazid (with pyridoxine) and rifampicin, OR
6 months of isoniazid (with pyridoxine)

514
Q

What are the findings on a chest X-ray for active tuberculosis?

A

Upper lobe cavitation is the classical finding of reactivated TB
Bilateral hilar lymphadenopathy

515
Q

What is the gold standard investigation for tuberculosis?

A

Sputum culture:
More sensitive than sputum smear and NAAT
Can test drug sensitivities

516
Q

What is the first line investigation for tuberculosis?

A

Sputum smear:
Inexpensive and rapid
3 specimens are needed
All mycobacteria stain positive (Zeihl-Neelsen stain)
Decreased sensitivity in HIV patients

517
Q

What is the management for active tuberculosis infection?

A

Rifampicin
Isoniazid
Pyrazinamide - only for first 2 months
Ethambutol - only for first two months

518
Q

What are the side-effects of rifampicin?

A

Orange urine
Hepatotoxicity

519
Q

What are the side effects of isonazid?

A

Peripheral toxicity - pyridoxine is used to prevent (vitamin B6)
Hepatotoxicity

520
Q

What are the side effects of pyrazinamide?

A

Hyperuricaemia causing gout
Hepatotoxicity

521
Q

What are the side effects of ethambutol?

A

Optic neuritis

522
Q

What is scarlet fever?

A

Scarlet fever is a reaction to erythrogenic toxins produced by Group A haemolytic streptococci (usually Streptococcus pyogenes)

523
Q

What is the incubation period of scarlet fever?

A

2-4 days

524
Q

How is scarlet fever spread?

A

Via the respiratory route by inhaling or ingesting respiratory droplets or by direct contact with nose and throat discharges, (especially during sneezing and coughing).

525
Q

What are the features of scarlet fever?

A

Fever: typically lasts 24 to 48 hours
Malaise, headache, nausea/vomiting
Sore throat
‘Strawberry’ tongue
Rash

526
Q

Describe the rash seen in scarlet fever?

A

Fine punctate erythema (‘pinhead’) which generally appears first on the torso and spares the palms and soles
‘Sandpaper’ texture

527
Q

What is the first line management for scarlet fever?

A

Penicillin V for 10 days

528
Q

What is the second line management for scarlet fever?

A

Azithromycin

529
Q

What are the rules surrounding scarlet fever and schooling?

A

Can return to school 24 hours after commencing antibiotics

Public health will need to be informed

530
Q

What is the most common complication of scarlet fever?

A

Otitis media

531
Q

What is toxic shock syndrome?

A

Staphylococcal toxic shock syndrome describes a severe systemic reaction to staphylococcal exotoxins, the TSST-1 superantigen toxin

532
Q

What are the features of toxic shock syndrome?

A

Fever
Hypotension
Rash -> Desquamation

533
Q

What is the management of toxic shock syndrome?

A

Clindamycin and benzylpenecillin

534
Q

What is Kawasaki disease?

A

Kawasaki disease is a type of vasculitis which is predominately seen in children

535
Q

What are the features of Kawasaki disease?

A

High grade fever >5 days

CRASH:
Conjunctival injection
Rash - bright red, cracked lips
Adenopathy - enlarge cervical lymph nodes
Strawberry tongue
Hands and feet rash - later peels

536
Q

What is the management for Kawasaki disease?

A

High-dose aspirin
IV imunoglobulins

537
Q

What is the main complication of Kawasaki disease?

A

Coronary artery aneurysm therefore an ECHO should be performed

538
Q

What are the main organisms that cause meningitis in neonates to 3 months old?

A

Group B Streptococcus: usually acquired from the mother at birth.
E. coli and other Gram -ve organisms
Listeria monocytogenes

539
Q

What are the main organisms that cause meningitis in 1 month to 6 year olds?

A

Neisseria meningitidis (meningococcus)
Streptococcus pneumoniae (pneumococcus)
Haemophilus influenzae

540
Q

What are the main organisms that cause meningitis in children over 6 years old?

A

Neisseria meningitidis (meningococcus)
Streptococcus pneumoniae (pneumococcus)

541
Q

What are the main features of meningitis?

A

Headache
Fever
Nausea/vomiting
Photophobia
Drowsiness
Seizures

Neck stiffness
Purpuric rash

542
Q

What is the management for meningitis for children under 3 months old?

A

IV amoxicillin (or ampicillin) + IV cefotaxime

543
Q

Who should be offered prophylaxis for meningitis?

A

Offered to households and close contacts of patients affected with meningococcal meningitis

544
Q

What is the management for viral meningitis?

A

Ceftriaxone and aciclovir intravenously

545
Q

What is the most common cause of viral meningitis in adults?

A

Non-polio enteroviruses e.g. coxsackie virus, echovirus

546
Q

What is the most common complication of meningitis?

A

Sensorineural hearing loss

547
Q

What is contraindicated in meningococcal septicaemia?

A

Lumbar puncture

548
Q

What is the management for meningitis for children over 3 months old?

A

IV cefotaxime (or ceftriaxone)

549
Q

What are the findings in CSF fluid for bacterial meningitis?

A

Cloudy
Low glucose (< 1/2 plasma)
High protein
10-5,000 polymorphs/mm³

550
Q

What are the findings in CSF fluid for viral meningitis?

A

Clear/cloudy
60-80% of plasma glucose
Normal/raised protein
15-1,000 lymphocytes/mm³

551
Q

What are the findings in CSF for tuberculosis meningitis?

A

Slight cloudy, fibrin web
Low glucose (< 1/2 plasma)
High protein
10-1,000 lymphocytes/mm³

552
Q

CSF fluid for suspected meningitis:

Cloudy
Low glucose (< 1/2 plasma)
High protein
10-5,000 polymorphs/mm³

What type of pathogen is involved?

A

Bacterial meningitis

553
Q

CSF fluid for suspected meningitis:

Clear/cloudy
60-80% of plasma glucose
Normal/raised protein
15-1,000 lymphocytes/mm³

What type of pathogen is involved?

A

Viral meningitis

554
Q

CSF fluid for suspected meningitis:

Slight cloudy, fibrin web
Low glucose (< 1/2 plasma)
High protein
10-1,000 lymphocytes/mm³

What type of pathogen is involved?

A

Tuberculosis meningitis

555
Q

When should dexamethasone NOT be given to children for meningitis?

A

Under 3 months old

556
Q

Define encephalitis?

A

Encephalitis describes inflammation of the brain parenchyma. It mostly affects frontal and temporal lobes

557
Q

What pathogen typically causes encephalitis?

A

Herpes simplex 1 (95%)

558
Q

What is the management for encephalitis?

A

IV acyclovir

559
Q

What type of organism is E. coli?

A

Gram negative rod

560
Q

What type of organism is Listeria monocytogenes?

A

Gram positive rod

561
Q

What type of organism is Neisseria meningitidis?

A

Gram negative diplococci

562
Q

What type of organism is Streptococcus pneumoniae?

A

Gram positive diplococci/chain

563
Q

What type of organism is Haemophillus influenzae?

A

Gram negative coccobacilli

564
Q

Suspected bacterial meningitis: an LP should be done before IV antibiotics, unless?

A

Cannot be done within 1 hour
Signs of severe sepsis or a rapidly evolving rash
Significant bleeding risk
Signs of raised intracranial pressure

565
Q

What are the four areas of developmental assessment?

A

Gross motor
Fine motor
Language delay
Social

566
Q

What should a child be able to do at 3 months in terms of gross motor milestones?

A

Little or no head lag on being pulled to sit
Lying on abdomen, good head control
Held sitting, lumbar curve

567
Q

What should a child be able to do at 6 months in terms of gross motor milestones?

A

Lying on abdomen, arms extended
Lying on back, lifts and grasps feet
Pulls self to sitting
Held sitting, back straight
Rolls front to back

568
Q

What should a child be able to do at 7-8 months in terms of gross motor milestones?

