A.1 Obstructive Lung Disease Flashcards
A.1 Obstructive Lung Disease
COPD - Chronic Obstructive Pulmonary Disease
Obstruction of airflow leading to air trapping in lungs. Airways may close prematurely, measured through lung volumes such as FRC, RV, and TLC.
A.1 Obstructive Lung Disease
Types of COPD:
Chronic Bronchitis: Characterized by a productive cough occurring most days for at least three consecutive months over two years.
Emphysema: Involves the destruction of alveolar walls, significantly impacting lung function.
A.1 Obstructive Lung Disease
Epidemiology:
Affects more males than females (2:3 male-to-female ratio).
Third leading cause of death globally.
A.1 Obstructive Lung Disease
Etiology:
Exogenous Factors:
Smoking: Primary cause (90% of cases).
Environmental pollution and occupational exposure.
Endogenous Factors:
Genetic predisposition (e.g., α1-Antitrypsin deficiency).
Antibody deficiencies affecting lung growth and development.
Conditions like primary ciliary dyskinesia (e.g., Kartagener syndrome).
A.1 Obstructive Lung Disease
Classification
GOLD utilizes the FEV1/FVC ratio (Tiffeneau-Pinelli index) to classify COPD.
Assessment includes symptom severity and history of exacerbations, which informs the GOLD stages and treatment options.
A.1 Obstructive Lung Disease
Emphysema Subtypes
Centrilobular Emphysema:
Most prevalent, especially among smokers; typically affects the upper lung zones and distal alveoli.
Panlobular Emphysema (Panacinar):
Less common; often associated with α1-antitrypsin deficiency; predominantly affects the lower lung zones.
Senile Emphysema:
Loss of pulmonary elasticity due to aging.
A.1 Obstructive Lung Disease
Pathophysiology:
Chronic Inflammation:
- Exposure to harmful stimuli leads to increased oxidative stress and the release of reactive oxygen species (ROS) by inflammatory cells.
- Involvement of goblet cells, macrophages, and CD8+ T lymphocytes contributes to the release of cytokines and the structural changes in lung parenchyma.
- There is an increase in goblet cell proliferation, mucus hypersecretion, and impaired ciliary function, resulting in chronic productive cough.
- A Reid index of less than 0.5 indicates chronic bronchitis, which reflects the thickness of the submucosal mucus layer in relation to the bronchial epithelium.
- Smooth muscle hyperplasia of the small airways can lead to pulmonary hypertension and cor pulmonale (right heart failure).
Tissue Destruction:
- Bronchial inflammation or other harmful factors increase protease activity, including α1-antitrypsin deficiency.
- This imbalance in protease activity leads to the following:
- Loss of elastic recoil and destruction of lung parenchyma.
- Changes in lung compliance and increased air trapping.
- Development of dead space, which can be assessed by DLCO and V/Q mismatch.
- Results in hypoxemia and hypercapnia.
A.1 Obstructive Lung Disease
Symptoms:
Symptoms may be minimal or nonspecific until the disease progresses to an advanced stage, including:
Chronic cough with sputum production.
Dyspnea and tachypnea (initial symptoms may be subtle, progressing to more evident signs).
Pursued lip breathing.
Expiratory wheezing, crackles, muffled breath sounds, and/course rhonchi on auscultation.
Cyanosis (due to hypoxemia).
Tachycardia.
A.1 Obstructive Lung Disease
Indicators of Advanced COPD:
Diaphragmatic Dysfunction:
Increased anterior-posterior chest diameter.
Respiratory Muscle Weakness:
Impairment of respiratory muscles (diaphragm included).
Hyperresonance on percussion:
Reduced diaphragmatic excursion and decreased lung expansion noted during respiratory assessment.
Diminished Breath Sounds:
Often described as “silent” lung.
A.1 Obstructive Lung Disease
Complications:
Right ventricular hypertrophy evident through clinical signs, indicating cor pulmonale.
Peripheral edema (often noted in the ankles) and hepatomegaly.
Risk of additional conditions such as hypoxemia and hypercapnia.
A.1 Obstructive Lung Disease
Physical Exam Findings:
Nail clubbing related to lung conditions (e.g., bronchiectasis, pulmonary fibrosis, lung cancer).
A.1 Obstructive Lung Disease
Diagnosis
Pulmonary Function Test (PFT):
- Spirometry and Body Plethysmography:
- Evaluate FEV1, FVC, and FEV1/FVC ratio.
- Post-bronchodilator test: FEV1/FVC ratio should be < 0.70.
Blood Gas Analysis and Pulse Oximetry:
- Assess for hypoxemia and hypercapnia.
Imaging Studies:
- Chest X-ray:
- Notes: Increased AP diameter, flat diaphragms, and hyperinflation.
- Chest CT:
- Used for differential diagnosis (Dx).
Laboratory Tests:
- Complete Blood Count (CBC):
- May show increased serum hematocrit.
