Pneumonia Flashcards
- Define pneumonia. What are the main causes and mechanisms behind lung consolidation?
Answer:
Definition: Pneumonia is an inflammation of the lung parenchyma, often due to infection but sometimes from non-infectious causes like toxins or aspiration.
Main Causes:
Infectious: Bacteria (e.g., Streptococcus pneumoniae), viruses (e.g., Influenza), fungi.
Non-infectious: Inhalation of chemicals, aspiration of gastric contents.
Mechanisms:
Infection triggers an innate immune response (early) and an adaptive immune response (later).
Lung consolidation occurs due to alveolar spaces filling with exudate (protein-rich fluid) and inflammatory cells, replacing air and causing solidification (“hepatisation”).
- Differentiate between lobar pneumonia and bronchopneumonia.
== lobar pneumonia
Patient Profile/Distribution/ Main Causative Agent/ Tissue Damage/Progression
Healthy adults (20–50 years)
Entire lobe consolidated, usually unilateral
Streptococcus pneumoniae (95%)
Minimal structural destruction
Follows 4 classical stages (Congestion → Red Hepatisation → Grey Hepatisation → Resolution)
- Differentiate between lobar pneumonia and bronchopneumonia.
== bronchopneumonia
Patient Profile/Distribution/ Main Causative Agent/ Tissue Damage/Progression
Extremes of age (infants, elderly) or debilitated patients
Patchy consolidation, often bilateral
Staphylococci, Streptococci, Haemophilus influenzae
Significant alveolar and bronchiolar destruction
Patchy, may coalesce; destructive changes
Describe the four stages of bacterial pneumonia in detail.
Answer:
* 1. Congestion (Day 1):
o Heavy, boggy lungs.
o Vascular engorgement.
o Fluid (transudate progressing to exudate) fills alveoli.
o Bacterial proliferation.
* 2. Red Hepatisation (Days 2–4):
o Alveoli packed with neutrophils, red blood cells, and fibrin.
o Lung appears liver-like, red, and firm.
* 3. Grey Hepatisation (Days 5–9):
o RBCs disintegrate.
o Dominance of neutrophils and macrophages.
o Lung appears grey-brown.
* 4. Resolution (After Day 9–10):
o Macrophages digest and remove debris.
o Normal lung architecture restored if successful.
- Why do people get pneumonia despite having defense mechanisms in the lungs?
Answer: Defense failures occur due to:
* Decreased defenses:
Impaired cough reflex (e.g., CNS depression).
Dysfunction of mucociliary clearance.
Impaired phagocytic activity (e.g., alveolar macrophages).
* Increased vulnerability:
Excessive edema.
Excessive secretions.
* Presence of infections:
Viral infections compromise barriers and immunity.
Hospital-acquired infections (nosocomial).
* Organism virulence and dose: Highly virulent pathogens or overwhelming inoculum.
What are the complications of pneumonia?
- Abscess formation: Especially with Staphylococcus, Klebsiella, and Type 3 pneumococci.
- Pleural involvement:
Pleurisy.
Empyema (pus in pleural cavity).
Pneumothorax (lung collapse from air in pleural space). - Fibrosis: Chronic inflammation leading to fibrotic lung tissue.
- Haematogenous spread: Leading to infective endocarditis, pericarditis, brain abscesses, or septic arthritis.
What is atypical pneumonia and how does it differ from typical bacterial pneumonia?
Answer:
* Etiology: Caused mainly by viruses (Influenza, RSV, COVID-19) and some bacteria (e.g., Mycoplasma pneumoniae, Chlamydia pneumoniae).
* Histology:
Few neutrophils, mainly mononuclear cells (lymphocytes, monocytes).
Interstitial inflammation rather than alveolar exudate.
* Clinical Course:
Less alveolar filling.
Risk of secondary bacterial infection.
* Complications: Can lead to ARDS (Acute Respiratory Distress Syndrome) and V-Q mismatch (ventilation-perfusion imbalance).
