LUNGS – NORMAL STRUCTURE

Anatomy

Right lung: 375–550 g (avg. 450 g), 3 lobes (upper, middle, lower), 2 fissures (narrow grooves, clefts)
Left lung: 325–450 g (avg. 400 g), 2 lobes (upper, lower), 1 fissure. Middle lobe represented by lingula (tongue-like projection of the superior lobe that overlaps the heart)
Airway pathway:
Trachea → Right/Left Main Bronchi → Segmental bronchi → Terminal bronchioles → Acinus (functional unit).
Acinus structure:

Respiratory bronchioles
Alveolar ducts
Alveolar sacs (alveoli)

Airway Wall Composition

Trachea/bronchi: Cartilage, smooth muscle, mucous glands.
Bronchioles: Smooth muscle only; no cartilage/mucous glands.

Blood Supply

Dual supply:
- Pulmonary arteries: Deoxygenated blood.
- Bronchial arteries: Oxygenated blood.

🧬 Histology

Bronchi/Bronchioles: Lined by pseudostratified ciliated columnar epithelium with goblet cells (decrease toward bronchioles).

Bronchioles: No goblet cells; have Clara cells (secrete lysozyme).
Alveolar wall (septum):

Capillary endothelium (Single layer of squamous endothelial cells resting on a basement membrane.)
Basement membrane + scant interstitium (the connective tissue framework (collagen, fibroblasts, extracellular matrix, small vessels) that lies between functional units of an organ).
Alveolar epithelium:
- Type I pneumocytes: 95%, gas exchange.
- Type II pneumocytes: Microvilli, secrete surfactant, proliferate to replace Type I.
Alveolar macrophages

💨 Functions

Gas exchange (O₂ in, CO₂ out)
Clearance of inhaled pollutants via mucociliary action, macrophages
Pulmonary circulation affects and is affected by heart diseases.

PAEDIATRIC LUNG DISEASE

1. Congenital Cysts

Defects in bronchial cartilage, elastic tissue/muscle → cysts. (If these structures are deficient, abnormal, or destroyed: The bronchial lumen dilates abnormally. Over time, these dilated, weakened airways form cystic spaces.)
Large cyst = Pneumatocele
Multiple small cysts = Sponge-like lung appearance.
May rupture → pneumothorax (air in the pleural cavity) or hemoptysis (coughing up blood or blood-stained sputum)

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

ARDS is a life-threatening form of acute respiratory failure characterized by diffuse lung injury, severe hypoxemia, and non-cardiogenic pulmonary edema due to increased alveolar–capillary permeability. Also called Hyaline Membrane Disease (HMD)

Types

Neonatal ARDS
Adult ARDS (Diffuse Alveolar Damage)

🌬️ Clinical Features

Neonatal ARDS: Dyspnea (labored breathing), cyanosis, rapid breathing post-birth; often fatal.
Adult ARDS: Sudden respiratory failure, cyanosis, poor response to oxygen.

Etiology

Neonatal ARDS:

Prematurity – most important (↓ surfactant production). (a lipoprotein complex secreted by Type II alveolar epithelial cells (pneumocytes) in the lungs)
Infants of diabetic mothers – insulin antagonizes cortisol, delaying surfactant synthesis.
Caesarean delivery without labor – labor stress normally increases fetal cortisol → surfactant release; absent in elective C-section.
Male sex – males more susceptible (M:F ≈ 2:1).
Birth asphyxia / perinatal hypoxia – impairs surfactant function.
Maternal sedation/anesthesia – depresses fetal respiration and surfactant release.
Idiopathic cases – sometimes occurs without obvious risk factor.

Adult ARDS:

Shock (trauma, sepsis, burns)
Viral infections
Pancreatitis (release of activated pancreatic enzymes (trypsin, elastase, phospholipase) into circulation. These enzymes damage pulmonary capillary endothelium → ↑ vascular permeability.)
Toxins, narcotics, radiation
Drugs (salicylates, colchicine)

Pathogenesis

Neonatal:

↓ Surfactant (from Type II cells) → ↑ surface tension → Atelectasis (Loss of lung volume caused by inadequate expansion of air spaces)
Leads to: ↓ ventilation → Ischemia → Hyaline membrane formation

Adult:

Trigger (sepsis, trauma, infections, pancreatitis, drugs, etc.) →
1. Cytokine Imbalance
  - ↑ Pro-inflammatory cytokines: IL-1, IL-8, TNF
  - Recruit & activate neutrophils
2. Neutrophil-mediated Injury
  - Release proteases, oxidants, leukotrienes
  - → Endothelial & epithelial damage
3. Alveolar–Capillary Barrier Injury
  - ↑ Vascular permeability → Pulmonary edema (protein-rich)
  - Fibrin + necrotic debris → Hyaline membrane formation
4. Repair/Organizing Phase
  - Fibrogenic cytokines (TGF-α, PDGF)
  - → Fibrosis & stiff lungs
End Result
- Alveolar & capillary damage
- Poor compliance (stiff lungs)
- Refractory hypoxemia (does not improve with O₂)
- Respiratory failure

Morphology

Gross:

Lungs: Heavy, airless, sink in water

Microscopy:

Collapsed + dilated alveoli
Necrotic epithelium, eosinophilic hyaline membranes (fibrin + debris)
Oedema, congestion, intra-alveolar hemorrhage
Type II pneumocyte proliferation
Organizing stage: Interstitial fibrosis

Consequences

Death: High neonatal mortality (esp. <1kg); adult ARDS has poor prognosis
Resolution: Possible with supportive care/ventilation

3. Bronchopulmonary Dysplasia (BPD)

Chronic lung disease in neonates (especially preterm infants) who required prolonged oxygen therapy + mechanical ventilation for neonatal ARDS.
Causes / Pathogenesis
- Oxygen toxicity → free radical injury.
- Barotrauma → mechanical ventilation injury.
- Repeated alveolar/capillary damage → abnormal repair → fibrosis & airway remodeling.
Clinical Features
- Persistent respiratory distress lasting 3–6 months after birth.
- Tachypnea, hypoxemia, difficulty weaning from oxygen/ventilator.
- May progress to pulmonary hypertension & cor pulmonale.
Microscopy / Pathology
- Fibrous thickening of alveolar walls.
- Bronchiolitis with inflammatory infiltrates.
- Peribronchial fibrosis.
- Emphysematous changes (over-distension of alveoli).
- Squamous metaplasia in bronchioles (abnormal epithelial repair).

