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MRCPCH Clinicals > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Common organisms causing croup

A

Parainfluenza virus
Human metapneumovirus
RSV
Influenza

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2
Q

Common organisms causing bronchiolitis

A 
RSV in 80%
Human metapneumovirus
Parainfluena
Rhinovirus
Adenovirus
Mycoplasma pneumoniae
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3
Q

What is asthma?

A

Chronic inflammatory disease of airways where airway inflammation leads to airway oedema, and hyperactivity resulting in reversible bronchoconstriction

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4
Q

Management of acute asthma

A 
Positioning
Oxygen
Salbutamol
Ipratropium bromide
Steroids (pred or hydrocortisone)
IV magnesium sulphate
IV salbutamol
Theophylline
IV adrenaline
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5
Q

What kind of drug is ipratropium bromide?

A

Anticholinergic

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6
Q

What kind of drug is salbutamol?

A

Beta 2 agonist

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7
Q

What is the purpose of ipratropium bromide in management of asthma?

A

Augments the action of the beta-2 agonists

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8
Q

What kind of drug is montelukast?

A

Leukotriene receptor antagonist

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9
Q

What are some examples of long acting beta-2 agonists?

A

Salmetero, eformoterol

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10
Q

When should a LABA not be used?

A

Children under 5 or as first line prevention

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11
Q

What is omalizumab?

A

Murine recombinant monoclonal antibody

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12
Q

What is the mechanism of action of omalizumab?

A

Blocks IgE which suppresses early- and late-phase allergic responses and sputum eosinophilia

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13
Q

What is the mechanism of action of tiotropium?

A

Long acting anticholinergic drug

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14
Q

What are the BTS guidelines for asthma management (non acute)?

A
  1. SABA
  2. Low dose inhaled steroid
  3. If >5: LABA, increase steroid, then LTRA
    If <5: LTRA
  4. Increase steroid again
  5. Regular oral steroid and refer to resp
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15
Q

What is the definition of bronchopulmonary dysplasia?

A

Oxygen requirement beyond 36 weeks post conceptual age

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16
Q

What is the mechanism of action of caffeine for neonates?

A
  1. Decreases CNS effects of adenosine
  2. Stimulates breathing by:
    - Enhancing CO2 sensitivity
    - Increasing diaphragmatic activity
    - Increasing minute ventilation
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17
Q

What makes premature babies at risk of BPD?

A
  • Premature antioxidant system
  • Surfactant deficiency
  • Very compliant chest wall
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18
Q

What is the pathophysiology of BPD?

A
  • Developmental arrest of alveologenesis and vasculogenesis
  • dysregulated angiogenesis
  • Leads to large, simplified alveoli and dysmorphic lung vasculature
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19
Q

What is the prognosis for BPD?

A

50% rehospitalised in first 2 years

More likely to have hyper-reactive airways and respiratory tract infections

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20
Q

What is croup?

A

Viral laryngotracheobronchitis

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21
Q

Which organisms cause croup?

A

Parainfluenza
Influenza
RSV
Rhinovirus

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22
Q

In what age is croup commonest?

A

6 months to 5 years

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23
Q

Is croup more common in girls or boys?

A

Boys

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24
Q

What is the management for croup?

A

Steroids
Inhaled budesonide
Nebulised adrenaline
Intubate

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25
Q

Treatment for tuberculosis?

A

RIPE:
Rifampicin + isoniazid (6 months)
Pyrazinamide + ethambutol (2 months)

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26
Q

Side effects of rifampicin

A

Orange urine/tears
Hepatic enzyme induction
Abnormal LFTs

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27
Q

Side effects of isoniazid

A

Abnormal LFTs

Peripheral neuropathy

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28
Q

Side effects of pyrazinamide

A

Liver toxicity

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29
Q

Side effects of ethambutol

A

Visual disturbance

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30
Q

Which TB drug should be avoided in very young children?

A

Ethambutol

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31
Q

What drug can be given as prophylaxis for a neonate born to a mother with active TB?

A

Isoniazid

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32
Q

What are the 3 types of CCAM?

A

Type 1 - single or multiple large cysts
Type 2 - multiple small cysts
Type 3 - solid mass

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33
Q

What is a congenital lobar sequestration?

A

Mass of non-functional lung with abnormal communication with airway, usually supplied by systemic circulation

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34
Q

Which lobes of the lung are most commonly affected by congenital lobar sequestration?