- Testing for Alpha-1 Antitrypsin Deficiency (AATD):
- Recommended for all COPD patients, irrespective of age or ethnicity.
- Liver Biopsy:
- Evaluates for PAS-positive, spherical inclusion bodies in peripheral hepatocytes.
Microbiological Evaluation:
- Gram Stain and Sputum Culture:
- Important in suspected pulmonary infections (e.g., new infiltrate on chest X-ray).
Electrocardiogram (ECG):
- May show signs of P. pulmonale, including low amplitude of QRS complexes and poor R wave progression.
A.1 Obstructive Lung Disease
Treatment:
- Cessation of Tobacco Use: This is the most effective step to slow the decline in lung function.
- Medical Treatment according to GOLD:
- Patient Group A (1 or fewer symptoms):
- Initial Treatment: Any bronchodilator, such as a SABA (short-acting beta agonist) or short-acting bronchodilator.
- Subsequent Escalation: Consider adding LAMA (long-acting muscarinic antagonist) or LABA (long-acting beta agonist).
- Patient Group B (Mild symptoms):
- Initial Treatment: LABA and LAMA.
- Subsequent Escalation: Add ICS (inhaled corticosteroids) if necessary.
- Patient Group C (Moderate symptoms):
- Initial Treatment: LAMA.
- Subsequent Escalation: Consider adding ICS, especially for patients with a high eosinophil count.
- Patient Group D (Severe symptoms):
- Initial Treatment: LAMA plus ICS.
- Subsequent Escalation: Consider systemic corticosteroids or other therapies as needed.
A.1 Obstructive Lung Disease
Complications:
Chronic respiratory failure is noted when pO2 is less than 60 mm Hg.
There may be instances of acute exacerbation.
Cor pulmonale can occur, potentially leading to secondary spontaneous pneumothorax due to the rupture of bullae, particularly in those with bullous emphysema.
A.1 Obstructive Lung Disease
Bronchiectasis
Bronchiectasis is caused by either inadequate clearance of secretions, airway obstruction, or impaired host defenses, which can lead to permanent dilation of the airways.
A.1 Obstructive Lung Disease
Etiology
Bronchiectasis
Pulmonary Infections:
Infections (e.g., bacterial, viral, fungal) associated with conditions such as pneumonia or post-infectious bronchiectasis (e.g., following severe viral illness or Sjögren syndrome, Crohn disease).
Disorders of Ciliary Motility:
Conditions such as Cystic Fibrosis (CF):
Primary ciliary dyskinesia (PCD) / Kartagener syndrome.
Obstruction:
Airway blockage or damage leading to impaired mucus clearance (e.g., tumors, foreign bodies).
Immunodeficiencies:
Examples include situations where the immune response is compromised, like immunodeficiency syndromes.
A.1 Obstructive Lung Disease
Clinical Features
Bronchiectasis
Bronchiectasis should be considered in patients with chronic cough and copious sputum production.
Symptoms:
Chronic productive cough, often with the production of sputum.
Associated signs include crackles, hemoptysis, wheezing, and bronchial breath sounds.
Dyspnea:
Shortness of breath, which may worsen during exertion.
Expectoration:
A possible yellow or green, foul-smelling sputum, often indicating infection.
Clubbing of Nails:
Finger clubbing may be present due to chronic hypoxia or lung disease.
A.1 Obstructive Lung Disease
Diagnostics
Bronchiectasis
Chest X-ray:
Preferred initial test to look for:
“Tram track” lines.
Thin-walled cysts (potentially with air-fluid levels).
In advanced stages, can reveal honeycombing.
High-Resolution Computed Tomography (HRCT):
Confirmatory test for bronchiectasis, showing:
Dilated bronchi with thickened walls.
Cysts, particularly located in the lower lobes, and evidence of honeycombing.
A.1 Obstructive Lung Disease
Treatment:
Bronchiectasis
Management:
- Cannot be cured, but symptoms and progression can be managed. The underlying causes should also be addressed.
Conservative Approaches:
- Bronchopulmonary hygiene and chest physiotherapy.
- Antibiotic therapy for exacerbations and prevention.
- Smoking cessation.
- Vaccinations:
- Annual influenza vaccine and pneumococcal vaccine.
Medications:
- Corticosteroids and nebulized hypertonic saline may be beneficial.
A.1 Obstructive Lung Disease
Invasive Procedures:
Bronchiectasis
Surgical options:
Resection of bronchiectatic tissue or lobectomy may be indicated, particularly if pulmonary hemorrhage or significant bronchial obstruction is present.
Pulmonary artery embolization:
For those with complications related to bronchiectasis.
Lung transplantation:
Considered for end-stage disease.
A.1 Obstructive Lung Disease
Complications
Bronchiectasis
Recurrent bronchopulmonary infections leading to COPD and respiratory failure.
Pulmonary hemorrhage (e.g., hemoptysis).
Lung abscess.