A

Sits without support (Refer at 12 months)

569
Q

What should a child be able to do at 9 months in terms of gross motor milestones?

A

Pulls to standing
Crawls

570
Q

What should a child be able to do at 12 months in terms of gross motor milestones?

A

Cruises
Walks with one hand held

571
Q

What should a child be able to do at 13-15 months in terms of gross motor milestones?

A

Walks unsupported (Refer at 18 months)

572
Q

What should a child be able to do at 18 months in terms of gross motor milestones?

A

Squat to pick up a toy

573
Q

What should a child be able to do at 2 years in terms of gross motor milestones?

A

Runs
Walks upstairs and downstairs holding on to rail

574
Q

What should a child be able to do at 3 years in terms of gross motor milestones?

A

Rides a tricycle using pedals
Walks up stairs without holding on to rail

575
Q

What should a child be able to do at 4 years in terms of gross motor milestones?

A

Hops on one leg

576
Q

What should a child be able to do at 3 months in terms of speech and hearing milestones?

A

Quietens to parents voice
Turns towards sound
Squeals

577
Q

What should a child be able to do at 6 months in terms of speech and hearing milestones?

A

Double syllables ‘adah’, ‘erleh’

578
Q

What should a child be able to do at 9 months in terms of speech and hearing milestones?

A

Says ‘mama’ and ‘dada’
Understands ‘no’

579
Q

What should a child be able to do at 12 months in terms of speech and hearing milestones?

A

Knows and responds to own name

580
Q

What should a child be able to do at 12-15 months in terms of speech and hearing milestones?

A

Knows about 2-6 words (Refer at 18 months)
Understands simple commands - ‘give it to mummy’

581
Q

What should a child be able to do at 2 years in terms of speech and hearing milestones?

A

Combine two words
Points to parts of the body

582
Q

What should a child be able to do at 2.5 years in terms of speech and hearing milestones?

A

Vocabulary of 200 words

583
Q

What should a child be able to do at 3 years in terms of speech and hearing milestones?

A

Talks in short sentences (e.g. 3-5 words)
Asks ‘what’ and ‘who’ questions
Identifies colours
Counts to 10 (little appreciation of numbers though)

584
Q

What should a child be able to do at 4 years in terms of speech and hearing milestones?

A

Asks ‘why’, ‘when’ and ‘how’ questions

585
Q

What should a child be able to do at 3 months in terms of fine motor and vision milestones?

A

Reaches for object
Holds rattle briefly if given to hand
Visually alert, particularly human faces
Fixes and follows to 180 degrees

586
Q

What should a child be able to do at 6 months in terms of fine motor and vision milestones?

A

Holds in palmar grasp
Pass objects from one hand to another
Visually insatiable, looking around in every direction

587
Q

What should a child be able to do at 9 months in terms of fine motor and vision milestones?

A

Points with finger
Early pincer

588
Q

What should a child be able to do at 12 months in terms of fine motor and vision milestones?

A

Good pincer grip
Bangs toys together

589
Q

Describe fine motor and vision milestones for children using bricks?

A

15 months - Tower of 2
18 months - Tower of 3
2 years - Tower of 6
3 years - Tower of 9

590
Q

Describe fine motor and vision milestones for children with drawing?

A

18 months - Circular scribble
2 years - Copies vertical line
3 years - Copies circle
4 years - Copies cross
5 years - Copies square and triangle

591
Q

Describe fine motor and vision milestones for children in terms of a book?

A

15 months - Looks at book, pats page
18 months - Turns pages, several at time
2 years - Turns pages, one at time

592
Q

Describe the generic social behaviour and interaction milestones?

A

6 weeks - Smiles (Refer at 10 weeks)
3 months - Laughs, enjoys friendly handling
6 months - Not shy
9 months - Shy, takes everything to mouth

593
Q

Describe social behaviour and interaction milestones in terms of feeding?

A

6 months - May put hand on bottle when being fed
12-15 months - Drinks from cup + uses spoon, develops over 3 month period
2 years - Competent with spoon, doesn’t spill with cup
3 years - Uses spoon and fork
5 years - Uses knife and fork

594
Q

Describe social behaviour and interaction milestones in terms of dressing?

A

12-15 months - Helps getting dressed/undressed
18 months - Takes off shoes, hat but unable to replace
2 years - Puts on hat and shoes
4 years - Can dress and undress independently except for laces and buttons

595
Q

Describe social behaviour and interaction milestones in terms of play?

A

9 months - Plays ‘peek-a-boo’
12 months - Waves ‘bye-bye’, plays ‘pat-a-cake’
18 months

596
Q

Define epilepsy?

A

Epilepsy is a common neurological condition characterised by recurrent seizures

597
Q

How is a seizure classified?

A
  1. Where seizures begin in the brain
  2. Level of awareness during a seizure
  3. Other features of seizures
598
Q

What is a focal seizure?

A

Start in a specific area, on one side of the brain.
The level of awareness can vary in focal seizures.
Can also be either motor or non-motor.

599
Q

What is a generalised seizure?

A

Involve networks on both sides of the brain at the onset.
Consciousness lost immediately.
Can be further subdivided into motor (e.g. tonic-clonic) and non-motor (e.g. absence)

600
Q

What are the different types of generalised seizures?

A

Tonic-clonic (grand mal)
Tonic
Clonic
Typical absence (petit mal)
Myoclonic
Atonic

601
Q

What is a focal to bilateral seizure?

A

Starts on one side of the brain in a specific area before spreading to both lobes

602
Q

What is a postictal phase in a seizure?

A

Where the person is confused, drowsy and feels irritable or depressed for around 15 minutes

603
Q

What is a tonic seizure?

A

The muscles become stiff and flexed, which can cause the patient to fall, usually backwards

604
Q

What is an atonic seizure?

A

Aka drop attacks. The muscles suddenly relax and become floppy, which can cause the patient to fall, usually forward.

605
Q

What is a clonic seizure?

A

Clonic seizures: violent muscle contractions (convulsions)

606
Q

What is a tonic-clonic seizure?

A

There is loss of consciousness andtonic(muscle tensing) andclonic(muscle jerking) episodes. Typically the tonic phase comes before the clonic phase.

607
Q

What is a myoclonic seizure?

A

Short muscle twitches. The patient usually remains awake during the episode.
Typically happen in children as part ofjuvenile myoclonic epilepsy.

608
Q

What is an absence seizure?

A

Aka petit mal seizures, impaired awareness or responsiveness. Patient becomes blank and stares into space before returning to normal.

609
Q

What are the main investigations following a seizure?

A

Following their first seizure patients generally have both an electroencephalogram (EEG) and neuroimaging (usually a MRI)

610
Q

What is the management for generalised tonic-clonic seizures in males?

A

Sodium valproate

611
Q

What is the management for generalised tonic-clonic seizures in females?

A

Lamotrigine or levetiracetam

Girls aged under 10 years and who are unlikely to need treatment when they are old enough to have children or women who are unable to have children may be offered sodium valproate first-line

612
Q

What is the first line management for focal seizures?

A

Lamotrigine or levetiracetam

613
Q

What is the second line management for focal seizures?

A

Carbamazepine, oxcarbazepine or zonisamide

614
Q

What is the first line management for absence (petit mal) seizures?

A

Ethosuximide

615
Q

What is the second line management for absence (petit mal) seizures in males?

A

Sodium valproate

616
Q

What is the second line management for absence (petit mal) seizures in females?

A

Lamotrigine or levetiracetam

617
Q

What drug may exacerbate absence seizures?

A

Carbamazepine

618
Q

What is the management for myoclonic seizures in males?

A

Sodium valproate

619
Q

What is the management for myoclonic seizures in females?

A

Levetiracetam

620
Q

What is the management for tonic or atonic seizures in males?

