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5 Cards in this Set
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Interstitial Lung disease(nofc:by VP)
CXR is starting point for diagnosis. Widespread changes, involving both lung fields, though not equally. HX impt- dusts, chem., occup.Hx, Drugs (cytoxic, penicllin, gold, amiodarone), radiation, illnesses esp collagen vascular dz’s Sx Hx: most common breathlessness and dry cough (stretch R), review old CXR’s, rales, clubbing, exercise desturation PFT: restrictive pattern, ßDLCO · Diffuse thickened alv walls by inflamm, edema and/or fibrosis · CXR- interstitial changes, HresCT-suggest area for biopsy · Bronchoscopy- deseases whose histological characteristics can be seen on small specimens · BAL- infxns: PCP, inflamm cell type · Dx by transbronchial or open/thorcoscopic wedge biopsy (perform in active disease areas) · Ddx include asbestosis, silicosis, drugs, farmer’s lung, TB, IPF, collagen vasc. Dz, pulmonary vasculitis, and sarcoidosis, etc. |
Idiopathic Pulmonary Fibrosis
· Cryptogenic fibrosing alveolitis · 50 yo onset; 5 year mortality = 50% · progr pulm involvement w/cyanosis, cor pulmonale and respiratory failure; coarse linear densities with peripheral honeycomb pattern · Bibasilar end inspiratory crackles/rales- when alveoli open at the end of inspiration · Risks: Smoking, exp to wood/metal dust · Dx of exclusion · trt w/xplant, but immunosup. Good but objective responses in < 50% · UIP = IPFà usual interstitial pneumonia · AIP or Hamman- Rich Syndrome – rapid course; slower than infection but faster than IPF |
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Major clinical criteria for IPF:
· Exclusion of othr causes (RA), abnl PFT’s, bibasilar reticular abnls, ground glass opacities, have to have transbronchial biopsy or BAL with no features supporting alternative diagnosis · Age >50 yrs, insidious onset with DOE, duration >3mos, bibasilar inpiratory crackles Risk factors · Cigarettes, metal dust, wood dust, viruses, hered. Collagen Vascular Diseases · Differ from IPF b/c part of multisys. dz, seen prior to pulm involvement, pleural involvement common |
1. SLE
· Pleuritis/pleural effusion (common with coll vasc dz assoc w/ILD); occ, severe acute lupus pneumonitis, fibrosis less common, alveolar hem. · Diaphragmatic weakness 2. Rheumatoid Arthritis w/Pleuropulmonary Disease · Joint dz. usually precedes pulm; M >F · Pulm complications rare; pleural eff #1, but with IPF alone that is not common · Other sx present: fibrosing alveolitis/IPF, necrobiotic nodules/Caplan’s syndrome (coal), bronchiolistis obliterans, associated with ILD drug toxicity (tx for RA- gold, methotrexate, etc) 3. many other vasculitides can effect the resp sys. |
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Sarcoidosis
· Multisystem dz of unknown etiology; lung is primary player; char by noncaseating granulomas (follow lymphatic distribution); upper 2/3 lung · F>M; blacks>whites; usu <40 yo; Asx w/abn CXR · Disease does not usually prog linearly; good Px · Radiologic Stages: 0) Stage 0 – no CXR abn (sarcoid in other system) 1) Stage I – l.n. enlargement with asx and abnl CXR (KNOW most common!) · Fungal infxn, TB, lymphoma 2) Stage II – nodes + diffuse parenchymal changes · TB, IPF, lymphangitic CA, pneumoconiosis, PIE 3) Stage III – no nodes, diffuse changes · Same as 2 plus berylliosis, sceloderma, alveolar proteinosis 4) Stage IV – fibrosis · Same as stage 3 |
· Dx of excl, based on transbronchial biopsy + CXR bronchoscopy can make diagnosis because so diffuse
· Each stage has another diagnostic DDx that goes with it · Half spont remit (3yrs), quarter stable, quarter progress; Systemic vital organ involvementàCNS facial n. palsy, cardiac CHF, skin, ocular-uveitis, endocrine Ca2+, bone cysts, lytic or sclerotic lesions; trt w/immsupp. But if asx- observe |
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Pneumoconioses
· Lung disease resulting from inhalation of mineral/organic dust · Factors in dz: particle size, shape, clearance, exposure, duration of exposure, solubility, antigenicity, host factors · Hx: get details, details of occ. Exp.miner, insulator, welder, sandblaster, foundry worker) |
1) Asbestosis – WWII shipyard workers, refineries, demolition of old buildings, brake repair, insulation; irreg opacities in bilat lower lobes (plaques), calcified pleura, insidious >20 yrs, DOE, paroxysmal cough, cor pulmonale and resp failure in final states; asbestos bodies (type of Fe body – dumbbell shaped)
a) pulmonary fibrosis (asbestosis)- must have fibrosis to have asbestosis b) benign pleural dz (adhesions/plaques) c) bronchogenic CA – 50X Ý in smokers d) mesothelioma – assoc w/asbestos exp but NOT w/smoking, relationship so strong get compensations, male>female |
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2) Silicosis – chronic, nodular “simple silicosis” most commonà fibronodular lung dz caused by LT (5 yrs) exp to crystalline silica (seen on polarized light); upper lobe, hilar adenopathy (eggshell calci); Ýrisk for TB b/c TB loves upper lobes, no Ýrisk for lung CA (asbestos does!)
a) Natural hx variable- slowly progr dyspnea, cough, sputum, may be fairly asx, most common to have CXR abnl b) Dx: CXR and Hx, sometimes lung biop (granulomas), HRCT helpful |
Hypersensitivity Pneumonitis – inhalation of/sensitivity to organic dusts; varied Ag but clinical response same, “Farmer’s lung” – moldy hay, flu-like. Dyspnea, cough, diffuse nodular, patchy consolidation, always abnl PFT’s with ¯ DLCO and PaO2, Eitology?:? thermophilic actinomycetes in moldy hay, acute change
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