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3a Exam > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

Name 5 common causes of viral respiratory infections

A

Majority are viral:
- Respiratory syncytial virus (RSV)
- Rhinovirus
- Influenza
- Metapneumovirus
- Adenoviruses

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2
Q

Name 5 common causes of bacterial respiratory infections

A
  • Streptococcus pneumoniae
  • Haemophilus influenza
  • Moraxella catarrhalis
  • Bordetella pertussis
  • Mycoplasma pneumoniae
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3
Q

What are 5 risk factors for respiratory infections?

A
  • Parental smoking
  • Poor socioeconomic status (damp/overcrowded)
  • Poor nutrition
  • Male
  • Immunodeficiency
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4
Q

What is the clinical presentation of coryza?

A
  • Clear/mucopurulent nasal discharge
  • Nasal blockage
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5
Q

What are the most common pathogens that can cause corzya?

A

Rhinovirus
Coronaviruses
RSV

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6
Q

What is the management of coryza?

A

Paracetamol
Ibruprofen

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7
Q

What is Tonsillitis?

A

Form of pharyngitis where there is intense inflammation of the tonsils +/- purulent exudate

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8
Q

What are the most common pathogens that can cause pharyngitis?

A

Viral:
- Common cold viruses
- Adenoviruses
- EBV
Bacterial (older children):
- Group A beta-haemolytic strep

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9
Q

What is the clinical presentation of Tonsillitis?

A
  • Acute
  • Painful throat >48 hours
  • Dysphagia
  • Painful ears
  • Abdominal pain in small children
  • Headache
  • Voice changes
  • Erythema/inflamed tonsils + pharynx
  • Yellow exudate
  • Foul smelling breath
  • Fever
  • Swollen anterior cervical lymph glands
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10
Q

What is the management of Tonsillitis?

A

Symptomatic relief : Paracetamol and Ibruprofen
Abx indications: Penicillin V for 10 days:
- Marked systemic upset
- Unilateral peritonsillitis
- Rheumatic fever Hx
- Increased infection risk
- CENTOR > 3
Tonsillectomy: recurring cases

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11
Q

When would a Tonsillectomy be considered?

A

1) After >7 episodes of Tonsillitis
2) OSA or sleep-deprived breathing

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12
Q

What is the CENTOR criteria?

A

Calculates probability tonsillitis is is due Strep
4 criteria:
1) Tonsillar exudate
2) Tender anterior cervical lymphadenopathy
3) Fever
4) Absence of cough

3+ = Strep infection + Abx

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13
Q

Criteria for Tonsillitis referral?

A

Difficulty breathing
Clinical dehydration
Abscess
Systemic illness/sepsis
Suspected sinister cause

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14
Q

What is Quinsy?

A

Peritonsillar abscess (complication of tonsillitis)

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15
Q

What is the clinical presentation of Quinsy?

A

Sore throat
Dysphagia
Uvula deviation
Trismus (lockjaw)

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16
Q

What is Acute Otitis media?

A

Infection of the middle ear

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17
Q

What causes Acute otitis media?

A

Viruses e.g. RSV and rhinovirus

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18
Q

Why is acute otitis media common in children?

A

Short horizontal eustachian tubes + mucosal discharge

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19
Q

What is the clinical presentation of Acute Otitis media?

A

Rapid onset ear pain (due to bulging of tympanic membrane)
Pyrexia
Otorrhoea
Coryzal symptoms
Loss of hearing
Balance issues and vertigo

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20
Q

What investigations are ordered for acute otitis media?

A

Otoscopy:
-Bulging, red inflamed tympanic membrane
- Otorrhoea: perforation

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21
Q

What is the management of Acute Otitis media?

A

> 4 days of no symptoms: Amoxicillin / Erythromycin
Grommet insertion if recurrent

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22
Q

What is the function of a grommet?

A

A grommet keeps the middle ear aerated and prevents the accumulation of fluid

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23
Q

What is the leading cause of hearing loss in children?

A

Otitis media with effusion/glue ear

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24
Q

What causes glue ear?

A

Infection!
45% follow AOM

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25
Q

Give 3 causes of conductive hearing loss.

A
  1. Glue ear
  2. Ear wax
  3. Otitis media
  4. Perforated ear drum
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26
Q

Give 3 potential consequences of hearing loss

A
  1. Speech and language delay
  2. Social problems e.g. behavioural issues
  3. Academic underachievement
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27
Q

What is sinusitis?

A

Inflammation of the paranasal sinuses

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28
Q

What causes sinusitis?

A

Viruses e.g. RSV and rhinovirus

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29
Q

What is the clinical presentation of sinusitis?

A

Short symptoms suggest viral (<10 days)
Purulent nasal discharge
Nasal obstruction
Facial pain/pressure and swelling

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30
Q

How is sinusitis managed?

A

Paracetomol and ibuprofen: symptomatic relief
Amoxicillin/ doxycycline: if bacterial
Avoid antihistamines: may thicken secretions

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31
Q

What is Stridor?

A

Inspiration + upper airways + narrowing

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32
Q

Signs of upper airway obstruction?

A
  • Stridor
  • Hoarseness
  • Barking cough (sea lion)
  • Dyspnoea
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33
Q

How is the severity of upper airway obstruction assessed?

A

Degree of chest retraction and degree of stridor

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34
Q

What should you avoid in a suspected upper airway obstruction?

A

Avoid examination using a spatula as this may precipitate total obstruction

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35
Q

Describe why hoarseness occurs

A

Inflammation of the vocal cords

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36
Q

What is Croup otherwise known as?

A

Laryngotracheobronchitis

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37
Q

What is Croup?

A

URTI → mucosal inflammation and increased secretions → larynx oedema

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38
Q

Where is oedema dangerous in Croup?

A

Subglottic area → critical narrowing of the trachea

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39
Q

What are viral causes Croup?

A

Parainfluenza 1, 2, 3 (most common)
Metapneumovirus
RSV
Influenza

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40
Q

When is Croup most common?

A

Autumn time
6 months- 6 years old; peak incidence ≈2 years old

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41
Q

What is the clinical presentation of Croup?

A
  • Barking cough (worse at night)
  • Harsh stridor
  • Hoarse voice
  • Preceding non specific viral URTI
  • Increased work of breathing
  • Coryza: low grade fever
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42
Q

What is the management of Croup?

A

Conservative
Oral dexamethasone 1.8mg (0.15mg/kg)

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43
Q

What are signs of severe Croup?

A

Cyanosis

Altered consciousness

Rising HR/RR

Restlessness

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44
Q

What is Bacterial Tracheitis?

A

Pseudomembranous croup is an uncommon but dangerous disease very similar to severe croup

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45
Q

How is Bacterial Tracheitis different to Severe Croup?

A
  • High fever
  • Appears toxic
  • Tracheal tenderness
  • Rapidly progressive airways obstruction (thick exudate cant be cleared by coughing)
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46
Q

What is bacterial tracheitis caused by?

A

S. aureus
Strep Group A
H. influenzae

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47
Q

What is the management of bacterial tracheitis?

A

IV Vancomycin

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48
Q

What is Acute Epiglottitis?

A

Inflammation and localised oedema of the epiglottis
Life-threatening airway obstruction

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49
Q

What causes Epiglottitis?

A

Haemophilus influenza type B

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50
Q

What affect has Hib immunisation had on the incidence of epiglottitis?

A

> 99% reduction in cases
Most common in ages 2-7 years

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51
Q

What is the clinical presentation of Acute Epiglottitis?

A
  • Intense swelling of epiglottis
  • Onset very acute
  • High fever
  • Dysphagia and speech difficulty due to pain
  • Drooling
  • Stridor
  • Minimal cough
  • Tripod position
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52
Q

In what position would you expect a child with trachea obstruction to be in?

A

Immobile
Upright
Open mouth to optimise the airway

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53
Q

How is epiglottitis diagnosed?

A

Laryngoscopy

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54
Q

What should you never do when suspecting obstruction of the respiratory tract/acute epiglottitis?

A

Do not examine throat with spatula or lie the child down
Do not upset
Do not cannulate

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55
Q

What is the management of Acute Epiglottitis?

A

IV Abx: Cefotaxime
Intubate
Supplemental O2
Corticosteriods (dexamethasone)
Tracheostomy: if complete obstruction

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56
Q

What is the difference between Croup and Acute Epiglottitis in terms of:
1) Onset
2) Cough
3) Preceding coryza
4) Able to drink

A

Croup:
1) Days
2) Severe barking cough
3) Preceding coryza
4) Can drink

Acute Epiglottitis:
1) Hours
2) Absent/minor cough
3) No preceding coryza
4) Can’t drink

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57
Q

What is the difference between Croup and Acute Epiglottitis in terms of:
1) Drooling
2) Appearance of child
3) Fever
4) Stridor and voice/cry

A

Croup:
1) None
2) Unwell appearance
3) Fever <38.5
4) Harsh stridor with hoarse cry

Acute Epiglottitis:
1) Drooling
2) Toxic, very unwell
3) Fever >38.5
4) Soft whispering stridor, muffled cry/reluctant to speak

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58
Q

What is the main difference between Croup and Bronchiolitis?

A

Croup = stridor + Parainfluenza virus B
Bronchiolitis = wheeze + RSV

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59
Q

What is Whooping Cough (Pertussis)?

A

URTI

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60
Q

What causes whooping cough?

A

Bordetella pertussis: Gram- coccobacillus

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61
Q

How is whooping cough transmitted?

A

Inhaled droplets

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62
Q

How long do Whooping Cough symptoms last?

A

6-8 weeks

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63
Q

What is the first stage of whooping cough?

A

Catarrhal

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64
Q

What is the clinical presentation of the Catarrhal stage (1st stage) in Whooping Cough?

A
  • Malaise
  • Conjunctivitis
  • Nasal discharge
  • Sore throat
  • Dry cough
  • Mild fever
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65
Q

What is the second stage of Whopping Cough?

A

After two weeks of the catarrhal phase →Paroxysmal coughing stage (barking cough)

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66
Q

Describe the Paroxysmal coughing stage in Whooping Cough

A

Dry hacking cough that is worse at night and after feeds
Coughing episodes followed by characteristic ‘whoop’
→ loss of consciousness

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67
Q

What is the characteristic ‘whoop’ in whooping cough?

A

Inspiration against a closed glottis
Child chokes, gasps and face reddens

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68
Q

What can happen post-cough in Whooping Cough?

A

Vomiting
Apnoea
Cyanosis
Coughing fits → Subconjunctival haemorrhage/anoxia → seizures/syncope

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69
Q

What investigations are ordered for Whooping Cough?

A
  • Notifiable disease
  • Nasopharyngeal swabs: PCR
  • Bacterial culture: MCS
  • Oral anti-pertussis IgG
  • Marked lymphacytosis= COMMON
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70
Q

What is the management for Whooping Cough?

A

Hospitalised: if <6 months (risk of apnoea)
10-14 days incubation
Off school for 48 hours after Abx commencement:
- Macrolides: Azithromycin or Erythromycin
- Erythromycin: pregnant women

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71
Q

What is Bronchiolitis?

A

LRTI following a URTI
Inflammation and infection in the bronchioles

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72
Q

Who is affected by Bronchiolitis?

A

Commonest lung infection in infants (peaks at 3-6 months)
Rare in those aged >1 years

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73
Q

What makes bronchiolitis more severe?

A

Congenital heart defects
Cystic Fibrosis
Down’s syndrome

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74
Q

What are 5 causes of bronchiolitis?

A

Respiratory syncytial virus (RSV): 80%of cases
Metapneumovirus
Parainfluenza
Rhinovirus
Adenovirus

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75
Q

What are the causes of severe bronchiolitis?

A

RSV + Metapneumovirus dual infection

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76
Q

What are the risk factors for bronchiolitis?

A
  • Premature/low birth weight
  • Cystic Fibrosis
  • Congenital heart disease
  • Down’s syndrome
  • Immunocompromised
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77
Q

What is the clinical presentation of bronchiolitis?

A

Coryza precedes dry cough
Tachycardia
Signs of respiratory distress
Dyspnoea
Tachypnoea
Poor feeding
Mild fever (under 39ºC)
Apnoeas episodes
Wheeze and crackles
Cyanosis
Sub/ intercostal recession
Hyperinflation of chest:
-Prominent sternum
-Liver displaced downwards

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78
Q

When should a child be admitted for bronchiolitis?

A
  • Infrequent feeding
  • Respiratory distress
  • Hypoxia
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79
Q

What investigations are ordered for bronchiolitis?

A

Pulse oximetry
Viral throat swab
ABG
FBC
CXR: excludes pneumothorax

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80
Q

What is the management of Bronchiolitis?

A

Oxygen therapy
Supportive (NG nutrition, fluids, temp control)
Ventilation (CPAP)
Palivizumab prophylaxis
Ribavarin: if high risk

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81
Q

What is Ribavirin?

A

Antiviral against RSV
Used against Hep C (+ interferons/ simeprevir, sofosbuvir) and haemorrhagic fevers

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82
Q

What should be given if SpO2 <92%?

A

High flow humidified oxygen via nasal cannulae

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83
Q

What is pneumonia?

A

Inflammation of the lungs

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84
Q

How is a HA pneumonia defined?

A

Pneumonia that develops within 48 hours of admission

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85
Q

What criteria is used to assess pneumonia severity?

A

CURB-65:**

Confusion

Urea >7

Respiratory rate ≥ 30

Blood pressure < 90 systolic or ≤ 60 diastolic.

Age ≥65

Score 0/1: consider treatment at home

Score ≥ 2: consider hospital admission and dual antibiotics

Score ≥ 3: consider intensive care assessment

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86
Q

What causes pneumonia in newborns?

A

Group B strep: maternal
Gram negative enterococci

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87
Q

What causes pneumonia in infants and young children?

A

S. pneumoniae
Haemophilus influenza B
S. Aureus (infrequent but serious)

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88
Q

What are viral causes of pneumonia?

A

RSV
Influenza A/B
Parainfluenza
Adenovirus

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89
Q

What are atypical causes of stroke?

A

Mycoplasma pneumoniae
Chlamydia pneumoniae

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90
Q

What is the clinical presentation for pneumonia?

A

Productive cough +/- haemoptysis
- Non-productive cough = atypical infection
High fever (> 38.5ºC)
Tachypnoea
Tachycardia
Hypoxia
Hypotension
Increased work of breathing
Lethargy
Delirium (acute confusion associated with infection)
Pleuritic chest pain
Poor feeding
Respiratory distress

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91
Q

What are the chest signs of pneumonia?

A

Bronchial breathing (loud breathing due to turbulent blood flow)
Focal coarse crepitations (crackles from purulence)
Dullness to percussion

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92
Q

How is pneumonia diagnosed?

A

Pulse oximetry
Sputum and blood MCS
FBC: CRP
CXR: consolidations

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93
Q

What is the management of pneumonia?

A

If resp distress/O2 <92%: admit to hospital
Oxygen
IV fluids
If acutely unwell: IV benzylpenicillin
ORAL Abx for newborns: amoxicillin

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94
Q

What is the clinical presentation of respiratory distress?

A
  • Raised respiratory rate
  • Use ofaccessory musclesto breath
  • Intercostalandsubcostal recessions
  • Nasal flaring
  • Head bobbing
  • Tracheal tugging
  • Cyanosis(due to low oxygen saturation)
  • Abnormal airway noises
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95
Q

What criteria is used to differentiate transudates from exudates in a pleural effusion?

A

Lights

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96
Q

What are crackles?

A

Inspiration + nonmusical + heard when air is forced through passages blocked by exudates

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97
Q

What is Wheeze?

A

Expiration + musical + narrowing of smaller airways (e.g bronchioles)

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98
Q

What is ronchi?

A

Expiration + coarse sounds + narrowing of tracheobronchial passages

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99
Q

What is asthma?

A

Chronic lung condition where airways inflame in response to hypersensitivity (IgE)

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100
Q

What are the two types of wheeze in asthma?

A

Transient early wheeze
Persistent and recurrent wheeze

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101
Q

What is transient early wheeze in asthma?

A

Viral associated wheeze: e.g. RSV
Small airways obstructed due to inflammation
More common in males
Resolves by 5 years old

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102
Q

What is persistent and recurrent wheeze in asthma?

A

Presence of IgE to common inhalant allergens (Atopic Asthma)
FHx
Associated with eczema, hayfever and food allergies

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103
Q

What is the pathophysiology of asthma symptoms?

A

Bronchial inflammation leads to:
1) Oedema
2) Excessive mucous production
3) Infiltration of cells

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104
Q

What does bronchial inflammation lead to in asthma?

A

Airway narrowing and reversible airflow obstruction

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105
Q

What cells infiltrate the bronchials in asthma?

A

Eosinophils
Neutrophils
Mast cells
Lymphocytes

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106
Q

What are the risk factors for asthma?

A

Low BW
FHx
Bottle fed
Atopy
Male
Pollution
ADAM33 Gene
Samter’s triad:
- Asthma
- Nasal polyps
- Aspirin insensitivity

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107
Q

What can trigger asthma?

A

Pollen
Dust
Feathers
Exercise
Pollution
Cold air
Illness (viruses)

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108
Q

What is the clinical presentation of asthma?

A

Dyspnea: dinural (worse at night and in the morning)
Dry cough
Expiratory polyphonic wheeze
Chest tightness
Hx of atopic conditions and triggers
Symptoms improve with bronchodilators
SILENT CHEST RED FLAG = exacerbation

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109
Q

What are the investigations for asthma?

A

Spirometry:
-FEV1/FEC: <70% of predicted
-FEV1: reduced
-Bronchodilator reversibility (BDR): increases FEV1 by ≥12%+ ≥200ml volume
CXR
FBC: raised eosinophil count = inflammation from allergic reaction
Direct bronchial challenge test: histamine
Allergy testing
PEFR diary: diurnal variation
- >20% predicted 3/7 days
Fractional exhaled nitric oxide (FeNO):>40 ppb (measures lung inflammation)

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110
Q

How would you assess the severity of asthma on a spirometer?

A

FEV1/FVC:
>70%: Mild
60-69%: Moderate
50-59%: Moderately Severe
35-49%: Severe
<34%: Very Severe

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111
Q

What is the treatment of asthma in those aged 5-16?