A

Sodium valproate

621
Q

What is the management for tonic or atonic seizures in females?

A

Lamotrigine

622
Q

What is a febrile convulsion?

A

Febrile convulsions are seizures provoked by fever in otherwise normal children

623
Q

What is a simple febrile convulsion?

A

< 15 minutes
Generalised seizure
No reoccurrence
Complete recovery within the hour

624
Q

What is a complex febrile seizure?

A

15-30 minutes
Focal seizure
May have repeated seizures

625
Q

What is febrile status epileptics?

A

> 30 minutes in duration

626
Q

What is the management for recurrent febrile convulsions in the community?

A

Benzodiazepine rescue medication:
Rectal diazepam
Buccal midazolam

627
Q

What is the management for status epilepticus convulsions in the community?

A

Benzodiazepine rescue medication:
Rectal diazepam
Buccal midazolam

628
Q

What is the rescue management for status epilepticus convulsions in a hospital setting?

A

IV lorazepam

629
Q

Define autism?

A

A triad of communication impairment + impairment of social relationships + ritualistic behaviour

630
Q

A triad of communication impairment + impairment of social relationships + ritualistic behaviour would indicate what?

A

Autism

631
Q

What is ADHD?

A

A condition incorporating features relating to inattention and/or hyperactivity/impulsivity that are persistent.

632
Q

What would some features of inattention be?

A

Does not follow instructions
Reluctant to engage in mentally-intense tasks
Easily distracted
Finds it difficult to sustain tasks
Finds it difficult to organise tasks or activities
Often forgetful in daily activities
Often loses things necessary for tasks or activities
Often does not seem to listen when spoken to directly

633
Q

What would some features of hyperactivity be?

A

Unable to play quietly
Talks excessively
Does not wait their turn easily
Will spontaneously leave their seat when expected to sit
If often ‘on the go’
Often interruptive or intrusive to others
Will answer prematurely, before a question has been finished
Will run and climb in situations where it is not appropriate

634
Q

What is the first-line management for ADHD?

A

10 week period of ‘watch and wait’ to observe whether symptoms change or resolve

635
Q

What are the conditions of providing pharmacological therapy for patients with ADHD?

A

Used as a last resort, and is only available to those that are aged 5 and over.

636
Q

What is the first line pharmacological treatment for ADHD in children?

A

Methylphenidate on a 6 week trial basis

637
Q

What type of drug is methylphenidate?

A

It is a CNS stimulant which primarily acts as a dopamine/norepinephrine reuptake inhibitor

638
Q

What are some side effects of methylphenidate?

A

Abdominal pain, nausea and dyspepsia.
In children, weight and height should be monitored every 6 months

639
Q

What are the first line pharmacological agents for ADHD in adults?

A

Methylphenidate or lisdexamfetamine are first-line options.
Switch between drugs if the other fails

640
Q

What is the second line pharmacological agent for ADHD in children?

A

Lisdexamfetamine

641
Q

What is a third line pharmacological agent for ADHD in children?

A

Dexamfetamine - only in those who have benefited from lisdexamfetamine, but who can’t tolerate its side effects.

642
Q

What is a MAJOR side effect of methylphenidate and lisdexamfetamine?

A

Cardiotoxicity - Perform a baseline ECG before starting treatment, and refer to a cardiologist if there is any significant past medical history or family history, or any doubt or ambiguity.

643
Q

Is ADHD more common in boys or girls?

A

Boys by a ratio of 4:1

644
Q

How many features must a 16 year old have if they are to be diagnosed with ADHD?

A

Up to 16 years old - 6 features must be present.

645
Q

How many features must a patient have if they are older than 17 years old, to be diagnosed with ADHD?

A

Over 17 years old - 5 features must be present.

646
Q

What is the most common cause of child and adolescent admission to psychiatry wards?

A

Anorexia nervosa

647
Q

What is anorexia nervosa?

A

Anorexia nervosa (AN) is an eating disorder characterised by restriction of caloric intake leading to low body weight, an intense fear of gaining weight, and a body image disturbance

648
Q

What is first line management for anorexia nervosa in children?

A

Anorexia focussed family therapy

649
Q

What is second line management for anorexia nervosa in children?

A

Individual eating-disorder-focused cognitive behavioural therapy (CBT-ED)

Is first line in adults.

650
Q

What is bulimia nervosa?

A

Bulimia nervosa is a type of eating disorder characterised by episodes of binge eating followed by intentional vomiting or other purgative behaviours such as the use of laxatives or diuretics or exercising

651
Q

What is the management for bulimia nervosa?

A

Referral for specialist care
Bulimia-nervosa-focused family therapy (FT-BN)

Eating-disorder-focused cognitive behavioural therapy (CBT-ED)
Bulimia-nervosa-focused guided self-help for adults

652
Q

What pharmacological agent is currently liscensed for bulimia nervosa?

A

High dose Fluoxetine

653
Q

What signs may be seen on a patient with bulimia nervosa?

A

Russel’s sign - calluses on the knuckles or back of the hand due to repeated self induced vomiting
Erosion of teeth

654
Q

Define cryptorchidism?

A

A congenital undescended testis is one that has failed to reach the bottom of the scrotum by 3 months of age

655
Q

What are the reasons for correction of cryptorchidism?

A

Reduce risk of infertility
Allows the testes to be examined for testicular cancer
Avoid testicular torsion
Cosmetic appearance

656
Q

What is the management of cryptorchidism?

A

Orchidopexy at 6- 18 months of age

657
Q

What is testicular torsion?

A

Twist of the spermatic cord resulting in testicular ischaemia and necrosis.

658
Q

What are the features of testicular torsion?

A

Pain is usually severe and of sudden onset
May be referred to the abdomen
Nausea and vomiting

659
Q

On examination what would you see for testicular torsion?

A

Swollen, tender testis retracted upwards. The skin may be reddened
Cremasteric reflex is lost
Elevation of the testis does not ease the pain (Prehn’s sign negative)

660
Q

What is the management for testicular torsion?

A

Treatment is with urgent surgical exploration and bilateral orchiopexy (fixated to scrotal sac)

661
Q

Define precocious puberty?

A

‘development of secondary sexual characteristics before 8 years in females and 9 years in males’

662
Q

What are the two types of precocious puberty?

A
  1. Gonadotrophin dependent
  2. Gonadotrophin independent
663
Q

What is the cause of gonadotrophin dependent precocious puberty?

A

Due to premature activation of the hypothalamic-pituitary-gonadal axis
FSH & LH raised

664
Q

What is the cause of gonadotrophin independent precocious puberty?

A

Due to excess sex hormones
FSH & LH low

665
Q

How can size of testes indicate the cause of precocious puberty?

A

Bilateral enlargement = gonadotrophin release from intracranial lesion
Unilateral enlargement = gonadal tumour
Small testes = adrenal cause (tumour or adrenal hyperplasia)

666
Q

What is primary hypothyroidism?

A

There is a problem with the thyroid gland itself, for example an autoimmune disorder affecting thyroid tissue

667
Q

What is secondary hypothyroidism?

A

Usually due to a disorder with the pituitary gland (e.g.pituitary apoplexy) or a lesion compressing the pituitary gland

668
Q

What are the general features of hypothyroidism?

A

Weight gain
Lethargy
Cold intolerance
Constipation

669
Q

What are the skin features of hypothyroidism?

A

Dry (anhydrosis), cold, yellowish skin
Non-pitting oedema
Dry, coarse scalp hair, loss of later aspect of eyebrows (Queen Anne’s sign)

670
Q

What is the gynaecological feature of hypothyroidism?

A

Menorrhagia

671
Q

What are the neurological features of hypothyroidism?

A

Decreased deep tendon reflexes
Carpal tunnel syndrome

672
Q

What are the features of congenital hypothyroidism?

