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LUNGS PATHOLOGY 1 - Coggle Diagram

- - - - tobacco smoking (90%)
        
        environmental pollution (15%)
    - - emphysema
        
        irreversible enlargement of th airspaces distal to the terminal bronchiole, accompanied by destruction of their walls
        
        classification based on the segment of the respiratory units involved
        
        CENTRIACINAR
        
        airflow obstruction
        
        95% of COPD patients
        
        central / proximal parts of acini involvement
        
        sparing of distal alveoli
        
        PANACINAR
        
        airflow obstruction
        
        alpha1 antitrypsin deficiency association
        
        exacerbated by smoking
        
        uniformly enlarged acini
        
        paraseptal
        
        distal part of the acinus involved
        
        spontaneous pneumothorax in young adults
        
        cyst-like structures
        more adjacent to the pleura
        
        irregular
        
        irregularly involved acinus
        
        association with scarring
        
        compensatory
        
        distension of alveoli
        
        response to loss of lung substance elsewhere
        
        obstructive
        
        the lungs expand due to air trapping
        
        commonly caused by subtotal obstruction of an airway by a tumor or foreign object
        
        bullous
        
        large subpleural blebs / bullae
        
        often near the apex
        
        rupture of bullae --> pneumothorax
        
        interstitial
        
        entrance of air into the connective tissue of the lung, mediastinum, subcutaneous tissue
        
        caused by transient increases in intra-alveolar pressure
        
        pathogenesis
        
        release of proteases, which in the absence of alpha1 antitrypsin activity result in excessive digestion of elastic tissue
        
        destruction of alveolar walls and emphysema
        
        pathology
        
        macro
        
        lungs are enlarged because they are full of air
        
        micro
        
        disruption of alveolar walls
      - chronic bronchitis
        
        persistent cough with sputum production for at least 3 months in at least 2 consecutive years in the absence of any other identifiable cause
        
        pathogenesis
        
        esxposure to noxious or irritating inhaled substances, e.g. tobacco and dust from grain, cotton and silica
        
        mucus hypersecretion
        
        acquired cystic fibrosis factor regulator dysfunction
        
        inflammation
        
        infections
        
        pathology
        
        macro
        
        hyperemia, swelling and edema of mucous membranes, frequently accompanied by excessive mucinous or mucopurulent secretions
        
        sometimes heavy casts of secretions and pus fill the bronchi and bronchioles
        
        micro
        
        chronic inflammation of the airways
        
        thickening of the bronchiolar wall due to smooth muscle hypertrophy
        
        deposition of EC matrix in the muscle layer and peri-bronchial fibrosis
        
        goblet cell hyperplasia
        
        enlargement of the mucus-secreting glands of trachea and bronchi
        
        marked constriction of bronchioles, eventually developinf into obliteration of the lumen due to fibrosis (bronchiolitis obliterans)
    - - chronic cough with sputum production, slowly increasing dyspnea, superimposed infections
    - - spirometry with FEV1/FVC<0.7
    - - smoking cessation
        
        oxygen therapy
        
        long-acting bronchodilators with corticosteroids
        
        antibiotics
        
        physical activity
        
        bullectomy
        
        lung volume reduction surgery
        
        lung transplantation
    - - progression and death
        
        pulmonary hypertension
        
        cor pulmonare
        
        heart failure
        
        acute respiratory failure
        
        subpleural blebs breakage leading to fatal pneumothorax
  - - - airway inflammation is central and causes airway dysfunction partly through the release of potent inflammatory mediators and partly through remodeling of the airway wall
        
        early phase
        
        bronchoconstriction
        
        incresed mucus production
        
        variable degrees of vasodilation
        
        increased vascular permeability
        
        mast cells produce mediators which stimulate the subepithelial vagal receptors
        --> bronchoconstriction
        
        late phase
        
        recruitment of leukocytes (eosinophils, neutrophils) and T cells (Th2 and Th17)
    - - ATOPIC
        