A

Lower lobes, left

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35
Q

What are bronchogenic/duplication cysts?

A

Remnant of primitive foregut derived from abnormal tracheobronchial budding - they contain normal tracheal tissue filled with fluid

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36
Q

What is congenital lobar emphysema?

A

Overinflation of the lobe as a result of intrinsic deficiency of bronchial cartilage ± elastic tissue

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37
Q

Where does congenital lobar emphysema affect?

A

Rare in lower lobes - usually left upper or right middle/upper

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38
Q

How does congenital lobar emphysema present?

A

Asymptomatic
Respiratory distress in neonatal period
Chest asymmetry
Hyperresonance

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39
Q

How is congenital lobar emphysema managed?

A

Lobectomy if respiratory distress

Conservatively if mild symptoms

40
Q

What is congenital lobar emphysema often associated with?

A

1:6 have a cardiac abnormality

41
Q

What is Scimitar syndrome?

A

Hypoplastic right lung with anomalous venous drainage, usually to IVC or right atrium ± systemic collateral arterial supply

42
Q

What is the scimitar sign?

A

Vertical line caused by the right upper lobe pulmonary vein running into the IVC

43
Q

How does scimitar syndrome present?

A

Asymptomatic, or can lead to recurrent infections

44
Q

How is scimitar syndrome managed?

A

Surgical correction for vascular abnormality

45
Q

What is the incidence of CDH?

A

1:2500-3500 births

46
Q

On which side is CDH more common?

A

Left

47
Q

What is the prognosis of CDH?

A

20-40% mortality rate

48
Q

What is the cause of alveolar proteinosis?

A

Uncertain; some relate to deficiency of surfactant-associated protein B, some to gm-csf
Lipid-laden type II pneumocystis desquamate into the alveolar spaces

49
Q

What is the prognosis for alveolar proteinosis?

A

Almost universally fatal in infants, in older children lung lavage can help

50
Q

What is congenital pulmonary lymphangiectasia?

A

Rare dilatation of pulmonary lymphatics leading to severe neonatal respiratory distress and pleural effusions

51
Q

What is congenital pulmonary lymphangiectasia associated with?

A

Congenital cardiac disorders like obstructed venous drainage

52
Q

What causes obliterative bronchiolitis?

A

Viral infection, often adenovirus or myoplasma

Less often measles, RSV, or lung or bone marrow transplant

53
Q

What is the pathophysiology of obliterative bronchiolitis?

A

Severe widespread small airway obstruction eventually leading to pulmonary hypertension

54
Q

What is the radiological appearance in obliterative bronchiolitis?

A

Patchy areas of air trapping (honeycomb), patchy pruning of vascular markings, hyper inflated lungs

55
Q

What is the management of obliterative bronchiolitis?

A

In early stages may respond to bronchodilators or steroids, but often no treatment is successful

56
Q

What can obliterative bronchiolitis progress to?

A

Swyer-James or Macleod syndrome of unilateral hyper lucent lung with diminished vascularity

57
Q

What is the pathophysiology of haemosiderosis?

A

Repeated episodes of pulmonary haemorrhage lead to an accumulation of haemosiderin in the alveoli

58
Q

What causes haemosiderosis?

A

Uncertain - some are associated with CMPA, some with Goodpasture syndrome

59
Q

What are the symptoms of haemosiderosis?

A

Usually episodic fever, dyspnoea, wheeze ± haemoptysis

60
Q

How is haemosiderosis diagnosed?

A

By finding haemosiderin-laden macrophages in a BAL

61
Q

How is haemosiderosis managed?

A

Steroids

Hydroxychloroquine or other immunosuppressives, treat the anaemia and hypoxia

62
Q

What is the pathophysiology of pulmonary hypertension?

A

Chronic hypoxia leads to pulmonary vasoconstriction and arterial wall change

63
Q

What are the management options for pulmonary hypertension?

A 
High oxygen
Nitric oxide
Sildenafil
Prostacyclin
Nifedipine
64
Q

How is cystic fibrosis inherited?

A

Autosomal recessive - multiple mutations but most common is delta F508

65
Q

What is the cause of cystic fibrosis?