A

Prolonged neonatal jaundice
Delayed mental/physical milestones
Short stature
Puffy face
Hypotonia

673
Q

What is the most common cause of hypothyroidism in children?

A

Autoimmune thyroiditis

Most common in developing world - iodine deficiency

674
Q

What would a TFT show for hypothyroidism?

A

High TSH
Low T3
Low T4

675
Q

What is the management for hypothyroidism?

A

Levothyroxine

676
Q

What are the side-effects of thyroxine therapy?

A

Hyperthyroidism: due to over treatment
Reduced bone mineral density
Worsening of angina
Atrial fibrillation

677
Q

What is Kallmann’s syndrome?

A

Kallmann’s syndrome is a recognised cause of delayed puberty secondary to hypogonadotropic hypogonadism

678
Q

What is the inheritance pattern of Kallmann’s syndrome?

A

X-linked recessive
Therefore more common in males

679
Q

What is the pathophysiology behind Kallmann’s syndrome?

A

Thought to be caused by failure of GnRH-secreting neurones to migrate to the hypothalamus

680
Q

What are the key features of Kallmann’s syndrome?

A

‘delayed puberty’
Hypogonadism, cryptorchidism
ANOSMIA
Sex hormone levels are low
LH, FSH levels are inappropriately low/normal
Patients are typically of normal or above-average height
Cleft lip and palete

681
Q

What is the management for Kallmann’s syndrome?

A

Testosterone in males
Oestrogen-progestin supplementation in females

682
Q

Describe the LH and Testosterone results in: Klinefelter’s syndrome, Hypogonadotrophin hypogonadism, Androgen insensitivity syndrome?

A

Klinefelter’s syndrome - high LH and low test
Hypogonadotrophin hypogonadism - low LH and low test
Androgen insensitivity syndrome - high LH and normal/high test

683
Q

What is congenital adrenal hyperplasia?

A

Congenital adrenal hyperplasia (CAH) refers to a group of autosomal recessive disorders that impair adrenal steroid biosynthesis

684
Q

How does congenital adrenal hyperplasia cause symptoms?

A

The deficiency in cortisol production leads to compensatory overproduction of adrenocorticotropic hormone (ACTH) by the anterior pituitary.

Elevated ACTH levels increase the production of adrenal androgens, which can result in the virilization of female infants and affect genital development.

685
Q

What are the different types of congenital adrenal hyperplasia?

A

21-hydroxylase deficiency (90% - most common)
17-hydroxylase deficiency (very rare)
11-beta hydroxylase

686
Q

What is the investigation for congenital adrenal hyperplasia?

A

ACTH stimulation test - evaluates the adrenal gland’s response to ACTH, with abnormal increases in 17OHP indicating CAH

687
Q

What is the management for congenital adrenal hyperplasia?

A

Involves glucocorticoid replacement to reduce ACTH levels and minimize adrenal androgen production

688
Q

What are the features of 21-hydroxylase deficiency type congenital adrenal hyperplasia?

A

Virilization of female genitalia
Precocious puberty in males
Salt losing crisis

689
Q

What are the features of 11-beta-hydroxylase deficiency type congenital adrenal hyperplasia?

A

Virilisation of female genitalia
Precocious puberty in males
Hypertension
Hypokalaemia

690
Q

What are the features of 17-hydroxylase deficiency type congenital adrenal hyperplasia?

A

Non-virilising in females
Inter-sex in boys
Hypertension

691
Q

At what percentile of BMI would clinical intervention be considered for obesity in children?

A

91st

692
Q

At what percentile of BMI would assessment of co-morbidities be assessed in children?

A

98th

693
Q

What are the risk factors for obesity in children?

A

Lifestyle factors
Asian children
Female children
Taller children

694
Q

What are the classifications of overweight, clinical obesity and severe obesity for children / young adults?

A

Overweight: BMI 91st centile
Clinical obesity: BMI 98th centile
Severe obesity: BMI 99.6th centile

695
Q

Define alpha thalassaemia?

A

Alpha-thalassaemia is a autosomal recessive condition due to a deficiency of alpha chains in haemoglobin

696
Q

Where are the alpha-globulin genes located?

A

2 separate alpha-globulin genes are located on each chromosome 16

697
Q

Give an overview of alpha-thalassaemia where 1/2 alpha globulin alleles are affected?

A

If 1 or 2 alpha globulin alleles are affected then the blood picture would be hypochromic and microcytic, but the Hb level would be typically normal

698
Q

Give an overview of alpha-thalassaemia where 3 alpha globulin alleles are affected?

A

If are 3 alpha globulin alleles are affected results in a hypochromic microcytic anaemia with splenomegaly. This is known as Hb H disease

699
Q

Give an overview of alpha-thalassaemia where 4 alpha globulin alleles are affected?

A

If all 4 alpha globulin alleles are affected (i.e. homozygote) then death in utero (hydrops fetalis, Bart’s hydrops)

700
Q

What is the management for alpha-thalassaemia in severe cases?

A

Regular Blood Transfusions to maintain normal haemoglobin levels in severe cases.

Chronic transfusion therapy may lead to iron overload, hence iron chelation therapy with drugs like Deferasirox or Deferoxamine is necessary

701
Q

Define beta-thalassaemia?

A

Beta-thalassaemia trait is an autosomal recessive condition where there is deficiency in the production of the beta globulin chains of haemoglobin.

characterised by a mild hypochromic, microcytic anaemia..

702
Q

Where are the beta-globulin genes located?

A

Chromosome 11

703
Q

What is beta-thalassaemia trait?

A

Where there is a reduced beta chain due to either promotor region mutations or splice sites.

704
Q

What is beta-thalassaemia major?

A

Where there is absent beta chains due to either promotor region mutations or splice sites

705
Q

What are the features of beta-thalassaemia major?

A

Presents in the first year of life with failure to thrive and hepatosplenomegaly

706
Q

What is the management for beta-thalassaemia major?

A

Repeated blood transfusions
Iron chelation therapy due to potential of iron overload

707
Q

Define haemolytic disease of the newborn?

A

Also known as erythroblastosis fetalis, is a complex and potentially life-threatening condition arising from maternal-foetal blood group incompatibility.

708
Q

What are the investigations for beta-thalassaemia?

A

Hb electrophoresis:
HbA2 & HbF raised
HbA absent

FBC - Microcytic anaemia

709
Q

Define sickle cell anaemia

A

Sickle-cell anaemia is a genetic condition that results for synthesis of an abnormal haemoglobin chain termed HbS

710
Q

In what demographic is sick-cell anaemia more common and why?

A

It is more common in people of African descent as the heterozygous condition offers some protection against malaria

711
Q

When do features of sickle-cell anaemia develop and why?

A

Symptoms in homozygotes don’t tend to develop until 4-6 months when the abnormal HbSS molecules take over from fetal haemoglobin

712
Q

What is the pathophysiology behind sick-cell anaemia?

A

Polar amino acid glutamate is substituted by non-polar valine in each of the two beta chains (codon 6).
This decreases the water solubility of deoxy-Hb causing them to polymerase and ‘sickle’ where they haemolyse and block small vessels

713
Q

What is the inheritance pattern of sickle cell anaemia?

A

Autosomal recessive

714
Q

What is the investigation for sickle-cell anaemia?

A

Hb electrophoresis
FBC
Blood film

715
Q

Define haemophilia, what is the inheritance pattern?

A

Haemophilia is an X-linked recessive disorder of coagulation due to an absence of a clotting factor depending on subtype

716
Q

What deficiency is there in haemophilia A?

A

Haemophilia A is caused by a deficiency in factor VIII

717
Q

What deficiency is there in haemophilia B?

A

Haemophilia B (also known as Christmas disease) is caused by a deficiency in factor IX

718
Q

What are the features of haemophilia?

