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PNEUMONIA - 25 Marks

1. Definition

• Tintinalli's Emergency Medicine, p. 484

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2. Classification

• Tintinalli's Emergency Medicine, p. 485

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3. Etiology (Common Organisms)

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4. Pathophysiology

1. Route of entry: Pathogens are inhaled or aspirated into the lungs. Aspiration is the more common route, especially in healthcare settings. Hematogenous spread (e.g., from bacteremia) is less common but occurs with S. aureus and Pneumococcus.
2. Alveolar filling: Organisms trigger an intense inflammatory response. The alveoli fill with exudate and WBCs - this is called consolidation.
3. Spread: Organisms spread along the bronchial tree or through pores between adjacent alveoli (pores of Kohn).
4. V/Q mismatch and hypoxemia: Consolidated areas are still perfused but not ventilated - creating a shunt effect (blood passes through unventilated lung). Studies show that in mild pneumonia, shunt = ~7.5% and low V/Q regions account for ~4.2% of perfusion. In severe pneumonia requiring ventilation, shunt rises to ~22%.

• Murray & Nadel's Respiratory Medicine, p. 960

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5. Risk Factors

• Aspiration risk: stroke, swallowing disorders, nasogastric tube, seizures, intubation
• Impaired mucociliary clearance: smoking, COPD
• Bacteremia risk: indwelling vascular devices, debilitation
• General: extremes of age, alcoholism, immunocompromise, malignancy

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6. Clinical Features

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7. Diagnosis

• Chest X-ray: Lobar/segmental consolidation (typical), bilateral patchy infiltrates (atypical/viral)
• CBC: Leukocytosis (bacterial), leukopenia (severe/viral)
• Blood cultures: Low yield in outpatients; recommended for ICU, leukopenia, cavitary lesions, asplenia, pleural effusion
• Sputum Gram stain + culture: Useful only with a good-quality specimen
• Urine Legionella antigen: For ICU patients, alcoholics, travelers
• ABG: If severe desaturation or respiratory distress
• Serum electrolytes, BUN, creatinine: For hospitalized patients

Differential includes: lung cancer, TB, pulmonary embolism, hypersensitivity pneumonitis, fungal infections.

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8. Severity Assessment - CURB-65

• Score 0-1: Treat as outpatient
• Score 2: Consider admission
• Score ≥3: Admit; consider ICU if score ≥4-5

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9. Treatment

Outpatient CAP (healthy, no comorbidities):

• Amoxicillin OR
• Azithromycin or Clarithromycin (macrolide) if typical organisms suspected

Inpatient (non-ICU):

• Beta-lactam (ampicillin-sulbactam, ceftriaxone) + macrolide, OR
• Respiratory fluoroquinolone (levofloxacin, moxifloxacin) alone

Inpatient (ICU/severe CAP):

• Beta-lactam + azithromycin or fluoroquinolone

Pseudomonas risk (HCAP/VAP):

• Anti-pseudomonal beta-lactam (piperacillin-tazobactam) + fluoroquinolone (ciprofloxacin)
• Add vancomycin or linezolid if MRSA risk

Supportive:

• Supplemental oxygen, IV fluids, analgesia
• Consider ICU if: sepsis, mechanical ventilation needed, RR markedly elevated, PaO₂/FiO₂ ≤250, multilobar infiltrates, confusion

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10. Complications

• Parapneumonic effusion / empyema - needs drainage
• Lung abscess - especially with aspiration
• Bacteremia and sepsis
• Respiratory failure / ARDS
• Pleural effusion (causes additional hypoxemia via shunt)

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CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) - 25 Marks

1. Definition

• Robbins Basic Pathology, p. 495; Katzung Pharmacology 16e, p. 565

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2. Epidemiology

• 3rd most common cause of death in the United States
• Costs >$40 billion per year in direct and indirect healthcare costs in the US
• Occurs in older patients with a history of smoking; about 15-30% of habitual smokers develop overt COPD (though radiographic changes occur in a much higher proportion)

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3. The Two Main Components

A. Emphysema

• Definition: Enlargement of air spaces distal to terminal bronchioles caused by destruction of elastic support structures (alveolar walls) by proteases (especially elastase) released from inflammatory cells (mainly neutrophils)
• Mechanism: Protease-antiprotease imbalance. Normally, alpha-1-antitrypsin (AAT) inhibits neutrophil elastase. Smoking increases protease activity AND inactivates AAT
• Subtypes:
  • Centriacinar (centrilobular): Most common; smoking-related; affects central/proximal parts of the acinus
  • Panacinar (panlobular): Affects the whole acinus; classically seen in alpha-1-antitrypsin (AAT) deficiency
• Features: Increased chest volume, severe dyspnea, relatively preserved blood oxygenation at rest ("Pink Puffer")
• Robbins Basic Pathology, p. 495