A

Mutation affects cystic fibrosis transmembrane conductance regulator (CFTR), which is a cyclic AMP regulated chloride channel on the apical surface of epithelial cells which also inhibits the epithelial sodium channel. In CF, the respiratory epithelium therefore fails to secrete chloride ions (fails to absorb in the sweat gland, hence the high sweat chloride), and hyper absorbs sodium ions and hence H2O. Secretions are viscid and the airway surface is dehydrated.

66
Q

What are the pathophysiological features of CF?

A

Dehydration of mucus and airway surface liquid
Disturbed mucociliary clearance
Increased risk of airway infection
Inflammation associated with progressive lung disease

67
Q

What is the incidence of CF?

A

Carriers are 1:25, disease is in 1:2500 births of white babies

68
Q

What is ABPA?

A

Complex hypersensitivity reaction in response to colonisation of airways with Aspergillus fumigatus

69
Q

Who gets ABPA?

A

Almost exclusively people with asthma or CF

70
Q

What is the pathophysiology of ABPA?

A

Mucoid impaction of bronchi
Eosinophilic pneumonia
Bronchocentric granulomatosis

71
Q

What are the symptoms of ABPA?

A

Recurrent exacerbations of fever, malaise, expectoration of brownish mucus plugs, wheeze, rhinosinusitis

72
Q

What is the management of ABPA?

A

Steroids
Antifungals e.g. itraconazole
Omalizumab may be useful if recurrent

73
Q

How is ABPA diagnosed?

A

Establishing sensitisation to Aspergillus antigens

74
Q

How is CF diagnosed?

A

Guthrie tests immune reactive trypsin, which will be high
Sweat test
Genetic testing

75
Q

What is a diagnostic sweat test value?

A

> 60mmol/l chloride in at least 100mg sweat

76
Q

How is primary ciliary dyskinesia inherited?

A

Autosomal recessive

77
Q

How common is primary ciliary dyskinesia?

A

1:15,000 births

78
Q

How does primary ciliary dyskinesia present?

A 
Neonatal respiratory distress and rhinorrhoea
Recurrent LRTIs
Sinus disease
Glue ear
Male infertility and female subfertility
79
Q

What other conditions can primary ciliary dyskinesia be associated with?

A

40% have dextrocardia ± abdominal situs inversus (Kartagener syndrome)

80
Q

How is primary ciliary dyskinesia diagnosed?

A

Nasal brushing for ciliary beat frequency, assessment of beat coordination and structure
Low exhaled/nasal nitric oxide

81
Q

Which genes are implicated in primary ciliary dyskinesia?

A

DNAI1 and DNAH5 - identified in 40% of families with PCD

82
Q

What is the treatment for primary ciliary dyskinesia?

A

Physiotherapy
Antibiotics
ENT and hearing assessment
Genetic counselling

83
Q

What is the incidence of OSA?

A

2%

84
Q

What is the peak age for OSA?

A

2-8 years

85
Q

What are the contributing factors to OSA?

A

Increased upper airway resistance
Decreased neuromuscular activation
Altered ventilatory control
Changed arousal thresholds

86
Q

What are the features of OSA?

A

Repetitive collapse of the pharyngeal airway
Intermittent hypercarbic hypoxia
Recurrent transient arousal

87
Q

How is OSA diagnosed?

A

Polysomnography

88
Q

What are the symptoms of OSA?

A

Snoring, snorting
Sleep disturbance
Non-refreshing sleep
Daytime sleepiness

89
Q

What are the surgical options for OSA?

A

Adenotonsillectomy
Mandibular distraction
Maxillomandibular advancement
Tracheostomy

90
Q

What are the medical/conservative options for OSA?

A

Intranasal corticosteroids
Leukotriene antagonists
Weight loss
Ventilatory support

91
Q

How common is choanal atresia?

A

1:60-70,000 births

92
Q

What causes choanal atresia?

A

Failure of the breakdown of the bucconasal membrane, leading to complete obstruction of the nostril(s)

93
Q

Which conditions are cleft lip and palate associated with?

A

Pierre Robin sequence
Stickler sydrome
Edwards syndrome

94
Q

What cases a laryngeal cleft?

A

Failure of closure of the tracheo-oesophageal septum

95
Q

What is the serious complication of laryngeal haemangioma?

A

Can bleed copiously with instrumentation - topical adrenaline can then be used

96
Q

What causes tracheo oesophageal fistula?

A

Failure of normal development of the primitive foregut

MRCPCH Clinicals (17 decks)

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