Respiratory System – Pathology Notes

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Normal Anatomy & Histology of the Respiratory System

Foundation

1. Structural Overview

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Upper Respiratory TractNasal organ, pharynx, larynx (above cricoid cartilage)

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Lower Respiratory TractTrachea, bronchi, and lungs (below cricoid cartilage)

Nasal organ → Pharynx → Larynx
↓
Trachea Conducting
↓
L/R Bronchi → Bronchial tree
↓
Bronchiole (<1 mm)
↓
Terminal bronchiole (<0.5 mm)
↓
Respiratory bronchioles Respiratory
↓
Alveolar ducts → Alveolar sacs → Alveoli

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Key Concepts Lobule = unit supplied by a terminal bronchiole. Acinus = basic functional/respiratory unit = cluster from respiratory bronchiole onward. The pulmonary acinus is where gas exchange happens.

2. Trachea — Histological Layers

Mucosa

Epithelium + Lamina propria

Submucosa

Connective tissue, glands

Cartilage

C-shaped hyaline cartilage rings

Adventitia

Outermost fibrous layer

Epithelial cells of the airway (Pseudostratified ciliated columnar epithelium):

Ciliated cells — beat mucus toward pharynx
Goblet cells — secrete mucus
Basal cells — stem/progenitor cells
Small granular cells — neuroendocrine cells (important in small cell carcinoma)

3. Air-Blood Barrier

The ultimate site of gas exchange. Function: excrete CO₂ from blood and replenish O₂. Located in the alveolar wall.

4. Defense Mechanisms of the Respiratory Tract

Rhinothrix (nasal hairs) — physical baffle for large particles
Cilia-mucus transport system — mucociliary escalator; moves particles up
Local immunity — secretory IgA in respiratory secretions, complement (alexin), lysozyme
Alveolar macrophages — phagocytose particles/pathogens in alveoli

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Section 1 — Pneumonia

§ 1

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Classification By agent: bacterial, viral, fungal.
By distribution: Lobar pneumonia · Lobular (broncho)pneumonia · Interstitial pneumonia

A. Lobar Pneumonia

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EtiologyStreptococcus pneumoniae (most common). Predisposed by cold, fatigue.

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Typical PatientAdults 30–50 years, previously healthy.

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PathogenesisBacteria → proliferate in alveoli → capillary dilatation → serous exudates → spread via Kohn's pores → entire lobe involved.

Morphology — Type: Diffuse exudative (fibrinous) inflammation in alveoli. Involves a large portion or entire lobe.

Four Classical Pathological Stages:

Stage 1 · Day 1–2

Congestion

Diffuse serous inflammation. Lobe: heavy, dark red, boggy. Frothy red fluid squeezed out. Micro: vascular congestion, proteinaceous fluid, scattered neutrophils, many bacteria in alveoli.

Stage 2 · Day 3–4

Red Hepatization

Lobe: red, firm, liver-like. Alveoli packed with fibrin, red cells, neutrophils, bacteria. Interalveolar congestion persists. Pleura may show fibrinous exudate.

Stage 3 · Day 5–6

Gray Hepatization

Lobe: dry, gray, firm, liver-like. Congestion diminished. Alveoli distended with fibrin + many neutrophils but fewer bacteria. Capillaries appear compressed.

Stage 4 · After 1 week

Resolution

Favorable outcome. Consolidated exudate undergoes enzymatic degradation; macrophages clear debris. Normal structure restored.

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Why we rarely see all stages todayAntibiotic therapy interrupts the natural sequence.

Clinical Features:

Cough, fever, "rusty" sputum (hemosiderin from RBC degradation by macrophages)
Pleuritic pain and pleural friction rub (fibrinous exudate in visceral pleura)
Sudden onset with chills, dyspnea, chest pain, productive sputum

Complications:

Pulmonary carnification — failure to resolve; organized to brown flesh-like fibrous tissue (due to ↓ neutrophil proteinase or ↑ fibrin exudate)
Empyema (pus in pleural cavity)
Abscess formation
Septicemia / pyemia
Infectious (toxic) shock

B. Lobular Pneumonia (Bronchopneumonia)

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EtiologyPyogenic bacteria: staphylococci, streptococci, pneumococci.

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Typical PatientChildren, elderly, debilitated (immunocompromised) patients.

