COPD Flashcards

1
Q

What is COPD?

A
  • COPD is a common, preventable and treatable disease
  • characterized by the presence of persistent respiratory symptoms and airflow limitation
  • secondary to airway and alveolar abnormalities resulting from exposure to noxious particles or gases
  • influenced by host factors including abnormal lung development
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2
Q

Airflow obstruction and COPD?

A

not fully reversible

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3
Q

COPD spectrum of abnormalities?

A
  1. emphysema
  2. chronic bronchitis
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4
Q

What is emphysema?

A

Permanent dilatation and wall destruction of airspaces distal to the terminal respiratory bronchioles

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5
Q

What is chronic bronchitis?

A
  • Inflammation of the airways
  • large airway involvement leads to mucosal thickening and mucus hypersecretion
  • smaller bronchioles involvement produces airflow obstruction
  • Chronic productive cough for at least 3 months of two consecutive years
  • absence of other diseases causing sputum production.
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6
Q

Modifiable Risk factors for COPD?

A

cigarette smoking
- most common risk factor worldwide, representing the principal cause in up to 90% of patients
- Effects of smoking on lung function decline are dose dependent (airflow obstruction is directly proportional to the smoking pack years)

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7
Q

Genetic risk factors for COPD?

A

α1-Antitrypsin Deficiency
- Autosomal dominant mutations of SERPINA1 gene on chromosome 14

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8
Q

Non-modifiable risk factors for COPD?

A
  1. Occupational exposure
    - mining and chronic dust e.g. silica, cotton
  2. Biomass Fuel
  3. HIV infection in smokers
  4. Second Hand Cigarette Smoking
  5. Ambient air pollution
  6. Airway hyperresponsiveness
  7. Preterm birth
  8. Respiratory infections e.g. PNA, TB and Bronchiectasis
  9. Children born to smoking mothers
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9
Q

Pathogenesis of COPD?

A
  1. Chronic exposure to cigarette smoke in genetically susceptible individuals triggers inflammatory and immune cell recruitment within large and small airways and in the terminal air spaces of the lung
  2. Inflammatory cells release proteinases that damage the extracellular matrix supporting airways, vasculature, and gas exchange surfaces of the lung
  3. Structural cell death occurs through oxidant-induced damage, cellular senescence, and proteolytic loss of cellular-matrix attachments leading to extensive loss of smaller airways, vascular pruning, and alveolar destruction
  4. Disordered repair of elastin and other extracellular matrix components contributes to air space enlargement and emphysema
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10
Q

Pathological changes in COPD?

In Emphysema

A
  1. Panacinar emphysema is characteristic of AAT deficiency and is typically more severe in the lower Lobes
  2. Centriacinar emphysema is common in cigarette smokers and rare in nonsmokers
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11
Q

Clinical features?

A
  1. Dyspnea on exertion (or at rest) that is progressively worsening over time.
  2. Chronic cough
  3. Sputum production
  4. Weight loss with end-stage COPD.
  5. Morning headaches
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12
Q

Important things to note in history of COPD?

A
  1. Past Medical Hx
    - Other underlying lung pathology
  2. Social hx:
    - Cigarette smoking (Active/ passive)
    - Environmental exposures (home/ occupational)
    - Biomass fuel
  3. Family history
    - Genetic predisposition
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13
Q

General exam findings?

A
  1. Cyanosis
  2. Nicotine staining fingers
  3. Wasting
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14
Q

Respiratory exam findings?

A
  1. Inspection:
    - Hyper inflated ‘barrel chest’
    - Accessory muscle use and tachypnoea
  2. Palpation:
    - Reduced chest expansion
    - Hoover’s sign: Drawing in of the lower intercostal muscles with inspiration.
  3. Percussion: Hyperresonance
  4. Auscultation:
    - expiratory wheeze
    - Prolonged expiration
    - Reduced breath sounds
    - crackles
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15
Q

Complications of COPD?

A

CVS changes
1. Tachycardia
2. Loud P2 in pulmonary HTN
3. Elevated JVP
4. Peripheral edema

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16
Q

Chest imaging findings?

A
  1. Increased lung volumes
  2. Relatively depressed diaphragms
  3. Straightened left heart border
  4. Tear drop heart shadow
  5. an increased AP chest diameter
17
Q

Pulmonary function test results in COPD?