A
  1. SABA PRN (short acting beta 2 agonist) (blue reliever): e.g. salbutamol
    • low dose ICS daily if uncontrolled (brown preventer): e.g. beclomethasone
    • LTRA(leukotriene receptor antagonist): e.g. montelukast
    • LABA if uncontrolled (green-purple long acting beta 2 agonist): salmetrol
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112
Q

What is the treatment of asthma in those <5?

A

1) SABA
2) 8 week moderate dose ICS trial
3) Add LTRA

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113
Q

What is the treatment of severe asthma attack?

A

O SHIT ME:
Oxygen
Salbutamol (nebulised)
Hydrocortisone IV/ oral prednisolone
Ipratropium bromide (nebulised)
Theophylline IV
Magnesium sulphate IV
Escalate

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114
Q

What is Kartagener syndrome?

A

Rare, autosomal recessive genetic ciliary disorder
Triad of situs inversus, chronic sinusitis and bronchiectasis
This leads to recurrent chest infections

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115
Q

What is cystic fibrosis?

A

Autosomal recessive multi-system disease of water and salt transport affecting the mucosal glands

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116
Q

What gene is defective in cystic fibrosis?

A

Autosomal recessive mutations with cystic fibrosis transmembrane conductance regulator gene on chromosome 7 (CFTR)

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117
Q

What is the pathophysiology of cystic fiborosis?

A

CFTR gene is a critical chloride channel:
1) Decreased excretion of chloride into the airway lumen and an increased reabsorption of sodium into the epithelial cells
2) Less excretion of salt → less excretion of water and increased viscosity/tenacity of airway secretion

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118
Q

What is the clinical presentation of cystic fiborosis?

A

Meconium ileus
Recurrent respiratory tract infections
Pancreatitis
Steatorrhoea
Salty skin
Poor weight and height: malnutrition due to malabsorption leads to **failure to thrive **and slow growth
Chronic thick productive cough
Clubbing
Dysponea
Crackles and wheeze
Abdominal pain and bloating
Nasal polyps
Male almost always infertile
Secondary amenorrhoea in females
Arthropathy
DM

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119
Q

How would you diagnose cystic fiborosis?

A
  • Newborn blood spot testing: immunoreactive trypsinogen test (mucus prevents trypsinogen from reaching the intestines and causes build up in blood)
  • SWEAT TEST: sodium >60mmol/L
  • Genetic testing
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120
Q

What microbes colonise the lungs in CF?

A

Younger: S. aureus, S. pneumoniae
EVENTUALLY >90% will have pseudomonas aeruginosa

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121
Q

How is cystic fibrosis managed?

A

Salbutamol + ICS
Lung transplant if FEV1 <30% expected
Pseudomonas Aeruginosa abx: nebulised tobramycin
Inhalation of recombinant human deoxyribonuclease (rhDNAse)
Mucolytics (dornase alfa or Acetylcysteine)
Hypertonic saline by inhalation (hydrators)
Amiloride (inhibits sodium transport)
Airway clearance techniques: chest physiotherapy, exercise and postural drainage.
PERT (pancreatic enzyme replacement therapy)

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122
Q

What are the 3 categories of Congenital Heart Disease?

A

1) Holes/connections
2) Narrowing/stenosis
3) Complex (right→left shunt)

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123
Q

What is the most common congenital heart defect of:
Valves?
Septums?

A

Bicuspid aortic valve
VSD

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124
Q

Give some examples of ‘holes/ connections of CHD?

A

ASD
PDA
VSD
AVSD

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125
Q

Which congenital heart lesion involves the mixing of oxygenated and deoxygenated blood?

A

AVSD

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126
Q

What are the most common left → right shunt CHDs?
How do they present?

A

VSD
PAD
ASD
AVSD
BREATHLESS (acyanotic)

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127
Q

Describe the management for CHD that cause a L->R shunt

A

Stabilise the patient
Increase calorie intake
NG tube
Diuretics and ACEi to prevent HF symptoms
Surgical repair

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128
Q

Give some examples of ‘narrowing/ stenosis’ in CHD?

A

Coarctation of the aorta (collapse with shock)
AS
PS

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129
Q

What are the most common right → left shunting CHD?
How to they present?

A

Tetralogy of Fallot
Transposition of the great arteries
BLUE (cyanotic)

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130
Q

What does right → left shunts cause?

A

Cyanosis

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131
Q

What is the pathophysiology of Eisenmenger’s syndrome?

A

Pulmonary pressure exceeds systemic pressure
Reverses shunt→ cyanosis (left→ right becomes right→left shunt)

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132
Q

What are the features of an innoSent murmur (5 S’s)

A

Soft
Systolic
aSymptomatic
left Sternal edge
normal heart Sounds

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133
Q

What sre investigations for CHD?

A

FBC
CXR
PaO2
Echo +/- cardiac catheterisation

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134
Q

What are causes of atrial septal defects?

A

Foetal alcohol syndrome
Trisomy 21

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135
Q

Name the three types of atrial septal defects

A
  • Ostium Secondum 90%
    (high hole)
  • Ostium Primum (10% low hole)
  • AVSD
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136
Q

Listening to S2:

If it is split (double) during inspiration and single during expiration what does it mean?

A

Normal!

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137
Q

Listening to S2:
If it is split (double) all the time what does it mean?

A

ASD

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138
Q

Listening to S2:
If it is never split (double) what does it mean?

A

All other CHDs

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139
Q

What is the clinical presentation of atrial septal defects?

A

Asymptomatic
Fixed and widely split S2
Ejection systolic murmur in pulmonary area
Palpitations

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140
Q

What are the investigations for atrial septal defect?

A

CXR
ECG

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141
Q

What is the management of atrial septal defects?

A

Surgery

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142
Q

What is patent ductus arteriosis?

A

Tube between the aorta and pulmonary artery that fails to close 1 month after birth

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143
Q

What is the clinical presentation of patent ductus arteriosis?

A
  • Poor feeding (failure to thrive)
  • Tachypnoea
  • Active precordium
  • Thrill
  • Hepatomegaly
  • Oedema
  • Pneumonias
  • CCF + pulmonary hypertension
  • LOUD S2
  • Large, bounding collapsing pulse (Gallop rhythm)
  • Heaving apex beat
  • Left subclavicular thrill
  • Continuous machinery murmur pulmonary area
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144
Q

How is patent ductus arteriosis investigated?

A

ECG and CXR: normal
Echo: ensures no duct dependant circulation (e.g in pulmonary atresia)

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145
Q

What is the management of patent ductus arteriosis?

A

Ibuprofen/Indomethacin (prostaglandin inhibitor): closes duct
SURGERY after 1 year: bacterial endocarditis risk

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146
Q

What complication can ventricular septal defects cause?

A

High risk of bacterial endocarditis

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147
Q

What is the clinical presentation ventricular septal defects?

A

Poor feeding and FTT
Tachypnoea
Thrill
Hepatomegaly
Oedema
Harsh loud pansystolic mumur best heard in LLSE +/- thrill
Gallop rhythm
Active pre-cordium

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148
Q

What are the investigations for ventricular septal defects?

A

Echo: precise defect
ECG: hypertrophy
CXR:
- Cardiomegaly
- Pulmonary oedema
- Enlarged pulmonary arteries

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149
Q

What is the management for ventricular septal defects?

A

Muscular VSDs: 30% close spontaneously
Heart failure: Diuretics
Additional calorie input
Surgery: prevents pulmonary capillary bed damage due to pulmonary HTN and high blood flow

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150
Q

AVSD is a common defect in people with which chromosomal abnormality?

A

Trisomy 21

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151
Q

What are the clinical features of AVSD?

A

Poor feeding
Tachypnoea
Hepatomegaly
Oedema
Failure to thrive
No murmur
Thrill
Gallop rhythm
Present at antenatal US scan
Cyanosis at birth/ heart failure at 2-3 weeks
Often detected by echo check up in Down’s

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152
Q

What is the management of AVSD?

A

Treat heart failure
Surgical repair: at 3-6 months

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153
Q

What is Coarctation of the Aorta?

A

Arterial duct tissue encirculing the aorta at the point it inserts into the duct:
1) Constricts aorta when duct closes
2) Obstruction to LV outflow

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154
Q

What is the clinical presentation of Coarctation of the Aorta?

A

When ductus arteriosus closes; acute circulatory collapse:
Weak femoral pulses
Radio-femoral delay
Ejection systolic murmur
Difference in pre and post-ductal saturations
Heart failure
Metabolic acidosis

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155
Q

How is Coarctation of the Aorta investigated?

A

4 limb BP
CXR: cardiomegaly

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156
Q

How is Coarctation of the Aorta managed?

A

Surgical repair: by 5 years old

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157
Q

What is Aortic Stenosis?

A

Aortic valve leaflets partly fused together- restricted exit from LV

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158
Q

What is the clinical presentation of Aortic Stenosis?

A
  • Ejection systolic murmur: URSE!
  • Palpable carotid thrill in suprasternal region
  • LVH
  • Critical AS: severe heart failure
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159
Q

What is the investigation for Aortic Stenosis?

A

Radiograph: prominent LV
ECG

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160
Q

What is the management of Aortic Stenosis?

A
  • Regular echos
  • Balloon valvotomy/dilation
  • Valve replacement: surgery
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161
Q

What is pulmonary stenosis?

A

Pulmonary valve leaflets partly fused together which restricts exit from the RV

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162
Q

What is the presentation of pulmonary stenosis?

A

Systolic ejection murmur in ULSE that can radiate to the back
Right ventricular heave

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163
Q

How is pulmonary stenosis investigated?

A

ECG: upright T wave/ RV hypertrophy
CXR

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164
Q

How is pulmonary stenosis managed?

A

Transcathether balloon dilation

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165
Q

What is the pathophysiology of transposition of the great arteries?

A

1) Aorta connected to RV
2) Pulmonary artery connected to LV (deoxygenated blood to body)
3) Incompatible with life (often have naturally occurring ASD,VSD, PDA)

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166
Q

What is the clinical presentation of transposition of the great arteries?

A
  • Cyanosis
  • S2: loud and singular
  • Reduced sats
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167
Q

How is transposition of the great arteries investigated?

A

CXR: narrow upper mediastinum ‘egg on side’ appearance of cardiac shadow
Echo: abnormal arterial connections
Check for 22q deletion

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168
Q

What is the management of transposition of the great arteries?

A

Maintain patency of ductus arteriosus: prostaglandin infusion
Balloon atrial septostomy
Surgery: arterial switch procedure in first few days of life

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169
Q

What genetic disorders is Tetralogy of Fallot associated with?

A

Down’s syndrome
22q deletions

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170
Q

What are the 4 features of Tetralogy of Fallot?

A

1) VSD
2) Overriding aorta
3) Pulmonary stenosis
4) RVH

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171
Q

What is the clinical presentation of Tetralogy of Fallot?

A
  • Cyanotic
  • Breathlessness
  • Acidosis
  • Collapse
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172
Q

How is Tetralogy of Fallot investigated?

A

Echo
CXR: small, up tilted, boot shaped apex
Harsh systolic murmur: LLSE

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173
Q

How is Tetralogy of Fallot investigated?

A

Close VSD and relieve right ventricular outflow tract obstruction: shunt to increase pulmonary blood flow

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174
Q

What is Ebstein’s Anomaly?

A

Posterior leaflets of tricuspid valve displaced anteriorly

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175
Q

What causes Ebsteins Anomaly?

A

Lithium in pregnancy (e.g bipolar mum)

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176
Q

What heart problems can develop due to Ebstein’s Anomaly

A

Tricuspid regurgitation
Tricuspid Stenosis
RA enlargement

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177
Q

What murmur is heard in tricuspid regurgitation?

A

Pan-systolic

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178
Q

What murmur is heard in tricuspid stenosis?

A

Mid-diastolic

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179
Q

Name 3 CHDs associated with Turner syndrome

A

Coarctation of the aorta
Aortic stenosis
Aortic dissection

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180
Q

Name 3 CHDs associated with Down’s syndrome

A

AVSD
Tetralogy of Fallot
VSD

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181
Q

Name 3 CHDs associated with Down’s syndrome

A

AVSD
Tetralogy of Fallot
VSD

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182
Q

What is Kawasaki disease?

A

Idiopathic systemic vasculitis that most commonly effects children aged 6 months-5 years

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183
Q

What is the major complication of Kawasaki Disease?

A

Coronary artery aneurysm formation

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184
Q

What is the clinical presentation of Kawasaki Disease?

A

MyHEART:
Mucosal Involvement:-inflamed dry lips/ strawberry tongue
Hand and feet swelling
Eye: bilateral conjunctivitis
lymphAdenopathy (cervical)
Rash
Temperature: >5 days of high° fever

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185
Q

What are the three phases of Kawasaki Disease?

A

1) Acute febrile (1-2 weeks)
Fever + 4 of criteria (MyHEART)
2) Subacute: remission of fever (4-6 weeks)
development of coronary artery aneurysms
3) Convalescent (6-12 weeks)
Resolution of clinical signs + normalisation of inflammatory markers

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186
Q

How is Kawasaki disease investigated?

A

Echo is essential: coronary artery pathology
FBC:
- High ESR, CRP WCC
- High Platelets
LFT: high AST and hypoalbuminemia
High a1-antitrypsin
Bilirubin
High Urinalysis: raised WCC without infection

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187
Q

What is the management of Kawasaki Disease?

A

Aspirin (reduce the risk of aneurysms and thrombosis)
IV Immunoglobulins
Echo: 6 weeks later to check for aneurysms
Infliximab (anti-TNF): if permanent inflammation

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188
Q

What is Henoch-Schonlein purpura?

A

HSP is an IgA mediated, autoimmune hypersensitivity vasculitis of childhood

(Skin, joint, gut, kidneys)

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189
Q

What are the risk factors for Henoch-Schonlein purpura?

A

Infections (group A strep, mycoplasma and EBV)
Vaccinations
Exposure to allergens, cold and pesticides
Insect bite

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190
Q

What is the clinical presentation of Henoch-Schonlein purpura?

A
  • Fever
  • Rash
  • Abdominal pain/symptoms
  • Renal involvement
  • Arthritis
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191
Q

What are the investigations for Henoch-Schonlein purpura?

A

Urinanalysis: protein/haematuria
Raised ESR
Raised serum IgA
Raised WCC
Increased anti-streptolysin O titrates: detects Group A Strep

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192
Q

What is the classic triad in Henoch-Schonlein purpura?

A

1) Purpura (non-blanching)
2) Arthritis/arthralgia
3) Abdominal pain

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193
Q

What is the treatment for Henoch-Schonlein purpura?

A

NSAIDs: joint pain
Corticosteroids: arthralgia
Most recover in 2 months

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194
Q

What is infective endocarditis?

A

Infection of valves/endocardium → destruction due to infective organisms forming vegetation

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195
Q

What is the most common cause of infective endocarditis?

A

S. viridans

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196
Q

What are the risk factors for infective endocarditis?

A

IV drug users
Prosthetics
Structural heart defects

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197
Q

What is the clinical presentation of infective endocarditis?

A

Any kid with fever and significant cardiac murmur
Weight loss
Night sweats
Anaemia: unexplained
Petechiae
Clubbing
Splinter haemorrhages (due to small septic emboli)
Osler’s nodes (nodules from inflammation)
Janeway lesion (flat from small septic emboli)

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198
Q

How is infective endocarditis diagnosed?

A

Blood cultures: take 3+ samples within first 24h in hospital
Echo: confirms presence of vegetations
High ESR: (monitors treatment)

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199
Q

How is infective endocarditis managed?

A

Abx:
Empirical: Amoxicillin (rifampicin if prosthetic valve) + gentamycin + vancomycin
Once known
Streps: IV penicillin and gentamycin for 6 weeks
Valve replacement/debridement

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200
Q

What should you always suspect if purpura is non blanching?

A

Meningococcal disease: septicemia

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201
Q

What is Rheumatic Fever?

A

Systemic febrile illness + Pharyngitis (occurs 2-4 weeks after infection)
Autoimmune condition triggered group A B-haemolytic strep

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202
Q

What is the Jones diagnostic criteria in rheumatic fever?

A

1/2 major + 2 minor plus evidence of preceding strep infection (scarlet fever/ throat swab/ high serum ASO antibody titre, ECHO, ECG or CXR)
JONES FEAR: mnemonic of criteria

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203
Q

What are the major and minor signs of Rheumatic Fever?

A

JONES FEARP:
JONES: Major
- Joint arthritis: polyarthritis
- Organ inflamation: Carditis(+ve echo, changed murmur, CCF, cardiomegaly)
- Nodules subcutaneous
- Erythema marginatum
- Sydenham’s chorea- neurological manifestation

FEARP: Minor
- Fever
- ECG PR interval <0.2s
- Arthralgia pain
- Raised ESR/ CRP
- Previous rheumatic fever/ rheumatic heat disease

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204
Q

What is the management of Rheumatic Fever?

A

Aspirin + Prednisolone: carditis (be careful of Reye’s syndrome)
Benzylpenicillin → Penicillinn V 10 days: Pharyngitis
NSAIDS: joint pain
Prednisolone: synderham’s Chorea

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205
Q

What is chicken pox?

A

Highly infectious disease caused by varicella zoster virus (VZV)

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206
Q

What does reactivation of VZV lead to?

A

Reactivation of dormant virus after a bout of chicken pox leads to herpes zoster (shingles) in posterior root ganglia

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207
Q

What are the risk factors for chicken pox?

A
  • Immunocompromised
  • Older age
  • Steroid use
  • Malignancy
  • Dangerous in neonates and to the foetus if contracted in pregnancy
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208
Q

How long are you infectious for in chicken pox?

A

Infective from 4 days prior to rash until all lesions have scabbed (day 5)

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209
Q

What is the clinical presentation of chicken pox?

A
  • T 38-39°
  • Headache
  • Malaise
  • Coryzal symptoms
  • Crops of vesicles (itchy)
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210
Q

Where are the vesicles normally found in chicken pox?

A

Mostly on the head, neck and trunk
Very sparse on the limbs

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211
Q

What is the cycle of a vesicle in chicken pox?

A

1) Macule
2) Papule
3) Vesicle (red surround)
4) Ulcers
5) Crust

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212
Q

What does redness around the lesion suggest in chicken pox?

