PNEUMONIA Flashcards
Risk Factors for Pathogens Resistant to Usual Therapy for CAP.
- Hospitalization 2 or more days in previous 90 days
- Use of antibiotics in previous 90 days
- Immunosuppresion
- Nonambulatory status
- Tube feedings
- Gastric acid suppression
- Severe COPD or bronchiectasis
Multidrug-resistant gram-negative bacteria and MRSA
Risk Factors for Pathogens Resistant to Usual Therapy for CAP.
- Cavity infiltrate or necrosis
- Gross hemptysis
- Erythematous rash
- Concurrent influenza
- Young, previously healthy status
- Summer-month onset
CA-MRSA
Risk Factors for Pathogens Resistant to Usual Therapy for CAP.
- Hospitalization 2 or more days in previous 90 days
- Use of antibiotics in previous 90 days
- Chronic hemodialysis in previous 30 days
- Documented prior MRSA colonization
- Congestive heart failure
- Gastric acid suppression
Nosocomial MRSA
Mechanical Factors of CAP
- hair and turbinates of the nares
- branching architecture of the tracheobronchial tree
- gag and cough reflex
- normal flora adhering to mucosal cells of the oropharynx
Microorganisms access to the lower respiratory tract by:
– microaspiration from the oropharynx
– small-volume aspiration occurs frequently during sleep
– hematogenous spread
– contiguous extension from an infected pleural or mediastinal space
When the capacity of the alveolar macrophages to ingest or kill the microorganisms is exceeded this become manifested.
clinical pneumonia
Host inflammatory response trigger the clinical syndrome of pneumonia
– release of inflammatory mediators (IL6 and TNF)
fever
host inflammatory response trigger the clinical syndrome of pneumonia
- chemokines (IL 8 and GCSF) -> release of neutrophils
peripheral leukocytosis and increased purulent secretions
Host inflammatory response trigger the clinical syndrome of pneumonia
- Inflammatory mediators released by macrophages and the newly recruited neutrophils
alveolar capillary leak
Host inflammatory response trigger the clinical syndrome of pneumonia
- erythrocytes cross the alveolar–capillary membrane
hemoptysis
Host inflammatory response trigger the clinical syndrome of pneumonia
- capillary leak
radiographic infiltrate and rales
Host inflammatory response trigger the clinical syndrome of pneumonia
- alveolar filling
hypoxemia
Host inflammatory response trigger the clinical syndrome of pneumonia
- increased respiratory drive in the systemic inflammatory response syndrome
respiratory alkalosis
– presence of erythrocytes in the cellular intra-alveolar exudate
– neutrophil influx is more important with regard to host defense
– bacteria are occasionally seen in pathologic specimens collected during this phase
Red hepatization phase
– no new erythrocytes are extravasating, and those already present have been lysed and degraded
– neutrophil is the predominant cell, fibrin deposition is abundant, and bacteria have disappeared
– corresponds with successful containment of the infection and improvement in gas exchange
Gray hepatization
- presence of a proteinaceous exudate—and often of bacteria—in the alveoli
Edema
– macrophage reappears as the dominant cell type in the alveolar space
– debris of neutrophils, bacteria, and fibrin has been cleared, as has the inflammatory
response
Resolution
Most common etiology of CAP
Streptococcus pneumoniae
Atypical pathogens
– Mycoplasma pneumoniae,
– Chlamydia pneumoniae
– Legionella species
– respiratory viruses