PNEUMONIA – DEFINITION

Pneumonia is acute inflammation of the lung parenchyma distal to the terminal bronchioles (includes alveolar ducts, sacs, and alveoli).
Pneumonitis is another term used synonymously.
Consolidation: Solidification of lung tissue, seen grossly or radiologically in pneumonia due to accumulation of exudate, inflammatory

PATHOGENESIS

Microorganisms enter the lungs through:

Inhalation from the air; Breathing in infectious droplets, dust, or aerosols containing bacteria, viruses, or fungi.
Aspiration from oropharynx/nasopharynx; Microbes from the upper respiratory tract secretions aspirated into lungs, especially in impaired consciousness, alcoholics
Hematogenous spread (bloodstream); Secondary to bacteremia or septicemia from another focus (endocarditis, abscess, IV drug use).
Direct spread from adjacent infection; Extension from nearby infected sites such as pleura, mediastinum, or chest wall.

DEFENSE MECHANISMS OF LUNGS

Nasopharyngeal filtering; The nasal hairs filter large particles (>10 µm). Air turbulence in the upper respiratory tract traps dust and microbes in mucus. Sneezing and coughing expel trapped materials.
Mucociliary clearance; Lined by ciliated columnar epithelium and goblet cells. Goblet cells produce mucus that traps inhaled particles. Ciliary beating moves the mucus layer upwards toward the pharynx, where it is swallowed or expectorated.
Alveolar macrophages; Act as first line of defense in distal airspaces. Phagocytose bacteria, dust, and dead cells.
Immunoglobulins; IgG: predominant in alveolar lining fluid; important in opsonization and complement activation. IgE: involved in defense against parasites and in allergic reactions.

PREDISPOSING FACTORS

Altered consciousness (e.g. coma, trauma, seizures, alcoholism).
Depressed cough reflex (e.g. post-surgery, neuromuscular disease).
Impaired mucociliary transport (e.g. smoking, viral infections).
Alveolar macrophage dysfunction (e.g. hypoxia, malnutrition); defective phagocytosis and cytokine signaling → inadequate local defense.
Endobronchial obstruction (e.g. tumor, mucus plugs); obstruction prevents clearance → stasis of secretions → secondary bacterial infection.
Leucocyte dysfunctions (e.g. AIDS, chemotherapy).

CLASSIFICATION OF PNEUMONIAS

Based on Anatomic Involvement

Lobar Pneumonia (an entire lobe of the lung)
Bronchopneumonia (Lobular pneumonia); Patchy multifocal consolidation around bronchioles, often involving multiple lobes, especially basal lobes.
Interstitial Pneumonia (Atypical); Diffuse, patchy inflammation mainly involving alveolar septa and interstitium, without alveolar exudate.

Etiologic Classification

A. Bacterial Pneumonias

Lobar pneumonia
Bronchopneumonia

B. Viral and Mycoplasmal Pneumonias

Primary atypical pneumonia (caused by atypical pathogens (not the usual pyogenic bacteria)).

C. Other Types

Pneumocystis pneumonia
Legionella (Legionnaire’s disease)
Aspiration pneumonia (Pulmonary infection resulting from inhalation of gastric contents, oropharyngeal secretions)
Hypostatic pneumonia; pneumonia in the dependent portions of lungs (posterior/basal lobes), due to stasis of secretions in bedridden/debilitated patients
Lipid pneumonia; caused by accumulation of lipids (oils/fats) within the alveoli, leading to chronic inflammatory reaction. mineral oil (used as laxative), oily nose drops, ghee, petroleum jelly, occupational exposure (oil sprays). Also occurs when lipids are released from degenerating cells or obstructed airways seen in chronic lung obstruction (tumor), lipid storage diseases, post-radiation injury.

A. BACTERIAL PNEUMONIA

1. LOBAR PNEUMONIA

Definition: Acute bacterial infection affecting part/whole of one or more lobes.

Common Pathogens:

Streptococcus pneumoniae (90% of cases)
Staphylococcus aureus
β-hemolytic streptococci
Klebsiella pneumoniae, Haemophilus influenzae, E. coli, Pseudomonas

Stages of Lobar Pneumonia (Laennec’s Stages)

1. Congestion (1–2 days)

Gross: Dark red, heavy, blood-stained frothy fluid
Microscopy: Dilated capillaries, oedema, few neutrophils, bacteria

2. Red Hepatisation (2–4 days)

Gross: Liver-like red, firm, airless lung
Microscopy: Fibrin, many neutrophils, red cells, engulfed bacteria

3. Grey Hepatisation (4–8 days)

Gross: Grey, firm, granular, dry cut surface
Microscopy: More fibrin, fewer neutrophils/RBCs, macrophages begin to appear

4. Resolution (after day 8–9 or early with antibiotics)

Gross: Frothy, grey-red fluid, softening from center
Microscopy: Macrophages predominant, removal of exudate, lung aeration restored

Complications of Lobar Pneumonia

Organization → Fibrous lung (carnification); Normally, in lobar pneumonia, after the stage of red and grey hepatization, the exudate in alveoli gets digested and removed by macrophages, leading to resolution. But sometimes, the fibrin-rich exudate is not removed. Instead, it undergoes organization. Fibroblasts grow into the alveolar spaces, replacing the exudate with fibrous tissue.As a result, the affected part of lung becomes dense, firm, and airless, resembling red meat → hence the term carnification.
Pleural effusion (abnormal accumulation of fluid in the pleural cavity)→ May resolve or form adhesions
Empyema → Pus in pleural cavity
Lung abscess; A localized area of suppuration and necrosis in the lung, leading to formation of a cavity filled with pus.
Metastatic infection → Pericarditis, endocarditis, meningitis, brain abscess

Clinical Features

Sudden onset, chills, fever, pleuritic chest pain
Productive cough (mucoid/purulent/bloody)
Neutrophilic leucocytosis
X-ray: Lobar consolidation
Sputum culture guides treatment
Good response to antibiotics (within 48–72 hours)

2. BRONCHOPNEUMONIA (Lobular Pneumonia)

Definition: Patchy bacterial infection around terminal bronchioles and alveoli

Common in:

Infants & elderly
Post-viral infections (e.g. influenza, measles)
Bedridden, debilitated patients

Causative Organisms:

Staphylococci, Streptococci, Pneumococci
Klebsiella pneumoniae, Haemophilus influenzae, Pseudomonas

Morphology:

Gross: Patchy red/grey dry lesions (3–4 cm), lower zones, bilateral
Microscopy:
- Acute bronchiolitis
- Neutrophil-rich exudate in alveoli
- Septal (thin walls of connective tissue that separate adjacent alveoli) thickening, oedema in less affected areas

Complications:

