Pulmonary Infection Pathology Flashcards
Pulmonary
Host Defenses
- Physical barriers
- Nasal turbinates, epiglottis, larynx
- Dichotomously branching conducting airways
- Anatomic barrier
- Mucociliary clearance
- Coughing
- Antibaterial activity of bronchial secretions
- Lysozyme, lactoferrin, sIgA
- Defenses in alveolar spaces
- Surfactant ⇒ antibacterial activity
Pulmonary Infection
Risk factors
- Intubation
- Malnutrition
- Cigarette smoke & other noxious fumes
- Congenital structual defects of cilia
- LOC or anesthesia
- Pulmonary congestion, edema, emphysema
- Immunosuppression
Routes of Infection
- Inhalation of infectious droplets
- Aspiration of oral/gastric contents
- Hematogenous
Pulmonary Consolidation
When alveoli filled with supprative exudates
PNA
Patterns
Lobar PNA
Involves one or more lobes uniformly
Strep. pneumoniae most common cause
Bacterial PNA
Inflammatory Stages
- Congestion
- Red hepatization
- Gray hepatization
- Resolution vs organization
Congestion
Stage 1:
Red Hepatization
Stage 2:
Grey Hepatization
Stage 3:
Resolution
Stage 4:
Exudates resolves or undergoes organization.
Organizing PNA
- Virulent organisms damaged basement membrane
- Activates repair reaction
- Influx of fibroblasts ⇒ collagen secretion
- Exudates become organized
Bronchopneumonia
Lobular, patchy, non-uniform distribution of consolidation
Caused by many pathogens:
- Gram ⊕
- S. aureus, S. pneumoniae, S. pyogenes, H. inluenzae
- Gram ⊖
- P. aeruginosa, Enterobacteriaceae, L. pneumophila
Bronchopneumonia
Gross Appearance
Granular consolidation, often adjacent to major airways.
Seen as pale-colored, firm nodules.
Bronchopneumonia
Microscopic Appearance
Alveoli filled with edema, extravasated RBCs, bacteria, PMN, and alveolar Mφ.
Can see virulent organisms, likely to organize:
S. aureus ⇒ microabscesses, results in permanent lung damage
P. aeruginosa ⇒ vasculitis, necrosis