Resp Pneumonias Flashcards
Define pneumonia. What is the main cause?
Answer:
Pneumonia is an inflammation of the lung parenchyma, typically due to an infection. It results in consolidation, meaning the alveolar spaces are filled with fluid and cells, replacing air. Most commonly, it is caused by bacteria, although viruses and fungi can also be responsible.
Compare lobar pneumonia and bronchopneumonia. List three key differences.
Age group, Distribution, Common organisms
Lobar Pneumonia: Healthy, middle-aged adults; Entire lobe (diffuse, confluent); Streptococcus pneumoniae (95%)
Bronchopneumonia: Extremes of age, debilitated patients; Patchy, multifocal, bilateral; Staph, Strep, H. influenzae, E. coli
List and describe the four classical stages of lobar pneumonia.
Answer:
Congestion (Day 1): Vascular engorgement, transudate in alveoli, few neutrophils, early bacterial multiplication
Red hepatization (Days 2–4): RBCs and neutrophils fill alveoli, exudation, fibrin deposition
Grey hepatization (Days 5–9): RBCs breakdown, dense neutrophilic exudate, macrophage infiltration begins
Resolution (> Day 10): Macrophages clear debris, resorption of exudate, tissue returns to normal
Explain why patients with impaired defenses are more prone to pneumonia.
Answer:
Normal defense mechanisms (cough reflex, mucociliary clearance, macrophages) can be impaired due to:
CNS depression or coma (↓ cough reflex)
Smoking or viral infections (↓ ciliary function)
Immunosuppression (↓ phagocytic activity) This allows pathogens to colonize and invade alveoli, leading to infection.
Which feature distinguishes bronchopneumonia from lobar pneumonia histologically?
Answer:
Tissue destruction is a key feature of bronchopneumonia, with necrosis of alveolar and bronchiolar walls, liquefactive necrosis, and possible massive hemorrhage. Lobar pneumonia preserves architecture but fills alveoli with exudate.
What are the complications of bacterial pneumonia?
Answer:
Abscess formation (esp. with Staph, Klebsiella)
Pleural involvement: pleurisy, empyema, pneumothorax
Fibrosis from chronic inflammation
Sepsis: hematogenous spread to brain, joints, kidneys, etc.
Pericarditis: if bacteria invade heart structures
Describe the pathogenesis of atypical pneumonia.
Answer:
Caused by viruses (e.g., influenza, RSV, SARS-CoV-2) or mycoplasma
Interstitial involvement, not alveolar filling
Lymphocytes and monocytes predominant; few neutrophils
Cytopathic effects may destroy epithelium
May lead to ARDS or secondary bacterial infection
Why does red hepatization occur in pneumonia?
Answer:
Due to vascular leakage, RBCs extravasate into alveoli alongside fibrin and neutrophils, giving the lung a liver-like appearance and texture. It reflects intense inflammation.
What immune cells dominate each phase of pneumonia?
Answer:
Early (congestion/red hepatization): Neutrophils dominate
Grey hepatization/resolution: Macrophages increase to clear debris
Atypical pneumonia: Mononuclear cells (lymphocytes, monocytes)
Explain how atypical pneumonia differs in radiology and histology from typical bacterial pneumonia.
Answer:
Radiology: Diffuse or patchy interstitial infiltrates
Histology: Thickened interstitium, little/no alveolar exudate, sparse neutrophils
Cause: Intracellular pathogens (viruses, mycoplasma)
Why is the alveolar architecture preserved in lobar pneumonia but destroyed in bronchopneumonia?
Answer:
In lobar pneumonia, Streptococcus pneumoniae does not release exotoxins, so inflammation is intense but non-destructive.
In bronchopneumonia, pathogens like Staph aureus release exotoxins, leading to liquefactive necrosis, destroying tissue.
Describe the appearance and significance of “grey hepatization.”
Answer:
Appears grey due to fewer RBCs, more neutrophils, macrophages, and fibrin
Indicates peak of inflammation with exudate consolidation
Precedes resolution stage