Bronchiolar fibrosis → Bronchiectasis (permanent abnormal dilatation of bronchi and bronchioles, caused by destruction of muscle and elastic tissue due to chronic necrotizing infections.)
Other complications similar to lobar pneumonia

Clinical Features:

History of prior illness or infection
Starts as bronchitis, progresses to pneumonia
Blood: Neutrophilic leucocytosis
X-ray: Patchy, mottled opacities in lower zones

Comparison Table – Lobar vs Bronchopneumonia

Feature	Lobar Pneumonia	Bronchopneumonia
Definition	Involves entire or part of lobe	Patchy infection of bronchioles & alveoli
Age	Adults	Infants & elderly
Predisposing factors	Healthy individuals	Chronic illness, viral infections
Common organisms	Pneumococcus, Klebsiella	Staph, Strep, H. influenzae
Pathology	4 classic stages	Patchy consolidation
X-ray	Consolidation	Mottled opacities
Prognosis	Good	Variable, complications more likely
Complications	Less common	Bronchiectasis, others

B. VIRAL & MYCOPLASMAL PNEUMONIA (Primary Atypical Pneumonia)

Definition: Inflammation confined to interstitial tissue of lungs. No alveolar exudate.

Etiology:

Respiratory Syncytial Virus (RSV) (common)
Mycoplasma pneumoniae
Influenza, adenovirus, rhinovirus, CMV, coxsackievirus
Psittacosis (Chlamydia), Q fever (Coxiella)

Morphologic Features

Gross:

Lungs: Heavy, congested, with patchy to diffuse consolidation
Frothy/bloody fluid on cut surface
Mild or absent pleural reaction

Microscopy:

Interstitial inflammation: Thickened alveolar walls with mononuclear cells (lymphocytes, macrophages, plasma cells)
Necrotising bronchiolitis
Reactive hyperplasia: Multinucleate giant cells (syncytia)
Alveolar changes: Oedema, fibrin, hyaline membrane (if severe or bacterial superinfection)

Complications

Superimposed bacterial infection
Severe cases: Interstitial fibrosis

Clinical Features

Starts with upper respiratory symptoms (cold, fever, headache, muscle aches)
Then dry, hacking cough (A short, dry, frequent, non-productive cough, often irritating and persistent)
Blood: Neutrophilic leucocytosis
X-ray: Patchy/diffuse consolidation
Cold agglutinin (Autoantibodies (usually IgM) that bind to red blood cells (RBCs) at cold temperatures (typically 0–4°C, sometimes up to 30°C). They cause agglutination (clumping) and sometimes hemolysis when blood is cooled.) titers ↑ in Mycoplasma and adenovirus
Difficult to isolate organism

C. Other Types of Pneumonias

This category includes infective pneumonias like Pneumocystis carinii and Legionella pneumonia, as well as non-infective types such as aspiration, hypostatic, and lipid pneumonia.

1. Pneumocystis carinii Pneumonia (PCP)

Cause: Pneumocystis carinii (now P. jirovecii) – a fungus found widely in the environment.
Mode of transmission: Inhalation (opportunistic infection).
Affected groups:
- Neonates
- Immunosuppressed individuals (e.g. HIV/AIDS, chemotherapy, organ transplant, malnutrition, agammaglobulinemia).
- Commonest infection in HIV/AIDS patients.

Morphologic Features:

Gross: Lungs are consolidated, dry, and gray.
Microscopy:
1. Interstitial pneumonitis with mononuclear infiltrate in alveolar walls.
2. Alveoli filled with pink frothy fluid containing organisms.
3. Gomori Methenamine Silver (GMS) stain reveals:
  - Oval or crescentic cysts (~5 μm)
  - Tiny black dot-like trophozoites.
4. No significant inflammatory exudate.

Clinical Features:

Rapid onset dyspnea (difficulty in breathing), tachycardia, cyanosis, non-productive cough.
Fatal in 1–2 weeks if untreated.
Chest X-ray: Diffuse alveolar and interstitial infiltrates.

2. Legionella Pneumonia (Legionnaire’s Disease)

Cause: Legionella pneumophila – Gram-negative bacillus.
Source: Contaminated water (e.g., cooling towers, drinking water).
Predisposing Factors: Immunodeficiency, corticosteroids, old age, smoking.

Morphologic Features:

Gross: Widespread bronchopneumonia, pleural effusion common.
Microscopy:
1. Intra-alveolar exudate – early neutrophils, later macrophages.
2. Septal epithelial hyperplasia and thrombosis.
3. Organisms seen in macrophages (special stains, immunofluorescence).

Clinical Features:

Malaise, headache, myalgia → fever, chills, cough.
Bacteremia may lead to:
- Abdominal pain, diarrhea, proteinuria, mild liver dysfunction.

3. Aspiration (Inhalation) Pneumonia

Cause: Inhalation of food, gastric contents, oropharyngeal material.
Risk Factors: Unconsciousness, intoxication, neurological disorders, tumors, infants, tracheoesophageal fistula.

Morphologic Types:

Sterile Aspirate (e.g., gastric acid):
- Chemical pneumonitis
- Hemorrhagic edema
- Cyanosis, shock, bloody sputum
Non-Sterile Aspirate:
- Bronchopneumonia with necrosis
- Granulomas with foreign body giant cells; A chronic inflammatory response characterized by an aggregate of activated macrophages (epithelioid cells), often surrounded by lymphocytes. Sometimes contain multinucleated giant cells. Formed when macrophages fuse around a large, indigestible material (foreign body).

4. Hypostatic Pneumonia

Cause: Stagnation of fluid in basal/posterior lung parts in debilitated patients.
Common in: Bedridden, comatose, or elderly patients.
Mechanism: Accumulated fluid gets infected by URT flora → pneumonia.

5. Lipid Pneumonia

Two Types:
1. Exogenous: Aspiration of oily materials (nasal drops, paraffin, oily vitamins).
2. Endogenous: Tissue breakdown due to obstruction (cancer, TB, bronchiectasis).

Morphologic Features:

Gross: Right lung often affected; golden-yellow consolidated areas.
Microscopy:
- Foamy macrophages in alveoli (lipid-filled)
- Granulomas with foreign body giant cells

Lung Abscess

Definition: Localized necrosis with suppuration (the process of pus formation) of lung tissue.

Types:

Primary: In normal lung; mostly due to aspiration.
Secondary: Complication of other lung diseases or systemic infections.

