PULMONARY PATHOLOGY
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Transcript of PULMONARY PATHOLOGY
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PULMONARY PATHOLOGYPULMONARY PATHOLOGY
Prof Frank Carey
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General ApproachGeneral Approach
Understanding mechanisms of disease Emphasizing the role of the pathologist in
diagnosis
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Functional Classification of Functional Classification of Lung DiseaseLung Disease
Distinctive clinical and physiological features define:
Obstructive lung disease Restrictive lung disease
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Airway Narrowing/ObstructionAirway 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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Main Categories of Obstructive Main Categories of Obstructive DiseaseDisease
Asthma Chronic obstructive pulmonary disease
(COPD/COAD/COLD)
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Chronic Obstructive DiseaseChronic Obstructive Disease
Chronic bronchitis Emphysema
Symptomatic patients often have both
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Chronic BronchitisChronic Bronchitis
Cough 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 BronchitisChronic 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 BronchitisChronic Bronchitis
Non-reversible obstruction In some patients there may be a reversible
(“asthmatic”) component
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Normal vs. Chronic BronchitisNormal vs. Chronic Bronchitis
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Small airways in Chronic Small airways in Chronic BronchitisBronchitis
More important than traditionally realised Goblet cell metaplasia, macrophage
accumulation and fibrosis around bronchioles may generate functional obstruction
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EmphysemaEmphysema 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)Emphysema (types)
Centriacinar (centrilobular) Panacinar Others (e.g. localised around scars in the
lung)
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EmphysemaEmphysema Difficult to diagnose in life (apart from in
extremis) Radiology (CT) can show changes in lung
density Correlation with function known from
autopsy studies
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EmphysemaEmphysema
“Dilatation” is due to loss of alveolar walls (tissue destruction)
Appears as “holes” in the lung tissue
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Normal lungNormal lung
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Centriacinar emphysemaCentriacinar emphysema
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Panacinar emphysema 1Panacinar emphysema 1
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Panacinar emphysema 2Panacinar emphysema 2
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EmphysemaEmphysema
How do these changes relate to functional deficit?
Poorly at macroscopic level Better with microscopic measurement
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NormalNormal
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Early emphysemaEarly emphysema
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Emphysema Impairs Emphysema Impairs Respiratory FunctionRespiratory Function
Diminished alveolar surface area for gas exchange
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)Loss of surface area (emphysema)
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Loss of support on bronchiolar wallsLoss of support on bronchiolar walls
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As disease advances….As disease advances….
Pa O2 leads to:
Dyspnoea and increased respiratory rate Pulmonary vasoconstriction (and
pulmonary hypertension)
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Epidemiology of COPDEpidemiology of COPD
Smoking Atmospheric pollution Genetic factors
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Pathophysiology of Pathophysiology of EmphysemaEmphysema
High rate of emphysema in the rare genetic condition of 1 antitrypsin deficiency
THE PROTEASE/ANTIPROTEASE HYPOTHESIS
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Elastic TissueElastic 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…..Tobacco smoke…..
Increases nos. of neutrophils and macrophages in lung
Slows transit of these cells Promotes neutrophil degranulation Inhibits 1 antitrypsin
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Bronchial AsthmaBronchial Asthma
A chronic inflammatory disorder characterised by hyperreactive airways leading to episodic reversible bronchoconstriction
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AsthmaAsthma Extrinsic - response to inhaled antigen
Intrinsic - non-immune mechanisms (cold, exercise, aspirin)
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Immunological Mechanisms 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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PathologyPathology Narrowed oedematous airways Mucus plugs Inflammatory cells (lymphocytes, plasma
cells, eosinophils) Epithelial cell damage
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Mucosal oedemaMucosal oedema
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Mucus plugsMucus plugs
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Mucus plug/inflammationMucus plug/inflammation
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InflammationInflammation
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Inflammation/epithelial damageInflammation/epithelial damage