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DistributionMultifocal, bilateral, basal lung predominance. Centered around small bronchi and bronchioles → hence "bronchopneumonia".

Pathological Changes:

Gross: lower lobes, dispersed elevated focal areas of consolidation and suppuration. Severe cases → confluent bronchopneumonia.
Microscopy (LM): suppurative, neutrophil-rich exudate fills bronchi, bronchioles, adjacent alveoli; walls show vascular congestion and edema; alveolar spaces show proteinaceous edema; compensatory emphysema in adjacent areas.
Pleural involvement less common than lobar pneumonia.

Clinical Features: Fever, cough, purulent sputum. Often aggravates pre-existing illness.

Complications:

Respiratory failure
Heart failure (toxins → myocardial damage + hypoxia → pulmonary artery spasm → right heart overload)
Abscess, pyemia, empyema
Bronchiectasis

Lobar vs Lobular Pneumonia — High-Yield Comparison

Feature	Lobar Pneumonia	Lobular (Broncho)pneumonia
Causative agent	Pneumococcus (S. pneumoniae)	Pyogenic bacteria (Staph, Strep, Pneumo)
Typical age	30–50 yrs, healthy adult	Children, elderly, debilitated
Distribution	Entire lobe (diffuse)	Patchy, multifocal, bilateral, basal
Nature of inflammation	Fibrinous (exudative)	Suppurative (purulent)
Stages	4 classic stages, ~7–10 days	No classic stages
Pleural involvement	Common	Less common
Key complications	Carnification, lung abscess, septicemia, toxic shock	Lung abscess, pyothorax, bronchiectasis, heart failure, respiratory failure
Clinical onset	Sudden, chills, fever, rusty sputum	Fever, cough, purulent sputum

C. Viral Pneumonia

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PathogensInfluenza virus, RSV (respiratory syncytial virus), adenovirus, parainfluenza virus.

Pathological Changes:

Gross: lungs slightly enlarged, edematous
Microscopy: Interstitial pneumonia pattern — alveolar walls widened and edematous, infiltrated with mononuclear cells (lymphocytes, monocytes). Alveolar spaces contain little fluid with occasional mononuclear cells.
Viral inclusion bodies — diagnostic feature: round/oval, erythrocyte-like in size, mostly eosinophilic, with halos. Examples:
- CMV (Cytomegalovirus): located in nucleus
- Measles virus: located in cytoplasm
Hyaline membrane formation → less sputum, dyspnea
Multinucleated giant cells (from alveolar epithelium)

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Inclusion bodies — formationFormed by aggregation of complete virus particles or unassembled virus subunits, or reaction products of host cells to viral infection (without actual virus particles).

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Section 2 — COPD & Pulmonary Emphysema

§ 2

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COPD DefinitionA group of conditions sharing dyspnea with chronic/recurrent obstruction to airflow. Major types: chronic bronchitis, emphysema, bronchiectasis, asthma.

A. Pulmonary Emphysema

Definition: Abnormal permanent enlargement of airspaces distal to the terminal bronchiole, accompanied by destruction of their walls without obvious fibrosis.

Etiology & Pathogenesis

Key Mechanism: Two critical imbalances working together (additive effects):

Imbalance 1

Protease–Antiprotease Imbalance

Smoking → ↑ elastase activity
α₁-antitrypsin (α₁AT) deficiency → ↓ anti-elastase → elastic fiber damage
α₁AT deficiency can be congenital OR "functional" (due to oxidative inactivation by smoking)

Imbalance 2

Oxidant–Antioxidant Imbalance

Smoking → oxidants → inactivate α₁AT (functional deficiency)
Combines with protease imbalance → additive tissue damage

Also contributing: Obstructive ventilatory dysfunction of bronchioles → narrowing.

Types of Emphysema (by anatomic distribution within the lobule)

Type	Location of Dilation	Key Association
1. Centriacinar	Respiratory bronchioles dilate (central part of acinus)	Cigarette smoking; most common; not α₁AT deficiency
2. Panacinar	Entire acinus uniformly enlarged (respiratory bronchiole → terminal alveoli)	α₁-antitrypsin deficiency
3. Distal acinar (paraseptal)	Adjacent to pleura and lobular connective tissue septa; margins of lobules most affected	Spontaneous pneumothorax in young adults; bulla formation
4. Irregular	Irregular; associated with scarring	Healed inflammatory diseases; clinically asymptomatic; most common form overall