Etiology:

Organisms: Streptococci, staphylococci, Gram-negative bacteria.
Sources:
- Aspiration (infected material, food)
- Preceding infections (e.g., TB, bronchiectasis)
- Bronchial obstruction (tumor, foreign body)
- Septic embolism; A type of embolism in which fragments of infected material (usually containing bacteria, fungi, or other microorganisms) break off from a primary infectious focus and travel through the bloodstream, lodging in distant sites. These emboli cause both vascular obstruction and secondary infection/abscess formation.

Morphologic Features:

Site: Right lung, lower part of upper lobe or apex of lower lobe.
Gross:
- Single (primary) or multiple (secondary) cavities (mm to 5–6 cm)
Microscopy:
- Suppurative exudate
- Chronic inflammatory infiltrate
- Fibrocollagenous wall in chronic abscess

Clinical Features:

Fever, malaise, weight loss, purulent sputum, hemoptysis

Fungal Infections of Lung

More common than TB in the US; serious in immunocompromised.

1. Aspergillosis

Cause: Aspergillus fumigatus
Forms: Allergic bronchopulmonary aspergillosis, aspergilloma, necrotizing bronchitis
High risk: Leukemia, HIV/AIDS
Gross: Fungal ball (A mass of fungal hyphae, inflammatory cells, fibrin, and necrotic debris) in preexisting cavities
Microscopy:
- Septate hyphae with acute angle branching
- PAS and silver stain positive
- Chronic inflammation in cavity wall

2. Mucormycosis

Cause: Mucor, Rhizopus
Seen in: Diabetic ketoacidosis
Features:
- Broad, non-septate hyphae
- More destructive than aspergillosis

3. Candidiasis

Cause: Candida albicans
Commensal → pathogenic in immunosuppression
May invade blood vessels (angioinvasion)

4. Histoplasmosis

Cause: Histoplasma capsulatum (inhalation of bird droppings)
Lesions: Ghon’s complex-like

5. Cryptococcosis

Cause: Cryptococcus neoformans (pigeon droppings)
Lesions: Granuloma in lung, may cause meningitis

Pulmonary Tuberculosis (TB)

Type of Inflammation: Chronic Granulomatous Inflammation

1. Causative Agent

Mycobacterium tuberculosis
Strict aerobe; thrives in oxygen-rich tissues (e.g., lung apex)
Human strains: M. tuberculosis hominis, M. bovis (rare), M. africanum, etc.

2. Morphology of Granuloma (Tubercle)

A fully-developed tubercle is ~1 mm in diameter and shows:

Central caseation necrosis (cheese-like)
Surrounding epithelioid cells
Langhans’ giant cells (20+ nuclei arranged peripherally)
Peripheral lymphocytes
fibroblasts and fibrosis

3. Cellular Components of TB Granuloma

Epithelioid cells: Modified macrophages; pale eosinophilic cytoplasm; weakly phagocytic.
Multinucleated giant cells: From fusion of epithelioid cells.
- Langhans’ type (TB): nuclei in horseshoe/ring.
Lymphocytes: Cell-mediated immunity
Plasma cells: Humoral response
Necrosis: Central caseation (necrosis in which the dead tissue has a soft, white “cheese-like” appearance)
Fibrosis (excessive deposition of collagen-rich connective tissue): Healing response

4. Diagnostic Methods

Ziehl-Neelsen stain: Acid-fast bacilli (AFB)
Culture: Lowenstein-Jensen medium (6 weeks)
PCR: Rapid, sensitive
Fluorescent stains

5. Hypersensitivity & Immunity

Type IV hypersensitivity (cell-mediated)
Tuberculin (Mantoux) test: PPD injection → ≥15mm induration in 72 hrs indicates previous exposure

6. Evolution of Tubercle (Granuloma)

Neutrophils arrive but fail
Macrophages dominate
T/B cells activated → CD4+ cells induce granuloma formation
Epithelioid cells form, fuse into giant cells
Lymphocytes + fibroblasts surround
Caseation necrosis appears (7–14 days)
Possible fate:
- Liquefaction → cold abscess
- Sinus formation (A sinus in pathology is an abnormal tract lined by granulation tissue that connects a focus of suppuration (pus/abscess) to the body surface or another epithelial surface.)
- Coalescence → fibrosis (When multiple small granulomas join together. They merge into a larger mass of inflammatory tissue. After coalescence, the healing process involves fibroblast proliferation and collagen deposition. This leads to fibrosis (scar tissue formation). Fibrosis replaces normal parenchyma → causes structural distortion and loss of function.
- Calcification or ossification (When tissues undergo chronic inflammation, necrosis, or healing, they may end up with mineral deposition)

7. Types of Tuberculosis

A. Primary Tuberculosis (Ghon’s Complex)

Occurs in non-sensitized individuals
Common in children
Three components:
1. Ghon’s focus: Subpleural lesion (lung)
2. Draining lymphatics: Show tubercles (tiny granulomas)
3. Hilar lymphadenopathy: Caseation
Fate:
- Healing → fibrosis/calcification
- Progression → active spread or miliary TB (disseminated form of tuberculosis)
- Reactivation → secondary TB

B. Secondary Tuberculosis (Reactivation or Reinfection)

In previously sensitized individuals
Often in lung apex (high O₂)
Lesions: Caseating granulomas with peripheral fibrosis
Can arise from:
- Reactivation of dormant focus
- Fresh exogenous infection

8. Spread of Tuberculosis

Local: Macrophage migration
Lymphatic: Regional lymph nodes
Haematogenous: Miliary TB (liver, spleen, kidney, brain)
Natural passages:
- Pleura → pleurisy
- Larynx → laryngitis
- GI tract → ileocaecal TB
- Kidney → bladder

9. Atypical Mycobacteria (Non-Tuberculous Mycobacteria)

Environmental mycobacteria; acid-fast
Include: M. avium, M. kansasii, M. fortuitum, M. ulcerans
Less virulent, not spread person-to-person
Classified as:
- Rapid growers: M. fortuitum, M. chelonae
- Slow growers

10. HIV-Associated Tuberculosis

High incidence in HIV/AIDS patients
Presents with sputum smear-negative but culture-positive TB
More extrapulmonary involvement: Lymph nodes, pleura, meninges

📌 Chronic Obstructive Pulmonary Disease (COPD)

➤ Definition:

Group of chronic lung diseases with obstructed airflow at various levels, resulting in lung function disability.

➤ Major Types:

Chronic bronchitis
Emphysema
Bronchial asthma
Bronchiectasis

Chronic Bronchitis

Definition

Chronic bronchitis is defined as a persistent cough with sputum (expectoration) for at least 3 months in a year, for 2 consecutive years.
It is one of the major forms of COPD (Chronic Obstructive Pulmonary Disease).