A

Bacterial superinfection

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213
Q

What is the ddx of chicken pox?

A
  • Shingles: only one dermatome distribution
  • Generalised herpes zoster/ simplex
  • Dermatitis herpetiformis
  • Impetigo
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214
Q

What investigations are ordered for chicken pox?

A
  • Clinical
  • Fluorescent antibody tests: IgM and IgG
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215
Q

What is the management of chicken pox?

A

Calamine lotion
Antivaricella: zoister immunoglobulin
Acyclovir: if high risk
Flucloxacillin: in bacterial superinfection
5 days off school for kids

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216
Q

What is measles?

A

Acute viral infection caused by single stranded RNA morbillivirus from the paramyxovirus family

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217
Q

How is measles transmitted?

A

Respiratory droplets

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218
Q

What is the incubation time for measles?

A

7-12 days

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219
Q

How long are you infectious for in measles?

A

From prodrome until 4 days after the rash of measles appear

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220
Q

What is the cause of measles?

A

RNA Morbillivirus from the paramyxovirus

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221
Q

What is the clinical presentation of measles?

A

1) Incubaction period: usually asymptomatic

2) Prodrome: pyrexia, malaise, anorexia, conjunctivitis, cough, coryza and koplik spots (blue-white spots on inside of mouth opposite to molars)

3) Exanthem: Erythematous maculopapular non-itchy rash which becomes blotchy and confluent (lasts 3 days and leaves behinds a brown discolouration) + High fever

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222
Q

What investigations for measles?

A

IgM & IgG positive
Salivary swab/serum sample: for measles specific immunoglobulin (within 6 weeks of onset)
Salivary swab: RNA detection

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223
Q

What is the management of measles?

A

Paracetamol/ Ibuprofen + fluids

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224
Q

What are the complications of measles?

A

More common if <5 years or >20 years:
- Otitis media
- Croup/ tracheitis
- Pneumonia
- Encephalitis

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225
Q

What is the complication of vitamin A deficiency in measles?

A

Blindness

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226
Q

What is the most common cause of death in measles?

A

Pneumonia

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227
Q

What is subacute sclerosing panencephalitis?

A

7-13 years post measles: chronic complication

Progressive changes in behaviour, myoclonus, dystonia, dementia → death

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228
Q

What is the risk of measles during pregnancy?

A

Miscarriage, prematurity and low birthweight

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229
Q

What is scarlet fever?

A

Disease of streptococcus pyogenes (group A strep) exotoxins usually following tonsillitis

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230
Q

Who does scarlet fever affect?

A

<10 yr olds
Unusual in <2 yr olds

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231
Q

How does scarlet fever present?

A
  • Acute tonsillitis and fever → rash 24-48 hours after
  • Strawberry tongue
  • Flushed face
  • Cervical lymphadenopathy
  • Scarletiniform rash: Red, ‘pin-prick’ blanching sandpaper rash on chest outwards
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232
Q

How is scarlet fever investigated?

A

Clinical
Throat swab
Antigen detection kits:
- Strep antibody tests

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233
Q

What is the management of Scarlet fever?

A

Penicillin/ Azithromycin: 10 days
Rest
Fluids
Paracetamol/ibuprofen

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234
Q

What are the complications of scarlet fever?

A
  • Syndenhams Chorea
  • Otitis media
  • Rheumatic fever
  • Glomerulonephritis
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235
Q

What causes rubella?

A

RNA virus: Rubivirus Togaviridae

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236
Q

How is rubella transmitted?

A

Inhaled droplets

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237
Q

What is the incubation period of rubella?

A

14-21 days

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238
Q

How long are you infectious for in rubella?

A

5 days before and 5 days after start of rash

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239
Q

What is the clinical presentation of rubella?

A
  • Lethargy
  • Low grade fever
  • Headache
  • Mild conjunctivitis
  • Anorexia
  • Pink-red maculopapular rash
  • Suboccipital lymphadenopathy
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240
Q

How is rubella investigated?

A

PCR testing
Saliva: rubella IgM in saliva
FBC: low WBC, high lymphocytes and thrombocytopenia

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241
Q

How is rubella managed?

A

MMR vaccine
Paracetamol: for fever

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242
Q

What is congenital rubella caused by?

A

When a mother is infected with rubella during pregnancy

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243
Q

How does congenital rubella present?

A

Weeks 1-4 = blindness (congenital cataracts + glaucoma)

Weeks 4-8 = congenital heart disease (PDA)

Weeks 8-12 = deafness

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244
Q

What is slapped cheek syndrome (erythema infectiosum)?

A

Parvovirus B19 transmitted through droplets

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245
Q

What are the prodrome symptoms of slapped cheek syndrome (erythema infectiosum)?

A

≈1 week:
- Mild
- Headache, rhinitis, sore throat, fever, malaise
THEN l ≈1 week asymptomatic

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246
Q

What happens after a week of no symptoms (prodrome) in slapped cheek syndrome (erythema infectiosum)?

A

Classic ‘slapped cheek’ rash: erythematous macular morbilliform rash develops on the limbs 1-4 days after the facial rash
Arthralgia

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247
Q

How is slapped cheek syndrome (erythema infectiosum) investigated?

A

B19 specific IgM: current or recent infection
B19 specific IgG: immunity
PCR

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248
Q

What is the management of slapped cheek disease?

A

Conservative

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249
Q

What is impetigo?

A

Acute superficial bacterial skin infection

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250
Q

What is the main cause of impetigo?

A

S. aureus

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251
Q

What does Impetigo look like?

A

Well defined lesions
Honey/golden coloured crusts on erythematous base
Systemic symptoms: Lymphadenopathy, mild fever and malaise

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252
Q

How is impetigo managed?

A

Topical fusidic acid
Oral flucloxacillin: if severe

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253
Q

What is meningitis?

A

Inflammation of the leptomininges

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254
Q

What are the causes of meningitis?

A

Neonates: GBS, E.coli, lysteria monocytogenes.
1m-6 years: Neisseria meningitidis, S.pneumoniae, H.influenzae.
> 6 years: Neisseria meningitidis.

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255
Q

What are the risk factors for meningitis?

A
  • Immunocompromised
  • Crowding
  • Endocarditis
  • DM
  • Alcoholism and cirrhosis
  • IV drug abuse
  • Renal/adrenal insufficiency
  • Malignancy
  • Sickle cell disease
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256
Q

What is the pathophysiology of meningitis?

A

BACTERIAL:
1) The pia-arachnoid is congested with polymorphs causing a layer of pus to form

VIRAL:
1) Lymphocytic inflammatory CSF without pus formation
2) No polymorphs/ adhesions
3) Little or no cerebral oedema unless encephalitis develops

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257
Q

Who does meningitis affect?

A

Common in infants, children or elderly

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258
Q

Which is more common, viral or bacterial meningitis?

A

Viral > Bacterial

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259
Q

What is the clinical presentation of meningitis?

A

Septic signs occur before meningeal signs:
-Malaise, fever, headache, temperature, rigor, vomiting
- Tachycardia
- Tachyponea
- Hypotension
- Poor feeding
- Abnormal cry
Meningeal signs are late and less common in young children:
Classic= headache + fever + neck stiffness + photophobia + Malaise, fever, headache, temperature, rigor, vomiting
+ve Kernigs (resistance to extending knee when hip is flexed)
+ve Brudzinki’s (neck flexion = hip flexion)

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260
Q

What are the investigations for meningitis?

A

DO NOT DELAY TREATMENT OVER INVESTGATIONS
Blood Cultures
EDTA blood for PCR
Throat swabs
- Lactate
- FBC
- Glucose
- U&Es

LP immediately:

Appearance:

Bacteria: cloudy

Virus: normal

Protein:

Bacteria: high

Virus: mildly raised or normal

Glucose:

Bacteria: low

Virus: normal

WCC:

Bacteria: high and PMN

Virus: high and lymphocytes

Culture and sensitivity:

Bacteria: positive

Virus: positive

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261
Q

If meningitis is suspected what must be given immediately to:

<3m?

> 3m-18years?

In GP before hospital?

A

High flow O2
Abx:
<3m= Cefotaxime + Amoxicillin + Aciclovir
>3m= Ceftriaxone + Dexamethasone (reduces inflammation)
In GP = Benzylpenicillin (Cefotaxime if allergic)

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262
Q

What is Coxsackie’s disease (Hand, Foot and Mouth)?

A

Viral illness commonly causing lesions involving the hands, foot and mouth

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263
Q

How is Coxsackie’s disease (Hand, Foot and Mouth) transmitted?

A

Feacal-oral route

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264
Q

What causes Coxsackie’s disease (Hand, Foot and Mouth)?

A

Coxsackievirus A16
Enterovirus 71

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265
Q

Who is most affected by Coxsackie’s disease (Hand, Foot and Mouth)?

A

<10 yrs old
Outbreaks common in nurseries, schools and childcare centres

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266
Q

What is the clinical presentation of Coxsackie’s disease (Hand, Foot and Mouth)?

A
  • Fever
  • Malaise
  • Loss of appetite
  • Sore mouth/throat
  • Cough
  • Abdo pain
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267
Q

Describe the mouth lesions in Coxsackie’s disease (Hand, Foot and Mouth)?

A

On buccal mucosa, tongue or hard palate
Begin as macular lesions that progress to vesicles which then erode
Yellow ulcers surrounded by red haloes

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268
Q

Describe the skin lesions found in Coxsackie’s disease (Hand, Foot and Mouth)

A

Palms, soles and between fingers/ toes
Erythematous macules but rapidly progress to grey vesicles with an erythematous base

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269
Q

How is Coxsackie’s disease (Hand, Foot and Mouth) diagnosed?

A

Clinical diagnosis
Swab lesions
PCR

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270
Q

How is Coxsackie’s disease (Hand, Foot and Mouth) managed?

A

Fluid intake
Soft diet
Paracetamol/Ibuprofen
If mouth is very painful, use topical agents e,g, lidocaine oral gel
Stay off school until better

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271
Q

What is encephalitis?

A

Inflammation of brain parenchyma
Usually caused by infection (normally viral)

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272
Q

What is the clinical presentation of encephalitis?

A
  • Flu like prodrome: often self-limiting
  • Reduced GCS
  • Odd behaviour
  • Vomiting
  • Focal neurological symptoms
  • Fits/ focal seizures
  • Fever
  • Meningism symptoms
  • Headache
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273
Q

What are the investigations for encephalitis?

A
  • CSF, MC&S and PCR
  • Bloods
  • Stool (enteroviruses)
  • Urine
  • LP
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274
Q

What is the management of encephalitis?

A

Anciclovir: if HSV suspected/confirmed
Dexamethasone: treats high ICP

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275
Q

What is tuberculosis?

A

A granulomatous disease caused by Mycobacterium tuberculosis

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276
Q

How does TB spread from person to person?

A

Inhaled droplets

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277
Q

When should you suspect tuberculosis?

A

Overseas contact
HIV +ve
Odd CXR

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278
Q

What is the 15 clinical presentation of tuberculosis?

A

Anorexia
Low fever
Failure to thrive
Malaise
Cough +/- haemoptysis
Erythema nodosum
Lymph nodes: a cold abscess (firm, painless and no red inflammation)
Constitutional symptoms
Spinal TB: pain
Dyspnea: gradually as lungs become damaged
Clubbing
Lupus vulgaris: apple jelly nodules
Auscultation: possible crackles
Haematuria, increased frequency and nocturia
Pyuria in the absence of a positive culture = sterile pyuria

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279
Q

How is TB diagnosed?

A

3x sputum culture + Ziehl-Neelsen stain smear on Lowenstein Jensen medium: will turn red if acid-fast bacilli
Chest X-ray: millet seeds, consolidation, hilar lymphadenopathy and pleural effusions
Tuberculin tests
Mantoux Test: if latent
- < 6mm or >15mm =give BCG
Interferon-Gamma Release Assays (IGRAs): if latent

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280
Q

What is the management of TB?

A

Rifampicin (6 months)
Isoniazid (6 months)
Pyrazinamide (2 months)
Ethambutol (2 months)

BCG vaccine: if high risk

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281
Q

What is the BCG vaccine?

A

Limited protection against TB and leprosy in high risk groups

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282
Q

When is the BCG vaccine contradicted?

A
  • Previous BCG vaccination
  • Hx TB
  • HIV
  • Pregnancy
    • tuberculin test
  • NO EVIDENCE FOR EFFICACY >35
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283
Q

What are the complications of TB?

A

1) Pleural effusion
2) Pericardial effusion
3) Lung collapse
4) Lung consolidation

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284
Q

What are the side-effects of Rifampicin?

A

Hepatitis
“red-an-orange-pissin and tears”
Flu like symptoms
Impaired COCP function

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285
Q

What are the side-effects of Isoniazid?

A

Hepatitis
I’m-so-numb-azid: paraesthesia
Agranulocytosis

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286
Q

What are the side-effects of Pyrazinamide?

A

Hyperuricaemia – GOUT
Arthralgia
Myalgia
Hepatitis

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287
Q

Side-effects of Ethambutol?

A

“Eye-thambutol”: colour blindness (Optic Neuritis)

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288
Q

What is the treatment of latent TB?

A

Normal treatment + Isoniazid for 6 months

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289
Q

What is HIV?

A

A retrovirus (RNA virus) that infects cells of the immune system

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290
Q

What are the HIV strains?

A

Two strains:
HIV-1 (more common)
HIV-2

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291
Q

How is HIV transmitted?

A

Infected bodly fluids:
1. Sexual:most cases. MSM have a higher risk
2. Parenteral:via needlestick or needle sharing
3. Vertical:via breastfeeding or vaginal delivery

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292
Q

What is the presentation of HIV and AIDS?

A

Acute infection:

Asymptomaticorflu-like illness

Clinical latency:

May be asymptomaticorpresent with non-AIDS defining illnesses:

Fever and night sweats

Persistent lymphadenopathy
Parotid enlargement
Hepatosplenomegaly
Persistent diarrhoea
Reduced platelets
Weight lost

Opportunistic infections: e.g. thrush

AIDS:

AIDS-defining illness

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293
Q

When should HIV be diagnosed in childhood?

A

AIM: Before 1st birthday
Tests at 3&6 months:
- HIV viral PCR
- ELISA: HIV antibody, p24 antigen test and IgA
Monitor CD4 T-cell count and viral load

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294
Q

What is the management for HIV?

A

Treatment aim: normal CD4 count
andundetectable viral load

Highly Active Anti-Retrovirus therapy (HAART)

Prophylactic co-trimoxazole

Pre+post exposure prophylaxis: zidovudine

Vaccinations

Condoms and regular HIV tests

Pre-test and post-test counselling

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295
Q

When should HAART begin in HIV?

A

Those with AIDs defining conditions/CD4 <15%

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296
Q

What is the pathophysiology of toxic shock syndrome?

A

S. aureus + Group A strep

Toxin acts is a super antigen that can cause organ dysfunction

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297
Q

What is the clinical presentation of toxic shock syndrome?

A
  • Fever >39°
  • Hypotension
  • Diffuse erythematous, macular rash
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298
Q

What is the management of toxic shock syndrome?

A

Intensive care
Infected areas: surgically debrided
Abx: Ceftriaxone + Clindamycin

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299
Q

What are strawberry marks?

A

Cavernous haemangioma
Self limiting
Concerning if over eye and in airway

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300
Q

What is a Port Wine Stain?

A

Permanent capillary haemangioma

Present in Sturge-Weber Syndrome

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301
Q

What is Sturge-Weber Syndrome?

A

Too many capillaries in the meninges
Area of face innervated by trigeminal nerve affected by Port Wine Stain

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302
Q

What syndrome are moles common in? (Naevi)

A

Turner’s

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303
Q

What are mongolian blue spots?

A

Non- caucasian ancestry

Congential dermal melanocytosis

Lower back/ buttocks

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304
Q

What are cafe au lait spots?

A

Flat light brown patches on the skin

> 5 = Neurofibromatosis

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305
Q

What are Milia (milk spots)?

A

Sebaceous plugs from sweat glands

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306
Q

What is Urticaria (hives)?

A

‘Nettle-like’ rashes, raised and itchy patches

Allergen exposure

linked to child abuse if late presentation, symmetry and odd history

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307
Q

What are infantile urticaria?

A

Erythema toxicum neonatorum: benign red blotches that resolve spontaneously following birth

Histamine reaction

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308
Q

Key points to remember in chickenpox?

A

Dangerous in immunocompromised

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309
Q

Key points to remember in Measles?
(Prodromal CCCK)

A
  • Cough
  • Coryza
  • Conjunctivitis
  • Koplik spots (inside mouth)
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310
Q

Key points to remember in Parvovirus?

A

Slapped cheek

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311
Q

Key points to remember in Coxsackie?

A

Hand, foot and mouth

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312
Q

Key points to remember in Mumps?

A

Prodromal malaise
Parotids
Orchitis
Infertility

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313
Q

What is Molluscum contagiosum?

A

Pox like nodules that last for months
Harmless

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314
Q

What do you call a rash that accompanies a disease/ fever?

A

Exanthema

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315
Q

What rash is diabetes associated with?

A

Acanthosis nigricans

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316
Q

What is the cause of Congenital Toxoplasmosis?

A

Cat faeces infected with toxoplasma gondii

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317
Q

How does toxoplasmosis present?

A
  • Intracranial calcification
  • Microcephaly/hydrocephalus
  • Chorioretinitis
  • Cerebral palsy
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318
Q

How is Toxoplasmosis diagnosed?

A

Serology: >95% asymptomatic

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319
Q

How is toxoplasmosis treated?

A

Pyrimethamine + Sulphadiazine + Spiramycin

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320
Q

What is Toxocara?

A

Infection associated with eating dog faeces
Leads to blindness

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321
Q

What infections are associated with Cat + Dog faeces?

A

Cat: Toxoplasmosis (fits, deafness)

Dog: Toxocara (acquired blindness)

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322
Q

What is a TORCH infection and what does it stand for?

A

Infection to the developing foetus/ newborn by any of:
Toxoplasmosis
Other agents ( Syphillis, Varicella- zoster and Parvovirus B19
Rubella (german measles)
Cytomegalovirus
Herpes simplex

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323
Q

What is the most common congenital infection in the U.K?

