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Pathology of the lung
C.Murtono
Demo pada blok Respirasi
FKUAJ
Normal Lung
Normal Lung
Common Cold
• Infection, inflammation can spread– Laryngitis– Bronchitis
• Treatment is symptomatic– Acetaminophen– Decongestant– Antihistamine– Humidifiers– Are antibiotics prescribed?
Secondary Bacterial Infections
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
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
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
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
Lobar Pneumonia
• Streptococcal pneumoniae, pneumococcal
• Infection localized in 1 or more lobes
Consolidation
Lobar Pneumonia – Gray hep…
Lobar Pneumonia:
Broncho-pneumonia
Broncho-pneumonia
Broncho-pneumonia
Bronchopneumonia:
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.
Lung Abscess:
Lung Abscess:
Lung Fungal Abscess: Candida
Normal Lung vs. Cancerous Lung
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
Bronchogenic Carcinoma
Lung Cancer—Diagnostic Tests
• Chest X-rays
• Bronchoscopy
• Pulmonary function tests
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
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
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
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
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.
Ghon Complex
Tuberculous Granuloma
Granuloma or LH giant cell is not pathagnomonic of TB…!
• Foreign body granuloma.• Fat necrosis.• Fungal infections.• Sarcoidosis.• Crohns disease.
Caseation Necrosis
Miliary TB• Millet like – grain.• Extensive micro
spread.• Through blood or
bronchial spread• Low immunity• Pulmonary or
Systemic types.
Miliary TB
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.
Cavitary Secondary TB
Lung TB - Cavitation
AFB - Ziehl-Nielson stain