Etiopathogenesis (Causes & Mechanism)

The disease is mainly caused by long-term irritation of the airways:

Smoking (most important cause):
- Reduces ciliary activity → poor mucus clearance
- Reduces alveolar macrophage function → impaired defense
- Increases size & number of mucus glands (hypertrophy + hyperplasia)
- Causes bronchial obstruction & reflex bronchoconstriction
Air Pollution:
- Sulfur dioxide, nitrogen dioxide, dust act as irritants.
Occupational Exposure:
- Long-term exposure to dust (e.g., cotton mills, coal mines).
Infections:
- Usually secondary bacterial or viral infections → worsen disease.
Genetic / Familial Factors:
- Family history, passive smoking may contribute.

Morphologic Features

Gross:
- Bronchial walls are thickened, swollen (oedematous) with mucus plugs filling the lumen.
Microscopic:
- Submucosal gland enlargement.
- Goblet cell hyperplasia & squamous metaplasia of bronchial epithelium (Replacement of the normal respiratory columnar ciliated epithelium with stratified squamous epithelium).
- Mucus plugging inside bronchioles.
- Mild chronic inflammation of the bronchial wall.

Clinical Features

Persistent, productive cough (sputum daily).
Recurrent chest infections.
Dyspnea (shortness of breath) especially on exertion.
"Blue Bloaters":
- Cyanosis (bluish discoloration due to hypoxemia).
- Fluid retention → edema.
- May progress to cor pulmonale (right-sided heart failure).
Chest X-ray: Enlarged heart and prominent pulmonary vessels.

Emphysema

Definition

A chronic lung disease characterized by:
- Permanent enlargement of distal airspaces (respiratory bronchioles, alveolar ducts, alveoli).
- Destruction of alveolar walls without significant fibrosis.
It is a distinct clinicopathologic entity separate from chronic bronchitis, though both often coexist in COPD.

Types of True Emphysema

Centriacinar (Centrilobular)
- Involves central/proximal parts of acini (respiratory bronchioles).
- Distal alveoli spared.
- Strongly linked to smoking and most common in upper lobes.
Panacinar (Panlobular)
- Involves entire acinus (from bronchiole to terminal alveoli).
- Associated with α1-antitrypsin deficiency.(It inhibits neutrophil elastase, preventing destruction of alveolar walls.)
- Affects lower lobes more.
Paraseptal (Distal Acinar)
- Involves distal acinus, adjacent to septa.
- Associated with spontaneous pneumothorax in young adults due to rupture of bullae/subpleural blebs or bullae (air-filled spaces).
Irregular
- Involves acini irregularly
- Common, often asymptomatic.
Mixed (Unclassified)
- Shows features of multiple types.

Etiopathogenesis

📌 Protease-Antiprotease Hypothesis

Normal lungs:
- α1-antitrypsin (α1-AT) inhibits neutrophil elastase, preventing alveolar damage.
In α1-AT deficiency:
- Elastase unchecked → alveolar wall destruction.
- Leads to panacinar emphysema (esp. lower lobes).
Smoking:
- Inactivates α1-AT (oxidative stress).
- Attracts neutrophils, ↑ elastase release.
- Therefore, smoking accelerates emphysema.

Pathology

Gross:
- Overinflated, pale lungs.
- Subpleural bullae and blebs (air-filled spaces).
Microscopic:
- Enlarged airspaces.
- Destroyed alveolar septa.
- Loss of elastic tissue.
- Mild chronic inflammation.

Clinical Features (Predominant Emphysema)

Dyspnea: Progressive, often first symptom.
Cough: Appears late, with scanty sputum.
Barrel-shaped chest: Due to hyperinflation.
Weight loss: Common due to ↑ work of breathing.
Late stage: Cor pulmonale and respiratory failure.
CXR: Hyperlucent lungs (Lungs appear darker on X-ray because they contain more air than normal), flattened diaphragm (Diaphragmatic domes lose their normal rounded contour and appear depressed/flat), small vertical heart (Hyperinflated lungs compress and push the mediastinum and heart vertically).

Bronchial Asthma

Definition: Hyperresponsive airways leading to reversible airway narrowing
Symptoms: Dyspnoea, cough, wheezing (high-pitched, whistling sound produced during breathing)
Severe form: Status asthmaticus (A prolonged, severe asthma attack lasting for hours to days. Characterized by severe airflow obstruction, hypoxemia. Unresponsive to usual therapy)
Epidemiology:
- ~4% in US
- 50% cases begin before age 10

Types of Asthma

Feature	Extrinsic (Atopic/Allergic)	Intrinsic (Non-atopic)
Age	Childhood	Adult
Allergy History	Present	Absent
Allergens	Present	Absent
Serum IgE	Elevated	Normal
Nasal polyps/Chronic bronchitis	Absent	Present
Drug Sensitivity	Rare	Often (e.g. Aspirin)

Pathogenesis

Extrinsic Asthma:
- IgE-mediated Type I hypersensitivity
- Triggered by allergens (e.g., dust, pollen)
- Acute Phase: Mast cells → histamine, leukotrienes → bronchospasm, edema, mucus
- Late Phase: Eosinophils, neutrophils → prolonged inflammation
Intrinsic Asthma:
- Triggered by infections (esp. viral), cold, stress, drugs (e.g., aspirin)
- No IgE involvement
Mixed Type: Overlapping features

Morphology

Gross: Overinflated lungs, mucus plug occlusion
Microscopy:
1. Thickened basement membrane
2. Submucosal gland & smooth muscle hypertrophy
3. Inflammatory infiltrates (eosinophils, lymphocytes)

Clinical Features

Dyspnoea, wheezing, and cough
Eosinophilia in blood and sputum
Chronic asthma may lead to cor pulmonale

Bronchiectasis

Definition
- Permanent, abnormal, and irreversible dilatation of bronchi/bronchioles (>2 mm in diameter).
- Results from chronic infection and obstruction causing destruction of the bronchial wall.
Etiology & Pathogenesis
Two main mechanisms:
1. Obstruction
  - Tumors, foreign bodies.
  - Obstruction → impaired clearance → infection → wall destruction.
2. Infection
  - Severe necrotizing pneumonia or TB → bronchial wall damage → dilatation.
  - Often infection + obstruction act together.
Associated Conditions
- Congenital / Hereditary:
  - Congenital bronchiectasis.
  - Cystic fibrosis → thick mucus, recurrent infections.
  - Immotile cilia syndrome (Kartagener’s syndrome) → defective mucociliary clearance.
- Obstructive causes:
  - Tumors, foreign body aspiration.
- Secondary to infections:
  - Staphylococcal pneumonia, TB, pertussis.
Morphology
Gross
- Usually affects lower lobes (gravity favors drainage and infection).
- Dilated bronchi often extend to pleural surface.
- Types:
  - Cylindrical – uniform tube-like dilatation.
  - Fusiform – spindle-shaped dilatation.
  - Saccular (cystic) – balloon-like dilatation.
  - Varicose – irregular dilatation with alternating constriction.
Microscopy
- Ulceration or squamous metaplasia of epithelium.
- Inflammatory infiltrates in wall.
- Destruction of smooth muscle & elastic tissue.
Clinical Features
- Chronic productive cough with copious, foul-smelling purulent sputum (often layered: frothy → mucopurulent → purulent).
- Haemoptysis (sometimes massive).
- Recurrent pneumonias.
- Dyspnoea, fever, malaise.
Complications