A

Cytomegalovirus (CMV)

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324
Q

What is the clinical presentation of CMV?

A
  • Growth retardation
  • Microcephaly
  • Hepatosplenomegaly
  • Hepatitis
  • Anaemia/jaundice/ thrombocytopenia
  • IUGR
  • Chorioretinitis
  • Motor and cognitive impairment
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325
Q

What is the management of Syphillis?

A

Benzylpenicillin

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326
Q

What is the clinical presentation of Herpes Simplex?

A

Blindness
Low IQ
Epilepsy
Jaundice
Respiratory distress
30% die even when treated

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327
Q

What is the management of herpes simplex virus?

A

Acyclovir

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328
Q

What is Eczema?

A

Chronic atopy leading to epidermis inflammation:
includes atopic dermatitis and contact dermatitis

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329
Q

How common is Eczema?

A

15-20% of children
Increasing incidence

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330
Q

What is the management for eczema?

A

Emollients

Topical corticosteroids

Antihistamines

Phototherapy

Systemic immunosuppression

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331
Q

What is Eczema Herpeticum?

A

Severe infection of skin (HSV 1+2)
Potentially life threatening

More common in kids with eczema

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332
Q

How is Eczema Herpeticum treated?

A

Acyclovir

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333
Q

What is Stevens-Johnson syndrome (SJS)?

A

Epidermal necrosis due to hypersensitivity

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334
Q

Causative drugs of Stevens- Johnson Syndrome?

A
  • Sulfonamides
  • Anti-epileptics
  • Penicillin
  • NSAIDs
335
Q

What is the presentation of Stevens-Johnson Syndrome?

A

Painful erythematous macules
Severe mucosal ulceration

336
Q

What is the treatment for Stevens-Johnson Syndrome?

A

Steroids
Immunoglobulins
Immunosuppressant

337
Q

What is anaphyplaxis?

A

Type 1 hypersensitive reaction: IgE simulates mast cell degranulation
Life threatening

338
Q

What may bring on the IgE mediated reaction in anaphylaxis?

A

Foods
Insect sting
Drugs
Latex
Exercise
Inhaled allergens

339
Q

What are the fatal causes of anaphylaxis in adults?

A

Mainly nuts

340
Q

What are the main features of anaphylaxis?

A

Occurs within minutes of drug exposure and lasts 1-2 hours

Flushing: vasodilation

Angio-oedema: increased vascular permeability- fluid centrally shifted peripherally

Central cyanosis

Wheeze, dyspnea: bronchoconstriction

Urticaria

Anaphylactic shock

Cardiac arrest

341
Q

How is anaphylaxis diagnosed?

A

ABCDE
ECG
Mast cell tryptase
ABG

342
Q

What is the management of anaphylaxis?

A

ABCDE
IM Adrenaline: second dose after five minutes if no response
- <6 months: 0.01mg
- 6m-6 years: 0.15mg
- 6-12 years: 0.3mg
- >12 years: 0.5mg
If anaphylactic shock: IV adrenaline
IV Antihistamine (chlorphenamine 10mg)
IV HydrocortisoneSalbutamol if wheeze
IV fluids
High flow O2
Monitor pulse oximetry, ECG, BP

343
Q

Define failure to thrive

A

Poor growth rate or weight falling 2 centile lineS

344
Q

What is the key determinant in questioning the health of a child?

A

Growth

345
Q

What is the most common causes of failure to thrive?

A

Inadequate calorie intake:
- Poor breastfeed technique
- Poverty
- Unsuitable food offered
- Neglect

346
Q

What are the 4 Domains of childhood development?

A

1) Gross motor
2) Fine motor and vision
3) Speech, language and hearing
4) Social

347
Q

What is developmental surveillance in childhood?

A

Following child over time: incorporated into well-child checks, general physical examination and routine immunisation visits

348
Q

Define developmental delay

A

Along normal route, but takes longer to reach milestones

349
Q

Define developmental disorders

A

Does not follow normal pattern
Impairment

350
Q

What are the biological and environmental risk factors for developmental disorders?

A

Biological:
- Prematurity
- Low birth weight
- Birth asphyxia
- Hearing/vision impairment
Environmental:
- Poverty
- Poor parental education
- Maternal alcohol/drugs

351
Q

Name the 11 primitive reflexes

A

A M L PPPP R S T:
Atonic neck reflex

Moro reflex

Landau reflex

Plantar grasp reflex

Palmar grasp reflex

Parachute reflex

Positive support reflex

Rooting reflex

Stepping reflex

Trunk incurvation

352
Q

What are the ‘Palmar’ and ‘plantar’ grasp reflexes?

A

Touch hand/soles and baby will grasp/curl toes

353
Q

When should the Palmar’ and ‘plantar’ grasp reflexes be seen?

A

Palmar = until 6 months

Plantar = until 9-12 months

354
Q

What is the ‘stepping’ reflex?

A

1) Hold baby upright with one sole on table top
2) Hip and knee will flex and other foot step forward

355
Q

When should the ‘stepping reflex be seen?

A

6 weeks

356
Q

What is the ‘moro’ reflex?

A

1) Hold baby supine and abruptly lower the body about 2 feet
2) Arms will abduct/extend and legs flex

357
Q

When should the ‘moro’ reflex be seen?

A

Until 2 months

358
Q

What is the ‘tonic-neck’ reflex?

A

1) baby supine, turn head to one side and hold jaw on shoulder
2) Arms/legs the heads turned to will extend and opposite will flex

359
Q

When should the ‘tonic-neck’ be seen?

A

Until 6 months

360
Q

What is the ‘sucking and rooting’ reflex?

A

1) Stroke perioral skin at corner of the mouth
2) Mouth will open and baby will turn head toward stimulus and suck

361
Q

When should the ‘sucking and rooting’ reflex be seen?

A

Until 4 months

362
Q

What is the ‘trunk incurvation’/Galant’s reflex?

A

1) Support baby prone and stroke one side of the back
2) Spine will curve towards stimulated side

363
Q

When should the ‘trunk incurvation’/ Galant’s reflex be seen?

A

0-2 months

364
Q

What is the ‘Landau’ reflex?

A

1) Suspend baby prone
2) Head will lift up and the spine will straighten

365
Q

When should the ‘Landau’ reflex be seen?

A

0-6 months

366
Q

What is the ‘Parachute’ reflex?

A

1) Suspend baby prone and slowly lower the head towards a surface
2) Arms and legs will extend in a protective fashion

367
Q

When should the ‘Parachute’ reflex be seen?

A

8 months onwards

368
Q

What is the ‘Positive support’ reflex ?

A

1) Hold baby upright until feet touch a surface
2) Hips, knees and ankles will extend and partially bear weight for 20/30 seconds

369
Q

When should the ‘Positive support’ reflex be seen?

A

0-6 months

370
Q

What are the postural reflexes?

A
  • Parachute
  • Positive support
  • Landau
  • Neck/head righting reflexes
  • Lateral propping
371
Q

What does persistence of primitive reflexes and lack of development of postural reflexes show?

A

Motor neuron abnormalities in infants

372
Q

Define childhood disability

A

Physical or mental impairment preventing children from going about daily life

373
Q

Name two examples of childhood disability

A

1) Down’s syndrome
2) Cerebral Palsy

374
Q

What is Cerebral Palsy?

A
  • A permanent neurological problem resulting from damage to the brain around the time of birth
  • Lesions are non-progressive, but manifest clinically overtime
375
Q

What are the main domains affected in Cerebral Palsy

A
  • Cognition
  • Communication
  • Perception
  • Sensation
  • Behaviour
  • Seizures
376
Q

What are the causes of antenatal Cerebral Palsy?

A

Antenatal e.g vascular occlusion/congenital infection (CMV, toxoplasmosis or rubella) (majority)

Birth asphyxia/trauma

377
Q

What are post-natal causes of Cerebral Palsy?

A
  • Meningitis/encephalitis/encephalopathy
  • Head trauma
  • Intraventricular haemorrhage
378
Q

What are the clinical motor presentations of Cerebral Palsy?

A
  • Abnormal limb/trunk posture and tone
  • Delayed motor milestones
  • Abnormal gait
379
Q

What are the non-motor presentations of Cerebral Palsy?

A
  • Feeding difficulties
  • Learning difficulties
  • Epilepsy
  • Language/speech difficulties
  • Persistent primitive reflexes
380
Q

How is functional ability described/assessed in Cerebral Palsy?

A

Gross Motor Function Classification System (GMFCS)

381
Q

What is the GMFCS?

A

Gross Motor Function Classification System I-III:
- Measures child’s functional ability following diagnosis of cerebral palsy

382
Q

What are the 5 levels of the GMFCS in Cerebral Palsy?

A

Level 1: walks without limitation

Level 2: walks with limitations

Level 3: walks using handheld mobility device

Level 4: self mobility with limitations (may use powered mobility)

Level 5: manual wheelchair transportation

383
Q

How is Cerebral Palsy diagnosed?

A

Clinicaly
MRI: identifies cause

384
Q

What are the 4 clinical subtypes of Cerebral Palsy?

A
  • Spastic (majority)
  • Dyskinetic
  • Ataxic
  • Mixed
385
Q

Describe Spastic Cerebral Palsy

A
  • Damage to UMN pathway
  • Limb tone persistently increased (spastic)
  • Brisk deep tendon reflexes
  • Clasp knife reflexes
386
Q

What are the 3 different types of Cerebral Palsy?

A

1) Hemiplegia
2) Diplegia
3) Quadriplegia

387
Q

What is quadriplegia associated with in Cerebral Palsy?

A
  • Seizures
  • Low IQ
  • Swallowing difficulties
388
Q

Describe Dyskinetic

A

Movements of involuntary control
Muscle tone variable
Chorea
Athetosis
Dystonia

389
Q

What is Chorea?

A

Jerky movements

390
Q

What is Athetosis?

A

Slow writhing movements distally: e.g. fanning fingers

391
Q

What is Dystonia?

A

Twisting appearance from simultaneous contraction of agonist and antagonist muscle groups

392
Q

What damage is associated with Ataxic Cerebral Palsy?

A

Cerebellum damage

393
Q

Describe Ataxic

A
  • Poor balance
  • Delayed motor development
  • Hypo/hypertonia
  • Uncoordinated, intention tremor and ataxic gait (evident later on)
394
Q

What is Ataxia?

A

Lack of voluntary co-ordination of muscle movements that can include ataxic gait, speech and abnormal eye movements

395
Q

What damage is associated with Dyskinetic Cerebral Palsy?

A

Basal ganglia damage

396
Q

What is the treatment for spasticity (hypertonia) Cerebral Palsy?

A

Oral Diazepam
Baclofen
Botulinum toxin (botox): relaxes muscles

397
Q

Who is involved in managing Cerebral Palsy?

A
  • Physiotherapist
  • Speech Therapist
  • Occupational Therapist
  • Orthoptist/ Audiologist
  • Dietitian
  • Social worker
398
Q

What gene mutation causes Down’s Syndrome?

A

Trisomy 21

399
Q

What are the risk factors for Down’s syndrome?

A

FHx
Old maternal age: >35

400
Q

What is the clinical presentation of Down’s syndrome (excluding facial features)?

A

Deafness
Blindness
Hypothyroidism
Dementia
Learning disability
Hypotonia
Short stature
CHD
Atlantoaxial instability
ALL

401
Q

What are the facial features of Down’s syndrome (excluding facial features)?

A
  • Epicanthic folds (inner corner of eye)
  • Protruding tongue
  • Small low set ears
  • High arched palate
  • Palpebral fissures (eyes at angle)
  • Single palmar crease
  • Brachycephaly (flat head)
  • Brushfield spots (white spots in eyes)
402
Q

What is Edward’s Syndrome?

A

Trisomy 18

403
Q

Who is mainly affected by Edward’s Syndrome?

A

Females

404
Q

What is the clinical presentation of Edward’s syndrome?

A

Severe psychomotor + growth retardation in those that survive 1st year of life:
- Micrognathia
- Low set ears
- Rocker bottom feet
- Overlapping of fingers
- Learning disabilities

405
Q

What is Patau’s Syndrome?

A

Severe physical and mental congenital abnormalities due to Trisomy 13
Can cause Holoprosencephaly

406
Q

What is the clinical presentation of Patau’s Syndrome?

A

Microcephalic
Microphthalmia (one small eye)
Hypotelorism (decreased distance between eyes)
Cleft lip/palate
Scalp lesions
Rocker bottom feet
CHD
IUGR and low BW
Severe learning difficulties

407
Q

What is Holoprosencephaly?

A

Brain doesn’t divide into two halves

408
Q

What is the management of Patau’s Syndrome?

A

Death within 7-10 days

409
Q

Define genetic imprinting

A

Only one copy of a gene is expressed

410
Q

Give two examples of Genomic imprinting

A

Angelmans syndrome

Prader Willi syndrome

411
Q

What are Minosomy disorders?

A

Absence of one member of a pair of chromosome

412
Q

Give an example of a Minosomy disorder?

A

Turner’s syndrome

413
Q

Give 5 examples of Trisomy disorders

A

Downs
Edwards
Pataus
XXX syndrome
Klinefelter’s

414
Q

Give 4 examples of Autosomal Dominant conditions

A

Huntingtons
Neurofibromatosis
Hereditary spherocytosis
Marfans

415
Q

Give 3 examples of Autosomal recessive conditions

A

CF
Albinism
PKU (phenylketouria)

416
Q

Give examples of X linked inheritance conditions

A

Duchenne’s muscular dystrophy
Red-green colour blindness
G6PD deficiency
Haemophilia A/B

417
Q

What is Prader-Willi Syndrome?

A

Loss of functional genes on the proximal arm of the chromosome 15 inherited from the father

First human disorder attributed to genomic imprinting

418
Q

What causes Prader-Willi Syndrome?

A

Deletion in the paternally inherited chromosome 15 or maternal uniparental disomy 15

OPPOSITE TO ANGELMAN’S

419
Q

What is the clinical presentation of Prader-Willi Syndrome?

A

Infant: Genital hypotonia, development delay and failure to thrive/ poor feeding, and blue eyes blonde hair

Adolescence: Obesity, learning disabilities, behavioural difficulties and hyperphagia (always hungry)

420
Q

Why do patients have hyperphagia in Prader-Willi Syndrome?

A

Raised ghrelin

421
Q

What is the management of Prader-Willi Syndrome?

A

Growth Hormonea
Anti-psychotics: Olanzapine
SSRI’s

422
Q

What is Angelman’s Syndrome?

A

Genetic imprinting disorder
Due to maternal deletion of chromosome 15

OPPOSITE OF PRADER WILLI

423
Q

What is the clinical presentation of Angelman’s Syndrome?

A

Fascination with water
Happy demeanour
Dysmorphic features: widely spaced teeth
Learning disability
Speech impairment
Ataxia (broad based gait)
Strabismus
Drooling
Epilepsy
Microcephaly
V similar to autism

424
Q

How is Angelman’s syndrome diagnosed?

A

Chromosomal analysis
Fluorescence in situ hybridisation (FISH): deletions

425
Q

How is Angelman’s Syndrome managed?

A

Behavioural modification programmes
Speech therapy
Physiotherapy
Parental education
Anti-convulsants for Epilepsy: valproate/ clonazepam

426
Q

What is Turner’s Syndrome?

A

Loss/abnormality of the second X chromosome (45 XO)

427
Q

What is there a increased risk of in Turner’s Syndrome?

A

Increased risk of CHD
Renal malformations
Hearing loss
Osteoporosis
Obesity
Diabetes
Atherogenic lipid profile

428
Q

What is the clinical presentation of Turner’s Syndrome?

A

Short stature
Webbed neck
Cubitus valgus (increased carrying angle)
Widely spaced nipples
Almost all infertile
Delayed puberty
Ovarian failure
Low posterior hairline
High arching palate
Recurrent otitis media
CV and renal malformations

429
Q

What is Turner’s Syndrome associated with?

A

Autoimmune conditions:
Thyroid
Diabetes
Coeliac
Crohn’s

430
Q

How is Turner’s Syndrome diagnosed?

A
  • Amniocentesis or chorionic villous sampling
  • Chromosomal analysis
431
Q

How is Turner’s Syndrome managed?

A

Short stature: recombinant human growth hormone
Oestrogen + progesterone (12 years): to initiate puberty, prevent osteoporosis and regulate the menstrual cycle
Fertility treatment

432
Q

What is the cause of Noonnan’s Syndrome?

A

Autosomal dominant mutations in the RAS/ MAPK pathway

60% are new spontaneous mutations

433
Q

What is the clinical presentation of Noonnan’s Syndrome?

A

Learning disability
Cryptorchidism
Pectus excavatum
Pulmonary stenosis
Short stature
Broad forehead
Downward sloping eyes with ptosis
Hypertelorism (wide space between the eyes)
Prominent nasolabial folds
Low set ears
Webbed neck
Widely spaced nipples

434
Q

What is Neurofibromatosis?

A

Autosomal dominant disorder of benign neuromas that encompasses NF1, NF2 and Schwannomatosis

435
Q

What is NF1?

A

NF1 gene defect on chr 17: Skin lesions
More common then NF2

436
Q

What is NF2?

A

NF2 gene defect on chr 22: bilateral acoustic neuromas (schwannomas, meningiomas and ependymonas)
Less common

437
Q

What is the diagnostic criteria for NF1 (neurofibromatosis)?

A

2/7 = diagnosis
** CRABBING**
Café-au-lait spots (6+) (>5mm kids, >15mm adults)
Relative with NF1
Axillary or inguinal freckles (skin folds)
Bony dysplasia e.g. Bowing of a long bone or sphenoid wing dysplasia (absence of bone around eyes)
Iris hamartomas (Lisch nodules yellow-brown spots in eyes) (2 or more) are yellow brown spots on the iris
Neurofibromas (2 or more) or 1 plexiform neurofibroma
Glioma of the optic nerve

438
Q

What is the presentation of NF2 (neurofibromatosis)?

A

Hearing loss
Tinnitus
Balance problems
Bilateral schwannomas

439
Q

What is the key difference between NF1 and NF2?

A

Rarely >6 cafe-au-lait spots in NF2

440
Q

What is the management of Neurofibromatosis?