How does the immune response contribute to lung damage in pneumonia?
Answer:
* Immunopathology:
o Host’s inflammatory response intended to eliminate pathogens inadvertently causes tissue injury.
o Massive exudate formation leads to hepatization (seen in lobar pneumonia).
o In bronchopneumonia, intense immune response can destroy alveolar and bronchiolar walls, leading to liquefactive necrosis.
What is hepatisation?
Solidification of the lung, making it liver-like due to fluid/cell infiltration.
Dominant cell in early pneumonia?
Neutrophils.
Dominant cell in viral pneumonia?
Mononuclear cells (lymphocytes, monocytes).
Complication specific to bronchopneumonia?
Tissue destruction with massive hemorrhage.
What bacteria causes 95% of lobar pneumonia?
Streptococcus pneumoniae.
Describe the temporal progression of lobar pneumonia through its four classical stages.
Pneumonia, particularly lobar pneumonia, progresses through four stages:
1. Congestion (0–24 hours):
o Bacterial multiplication.
o Vascular engorgement with fluid (transudate then exudate) into alveoli.
o Early neutrophil infiltration.
- Red Hepatisation (Day 2–4):
o Extensive exudation with red blood cells, neutrophils, and fibrin filling alveoli.
o Lung becomes firm and red, resembling liver tissue. - Grey Hepatisation (Day 5–9):
o Decreased red blood cells.
o Alveoli filled mainly with neutrophils, macrophages, fibrin.
o Lung appears grey-brown. - Resolution (>Day 9–10):
o Macrophages digest debris and fibrin.
o Clearance via lymphatics or expectoration.
o Restoration of lung architecture if successful.
Explain how the interaction between bacteria and the host immune response leads to the formation of lobar or bronchopneumonia.
Model Answer:
* In Lobar Pneumonia:
o Highly virulent bacteria (e.g., encapsulated Streptococcus pneumoniae) trigger a robust immune response.
o Massive exudation fills alveoli across an entire lobe.
o Minimal tissue destruction due to efficient containment.
* In Bronchopneumonia:
o Less virulent bacteria or compromised immunity.
o Patchy infiltration begins around bronchioles, often leading to destruction of bronchiolar and alveolar walls.
o Lesions can become confluent over time.
Thus, host immune competency and bacterial virulence govern the pathological pattern.
What are the key histological and clinical bacterial pneumonia
Bacterial Pneumonia (Typical)
Neutrophils predominate
Filled with exudate and inflammatory cells
Severely impaired by alveolar filling
Sudden high fever, productive cough (yellow-green sputum)
Streptococcus pneumoniae, Staphylococcus aureus
What are the key histological and clinical viral pneumonia
Viral Pneumonia (Atypical)
Mononuclear cells (lymphocytes, macrophages) predominate
Little alveolar involvement, mainly interstitial inflammation
Impaired by thickened alveolar walls
Mild fever, dry cough, myalgia, fatigue
Influenza virus, RSV, SARS-CoV-2, Mycoplasma pneumoniae
List and explain the major complications that can arise from pneumonia.
✅ Model Answer:
* Abscess Formation:
o Due to tissue necrosis and liquefaction, often with Staphylococcus aureus and Klebsiella pneumoniae.
* Pleural Complications:
o Pleurisy: Inflammation of pleural surfaces.
o Empyema: Pus accumulation in the pleural cavity.
o Pneumothorax: Air enters pleural space due to rupture, collapsing lung.
* Fibrosis:
o Chronic inflammation can lead to lung fibrosis and reduced lung compliance.
* Sepsis and Haematogenous Spread:
o Dissemination of bacteria leading to infections in heart valves (endocarditis), pericardium (pericarditis), brain (abscess), joints (septic arthritis), or kidneys.
* Secondary bacterial infections:
o Particularly following viral pneumonias (e.g., secondary bacterial bronchopneumonia after influenza).