A

COPD shows obstructive airway disease pattern, FEV1/FVC < 0.7, which is not reversible
- FEV1 determines the severity of obstruction.
Note: If FEV1 and FVC are partially reversible, then an asthmatic component is present

18
Q

GOLD classification of severity of COPD?

A
  1. mild COPD
    - FEV1/FVC <0.7
    - FEV1 >80% predicted
  2. moderate COPD
    - FEV1/FVC <0.7
    - FEV1 <80 but >50% of predicted
  3. severe COPD
    - FEV1/FVC <0.7
    - FEV1 <50% but >30% of predicted
  4. very severe COPD
    - FEV1/FVC <0.7
    - FEV1 <30% of predicted or
    - FEV1< 50% with respiratory failure or right sided heart failure
19
Q

What other investigations can you do in COPD?

A
  1. Arterial blood gases
    - hypercapnia
    - respiratory acidosis
    - hypoxemia
  2. FBC (polycythaemia)
    - EPO mediated rise in HCT in response to prolonged hypoxia
20
Q

Modified medical research council dyspnea scale?

A

0 - not troubled by breathlessness except on strenuous exercise
1 - short of breath when hurrying or walking up a slight hill
2 - walks slower than contemporaries on the level because of breathlessness or has to stop for breath when walking at own pace
3 - stops for breath after walking 100m or after a few minutes on the level
4 - too breathless to leave the house or breathless when dressing or undressing

21
Q

Long term treatment of COPD?

A
  1. bronchodilators
  2. inhaled corticosteroids - reduce exacerbations
  3. theophylline e.g. aminophylline
  4. phosphodiesterase 4 inhibitors e.g. roflumilast
  5. prophylactic antibiotics e.g. azithromycin in frequent exacerbations
  6. A1AT augmentation therapy
22
Q

Bronchodilator drugs?

A
  1. Beta agonists e.g. salbutamol, formoterol
  2. Anticholinergics e.g. ipratropium, tiotropium
23
Q

Non-pharmacotherapy long term treatment?

A
  1. Pulmonary rehabilitation
  2. Lung volume reduction surgery
  3. Lung transplant
  4. Vaccination (Pneumococcal, COVID, Influenza)
  5. Nutritional support and counselling
24
Q

What interventions can improve survival?

A
  1. Smoking Cessation
  2. oxygen therapy in chronically hypoxemic patients
  3. lung volume reduction surgery (LVRS) in selected patients with emphysema
25
Q

What are acute exacerbations in COPD?

A

Worsening of respiratory symptoms such as dyspnea, cough, sputum production

26
Q

What triggers acute exacerbations?

A
  1. Infections
  2. Poor drug adherence
  3. Heart Failure
  4. Pulmonary embolism
27
Q

Causes of infections in acute exacerbations?

Low vs high risk groups?

A
  1. Viral or Bacterial
    e.g. H. influenza, S. Pneumoniae, Moraxella Carthallis and rarely Chlamydia pneumoniae
  2. High risk groups (>4 exacerbations/year; GOLD class 3/4 or with comorbidities)
    - risk of infection with klebsiella and pseudomonas
28
Q

Management of acute exacerbations?

A
  1. antibiotic therapy
  2. systemic corticosteroids
  3. bronchodilators
  4. theophyllines
  5. oxygen therapy
29
Q

Antibiotic therapy in management of acute exacerbations?

Low vs high risk groups?

A

For low risk groups, use:
1. Second generation macrolide e.g. Azithromycin
2. Second or 3rd generation cephalosporin e.g. Ceftriaxone
3. Doxycycline
4. Ampicillin
5. Cotrimoxazole
For high risk groups, use:
1. Quinolones
2. B-lactam lactamase inhibitors e.g. Ciprofloxacin, Clavuronic Acid, Tazobactam

30
Q

Oxygen therapy in management of acute exacerbations?

A
  1. target 88-92% O2 saturation
  2. Mechanical ventilation in respiratory acidosis
  3. Risk of impairing hypoxic drive in respiratory center and development of CO2 narcosis
31
Q

Complications of oxygen therapy in COPD?

A

Danger of hypercapnic respiratory failure
1. Chronic hypercapnia leads to loss of sensitivity to raised CO2 levels
2. Rely on hypoxia for respiratory drive
- If you give oxygen, patients may lose hypoxic drive

32
Q

Indications for long term supplemental O2?

A
  1. PaO2< 55mmHG and saturation < 88%
  2. PaO2 55-59mmHg 88-92% with cor pulmonale, polycythemia