A

Intervene when tumours produce pressure symptoms or suggestive of malignant change
Surgery

441
Q

What is Fragile X Syndrome (Martin-Bell)?

A

Mutation in the FMR1 (fragile X mental retardation 1) gene on the X chromosome

442
Q

What causes Fragile X Syndrome (Martin-Bell)?

A

FMR1 gene includes a CCG repeat
As its passed from each generation it lengthens
Once it reaches >200 no fragile X protein is made
TRINUCLEOTIDE REPEAT DISORDER

443
Q

What condition is due to a CCG repeat?

A

Fragile X syndrome

444
Q

What are the clinical presentation of Fragile X Syndrome (Martin-Bell)?

A

Delayed speech + language
Macro-orchidism
Macrocephaly
Large ears
Long narrow face
Hypermobile joints
ADHD
Seizures
Autism

445
Q

What are the investigations for Fragile X Syndrome (Martin-Bell)?

A

Molecular genetic testing of FMR1 gene

446
Q

What is the management of Fragile X Syndrome (Martin-Bell)?

A

Minocycline: improves behaviour

447
Q

What is Klinefelter Syndrome?

A

Additional X chromosome (47XXY)
Chief genetic cause of hypogonadism

448
Q

What is the clinical manifestation of Klinefelter Syndrome?

A

Gyaecomastia
Azoospermia
Tall
Macro-orchidism
Reduced pubic hair

449
Q

What is the management of Klinefelter Syndrome?

A

Testosterone injections
Advanced IVF techniques: fertility
Mastectomy (gynaecomastia)

450
Q

What is Autism?

A

Neurodevelopmental disorder of social interaction, repetitive behaviour and communication impairments

451
Q

Define Autism

A

Abnormal development manifesting before the age of 3

452
Q

What are 3 characteristics of abnormal functioning in Autism?

A

1) Reciprocal social interaction
2) Impairment of language and communication
3) Restricted, repetitive behaviour

453
Q

In autism, how many diagnosed are male?

A

75% male

454
Q

What is the clinical presentation of Autism?

A
  • Communication difficulties
  • Social interaction
  • Difficulties with imagination/ rigidity of thought
455
Q

What are 5 examples of social interaction difficulties seen in autism?

A
  • No desire to interact with others
  • Oblivious to others feelings
  • No understanding of unspoken social rules
  • Lack of empathy
  • Poor eye contact
456
Q

What are 5 examples of behavioural difficulties in autism?

A

Restrictive/ repetitive movements: self-stimulating e.g. hand-Flapping or rocking
Obsessive fixations
Inability to play/write imaginatively
Same questions

457
Q

What are examples of communication difficulties in Autism?

A

Repeats speech
Disordered language
Poor non-verbal communication
No social awareness, unable to start up or keep a conversation

458
Q

What medical problems are associated with Autism?

A

Epilepsy
Visual and hearing
Mental health (ADHD, depression and anxiety)

459
Q

What is the management for Autism?

A

Early behavioural intervention
Education for parents
Support in schools
Risperidone: aggression/irritability
Melatonin: sleep difficulties
SSRI’s: repetitive behaviours

460
Q

What is the treatment for Aggression/irritability in Autism?

A

Risperidone

461
Q

What treats sleep difficulties in Autism?

A

Melatonin

462
Q

What treats repetitive behaviours in Autism?

A

SSRI’s

463
Q

What is Aspergers Syndrome?

A

Pervasive development disorder which lies within the autistic spectrum.

464
Q

What is the ratio of Boys:Girls in Asperger’s Syndrome?

A

Boys:Girls
8:1

465
Q

What are the 3 key differences between Autism and Asperger’s Syndrome?

A
  • Lack of delayed cognition and language
  • Aspergers are above average intelligent
  • Aspergers are more likely to seek social interaction and share activities/ friendships
466
Q

What is the clinical manifestation of Asperger’s Syndrome?

A
  • Obsessed with complex subjects
  • Concrete thinking
  • Pedantic
  • Normal speech
  • Clumsiness
  • Solitary but socially aware
  • Poor sleep patterns
467
Q

What is attention deficit hyperactivity disorder (ADHD) ?

A

Persistant and extreme hyperactivity and attention deficit

468
Q

What are causes of ADHD?

A

Prematurity
Fetal alcohol syndrome

469
Q

What are the 3 core symptoms of ADHD?

A
  • Hyperactivity
  • Inattention
  • Impulsivity
470
Q

What criteria must be met for a diagnosis of ADHD?

A

1) Present before 12
2) Developmentally inappropriate
3) Severel symptoms in multiple settings
4) Clear effect on social/academic/ occupational functioning

471
Q

How many inattentive and hyperactive symptoms must be evident for a diagnosis of ADHD?

A

6/9: inattentive

6/9: hyperactive/impulsive symptoms

472
Q

What are the 9 inattentive symptoms of ADHD?

A

1) Easily distracted
2) Does not appear to be listening when spoken to
3) Has difficulty sustaining attention
4) Avoids/ dislikes sustained mental effort
5) Forgetful in daily activities
6) Difficulty following instructions/ fails to complete tasks
7) Difficulty organising tasks
8) Careless mistakes/ lack of attention to detail
9) Loses important items

473
Q

What are 3 impulsive symptoms present in ADHD?

A

1) Blurts out answers
2) Has difficulty awaiting turn
3) Interrupts / intrudes others

474
Q

What are 6 hyperactive symptoms present in ADHD?

A

1) Squirms/ fidgets
2) Cannot remain seated
3) Runs/ climbs in inappropriate situations
4) Often ‘on the go’
5) Talks excessively
6) Cannot perform leisure activities quietly

475
Q

What is the management of ADHD?

A

Diet and exercise
Methylphenidate (ritalin); 6 week trial + monitor growth

476
Q

What is syncope?

A

Sudden reduction in cerebral perfusion with oxygenated blood

477
Q

What is a seizure?

A

Transient occurence of signs/symptoms due to abnormal excessive neuronal activity in the brain

478
Q

How are seizures treated?

A

Diazepam or Lorazepam if >5 min

479
Q

SYNCOPE VS SEIZURE

Triggers

A

Seizure:
Flashing lights/ hyperventilation

Syncope:
Upright, exertion, blood, needles

480
Q

SYNCOPE VS SEIZURE

Prodrome

A

Seizure:
Typical aura

Syncope:
Nausea, sweating or palpitations

481
Q

SYNCOPE VS SEIZURE

Duration

A

Seizure:
Variable

Syncope:
1-30s

482
Q

SYNCOPE VS SEIZURE

Convulsive jerks

A

Seizure:
Common + prolonged

Syncope:
Less common + brief

483
Q

SYNCOPE VS SEIZURE

Incontinence

A

Seizure:
Common

Syncope:
Uncommon

484
Q

SYNCOPE VS SEIZURE

Tongue bite

A

Seizure: Common

Syncope: rare

485
Q

SYNCOPE VS SEIZURE

Colour?

A

Seizure:
Partial- pale
Tonic clonic- red,blue

Syncope:
Very pale

486
Q

SYNCOPE VS SEIZURE
Post-ictal phase

A

Seizure:
Yes + slow + confused

Syncope:
No + rapid orientation

487
Q

What are febrile seizures?

A

Seizures occurring in children aged 6m-6 years with fever and raised temperature (>37.8°)

488
Q

What is a simple febrile seizure?

A
  • Generalised tonic-clonic
  • <15 mins
  • Occurs once during illness
  • Should be recovered/drowsy within 1 hr
489
Q

What is a complex febrile seizure?

A

Focal or partial seizures
May reoccur during same febrile illness
>15 mins

490
Q

How long is a febrile status epilepticus seizure?

A

> 30 mins

491
Q

What can cause febrile seizures?

A
  • Metabolic (electrolytes/glucose)
  • Viral (meningo)
  • CNS lesion
  • Epilepsy
  • Trauma
492
Q

When should you urgently refer febrile seizures?

A

1) First febrile seizure
2) >5 min duration
3) Drowsy >1 hour after seizure
4) Previous history of:
- <18 months
- Complex seizure
- On Abx

493
Q

When should a LP be considered in febrile seizures?

A

Aged <18m

494
Q

Contra- indications of LP?

A
  • Reduced consciousness
  • Septicaemic shock
  • Likely invasie meningococcal
  • Signs of raised ICP
  • Focal neurology
  • Bleeding tendency
495
Q

Why wait 12 hours before taking a LP?

A

To make sure you don’t have a bloody tap

496
Q

What are reflex anoxic seizures?

A

Paroxysmal, self limiting brief asystole (<15s) that occurs in infants (6m- 2yrs) due to common triggers such as:
- Pain
- Cold foods
- Fright
- Fever

497
Q

What is the pathophysiology of reflex anoxic seizures?

A

When a child is startled, strong signals from the vagus nerve cause the heart to stop beating

498
Q

What is the clinical presentation of reflex anoxic seizures?

A

Stops breathing
Stiff/rigidity
Incontinence
Pale/blue
NO tongue bite

499
Q

What is the management of reflex anoxic seizures?

A

Check ferritin + treat
No drugs needed
Pacemaker
Child usually grows out of it

500
Q

What is epilepsy?

A

Tendency to have seizures: transient episodes of abnormal electrical activity in the brain.

Symptom: not a true condition

Diagnosed after a minimum of 2 seizures

501
Q

What can cause epilepsy?

A

Usually none found
Infection
Hypo (glucose, Na, Ca, Mg)
Trauma
Metabolic defects
CNS tumour
Lights
Exercise

502
Q

What are the main 2 broad classifications of epilepsy?

A

Generalised (both hemispheres)

Focal/Partial (one hemisphere + start in the temporal lobe)

503
Q

Describe absent epilepsy (7 points)

A

1) Transient LoC <30s
2) Abrupt onset and no motor phenomena apart from eyelid flickering
3) Precipitated by hyperventilation
4) Stare momentarily and stop moving
5) No recall but knows they’ve missed something
6) 2/3rds female
7) 4-12 yrs old

504
Q

What are the 5 types of generalised seizures?

A

Absent
Myoclonic
Tonic
Tonic-clonic
Atonic

505
Q

What are the 4 types of partial/focal seizures?

A

Frontal
Temporal
Parietal
Occipital

506
Q

Describe myoclonic seizures

A

Brief, repetitive jerking movements of limbs, neck or trunk

507
Q

What is are hiccups?

A

Non-epileptic myoclonic seizure of diaphragm

508
Q

Describe a tonic seizures

A

Tone increase (muscle tensing)

509
Q

Describe the tonic phase of Tonic-clonic seizures

A
  • Rigid
  • Fall to ground
  • Stop breathing/cyanosis
510
Q

Describe the clonic phase of Tonic-clonic seizures

A
  • Rhythmic contractions
  • Limb jerking
  • Irregular breathing
  • Saliva/ cyanosis
  • Tongue bite/incontinence
511
Q

What follows a tonic-clonic seizure and how long do they last?

A

Deep sleep/unconsciousness for up to several hours

512
Q

Describe an atonic seizure

A

Transient loss of muscle tone causing drop to the floor or drop of head

513
Q

Describe a frontal seizure

A

Motor phenomena (clonic)

Asymmetrical

514
Q

Describe a parietal seizure

A

Contralateral altered sensation

515
Q

Describe a temporal seizure

A
  • Auditory/ smell/ taste phenomena
  • Lip smacking/ plucking clothes
  • Longer seizures
  • Deja vu
516
Q

Describe a occipital seizure

A

Vision distortion

517
Q

How is epilepsy diagnosed?

A

EEG: within 24 hours
MRI head: focal lesions
Bloods: Glucose + Electrolytes
CK: raised in true epileptics after clonus and tonic seizures vs normal in pseudoseizures

518
Q

What is the management of generalised seizures?

A

Trigger education
1st line: sodium valproate
TERATOGENIC
Increases GABA activity
Used by most other types as well

519
Q

What is the management of focal seizures?

A

Carbamazepine (only epilepsy to use this)

520
Q

What is the management of prolonged seizures?

A

Rectal diazepam

521
Q

What is status epilepticus?

A

Seizure >30 minutes

OR

Multiple seizures, without regaining consciousness, lasting >30 minutes

Brian swells and can cause herniation due to electrolyte imbalance from the firing neurons metabolic demand not being met

522
Q

What is the management of status epilepticus?

A

ABCDE:
- Secure airway
- IV access
- Check BP
- Check temp
- Check glucose

Drugs:
- Lorazepam IV (5 min (Benzodiazepine increases GABA activity))
- Lorazepam IV (15 min)
- Phenytoin IV (>20 min)
- GA e.g. Propofol (>30 min) + Refer to PICU

523
Q

What are 3 components of infantile spasms/west syndrome?

A

1) Infantile spasms
2) Hypsarrhythmia (chaotic EEG)
3) Learning disability

524
Q

What is the clinical presentation of infantile spasms/west syndrome?

A

Learning disability
Hypopigmented skin lesions
Growth restriction
Spasms: 5-10 seconds + just before/ after sleep
- Clusters of head nodding/trunk jerks

525
Q

What are the investigations for infantile spasms/west syndrome?

A

EEG: hypsarrhythmia

526
Q

What is the management of infantile spasms/west syndrome?

A

Vigabatrin
ACTH (daily IM)
Prednisolone
PROGNOSIS IS POOR

527
Q

What is Tuberous Sclerosis?

A

Multi-system hamartomas

528
Q

What causes Tuberous Sclerosis?

A

TSC1 (chr 9 hamartin) or TSC2 (chr 16 tuberin)
Autosomal dominant mutations regulating cell growth

529
Q

What is the clinical manifestation of Tuberous Sclerosis?

A

Epilepsy
Learning disability
Poliosis: white patches of hair
Angiofibromas: skin coloured papules over the nose and cheeks
Ash leaf spots
Cafe-au-lait spots
Shagreen patches: thick, dimpled pigemented skin
Subungual fibromata

530
Q

What type of epilepsy is seen in Tuberous Sclerosis?

A

Focal seizures and infantile spasms occur in infancy 2° to tuber formation in the brain

531
Q

How is Tuberous Sclerosis diagnosed?

A

Clinical
EEG: epilepsy
MRI head: cortical tubers

532
Q

What is the management of Tuberous Sclerosis?

A

Treat complications
Vigabatrin

533
Q

What type of genetic defect is Muscular Dystrophy?

A

X-linked recessive

Mutation to gene encoding dystrophin

534
Q

What is dystrophin?

A

Strengthens muscle fibres

535
Q

What are the two types of Muscular Dystrophy?
Which is more severe?

A

Duchenne: loss of Dystrophin (more severe)

Becker: misshapen dystrophin

536
Q

What is the clinical presentation of Muscular Dystrophy?

A
  • 1-6 yrs old: Duchenne
  • 10-20yrs old: Becker
  • Waddling clumsy gait
  • Calf pseudohypertrophy
  • Classic gower manoeuvre (on fours getting up)
  • Respiratory impairment
  • Wheelchair: 9-12 yrs old
  • Scoliosis
  • Osteoporosis
537
Q

What is the Gower Manoeuvre?

A

Using hands to crawl up from a sitting position to a standing position

538
Q

What are the investigations for Muscular Dystrophy?

A

Raised: creatinine kinase
Muscle biopsy:
- Abnormal fibres surrounded fat/fibrous tissue

539
Q

What is the management of Muscular Dystrophy?

A

Exercise: maintains muscle power and mobility, and delays scoliosis
Prednisolone: slows muscle strength and function decline
Creatine supplementation

540
Q

What is gastroenteritis?

A

Inflammation from the stomach to the intestines: causes nausea, vomiting and diarrhoea that lasts <14 days

541
Q

What are the common causes of gastroenteritis in children and adults?

A

Children= Rotavirus
Adults = Noravirus

542
Q

How many deaths of children/year are due to rotavirus (gastroenteritis)?

A

600k

Vaccine is part of the schedule

543
Q

What are risk factors for gastroenteritis?

A

Poor hygiene
Immunocompromised
Poorly cooked food

544
Q

What is the clinical manifestation of gastroenteritis?

A

Diarrhoea
Blood: likely bacterial
Fever, fatigue, headache and myalgia
N&V
Abdo cramping

545
Q

What is the concern with a child with gastroenteritis?

A

Dehydration → shock

546
Q

What are the investigations for gastroenteritis?

A

FBC:

Low MCV: +/- Fe deficiency

High MCV: if alcohol abuse/decreased B12 absorption

Raised WCC: if parasitic cause

Raised ESR + CRP

U&E: indicates dehydration

Stool Feacal occult blood + MCS:

Bacteria/parasites/C. Diff

Abdominal x-ray: toxic megacolon indicates C. difficile

547
Q

What is the management of gastroenteritis?

A

Isolate 48 hrs
Oral rehydration (Dioralyte)
Avoid sugary drinks
Anti-emetics (metoclopramide, 5HT3 Receptor antagonist and 5HT4 agonist)
Anti-motility agents (loperamide hydrochloride)
Abx
Stop C antibiotics: if pseudomembranous colitis

548
Q

What is a common complication of gastroenteritis?

A

Transient lactose intolerance

549
Q

How would you manage transient lactose intolerance?

A

1) Lactose-free diet
2) Slowly reintroduce lactose after a few months

550
Q

What are signs of Post-Infective lactose Intolerance?

A
  • Weight loss
  • Stools green and frothy
  • Increased frequency
551
Q

Give 3 causes of lactose intolerance

A

1) Primary: lactase deficiency
2) Secondary: due to small intestine injury from e.g. infection, coeliac or IBD
3) Post-infective lactose intolerance.

552
Q

What test can be done to check for lactose intolerance?

A

Stool: non-absorbed sugars
Hydrogen breath test

553
Q

What is colic?

A

Infant who isn’t sick or hungry cries for:
>3 hours a day
>3 days/week
>3 weeks

554
Q

What immunoglobulin is Cows Milk Allergy associated with?

A

IgG & IgE

555
Q

What is cow’s milk protein allergy?

A

A IgE mediated hypersentivity reaction to milk

556
Q

What is the clinical presentation of Cow’s milk protein allergy?

