ĐĎॹá>ţ˙ IKţ˙˙˙H˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙˙ěĽÁ5@ đż0ą bjbjĎ2Ď2 +4­X­Xą˙˙˙˙˙˙ˆ2222222FÎ0Î0Î0Î0 Ú0<F5ś"1"1"1"1"1"1"1"1˜4š4š4š4š4š4š4$Ď5R!8jž42 2"1"1 2 2ž422"1"1Ó4Ĺ3Ĺ3Ĺ3 22"12"1˜4Ĺ3 2˜4Ĺ3Ĺ3Ű34S22|4"11 ŔŁSwcĽÁÎ0 2"l4˜4é405t4‹8+2‹8|4FF2222‹82|4"1"D1Ĺ3\1p1™"1"1"1ž4ž4FFÄ Äť3 FF DIFFUSE LUNG DISEASE Interstitial Lung Disease It is the result of injury to structures in the alveolar space, interstitial space, or both PATHOLOGY Alveolar cell injury Altered permeability in the alveolocapillary inter phase Alveolar exudation Infiltration of interstitial spaces by mononuclear cells, neutrophils and other cells Increase in the thickness of the pulmonary interstitium Capillary damage causes increased permeability and edema formation Interstitial fibrosis PHYSIOLOGY “Restrictive Defect” Lung Volumes - decreased TLC, VC, and RV decreased Airflow rates - near normal Lung compliance is decreased and elastic recoil is increased DLCO is decreased early in the course Exercise induced hypoxemia Hypocarbia in early stages Hypercarbia in late disease (Respiratory Exhaustion) ROENTGENOLOGY HRCT Scan: Shows characteristics findings Pulmonary Langerhans Cells Granulloma: Nodular cystic spaces in the upper lung field Idiopathic Pulmonary Fibrosis: Subpleural honey combing Lymphangioleiomyomatosis Well defined cystic spaces in the lung parenchyma CXR: Alveolar pattern Interstitial pattern combination of alveolar - interstitial patterns CLASSIFICATION OF DIFFUSE Pulmonary Diseases IDIOPATHIC PULMONARY FIBROSIS Cryptogenic Fibrosing Alveolitis Rare Disorder Diffuse Fibrosis throughout the Lung fields Late middle age Most common cause of chronic diffuse interstial Lung disease Some studies indicate that Hepatitis C virus infection is an etiologic factor PATHOGENESIS Complex Macrophages activated by several factors Production of growth factors e.g. Fibronectin, platelet-derived growth factor (PDGF), TGT-B, IGF-I Deposition of collagens type I and III CLINICAL FEATURES Progressive Breathlessness Frequent Coughing Fatigue Anorexia Weight loss Arthralgias PHYSICAL FINDINGS Cyanosis Tachypnea at rest Clubbing of the fingers and toes (without hypertrophic osteoarthropathy) Dry crackles, or coarse crackles on inspiration (Auscultation), heard at the Lung bases Accentuated pulmonic second sound Signs of RHF IMAGING CXR- Diffuse reticular or reticulonodular markings (lower Lung zones) High Resolution CT- “Ground Glass” appearance of the lower Lung fields (stage of alveolitis) Nodular Infiltrates Honey Combed or Swiss Cheese appearance (end stage disease) Iinear opacities Ring shaped opacities Lung field contracted LABORATORY EXAMINATION ESR elevated Circulating immune - complex titers 50% Serum immunoglobins Cryoimmunoglobulins RF (Rhematoid factors) 30% ANA (Antinuclear antibody) 35% LUNG FUNCTION TESTS Advanced Disease TLC VC RV FEV1/FVC Ratio-Normal or increased DLCO - Reduced by 30% - 50% Bronchoscopy Sarcoidosis - Yield 80% BAL Useful information about cells+proteins LUNG BIOPSY Histologic Evaluation Good Microbial Cultures Immunofluorescence and eleetnn-microscope studies Analysis of inorganic substances DIAGNOSTIC APPROACH Occupational and environmental history Prior chest films review check for multi system disease process, new medication, neurologic status (aspiration and infection) Chest X-ray / HRCT chest scan Pulmonary function test / DLCO Arterial Blood gases (desatuiration with exercise) Fiberoptic bronchoscopy (1st invasive procedure) Transbronchial biopsy / BAL Imaged thorascopic or open lung biopsy TREATMENT Oral prednisone 1mg / kg / d * 8 week maintenance level 0.25 mg / kg / day * 6 months Immosuppression with cyclophosphamide if disease is progressive (Addition) dose 1mg / kg / day Pulsed doses of cyclophosphamide given biweekly Azathioprine Colchicine 0.6 mg / day (inhibit macrophage produced fibroblast growth factors) Discontinue cigarette smoking Supplemental oxygen therapy Diureties Bronchodilator’s Narcotic containing antitussive medication Management of infection during immno suppression Prophylactic use of pneumococcal and influenza vaccines Lung transplantation IDIVIDUAL FORMS OF ILD ILD associated with collagen vascular disorders Systemic Lupus Erythematosus Half of the patients with SLE ultimately develop overt lung disease Pleuritis, pleural effusion, Acute pneumouitis (most frequent) Chromic progressive ILD (uncommon) abnormal DLCO Lymphocytic alveolitis (better response to treatment) End RHEUMATOID ARTHRITS Pleural disease (effusion and subpleural noduls) Parenchymal nodular infiltrates Diffuse interstitial fibrosis ILD can develop before joint disease becomes evident (in men) High titers of rheumatoid factor Broncholitis obliterans with organizing puemonia have been reported Patient who receives methotrexate or gold must be differentiated Penicillamine therapy broncholitis obliterans ANKYLOSING SPONDYLITIS Bilateral upper lobe fibrosis Fibrocavitary disease, may develop late in the course SYSTEMIC SCLEROSIS Radiographic evidence of lung involvement Cutaneous scleroderma can involve the anterior chest wall and abdomen restrictive lung disease SJOGREN’S SYNDROME SYNDROMES OF ILD WITH PULMONARY HEMORRIAGE Recurrent hemoptysis, dysprea and hypoxemia with diffuse alveolar opacities on chest radiography SLE, wegener’s granulomatosis, behcet’s disease, allergic churg- strauss granulomatosis, Henoch- schonlein purpura, mixed cryoglobinemia Serologic test ANA, Anti GBM antibody and complement Renal biopsy and lung biopsy may be repaired for definite diagnosis e-g GOOD PASTUR’S SYNDROME Pulmonary hemorrhage and glumerulonephritis are the features Anti bodies to renal glomeraular and lung alveolar basement membranes IDIOPATHIC PULMONARY HEMOSIDEROSIS Diagnosis of exclusion Lung biopsy is necessary (rule out) inflammatory injury) Children and young adults are usually affected Clinical course fulminant mild Glucocorticoid treatment to control bleeding acutely PULMONARY ALVEOLAR PROTEINOSIS Alveoli are filed with grammar material that stains with periodic acid schiff reagent (PAS) (Primary VS secondary) secondary can be associated with inhaled dust exposure (silica and aluminium) malignancy, and chronic infection intraalveolar material surfactant phospholid, LDH, proteins and Igs whole lung lavage provides long term benefits LYMPHOCYTIC INFILTRATIVE DISORDERS Behave as low grade lymphoma diffuse interstitial infiltration with lymphocytes and plasma cells Autoimmune disease or dysproteinemia exists /Œ–ç ń & 4 > ^ … ´ Ô î  < @ ™ ł Ć ă ä  Ű č Ľś! 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