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Pathology of the Lung

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Pathology of the lung C.Murtono Demo pada blok Respirasi FKUAJ
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Page 1: Pathology of the Lung

Pathology of the lung

C.Murtono

Demo pada blok Respirasi

FKUAJ

Page 2: Pathology of the Lung

Normal Lung

Page 3: Pathology of the Lung

Normal Lung

Page 4: Pathology of the Lung

Common Cold

• Infection, inflammation can spread– Laryngitis– Bronchitis

• Treatment is symptomatic– Acetaminophen– Decongestant– Antihistamine– Humidifiers– Are antibiotics prescribed?

Page 5: Pathology of the Lung

Secondary Bacterial Infections

Page 6: Pathology of the Lung

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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Page 8: Pathology of the Lung

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

Page 11: Pathology of the Lung

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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Page 14: Pathology of the Lung

Lobar Pneumonia

• Streptococcal pneumoniae, pneumococcal

• Infection localized in 1 or more lobes

Page 15: Pathology of the Lung

Consolidation

Page 16: Pathology of the Lung

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

Page 21: Pathology of the Lung

Bronchopneumonia:

Page 22: Pathology of the Lung

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.

Page 23: Pathology of the Lung

Lung Abscess:

Page 24: Pathology of the Lung

Lung Abscess:

Page 25: Pathology of the Lung

Lung Fungal Abscess: Candida

Page 26: Pathology of the Lung

Normal Lung vs. Cancerous Lung

Page 27: Pathology of the 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

Page 28: Pathology of the Lung

Bronchogenic Carcinoma

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Page 30: Pathology of the Lung

Lung Cancer—Diagnostic Tests

• Chest X-rays

• Bronchoscopy

• Pulmonary function tests

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Page 33: Pathology of the Lung

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

Page 34: Pathology of the Lung

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

Page 35: Pathology of the Lung
Page 36: Pathology of the Lung
Page 37: Pathology of the Lung

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

Page 38: Pathology of the Lung
Page 39: Pathology of the Lung
Page 40: Pathology of the Lung
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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

Page 42: Pathology of the Lung

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.

Page 43: Pathology of the Lung

Ghon Complex

Page 44: Pathology of the Lung

Tuberculous Granuloma

Page 45: Pathology of the Lung

Granuloma or LH giant cell is not pathagnomonic of TB…!

• Foreign body granuloma.• Fat necrosis.• Fungal infections.• Sarcoidosis.• Crohns disease.

Page 46: Pathology of the Lung

Caseation Necrosis

Page 47: Pathology of the Lung

Miliary TB• Millet like – grain.• Extensive micro

spread.• Through blood or

bronchial spread• Low immunity• Pulmonary or

Systemic types.

Page 48: Pathology of the Lung

Miliary TB

Page 49: Pathology of the Lung

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.

Page 50: Pathology of the Lung

Cavitary Secondary TB

Page 51: Pathology of the Lung

Lung TB - Cavitation

Page 52: Pathology of the Lung

AFB - Ziehl-Nielson stain

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Page 54: Pathology of the Lung

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