A

Vomiting
Abdominal pain
Diarrhoea
Malabsorption
Intestinal bleeding
Bloating
Allergy symptoms: urticaria and lip swelling
Anaphylaxis

557
Q

How is cows milk protein allergy diagnosed (CMPI)?

A

RAST test: skin prick blood test to measure IgE specific antibodies in the blood

558
Q

What is the management of Cows Milk Protein Allergy?

A

Breast feeding mothers: avoid dairy products
Use special hydrolysed formulas
Adrenaline in severe reactions
Antihistamines
Normally resolved by 5 years old

559
Q

What is toddlers diarrhoea?

A

Most common cause of loose stools in preschool children

560
Q

What causes toddlers diarrhoea?

A

Intestinal motility delay
Often undigested vegetables + mucus

561
Q

How is toddlers diarrhoea treated?

A

Improve diet:
High fat (whole milk)
Normal fibre
Reduce fruit juice

562
Q

What is Coeliac disease?

A

Gluten sensitive enteropathy: damaging immunological response to proximal small intestine mucosa

563
Q

What antibodies are involved in coeliac disease?

A

Anti-endomysial IgA (Anti-EMA IgA)
Anti-tissue transglutaminase (Anti-TTG IgA)

564
Q

What genes is Coeliac Disease associated with?

A

HLA DQ2
DQ8

565
Q

What are the risk factors for Coeliac Disease?

A

Downs
T1DM
Autoimmune thyroid disease

566
Q

What is the clinical presentation of Coeliac Disease?

A

GLIAD:

GI Malabsorption

Failure to thrive in children

Fatigue and weakness

Diarrhoea
Abdominal pain

Lymphoma and Carcinoma

Enteropathy-associated T-cell lymphoma

Small bowel adenocarcinoma

Immunulogical

IgA deficiency

T1DM

Primary biliary cholangitis
Aphthous ulcers

Anaemia

Hyposplenism
Iron deficiency

Dermatological

Dermatitis herpetiformis (itchy rash in response to gluten)
Dental enamel defects

567
Q

What are the investigations for Coeliac Disease?

A

Oesophago-gastro-duodenoscopy (OGD) and duodenal biopsy:
-Crypt hypertrophy
- Intraepithelial lymphocytes
- Villous atrophy
- Lamina propria infiltration

Antibodies:
- Anti-EMA IgA
- Anti-TTG IgA
- Blood smear and FBC

568
Q

What is Crohn’s disease?

A

IBD of transmural inflammation of the GIT (from mouth → anus)

Terminal ileum + colon most affected

569
Q

What antibody is associated with Crohn’s?

A

ASCAs

570
Q

What is NEST in Crohns?

A

NESTS:

No blood or mucus (less common)

Entire GI tract

Skip lesions on endoscopy

Terminal ileum most affected and Transmural inflammation

Smoking is a risk factor

571
Q

What is the clinical presentation of Crohn’s Disease?

A

Relapsing and remitting course
Abdominal pain and tenderness: RLQ (ileum and may mimic appendicitis)
Systemic symptoms:
-Diarrhoea (not bloody)
-Anaemia
-Pyrexia
-Malaise
-Weight loss
Aphthous ulcer
Erythema nodosum + pyoderma gangrenosum
Arthritis and spondylitis
- Episcleritis
- Osteoporosis
Finger clubbing
Uveitis
Glossitis
Failure to thrive
Perianal abscesses, fistulae, tags or strictures

572
Q

What is Erythema Nodosum?

A

Inflammation of the fatty layer of skin

Reddish, painful, tender lumps

573
Q

How is Crohn’s Disease diagnosed?

A

Faecal calprotectin:: raised (indicates intestinal inflammation)
Colonscopy and biopsy:
- Transmural inflammation
- Deep ulcers
- Skip lesions
- Cobblestone mucosa
FBC
ASCA
Serum B12, folate and iron: low

574
Q

What are the Macroscopic and Microscopic histopathological findings of Crohn’s?

A

Macroscopic:
-Affects any part of GIT
-Oral and perianal disease
-Discontinuous involvement (skip lesions)
-Deep ulcers and fissures in mucosa (cobblestone appearance)

Microscopic:
-Transmural inflammation
-Non-ceasing Granulomas present 50%

575
Q

What is the management of Crohn’s Disease?

A

Smoking cessation
Inducing remission:
- Corticosteroids manage attacks: budesonide (mild), prednisolone (moderate) or hydrocortisone (severe)
- Refractory: Anti-TNF (INFLIXIMAB)
- Peri-anal disease – abx (METRONIDAZOLE)

Maintaining remission:
- Immunosuppressants: azathioprine
- Mercaptopurine (chemotherapy)

Anaemia: iron, B12 or folate deficiency should be treated

Surgery

576
Q

What is Ulcerative Colitis?

A

Chronic IBD of submucosal ulcers from the colon →rectum (mainly distal colon)

577
Q

What antibody is associated with Ulcerative Colitis?

A

pANCA

578
Q

What is CLOSE UP in ulcerative colitis?

A

CLOSE UP:

Continuous inflammation

Limited to colon and rectum

Only superficial mucosa affected

Smoking is protective

Excrete blood and mucus

Useaminosalicylates

Primary Sclerosing Cholangitis: in the majority of patients

579
Q

What is the clinical presentation of Ulcerative Colitis?

A

Abdominal discomfort, tenderness and distention
Tenesmus and faecal urgency
Erythema nodosum + pyoderma gangrenosum
Arthritis and spondylitis
Finger clubbing
Uveitis
Systemic symptoms:
- Diarrhoea (Blood +/- mucus PR)
- Anaemia
- Pyrexia
- Malaise
- Weight loss

580
Q

How is Ulcerative Colitis diagnosed?

A

Faecal calprotectin: raised

Colonoscopy and biopsy

Bloods:

-FBC: low Hb and high WCC

-LFTs: low albumin

-CRP/ES: high during flares

-Serum B12, folate and iron: low

-pANCA

Stool:

  • MCS
  • C. Diff Test (CDT)
    CT (perforation or megacolon)
581
Q

What are the Macroscopic and Microscopic histopathological findings of Ulcerative Colitis?

A

Macroscopic:
- Affects only colon

  • Begins in rectum and extends proximally
  • Continuous involvement
  • Red mucosa (bleeds easily)
  • Ulcers and pseudopolyps (regenerating mucosa)

Microscopic:

  • Mucosal and submucosal inflammation
  • No granulomata
  • Goblet cell depletion
  • Crypt abscesses
582
Q

What is the management of Ulcerative Colitis?

A

5-aminosalicylic acid (5-ASA): e.g. olsalazine reduces inflammation and maintains remission

Glucocorticoid: e.g prednisolone if not responsive to 5-ASA

Immunosuppressants: azathioprine/mercaptopurine (chemotherapy) +/- ciclosporin (DMARDs)

Admit if acute and severe with fluids

Surgery

583
Q

What is Kwashiorkor malnutrition?

A

Low protein + essential amino acids intake

584
Q

What is the clinical presentation of Kwashiorkor malnutrition?

A
  • Oedema
  • Hair changes
  • Mental changes
585
Q

What is the treatment of Kwashiorkor malnutrition?

A

Increase protein + vitamins diet

586
Q

What is Marasmus?

A

Malnutrition due to lack of calories from all energy sources

587
Q

What is Intussusception?

A

Most common cause of intestinal obstruction (atresia)
One segment of the bowel invaginates the other

588
Q

Where is Intussusception likely to occur?

A

Ileocaecal

589
Q

Who is most likely to get intussusception?

A

Male aged 6-18m

590
Q

What is the clinical presentation of Intussusception?

A

Sudden
Paroxysms of colicky abdominal pain
Early bile stained vomit
RUQ mass (sausage shape)
RED CURRENT JELLY stools

591
Q

How is intussusception diagnosed?

A

USS: ‘target sign’.
X ray + barium contrast:
- Dilated loops of bowel close to the obstruction
- Collapsed loops of bowel far from the obstruction
- Absence of air in the rectum

592
Q

What is the treatment of intussusception?

A

Immediate IV fluid resus
Analgesia: e.g. morphine
Interventional radiology: rectal air insufflation
Surgery

593
Q

What is Pyloric Stenosis?

A

Narrowing of the pyloric sphincter prevents food from travelling from the stomach → duodenum

594
Q

What is the clinical presentation of Pyloric Stenosis?

A
  • Projectile vomiting after feeding
  • No bile
  • Constipation
  • Weight loss
  • Visible gastric peristalsis (LUQ)
  • Firm mass in upper abdomen that feels like a large olive on test feed
595
Q

What are the metabolic signs of Pyloric Stenosis?

A
  • Metabolic alkalosis
  • Hyponatraemia
  • Hypochloraemia
  • Hypokalaemia
596
Q

What are the investigations for Pyloric Stenosis?

A

Abdominal US: thickened pylorus sphincter
U+E
Blood gas

597
Q

What is the management of Pyloric Stenosis?

A

IV fluids: rehydrate + correct electrolyte disturbance
Stop feeding to stop vomiting
Ramstedt’s Pyloromyotomy

598
Q

What is it Necrotising Enterocolitis (NEC)?

A

Inflammatory bowel necrosis
Most common GI emergency in neonates
(Tends to affect premature)

599
Q

What are the risk factors for Necrotising Entercolitis?

A
  • Prematurity
  • IUGR
  • PDA
600
Q

What is the clinical presentation of Necrotising Enterocolitis?

A
  • Feeding problems
  • Abdominal distension
  • N&V
  • Bloody mucoid stool and bilious vomiting
601
Q

How is Necrotising Enterocolitis diagnosed?

A

Abdo X-ray:
- Portal venous gas
- Dilated loops of bowel
- Bowel wall oedema (thickened bowel walls)
- Pneumatosis intestinalis (gas in the bowel)
- Pneumoperitoneum (free gas in the peritoneal cavity indicates perforation)
Blood tests:
-FBC: thrombocytopenia and neutropenia
-CRP
-CBG: metabolic acidosis
-Blood culture: sepsis

602
Q

What is the treatment for Necrotising Enterocolitis?

A

Nil by mouth
IC fluids
Total parenteral nutrition (TPN)
IV Cefotaxime/ Vancomycin for 10-14 days
Surgical emergency

603
Q

What are the complications of Necrotising Enterocolitis?

A

Death of the bowel tissue → bowel perforation.
Bowel perforation → peritonitis and shock

604
Q

What is chronic constipation?

A

Constipation lasting >6 months

605
Q

What investigation is key when investigating constipation?

A

AXR

606
Q

What is Hirschprung’s disease?

A

Absent bowel movements due to missing nerve cells (ganglia) in myenteric plexus segment of the colon

607
Q

What is the clinical presentation of Hirschprung’s disease?

A
  • No bowel movements in 1st 48hrs = Meconium Ileus intestinal
  • Vomiting bilious green
  • Absolute constipation
  • Bowel sounds tinkling → absent
608
Q

Which intestinal atresia is the only type to cause abdominal distension following birth?

A

Meconium Ileus

609
Q

What are the complications of Hirschprung’s disease?

A

GI perforation (Short gut syndrome after surgery)

610
Q

How is Hirschpring’s disease diagnosed?

A

X ray + barium contrast:
- Dilated loops of bowel close to the obstruction
- Collapsed loops of bowel far from the obstruction
- Absence of air in the rectum
Rectal biopsy: absence of ganglionic cells

611
Q

What is the management of Hirschprung’s Disease?

A

Bowel washouts/irrigation
Bypass surgery/ ileostomy//colostomy surgical of the aganglionic section of bowel

612
Q

Why do neonates have higher bilirubin levels than adults?

A

1) Higher concentration of RBCs with short lifespan
2) RBCs breakdown → unconjugated bilirubin
3) Unconjugated bilirubin becomes conjugated in liver → liver immaturity → slower conjugation

613
Q

What may be the possible cause of jaundice in neonates at:

<24 hours?

> 14 days?

A

Conjugated jaundice in the first 24 hours of life is always pathological:

<24hrs = Rhesus haemolytic disease (+ve Coombs test)

> 14 days = Biliary atresia (pale stools)

614
Q

What are the risk factors for Jaundice?

A
  • Low BW
  • Prematurity
  • Breast fed babies
  • Maternal diabetes
  • FHx
615
Q

What is the clinical presentation of Jaundice?

A

First seen normally on forehead and face
Neuro signs:
- Change in muscle tone, altered crying
- Pale stools and dark urine

616
Q

What is the name of continued high levels of unconjugated jaundice?

A

Kernicterus

617
Q

What is the treatment of unconjugated jaundice?

A

Phototherapy
Exchange transfusion

618
Q

What is Kernicterus?

A

High levels of unconjugated bilirubin
Acute bilirubin encephalopathy that can cause:
- Athetoid movements
- Deafness
- Low IQ

619
Q

What can Kernicterus be prevented by?

A

Jaundice treatments

620
Q

What is gastrooesophageal reflux disease (GORD)?

A

Reflux of stomach contents through the lower oesophageal sphincter and into the oesophagus to irritate the lining

621
Q

What are symptoms of gastrooesophageal reflux disease (GORD)?

A

Distress after feeds/failure to feed & thrive
Apnoea
Heartburn
Worse lying down
Related to meals
Relieved by antacids
Burning retrosternal pain
Dyspepsia
Acid regurgitation + Water brash
Bloating
Nocturnal cough
Hoarse voice
Odonophagia and dysphagia

622
Q

What are the investigations for GORD?

A

PPI trial: symptoms relieved
Endoscopy

623
Q

What is the management of GORD?

A

Avoid over-feeding
Thicken feeds e.g. carobel
Raise head of bed
Hold head whilst feeding
Small regular meals (not soon before bed)
Smoking cessation/alcohol reduction
Avoid hot drinks and spicy foods
Stop drugs: NSAIDs, steroids, CCBs or nitrates
Antacid + Na/Mg alginate (Gaviscon)
PPI: lansoprazole
- 11 month PPI: undiagnosed dyspepsia
- 2 months PPI: endoscopically confirmed GORD
Nissen fundoplication

624
Q

If GORD does not resolve in 6-9 months what can be done?

A

Fundoplication if still failure to thrive / severe oesophagitis

625
Q

What is Meckel’s Diverticulum?

A

Malformation of GI tract (bulge in distal ileum)

626
Q

What is Meckel’s Diverticulum rule of 2’s?

A

2% of population
2 feet from ileocaecal valve
2 different mucosa
Affects <2 year old
Males 2x than females
≤2 inches
2% are symptomatic
2 types of the mucosal lining

627
Q

How is Meckel’s Diverticulum diagnosed?

A

Always considered when patients have haemorrhage or obstruction
Technetium scan: a spot
CT scan: if volvulus/intusseception

628
Q

When should a Diverticula be resected?

A

> 2cm
Narrow neck
Fibrous band to abdominal wall
Inflamed/ thickened

629
Q

What can congenital diaphragmatic hernia lead to?

A

Impaired lung development:
- Pulmonary hypoplasia
- Pulmonary hypertension

630
Q

What is Gastroschisis?

A

Evisceration of abdominal contents
> 5cm opening

631
Q

What is Biliary Atresia?

A

Congenital condition where the bile duct is narrowed/absent (extra/intra-hepatic a biliary tree scaring)
Results in cholestasis

632
Q

What is the clinical presentation of Biliary Atresia?

A

Elevated unconjugated/conjugated bilrubin = jaundice after birth
Splenomegaly
Pale stools/ dark urine

633
Q

What are the investigations for Biliary Atresia?

A
  • Fasting abdominal US: contracted/absent gallbladder
  • Laparotomy
  • Transcutaneous bilirubin: raised conjugated bilirubin
  • LFT’s: abnormal
  • ERCP imaging: fails to outline a normal biliary tree
634
Q

What is the treatment for Biliary Atresia?

A

Kasai procedure

635
Q

What are causes of increased interstitial fluid?

A

Lymph drainage: lymphoedema (eg congenital, blockade)
Venous pressure and drainage: venous obstruction e.g
thrombosis
Lowered oncotic pressure (low albumin / protein):
- Malnutrition
- Decreased liver production
- Increased loss e.g. gut or Kidney (nephrotic syndrome)
Salt and water retention:
- Heart failure
- Kidney: impaired GFR

636
Q

What is nephrotic syndrome?

A

A group of symptoms where the glomerulus basement membrane becomes highly permeable to protein:
- Proteinuria: filtration barrier becomes disrupted and more permeable
- Hypoalbuminaria: albumin is lost in urine →peripheral and periorbital oedema
- Hypertension
- Peripheral oedema

637
Q

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

A

Minimal change disease

638
Q

What triad is found in Nephrotic Syndrome?

A

Heavy proteinuria:
▪ First morning urine (protein:creatinine) >1g/m2/24 hrs

Hypoalbuminaemia:
▪ Fluid retention and oedema <25-30

Oedema:
▪ Pitting oedema and gravitational

Can also have Hyperlipidaemia

639
Q

What are the investigations of Nephrotic Syndrome?

A

Urinalysis (dipstick = UTI, MC&S = protein)
24 hour urine collection
Protein levels >3.5mg
Renal biopsy
BP
Low serum albumin
Low Anti-TIII = prone to renal vein thrombosis/ DVT/ PE
Antistreptolysin O and anti-DNAse B titres
Throat swab

640
Q

What are the 3 types of Nephrotic Syndrome?

A

Congenital (<1 year)
Steroid sensitive
Steroid resistant

641
Q

What are signs of steroid sensitive Nephrotic Syndrome?

A

1) Normal BP: renal function
2) No haematuria
3) No nephritis
4) Histology: minimal change disease

642
Q

What are the signs of steroid resistant Nephrotic Syndrome?

A

1) Elevated BP: impaired renal function
2) Haematuria
3) Nephritis
4) Histology: underlying glomerulopathy/ basement membrane abnormality

643
Q

What is the treatment of Steroid Sensitive Nephrotic Syndrome?

A

1st: Prednisolone

2nd: Renal biopsy if unresponsive

644
Q

What is the treatment of steroid resistant Nephrotic Syndrome?

A

Diuretics/ACE-I = oedema
NSAIDs: reduce proteinuria

645
Q

What is nephritic syndrome?

A

A collection of signs and symptoms that occur as a result of kidney inflammation
It is NOT a diagnosis, but a clinical picture.
Leads to glomerular basement membrane damage:

  • Haematuria
  • Hypertension
  • Oedema
646
Q

What are the causes of Nephritic syndrome?