A

Haemoarthroses
Haematomas
Prolonged bleeding after surgery or trauma

719
Q

What are the investigations for haemophilia?

A

FBC - normal platelets
Bleeding time, thrombin time, prothrombin time normal
Activated partial thromboplastin time (APTT) is prolonged

720
Q

What is the management for haemophilia?

A

Avoid contact sports and medicines that promote bleeding e.g. aspirin
IV clotting factors - may be an immune response (15%)
Desmopressin
Tranexamic acid

721
Q

What is the most common inherited bleeding disorder?

A

Von Willebrands disease

722
Q

Define von Willebrands disease?

A

An inherited bleeding disorder usually due to a reduced quantity or reduced quality of von Willebrand factor

723
Q

What is the inheritance pattern of von Willebrands disease?

A

Autosomal dominant

724
Q

What is the role of von Willebrand factor?

A

Promotes platelet adhesion to damaged endothelium
Carrier molecule for factor VIII

725
Q

What are the investigations for von Willebrands disease?

A

Prolonged bleeding time
APTT may be prolonged
Factor VIII levels may be moderately reduced
Defective platelet aggregation with ristocetin

726
Q

What is the management for von Willebrands disease?

A

Tranexamic acid
Desmopressin
Factor VIII concentrate

727
Q

What is ITP?

A

Immune (or idiopathic) thrombocytopenic purpura (ITP) is an immune-mediated reduction in the platelet count.
It is an example of a type II hypersensitivity reaction

728
Q

What may cause ITP in children?

A

ITP in children is typically more acute than in adults and may follow an infection or vaccination

729
Q

What are the features of ITP?

A

Bruising
Petechial or purpuric rash

730
Q

What are the investigations for ITP?

A

FBC - isolated thrombocytopaenia
Blood film

731
Q

What is the management for ITP?

A

TP resolves in around 80% of children with 6 months, with or without treatment

732
Q

Define sideroblastic anaemia?

A

Sideroblastic anaemia is a condition where red cells fail to completely form haem

733
Q

What is the congenital cause of sideroblastic anaemia?

A

Delta-aminolevulinate synthase-2 deficiency

734
Q

What are the investigations for sideroblastic anaemia?

A

FBC - hypochromic microcytic anaemia
Iron studies: ferratin, iron, transferrin saturation are all high

735
Q

What is the most common anaemia?

A

Iron deficiency anaemia

736
Q

What demographic has the highest incidence of iron deficiency anaemia?

A

Preschool-age children

737
Q

What are the features of iron deficiency anaemia?

A

Fatigue
SOB on exertion
Pallor
Palpitations
Koilonychia - spoon shaped nails
Angular stomtatitis

738
Q

What are the investigations for iron deficiency anaemia?

A

FBC - hypochromic microcytic anaemia:

Low serum Ferratin
Low serum Iron
Low Transferrin
Total iron binding capacity will be high

Anti-Transglutaminase Antibody (TTG) antibodies to rule out Coeliac disease

739
Q

What is the management for iron deficiency anaemia?

A

Treat underlying cause

Oral iron supplementation - ferrous sulphate or ferrous fumarate

IV iron (ferric carboxymaltose) if cannot give above

Blood transfusion in severe cases

740
Q

Define acute lymphoblastic leukaemia?

A

Acute lymphoblastic leukaemia (ALL) is the most common malignancy affecting children and accounts for 80% of childhood leukaemias.

741
Q

What is the peak incidence age of ALL?

A

The peak incidence is at around 2-5 years of age.

742
Q

What are the classical features of ALL?

A

Anaemia: lethargy and pallor
Neutropaenia: frequent or severe infections
Thrombocytopenia: easy bruising, petechiae

743
Q

What are the different types of ALL?

A

Common ALL (75%), CD10 present, pre-B phenotype
T-cell ALL (20%)
B-cell ALL (5%)

744
Q

What are some management agents for ALL?

A

Vincristine
Corticosteroids
Anthrayclines
Methotrexate

745
Q

What is Wilm’s tumour?

A

Wilms’ tumour aka. nephroblastoma is a specific type of tumour affecting the kidney in children, typically under the age of 5 years

746
Q

What are the classic features of Wilm’s tumour?

A

May often present as a mass associated with haematuria
Pyrexia may occur in 50% of patients

747
Q

Where does Wilm’s tumour often metastasise?

A

Lungs

748
Q

What is the management for Wilm’s tumour?

A

Nephrectomy

749
Q

Define neuroblastoma?

A

A malignant tumour arising from the embryological neural crest element of the peripheral sympathetic nervous system

750
Q

What is the most common site of neuroblastoma?

A

Neural crest tissue in the adrenal glands

751
Q

What are some features of neuroblastoma?

A

Abdominal mass
Pallor, weight loss
Bone pain, limp
Hepatomegaly

752
Q

What are the investigations for neuroblastoma?

A

Urinary vanillylmandelic acid (VMA) and homovanillic acid (HVA) levels - both raised
Calcification may be seen on abdominal x-ray
Biopsy

753
Q

What is retinoblastoma?

A

Retinoblastoma is the most common ocular malignancy found in children

754
Q

What is the inheritance pattern of a dysfunctional Rb gene?

A

Autosomal dominant

755
Q

What is the pathophysiology behind retinoblastoma?

A

Caused by a loss of function of the retinoblastoma tumour suppressor gene on chromosome 13

756
Q

What are the possible features of retinoblastoma?

A

Absence of red-reflex, replaced by a white pupil (leukocoria) - the most common presenting symptom
Strabismus
Visual problems

757
Q

What are the management options for retinoblastoma?

A

Enucleation is NOT the only option
Depending on how advanced the tumour is other options include external beam radiation therapy, chemotherapy and photocoagulation

758
Q

What are the benign bone tumours?

A

Osteoma
Oestochondroma (exotosis)
Giant cell tumour
Osteoblastoma

759
Q

What are the malignant bone tumours?

A

Osteosarcoma
Ewing’s sarcoma
Chondrosarcoma

760
Q

Define osteoma?

A

Benign ‘overgrowth’ of bone, most typically occuring on the skull

761
Q

What is the most common benign bone tumour?

A

Osteochondroma (exotosis)

762
Q

Define osteochondroma?

A

Cartilage-capped bony projection on the external surface of a bone

763
Q

What is the most common malignant bone tumour?

A

Osteosarcoma

764
Q

Define osteosarcoma?

A

A malignant bone tumour that occurs most frequently in the metaphyseal region of long bones prior to epiphyseal closure, with 40% occuring in the femur, 20% in the tibia, and 10% in the humerus

765
Q

What would an X-ray of osteosarcoma show?

A

Codman triangle (from periosteal elevation) and ‘sunburst’ pattern

766
Q

Codman triangle and ‘sunburst’ pattern on an X-ray would indicate what?

A

Osteosarcoma

767
Q

Define Ewing’s sarcoma?

A

Small round blue cell tumour

768
Q

Where does Ewing’s sarcoma most commonly arise?

A

Occurs most frequently in the pelvis and long bones

769
Q

What would Ewing’s sarcoma show on an X-ray?

A

Onion skin appearance

770
Q

Onion skin appearance on an X-ray would indicate what?

A

Ewing’s sarcoma

771
Q

Define hepatoblastoma?

A

Hepatoblastomas are the most common primary malignant liver tumor in pediatric patients

772
Q

What is the management for hepatoblastoma?

A

Surgical resection - first line
Cisplatin chemotherapy
Liver transplant

773
Q

What is the most common primary brain tumour in children?

A

Pilocytic astrocytoma

774
Q

What would pilocytic astrocytoma show on histology?

A

Rosenthal fibres (corkscrew eosinophilic bundles)

775
Q

Define medulloblastoma?

A

A medulloblastoma is an aggressive paediatric brain tumour that arises within the infratentorial compartment. It spreads through the CSF system

776
Q

What is the management for medulloblastoma?

