Pathology of the Lung

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