Download - Pulmonary Pathology
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Pulmonary Pathology
Obstructive Airways Disease
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Respiratory disease
• Pulmonary diseases (especially infective) together with gastrointestinal infection are the commonest cause of death in the developing world
• Pulmonary disease is almost entirely environmental rather than genetic
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Basic anatomy!
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The respiratory acinus• Cartilage is present to
level of proximal bronchioles
• Beyond terminal bronchiole gas exchange occurs
• The distal airspaces are kept open by elastic tension in alveolar walls
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Function of lungs….
• Gas exchange (O2, CO2)– Depends on compliance (stretchability) of
lungs– Can only occur in alveoli that are both
ventilated and perfused
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Ventilation-perfusion defects
• Alveoli that are ventilated but not perfused is ventilatory “dead space”
• Alveoli that are perfused but not ventilated leads to “shunting” of non-oxygenated blood from pulmonary to systemic circulation ( a mechanism of cyanosis)
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Spirometry (pulmonary physiology)
• FEV1: volume of air blown out forcibly in 1 second. A function of large airways. Dependent on body size.
• Vital capacity (VC): total volume of expired air. Ratio FEV1/VC compensates for body size
• Tco (transfer factor): absorption of carbon monoxide in 1 breath (gas exchange)
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Functional Classification of Lung Disease
Distinctive clinical and physiological features define:
• Obstructive lung disease: decreased FEV1 and FEV1/VC
• Restrictive lung disease: decreased FEV1. Normal FEV1/VC. Decreased Tco.
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Respiratory failure (causes)
• Ventilation defects (CNS, neuromuscular defects, drugs)
• Perfusion defects (cardiac failure, pulmonary emboli)
• Gas exchange defects (fibrosis, consolidation, emphysema)
Lead to hypoxia and hypercapniaOften more than factor one will operate
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Airway Narrowing/Obstruction
• Muscle spasm• Mucosal oedema (inflammatory or
otherwise• Airway collapse due to loss of support• (Localised obstruction due to tumour or
foreign body)
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Localised obstruction
• Collapse• Lipid pneumonia• Infection• Bronchiectasis (if
longstanding)
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Main Categories of (diffuse) Obstructive Disease
• Asthma• Chronic obstructive pulmonary disease
(COPD/COAD/COLD)
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Chronic Obstructive Disease
• Chronic bronchitis• Emphysema
Symptomatic patients often have both
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Bronchial Asthma
A chronic inflammatory disorder characterised by hyperreactive airways leading to episodic reversible bronchoconstriction
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Asthma
• Extrinsic - response to inhaled antigen
• Intrinsic - non-immune mechanisms (cold, exercise, aspirin)
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Immunological Mechanisms
Type hypersensitivity - allergen binds to IgE on surface of mast cells
• Degranulation (histamine)– muscle spasm– inflammatory cell influx (eosinophils)– mucosal inflammation/oedema
• Inflammatory infiltrate tends to chronicity
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Pathology of asthma
• Airway inflammation with mucosal oedema• Mucus plugging
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Mucosal oedema
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Mucus plugs
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Mucus plug/inflammation
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Inflammation
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Inflammation/epithelial damage
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Chronic Obstructive Pulmonary Disease
• Chronic bronchitis• Emphysema
A smokers diseaseSymptomatic patients usually have both
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COPD
• In top 5 causes of death in Europe/N. America
• Clinical course characterised by infective exacerbations (Haemophilus influenzae, Streptococcus pneumoniae)
• Death by respiratory failure or heart failure (“cor pulmonale”)
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Chronic BronchitisCough productive of sputum on most
days for 3 months of at least 2 successive years
• An epidemiological definition• Does not imply airway inflammation
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Chronic Bronchitis
• Chronic irritation defensive increase in mucus production with increase in numbers of epithelial cells (esp goblet cells)
• Poor relation to functional obstruction• Role in sputum production and increased
tendency to infection
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Chronic Bronchitis
• Non-reversible obstruction• In some patients there may be a reversible
(“asthmatic”) component
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Normal vs. Chronic Bronchitis
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Small airways in Chronic Bronchitis
• More important than traditionally realised• Goblet cell metaplasia, macrophage
accumulation and fibrosis around bronchioles may generate functional obstruction
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Emphysema
• Increase beyond the normal in the size of the airspaces distal to the terminal bronchiole
• Without fibrosis
The gas-exchanging compartment of the lung
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Emphysema (types)
• Centriacinar (centrilobular)• Panacinar• Others (e.g. localised around scars in the
lung)
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Emphysema
• Difficult to diagnose in life (apart from late disease – enl;arged “barrel chest”)
• Radiology (CT) can show changes in lung density
• Correlation with function known from autopsy studies
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Emphysema
• “Dilatation” is due to loss of alveolar walls (tissue destruction)
• Appears as “holes” in the lung tissue
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Normal lung
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Centriacinar emphysema
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Panacinar emphysema 1
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Panacinar emphysema 2
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Emphysema
How do these changes relate to functional deficit?
• Poorly at macroscopic level• Better with microscopic measurement
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Normal
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Early emphysema
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Emphysema Impairs Respiratory Function
• Diminished alveolar surface area for gas exchange (decreased Tco)
• Loss of elastic recoil and support of small airways leading to tendency to collapse with obstruction
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Loss of surface area (emphysema)
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Loss of support on bronchiolar walls
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As disease advances….
Pa O2 leads to:
• Dyspnoea and increased respiratory rate• Pulmonary vasoconstriction (and
pulmonary hypertension)
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Epidemiology of COPD
• Smoking• Atmospheric pollution• Genetic factors
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Pathophysiology of Emphysema
High rate of emphysema in the rare genetic condition of 1 antitrypsin deficiency
• THE PROTEASE/ANTIPROTEASE HYPOTHESIS
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Elastic Tissue
• Sensitive to damage by elastases (enzymes produced by neutrophils and macrophages)
1 antitrypsin acts as an anti-elastase
Imbalance in either arm of this system predisposes to destruction of elastic alveolar walls (emphysema)
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Tobacco smoke…..
• Increases nos. of neutrophils and macrophages in lung
• Slows transit of these cells• Promotes neutrophil degranulation• Inhibits 1 antitrypsin