pulmonary pathology
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Pulmonary Pathology. Obstructive Airways Disease. 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. - PowerPoint PPT PresentationTRANSCRIPT
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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