A

Categorised into 3 groups:

Type III hypersensitivity:

  • Post-streptococcal glomerulonephritis
  • IgA nephropathy
  • Diffuse proliferative glomerulonephritis

Multiple causes:

  • Membranoproliferative glomerulonephritis
  • Rapidly progressive glomerulonephritis
  • Defect in collagen synthesis:

Alport syndrome

647
Q

What are the clinical features of Acute Glomerulonephritis?

A

Haematuria
Proteinuria
Decreased urine output (salt and water retention = HTN)
Impaired GFR (Increased Creatinine)
Oedema
Hypertension
Abdominal pain
Rash

648
Q

How is Acute Glomerulonephritis investigated??

A

FBC: mild normochromic +normocytic anaemia
U&Es: increased urea + creatinine, hyperkalaemia + acidosis
Low C3 + normal C4 complement
Renal biopsy
Urinalysis:
- Haematuria
- Red blood cell casts
- Proteinuria (<3.5g per day)
Microscopy: RBC casts

649
Q

What is the management of Acute Glomerulonephritis?

A

Fluid balance (salt restriction + diuretics)
Blood pressure control (ACEi/ARB)
Correct electrolyte imbalance (potassium/ acidosis)
Penicillin: if infection

650
Q

What is Alport Syndrome?

A

X linked recessive disorder associated with hearing loss, ocular defects and progressive kidney disease

Almost always has haematuria

651
Q

What are the terms for upper and lower UTI’s?

A

Upper = Pyelonephritis
Lower = Cystitis

652
Q

What are the main causative organism of UTI’s?

A

E.coli

Klebsiella

653
Q

What is the clinical presentation cystitis?

A

> 6 weeks of:
-Suprapubic pain: worse with a full bladder and relieved by emptying the bladder
-Changes in storage and voiding e.g. bedwetting
- Dysuria
- Suprapubic burning
- Worse during menstruation
- Changes in urineappearance/consistency e.g. cloudy, foul and - haematuria
- Confusion

654
Q

What is the clinical presentation of Pyelonephritis?

A

Similar presentation to lower UTIs + triad of:
1) High fever and rigors
2) Loin-groin/back pain
3) N&V

655
Q

What could dysuria alone mean?

A

Vulvitis in girls

Balanitis in boys

656
Q

What are the investigations for UTI’s?

A

Urinalysis dipstick: only if >3m olds
- Leukocyte esterases
- Nitrites
- Haemoglobin
MSU MCS: mid stream (<3m olds can only use this)
- RBCs
- WBCs
- Bacteria
- Inflammatory markers
Vaginal swab and NAAT: STI
LP
Blood cultures
USS: KUB
DMSA: to asses scarring if pyelonephritis
MCUG: reflux

657
Q

What is the management of UTI’s?

A

IV cefuroxime for 7 days:
THEN
< 3m old: IV Amoxicillin and Gentamycin
> 3m old: Trimethoprim THEN Nitrofurantoin if no response

658
Q

What is Vesicoureteric reflux?

A

Anomaly of vesicoureteric junction where the ureters are displaced laterally and enter bladder directly = not at an angle → back flow

659
Q

What can VUR cause?

A

Incomplete emptying = increase risk of UTI (cystitis)
Renal damage: if high pressure/infrarenal reflux

660
Q

How is VUR diagnosed?

A

Micturating cystourethrogram

661
Q

What is a AKI?

A

Acute decline in kidney function → rise in serum creatinine and/or fall in urine output

662
Q

What are Pre-renal causes of AKI?

A
  • Hypovolaemia (nephrotic syndrome, gastroenteritis and haemorrhage)
  • Circulatory failure
663
Q

What are Renal causes of AKI?

A

Vascular: haemolytic uraemia syndrome/vasculitis

Tubular: acute tubular necrosis

Glomerular: glomerulonephritis

Interstital: pyelonephritis

664
Q

What are Post-renal causes of AKI?

A

Obstruction
Congenital: posterior urethral valves
Acquired: blocked urinary catheter

665
Q

What are secondary causes of AKI?

A

Cardiac surgery
Bone marrow transplant
Toxicity: DRUGS (NSAIDs, vancomycin, acyclovir or aminoglycosides)

666
Q

How are AKI’s diagnosed?

A

Urinary output < 0.5ml/kg/hr for >6 hours

Serum creatinine increased by ≥50% in the past week

Serum creatinine increase by ≥25 µmol/l in 48 hours

Hyperkalaemia

667
Q

What is the management of AKI?

A

Fluids
Furosemide: If urine osmolality low
Renal replacement therapy: if pulmonary oedema/HTN/ not responding to tx

668
Q

What is the management of Hyperkalaemia?

A

Calcium resonium (mild)
IV calcium gluconate (if ECG changes)
Insulin + dextrose (removes K from body)
Diuretics/Dialysis (removes K from body)

669
Q

What is chronic kidney disease?

A

Deterioration of renal function for >3 months

Defined as: eGFR <60, proteinuria or ≥3mg/mmol albumin:creatine ratio

670
Q

What are the causes of CKD?

A
  • Congenital dysplastic kidney
  • Chronic pyelonephritis
  • Glomerulonephritis
  • HTN
  • Adult PKD
  • Diabetic nephropathy
671
Q

What is the clinical presentation of CKD?

A
  • Anorexia/lethargy
  • Polydipsia/polyuria
  • Hypertension
  • Retinopathy
  • Anaemia
  • Failure to thrive
  • Seizures
  • Renal Ricketts
  • Pruritus (itching) (unfiltered phosphorus)
672
Q

What are the investigations for CKD?

A

eGFR:

  • <60 mL/min/1.73m^2

Renal chemistry:

  • Creatinine: high
  • Urea: high
  • Electrolyte abnormalities

Urinalysis:

  • Haematuria +/- proteinuria +/- albuminuria
673
Q

What is the management of CKD?

A

Oralsodium bicarbonate: treats metabolic acidosis

Ironsupplementation andEPO: treats anaemia

Vitamin D

Dialysis

Renal transplantation

674
Q

What is the pathophysiology of T1DM?

A

Autoimmune disorder:
T-cell mediated B-cell destruction in the Islets of Langerhan leading to absolute Insulin Deficiency

675
Q

What % of childhood diabetes is type 1?

A

97%

676
Q

What is the pathophysiology of T2DM?

A

Decreased insulin secretion +/- increased resistance

677
Q

What is the action of insulin?

A

1) Stimulates glycogen formation from glucose in the liver
2) Stimulates glucose uptake from blood → cells
3) Lowers blood sugar

678
Q

What are the investigations for DM?

A

Diabetes:
Random blood glucose: ≥11 mmol/L
- Finger-prick
HbA1C: ≥48 mmol/L
- Average BM over 2-3 months
Random plasma glucose: ≥11 mmol/L
OGTT: ≥11.1 mmol/L
Fasting plasma glucose: ≥7.0. mmol/L
1. Fasting BM
2. 75g glucose
3. Second BM 2 hours later

Pre-diabetes:

HbA1C: ≥42-48 mmol/L

Impaired glucose tolerance: ≥7.8 - 11.1 mmol/L

Impaired fasting glucose: ≥6.1 - 6.9 mmol/L
Asymptomatic:
Same as above on TWO SEPARATE OCCASIONS

679
Q

How does the body respond when insulin is not working efficiently?

A

Gluconeogenesis = produce glucose from amino acids/muscle breakdown

Ketogenesis = fatty acids converted to ketones

680
Q

What is the clinical presentation of diabetes?

A

Weight loss /lean/low BMI (Type 1)

Weight gain (Type 2)

Polyuria

Polydipsia

Lethargy

Impaired growth

Reduced visual acuity

Recurrent infections: e.g. balantitis/pruititus vulvae from repeat candida infections

Acanthosis nigricans

Diabetic foot:
- Pulseless peripherals
- Calluses
- Ulceration
- Charcot join

681
Q

What is the management of diabetes?

A

TYPE 1
1st line: Insulin

TYPE 2
1st line: lifestyle and diet advice (increase exercise, stop smoking, vegetables and oily fish, low carbohydrate and high fibre)

2nd line: metformin

3rd line: metformin + another anti-diabetic (eg. sulfonylureas)

4th line >58 mmol/mol despite treatment: triple therapy (i.e +DPP-4i)

5th line: intermediate-acting insulin + metformin

682
Q

What is the clinical presentation of DKA?

A
  • Vomiting
  • Reduced consciousness
  • Acetone/fruity smell to their breath
  • Kussmaul respiration: deep laboured breathing in an attempt to reverse metabolic acidosis
683
Q

What are the investigation results of DKA?

A

Hyperglycaemia = >7mmol/L

Acidosis pH <7.3

Ketones in urine

684
Q

What is the management of DKA?

A

FIG-PICK

Fluids (over 48 hours) 0.9% NaCl.

Insulin 0.1units/kg/h (fixed rate infusion 1hr after giving fluids )

Glucose

Potassium

Infection

Chart: hourly blood glucose and ECG

Ketones

Avoid bicarbonate as increases risk of cerebral oedema

685
Q

What are clinical features of hypoglycaemia?

A
  • Irritable
  • Sweaty
  • Headache
  • Pallor
  • Drowsy
  • Slurred speech
  • Convulsions
686
Q

How is T3 and T4 produced?

A

1) Hypothalamus secretes thyrotropin-releasing hormone (TRH)
2) Anterior pituitary secretes thyroid-stimulating hormone (TSH)
3) Thyroid releases T3 and T4

687
Q

What are congenital and acquired causes of hypothyroidism?

A

Congenital:
- Dysgenesis
- Dyshormonogenesim
Acquired:
- Prematurity
- Iodine deficiency
- Hashimoto’s Thyroiditis (autoimmune)
- De Quervains thyroiditis
- Drugs

688
Q

What antibodies can be found in Hashimoto’s?

A

Thyroid peroxidase antibodies (Anti-TPO)
Anti-thyrogobulin (Anti-TgAb)

689
Q

What drugs can cause Hypothyroidism?

A

Lithium

Amiodarone

690
Q

What is the clinical presentation of hypothyroidism?

A

Menorrhagia
Myxoedema: autoimmune hypothyroidism

METABOLIC

Marcocytosis

Oedema (incl orbital)

Thyroid goiter

Anaemia

Bradycardia

Obesity

Lateral eyebrow loss

Irregular menstruation

Constipation
Learning difficulties

(Congenital normally picked up on screening and asymptomatic)

691
Q

What are the investigations for hypothyroidism?

A

Thyroid function test:
Primary hypothyroidism: ↑ TSH, ↓ T3 & T4
Secondary hypothyroidism: ↓ TSH, ↓ T3 & T4

ESR and CRP: de Quervain’s thyroiditis

Anti-TPO and Anti-TgAb: hashimotos thyroiditis
Guthrie test (heel-prick): IDENTIFIES CONGENITAL COAUSES

692
Q

What is the management for hypothyroidism?

A

Levothyroxine (replacement T4)

693
Q

What are the causes of hyperthyroidism?

A

Grave’s disease (autoimmune)
Toxic multi-nodular goitre
De Quervains thyroiditis
Drugs

694
Q

What antibodies can be found in Grave’s disease (hyperthyroidism)?

A

Anti-TSH receptor antibodies (Anti-TSH)

695
Q

What drugs can cause Hyperthyroidism?

A

Amiodarone

696
Q

What are the most common causes of Thyrotoxicosis?

A

Graves Disease

Thyroid Eye Disease

Amiodarone

697
Q

What is the clinical presentation of hyperthyroidism?

A

General: THYROIDISMG

Tremor

Heart rate increase

Yawning

Restless

Oligomenorrhoea

Irritability

Diarrhoea

Intolerance to heat

Sweating

Muscle wasting (weight loss)

Goitre

Grave’s disease:

  • Diffus Goitre
  • Grave’s eye disease
  • Pretibial myoexoedema (musin deposits in skin)
  • Bilateral exophthalmos

Toxic multi-nodule goitre:

  • Goitre with firm nodules
698
Q

What are the investigations for hyperthyroidism?

A

Thyroid function test: ↓ TSH, ↑ T3 & T4
ESR and CRP: de Quervain’s thyroiditis
Anti-TSH
Anti-TPO
Anti-TgAb

699
Q

What is the management for hyperthyroidism?

A

Grave’s disease:
- Carbimazole (anti-thyroid drug): titration-block or block and replace

General:
- Radioactive iodine
- Beta blockers: e.g. propranolol for symptomatic relief
- Surgical resection

700
Q

What is the management of Thyroid storm/crisis?

A
  • IV hydrocortisone
  • IV Fluids
  • Propanolol
701
Q

What is Congenital Adrenal Hyperplasia?

A

1) Autosomal recessive mutation in chr 6
1) Defective 21-hydroxylase enzyme
1) Less gluco+ mineralocorticoids produced
1) More testosterone made

702
Q

What is the clinical manifestation of Congenital Adrenal Hyperplasia?

A

Hyponatraemia
Hypoglycaemia
Hyperkalaemia

703
Q

How is Congenital Adrenal Hyperplasia diagnosed?
How is it diagnosed?

A

SALT-LOSERS: (no aldosterone production)
- Hyponatraemia
- Hypoglycaemia
- Hyperkalaemia
- Metabolic acidosis
- Hypoglycaemia
- Elevated 17alpha-hydroxyprogesterone

704
Q

What is the management of Congenital adrenal hyperplasia?

A

IV fluids: restores electrolyte levels
Glucocorticoids: fludrocortisone
Cortisol: IV hydrocortisone

705
Q

What is Kallmann’s?

A

Hypogonadotrophic hypogonadism causing:
- Delayed puberty
- Anosmia

706
Q

Define precocious puberty

A

Development of secondary sexual characteristics before:
- 8 years in females
- 9 years in males

707
Q

What is Thelarche?

A

First stage of breast development

708
Q

What is Adrenarche?

A

Maturation of the adrenal gland → androgen production → body odour and mild acne

709
Q

What is pubarche?

A

Growth of pubic hair

710
Q

What is the first sign of puberty in girls?

A

Thelarche

711
Q

What is the first sign of puberty in boys?

A

First ejaculation and testicular size >3ml

712
Q

Define delayed puberty

A

The absence of secondary sexual characteristics by age 14 or 16

713
Q

What must you rule out as a cause of delayed puberty in girls?

A

Turner syndrome (45X0)

714
Q

What is the likely cause of delayed puberty in boys?

A

Constitutional delay (runs in the family)

715
Q

What must you rule out as a cause of precocious puberty in boys?

A

Brain tumour

716
Q

How would you treat precocious puberty?

A

GnRH super-agonists can be given to suppress pulsatility of GnRH secretion

717
Q

What is the Gonadotrophin pathway?

A

1) GnRH (from hypothalamus) → increased FSH+LH
2) Testes/ovaries → increased testosterone & oestrogen/progesterone → inhibited FSH/LH secretion

718
Q

What is Juvenile idiopathic arthritis (JIA)?

A

Joint swelling/stiffness
>6 weeks
Aged <16
No other cause is identified

719
Q

How is Juvenile idiopathic arthritis (JIA) classified?

A

Oligoarticular: 1-4 joints in first 6 months
Polyarticular RF -ve: 5+ joints in first 6 months
Polyarticular RF +ve: 5+ joints in first 6 months /+ve RF seen on two occasions
Systemic onset JIA: Arthritis + 2 weeks fever
Psoriatic: arthritis + psoriasis

720
Q

What symptoms are associated with Juvenile idiopathic arthritis (JIA)?

A

Fluctuating fever
Salmon-pink rash
Uveitis
Pain
Morning stiffness
Swelling
Psoriasis
Dactylitis
Nail pitting
Rash
Uveitis

721
Q

What are the complications of Juvenile idiopathic arthritis (JIA)?

A

Chronic anterior uveitis

Growth failure

Osteoporosis

722
Q

What are the investigations of Juvenile idiopathic arthritis (JIA)?

A

MCV: normocytic anaemia
FBC:
- Raised: WCC, CRP, ESR, platelets and serum ferritin.
RF / HLA-B27
MSK examination
X-rays

723
Q

What is the management of Juvenile Idiopathic arthritis (JIA)?

A

NSAIDs
Analgesics
Corticosteroid tablets/injections
DMARDs (e.g. methotrexate)
TNFi (infliximab)
IL 6 inhibitor (tocilizumab)

724
Q

What is juvenile-onset systemic lupus erythematosus (JSLE)?

A

Chronic autoimmune disease affecting every organ of the body
Relapsing and remitting

725
Q

What is the clinical manifestation of juvenile-onset systemic lupus erythematosus (JSLE)

A

SOAP BRAIN MD
Serositis (pleuritis/pericarditis)
Oral ulcers
Arthritis
Photosensitivity

Blood (pancytopenia)
Renal (proteinuria)
ANA +ve (anti-nuclear antibody)
Immunological
Neurological (psych/seizures)

Macular rash (salmon-pink)
Discoid rash

726
Q

What is the treatment for juvenile-onset systemic lupus erythematosus (JSLE)?

A

No cure
Avoid sun and use sunscreen
Corticosteroid (prednisolone)
DMARD (hydroxychloroquine)
NSAIDs

727
Q

What is Osteomyelitis?

A

Inflammation of the bone/bone marrow
Normally limited to one bone, but can be at multiple sites
Can be in periphery or axial skeleton

728
Q

Where are the most common sites of Osteomyelitis?

A

Distal femur

Proximal tibia

729
Q

What are the most common causes of bacterial Osteomyelitis?

A

S. Aureus

H. influenza

Group A beta haemolytic strep

730
Q

What are the clinical manifestations of Osteomyelitis?

A

Severe pain

Immobile limb (pseudo paresis)

Swollen over area

Acute febrile illness (lethargy/high temp)

731
Q

What are the investigations for Osteomyelitis?

A

X-ray
MRI
Blood cultures
FBC: Raised WCC/CRP

732
Q

What is the treatment for Osteomyelitis?

A

1) >3m old = 7 days IV Cefuroxime
2) THEN + 5 weeks oral (if tolerated and CRP <10):
- Flucloxacillin: S.aureus
- Co-amoxiclav: if unsure

733
Q

What is septic arthritis?