A

Surgical resection and chemotherapy

777
Q

What is the most common paediatric supratentorial tumour?

A

Craniopharyngioma

778
Q

Define craniopharyngioma?

A

A solid/cystic tumour of the sellar region that is derived from the remnants of Rathke’s pouch

779
Q

What is the management of craniopharyngioma?

A

Surgical resection of tumour
With or without postoperative radiotherapy.

780
Q

Define Kleinfelter syndrome?

A

Klinefelter syndromeoccurs when amalehas anadditional X chromosome, making them47 XXY.

781
Q

What are the classical features of Kleinfelter syndrome?

A

Taller height
Wider hips
Gynaecomastia
Small testicles
Reduced libido
Infertility

782
Q

What are some of the management options for Kleinfelter syndrome?

A

Testosterone injections
Breast reduction surgery

783
Q

Define Turner syndrome?

A

Turner’s syndrome is a chromosomal disorder caused by either the presence of only one sex chromosome (X) or a deletion of the short arm of one of the X chromosomes.

784
Q

What are the classical features of Turner’s syndrome?

A

Short stature
Widely spaced nipples
Webbed neck
Bicuspid aortic valve
Coarctation of the aorta
Primary amenorrhoea

785
Q

What is the most serious long-term health complication of Turner’s syndrome?

A

Aortic dilatation and dissection

786
Q

What autoimmune conditions have an increased incidence in Turner’s syndrome?

A

Autoimune thyroiditis
Crohn’s disease

787
Q

What are trisomy 13, 18 and 21 also known as?

A

Patau syndrome
Edward syndrome
Down syndrome

788
Q

What parameters are measured in the combined test?

A

Nuchal translucency measurement
Serum B-HCG
Pregnancy-associated plasma protein A (PAPP-A)

789
Q

When is the combined test performed in pregnancy?

A

11-13+6 weeks.

790
Q

What parameters are measured in the quadruple test?

A

Alpha-feto protein.
Serum B-HCG
Unconjugated oestriol
Inhibin A

791
Q

When is the combined test performed in pregnancy? Why would a combined test not be offered?

A

If women book later in pregnancy the quadruple test should be offered between 15 - 20 weeks.

792
Q

What would the results be for a combined test be for Down syndrome?

A

Increased hCG
Decreased PAPP-A
Thickened nuchal transparency

793
Q

What would the results be for a combined test be for Edward syndrome?

A

Increased hCG (lower than that of Down syndrome)
Decreased PAPP-A
Thickened nuchal transparency

794
Q

What would the results be for a combined test be for Patau syndrome?

A

Increased hCG (lower than that of Down syndrome)
Decreased PAPP-A
Thickened nuchal transparency

795
Q

What would the results be for a quadruple test be for Down syndrome?

A

Decreased alpha-feto protein.
Decreased unconjugated oestriol
Increased Serum B-HCG
Increased inhibin A

796
Q

What would the results be for a quadruple test be for Edwards syndrome?

A

Decreased alpha-feto protein.
Decreased unconjugated oestriol
Decreased Serum B-HCG
Normal inhibin A

797
Q

What would the results be for a quadruple test be for Patau syndrome?

A

Increased alpha-feto protein.
Normal unconjugated oestriol
Normal Serum B-HCG
Normal inhibin A

798
Q

What would a result of increased hCG , decreased PAPP-A, thickened nuchal transparency indicate for the combined test?

A

Down syndrome.

799
Q

What would a result of moderately increased hCG , decreased PAPP-A, thickened nuchal transparency indicate for the combined test?

A

Edward syndrome or Patau syndrome.

800
Q

What would a result of decreased alpha-feto protein, decreased unconjugated oestriol, increased Serum B-HCG, increased inhibin A indicate for the quadruple test?

A

Down Syndrome

801
Q

What would a result of decreased alpha-feto protein, decreased unconjugated oestriol, decreased Serum B-HCG, increased inhibin A indicate for the quadruple test?

A

Edwards syndrome.

802
Q

What would a result of increased alpha-feto protein, normal unconjugated oestriol, normal Serum B-HCG, normal inhibin A indicate for the quadruple test?

A

Neural tube defects

803
Q

What type of genetic disease is fragile X syndrome?

A

Trinucleotide repeat disorder.

CGG repeats

804
Q

What is the pathophysiology behind fragile X syndrome?

A

CGG repeat expansions can lead to DNA hypermethylation and cause reduced production of the fragile X mental retardation protein (FMRP), critical for normal brain development

805
Q

What is the pattern of inheritance of Duchenne muscular dystrophy?

A

X-linked recessive inherited disorder in the dystrophin genes required for normal muscular function.

806
Q

What are the classical features of Duchenne muscular dystrophy?

A

Progressive proximal muscle weakness from 5 years
Calf pseudohypertrophy
Gower’s sign: child uses arms to stand up from a squatted position
30% of patients have intellectual impairment

807
Q

What are the investigations for Duchenne muscular dystrophy?

A

Raised creatinine kinase
Genetic testing is GOLD STANDARD

808
Q

What is Angelman’s syndrome?

A

Angelman Syndrome is a rare genetic disorder caused by the loss of function of the UBE3A gene which affects normal brain development.

809
Q

Why are both Angelman’s syndrome and Prader-Willi syndrome considered imprinting disorders?

A

The paternal copy of the gene is imprinted and usually inactive in the brain so requires a working maternal copy for Asherman’s syndrome.

Prader-Willi syndrome - chromosome 15q11-q13 region is normally paternally inherited as they are inactivated on the maternal chromosome.

810
Q

What is Noonan syndrome?

A

Noonan syndrome is an autosomal-dominant inherited disorder which affects the RAS/MAPK pathway

811
Q

What is William syndrome?

A

William’s syndrome is an inherited neurodevelopmental disorder caused by a microdeletion on chromosome 7

812
Q

What are the classic features of William syndrome?

A

Very sociable personality, the starburst eyes and the wide mouth with a big smile.

813
Q

What are the associated conditions with William syndrome?

A

Supravalvular aortic stenosis and hypercalcaemia

814
Q

Define osteogenesis imperfecta?

A

More commonly known as brittle bone disease, is a group of disorders of collagen metabolism resulting in bone fragility and fractures

Most common is type 1, also less severe

815
Q

What is the inheritance pattern of osteogenesis imperfecta?

A

Autosomal dominant

816
Q

What is the pathophysiology behind osteogenesis imperfecta

A

Abnormality in type 1 collagen due to decreased synthesis of pro-alpha 1 or pro-alpha 2 collagen polypeptides

817
Q

What are the features of osteogenesis imperfecta?

A

Presents in childhood
Fractures following minor trauma
Blue sclera
Deafness secondary to otosclerosis
Dental imperfections are common

818
Q

What would blood show in osteogenesis imperfecta?

A

Adjusted calcium, phosphate, parathyroid hormone and ALP results are usually normal in osteogenesis imperfecta

819
Q

What is the management for osteogenesis imperfecta?

A

Bisphosphonates
Vitamin D supplementation

820
Q

What is rickets?

A

Rickets is a term that describes inadequately mineralised bone in developing and growing bones

821
Q

What are the risk factors for rickets?

A

Dietary deficiency of calcium, for example in developing countries
Prolonged breastfeeding
Unsupplemented cow’s milk formula
Lack of sunlight - Vitamin D deficency

822
Q

What are the classical features of rickets in younger children?

A

Aching bones and joints
Bow legs (genu varum)
Rickety rosary - swelling at costochondral joint
Kyphoscoliosis
Craniotabes

823
Q

What are the classical features of rickets in older children?

A

Aching bones and joints
Knock knees (genu valgum)
Rickety rosary - swelling at costochondral joint
Kyphoscoliosis
Harrison’s sulcus

824
Q

What are the investigations for rickets?

