Pathophysiology: Inoculation of the respiratory tract by infectious organisms leads to an acute inflammatory response in the host that is typically

1-2 weeks in duration. This inflammatory response differs according to the type of infectious agent present. Viral Infection These are characterized by the accumulation of mononuclear cells in the submucosa and perivascular space, resulting in partial obstruction of the airway. They clinically manifest as wheezing and crackles. Disease progresses when the alveolar type II cells lose their structural integrity and surfactant production is diminished, a hyaline membrane forms, and pulmonary edema develops. Bacterial Infection The alveoli fill with proteinaceous fluid, which triggers a brisk influx of red blood cells and polymorphonuclear cells (red hepatization) followed by the deposition of fibrin and the degradation of inflammatory cells (gray hepatization). During resolution, intra - alveolar debris is ingested and removed by the alveolar macrophages. This consolidation leads to decreased air entry and dullness to percussion. Inflammation in the small airways leads to crackles. Wheezing is less common than in viral infections. Inflammation and pulmonary edema resulting from these infections causes the lungs to become stiff and less distensible, thereby decreasing tidal volume. The patient must increase his respiratory rate to maintain adequate ventilation. Pathophysiology

Etiologic Agent: Factors: Bacteria Virus

Predisposing Elderly Hospitalization Immobilization Immune Defficiency Long Term Illness

Smoking Microorganism enter alveolar Spaces by droplet inhalation Inflammation occurs Alveolar fluid increase Ventilation decreases as secretion thicken Bronchopneumonia Empyema (collection of pus & liquid

From infected tissue) Lung Abscess (collection of pus, inflammation & destruction of tissue) Cancer of the lung Death

Pleurisy (Inflammation of membrane)