Lung Diseases: An Overview

Lung Diseases: An Overview

I. Obstructive Lung Diseases

• Emphysema:

• Mechanism: Loss of lung parenchyma leading to decreased elasticity, trapping air.

• Asthma:

• Allergic Asthma:

• Population: Children, often associated with fever or eczema.

• Mechanism: Type I hypersensitivity reaction.

• Early Phase: Release of mediators causing edema and increased permeability.

• Late Phase: Release of enzymes from eosinophils and neutrophils.

• Grossly: Increased lung size, mucus plugs obstructing bronchioles.

• Microscopically: Smooth muscle hypertrophy, increased basement membrane collagen, eosinophil infiltration.

• Characteristics:

• Presence of Charcot-Leyden crystals and Curschman spirals.

• Reduced FEV1/FVC.

• Decreased PCO2.

• False Positive: Allergic asthma has eosinophils.

• Non-allergic Asthma:

• Population: Adults.

• Chronic Bronchitis:

• Definition: Cough for 3 months in 2 consecutive years.

• Grossly: Mucus plugs obstructing bronchioles.

• Microscopically: Increased Reid index.

• Characteristics: Metaplasia of bronchial epithelium to goblet cells.

• Bronchiectasis:

• Main Process: Infection and obstruction.

• Pathogenesis: Destruction of smooth muscle and elastic fibers of the bronchioles.

• Grossly: Occurs in lower lobes, more common in the right lung.

• Microscopically: Inflammation and destruction of smooth muscle tissue.

• Complications: Hemoptysis, pulmonary hypertension, abscess formation, bronchiectatic bulla formation.

II. Restrictive Lung Diseases

• Restrictive Lung Disease:

• Histologically: Diffuse alveolar damage.

• Alternative name: Interstitial lung disease.

• Stages of Diffuse Alveolar Damage: Exudation, cellular proliferation, fibrosis.

• Acute Restrictive Lung Disease:

• Grossly: Firm lungs.

• Microscopically: Hyaline membrane in exudative stage, type II pneumocyte proliferation, fibrosis.

• Clinically: Severe dyspnea, pink frothy sputum within the first 72 hours.

• Causes: Severe lung infection, aspiration, sepsis, severe trauma with shock.

• Chronic Restrictive Lung Disease:

• Characteristics: Normal FEV1/FVC, decreased gas exchange.

• Causes: Autoimmune, drugs, occupational, idiopathic.

III. Pneumonia

• Typical Community-Acquired Pneumonia:

• Includes: Bronchopneumonia, lobar pneumonia.

• Resolution Stage of Lobar Pneumonia: Many new blood vessels in alveolar walls.

• Atypical Community-Acquired Pneumonia:

• Microscopically: Interstitial lymphocytic infiltration, diffuse alveolar damage.

• Characteristics: Viral etiology.

• Radiation Pneumonitis:

• Early Stage: Similar to diffuse alveolar damage.

• Late Stage: Atypical cells, dysplasia, multinucleation.

IV. Lung Cancer

• Lung Cancer: All are malignant, most common is adenocarcinoma.

• Adenocarcinoma:

• Common in: Females, less associated with smoking.

• Morphology: Papillary and solid forms.

• Squamous Cell Carcinoma:

• Invades: Hilum lymph nodes, distant metastasis late.

• Small Cell Carcinoma:

• Location: Central, along bronchi, early metastasis.

• Nuclei: Small, hyperchromatic, salt and pepper pattern, scant cytoplasm.

• Peripheral Carcinoma:

• Includes: Adenocarcinoma, bronchioloalveolar carcinoma.

• Carcinoma with Lambert-Eaton Myasthenic Syndrome:

• Small Cell Carcinoma.

• Bronchial Carcinoid Tumor:

• Origin: Neuroendocrine cells.

• Grossly: Polypoid tumor protruding into the lumen of the bronchus.

• Microscopically: Normal lining epithelium, nests of cells, organoid pattern, fibrous stroma with blood vessels.

• Diagnosis: Immunohistochemical staining.

V. Pulmonary Tuberculosis

• Primary Tuberculosis: Ghon complex, granuloma in the lung periphery (near the interlobar fissure).

• Secondary Tuberculosis: At the lung apex due to aerobic nature of Mycobacterium tuberculosis.

• Progressive Primary Tuberculosis: Develops bronchiectasis in immunocompromised patients.