Pneumonia Pathophysiology

1. Pneumonia Pathophysiology Alveolar Microbial Proliferation + Host Response via Oropharyngeal Aspiration Droplet Inhalation Hematogenous Contiguous Spread

2. Pneumonia Pathophysiology Congestion – with the presence of a proteinaceousexudate—and often of bacteria—in the alveoli. Rarely evident in clinical or autopsy specimens because it is so rapidly followed by Red Hepatization – with the presence of erythrocytes in the intraalveolarexudate, neutrophils also present for host defense, and bacteria are occasionally seen in cultures. Gray Hepatization – with no new erythrocytes, those already present have been lysed and degraded; neutrophils predominate, fibrin deposition abundant, bacteria have disappeared. Corresponds with successful containment of the infection and improvement in gas exchange. Resolution – macrophages predominate, neutrophil, bacteria, and fibrin debris have been cleared, as has the inflammatory response. Describes best pneumococcal pneumonia

4. EA-TEF Pathophysiology The esophagus and trachea share a common embryologic origin. They typically divide into separate tubes by approximately 36 days gestation. Failure to separate can result in a spectrum of anomalies. Mice deficient in the Sonic-hedgehog signaling pathway develop a phenotype which includes EA-TEF. Sonic-hedgehog transcripts were absent in human esophageal samples obtained from infants with TEF. Tissue obtained from the fistula tract were found to express Thyroid transcription factor one (TTF-1) and fibroblast growth factor FGF-10), suggesting that the fistula is of respiratory origin. A genetic basis for EA-TEF has not been definitively established, but reports indicate that this anomaly may occur in several generations of the same family. Twin studies also demonstrate the presence of esophageal atresia in sets of dizygotictwins.