Condition Macroscopic Microscopic Pathophysiology Chronic

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Condition Macroscopic Microscopic Pathophysiology Chronic Powered By Docstoc
					Condition                Macroscopic                                   Microscopic                                  Pathophysiology
                                                       Chronic Obstructive Pulmonary Diseases
Chronic Bronchitis       -   Hyperemia, swelling and oedema of the    - chronic inflammation of the airways         -   Chronic irritation by inhaled
- productive cough at        mucous membranes                             (predominantly lymphocytes)                   substances (Tobacco, cotton,
   least 3/12 in at      -   Accompanied by excessive mucinous to     - Enlargement of mucus-secreting                  silica)
   least 2 consecutive       mucopurulent secretions layering the         glands of the trachea / bronchi           -   Hypersecretion of mucus & SM
   years                     epithelial surfaces                      - Assess enlargement by Reid index                spasm
- smoking is important   -   Sometimes → heavy casts of secretions        (ratio of the thickness of the mucous     -   → obstruction
                             & pus fill the airways                       gland layer to the thickness of the       -   → ↑ airway resistance
                                                                          wall btw the epithelium & cartilage)      -   V/Q mismatch
                                                                      - Bronchial epithelium → squamous             -       ↑ed shunting (perfusion of
                                                                          metaplasia & dysplasia                        unventilated areas)
                                                                      - Marked narrowing of bronchioles →           -   → Hypoxemia
                                                                          goblet cell metaplasia, mucus
                                                                          plugging, inflammation, fibrosis,
                                                                          smooth muscle hyperplasia
                                                                      - Tobacco MΦ’s
Panacinar                -    Voluminous lungs, often overlapping the   -   Abnormal fenestrations in the walls     -  Protease-antiprotease theory
                              heart                                         of the alveoli                          -  Alveolar destruction results from
                         -    Acinus uniformly enlarged from resp       -   Complete destruction of septal walls       an imbalance btw proteases (NΦ
                              bronchiole to terminal alveoli            -   Pores of Kohn are so large, that the       & MΦ elastase) & antiprotease
                         -    Usu lower zones & in the anterior             septa appear to be floating                (α1-AT)
                              margins of the lung                       -   Fusion of adjacent alveoli → blebs or   - NΦ elastase → digests lung
Centriacinar             -   Upper 2/3 of lungs most affected,              bullae                                  Nicotine
                             particular apical segment                  -   Often the resp bronchioles and          - Direct chemoattractant effect
                         -   Involves central and proximal parts of         vasculature of the lung are deformed    - ROS → inactivation of α1-AT
                             the acini (resp bronchioles)                   and compressed by the distortion of        (functional α1-AT deficiency)
                         -   Both Emphysematous & normal airspaces          the airspaces (↓ed radial traction)
                             exist in the same acinus
Paraseptal               -   Effects distal alveolar spaces
                         -   Most striking adjacent to pleura, along
                             the lobular connective tissue septa & at
                             margins of the lobules
Asthma                   -   Overdistended lungs due to overinflation   -   Mucus plugs contain whorls of shed      -   Genetic predisposition to atopy
                         -   Small areas of atelectasis                     epithelium → Curschmann spirals         -   Bronchial hyper-responsiveness
                         -   Occlusion of bronchi & bronchioles by       - Numerous EΦ & Charcot-leyden             -   Stimulus
                             thick, tenacious mucus plugs                   crystals (collection of crystalloid     -     hypersensitivity rxn
                                                                            made up of EΦ membrane protein)         -     ↑ mucus & ↑ SM
                                                                         - Thickened epithelial BM                  -     Obstruction
                                                                         - Oedema & an inflammatory infiltrate      -      ↑ airway resistance
                                                                            in the bronchial walls                  -     V/Q mismatch
                                                                         - ↑ size of submucosal glands              -     hypoxemia
                                                                         - Hypertrophy of bronchial SM
                                                         Pulmonary Diseases of Vascular Origin
Pulmonary Oedema         -   Lungs become heavy & wet and               - Engorged capillaries & filling of the     -  LHF, volume overload, pulmonary
                             subcrepitant → not quite crepitant            intra-alveolar airspaces by a granular      vein obstruction
                         -   Fluid accumulates esp in the dependent        pink precipitate                         - Infection: pneumonia