🧠 Memory Aid — Types of Emphysema

C – P – D – I

Centriacinar (Smoking) · Panacinar (α₁AT deficiency) · Distal acinar (Pneumothorax) · Irregular (Scarring)

Morphology

Gross:

Enlarged, blunt margins
Pale/gray-white, soft, without elasticity
Honeycomb-like appearance

Microscopy (LM):

Large, irregular air spaces
Markedly reduced number of alveolar walls
Thinning and destruction of alveolar septa
Septal capillaries compressed and bloodless
With advanced disease: adjacent alveoli coalesce → large airspaces

Clinical Features

Insidious onset of dyspnea (pulmonary dysfunction)
Barrel-shaped chest (enlarged lungs)
Risk of pneumothorax (bulla rupture)
Secondary pulmonary hypertension — from hypoxia-induced vascular spasm + loss of capillary surface area from alveolar destruction
Right-sided heart failure (cor pulmonale)

B. Chronic Bronchitis (Key Microscopic Features)

Hypertrophy of mucous glands (Reid index >0.5)
Goblet cell hyperplasia
Squamous metaplasia of epithelium
Infiltration of inflammatory cells

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Section 3 — Silicosis (Pneumosilicosis)

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Definition: An occupational disease caused by prolonged (5–10 years) inhalation of silica particles (silicon dioxide, SiO₂), deposited in the lung. It is the most important pneumoconiosis due to chronic, nodular, dense pulmonary fibrosis and high risk of tuberculosis co-infection.

Etiology

Inhalation of SiO₂ particles < 5 μm (reach alveoli).

Common occupational exposures:

Mining (gold, tin, copper, coal) and quarrying
Sandblasting
Metal grinding
Manufacture of ceramics

Pathogenesis

SiO₂ particles inhaled → engulfed by alveolar macrophages

SiO₂ enters lysosomes → forms hydrated silica

Hydrated silica damages lysosomal membrane

Macrophage undergoes necrosis → releases SiO₂

SiO₂ is released back into tissue and re-engulfed → vicious cycle

Necrotic macrophages release many cytokines

Stimulate fibroblast proliferation and collagen deposition

Result: Chronic inflammation and progressive fibrosis of lung

Morphology

Earlier Stage

Cellular silicotic nodules in upper lung
Fibrous nodules with hyaline change

Advanced Stage

Collagenous nodules
Hyalinized whorls of collagen with scant inflammation
Diffuse fibrosis in interstitium: alveolar septa, around blood vessels and bronchioles
Calcification or coal-blackening may be present
Nodules start small in upper lung, grow larger and more diffuse

Complications

Pulmonary tuberculosis — most important complication; silicosis + TB = "silicotuberculosis"
Right-side heart failure (chronic cor pulmonale)
Emphysema and spontaneous pneumothorax

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Section 4 — Chronic Cor Pulmonale

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Definition: Right ventricular hypertrophy, dilation, and potentially failure secondary to pulmonary hypertension caused by disorders of the lungs or pulmonary vasculature. Also called pulmonary hypertensive heart disease.

Etiology & Pathogenesis

COPD → ↓ blood vessels available → hypoxemia

Hypoxemia → pulmonary small artery spasm

↑ Resistance of lung circulation → ↑ pulmonary arterial pressure

Right heart works harder → hypertrophy → dilation → failure

Other causes: Disorders affecting chest movement; diseases of pulmonary vessels.

Pathological Changes

Lung lesions:

COPD changes
Arteriole walls thickened (media and intima: collagenous, elastic fiber ↑)
Muscularization of arterioles
Capillary loss

Heart changes:

Right ventricular wall hypertrophy
Trabeculae and papillary muscles thickened
Hypertrophic myocardial cells microscopically

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Section 5A — Nasopharyngeal Carcinoma (NPC)

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Introduction

Origin

Nasopharyngeal epithelium

Geography

Common in China (esp. Guangdong, Zhujiang, Xijiang drainage), Indonesia, Malaysia, North Africa

Demographics

Male:Female = 2:1, peak age 40–50 years. Males predominate especially before age 45.