A

Low vitamin D levels
Reduced serum calcium - symptoms may results from hypocalcaemia
Raised alkaline phosphatase

825
Q

What is the management for rickets?

A

Oral vitamin D

826
Q

Define transient synovitis?

A

Transient synovitis is sometimes referred to as irritable hip. It generally presents as acute hip pain following a recent viral infection

827
Q

What is the most common cause of hip pain in children?

A

Transient synovitis

828
Q

What is the typical age group for transient synovitis?

A

3-8 years old

829
Q

What are the features of transient synovitis?

A

Limp / refusal to weight bear
Groin or hip pain
Low grade fever (high fever -> septic arthritis)

830
Q

What is the management for transient synovitis?

A

Symptomatic relief - NSIADs and paracetamol

831
Q

What are the most common joints affected in septic arthritis?

A

Hip, knee and ankle

832
Q

What are the features of septic arthritis?

A

Joint pain (swollen and erythematous)
Limp (decreased ROM)
High grade fever
Systemically unwell

833
Q

What are the investigations for septic arthritis?

A

Joint aspiration - Raised WCC
Raised CRP and ESR
Blood cultures

834
Q

What criteria is used to diagnose septic arthritis?

A

Kocher criteria:
Fever >38.5 degrees C
Non-weight bearing
Raised ESR
Raised WCC

835
Q

What is the Kocher criteria used for?

A

Diagnosis of septic arthritis

836
Q

What is the empirical management for septic arthritis?

A

Flucloxacillin first line
If allergy then clindamycin

837
Q

What is the management for MRSA septic arthritis?

A

Vancomycin

838
Q

What is the management for gongococcal septic arthritis?

A

Cefotaxime or ceftriaxone

839
Q

Define osteomyolitis?

A

Osteomyelitis describes an infection of the bone

840
Q

What is haematogenous osteomyelitis?

A

From bacteraemia
Monomicrobia
Most common in children

841
Q

What is non-haematogenous osteomyelitis?

A

Contiguous spread of infection from adjacent soft tissues to the bone or from trauma
Polymicrobial
Most common in adults

842
Q

What is the most common causative pathogen of osteomyelitis?

A

Staphylococcus aureus

843
Q

What is the most common causative pathogen of osteomyelitis in sickle cell patients?

A

Salmonella species

844
Q

What is the investigation of choice in osteomyelitis?

A

MRI

845
Q

What is the management for osteomyelitis?

A

Flucloxacillin for 6 weeks
Clindamycin if allergy

846
Q

Define Legg-Calve-Perthes disease?

A

A self-limiting disease of the femoral head comprising necrosis, collapse, repair, and re-modelling

847
Q

What is the phenotype of Legg-Calves-Perthes disease?

A

Short stature
Delayed bone age
Hyperactivity

848
Q

What is the investigation for Legg-Calves-Perthes disease?

A

Bilateral hip X-Ray

849
Q

Define discoid meniscus?

A

A discoid meniscus is an anatomical variant of the normal crescent-shaped meniscus. It is often thicker and is disc- or saucer-shaped

850
Q

What are the investigations for discoid meniscus and what would they show?

A

X-Ray:
Widened joint space
Squaring of the lateral femoral epicondyle
Cupping of the tibial plateau
Hypoplastic lateral tibial spine
MRI:
Bow-tie sign

851
Q

What is the management for discoid meniscus?

A

Asymptomatic does not require surgery
Surgery

852
Q

In what demographic is slipped capital femoral epiphysis classically seen?

A

Seen in children, classically seen in obese boys

853
Q

Define slipped capital femoral epiphysis?

A

Displacement of the femoral head epiphysis postero-inferiorly

854
Q

What are the features of slipped capital femoral epiphysis?

A

Hip, groin, medial thigh or knee pain
Loss of internal rotation of the leg in flexion
Bilateral slip in 20% of cases

855
Q

What is the investigation of choice for slipped capital femoral epiphysis and what would be a positive sign?

A

X-Ray - Ap and lateral view would show frog-leg

856
Q

What is the management for slipped capital femoral epiphysis?

A

Internal fixation: typically a single cannulated screw placed in the centre of the epiphysis

857
Q

What are the complications of slipped capital femoral epiphysis?

A

Osteoarthritis
Avascular necrosis of the femoral head
Chondrolysis
Leg length discrepancy

858
Q

Define osgood-shlatter disease?

A

Osgood-Schlatter disease (tibial apophysitis) is a type of osteochondrosis characterised by inflammation at the tibial tuberosity
More commonly affects boys

859
Q

What is the investigation of choice for osgood-shlatter disease?

A

X-Ray

860
Q

What is the management for osgood-shlatter disease?

A

Supportive - NSAIDs and Physiotherapy

861
Q

What are the risk factors for developmental dysplasia of the hip?

A

Female sex: 6 times greater risk
Breech presentation

Positive family history
Firstborn children
Oligohydramnios
Birth weight > 5 kg

862
Q

Is left or right developmental dysplasia of the hip more common?

A

Slightly more common in left
20% of time it is bilateral

863
Q

What infants require screening for developmental dysplasia of the hip?

A

First-degree family history of hip problems in early life
Breech presentation at or after 36 weeks gestation
Multiple pregnancy

864
Q

Outline a clinical examination for developmental dysplasia of the hip?

A

Barlow test: attempts to dislocate an articulated femoral head
Ortolani test: attempts to relocate a dislocated femoral head

Symmetry of leg length
Level of knees when hips and knees are bilaterally flexed
Restricted abduction of the hip in flexion

865
Q

What is the investigation of choice for developmental dysplasia of the hip?

A

Ultrasound to confirm diagnosis
X-Ray is above 4.5 months old

866
Q

What is the management for developmental dysplasia of the hip?

A

Most will spontaneously stabilise by 3-6 weeks of age
Pavlik harness in children <4-5 months
Older children may require surgery

867
Q

Define juvenile idiopathic arthritis?

A

Juvenile idiopathic arthritis (JIA) describes a group of chronic paediatric inflammatory arthritides characterised by onset before 16 years of age and the presence of objective arthritis (in one or more joints) for at least 6 weeks

868
Q

What are the five types of juvenile idiopathic arthritis?

A

Systemic JIA
Polyarticular JIA
Oligoarticular JIA
Enthesitis related arthritis
Juvenile psoriatic arthritis

869
Q

What will investigations show for systemic JIA?

A

Antinuclear antibodies - negative
Rheumatoid factors - negative
CRP - raised
ESR - raised
Platelets - raised
Serum ferritin - raised

870
Q

What is the key complication of systemic JIA?

A

Macrophage activation syndrome (MAS)

871
Q

What are the features of classical systemic JIA?

A

Salmon-pink rash
Fevers
Joint pain

872
Q

Define polyarticular JIA?

A

Polyarticular JIA involves idiopathic inflammatory arthritis in 5 joints or more

873
Q

What are the features of polyarticular JIA?

A

The inflammatory arthritis tends to be symmetrical and can affect the small joints of the hands and feet, as well as the large joints such as the hips and knees

874
Q

What will investigations show for polyarticular JIA?

A

Most children are negative for rheumatoid factor and are described as “seronegative’
Seropositive patients tend to be older children and adolescents

875
Q

Define oligoarticular JIA?

A

Also known as pauciarticular JIA
Usually it only affects a single joint, which is described as a monoarthritis
It occurs more frequently in girls under the age of 6 years

876
Q

What are the features of oligoarticular JIA?

A

It tends to affect the larger joints, often the knee or ankle
Classically associated with anterior uveitis - ophthalmology referral

877
Q

What will investigations show for oligoarticular JIA?

A

Rheumatoid factor - negative
Antinuclear antibodies - positive

878
Q

What is the management for JIA?

