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Medicine Respiratory > Obstructive Airways Disease > Flashcards

Obstructive Airways Disease Flashcards

1
Q

Obstructive vs restrictive disease

A

Obstructive = airways, restrictive = lungs

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2
Q

Examples of obstructive airway diseases

A

Asthma, emphysema and chronic bronchitis (COPD), asthma/COPD overlap syndrome

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3
Q

The asthma triad

A

Reversible airflow obstruction, airway inflammation, airway hyperresponsiveness

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4
Q

Dynamic evolution of asthma

A

Broncho-constriction (brief symptoms) → chronic airway inflammation (exacerbations, airway hyper responsiveness) → airway remodelling (fixed airway obstruction)

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5
Q

Hallmarks of remodelling in asthma in the basement membrane, submucosa and mucosa

A

Basement membrane - thickening
Submucosa - collagen deposits
Mucosa - hypertrophy

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6
Q

Inflammatory cascade in asthma

A

Inherited or acquired factors → eosinophilic inflammation → Mediators, TH2 cytokines → twitchy smooth muscle (hyperresponsiveness)

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7
Q

What can be used to treat each of the following steps in the inflammatory cascade in asthma?:

  1. Inherited or acquired factors
  2. Eosinophilic inflammation
  3. Mediators, TH2 cytokines
  4. Twitchy smooth muscle
A
  1. Avoidance of precipitant
  2. Anti-inflammatory medication (corticosteroids, cromones, theophylline)
  3. Leukotriene receptor agonists or antihistamines, monoclonal antibodies (anti-IgE, anti-IL5)
  4. Bronchodilators (beta-2 agonists, muscarinic antagonists)
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8
Q

Potential triggers of asthma

A

Allergens (animal dander, dust mites, pollen, fungi), exercise, viral infection, smoke, cold, chemicals, drugs (NSAIDs, Beta-blockers)

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9
Q

When is asthma generally worse?

A

At night and in the morning. Diurinal variability

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10
Q

Which antibody is increased in atopic asthma?

A

IgE

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11
Q

Which blood cell is associated with asthma?

A

Eosinophil

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12
Q

General steps in diagnosis of asthma

A
  • History and examination
  • Diurnal variability of peak flow
  • Reduced forced expiratory ratio - FEV/FEV1 ratio <75%
  • Reversibility to inhaled salbutamol (>15%)
  • Provocation testing - bronchospasm (through exercise, histamine/methacholine//mannitol)
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13
Q

Diurnal variations in peak flow rate in asthma

A

Generally peak flow is in the evening compared to the morning

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14
Q

Components associated with development of obstruction and ongoing disease progression in COPD

A

Mucociliary dysfunction, inflammation, tissue damage

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15
Q

Disease progression in COPD

A

Exposure to inhaled noxious particles and gases cause inflammation of the lungs that can lead to COPD if the normal protective and/or repair mechanisms are overwhelmed of defective
These aggravate the mucosal lining of airways and macrophages which release neutrophilic chemotactic factors
Macrophages and neutrophils release proteases which break down connective tissue and cause mucus hyper secretion and goblet cell hyperplasia
Cytotoxic T cells may also be involved in the inflammatory cascade

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16
Q

2 diseases that fall under the term COPD

A

Chronic bronchitis and emphysema

17
Q

Chronic bronchitis:

  • Characteristics
  • Reversible or irreversible?
A
  • Chronic neutrophilic inflammation, mucus hyper secretion, mucociliary dysfunction, altered lung microbiome, smooth muscle spasm and hypertrophy
  • Partially reversible
18
Q

Emphysema:

  • Characteristics
  • Reversible or irreversible?
A
  • Alveolar destruction, impaired gas exchange, loss of bronchial support
  • Irreversible
19
Q

ABCD assessment tool in COPD

A

Spirometrically confirmed diagnosis → assessment of airflow limitation (FEV1) → assessment of symptoms/risk of exacerbations (via exacerbation history)

20
Q

Airflow limitation in COPD:

  • GOLD 1
  • GOLD 2
  • GOLD 3
  • GOLD 4
A

GOLD 1 - FEV1 ≥80% predicted
GOLD 2 - FEV1 50-79% predicted
GOLD 3 - FEV1 30-49% predicted
GOLD 4 - FEV1 <30% predicted

21
Q

Chronic cascade in COPD

A
  • Progressive fixed airflow obstruction
  • Impaired alveolar gas exchange
  • Respiratory failure ↓PaO2, ↑PaCO2
  • Pulmonary hypertension
  • Right ventricular hypertrophy/failure (Cor pulmonare)
  • Death
22
Q

How to prevent further decline in lung volume in COPD

A

Stopping smoking

23
Q

What is asthma/COPD overlap syndrome

A

COPD with blood eosinophilia >4%

24
Q

Difference between COPD and asthma/COPD overlap syndrome

A
  • Blood eosinophilia >4%
  • Responds better to inhaled corticosteroids with respect to exacerbation reductions
  • More reversible to salbutamol
25
Q

Asthma treatment guidelines

A 
Step 1 (intermittent) - short acting beta-2-agonists
Step 2 (mild persistent) - add inhaled corticosteroids
Step 3 (moderate persistent) - add LABA/LAMA, add LTRA/Theo/cromone
Step 4 (Severe persistent) - add oral steroid, add anti-IgE, anti-IL5, anti-IL4-alpha
26
Q

Why may corticosteroids cause pneumonia in COPD?

A

Due to local immune suppression and impaired mucociliary clearance - especially with fluticasone

27
Q

When in COPD is prednisolone used?

A

Only for acute exacerbations

28
Q

Actions of a spacer device

A
  • Avoids coordination problems with pMDI
  • Reduces oropharyngeal and pharyngeal side effects
  • Reduces systemic absorption from a swallowed fraction
  • Acts as a holding chamber for aerosol
  • Reduces particle size and velocity
  • Improves lung deposition
29
Q

Anti-IgE:

  • In which obstructive condition is it used in?
  • How is it administered?
  • Which patients may receive this?
A
  • Asthma
  • Injection every 2-4 weeks
  • For patients with severe persistent allergic asthma despite max therapy
30
Q

Anti-IL5:

  • Which obstructive condition is it used in?
  • How is it administered?
  • Which patients may receive this?
A
  • Asthma
  • Injection every 4/8 weeks
  • For patients with severe refractory eosinophilic asthma despite max therapy
31
Q

Anti-IL4 alpha:

  • Which obstructive condition is it used in?
  • How is it administered?
  • Which patients may receive this?
A
  • Asthma
  • Injection every 2 weeks
  • For patients with severe refractory asthma despite max therapy

Medicine Respiratory (12 decks)

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