Clubbing of fingers and toes (due to chronic hypoxia).
Cor pulmonale (pulmonary hypertension → right heart failure).
Brain abscesses (via septic emboli).

Goodpasture’s Syndrome

Definition:
A rare, life-threatening autoimmune disorder characterized by a combination of:

Pulmonary hemorrhage (due to lung involvement)
Rapidly progressive glomerulonephritis (RPGN) (due to kidney involvement).

Pathogenesis

Caused by anti-glomerular basement membrane (anti-GBM) antibodies.
These antibodies target the non-collagenous domain of the α3 chain of type IV collagen, which is present in both:
- Glomerular basement membrane (kidneys)
- Alveolar basement membrane (lungs).
Binding of antibodies → complement activation → inflammation → tissue destruction.
Smoking, infections, or hydrocarbon exposure may trigger pulmonary involvement.

Microscopy / Histopathology

Lungs:
- Diffuse alveolar hemorrhage
- Necrosis and later fibrosis
- Numerous hemosiderin-laden macrophages in alveoli
Kidneys:
- Crescentic glomerulonephritis (RPGN pattern)
- Fibrinoid necrosis of glomerular capillaries
- Linear IgG and C3 deposition along GBM on immunofluorescence

Clinical Features

Typically affects young males (20–40 years), but can occur at any age.
Pulmonary symptoms:
- Hemoptysis (often massive, recurrent)
- Anemia (from blood loss)
- Dyspnea, cough, respiratory failure
Renal symptoms:
- Hematuria, proteinuria
- Rapidly progressive renal failure (RPGN)
Without treatment → progression to end-stage renal disease (ESRD).

Diagnosis

Serology: Circulating anti-GBM antibodies (ELISA).
Renal biopsy: Crescentic GN with linear IgG deposits on GBM.
Lung biopsy (rarely needed): Alveolar hemorrhage, antibody deposition.

Treatment

Plasmapheresis: removes anti-GBM antibodies.
Immunosuppression: corticosteroids to suppress autoantibody production.
Supportive: oxygen, dialysis if renal failure develops.
Prognosis: poor if diagnosis is delayed; early treatment improves outcomes.

Tumours of the Lungs

I. Overview

Lungs can be affected by both benign and malignant tumours.
Bronchogenic carcinoma accounts for 95% of all primary lung tumours.
The lungs are also the most common site for metastases from other cancers.

II. WHO Classification of Lung Tumours

A. Epithelial Tumours

These constitute the majority of primary lung neoplasms.

1. Benign Epithelial Tumours

Papillomas:
Arise from the bronchial epithelium. They are exophytic growths that project into the bronchial lumen.
- Squamous papilloma: composed of stratified squamous epithelium, may be associated with HPV infection.
- Glandular papilloma: rare, with mucin-secreting columnar cells.
Adenomas:
Benign gland-forming neoplasms that may arise from bronchial or alveolar epithelium.

2. Dysplasia and Carcinoma in Situ

Represents preinvasive epithelial changes characterized by cellular atypia, increased nuclear-cytoplasmic ratio, and mitotic activity.
If untreated, severe dysplasia or carcinoma in situ may progress to invasive bronchogenic carcinoma. These changes are typically seen in the bronchial epithelium of chronic smokers.

3. Malignant Epithelial Tumours (Bronchogenic Carcinomas)

B. Soft Tissue Tumours

Derived from the connective tissue of the lung.

Benign:
- Fibroma (from fibroblasts)
- Leiomyoma (smooth muscle origin)
- Lipoma (adipose tissue)
- Haemangioma (vascular origin)
Malignant: leiomyosarcoma, angiosarcoma

A sarcoma is a malignant tumour that arises from mesenchymal (connective tissue) cells, such as those forming bone, cartilage, muscle, fat, fibrous tissue, blood vessels, or supporting stroma.

C. Pleural Tumours

Benign Mesothelioma
Malignant Mesothelioma

Mesothelioma is a malignant tumor of the mesothelial cells that line the serosal surfaces of the body.

D. Miscellaneous Tumours

Carcinosarcoma: Contains both carcinoma (epithelial) and sarcoma (mesenchymal) elements.
Pulmonary Blastoma (A blastoma is a malignant tumor composed of immature, undifferentiated cells that resemble embryonic (precursor) cells of the tissue from which they arise)
Melanoma (tumour of melanocytes — the pigment-producing cells)
Lymphoma (malignant neoplasm of lymphoid tissue, originating from lymphocytes (B cells, T cells, or NK cells)

E. Secondary (Metastatic) Tumours

Metastatic deposits to the lungs are far more common than primary lung cancers.

Common primary sources: breast, colon, kidney, thyroid, bone, and uterus.
Usually multiple, peripheral, and round.
Spread occurs via hematogenous or lymphatic routes.

Bronchogenic Carcinoma (Primary Carcinoma of the Lung)

Bronchogenic carcinoma refers to malignant epithelial tumours arising from the bronchial or bronchiolar epithelium. It is the most common cause of cancer-related death worldwide in both men and women and remains a major public health concern due to its strong association with smoking.

