COPD Flashcards
1
Q
Define chronic obstructive pulmonary disease (COPD).
Say what airflow limiation due to
A
- COPD is a disease of progressive airflow limitation that is not fully reversible, associated with an abnormal inflammatory response of the lungs to noxious particles or gases, predeminantly inhaled cigarette smoke
- The airflow limitation is due to decreased outflow pressure (emphysema) plus increased airway resistance (chronic bronchitis/bronchiolitis)
2
Q
Describe the typical history of a patient with COPD
(symptoms)
A
Clinical presentation:
- Productive morning morning cough, following many years of ‘smoker’s cough’
- Increased frequenced of lower respiratory tract infections
- Slowly progressive dyspnoea with wheezing
- Respiratory failure
- Chronic heart failure (cor pulmonale): occurs late
3
Q
On examination what would you find with a patient with COPD?
A
Signs:
Mild disease:
- widespread disease
Severe disease:
- Observations:
- Tachypnoea
- Cyanosis
- Flapping tremor of outstretched hands (if CO2 retainer)
- Inspection
- Hyperinflation
- Intercostal recession on inspiration
- Lip pursing on expiration
- Signs of respiratory distress (tracheal tug, paradoxical breathing, accessory muscle use)
- Palpation:
- Poor chest expansion
- Percussion:
- Hyper-resonant throughout, loss of cardiac/hepatic dullness
- Auscultation:
- Decreased breath sounds, prolonged expiratory phase
- Polyphonic wheeze (many pitches)
4
Q
What are complications of COPD?
A
- Acute exacerbations
- Polycthaemia (the bone marrow cells produces too many red blood cells)
- Respiratory failure
- Cor pulmonale (the enlargement and failure of the right ventricle of the heart)
- Pneumothorax
- Lung carcinoma
5
Q
Emyphysema causes COPD as causes decreased outflow pressure and therefore cause airflow limitation.
Describe the pathology of emphysema
A
Emphysema:
- Dilation of any part of the respiratory acinus (air spaces (air spaces distal to the terminal bronchioles) with destructive changes in the alvelor walls
- There is an absence of any scarring (fibrosis)
- Tissue destruction is caused by increased secretion and activation of extracellular proteases by inflammatory cells
- The inflammatory cells are stimulated by noxious particles e.g. smoking
- In centrilobular emphysema (most common cause) these changes are limited to the central part of the lobule directly around the terminal bronchiole, with normal aveoli elsewhere
- Panacinar emphysema leads to destruction and distension of the whole lobule, which can happen in smokers but is more common in a1-antitrypsin deficiency
- Dilated air spaces >1cm are termed bullae
- Loss of connective tissue in the alveolar walls leads to a loss of elastic recoil of the lungs, leading to air entrapment in the lungs and inadequate ventilation
- The reduction in the area available for gas exchange means there is reduced oxygen uptake
6
Q
Chronic bronchitis and bronchiolitis causes COPD as causes increases airway resistance and therefore causes airflow limitation.
Describe the pathology of Chronic bronchitis and bronchiolitis
A
Chronic bronchitis:
- Daily cough with sputum for at least 3 months per year for two years
- The primary abnormality seen is abnormal amounts of mucus, which causes plugging of the airway lumen
- The hypersecretion is associated with hypertrophy and hyperplasia of brochial mucus-secreting glands
- Shown by Reid indec: the ratio of gland: wall thickness
- Inflammation not typically present, although frequent LRTIs develop with secondary inflammation and squamous metaplasia
Bronchiolitis
- Cigarette smokers also develop inflammation of the airways <2mm in diameter, i.e. the bronchioles, with macrophage and lymphoid cell infiltration
- This is actually the first pathological change in COPD
- It may lead to scarring and narrowing of the airways
7
Q
What are risk factors for COPD?
A
- Cigarette smoke exposure:
- Stimulates neutrophils to produce elastase
- Can inactivate a1-antitrypsin
- Directly causes mucous gland hypertrophy
- Occuptional exposure to dust
- a1-antitrysin deficiency
- Recurrent chest infections
- Low socioeconomic status
- Asthma/atopy (allergies)
8
Q
Blue bloaters and Pink puffers are patients with COPD who exhibit specific phyical signs as a result of COPD
What are they? Why do they occur?
A
Blue bloaters:
- Patients with severe chronic bronchitis/COPD become insensitive to CO2 and thus rely on their hypoxic drive to stimulate respiratory effort
- These patients are not particularly breathless, but are cyanosed and oedematous
- Suggestive of cor pulmonale
- A blood gas will show type 2 respiratory failure (low oxygen, retaining CO2)
- Oxygen should be given with care in these patients
Pink puffers:
- These patients remain sensitive to CO2, thus keep a low CO2 and a near normal O2
- They are tachypnoeic and tachycardic, using accessory muscles to increase their ventilation and are breathless but not cyanosed
- The patients are very thin as large amounts f calories are used to breath
- This can progress to type 1 respiratory failure
9
Q
Outline the investigation of a patient with suspected COPD
A
- Lung function tests will show evidence of airflow limitation – decrease in both FEV and FVC, and a reduction in the ratio, to below 70%.
- CXR often normal - useful in ruling out other pathology
- CT may outline bullae
- Hb, PCV and CRP may be raised
- ABG may be normal at rest
- Sputum examination normally not required.
- ECG and Echo useful if heart involvement suspected
- Alpha-1 antritrypsin investigation may be required in younger patients or non-smokers.
10
Q
What spirometry data will show restrictive patterns?
obstructive patterns?
A
Restrictive pattern:
- Decrease in FEV and FVC but maintenance of normal ratio
- (ballon get hard or is in a box, so you can’t blow it up as much, but air still flows out normally)
Obstructive pattern:
- Decrease in FEV, normal FVC, and so decrease in ratio
- (Ballon still blows up, but you’re squeezing the neck as the air flows out)