Etiology & Pathogenesis

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Three Factors

EBV (Epstein-Barr Virus) infection — most important
Environmental factors — nitrosamines (esp. salted fish containing dimethyl nitrosamine 1–3.5 mg/kg)
Genetic factors

Evidence for EBV role:

Raised antibody levels (especially IgA against EBV) in most NPC patients compared to controls and other cancer types
EBV DNA or RNA present in practically all tumor cells
EBV present in precursor lesions of NPC, but NOT in normal nasopharyngeal epithelium
Diagnostic markers: IgA vs VCA (viral capsid antigen) and IgG/IgA vs EA (early antigens)

Morphology — Location

Most commonly: nasopharyngeal roof → lateral wall → pharyngeal recess

Gross Types:

Nodular

Nodular mass

Cauliflower

Polypoid/cauliflower mass

Submucosa

Beneath mucosa, bulges inward

Infiltrative

Diffuse wall infiltration

Ulcerative

Surface ulceration

Histological Types

Type	Subtype	Key Features
Squamous Cell Carcinoma	Keratinizing (well differentiated)	Intercellular bridges + keratin pearls; resembles normal squamous epithelium
	Non-keratinizing: Differentiated (poorly differentiated)	Delamination of cancer nest cells obscure; obvious cellular atypia
	Non-keratinizing: Undifferentiated ← MOST COMMON	Vesicular nucleus cell carcinoma (lymphoepithelioma): large vesicular nuclei, 1–2 prominent nucleoli, abundant cytoplasm, indistinct borders, numerous lymphocytes intermixed. OR Small cell types (small round/spindle cells). Sensitive to radiotherapy → better prognosis but can be confused with lymphoma → use Reticulin stain + IHC (CK+ = carcinoma; LCA+ = lymphoma)
Adenocarcinoma	—	Glandular differentiation

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IHC to distinguish NPC vs LymphomaCK (Cytokeratin) positive = NPC (carcinoma) · LCA positive = Lymphoma

Spread & Metastasis

1. Direct Extension

Upward → base of skull
Lateral → auditory tube → middle ear
Forward → eye sockets, nasal cavity
Downward → hard and soft palate
Backward → cervical vertebrae
CN II–VI damage

2. Lymphatic Metastasis (Early)

Painless enlargement of upper deep cervical lymph nodes = FIRST signal / earliest symptom

3. Hematogenous Metastasis

Liver, lung, bone

Clinical Features

Cervical lymph node enlargement (painless) — often first sign
Nasal discharge with blood (epistaxis)
Nasal obstruction
Tinnitus, hearing loss (amblyacousia)
Headache
Cranial nerve damage (CN II–VI)

Treatment & Prognosis

Radiosensitive — radiotherapy is primary treatment
5-year survival: 50% in advanced cases; 80% for T1N0M0 (no LN or distant metastasis)
Early screening: detect serum IgA vs VCA

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Section 5B — Carcinoma of the Lung

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Epidemiology

No. 1 cancer in industrialized countries
2nd most common cancer in Asia-Pacific; leading cause of cancer death
Most common cancer in men aged 40–70; M:F = 2:1
Rising incidence in women (due to smoking)

Etiology & Pathogenesis

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1. Cigarette Smoking — Main Cause Heavy smokers have a 20-fold increase in incidence vs non-smokers.
Carcinogens in smoke: polycyclic hydrocarbons, aromatic amines, heavy metals (nickel).
Mechanism: loss of cilia → squamous metaplasia → dysplasia → carcinoma in situ → invasive carcinoma.

Industrial Carcinogens

Asbestos (best known), uranium, nickel, chromate, gold mining

Air Pollution

Ozone, oxides of nitrogen and sulfur

Molecular Genetics

c-myc (SCLC), K-ras (adenocarcinoma), P53 (most frequent), RB, p16; LOH on chromosome 3p (all types)

Gross Types (by Position)

Type	Location	Histology Association	Notes
Central (Hilar)	Major bronchi (1st–3rd order); 75% of cases	Squamous cell carcinoma (related to smoking)	Causes airway obstruction
Peripheral	Small bronchi/bronchioles; alveolar cells; periphery of lungs	Adenocarcinoma; common in women	Single or multiple nodules
Diffuse	Diffuse miliary nodules	2–5% of lung cancers	Mimics pneumonia/tuberculosis

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Early Lung Carcinoma: Tumor mass <2 cm, limited to intrabronchial or bronchial wall + surrounding tissue, no lymph node metastasis. Subtypes: intraluminal, infiltrative, peribronchial.

