Pathology of lung, pleura and upper airways Assoc. Professor Jan Laco, MD, PhD.
Pathology of the Lung
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Transcript of Pathology of the Lung
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Pathology of the lung
C.Murtono
Demo pada blok Respirasi
FKUAJ
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Normal Lung
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Normal Lung
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Common Cold
• Infection, inflammation can spread– Laryngitis– Bronchitis
• Treatment is symptomatic– Acetaminophen– Decongestant– Antihistamine– Humidifiers– Are antibiotics prescribed?
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Secondary Bacterial Infections
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Chronic Bronchitis—Pathophysiology
• Significant changes in bronchi– Irreversible and progressive
• Inflammation, obstruction, repeated infection, chronic coughing• Inflamed, swollen mucosa• Hypertrophy/plasia of mucus glands
– Increased secretions (increased # goblet cells)– Decreased ciliated epithelia
• Fibrosis and thickening of bronchial wall– Further obstruction; pooling of secretions
• Decreased oxygen– Cyanosis during cough
• Severe dyspnea and fatigue• Pulmonary hypertension and R CHF
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Sinusitis
• Secondary bacterial infection• Obstruct drainage in 1 or more paranasal sinuses• Common causative organisms
– Pneumococci– Streptococci– Haemophilus influenzae
• Exudate accumulates• Signs
– Nasal congestion, fever, sore throat• Diagnosis confirmed by radiograph, transillumination• Decongestants, analgesics• Antibiotics
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Classification of the Pneumonias
• Causative agent– Virus, bacteria, fungus– Lobar is typically bacterial
• Pneumococcus
• Anatomical distribution of lesion– Both lungs or lobar
• Pathophysiologic changes– Viral changes in interstitial tissue or alveolar septae– Pneumococcal alveoli inflamed and fluid filled
• Exudate
• Epidemiologic categories– Nosocomial– Community acquired
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Stages of Pneumonia
• Congestion– Inflammation and vascular congestion in alveolar wall
• Exudate forms in alveoli– Interferes with oxygen diffusion
• Consolidation– Neutrophils, RBCs, fibrin accum in exudate
• Form solid mass
• RBCs break down, infection resolves– Macrophages break down exudate
• Expectorated or resorbed
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Lobar Pneumonia
• Streptococcal pneumoniae, pneumococcal
• Infection localized in 1 or more lobes
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Consolidation
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Lobar Pneumonia – Gray hep…
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Lobar Pneumonia:
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Broncho-pneumonia
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Broncho-pneumonia
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Broncho-pneumonia
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Bronchopneumonia:
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Lung Abscess:
• Focal suppuration with necrosis of lung tissue• Strep, Staph & Gram negative & anaerobes• Mechanism:
– Aspiration– Post pneumonic– Septic embolism– Neoplasms
• Productive Cough, fever.• Clubbing• Complications: Systemic spread, septicemia.
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Lung Abscess:
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Lung Abscess:
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Lung Fungal Abscess: Candida
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Normal Lung vs. Cancerous Lung
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Lung Cancer—Pathophysiology
• First change– Metaplasia, change in epithelial tissue
• Smoking, chronic irritation• Reversible if irritation removed
– Loss of ciliated pseudostratified epithelium• More vulnerable to irritants
• Next– Dysplasia, carcinoma develop– Hard to detect
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Bronchogenic Carcinoma
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Lung Cancer—Diagnostic Tests
• Chest X-rays
• Bronchoscopy
• Pulmonary function tests
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Asthma
• Periodic episodes of severe but reversible bronchial obstruction
• Frequency may lead to irreversible damage and COPD
• 2 types– Extrinsic asthma
• Acute episodes triggered by type I hypersensitivities• Onset in childhood
– Intrinsic asthma• Onset during adulthood• Stimuli target hyperresponsive tissue = acute attack
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Asthma—Pathophysiology: Acute Attack
• Both types• Bronchi and bronchioles respond to stimulus
with 3 changes– Bronchoconstriction– Inflammation of mucosa with edema– Increased secretion of thick mucus in passageways
• Changes may result in partial or total obstruction of airways– Interferes with oxygen supply, air flow
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Emphysema—Pathophysiology
• Significant change is destruction of alveolar walls and spaces– Leads to lg, inflated alveoli
• Classified by specific location of changes– Ex: Distal alveoli emphysema– Ex: Bronchiolar emphysema
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Severe Emphysema
• Adjacent damaged alveoli • Lung appears full of holes• Frequent infection• Lg. belbs near lung
surface– May rupture
• Pneumothorax
• Pulmonary hypertension or R CHF
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Primary or Ghon’s Complex
• Primary tuberculosis is the pattern seen with initial infection with tuberculosis in children.
• Reactivation, or secondary tuberculosis, is more typically seen in adults.
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Ghon Complex
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Tuberculous Granuloma
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Granuloma or LH giant cell is not pathagnomonic of TB…!
• Foreign body granuloma.• Fat necrosis.• Fungal infections.• Sarcoidosis.• Crohns disease.
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Caseation Necrosis
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Miliary TB• Millet like – grain.• Extensive micro
spread.• Through blood or
bronchial spread• Low immunity• Pulmonary or
Systemic types.
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Miliary TB
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Cavitary Tuberculosis
• When necrotic tissue is coughed up cavity.
• Cavitation is typical for large granulomas.
• Cavitation is more common in the secondary reactivation tuberculosis - upper lobes.
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Cavitary Secondary TB
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Lung TB - Cavitation
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AFB - Ziehl-Nielson stain
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