A

NSAIDs
Steroids in oligoarthritis
DMARDS
Biological therapy - TNF-alpha inhibitors

879
Q

What DMARDs can be used in JIA?

A

Methotrexate
Sulfasalazine
Lefulonmide

880
Q

What TNF-alpha inhibitors can be used in JIA?

A

Etanercept
Infliximab
Adalimumab

881
Q

What is adolescent idiopathic scoliosis (AIS)?

A

A structural spinal deformity characterised by decompensation of the normal vertebral alignment during rapid skeletal growth in otherwise healthy children

882
Q

What is congenital torticollis?

A

Congenital muscular torticollis (CMT) is a neck deformity that involves shortening of the sternocleidomastoid (SCM) muscle resulting in limited neck rotation and lateral flexion.

883
Q

What vaccines are given at 2 months old?

A

Dont talk to weird people I hate
‘6-1 vaccine’ (diphtheria, tetanus, whooping cough, polio, Hib and hepatitis B)
Men B

884
Q

What vaccines are given at 3 months old?

A

Dont talk to weird people I hate
‘6-1 vaccine’ (diphtheria, tetanus, whooping cough, polio, Hib and hepatitis B)
PCV

885
Q

What vaccines are given at 4 months old?

A

Dont talk to weird people I hate
‘6-1 vaccine’ (diphtheria, tetanus, whooping cough, polio, Hib and hepatitis B)
Men B

886
Q

What vaccines are given at 12-13 months old?

A

Hib/Men C
MMR
PCV
Men B

887
Q

What vaccines are given at 3-4 years old?

A

Dont talk to weird people
‘4-in-1 pre-school booster’ (diphtheria, tetanus, whooping cough and polio)
MMR

888
Q

What vaccines are given at 12-13 years?

A

HPV vaccination to boys and girls

889
Q

What vaccines are given at 13-18 years old?

A

Don’t talk to people
‘3-in-1 teenage booster’ (tetanus, diphtheria and polio)
Men ACWY

890
Q

What is an APGAR score? When is it used?

A

The Apgar score is used to assess the health of a newborn baby.

Assessed at 1 and 5 minutes

891
Q

What does a APGAR score of 0-3 mean, 4-6 mean, and 7-10 mean?

A

0-3 is very low
4-6 is moderately low
7-10 good score

892
Q

What score is given for pulse in the APGAR scoring?

A

2 = >100
1 = <100
0 = No pulse

893
Q

What score is given for respiratory effort in the APGAR score?

A

2 = Strong, crying
1 = Weak, irregular
0 = Nil

894
Q

What score is given for colour in the APGAR score?

A

2 = Pink
1 = Body pink, extremities blue
0 = Blue all over

895
Q

What score is given for muscle tone in the APGAR score?

A

2 = Active movement
1 = Limb flexion
0 = Flaccid

896
Q

What score is given for reflex irritability in the APGAR score?

A

2 = Cries on stimulation. Sneezing / coughing
1 = Grimace
0 = Nil

897
Q

What causes respiratory distress syndrome?

A

Insufficient surfactant production and structural immaturity in neonates

898
Q

What are the risk factors for respiratory distress syndrome?

A

Male sex
Diabetic mothers
Caesarian section
Second born or premature twins

899
Q

What is the management for respiratory distress syndrome?

A

Antenatal steroids(i.e.dexamethasone)
Oxygen - assisted ventilation
Exogenous surfactant via endotracheal tube

900
Q

Define meconium aspiration syndrome?

A

Respiratory distress in the newborn as a result of meconium in the trachea

901
Q

What are. the risk factors for meconium aspiration syndrome?

A

Maternal hypertension
Pre-eclampsia
Chorioamnionitis
Smoking
Substance abuse

902
Q

Define TORCH infection?

A

Toxoplasmosis - Toxoplasma gondii
Others (Syphilis, Hepatitis B) - Treponema pallidum, Hepatitis B virus
Rubella - Rubella virus
Cytomegalovirus (CMV) - Cytomegalovirus
Herpes simplex - Herpes virus simplex (HSV)

903
Q

What are the causes of neonatal jaundice in the first 24 hours?

A

Rhesus haemolytic disease
ABO haemolytic disease
Hereditary spherocytosis
Glucose-6-phosphodehydrogenase

904
Q

Why may there be physiological jaundice in neonates 2-14 days old?

A

More red blood cells, more fragile red blood cells and less developed liver function.

905
Q

What is the investigation for neonatal jaundice?

A

Conjugated and unconjugated bilirubin

Unconjugated is raised in biliary atresia

906
Q

What is the management for neonatal jaundice?

A

Phototherapy - converts unconjugated bilirubin to more excretable products
Exchange transfusion

907
Q

Define kernicterus?

A

A term used to describe the clinical features of acute or chronic bilirubin encephalopathy and the pathological findings of deep yellow staining in the brain

908
Q

Define necrotising enterocolitis?

A

a disorder affectingpremature neonates, where part of thebowelbecomesnecrotic.It is a life threatening emergency.

Death of the bowel tissue can lead to bowelperforation. Bowel perforation leads toperitonitisandshock.

909
Q

Define gastroschisis?

A

Gastroschisis describes a congenital defect in the anterior abdominal wall just lateral to the umbilical cord

910
Q

What will an abdominal X-ray show for necrotising enterocolitis?

A

Dilated bowel loops (often asymmetrical in distribution)
Bowel wall oedema
Pneumatosis intestinalis (intramural gas)
Portal venous gas
Pneumoperitoneum resulting from perforation
Air both inside and outside of the bowel wall (Rigler sign)
Air outlining the falciform ligament (football sign)

911
Q

What is the investigation of choice for necrotising enterocolitis?

A

Abdominal X-ray

912
Q

What is the management for gastroschisis?

A

Vaginal delivery may be attempted
Newborns should go to theatre as soon as possible after delivery, e.g. within 4 hours

913
Q

Define exomphalos / omphalocoele?

A

In exomphalos (also known as an omphalocoele) the abdominal contents protrude through the anterior abdominal wall but are covered in an amniotic sac formed by amniotic membrane and peritoneum.

914
Q

What is the management for exomphalos / omphalocoele?

A

Caesarean section - reduces risk of sac rupture
A staged repair - due to lack of space and increased intra-abdominal pressure

915
Q

Define oesophageal atresia and tracheo-oesophageal fistula

A

Oesophageal atresia (OA) and tracheo-oesophageal fistula (TOF) are congenital malformations that result from the defective separation of the common embryologic precursors to both the oesophagus and trachea

916
Q

What is neonatal hypoglycaemia?

A

Normal term babies often have hypoglycaemia especially in the first 24 hrs of life but without any sequelae.

< 2.6 mmol/L is used in many guidelines

917
Q

What is a key risk factor for neonatal hypoglycaemia?

A

Pre-term (>37 weeks)

918
Q

What is the management for neonatal hypoglycaemia?

A

Asymptomatic:
Encourage normal feeding (breast or bottle)
Monitor blood glucose

Symptomatic:
Admit to neonatal unit
IV infusion of 10% dextrose

919
Q

What type of organism is listeria?

A

A food-borne infection caused by a motile, non-spore-forming, gram-positive bacillus

920
Q

What is the management for listeria infection?

A

Ampicillin with Gentamicin

921
Q

What is the management for listeria infection in pregnant individuals?

A

Trimethoprim/sulfamethoxazole

Should be avoided during the first trimester of pregnancy due to the effect on folic acid metabolism

922
Q

What is the most common deformity affecting orofacial structures?

A

Cleft lip and palate

923
Q

What are the most common variants of cleft lip and palate?

A

Isolated cleft lip (15%)
Isolated cleft palate (40%)
Combined cleft lip and palate (45%)

924
Q

What drugs may increase the risk of cleft lip and palate?

A

Anti-epileptic use

Phase 3a (8 decks)

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