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YR3 Respiratory > Asthma + allergic airway diseases > Flashcards

Asthma + allergic airway diseases Flashcards

1
Q

Define asthma

A

Chronic inflammatory airway disease characterised by intermittent, reversable airway obstruction and hyperreactivity

Type 1 hypersensitivity

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2
Q

In asthma, what 3 factors lead to airway obstruction?

A
  • Bronchial smooth muscle contraction, triggered by a variety of stimuli
  • Mucosal inflammation, caused by mast cell and basophil degranulation leading to inflammatory mediators
  • Increased mucus production → mucus plugging
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3
Q

Briefly explain the pathophysiology of asthma

A

2 major elements in the pathophysiology: inflammation and airway hyper-responsiveness (AHR).

Trigger → release of inflammatory mediators → activation + migration of inflammatory cells:

  • Th2 mediated lymphocytic response
  • eosinophils
  • basophils
  • mast cells
  • macrophages
  • NK cells

These cells migrate, causing inflammatory changes in the epithelium, hyper-secretion of mucus and increased smooth muscle responsiveness.

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4
Q

Explain the risk factors for asthma

A
  • Family history
  • Atopic history- eczema, atopic dermatitis, allergic rhinitis
  • Nasal polypoposis- associated with late-onset asthma
  • Common allergens:
    • cats, dogs
    • cockroaches, dust mites
    • fungal spores
    • tobacco smoke, fumes from chemicals (e.g., bleach)
    • pollen from trees, weeds, and grass.
  • Associations: obesity, GORD, obstructive sleep apnoea
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5
Q

Summarise the epidemiology of asthma

A
  • Affects 10% of children
  • Affects 5% of adults
  • Prevalence appears to be increasing
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6
Q

What are the presenting symptoms of asthma?

A

Symptoms precipitated by allergen exposure, exposure to cold air, tobacco smoke, or particulates

Worse with emotions such as laughing hard

  • dyspnoea
    • ​variation (worst in morning & evening)
  • cough
  • expiratory wheezes
    • Polyphonic, high-pitched expiratory wheezes

Ask about previous hospitalisation due to acute attacks - this gives an indication of the severity of the asthma

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7
Q

Recognise the signs of asthma on physical examination?

A
  • Tachypnoea
  • Use of accessory muscles
  • Prolonged expiratory phase
  • Polyphonic wheeze
  • Hyperinflated chest
  • Hyper-resonant percussion note
  • Reduced air entry
  • Nasal polyposis- single or multiple polyps in the nasal cavity
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8
Q

State the signs of: moderate/severe/life-threatening attack

A
  • Moderate Attack
    • PEFR: >50-75% predicted
  • Severe Attack
    • PEFR 35-50% predicted
    • Pulse > 110/min
    • RR > 25/min
    • Inability to complete sentences
  • Life-Threatening Attack
    • PEFR < 33% predicted
    • Silent chest
    • Cyanosis – PaO2 <8kPa, normal/high PaCO2 >4.6kPa, low pH <7.35
    • Bradycardia
    • Hypotension
    • Confusion
    • Coma
  • Near fatal:
    • raised PaCO2 +/- require mechanical ventilation
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9
Q

What investigations would you do for acute asthma?

A
  • Peak flow
  • Pulse oximetry
  • ABG –
    • normal or slightly low PaO2
    • low PaCO2 (hyperventilation) – if PaCO2 raised, transfer to HDU for ventilation
  • CXR - to exclude other diagnoses (e.g. pneumonia, pneumothorax)
  • FBC - raised WCC if infective exacerbation
  • CRP
  • U&Es
  • Blood and sputum cultures
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10
Q

What does flow spirometry show in:

a) asthma
b) COPD

A

ASTHMA

  • Flow spirometry shows only obstructive changes
  • drop in FEV1 <70% but normal FVC
  • i.e. a reduced rate of air flow but a normal lung capacity

COPD

  • Flow spirometry shows obstructive changes (i.e. drop in FEV1 <70%)
  • Also a degree of restrictive change (i.e. FVC <70%).
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11
Q

What investigations would you do for subacute asthma?

A

Spirometry

  • gold standard
  • FEV₁/FVC <80% of predicted
  • bronchodilator reversibility test- improvement of FEV₁ by >12%

Peak expiratory flow rate

  • least 3 days/week for several weeks - often shows diurnal variation with a dip in the morning (>20% variation)

CXR

  • shows hyperinflation
  • May show signs of infection in acute exacerbation or pneumothorax

Bloods

  • normal/raised eosinophils +/- neutrophilia
  • IgE level- allergen specific
  • Aspergillus antibody titres

Bronchial challenge test

  • direct (histamine, other constrictive agents) and indirect (activate mast cells)

Skin prick allergy testing

  • identify allergen and direct immunotherapy

Fractional exhaled nitric oxide (FeNO)

  • Reflective of the degree of eosinophilic inflammation
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12
Q

Outline the management of asthma

A

Stepwise management (add on to initial therapy, then reduce if under control as much as possible):

  1. Short acting beta agonist (SABA) + inhaled corticosteroid (ICS)
  2. SABA + ICS + Leukotriene receptor antagonist (LTRA)
  3. Long acting beta agonist (LABA) + ICS +/- LTRA
  4. LABA + ^^ICS +/- LTRA
    • increasing dose of ICS
  5. Theophyline, LAMA
    • ​​refer to asthma specialist

NOTE: there are 2 management algorithms- BTS and NICE.