Occult Lung Cancer: Cancer cells in sputum, no clinical symptoms, X-ray negative. Pathology shows carcinoma in situ or early infiltrative carcinoma. No lymphatic metastasis.

Histological Classification

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Clinical division (for treatment purposes): NSCLC 70–75% (surgery) vs SCLC 20–25% (chemotherapy)

1. Squamous Cell Carcinoma

More common in men; strongly correlated with smoking
Arise centrally in major bronchi (central/hilar type)
Preceded by squamous metaplasia → dysplasia → carcinoma in situ (preneoplastic lesion, may last years)
Gross: central mass; necrosis frequent; cavitation from necrotic material discharge
Spreads to local hilar lymph nodes first

2. Adenocarcinoma (Most Common Overall)

Has replaced squamous cell carcinoma as the most common primary lung tumor
Most common in women, lifetime non-smokers, and persons <45 years
Predominantly peripheral mass
Grows rapidly; early and widespread hematogenous metastasis

Subtypes:

Acinar adenocarcinoma
Colloid (mucinous) adenocarcinoma
Papillary adenocarcinoma
Micropapillary adenocarcinoma
Solid adenocarcinoma with mucin
Lepidic adenocarcinoma (tumor cells grow along alveolar walls)

3. Large Cell Carcinoma

Undifferentiated malignant epithelial tumors lacking cytologic features of SCLC and no glandular or squamous differentiation
Likely represents squamous or adeno that is so undifferentiated it can't be recognized by light microscopy
Cells: large nuclei, prominent nucleoli, moderate cytoplasm
Variants: giant cell, clear cell, spindle cell

4. Small Cell Carcinoma (SCLC) — Most Malignant

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Highest MalignancyMost malignant lung cancer; usually central/hilar; strongly linked to smoking.

Histology:

Oval or short spindle cells, "oat cell" shape
Dark staining nuclei, very little cytoplasm
Grow in nests or clusters separated by connective tissue
"Fake chrysanthemum-morph" structure

Origin & Special Features:

Derived from neuroendocrine cells of bronchial mucosa
Neurosecretory granules on EM
IHC: Chromogranin (+), Synaptophysin (+)
Secretes peptide hormones (ACTH, ADH) → paraneoplastic syndromes (e.g. hypercalcemia)

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SCLC ManagementAlready metastasized at diagnosis → NOT curable by surgery. Best treated with chemotherapy ± radiation. Grows rapidly, metastasizes early and widely.

NSCLC vs SCLC — Critical Comparison Table

Feature	NSCLC	SCLC
Cytoplasm	Abundant	Scant
Nuclei	Pleomorphic (large)	Small, dark
Chromogranin IHC	Negative	Positive
Synaptophysin IHC	Negative	Positive
Treatment	Surgery	Chemotherapy
Outcomes	Better	Worse
Molecular changes	P16, cyclinD1, K-ras	P53, RB mutations

Minor Histological Types

Mucoepidermoid carcinoma
Adenoid cystic carcinoma
Adenosquamous carcinoma
Sarcomatoid carcinoma

Clinical Features

Cough, weight loss, chest pain, dyspnea
Superior vena caval syndrome — if tumor compresses SVC: puffiness of face, phlebeurysma (visible veins) of neck/chest
Horner's syndrome (apical/Pancoast tumor → cervical sympathetic plexus): ipsilateral enophthalmos (sunken eye), ptosis (drooping eyelid), miosis (small pupil), anhydrosis (no sweating)
Brachial plexus involvement → pain in ulnar nerve distribution, hand muscle wasting

🧠 Horner's Syndrome Mnemonic — "PAM is Horny"

P·A·M·E

Ptosis · Anhydrosis · Miosis · Enophthalmos

Patterns of Spread

1. Direct Extension

Airway obstruction (central type); pericardial/pleural effusion; SVC compression (venous congestion); brachial and cervical sympathetic plexus (apical tumors)

2. Lymphatic Metastasis

Hilar LN → paratracheal LN → cervical LN → Virchow's node (left supraclavicular)

3. Hematogenous Metastasis

Liver, bone, adrenal glands, brain. May produce clinical symptoms BEFORE primary tumor is detected.

