PATHOLOGY

1. Define & Classify Obstructive Lung Disorders

Definition:
Obstructive lung disorders are diseases characterized by increased
resistance to airflow due to partial or complete obstruction at any level from
the trachea to the respiratory bronchioles.
Classification:
1. Chronic Obstructive Pulmonary Disease (COPD):
• Emphysema
• Chronic bronchitis
2. Asthma
3. Bronchiectasis
4. Cystic Fibrosis (some sources include this)

EMPHYSEMA
2. Define & Classify Emphysema
Definition:
Emphysema is defined as abnormal permanent enlargement of airspaces
distal to the terminal bronchioles, accompanied by destruction of their
walls, without obvious fibrosis.
Classification (based on anatomic distribution):
1. Centriacinar (Centrilobular) – most common, involves
respiratory bronchioles (upper lobes), strongly associated with smoking.
2. Panacinar (Panlobular) – involves entire acinus, more common in
lower lobes; associated with α1-antitrypsin deficiency.
3. Paraseptal (Distal acinar) – affects distal alveoli, associated with
spontaneous pneumothorax in young adults.
4. Irregular Emphysema – acinus irregularly involved, usually
associated with scarring (asymptomatic, incidental finding).
3. Etiopathogenesis of Emphysema
Etiology:
• Cigarette Smoking – main cause (increased neutrophils,
macrophages, oxidative stress)
 • α1-antitrypsin deficiency
• Environmental pollutants
Pathogenesis (Two major mechanisms):
1. Protease–Antiprotease Imbalance:• Neutrophils &
macrophages release proteases (elastase) which destroy alveolar walls.
• α1-antitrypsin neutralizes elastase; its deficiency leads to
unchecked tissue destruction.
2. Oxidative Stress:
• From smoke and inflammatory cells – inactivates antiproteases
and damages lung tissue
4. Clinical Features of Emphysema
• Progressive dyspnea (initially on exertion)
• Minimal cough, scanty sputum
• Barrel-shaped chest (hyperinflation)
• Use of accessory muscles of respiration
• “Pink puffers”: breathless, not cyanotic
• Weight loss due to increased work of breathing
• Prolonged expiration
• Complications: pneumothorax, pulmonary hypertension, cor
pulmonale
5. Morphology of Emphysema
Gross Features:
• Lungs appear large, voluminous, and pale
• Loss of normal sponginess
• Bulging of alveolar spaces
• Centriacinar type – more severe in upper lobes
• Panacinar type – more uniform involvement, lower lobes
Microscopy (Histology):
• Abnormally enlarged airspaces distal to terminal bronchioles
• Destruction of alveolar walls and septa
• Loss of capillary beds
• Thin, stretched alveolar walls (in early stages)
• No significant fibrosis
• Inflammatory infiltrates (macrophages, neutrophils)
• Pigment-laden macrophages (especially in smokers)⸻

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 LUNG CARCINOMA
Here’s a concise and structured answer based on Harsh Mohan and Robbins
Pathology textbooks regarding Lung Carcinoma (often asked in AP exams
like AP 15, AP 18):
a. Classification of Lung Carcinoma
Lung carcinomas are broadly classified into two major categories:
1. Non-Small Cell Lung Carcinoma (NSCLC) (~85% cases)
• Adenocarcinoma (most common overall, especially in non-
smokers)
• Squamous Cell Carcinoma
• Large Cell Carcinoma
2. Small Cell Lung Carcinoma (SCLC) (~15% cases)
New WHO classifications also recognize:
• Adenosquamous carcinoma
• Carcinoid tumors (typical & atypical)
• Large cell neuroendocrine carcinoma
• Sarcomatoid carcinomas
b. Etiopathogenesis & Clinical Features
Etiopathogenesis:
• Smoking: Strongest risk factor (esp. for SCLC & squamous cell
carcinoma)
• Environmental exposures:
• Radon gas, asbestos, air pollution
• Genetic mutations:
• Adenocarcinoma: EGFR, ALK, KRAS mutations
• SCLC: TP53, RB, MYC amplification
• Chronic inflammation: From COPD, pulmonary fibrosis
Clinical Features:
• Persistent cough, weight loss, hemoptysis
• Chest pain, dyspnea
• Hoarseness (recurrent laryngeal nerve involvement)
• Features of metastasis: Bone pain, CNS symptoms
• Often asymptomatic until advanced
c. Morphology
Gross:

