COPD Flashcards
COPD definition and etiology
Definition
Chronic obstructive pulmonary disease (COPD) is a type of progressive lung disease characterized by long-term respiratory symptoms and airflow limitation.
Clinicopathological definition :
1-Chronic bronchitis
2- emphysema
Etiology
1- Causes of chronic bronchitis:
-Smoking Is the most common cause e.g. cigar,pipe.shisha and cannabis
- Infections (viral or bacterial)
- Air pollution
- Allergy
2-Causes of emphysema
-1ry: Alfa 1 antitrypsin deficiency
-2ry: Infection –obstruction
-False: Senile –compensatory-congenital
Pathological Stages of chronic bronchitis
1- Simple chronic bronchitis
o Reversible
o Excessive mucus secretion
2- Mucopurulent chronic bronchitis
o Recurrent infection of bronchi
3- Obstructive chronic bronchitis
o Irreversible
o Narrowing
o Submucosal inflammatory cell infiltration and submucosal thickness
o Muscular hypertrophy
Pathological types of emphysema:
1) Centrilobular
2) Panlobular emphysema
3) Irregular emphysema: (scar emphysema)
Complications of COPD:
1-repeated chest infections
2- Pulmonary hypertension and cor pulmonale
3- Recurrent spontaneous pneumothorax.
4- Respiratory failure
COPD symptoms and Examination
Symptoms
● History of heavy smoking for many years.
● Chronic bronchitis (cough daily or most of the day for about 3 months/year for 2 successive years
● sputum production for many years.
● Often worse with winter after chest infection
● Morning productive Cough often present only on walking up at first, later cough occurs throughout the day.
● Sputum usually mucoid - becomes purulent with exacerbation of disease but not excessive.
● Dyspnea
● Insidious onset of breathlessness on exertion with wheezing or tightness of chest
Two classical phenotypes have been described:
● Type A emphysematous type ‘Pink puffers’:
-sensitivity of respiratory center is normal
-maintain a normal PaCO2.
-Severe dyspnea
● Type B bronchitic type ‘Blue bloaters’:
-develop hypercapnia which decrease sensitivity to respiratory center so no dyspnea, oedema and secondary polycythaemia.
-Chest pain
-Intercostal muscle strain due to cough
-Ankle oedema if complicated with cor pulmonale
● In practice, these phenotypes often overlap
-
General examination
-Tachypnea
-Puffiness of eye lid due to chronic cough
-Clubbing if associated bronchiectasis
-Congested neck veins due to( increased intrathoracic pressure ,cor pulmonale RVF)
-Pursing lips
-Cyanosis in severe hypoxia and flapping tremors if respiratory failure
Local examination
1-Inspection and palpation
● Large barrel shaped chest.
● Prominent accessory respiratory muscle in neck.
● Limited chest expansion
● Low, flat diaphragm causing costal margin retraction on inspiration
● Palpable liver due to:
-depressed by flat diaphragm(not tender)
-congested liver due to cor pulmonal (tender)
● Ascites in RT side heart failure
2-Percussion
● Central trachea
● Decrease TVF bilateral
● Hyperresonance with enchroment on cardiac and hepatic dullness
● Depressed liver
3-Auscultation
● . distant heart sound.
● Diminished Vesicular breath sound with Prolonged expiration with generalized wheezing.
COPD investigations and GOLD classification ?
- Chest x-ray:
In mild COPD, the plain chest X-Ray may well be normal but with advanced emphysema changes include:
● Large volume lungs (Hyperinflation).
● Low flat diaphragm.
● Thin ribbon heart shadow. - CT of the lung:
● Is indicated when there is doubt about the diagnosis of COPD. - ECG AND ECHO:
● To assess cardiac function - PFT spirometry:
●Decrease FEV1 less than 80 %
● Decrease FEV1/FVC ratio less than 70%
● FEV1 improvement after bronchodilator is less than 15%(unlike bronchial asthma the improvement is more than 15 %) - Diffusion test:
● Decrease CO transfer factor in severe cases - Hematocrit:
● Polycythemia can develop in the presence of chronic hypoxemia
-Arterial blood gas measurement:
● Decrease PO2 in type A
● Hypoxia with hypercapnia in type B
- Alpha -1- antitrypsin deficiency screening
-
GOLD Classification of COPD (based on post bronchodilator FEV1):
Stage I: Mild FEV1/FVC < 0.70
FEV1 ≥ 80% predicted
Stage II: Moderate FEV1/FVC < 0.70
FEV1 50 - 80% predicted
Stage III: Severe FEV1/FVC < 0.70
FEV1 30 - 50% predicted
Stage IV: Very Severe FEV1/FVC < 0.70
FEV1 < 30% predicted or FEV1 < 50% predicted and chronic respiratory failure
COPD management?
-Smoking cessation
-Mycolytics
-expectorant
-Bronchodilator
● Inhaled therapy is preferred.
SHORT ACTING BRONCHODILATORS:
● short acting B agonist ,salbutamol(inhaled or nebulizer)
SHORT ACTING ANTICHOLINERGIC AGENTS (ipratropium bromide)
LONG ACTING BRONCHODILATORS
● Long acting B agonist
● (salmeterol and formoterol) twice daily by inhalation
● Long acting anticholinergic (tiotropium bromide )once daily
-Theophylline is effective in COPD.
-Corticosteroids
Inhaled corticosteroids: These reduce the frequency and severity of exacerbations; they are recommended in patients with severe asthma Long-acting bronchodilators are commonly combined with inhaled glucocorticosteroids.
-Antibiotics and antivirals
Antibiotics or antivirals may be prescribed when you develop certain respiratory infections
-Vaccines: influenza vaccination and pneumococcal vaccination;
Non pharmacological treatment
Rehabilitation:
-Oxygen therapy
● Oxygen therapy, one of the principal non-pharmacologic treatments for severe cases
● In hypercapnia, low flow continues humidified oxygen is recommended to
avoid CO2 narcosis.
● (as hypercapnia decrease sensitivity of respiratory center so hypoxia is the main stimulus)
- Surgical treatment
● Bullectomy.
● Lung Transplantation
Acute exacerbation of COPD definition and ttt?
Definitions:
-Acute exacerbations of COPD These are characterised by an increase in symptoms and deterioration in lung function
-They are more common in severe disease and may be caused by bacteria, viruses or a change in air quality
-Respiratory failure and/or fluid retention may be present
Treatment:
- Many patients can be managed at home with the use of increased bronchodilator therapy, a short course of oral corticosteroids and appropriate, antibiotics
- Cyanosis, peripheral oedema or altered conscious level should prompt hospital referral.
-Oxygen therapy: High concentrations of oxygen may cause respiratory depression and worsening acidosis Controlled oxygen at 24% or 28% should be used, aiming for PaO2 >8 kPa (60 mmHg) (or SaO2 88-92%) without worsening acidosis.
-Bronchodilators:
o Nebulised short-acting β2-agonists and anticholinergics are used.
- Corticosteroids: Oral prednisolone (usually 30 mg for 5-10 days) reduces symptoms, improves lung function and shortens hospital stay.
- Prophylaxis against osteoporosis should be considered if frequent courses of corticosteroids are needed.
- Antibiotics: These are recommended for an increase in sputum purulence, sputum volume or breathlessness. An aminopenicillin or a macrolide should be used. Co-amoxiclav is only required in regions where β-lactamase-producing organisms are known to be common.
- Ventilatory support: In patients with persistent tachypnea and respiratory acidosis