Prognosis

Overall 5-year survival: ~9% (very poor)
Surgical resection of solitary NSCLC: 30–40% 5-year survival
SCLC: chemotherapy responsive but ultimately recurs; other types disappoint with chemotherapy
Key principle: Early discovery → early diagnosis → early treatment

Diagnosis Methods

Sputum cytology, pleural effusion cytology
Fiberoptic bronchoscope examination and biopsy
X-ray, CT scanning, MRI
Fine-needle aspiration (FNA) biopsy

Therapy

Surgery, radiation therapy, and chemotherapy (based on type and stage)

All 4 Histological Types — Quick Revision

Type	Gross	Association	Special Feature	Treatment
Squamous Cell Ca	Central; cavitation common	Smoking, men	Squamous metaplasia → dysplasia → CIS (preneoplastic)	Surgery (NSCLC)
Adenocarcinoma	Peripheral; multiple nodules	Women, non-smokers, <45 yrs	Most common type overall; rapid hematogenous spread; lepidic subtype	Surgery (NSCLC)
Large Cell Ca	Variable	None specific	Diagnosis of exclusion; undifferentiated	Surgery (NSCLC)
Small Cell Ca	Central/hilar; soft white tan	Smoking; young–middle aged men	Oat cell; neuroendocrine origin; paraneoplastic syndromes; Chrom(+) Synap(+)	Chemo ± RT (SCLC)

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Master Summary & High-Yield Points

Exam Focus

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Pneumonia — Must Know Lobar: S. pneumoniae · 4 stages · entire lobe · rusty sputum · carnification is key complication.
Lobular: pyogenic · multifocal · basal · suppurative · children/elderly.
Viral: interstitial pattern · inclusion bodies · hyaline membrane · mononuclear infiltrate.

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Emphysema — Must Know Centriacinar = smoking. Panacinar = α₁AT deficiency. Distal acinar = pneumothorax in young adults. Irregular = scarring. Two imbalances (protease-antiprotease + oxidant-antioxidant) = additive.

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Silicosis — Must Know SiO₂ <5 μm · macrophage–lysosome damage · vicious cycle · hyalinized whorls · #1 complication = TB · #2 = cor pulmonale.

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NPC — Must Know EBV association · IgA vs VCA for screening · undifferentiated type most common (lymphoepithelioma) · radiosensitive · first sign = painless cervical LN enlargement · CK+ (not LCA+) = NPC not lymphoma.

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Lung Cancer — Must Know NSCLC (surgery) vs SCLC (chemo). Adenocarcinoma = most common overall, women, non-smokers, peripheral. Squamous = men, smoking, central, cavitation. SCLC = oat cell, neuroendocrine, paraneoplastic, worst prognosis. Overall 5-yr survival = 9%. Adenoca = K-ras; SCLC = P53+RB mutations; Chromogranin/Synaptophysin +ve = SCLC.

Disease	Key Bug / Cause	Pathology Buzzword	Key Complication
Lobar pneumonia	S. pneumoniae	Fibrinous; 4 stages; red/gray hepatization	Carnification
Bronchopneumonia	Pyogenic bacteria	Suppurative; patchy; basal; peribronchial	Bronchiectasis, heart failure
Viral pneumonia	Influenza, RSV, etc.	Interstitial; inclusion bodies; hyaline membrane	Respiratory failure
Emphysema	Smoking / α₁AT↓	Permanent airspace enlargement; no fibrosis	Cor pulmonale
Silicosis	SiO₂ inhalation	Hyalinized collagen whorls; nodular fibrosis	TB, cor pulmonale
Cor pulmonale	COPD → pulmonary HTN	RV hypertrophy/dilation	RV failure
NPC	EBV, nitrosamines	Undifferentiated; lymphoepithelioma	Cranial nerve damage, hematogenous spread
Lung Ca (SqCC)	Smoking	Central; cavitation; keratin pearls	Airway obstruction
Lung Ca (Adeno)	Non-smoking, women	Peripheral; lepidic; glandular	Early hematogenous spread
Lung Ca (SCLC)	Smoking; neuroendocrine	Oat cells; Chromogranin/Synaptophysin+	Paraneoplastic syndrome; early metastasis

🫁 Diseases of the Respiratory System

Normal Anatomy & Histology of the Respiratory System

Section 1 — Pneumonia

Section 2 — COPD & Pulmonary Emphysema

Section 3 — Silicosis (Pneumosilicosis)

Section 4 — Chronic Cor Pulmonale

Section 5A — Nasopharyngeal Carcinoma (NPC)

Section 5B — Carcinoma of the Lung

Master Summary & High-Yield Points