B. Chronic Bronchitis

• Definition: Persistent productive cough for at least 3 consecutive months in at least 2 consecutive years (clinical definition)
• Mechanism:
  • Mucus overproduction: from hyperplasia of tracheal/large airway mucous glands and goblet cell metaplasia in surface epithelium
  • Airway obstruction: from small airway inflammation (bronchiolitis)
  • Ciliary dysfunction from toxic cigarette smoke products (acrolein is a potent inducer)
• Histology: Enlarged mucus-secreting glands, goblet cell metaplasia, inflammation, bronchiolar wall fibrosis
• Features: Productive cough, hypoxemia, hypercapnia, cyanosis ("Blue Bloater")
• Robbins Basic Pathology, p. 495-496; Fishman's Pulmonary Diseases, p. 143

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4. Pathophysiology

1. Airflow obstruction: Loss of elastic recoil (emphysema) + airway wall thickening (bronchitis) + mucus plugging → reduced FEV₁, normal or near-normal FVC → reduced FEV₁/FVC ratio (<0.70)
2. Mucus dysfunction: Mucin concentrations (MUC5AC and MUC5B) are dramatically elevated in COPD; small airway mucus occlusion correlates with degree of airflow obstruction and predicts longevity
3. Hyperinflation: Loss of elastic recoil → lungs trapped in hyperinflation. During exercise, insufficient expiratory time causes dynamic hyperinflation - end-expiratory lung volume fails to decline to normal
4. Dyspnea mechanism:
   • Decreased ventilatory capacity (increased airway resistance + reduced elastic recoil)
   • Increased ventilatory requirement (V/Q mismatch)
   • Dynamic hyperinflation reduces inspiratory reserve volume, impairs respiratory muscle function, and increases work of breathing
5. Hypoxemia and hypercapnia: Ventilation-perfusion mismatch → Type 1 respiratory failure in emphysema; hypoventilation in chronic bronchitis → Type 2 (hypercapnic) respiratory failure
6. Cor Pulmonale: Chronic hypoxia → pulmonary vasoconstriction → pulmonary hypertension → right heart failure

• Fishman's Pulmonary Diseases, p. 2256-2275; Costanzo Physiology

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5. Risk Factors

• Cigarette smoking - the single most important risk factor
• Alpha-1-antitrypsin deficiency - genetic cause (panacinar emphysema)
• Occupational dust/chemical exposure
• Air pollution
• Recurrent respiratory infections (especially in childhood)
• Passive smoking

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6. Clinical Features

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7. Investigations

• Spirometry (Gold standard):
  • FEV₁/FVC < 0.70 (post-bronchodilator) confirms obstruction
  • Reduced FEV₁
  • Normal or increased FVC (due to air trapping)
• GOLD Staging by FEV₁ (% predicted):
  • GOLD 1 (Mild): FEV₁ ≥80%
  • GOLD 2 (Moderate): 50-79%
  • GOLD 3 (Severe): 30-49%
  • GOLD 4 (Very Severe): <30%
• Chest X-ray: Hyperinflation, flattened diaphragm, increased AP diameter, bullae (emphysema); increased bronchovascular markings (bronchitis)
• CT chest: Detects emphysema, small airway disease, bullae
• ABG: PaO₂↓, PaCO₂↑ (in bronchitis/advanced disease)
• ECG/Echo: For cor pulmonale assessment
• Alpha-1-antitrypsin levels: Screen in young non-smokers with panacinar emphysema

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8. Treatment

Non-pharmacological:

• Smoking cessation - single most effective intervention that slows disease progression
• Pulmonary rehabilitation
• Vaccination (influenza annually, pneumococcal)
• Long-term oxygen therapy (LTOT) if PaO₂ ≤55 mmHg (or ≤60 with cor pulmonale) - only treatment proven to improve survival in severe COPD

Pharmacological:

ICS therapy in COPD: less central than in asthma; use is associated with increased risk of bacterial pneumonia; recommended only for severe obstruction, prior exacerbations, or high eosinophil count

• Katzung Pharmacology, p. 565-566

COPD Exacerbations (Acute Worsening):

• Triggers: viral infection (most common), bacterial infection, air pollution
• Treatment:
  1. Supplemental oxygen (target SpO₂ 88-92% in COPD to avoid suppressing hypoxic drive)
  2. Short-acting bronchodilators (nebulized salbutamol + ipratropium)
  3. Systemic corticosteroids (prednisolone 40 mg x 5 days)
  4. Antibiotics (amoxicillin, doxycycline, or azithromycin) - because COPD exacerbations frequently involve bacterial lower airway infection
  5. Non-invasive ventilation (NIV/BiPAP) - if hypercapnic respiratory failure (pH <7.35)
  6. Mechanical ventilation - last resort

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9. Complications

• Cor pulmonale - right heart failure from chronic hypoxia
• Polycythemia - secondary to chronic hypoxemia
• Spontaneous pneumothorax - rupture of bullae (emphysema)
• Pulmonary hypertension
• Respiratory failure - Type 1 (emphysema) or Type 2 (bronchitis)
• Lung cancer - independent risk from smoking

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10. Key Distinguishing Points: Pneumonia vs. COPD

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