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MRCPCH Clinicals > Respiratory > Flashcards

Respiratory Flashcards

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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
Treatment for tuberculosis?
RIPE: Rifampicin + isoniazid (6 months) Pyrazinamide + ethambutol (2 months)
26
Side effects of rifampicin
Orange urine/tears Hepatic enzyme induction Abnormal LFTs
27
Side effects of isoniazid
Abnormal LFTs | Peripheral neuropathy
28
Side effects of pyrazinamide
Liver toxicity
29
Side effects of ethambutol
Visual disturbance
30
Which TB drug should be avoided in very young children?
Ethambutol
31
What drug can be given as prophylaxis for a neonate born to a mother with active TB?
Isoniazid
32
What are the 3 types of CCAM?
Type 1 - single or multiple large cysts Type 2 - multiple small cysts Type 3 - solid mass
33
What is a congenital lobar sequestration?
Mass of non-functional lung with abnormal communication with airway, usually supplied by systemic circulation
34
Which lobes of the lung are most commonly affected by congenital lobar sequestration?
Lower lobes, left
35
What are bronchogenic/duplication cysts?
Remnant of primitive foregut derived from abnormal tracheobronchial budding - they contain normal tracheal tissue filled with fluid
36
What is congenital lobar emphysema?
Overinflation of the lobe as a result of intrinsic deficiency of bronchial cartilage ± elastic tissue
37
Where does congenital lobar emphysema affect?
Rare in lower lobes - usually left upper or right middle/upper
38
How does congenital lobar emphysema present?
Asymptomatic Respiratory distress in neonatal period Chest asymmetry Hyperresonance
39
How is congenital lobar emphysema managed?
Lobectomy if respiratory distress | Conservatively if mild symptoms
40
What is congenital lobar emphysema often associated with?
1:6 have a cardiac abnormality
41
What is Scimitar syndrome?
Hypoplastic right lung with anomalous venous drainage, usually to IVC or right atrium ± systemic collateral arterial supply
42
What is the scimitar sign?
Vertical line caused by the right upper lobe pulmonary vein running into the IVC
43
How does scimitar syndrome present?
Asymptomatic, or can lead to recurrent infections
44
How is scimitar syndrome managed?
Surgical correction for vascular abnormality
45
What is the incidence of CDH?
1:2500-3500 births
46
On which side is CDH more common?
Left
47
What is the prognosis of CDH?
20-40% mortality rate
48
What is the cause of alveolar proteinosis?
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
What is the prognosis for alveolar proteinosis?
Almost universally fatal in infants, in older children lung lavage can help
50
What is congenital pulmonary lymphangiectasia?
Rare dilatation of pulmonary lymphatics leading to severe neonatal respiratory distress and pleural effusions
51
What is congenital pulmonary lymphangiectasia associated with?
Congenital cardiac disorders like obstructed venous drainage
52
What causes obliterative bronchiolitis?
Viral infection, often adenovirus or myoplasma | Less often measles, RSV, or lung or bone marrow transplant
53
What is the pathophysiology of obliterative bronchiolitis?
Severe widespread small airway obstruction eventually leading to pulmonary hypertension
54
What is the radiological appearance in obliterative bronchiolitis?
Patchy areas of air trapping (honeycomb), patchy pruning of vascular markings, hyper inflated lungs
55
What is the management of obliterative bronchiolitis?
In early stages may respond to bronchodilators or steroids, but often no treatment is successful
56
What can obliterative bronchiolitis progress to?
Swyer-James or Macleod syndrome of unilateral hyper lucent lung with diminished vascularity
57
What is the pathophysiology of haemosiderosis?
Repeated episodes of pulmonary haemorrhage lead to an accumulation of haemosiderin in the alveoli
58
What causes haemosiderosis?
Uncertain - some are associated with CMPA, some with Goodpasture syndrome
59
What are the symptoms of haemosiderosis?
Usually episodic fever, dyspnoea, wheeze ± haemoptysis
60
How is haemosiderosis diagnosed?