In BTS, LTRA and LABA are switched around.

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13
Q

How can asthma be classified?

A

according to severity:

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14
Q

Outline how acute asthma attacks are managed

A
  1. A-E approach
    • 15l/min 100% O2
    • ABG
    • ECG to monitor for arrhythmias
  2. 5mg salbutamol nebulised every 15 mins
  3. 0.5mg ipratropium bromide nebulised
  4. IV hydrocortisone / PO prednisolone
  5. If no improvement: 1.2-2 mg IV Mg sulfate over 20mins AND get senior help
  6. If still no improvement: IV aminophylline
  7. If still no improvement: intubation and ventilation in ICU
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15
Q

What advice would you give to an asthmatic?

A
  • Teach proper inhaler technique
  • Explain important of PEFR monitoring – twice a day, keep diary
  • Help quit smoking
  • Avoid provoking factors
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16
Q

What are the possible complications of asthma?

A
  • Growth retardation
  • Airway remodelling leading to chronic inflammation and COPD
  • Oral candidiasis + dysphonia 2/2 use of ICS
  • Chest wall deformity (e.g. pigeon chest)
  • Recurrent infections
  • Pneumothorax
  • Respiratory failure
  • Death
17
Q

Summarise the prognosis for patients with asthma

A

Airway remodelling with irreversible airflow obstruction occurs early with persistent childhood asthma; in adults there is little change

  • Many children improve with age
  • Adult onset is usually chronic
18
Q
A
19
Q

Define extrinsic allergic alveolitis

A

Interstitial inflammatory disease of the distal gas-exchanging parts of the lung caused by inhalation of non-human protein

Also known as hypersensitivity pneumonitis.

distal = terminal bronchioles + alveoli

20
Q

What are the most common causative organisms of extrinsic allergic alveolitis?

A

Bacteria

Actinomycetes is responsible for:

  • Farmers lung
  • Bagassosis or sugar worker’s lung
  • mushroom pickers lung

Animal proteins

  • Pigeon/bird fancier’s lung- caused by blood on bird feathers and excreta
  • exposure to large farm animals

Fungi

Maltworker’s Lung - caused by barley or maltlings containing Aspergillus clavatus

21
Q

Explain the aetiology of extrinsic allergic alveolitis

A

In sensitised individuals, repetitive inhalation of the antigen provokes a hypersensitivity reaction

  • Varies on intensity + clinical course depending on the antigen
  • Acutely, alveoli are infiltrated with acute inflammatory cells
  • With chronic exposure, granuloma formation and obliterative bronchiolitis can occur
22
Q

Summarise the epidemiology of extrinsic allergic alveolitis

A
  • UNCOMMON
  • 2% of occupational lung disease
  • 50% of reported cases affect farm workers
  • Geographical variation
23
Q

WHat are the classifications of extrinsic allergic alveolitis?

A

Acute (develops over hours following exposure)

Sub-acute (develops over weeks to months following exposure)

Chronic (develops over months to years following exposure).

24
Q

What are the presenting symptoms of extrinsic allergic alveolitis ?

A

ACUTE

Presentation is that of a flu-like illness, including:

  • fever, chills
  • malaise
  • non-productive cough
  • dyspnoea

…beginning 6-18 hours after acute, high-level exposure

Typically episodic

CHRONIC

  • malaise
  • dyspnoea
  • productive cough

…over weeks to months = insidious onset

25
Q

What are the signs of extrinsic allergic alveolitis on physical examination?

A
  • ACUTE
    • Presentation is that of a flu-like illness
    • Rapid shallow breathing
    • Pyrexia
    • Bibasalar inspiratory crackles
  • CHRONIC
    • Fine diffuse inspiratory crackles
    • Clubbing

The diagnosis requires known exposure to a cause of HP

26
Q

What investigations would you do for extrinsic allergic alveolitis?

A

Bloods

  • FBC - neutrophilia, lymphopenia, ESR, hypoalbuminaemia in chronic
  • ABG - reduced PO2 + PCO2

Serology

  • Test for IgG to fungal or avian antigens
  • NOTE: these are not diagnostic because you may find these in normal individuals

Imaging

  • CXR- patchy, nodular infiltrates are observed in acute and sub-acute HP; fibrosis in chronic HP.
    • may be normal between episodes of acute
  • CT chest- ground glass attenuation + poorly defined micronodules
    • more accurate + diagnostic than CXR

Pulmonary function tests

  • acute = restrictive
  • chronic = mixed restrictive + obstructive
  • diffusing lung capacity of carbon monoxide = reduced

Bronchioalveolar lavage

  • Positive antibody + lymphocytosis (elevated CD8+ cells)
27
Q
A

YR3 Respiratory (6 decks)

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