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 • Squamous Cell Carcinoma: Central location, may cavitate
• Adenocarcinoma: Peripheral, firm gray-white mass
• Small Cell Carcinoma: Central, infiltrative, soft & friable
• Large Cell Carcinoma: Large, undifferentiated mass
Microscopy:
• Adenocarcinoma: Glandular differentiation, mucin production,
lepidic pattern (in situ)
• Squamous Cell Carcinoma: Keratin pearls, intercellular bridges
• Small Cell Carcinoma: Small cells, scant cytoplasm, nuclear
molding, high mitoses, necrosis
• Large Cell Carcinoma: Undifferentiated cells, no squamous or
glandular features
d. Complications & Paraneoplastic Syndromes
Complications:
• Local invasion: Pleura, pericardium, esophagus
• Superior vena cava syndrome
• Pancoast tumor: Invasion of apex causing Horner’s syndrome
• Effusions: Pleural or pericardial
• Metastasis: Liver, bone, brain, adrenals
Paraneoplastic Syndromes:
• SCLC:
• SIADH (→ hyponatremia)
• Cushing’s syndrome (ectopic ACTH)
• Lambert-Eaton Myasthenic Syndrome
• Squamous Cell Carcinoma:
• Hypercalcemia (PTHrP secretion)
• Others:
• Hypertrophic pulmonary osteoarthropathy
• Dermatomyositis

BRONCHIECTASIS
Here’s a concise, exam-ready summary of Bronchiectasis based on Harsh
Mohan and Robbins Pathologic Basis of Disease:
(a) Definition of Bronchiectasis
Bronchiectasis is a chronic necrotizing infection of the bronchi and
bronchioles leading to abnormal permanent dilation of these airways.

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(b) Etiopathogenesis & Clinical Features
Etiopathogenesis:
Bronchiectasis results from a cycle of airway obstruction and chronic
infection, leading to destruction of the bronchial wall.
Predisposing conditions:
1. Obstruction (tumor, foreign body, mucus plugs)
2. Congenital/hereditary conditions:
• Cystic fibrosis (most common in children)
• Primary ciliary dyskinesia (e.g., Kartagener syndrome)
• Immunodeficiency states
3. Infections:
• Severe or necrotizing pneumonia (e.g., TB, Staphylococcus)
• Measles, pertussis
These factors impair mucociliary clearance, promoting infection and
inflammation, causing destruction and dilation of bronchi.
Clinical Features:
• Persistent productive cough with copious purulent sputum
• Hemoptysis
• Dyspnea and wheezing
• Clubbing of fingers in chronic cases
• Recurrent respiratory infections
• Worse in the morning due to postural drainage
(c) Morphology
Gross:
• Dilated bronchi extending to the pleural surface
• Commonly involves lower lobes, especially bilaterally
• Airways appear cystic or varicose
• Filled with foul-smelling purulent material
Microscopy:
• Destruction of bronchial walls
• Ulceration and necrosis of epithelium
• Acute and chronic inflammation
• Replacement by fibrous tissue (fibrosis)
• Squamous metaplasia or epithelial hyperplasia
(d) Complications
• Recurrent infections and abscesses

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 • Hemoptysis (sometimes massive)
• Amyloidosis (rare)
• Cor pulmonale due to pulmonary hypertension
• Respiratory failure
• Metastatic brain abscesses (from septic emboli)
Let me know if you’d like a diagram or mind map summarizing this.

NEOPLASIA
Definition of Neoplasia:
According to Harsh Mohan and Robbins Basic Pathology, neoplasia is
defined as:
“Neoplasia is the uncontrolled, abnormal proliferation of cells that persists
even after the removal of the stimulus which initiated the change.”
The resulting mass of abnormal cells is called a neoplasm or tumor.
The term is derived from Greek: neo = new, plasia = growth.
Salient Features of Neoplasia (as described in Harsh Mohan and Robbins):
1. Uncontrolled Cell Proliferation:
Neoplastic cells proliferate autonomously without regard to regulatory
signals, leading to persistent growth even in the absence of stimuli.
2. Clonality:
Neoplasms arise from a single progenitor cell that has undergone genetic
changes, making the tumor monoclonal in origin.
3. Genetic Alterations:
Neoplasms are the result of genetic mutations in proto-oncogenes, tumor
suppressor genes, apoptosis regulators, and DNA repair genes.
4. Loss of Differentiation (Anaplasia):
Malignant neoplasms often show a lack of cellular differentiation, with cells
appearing primitive and atypical.
5. Loss of Normal Regulatory Mechanisms:
Neoplastic cells evade normal growth controls (e.g., contact inhibition,
apoptosis), enabling limitless replication.
6. Formation of a Mass (Tumor):
Neoplasia usually leads to the formation of a mass or swelling due to the
accumulation of abnormal cells.

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 7. Autonomous Growth:
The growth of neoplastic cells continues without dependence on normal
growth signals or the presence of the original triggering factors.
8. Benign vs. Malignant Behavior:
• Benign tumors: Well-differentiated, slow-growing, non-invasive,
and localized.
• Malignant tumors: Poorly differentiated, fast-growing, invasive,
and capable of metastasis.
9. Invasion and Metastasis (Malignant Neoplasms):
A hallmark of malignancy is the ability to invade adjacent tissues and spread
to distant sites via blood, lymphatics, or body cavities.
10. Angiogenesis:
Neoplasms stimulate the formation of new blood vessels to support their
growth and survival.