By finding haemosiderin-laden macrophages in a BAL
61
How is haemosiderosis managed?
Steroids | Hydroxychloroquine or other immunosuppressives, treat the anaemia and hypoxia
62
What is the pathophysiology of pulmonary hypertension?
Chronic hypoxia leads to pulmonary vasoconstriction and arterial wall change
63
What are the management options for pulmonary hypertension?
``` High oxygen Nitric oxide Sildenafil Prostacyclin Nifedipine ```
64
How is cystic fibrosis inherited?
Autosomal recessive - multiple mutations but most common is delta F508
65
What is the cause of cystic fibrosis?
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
What are the pathophysiological features of CF?
Dehydration of mucus and airway surface liquid Disturbed mucociliary clearance Increased risk of airway infection Inflammation associated with progressive lung disease
67
What is the incidence of CF?
Carriers are 1:25, disease is in 1:2500 births of white babies
68
What is ABPA?
Complex hypersensitivity reaction in response to colonisation of airways with Aspergillus fumigatus
69
Who gets ABPA?
Almost exclusively people with asthma or CF
70
What is the pathophysiology of ABPA?
Mucoid impaction of bronchi Eosinophilic pneumonia Bronchocentric granulomatosis
71
What are the symptoms of ABPA?
Recurrent exacerbations of fever, malaise, expectoration of brownish mucus plugs, wheeze, rhinosinusitis
72
What is the management of ABPA?
Steroids Antifungals e.g. itraconazole Omalizumab may be useful if recurrent
73
How is ABPA diagnosed?
Establishing sensitisation to Aspergillus antigens
74
How is CF diagnosed?
Guthrie tests immune reactive trypsin, which will be high Sweat test Genetic testing
75
What is a diagnostic sweat test value?
>60mmol/l chloride in at least 100mg sweat
76
How is primary ciliary dyskinesia inherited?
Autosomal recessive
77
How common is primary ciliary dyskinesia?
1:15,000 births
78
How does primary ciliary dyskinesia present?
``` Neonatal respiratory distress and rhinorrhoea Recurrent LRTIs Sinus disease Glue ear Male infertility and female subfertility ```
79
What other conditions can primary ciliary dyskinesia be associated with?
40% have dextrocardia ± abdominal situs inversus (Kartagener syndrome)
80
How is primary ciliary dyskinesia diagnosed?
Nasal brushing for ciliary beat frequency, assessment of beat coordination and structure Low exhaled/nasal nitric oxide
81
Which genes are implicated in primary ciliary dyskinesia?
DNAI1 and DNAH5 - identified in 40% of families with PCD
82
What is the treatment for primary ciliary dyskinesia?
Physiotherapy Antibiotics ENT and hearing assessment Genetic counselling
83
What is the incidence of OSA?
2%
84
What is the peak age for OSA?
2-8 years
85
What are the contributing factors to OSA?
Increased upper airway resistance Decreased neuromuscular activation Altered ventilatory control Changed arousal thresholds
86
What are the features of OSA?
Repetitive collapse of the pharyngeal airway Intermittent hypercarbic hypoxia Recurrent transient arousal
87
How is OSA diagnosed?
Polysomnography
88
What are the symptoms of OSA?
Snoring, snorting Sleep disturbance Non-refreshing sleep Daytime sleepiness
89
What are the surgical options for OSA?
Adenotonsillectomy Mandibular distraction Maxillomandibular advancement Tracheostomy
90
What are the medical/conservative options for OSA?
Intranasal corticosteroids Leukotriene antagonists Weight loss Ventilatory support
91
How common is choanal atresia?
1:60-70,000 births
92
What causes choanal atresia?
Failure of the breakdown of the bucconasal membrane, leading to complete obstruction of the nostril(s)
93
Which conditions are cleft lip and palate associated with?
Pierre Robin sequence Stickler sydrome Edwards syndrome
94
What cases a laryngeal cleft?
Failure of closure of the tracheo-oesophageal septum
95
What is the serious complication of laryngeal haemangioma?
Can bleed copiously with instrumentation - topical adrenaline can then be used
96
What causes tracheo oesophageal fistula?
Failure of normal development of the primitive foregut

MRCPCH Clinicals (17 decks)

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