A

Infection of the joint space: can lead to bone destruction

734
Q

What should you assume in a limping child?

A

Septic arthritis until proven otherwise

735
Q

What are the most common causes of septic arthritis?

A

1) S. aureus
2) H. influenza

736
Q

What is the clinical presentation of septic arthritis?

A

Suspected in all monoarthritic cases: especially the knee

Hot, swollen, painful and restricted joint

Acute

Systemic symptoms

737
Q

What are the investigations of septic arthritis?

A

Hot joint policy: presume patient has septic arthritis until its excluded
Aspirate synovial joint: **MCS, FBC & crystal examination
- WCC, CRP/ESR

738
Q

What is the management of septic arthritis?

A

Abx

Therapeutic joint aspiration

Analgesia

739
Q

What is Developmental dysplasia of the Hip (DDH)?

A

Neonatal hip joint abnormality

740
Q

What are the risk factors of Developmental dysplasia of the Hip (DDH)?

A
  • Female 6x more likely
  • Breech presentation
  • FHx
  • Firstborn child
  • Oligohydramnios
741
Q

What is the clinical presentation of Developmental dysplasia of the Hip (DDH)?

A

Asymmetry
Abnormal gait:
- Affected hip externally rotated
- Toe-Walking on affected side
- Waddling gait

742
Q

What are the investigations of Developmental dysplasia of the Hip (DDH)?

A

Barlow Test = attempt to dislocate femoral head posteriorly
Ortolani Test = attempt to relocate a dislocated femoral head
Dynamic US: early diagnosis important as if appropriately aligned in first few months = resolve spontaneously
USS:
- Femoral head coverage <50%
- Alpha angle <60 degrees
CT
MRI

743
Q

What is the management of Developmental dysplasia of the Hip (DDH)?

A

Most spontaneously stabilise in 3-6 weeks

Pavlik harness (flexion-abduction orthosis) if <4-5m old

744
Q

What is Perthe’s Disease?

A

Temporarily disrupted blood flow to femoral head causing avascular necrosis in children aged 4-8yrs

745
Q

What is the clinical presentation of Perthe’s Disease?

A

Hip/groin pain
Limp
Restricted hip movements
Referred pain to the knee

746
Q

How is Perthe’s Disease diagnosed?

A

Limited abduction and internal rotation
X-ray: abnormal ossification
Blood tests: excludes inflammation
Technetium bone scan
MRI

747
Q

What is the treatment of Perthe’s disease?

A

Bed rest
Traction
Crutches
Analgesia

748
Q

What is Slipped Upper femoral epiphysis (SUFE)?

A

Slipped capital femoral epiphysis
Femoral head slips through a growth plate fracture

749
Q

What is the clincal presentation of Slipped Upper femoral epiphysis (SUFE)?

A

Hip, groin, thigh or knee pain
Restricted internal rotation
Painful limp
Restricted range of hip movement
Hip kept in external rotation

750
Q

How is Slipped Upper femoral epiphysis (SUFE) diagnosed?

A

X-ray

751
Q

What is the treatment for Slipped Upper femoral epiphysis (SUFE)?

A

Surgical pinning of the hip

752
Q

What is Achondroplasia?

A

Autosomal dominant
Most common form of short-limb dwarfism due to REDUCED growth of cartilaginous bone

753
Q

What is the clinical presentation of Achondroplasia?

A
  • Large skull
  • Normal trunk
  • Short arms and legs
  • Short stature
  • Frontal bossing
  • Marked lumbar lordosis
  • Bow legs (genu varum)
  • Disproportionate skull
  • Foramen magnum stenosis
754
Q

What is osteoporosis?

A

Low bone density and micro-architectural defects in bone tissue with normal mineralisation

Increased bone fragility and susceptibility to fracture

755
Q

Define osteoporosis in children.

A

1) > 1 vertebral crush fracture
OR
2) Bone density 2 long bone fractures (before age 10) or >3 fractures (age 19).

756
Q

What are inherited and acquired causes of osteoporosis?

A

Inherited: osteogenesis imperfecta

Acquired: drug induced, malabsorption

757
Q

What is osteopenia?

A

Stage before osteoporosis: less severe

758
Q

What is the clinical presentation of osteoporosis?

A

Asymptomatic: with the exception of fractures

Common fragility fractures: vertebral crush, radial wrist (Colles’ fracture) and proximal femur

759
Q

What investigations should be ordered for osteoporosis?

A

Dual-energy X-ray absorptiometry (DEXA) scan: measures bone loss
- T score <2.5 = osteoporosis

760
Q

What is the management of osteoporosis?

A

Vitamin D and calcium supplements (AdCal-D3)

Stop smoking

HRT: to prevent fragility fracture in high risk women

Anti-resorptive drugs:
- Biphosphonates: alendronate (inhibits osteoclast activity)
- Oestrogen (promotes osteoblast formation)
- Denosumab
Anabolic drugs
- Parathyroid hormone receptor agonists

761
Q

What is Osteogenesis Imperfecta?

A

Autosomal dominant condition
Increased fragility of bone (collagen type 1 = bone/teeth)

762
Q

What is the clinical presentation of Osteogenesis Imperfecta?

A
  • Hypermobility
  • Blue/grey sclera(the “whites” of the eyes)
  • Triangular face
  • Short stature
  • Deafness
  • Dental problems
  • Bone deformities: bowed legs and scoliosis
  • Joint and bone pain
  • Fractures
  • Bruises
763
Q

What classification is used in osteogenesis imperfecta?

A

Sillence classification

764
Q

How is Osteogenesis Imperfecta investigated?

A

Clinical diagnosis
X-rays: diagnoses fractures and bone deformities
Genetic testing
Bone densitometry

765
Q

How is Osteogenesis Imperfecta treated?

A

IV pamidronate: reduces fracture incidence, increases bone mineral density, reduces pain and increases energy levels
Oramorph or IV morphine
Bisphosphates: alendronate to increase bone density
Vitamin D: prevents deficiency

766
Q

What is Rickets?

A

A disorder of bone mineralisation leading to bone weakness
Caused by vitamin D deficiency

767
Q

Whatis the clinical presentation of rickets?

A

Bowed legs
Knock knees
Rachitic rosary (expanded ribs)
Craniotabes (soft skull)
Delayed closure of the sutures
Frontal bossing
Delayed teeth
bowing of legs
Growth failure
Bone pain

768
Q

What are the investigations for Rickets?

A

Serum 25-hydroxyvitamin D: < 25 nmol/L
X-ray

769
Q

What is the management of Rickets?

A

Correct deficiency: i.e colecalciferol + calcium

770
Q

What Hb figures show anaemia in

Neonates?

1-12 months?

1-12 years?

A

Neonate: <140g/L

1-12months: <100g/L

1-12years: <110g/L

771
Q

What are causes of anaemia?

A

Impaired red cell production (Iron deficiency)
Increased red cell destruction (haemolytic disease of newborn, thalassaemias, sickle cell and G6PD deficiency)
Blood loss (meckel’s diverticulum and von willebrand disease)

772
Q

What is the clinical presentation of anaemia?

A

Jaundice → kernicterus
Oedema
Hepatosplenomegaly
Fatigue
Headaches
Dizziness
Pale skin
Conjunctival pallor
Angular cheilitis
Glossitis
Aphthous ulcers
Tachycardia

773
Q

What are causes of iron-deficiency?

A
  • Excessive bleeding (menorrhagia or GI bleed)
  • Poor dietary intake (poor feeding)
  • Malabsorption (CMPI)
  • Increased requirements (growth spurts or pregnancy)
774
Q

What is the clinical presentation of Iron deficiency anaemia?

A

Fatigue
Pica
Pale skin
Angular chelitis
Atrophic glossitis
Post-cricoid webs
Koilonychia
Brittle hair and nails
Hair loss

775
Q

What are the investigations for iron deficiency anaemia?

A

Hb
FBC
MCV: microcytic hypo chromic reticulocytes
Transferrin saturation: Increased in iron deficiency
Low ferritin and serum Fe

776
Q

What is the management of iron deficiency anaemia?

A

Treat cause:
Ferrous sulphate (oral iron therapy)
- May cause N/D/V, abdo pain and constipation
Iron rich diet
- Meat and dark green vegetables
Blood transfusion

777
Q

What is G6PD?

A

Enzyme essential for preventing oxidative damage to red cells

RBCs lacking G6PD = exposed to oxidant induced haemolysis

778
Q

How is G6PD transmitted?

A

X-linked

779
Q

What is the clinical presentation of G6PD?

A

Intermittant neonatal jaundice
Anaemia
Gallstones
Splenomegaly
Acute intravascular haemolysis (triad signs below):
- Dark urine
- Fever
- Flank pain

780
Q

What investigations are used for G6PD?

A

Blood film: Heinz bodies
G6PD enzyme assay

781
Q

What is the management of G6PD?

A

Avoid triggers

782
Q

What is sickle cell?

A

Autosomal recessive

Misshapen β-globin= HbS

RBC sickled, fragile and prone to haemolysis

Can get stuck in capillaries→ vaso-occlusive crisis

783
Q

What are the investigations for sickle cell disease?

A

Newborn screening with Guthrie heel prick:
- Screening is offered during pregnancy.
FBC:normocytic anaemia with reticulocytosis
Blood film:sickled RBCs, target cells and Howell-Jolly bodies
Hb electrophoresis and solubility: diagnostic (increased HbS and reduced/absent HbA)

784
Q

What is the management for sickle cell disease?

A

Hydroxycarbamide (chemotherapy increases HbF)

Blood transfusions

785
Q

How does HbS form?

A

Mutation on codon 6 of B-globulin gene
Change in AA sequence from: Glutamine → Valine

786
Q

What is β-Thalassemia?

A

Excess of alpha chains

Autosomal recessive HBB gene on chr 11

HbA2 RAISED = ANAEMIA

787
Q

What is the management of β-Thalassemia?

A

Long term folic acid

Bone marrow transplant

Regular transfusions

788
Q

What is hereditary spherocytosis?

A

Autosomal dominant mutations changes RBC shaped from concave to sphere
Shape sphere RBC get destroyed as they pass through the spleen
Causes haemolytic anaemia

789
Q

What can trigger spherocytosis?

A

Parvovirus infection

790
Q

How is hereditary spherocytosis diagnosed?

A

Clinically
FHx
Blood film: spherocytes
MCHC: raised
FBC: raised reticulocytes

791
Q

How can spherocytosis be treated?

A

Oral folic acid

Splenectomy: if severe

792
Q

What is Immune Thrombocyotpenic Purpura (ITP)?

A

Destruction of platelets by IgG autoantibodies

793
Q

What is the clinical presentation of Immune Thrombocyotpenic Purpura (ITP)?

A

Asymptomatic
Prolonged bleeding
Petachie
Purpura/bruising

794
Q

What is the management of Immune Thrombocyotpenic Purpura (ITP)?

A

Prednisolone & IV IgG
Rituximab(monoclonal antibody used in cancer)

795
Q

What are the investigations for Immune Thrombocyotpenic Purpura (ITP)?

A

Dx of exclusion
Low platelets!

796
Q

What is Von Willebrand Haemophilia?

A

Abnormality to vWF→ no adhesion between platelets and damaged endothelium→ excessive bleeding

797
Q

What is the management of vWF?

A

Tranexamic acid (stop excessive bleeding post surgery)
In response to bleeds: IV infusion of vWF, desmopressin or IV factor VII

798
Q

What is Acute Lymphoblastic Leukaemia (ALL)?

A

Lymphoblast proliferation in the bone marrow: B cell lineage

Associated with down syndrome

799
Q

What is the most common cancer in children?

A

Acute Lymphoblastic Leukaemia (ALL)

800
Q

What is the clinical presentation of Acute Lymphoblastic Leukaemia (ALL)?

A
  • Increased infections (leukopenia)
  • Bone and joint pain: due to marrow expansion
    Petechiae and epistaxis: due to thrombocytopenia
  • Hepatosplenomegaly (blast cells enlarge →abdominal distension)
  • Lymphodenopathy (settle in lymph nodes)

Abdominal fullness and pain: (due to hepatosplenomegaly)

B-cell symptoms (night sweats, fever and weight loss)

Pallor and Fatigue: anaemia

Failure to thrive

801
Q

What are the causes of Acute Lymphoblastic Leukaemia (ALL)?

A

[t(12;21] or [t(9;22)] mutations

802
Q

What are the investigations for Acute Lymphoblastic Leukaemia (ALL)?

A

FBC: pancytopenia

Blood film: blast cells

Bone marrow biopsy (CONFIRMS)

803
Q

What is the treatment for Acute Lymphoblastic Leukaemia (ALL)?

A

Chemotherapy
Allopurinol: tumour lysis syndrome from chemotherapy can release uric acid → Gout

Radiotherapy
Stem cell transplantation for:
- Girls: 2 years
- Boys: 3 years
Surgery

804
Q

What are the 5 stages of Chemotherapy?

A

1) Induction
2) Consolidation
3) Interim maintenance
4) Delayed intensification
5) Maintenance

805
Q

Give 5 late effects of cancer treatment in children

A

Endocrine related e.g. growth and development problems.
Intellectual.
Fertility problems.
Psychological issues.
Cardiac and renal toxicity

806
Q

What are neuroblastoma tumours?

A

Tumours arising from neural crest tissue in the adrenal medulla and sympathetic nervous system

807
Q

What is the clinical presentation of Neuroblastoma’s?

A

1) Abdo mass (can be anywhere on sympathetic chain)
2) METASTASES SYMPTOMS

808
Q

How are neuroblastoma’s diagnosed?

A

Raised urinary catecholamines
Biopsy
MIBG scan (radiolabelled tumour-specific agent)

809
Q

Describe the treatment for a neuroblastoma malignancy.

A

Chemotherapy
Radiotherapy
Surgery

810
Q

What is Wilm’s tumour?

A

Most common renal tumour in childhood that is:
- Unilateral
- Presents as asymptomatic abdominal mass

811
Q

What is the clinical presentation of a Wilm’s tumour?

A

Abdominal mass
Haematuria
Abdominal pain
Anorexia
Anaemia

812
Q

What are the investigations for Wilm’s tumour?

A

US
CT/MRI: staging
Biopsy: staging

813
Q

Describe the treatment for Wilm’s tumour

A

Chemotherapy
Nephrectomy
Radiotherapy

814
Q

What are signs of a raised ICP?

A

Headache
Change in behaviour
Nausea/vomiting
Over-sleepy
Papilloedema (may decrease visual acuity)

815
Q

What is retinoblastoma?

A

Malignant tumour of retinal cells (eye)
Mutated RB1on chr 13

816
Q

What is the clinical presentation of Retinoblastomas?

A
  • Loss of red-reflex: replaced by white pupil (leukocoria)
  • Pain around the eye
  • Poor vision
817
Q

How are retinoblastomas diagnosed?

A

MRI

818
Q

What is the management of retinoblastoma’s?

A

1st line: Laser therapy
Chemotherapy + radiotherapy
Phototherapy
Surgical repair/removal

819
Q

Name the 5 components of the traffic light system for an unwell child

A

CRACO
1) Colour (skin, lips, tongue)
2) Activity
3) Respiratory
4) Circulation/Hydration
5) Other

820
Q

Name high risk signs of an unwell child (Traffic light)

A

Colour :
- Pallor
- Blue

Activity :
- Not responding to social cues
- Does not stay awake
- High pitched cry

Respiratory :
- Grunting
- Tachypnoea
- Chest in-drawing
- RR >60

Circulation/Hydration :
- Reduced skin turgor
- Tachycardia

Other :
- Temperature
- Non-blanching rash
- Bulging fontanelle
- Neck stiffness
- Status epilepticus
- Focal signs/seizures

821
Q

What heart rate is a high risk sign for the following ages:

<12 months?

12-24 months?

2-5 yrs?

A

<12m: >160 bpm

12-24m: >150bpm

2-5yrs: >140bpm

822
Q

What temperature is a high risk sign for the following ages:

<3 months?

3-6 months?

A

<3m: >38°

3-6m: >39°

823
Q

What breathing rate is a high risk sign for the following ages:

6-12 months?

> 12 months?

A

6-12m: >50

> 12m: >40

824
Q

How do you calculate the rate at which to give maintenance fluids to a child?

A

100ml/Kg/day: for first 10Kg

50ml/Kg/day: for the next 10Kg

20ml/Kg/day: for every Kg after that

825
Q

What fluid would you give to a neonate?

A

0.9% Sodium Chloride + 5% glucose +/- KCl

826
Q

Why is it important to avoid rapid rehydration?

A

Cerebral oedema

827
Q

How much should you feed to a neonate?

A

150ml/Kg/day

828
Q

Radiology: give 5 ways in which imaging a child differs to imaging an adult?

A
  1. Size
  2. Growth plates
  3. Skill sutures
  4. Ossification
  5. Congenital problems e.g. dextrocardia and osteogenesis imperfecta
829
Q

What is Respiratory Distress Syndrome?

A

1) Insufficient surfactant production in immature lungs
2) Lung cannot provide body with enough oxygen due to surfactant disruption → to lung collapse

830
Q

What is the pathophysiology of respiratory distress syndrome?

A
  • Sepsis, pneumonia, trauma or aspiration
  • Premature birth: not enough surfactant produced
831
Q

What are the risk factors for RDS?

A

Prematurity
C-section

832
Q

What is the clinical presentation of RDS?

A

Tachypnoea: RR 40-60/ >60
Subcostal and intercostal recession
Stridor
Cyanosis

833
Q

What are the investigations for RDS?

A

Nasopharyngeal aspirate: PCR
Bloods: amylase, FBC, U+E, CRP
CXR: bilateral diffuse infiltrates, hyperinflation, air trapping and focal atelectasias
PCWP: pulmonary capillary wedge pressure (<19mmHg)
Pulse oximetry
ABG: Refractory hypoxaemia

834
Q

What is the treatment of respiratory distress syndrome?

A

Antenatal steroids (i.e. dexamethasone to induce foetal lung maturation)
O2
Intubate
CO2 monitoring
Endotracheal surfactant
Nasal CPAP
Mechanical ventilation + Intubation
Supplementary oxygen
Fluids

3a Exam (9 decks)

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