flashpath - lung - chronic bronchitis
TRANSCRIPT
FLASHPATHH a z e m A l i
CHRONIC BRONCHITIS
H a z e m A l i
CLINICAL
Chronic bronchitis is one of the “obstructive lung diseases” that include:• Emphysema
• Bronchiectasis
• Small-airway disease “bronchiolitis”
• Asthma
CLINICALObstructive airway
diseaseRestrictive airway
diseaseGeneral features Increase in resistance to
airflow due to obstruction at any level
Reduced expansion of lung parenchyma
Total lung capacity (TLC)
Increased Reduced
Forced Expiratory Volume in one second (FEV1)
Reduced Normal
CLINICAL• Emphysema and chronic bronchitis are often clinically
grouped together and referred to as chronic obstructive pulmonary disease (COPD)
• COPD is the 3rd leading cause of global death
• Usually due to cigarette smoking and air pollution
• Usually present in adults (> 45 years old) and more common in males
• Main symptom are dyspnea and cough
CLINICALPredominant Chronic
BronchitisPredominant Emphysema
Age 40 – 45 years old 50 – 75 years oldAppearance Blue Bloater Pink Buffer
Dyspnea Mild, Late Early, SevereCough Early
Copious sputumLate
Scanty sputumInfections Common Occasional
Respiratory Insufficiency
Repeated Terminal
Cor pulmonale Common Rare, TerminalRadiology Prominent vessels
Large heartHyperinflation
Small heartAirway Resistance Increased Normal or slightly
increasedElastic Recoil Normal Low
CLINICAL• Chronic bronchitis is:
– Chronic disease of large airways– Persistent “productive” cough– For at least 3 months– In at least 2 consecutive years– Without other apparent explanation
CLINICALLines of treatment:• Smoking cessation• Medications (Bronchodilators, Steroids)• Oxygen therapy and Ventilatory support• Antibiotics (for 2ry infections)• Lung transplantation (for end-stage diseases)
Main causes of death:• Coronary artery disease• Respiratory failure• Right-sided heart failure
PATHOGENESIS
SmokingAir pollution(initiate bronchitis)
• Interferes with ciliary action• Directly damages airway
epithelium• Inhibits ability of white blood
cells to clear bacteria
Infection(maintain bronchitis)
GROSS• Bronchi:
– Dilated– Filled with excessive mucus / pus
• Lung parenchyma:– Anthracosis– Emphysema
MICROSCOPYBronchi:• Mucus hypersecretion• Hypertrophy of submucosal glands
– Increased Reid index• Goblet cell hyperplasia• Squamous metaplasia, Dysplasia• Chronic inflammation
– No eosinophils
MICROSCOPYReid index• Ratio of
REMEMBER:• Measured at main or lobar bronchi• The epithelium should be parallel to the cartilage• Normal index up to 0.4• Chronic bronchitis > 0.4 (average 0.6)
MICROSCOPY• Other Smoking-related conditions:
– Anthracosis– Emphysema– Desquamative interstitial pneumonia– Respiratory bronchiolitis– Pulmonary eosinophilic granuloma
• “Langerhans cell histiocytosis”– Usual interstitial pneumonia
• Pulmonary hypertension
CYTOLOGYBenign bronchial cell changes1. Reactive changes
– Columnar, ciliated bronchial cells– Nuclear enlargement– Coarse chromatin– Prominent nucleoli
2. Creola bodies– Spherical 3D Clusters– Columnar, ciliated bronchial cells– Also seen in Asthma
• Charcot-leyden crystals• Curschmann's spirals• Eosinophils
Reta
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CYTOLOGY3. Goblet cell hyperplasia
– Large sheets or round clusters– Composed almost exclusively of goblet cells
• Abundant mucin-filled cytoplasm– Benign columnar, ciliated bronchial cells are also seen
• The bronchi are lined with ciliated or columnar epithelium with scattered gobletcells. Goblet cell hyperplasia is an indication of irritation, such as in bronchitis or asthma
Benign bronchial cells changes can mimic Adenocarcinoma:– LOSS OF CILIA– Do not rush for calling adenocarcinoma on just few small group of cells
• Especially with inflammatory background OR history of COPD, Asthma– Reactive changes resolve within 1 month wait and repeat cytology
CYTOLOGYOther injury-associated findings1. Bronchial reserve cell hyperplasia
– Tightly packed small cells – Scant cytoplasm– Smudged dark chromatin– Nuclear molding may be seen– No mitoses or necrosis
Bronchial reserve cell hyperplasia can mimic Small cell carcinoma:– LESS COHESIVE– MARKED MITOSIS / NECROSIS– CLINICAL HISTORY
CYTOLOGYOther injury-associated findings2. Reparative “re-epithelialization” of respiratory tract
– Flat, cohesive sheets– Abundant cytoplasm– Enlarged nuclei– prominent nucleoli– Mitoses
Reparative epithelium can mimic Non-Small cell carcinoma:– LESS COHESIVE– MARKED MITOSIS / NECROSIS– CLINICAL HISTORY
DIFFERENTIAL DIAGNOSIS
Chronic bronchitis
Bronchiectasis Asthma
Small-airway disease
“bronchiolitis”
Emphysema
Site B r o n c h u s Bronchioles AlveoliMajor
pathology
• Mucous gland hyperplasia
• Excess mucus
• Inflammation
• Airway dilation & scarring
• Thickened basement membrane
• Smooth muscle hyperplasia
• Excess mucus
• Inflammation(eosinophils)
• Inflammatory scarring & obliteration
• Airspace enlargement
• Wall destruction
• No fibrosis
Other obstructive lung diseases:
DIFFERENTIAL DIAGNOSISChronic Bronchitis Bronchial Asthma
Age Usually adults Any ageSmoking history Almost invariable PossibleCough Persistent
ProductiveIntermittentNon-productive
Breathlessness Persistent IntermittentNocturnal symptoms Uncommon CommonFamily history Uncommon
“unless family members smoke”
Common
Other allergic diseases Uncommon Common“eczema or allergic rhinitis”
Airflow obstruction Irreversible ReversibleSputum Macrophages
NeutrophilsCreola bodies
EosinophilsCharcot–Leyden crystalsCurschmann’s spiralsCreola bodies
DIFFERENTIAL DIAGNOSISChronic Bronchitis Bronchial Asthma
Gross Excess mucusBronchial dilatationAssociated emphysema
Mucous plugsHyperinflation but no emphysema
Airway inflammation CD8+ T cellsNeutrophils periodically
CD4+ T cellsEosinophilsMast cells
Airway epithelium IntactGoblet cell hyperplasiaSquamous metaplasia
Fragile with strippingGoblet cell hyperplasiaSquamous metaplasia
Basement membrane thickening
Mild to moderate Marked
Bronchial glands enlargement
Marked Moderate
Airway muscle hypertrophy
May be seen Marked
Major complications Cor pulmonale Allergic bronchopulmonary aspergillosis
DIFFERENTIAL DIAGNOSISOther causes of chronic cough• Lung carcinoma• Bronchiectasis• Cystic fibrosis• Congestive heart failure• Tuberculosis
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