Incidence and Classification

Most common cancer in men and leading cause of cancer deaths globally.
Peak incidence: Between 55–65 years of age.
Increasing incidence in women due to changing smoking patterns

Main Histologic Types (WHO Classification)

Squamous Cell Carcinoma
Small Cell Carcinoma (small, round to oval cells with scant cytoplasm, hyperchromatic nuclei, and finely granular)
Adenocarcinoma (currently the most common subtype)
Large Cell Carcinoma (composed of large polygonal cells that lack the cytologic and architectural features of squamous cell carcinoma, adenocarcinoma, or small cell carcinoma)
Adenosquamous Carcinoma

Therapeutic (Clinical) Classification

Category	Proportion	Includes	Clinical Note
Small Cell Carcinoma (SCC)	20–25%	Small (oat) cell types	Highly malignant, early metastasis, chemo-responsive
Non-Small Cell Carcinoma (NSCC)	70–75%	Squamous, Adenocarcinoma, Large Cell	Often treated by surgery ± chemo/radiation
Combined Patterns	5–10%	Mixed histologies	Intermediate behaviour

Etiology

1. Smoking (Most Important Factor)

Responsible for ~80% of lung cancers.
Dose-dependent risk: Heavy smokers have a 60–70× higher risk than non-smokers.
Risk decreases after cessation but never returns to baseline.
Strongest association: Squamous cell carcinoma and Small cell carcinoma.
Carcinogens in cigarette smoke: Polycyclic aromatic hydrocarbons, Nickel, arsenic, and formaldehyde, Reactive oxygen species and free radicals

2. Other Risk Factors

Air pollution (industrial emissions, diesel exhaust)
Occupational exposures (Asbestos, uranium, chromium, nickel, beryllium, arsenic)
Vitamin A deficiency: Impairs epithelial repair and promotes metaplasia.
Chronic scarring: From tuberculosis.
Genetic predisposition and familial clustering.

IV. Molecular Pathogenesis

Oncogene Activation

K-RAS, EGFR, BRAF, MYC, PIK3CA

Tumour Suppressor Gene Inactivation

p53, Rb, p16, and RASSF1A (on chromosome 3p)

Autocrine Growth Factors

Tumour cells secrete autocrine peptides promoting proliferation. Nicotine also promotes tumour growth through nicotinic acetylcholine receptors.

Inherited Susceptibility

Li-Fraumeni syndrome (p53 mutation) and Retinoblastoma (Rb mutation) increase risk.

Molecular Therapy Targets

Molecular Alteration	Targeted Therapy
EGFR mutation	EGFR-TKIs (Gefitinib, Erlotinib)
ALK rearrangement	ALK inhibitors (Crizotinib)
VEGF overexpression	Anti-VEGF (Bevacizumab)
PD-L1 expression	Immune checkpoint inhibitors
Proteomic profiling	Future precision diagnosis and individualized therapy

V. Morphologic Types

A. Gross Morphology

Type	Location & Features
Hilar (Central) Tumours	Arise from main or segmental bronchi; grey-white; may cause obstruction.
Peripheral Tumours	Often adenocarcinomas; occur near lung periphery; mucoid or fibrotic appearance; may invade pleura.

B. Histologic Types

1. Squamous Cell Carcinoma

Site: Central, arising in major bronchi.
Association: Strongly linked with smoking.
Microscopy: Keratinized, intercellular bridges, squamous differentiation.
Pathogenesis: Sequential changes—metaplasia → dysplasia → carcinoma in situ → invasive carcinoma.

2. Small Cell Carcinoma

Site: Central; highly malignant, neuroendocrine origin (Neuroendocrine cells receive neuronal input and respond by releasing hormones or peptide substances into the blood, affecting distant target organs. Scattered singly or in small clusters in the bronchial and bronchiolar epithelium. Serotonin (5-HT), Calcitonin)
Microscopy: Small round cells, scant cytoplasm, “salt-and-pepper” chromatin
Markers: Chromogranin, NSE, CD56 positive.
Behavior: Early metastasis, chemo-responsive but poor long-term survival.

3. Adenocarcinoma

Site: Peripheral; most common type in women and non-smokers.
Microscopy: Glandular differentiation or mucin production.
Mutations: EGFR, ALK, KRAS.

4. Large Cell Carcinoma

Undifferentiated malignant epithelial tumour lacking glandular or squamous features.
Cells: Large, polygonal with abundant cytoplasm, prominent nucleoli.

5. Adenosquamous Carcinoma

Contains both glandular and squamous components, each ≥10% of tumour.
Behavior: Highly aggressive, poor prognosis.

VI. Spread of Tumour

1. Direct Invasion: Tumour extends to bronchi, pleura, pericardium, or great vessels.

2. Lymphatic Spread

Sequential spread to: Hilar nodes → Mediastinal nodes → Supraclavicular nodes.

3. Haematogenous Spread

Common metastatic sites: Liver > Adrenals > Bones > Brain > Other organs.

Clinical Features

A. Local Symptoms

Cough, chest pain, dyspnea, hemoptysis, wheezing.
Bronchial obstruction → leads to pneumonia

B. Metastatic Symptoms

Bone pain, neurological deficits, seizures, or liver enlargement. Superior Vena Cava (SVC) syndrome (obstruction of the superior vena cava, resulting in impaired venous drainage from the head, neck, upper extremities, and upper thorax into the right atrium.) due to mediastinal invasion.

C. Paraneoplastic Syndromes

Lung cancers often produce ectopic hormones (Ectopic hormone production refers to the abnormal secretion of biologically active hormones or hormone-like substances by non-endocrine tumors.)

Hormone / Factor	Effect / Syndrome	Commonly Seen In
ACTH	Cushing’s syndrome	Small cell carcinoma
ADH	SIADH → Hyponatremia	Small cell carcinoma
PTHrP	Hypercalcemia	Squamous cell carcinoma
Calcitonin	Hypocalcemia	Small cell carcinoma
Gonadotropins	Gynaecomastia (benign enlargement of the male breast)	Small cell carcinoma

PLEURA

NORMAL STRUCTURE

Visceral pleura: Covers lungs and fissures
Parietal pleura: Lines chest wall, mediastinum, diaphragm
Pleural cavity: Thin space with <15 mL of clear fluid
Lining: Single layer of mesothelial cells with connective tissue beneath

PLEURAL INFLAMMATIONS (PLEURITIS)

Pleuritis (Pleurisy) refers to inflammation of the pleura — the serous membrane covering the lungs (visceral pleura) and lining the thoracic cavity (parietal pleura).
It may occur as a primary condition, but more commonly it is secondary to lung or systemic diseases.

1. Serous, Fibrinous, and Serofibrinous Pleuritis

Pathogenesis

Results from increased vascular permeability due to inflammation.
The pleural cavity accumulates serous fluid (clear yellow), or fibrin if inflammation is more intense.

Causes

Infectious: Tuberculosis, bacterial pneumonia, lung abscess.
Non-infectious: Pulmonary infarcts, autoimmune diseases (Rheumatoid arthritis, SLE), uraemia

Morphology

Serous pleuritis: Thin clear exudate with few cells.
Fibrinous pleuritis: Rough pleural surfaces covered with gray-white fibrinous exudate; “bread and butter” appearance.
Serofibrinous pleuritis: Combination of fluid and fibrin.

