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Page 1: Pneumonia

Aspiration from the oropharynx Pathogens inhaled as contaminated droplets Hematogenous spread, or by

contiguous extension from

an infected pleural or

mediastinal space

Etiologic Agent

When barriers are overcome or when the microorganisms are small

enough to be inhaled to the alveolar level

When the capacity of the alveolar macrophages to

ingest or kill the microorganisms is exceeded

Alveolar macrophages initiate the inflammatory

response to bolster lower respiratory tract defenses

Release of inflammatory

mediators: interleukin (IL)-1

and tumor necrosis factor

(TNF)

Fever

Chemokines: IL-8, GCSF Release of Neutrophils

Peripheral

leukocytosis and

increased purulent

secretions

Inflammatory mediators released by macrophages + neutrophils Alveolar

capillary leak

(initially

localized) Radiographic infiltrate

Hemoptysis

Hypoxemia

Rales

Alveolar Filling

+ Some bacterial pathogens

Severe Hypoxemia

Increased respiratory drive

in SIRS Respiratory Alkalosis

Dyspnea

If severe enough, the changes in lung

mechanics secondary to reductions in

lung volume and compliance and the

intrapulmonary shunting of blood may

cause the patient's death.

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