Inflammatory lung diseases (ARDS, pneumonia, tuberculosis) – etiology, pathogenesis, and clinical manifestations.
I. Acute Respiratory Distress Syndrome (ARDS)
Etiology
- Direct lung injury:
- Pneumonia.
- Aspiration of gastric contents.
- Pulmonary contusion.
- Inhalational injury (toxic gases, smoke).
- Indirect (systemic) injury:
- Sepsis (most common cause).
- Severe trauma with shock.
- Acute pancreatitis.
- Massive transfusions.
Pathogenesis
- Initial injury to alveolar-capillary membrane → increased permeability.
- Protein-rich fluid enters alveoli → pulmonary edema (non-cardiogenic).
- Surfactant dysfunction → alveolar collapse (atelectasis).
- Decreased lung compliance and severe V/Q mismatch → refractory hypoxemia.
- Neutrophil activation → release of proteases, ROS, cytokines → further damage.
Clinical manifestations
- Severe dyspnea and tachypnea.
- Cyanosis, hypoxemia not improving with oxygen (refractory).
- Bilateral diffuse infiltrates on imaging.
- Progression to respiratory failure.
II. Pneumonia
Etiolog y
- Community-acquired:
- Streptococcus pneumoniae (most common).
- Haemophilus influenzae.
- Atypical: Mycoplasma, Chlamydophila, Legionella.
- Hospital-acquired (nosocomial):
- Gram- negative bacilli (e.g., Klebsiella, Pseudomonas).
- MRSA.
- Aspiration pneumonia:
- Anaerobes from oral flora.
Pathogenesis
- Inhalation or aspiration of microorganisms.
- Overwhelms local defenses (ciliary dysfunction, macrophages).
- Alveolar inflammation → exudate fills alveoli → consolidation.
- Impaired gas exchange → hypoxemia.
Clinical manifestations
- Fever, chills.
- Productive cough (purulent sputum in bacterial; dry in atypical).
- Pleuritic chest pain.
- Dyspnea, tachypnea.
- Crackles, bronchial breath sounds on auscultation.
- In elderly: confusion, weakness.
III. Tuberculosis (TB)
Etiology
- Mycobacterium tuberculosis, transmitted by airborne droplets.
Pathogenesis
- Inhalation of bacilli → alveolar macrophage phagocytosis.
- Bacilli survive and replicate inside macrophages.
- Primary TB: usually asymptomatic or mild flu-like illness; Ghon complex (lung + hilar node).
- Latent TB: bacteria dormant, contained by immune response (granulomas).
- Reactivation (secondary TB): immune suppression or aging → bacilli multiply, especially in apical lungs → cavitary lesions