Clinical Features

Sharp chest pain
Pleural friction rub
Fever and mild dyspnea (difficult or uncomfortable breathing) may occur.

Outcome

Usually resolves completely with absorption of exudate.
Repeated or severe attacks → fibrosis (deposition of fibrous connective tissue mainly collagen in an organ or tissue as a reactive or reparative process) and pleural adhesions, causing restricted lung expansion.

2. Suppurative Pleuritis

A purulent infection of the pleural cavity characterized by accumulation of pus. Represents severe bacterial infection of the pleura.

Causes

Direct spread from lung infections (pneumonia, lung abscess, bronchiectasis (irreversible dilation of bronchi due to destruction of their wall).
Trauma or post-surgical contamination.
Haematogenous spread.

Morphology

Pleural cavity filled with thick yellow-green pus.
Pleural surfaces become covered with fibrinopurulent exudate

Complications

Pleural fibrosis and adhesion → restricted lung expansion.
Loculated empyema (pus trapped in pockets).
Sepsis if untreated.

Clinical Features

Fever, productive cough, pleuritic chest pain, dyspnea.

3. Haemorrhagic Pleuritis

Inflammatory pleuritis with bloody exudate in the pleural cavity.

Causes

Metastatic carcinoma or other malignant involvement of pleura.
Bleeding disorders (e.g., anticoagulant therapy, thrombocytopenia).
Rickettsial infections or viral diseases.
Occasionally secondary to TB

Clinical Features

Chest pain, dyspnea

Outcome

May resolve with treatment of the underlying cause, or progress to fibrosing pleuritis.

NON-INFLAMMATORY PLEURAL EFFUSIONS

1. Hydrothorax

Clear, serous fluid (transudate) in pleural cavity
Causes: CHF (most common), renal/liver failure, tumors
Findings: Often bilateral

2. Haemothorax

Pure blood in pleural cavity
Causes: Trauma, ruptured aortic aneurysm
Complication: Clotting → fibrosis if not drained promptly

PNEUMOTHORAX

Pneumothorax is the presence of air or gas in the pleural cavity, leading to partial or complete collapse of the affected lung. It results from breach of the visceral or parietal pleura, allowing air to enter the normally closed pleural space.

Under normal conditions, the pleural cavity maintains negative pressure, which keeps the lung inflated and adherent to the chest wall. When air enters the cavity, the negative pressure is lost, and the lung collapses.

Types of Pneumothorax

1. Spontaneous Pneumothorax

Occurs without external trauma.

(a) Primary Spontaneous Pneumothorax

Seen mostly in young, tall, thin males.
Caused by rupture of small subpleural blebs or bullae (air-filled spaces within or beneath the visceral pleura, resulting from localized destruction of alveolar walls), usually at the lung apex.

(b) Secondary Spontaneous Pneumothorax

Occurs in individuals with underlying lung pathology that weakens alveoli or pleura.
Common causes:

Emphysema
Asthma
Tuberculosis
Bronchiectasis
Lung abscess

May present with sudden chest pain and breathlessness due to collapse of diseased lung tissue.

2. Traumatic Pneumothorax

Results from penetrating or blunt injury to the chest wall, allowing air entry.
Causes include:

Rib fractures puncturing lung
Stab or gunshot wounds
Surgical or biopsy procedures

May be open (communication with outside air) or closed (air trapped within pleural cavity).

3. Therapeutic Pneumothorax

Historically induced intentionally to collapse the lung in treatment of pulmonary tuberculosis (before antibiotics).
The rationale was to “rest” the infected lung and allow healing.
Now obsolete due to effective anti-TB therapy.

Complication: Tension Pneumothorax

A medical emergency where air enters the pleural space on inspiration but cannot escape during expiration (one-way valve mechanism).
This causes progressive accumulation of air, leading to:

Increased intrathoracic pressure
Mediastinal shift to the opposite side
Compression of the lung and great vessels

Management

Immediate decompression by inserting a wide-bore needle into the 2nd intercostal space (midclavicular line) to release trapped air,
followed by chest tube drainage.

The Respiratory System

Anatomy

Airway Wall Composition

Blood Supply

🧬 Histology

💨 Functions

PAEDIATRIC LUNG DISEASE

1. Congenital Cysts

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

Types

🌬️ Clinical Features

Etiology

Neonatal ARDS:

Adult ARDS:

Pathogenesis

Neonatal:

Adult:

End Result

Morphology

Gross:

Microscopy:

Consequences

3. Bronchopulmonary Dysplasia (BPD)

Causes / Pathogenesis

Clinical Features

Microscopy / Pathology

PNEUMONIA – DEFINITION

PATHOGENESIS

DEFENSE MECHANISMS OF LUNGS

PREDISPOSING FACTORS

CLASSIFICATION OF PNEUMONIAS

Based on Anatomic Involvement

Etiologic Classification

A. BACTERIAL PNEUMONIA

1. LOBAR PNEUMONIA

Stages of Lobar Pneumonia (Laennec’s Stages)

1. Congestion (1–2 days)

2. Red Hepatisation (2–4 days)

3. Grey Hepatisation (4–8 days)

4. Resolution (after day 8–9 or early with antibiotics)

Complications of Lobar Pneumonia

Clinical Features

2. BRONCHOPNEUMONIA (Lobular Pneumonia)

Comparison Table – Lobar vs Bronchopneumonia

B. VIRAL & MYCOPLASMAL PNEUMONIA (Primary Atypical Pneumonia)

Morphologic Features

Complications

Clinical Features

C. Other Types of Pneumonias

1. Pneumocystis carinii Pneumonia (PCP)

Morphologic Features:

Clinical Features:

2. Legionella Pneumonia (Legionnaire’s Disease)

Morphologic Features:

Clinical Features:

3. Aspiration (Inhalation) Pneumonia

Morphologic Types:

4. Hypostatic Pneumonia

5. Lipid Pneumonia

Morphologic Features:

Lung Abscess

Types:

Etiology:

Morphologic Features:

Clinical Features:

Fungal Infections of Lung

1. Aspergillosis

2. Mucormycosis

3. Candidiasis

4. Histoplasmosis

5. Cryptococcosis

Pulmonary Tuberculosis (TB)

1. Causative Agent

2. Morphology of Granuloma (Tubercle)

3. Cellular Components of TB Granuloma

4. Diagnostic Methods

5. Hypersensitivity & Immunity

6. Evolution of Tubercle (Granuloma)

7. Types of Tuberculosis

A. Primary Tuberculosis (Ghon’s Complex)