        allergen sensitization and immune activation
        
        frequently in patints with allergic rhinitis / eczema
        
        IgE-mediated hypersensitivity reaction
        
        triggers: environmental allergens
      - NON-ATOPIC
        
        no evidence of allergen sensitization
        
        no IgE reaction
        
        respiratory infections due to viruses, e.g. rhinovirus, RSV
        
        air pollutants, e.g. tobacco smoke, sulfur dioxise, nitrogen dioxide
        
        innocuous events, e.g. exposure to cold and exercise
      - DRUG-INDUCED
        
        e.g. aspirin-sensitive asthma
      - OCCUPATIONAL
        
        fumes, e.g. epoxy, resins, plastics
        
        organic or chemical dusts, e.g. wood, cotton, platinum
        
        gases, e.g. toluene
        
        other chemicals, e.g. formaldehyde, penicillin
    - - acute airflow obstruction
        
        primarily attributed to bronchoconstriction, acute edema, mucus plugging
      - airway remodeling
        
        chronic irreversible airway obstruction
        
        thickening of airway wall
        
        sub-basement membrane fibrosis
        
        increased vascularoty
        
        increase in the size of the submucosal glands and number of airway goblet cells
        
        hypertrophy and/or hyperplasia of the bronchial wall muscle with increased EM
      - occlusion of bronchi and bronchioles by thick, tenacious mucus plugs, which often contain shedded epithelium
        
        Curschmann spirals: mucus plugs dense spiral-shaped from subepithelial mucous gland of ducts or brochioles
        
        Charcot-Leyden crystals: composed of eosinophil-derived protein galectin-10
  - - - congenital or hereditary conditions that predispose to chronic infections, including CF, intralobar sequestration of the lung, immunodeficiency states, primary ciliary dyskinesia and Kartagener syndrome
      - severe necrotizing pneumonia
      - bronchial obstruction (tumor, foreign body, mucus impaction)
      - immune disorders (RA, transplantation)
      - idiopathic, in which there is a dysfunctional host immunity to infectious agents leading to chronic inflammation
    - - cystic fibrosis: the primary defect in ion transport results in thick viscous secretions that impair muco-ciliary clearance and lead to airway obstruction
      - primary ciliary dyskinesia: ciliary dysfunction due to defects in ciliary proteins, preventing mucociliary clearance
      - allergic bronchopulmonary aspergillosis: intense airway inflammation with eosinophils and formation of mucus plugs
    - - macro
        
        dilated airways
        (up to 4x)
        
        bronchi and bronchioles visible to the pleural surfaces
        
        dilated bronchi appear cystic and filled with mucopurulent secretions
      - micro
        
        acute and chronic inflammatory exudation within the walls of bronchi and bronchioles
        
        desquamation of the lining epithelium
        
        extensive ulceration
        
        necrosis destroys the walls and forms lung abscesses
        in chronic cases, fibrosis of walls develop
        
        --> subtotal or total obliteration of bronchiolar lumina
    - - severe and persistent cough
        
        expectoration of sputum
        
        dyspnea and orthopnea
        
        hemoptysis
    - - antibiotics and physical therapy, surgery
- - - - clinical manifestation of severe ALI
    - - histologic manifestation of the disease
  - - - shock
        
        oxygen therapy
        
        sepsis
  - - - increasing inflammation and pulmonary damage
- - - - emboli are variable in size
      - distinguished from a post-mortem clot by the presence of the lines of Zahn in the thrombus
      - pulmonary infarct is classically hemorrhagic
        
        it appears as a raised, red-blue area in the early stages
        
        the apposed pleural surface is covered by a fibrinous exudate
        
        red cells becing to lyse in 48h
        
        the infarct becomes paler and eventually red-brown as hemosiderin is produced
        
        fibrous replacement begins at the margins as a gray-whit peripheral zone
        
        it eventually converts the infarct into a contracted scar
    - - prolonged bed rest
        
        leg surgery
        
        severe trauma
        
        congestive HF
        
        oral contraceptives
        
        disseminated cancer
        
        inherited forms of
        hypercoagulability
    - - 60-80% of emboli are clinically silent
        
