Pathophysiology · MU Sofia

81. Obstructive lung diseases (chronic bronchitis, emphysema) - etiology, pathogenesis, clinical manifestations.

Inside: 4 sections · 1 labelled picture · 13 flashcards · 1 min

Topic 81 of 168 in the MU Sofia syllabus for Pathophysiology (Medicine, Year 3). The free AceMed note covers it in 4 sections, about 202 words (1 min of reading), with 13 flashcards.

In this note

  1. Obstructive lung diseases (chronic bronchitis, emphysema) - etiology, pathogenesis, and clinical manifestations.
  2. Pathogenesis
  3. Clinical manifestations
  4. II. Emphysema

Obstructive lung diseases (chronic bronchitis, emphysema) - etiology, pathogenesis, and clinical manifestations.

Group of diseases characterized by increased airway resistance, leading to obstructed airflow, especially during expiration.

I. Chronic bronchitis

Etiology

  • Cigarette smoking (most common cause).
  • Air pollution, occupational dust and chemical exposure.
  • Recurrent respiratory infections.

Pathogenesis

  1. Chronic exposure to irritants → airway epithelial irritation.
  2. Mucous gland hyperplasia and goblet cell metaplasia → excessive mucus production.
  3. Impaired ciliary function → decreased mucus clearance.
  4. Airway narrowing and obstruction by thick mucus → air trapping.
  5. Chronic inflammation → fibrosis and smooth muscle hypertrophy.

Clinical manifestations

  • Chronic productive cough ("blue bloater").
  • Dyspnea on exertion (later stages).
  • Frequent respiratory infections.
  • Cyanosis (hypoxemia).
  • Peripheral edema (due to right heart failure — cor pulmonale).

II. Emphysema

Etiology

  • Smoking (major cause).
  • α₁- antitrypsin deficiency (genetic form).

Pathogenesis

  1. Inflammation and oxidative stress from smoking → activation of neutrophils and macrophages.
  2. Release of proteases (elastase) and reactive oxygen species → destruction of alveolar walls.
  3. Loss of elastic recoil and alveolar septa → permanent enlargement of airspaces distal to terminal bronchioles.
  4. Air trapping → hyperinflation → impaired expiratory airflow.
  5. Decreased alveolar surface area → impaired gas exchange.

Clinical manifestations

  • Progressive dyspnea ("pink puffer").
  • Minimal cough and scant sputum.
  • Weight loss (increased work of breathing).
  • Barrel- shaped chest (hyperinflation).
  • Use of accessory muscles.
  • Pursed- lip breathing (to prevent airway collapse).

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