                             basal regions of the lower lobe            - Chronic → interstitial fibrosis →         - Shock, trauma, sepsis, aspiration
                                                                           numerous haemosiderin laden MΦ           - etc…
ARDS                     -   Lungs diffusely firm                       - Signs of acute inflammation               - NΦ activation → Microvascular
- Characterised by       -   Red, boggy, heavy                          - Fibrin rich hyaline membranes in             damage
   DAD                   -   Acute DAD (oedema, hyaline membranes)         alveoli                                  - → ↑ permeability & alveolar
- CXR shows diffuse      -   organising stage → patchy areas of                                                        flooding
   alveolar infiltrate       interstitial fibrosis                                                                  - → Loss of diffusion capacity
                         -   Thickened alveolar septa                                                               - Type II pneumocyte damage →
                                                                                                                       widespread surfactant
                                                                                                                    - Exudate not easily resolved →
                                                                                                                       organisation w scarring
                                                                                                                    - Usu no demonstrable alterations
                                                             Diffuse Interstitial Lung Disease
Idiopathic Pulmonary      -   Pleural surfaces of the lung are           - Usual interstitial pneumonia              -   Regardless of the type of
Fibrosis                      cobberstoned → retraction of scars         - Areas of dense collagenous fibrosis w         interstitial disease or specific
                              along the interlobular septa                    relative normal lung & fibroblastic        cause → common manifestation
                          -   Cut surface shows fibrosis (firm rubbery        foci                                       is alveolitis
                              white areas)                                                                           -   Lung injury (eg inhaled agent,
Pneumoconioses                                                                                                           blood borne toxin, unknown)
- non-neoplastic lung reaction to inhaled organic / inorganic particulates & chemical fumes or vapors                -   Activate MΦ (via T & B cells)
                                                                                                                     -   → chemotaxis of NΦ → oxidant
Coal workers’             -   Prominent & numerous aggregates of coal    -   Dense collage & pigment                     proteases → injury to Type I
pneumoconioses (CWP)          dust laden MΦ’s forming coal macules       -   Center is often necrotic                    pneumocytes
- inhaled carbon is       -   Present esp in upper zones of the upper                                                -   → Fibrogenic & chemotactic
   engulfed by alveolar       & lower lobes                                                                              cytokines → ↑ fibroblasts →
   MΦ → accumulate in     -   Severe → fibrosis & scarring in areas of                                                   FIBROSIS
   connective tissue          dust accumulation                                                                      -   Alveoli are replaced w cystic
   along lymphatics                                                                                                      spaces → Honeycomb Lung
Asbestosis                                                               -   Asbestos bodies (dumbbell shaped
                                                                             bodies) → haemosiderin &
                                                                             glycoprotein coated asbestos fibres
Granulomatous -           -   Usu no demonstrable alterations            -   Classic non-caseating granuloma →       UNKNOWN
Sarcoidosis               -   Granulomas coalesce → small nodule that        composed of aggregate of tightly
                              is palpable or visible                         clustered epitheloid cells
                          -   Non-caseating, non-cavitated               -   Langerhan cells often present
                              consolidation of CXR                       -   Laminated concretions composed of
                          -   Lesions primarily along lymphatics,            calcium & proteins → Schaumann
                              bronchi & blood vessels                        bodies
                                                                         -   Stellate inclusions known as asteroid
                                                                             bodies enclosed within giant cells
Hypersensitivity          -   Affect small bronchioles; may be           -   Thickened alveolar walls + w/           -   Hypersensitivity rxn affecting
Pneumonitis (aka              exudate in lumen;                              infiltration of lymphocytes, plasma         lung parenchyma that occurs in
extrinsic allergic        -   Fibrosis in advanced disease                   cells + sometimes eosinophils +             response to inhaled organic dusts
alveolitis)                                                                  collection of histiocytes    can form   -   ‘extrinsic’ cf IPF – etiologic
                                                                             small granuloma in some areas               agent is external + identified

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