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:

Bronchopneumonia

Bronchopneumonia

Bronchopneumonia

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 CancerPathophysiology
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 CancerDiagnostic 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

AsthmaPathophysiology: 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

EmphysemaPathophysiology
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 Ghons 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