        5% cause acute cor polmonare, shock or death
        
        the remaining causesymptoms related to ventilation-perfusion mismatch and/or pulmonary infarction (dyspnea, pleuritic chest pain)
      - pathophysiologic consequences:
        
        respiratory compromisation due to non-perfused, although ventilated, segment
        
        hemodynamic compromise due to increased rsistance to pulmonary blood flow caused by the embolic obstruction
      - high risk of recurrence, in particular of embolism
        
        pulmonary hypertension
        
        cor pomlonare
  - - - medial hypertrophy
        
        intimal fibrosis of pulmonary arteries
        
        RV hypertrophy
    - - tuft of calìpillaries, producing a network that involves the lumina of dilated thin-walled, small arteries
      - possible extension outside of the vessel
      - more prominent in idiopathic and familial pulmonary hypertension
  - - - diffuse alveolar hemorrhage
        
        cough, hemoptysis and anemia
        
        unknown etiology
        
        immunologic mechanism ?
    - - circulating auto-Abs against basal membtane collagen IV
        
        lung and kidney are the most frequently involved organs
        
        hemoptysis and glomerulonephritis
        
        plasmapheresis and immunosuppressive therapy
    - - aka Wegener granulomatosis
        
        autoimmune disease
        
        TBLB for diagnosis
        
        necrosis, granulomatous lung vasculitis, hemorrhage, capillaritis and poosly formed granulomas
- - - - unknown etiology
      - symptoms
        
        dyspnea, tachypnea, end-inspiratory crackles and eventual cyanosis, without wheezing or other evidence of airway obstruction
      - pulmonary function studies
        
        reduction in DLCO, lung volume and compliance
      - RX
        
        bilateral lesions in the form of small nodules, irregular lines or ground-glass shadows, corresponding to areas of interstitial fibrosis
      - outcome
        
        diffuse fibrotic scarring of the lung, often referred to as end-stage lung or honeycomb lung
        
        eventually, secondary pulmonary hypertension and right-sided heart failure may result
    - - IDIOPATHIC PULMONARY FIBROSIS
        
        usual interstitial pneumonia
        
        diagnosis
        
        characteristic appearance on computed tomography scans
        
        histology
        
        macro
        
        cobble.stoned pleural surfaces
        
        retraction of scars along the interlobular septa
        
        firm, rubbery white areas of fibrosis, preferentially in the lower lobes, subpleural regions and interlobular septa
        
        micro
        
        temporary and spatial heterogeneity
        
        mild / absence of inflammatory cell infiltrate
        
        honeycombing
        
        fibroblastic foci
        
        pathogenesis
        
        clinically predisposed individuals, prone to aberrant repair of recurrent alveolar epithelial cell injuries caused by environmntal exposures
        
        clinic
        
        smokers
        
        elderly (>50y)
        
        rare familial forms
        
        outcome
        
        slow progressive respiratory failure
        
        acute exacerbations
        
        rapid downhill clinical course (ARDS)
        
        progressivly restrictive syndrome and respiratory failure
        
        non specific interstitial pneumonia
        
        fibrosing ILD, with a much better prognosis if compared to pts with UIP
        
        etiology
        
        idiopathic
        
        connective diseases-associated
        
        histology
        
        distinction between cellular and fibrosing patterns
        
        homogeneous distribution
        
        no patchy
        
        no fibroblastic foci, honeycombing, hyaline membranes and granulomas
        
        cellular pattern: mild-to-moderate chronic interstitial inflammation, containing lymphocytes and few plasma cells in a uniform or patchy distribution
        
        fibrosing pattern: diffuse or patchy interstitial fibrotic lesions of roughly the same stage of development
        
        clinic
        
        dyspnea and cough
        
        female not smokers in the 6th decade of life
        
        CT scan: reticular opacities, bilateral, symmetric, lower lobes predominance
        
        criptogenetic organizing pneumonia
        
        response to infection or inflammatory injury of the lung, leading to cough and dyspnea
        
        RX / CT: patchy subpleural or nodular areas of airspace consolidation
        
        histology
        
        polypoid plugs of loose organizing connective tissue (Masson bodies) within alveolar ducts, alveoli and often bronchioles
        
        no interstitial fibrosis or honeycombing
        
        DD: neoplastic nodules
        
        outcome
        
        spontaneous recover, treatment with oral steroids
        
        in the long term, it is dependent on the underlying disorder
      - SECONDARY
        
        connective tissue disease-associated
        
        pneumoconiosis
        
        drug reactions
        
        radiation pneumonitis