L11 - COPD Flashcards

1
Q

Define COPD

A
  • Characterised by persistent airflow limitation
  • usually progressive
  • and associated with an enhanced chronic inflammatory response.
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2
Q

Criteria for diagnosis of Chronic bronchitis

A

cough and sputum for atleast 3 consecutive months for 2 consecutive years.

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3
Q

Emphysema

A
  • Abnormal permanent enlargement of airspace distal to terminal bronchioles.
  • Bullae may form.
  • Accompanied by the destruction of alveolar walls and without obvious fibrosis.
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4
Q

Why may COPD cause increased sputum production and what is the consequence of this?

A
  1. Enlargement of mucus secreting glands.
  2. Increased number of goblet cells.
  3. Inflammatory cell infiltrate.
    - increased sputum production may lead to chronic bronchitis
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5
Q

Describe the consequence of loss of elastic tissue, inflammation and fibrosis in airway wall:

A
  • Premature airway closure.
  • Gas trapping
  • Dynamic hyperinflation.

This leads to changes in pulmonary and chest wall compliance.

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6
Q

Systemic features of COPD

A
  1. Muscular weakness: reflecting deconditioning (lack of muscle fitness), cellular changes in skeletal muscle.
  2. Increased circulating inflammatory markers
  3. Peripheral oedema: impaired salt and water excretion
  4. Altered fat metabolism contributing to weight loss
  5. Prevalence of osteoporosis
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7
Q

Describe effects of pulmonary hyperinflation?

A
  • Flattens diaphragmatic muscle
  • leads to increased horizontal alignment of intercostal muscles
  • respiratory muscles disadvantaged
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8
Q

First symptoms of COPD?

A
  • cough

- associated sputum production

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9
Q

Why do COPD patients often have pitting oedema?

A
  • Salt and water retention

- caused by renal hypoxia and hypercapnia (carbon dioxide retention)

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10
Q

How might we measure lung volume?

A

Determine hyperinflation.

Generally performed by helium dilution technique.

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11
Q

Limitations of helium dilution technique to measure lung volume?

A

May underestimate lung volume in those with severe COPD and large bullae.

Hence Body Plethysnography used.

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12
Q

When are oral glucocorticoids given?

A
  • Good for use during exacerberations.
  • However not for maintenance therapy
  • as may contribute to osteoporosis and impaired skeletal muscle.
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13
Q

State some ways of managing COPD?

A

Bronchodilators: breathlessness

Oral glucocorticoids

Oxygen therapy

Surgical intervention

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14
Q

When might surgical intervention be required in a patient with COPD?

A
  • bullectomy

- if large bullae compressing surrounding normal lung tissue.

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15
Q

Example of bronchodilator which may be given to patient with COPD?

A

Nebulished short acting B2 agonist combined with anti-cholingeric agent (salbutamol and ipratropium)

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16
Q

Cholinergic medication action

A

Category of phamaceutical agents that act upon the neurotransmitter ACH

17
Q

How might oxygen therapy be implemented?

A

High flow nasal cannulae HFNC

- provides very high gas flow of humidified oxygen and air.

18
Q

Role of CPAP

A
  • Helps recruit collapsed alveoli

- enhance clearance of alveolar fluid.

19
Q

Example of a longer acting drug

A

Includes muscarinic antagonists tiotropium - often given with B2 agonist such as salmeterol or formeterol.

20
Q

Idiopathic pulmonary fibrosis

A
  • Debilitating inflammatory disorder
  • results in scarring of lung tissue
  • and loss of elasticity.
  • thus lung expansion and gaseous exchange in alveoli are impaired.
21
Q

Treatment for idiopathic pulmonary fibrosis

A

Use anti-fibrotic agents

  1. Pirfenidone
    - immunosuppressant, reduces fibroblast proliferation
22
Q

Examples of drugs which may be used to tackle cough

A

Opoid analgesics

Codeine - mild cough supressant

23
Q

Cryptogenic organising pnuemonia

A

Clinical syndrome characterised by:

  • cough
  • low grade fever
  • breathlessness
  • lung consolidation.
24
Q

Describe pathology of normal lungs

A
  1. Alveoli are kept open by special structures called alveolar attachments (elastin)
  2. Airway lining not damaged
  3. Alveoli clear of excess mucus
  4. Air flows in and out without compromise
25
Q

Pathology of COPD

A
  1. Break down of alveolar attachments by elastase, leading to small airway collapse
  2. Inflammation and thickening of lining of airway tubules
  3. Excess mucus production blocks airways
  4. Airflow compromise
26
Q

Describe importance of Alpha 1 antitrypsin deficiency?

A1AT

A

A1AT - protein inhibitor Pi of elastase.
A1AT deficiency: high levels of elastase destroys elastin.

Cigarette smoke decreases activity of A1AT

1% of all COPD patients have A1AT deficiency

27
Q

What system controls the muscle tone of airways, breathing and lung function?

Describe the division of these symtpoms

A

Autonomic nervous system:

  1. Sympathetic branch
    - used noradrenaline
    - b2 receptor
    - bronchodilation
  2. Parasympathetic branch
    - ACH
    - M3 receptors
    - bronchoconstriction
    - basal mucus production
28
Q

Describe sites of action of muscarinic anatagonists?

A

Anticholingeric agents are more effective in the proximal airways.

29
Q

Describe sites of action of b2-adrenergic receptors?

A

b2 agonists are relatively more effective in the distal airways.

30
Q

Describe the overview of diagnosis of COPD?

A
  1. Resp symptoms: dyspnoea, sputum production, chronic cough
  2. Spirometry: confirms persistent airflow limitation.
  3. Clinical features of asthma are missing.
31
Q

State some oral pharmacological therapies for COPD?

A
  1. Oral corticosteroids
  2. Oral theophylline
  3. Oral mucolytic therpay
  4. Oral phosphodiesterase-4 inhibitors
32
Q

Oral mucolytic therapy

A

Considered for people with a chronic cough productive of sputum.

Only continue mucolytic therapy if there is symptomatic improvement.

33
Q

Definition of an exacerbation

A

A sustained acute-onset worsening of the person’s symptoms from their usual stable state.

34
Q

Symptoms of an exacerbation (4)

A
  1. Worsening breathlessness
  2. Cough
  3. Increased sputum
  4. Change in sputum colour