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34 Cards in this Set
- Front
- Back
Diffuse Parenchymal Lung Disease (Interstial Lung disease)
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Idiopathic interstitial lung pnumonias are the most common. They inclue UIPs, NSIP, BOOP, and DIP
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Non-specific interstitial pneumonia
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-More homogenous
-no honeycombing |
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Bronchiolitis obliterans organized pneumonia
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-Plugs of fibroblasts in airways
-CT shows areas of consolidation |
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Desquamative Interstitial Pneumonia
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-Alveolar spaces filled with alveolar macrophages
-Cigarete smoking related -No desquamation -Ground glass opacifications on CT |
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Hypersensitivity Pneumonitis
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-Only disease caused by inhalation of organic particles
-Abnormal immunological reaction of the lung to specific organic antigens -Size and amount of particle are key factors -Thermophilic actinomycetes, fungi, and bird droppings are the most common causes |
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Pathogenesis of hypersensitivity pneumonitis
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antigen exposure ->accumulation of inflammatory cells ->lymphocytic alveolitis in more chronic phases -> granuloma formation -> normal repair or end up with fibrosis from continued antigen exposure
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someone presents with acute fever, chills, dyspnea, cough. chest xray shows infiltrates
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Could be hypersensitivity pneumonitis.
-High resolution CT shows a lot of "ground glass opacifications" |
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Subacute Hypersensitivity presentation
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Symptoms evolve over weeks to months
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Chronic hypersensitivity pneumonitis presentation
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Same as IPF.
-persistent cough, shortness of breath, sputum production -HRCT may show fibrotic changes |
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Diagnosis of Hypersensitivity pneumonitis
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-Careful H&P
-PFTs show restrictive pattern -Diffusion impairment and hypoxemia -Imaging acutely shows ground glass opacifications and chronically shows more fibrotic tissue -May have serum precipitating antibodies -Lung biopsy is the gold standard. Will show honeycombing in lower lungs in chronic |
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Shipbuilder, construction, automotive, railroad
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Think Asbestosis!
-Asbestos is a naturally occuring minral with therm-insulating properties |
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What can asbestos do?
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Induces pleural disease, malignant mesothelioma, bronchogenic cancer, and asbestosis
-98% is the more benign chrysotile fiber |
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Define Asbestosis
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-Interstitial pneumonitis and fibrosis caused by exposure to asbestos fibers. The prevalence increase with duration and intensity of exposure.
-LATENCY PERIOD OF 15-20 YRS -Most cases are progressive |
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Describe the pathogenesis of asbestosis
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-Direct toxic effects
-Release of mediators by inflammatory cells causes more inflammatory cells, fibroblast proliferation, and loss of type I and II pneumocytes |
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Clinical findings of asbestosis
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-Progressive Dyspnea
-Bibasilar inspiratory crackels -clubbing of fingernails -PFTs show restriction and low DLCO -can have honeycomb appearance |
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Radiographic findings of Asbestosis
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-Pleural plaques
-Round atelectasis -Basilar disease -interlobar septal fibrosis and honeycombing in advanced cases |
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How do you diagnose asbestosis?
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-Reliable history of exposure with latency period
-Evidence of interstitial fibrosis -Asbestos fibers or bodies in biopsy are helpful but not necessary |
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Foundry work, tunneling, sandblasting, pottery making, manufacturers of brink, tiles, glass
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Silicosis!
-Chronic fibrosis disease of the lungs caused by inhalation of free silica dust |
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Acute silicosis
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presents like ARDS. from massive exposure
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Chronic or Simple Silica exposure
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More like IPF with chronic cough and dyspnea. Caused by exposure to low concentrations for 20 yrs or more
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Pathogenesis of Silicosis
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alveolar macrophages eat silica, get activated, release inflammatory mediators, and cause inflammation and fibrosis
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Someone comes in asymptomatic and you discover an abnormal chest xray and then restricted PFTs
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Think silicosis. Usually it is asymptomatic. 10-15% go on to develop "progressive massive fibrosis"
On CXR, there a upper zone micronodular opacities |
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Diagnosis of Silicosis
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-History of exposure
-Absence of other illnesses -Reticulo-nodular and nodular infiltrates -Upper lobe predominance |
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Associated illnesses with silicosis
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-Mycobacterial infections (TB)
-Connective Tissue Disease like Scleroderma -Lung Cancer |
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Coal workers pneumoconiosis
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-exposure to coal dust and silica
-asymptomatic, small nodual opacities on CXR- ALL OVER -Need history of exposure and CXR to diagnose -Doesn't usually go to end stage lung disease |
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ILD is associated with what?
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Connective Tissue Diseases
-unknown etiology -most associated with scleroderma and rheumatoid arthritis and least with lupus -The CTD probably causes the ILD in many cases |
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Discuss Rheumatoid arthritis
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-Chronic symmetric polyarthritis, usually insidious onset with fatigue, loss of appetite, vague aches and pains, morning stiffness
-joint deformities -bone erosion with sinovitis -soft tissue around joints is swollen -Subcutaneous nodules |
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ILD caused by RA
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-more common in men
-infiltrates at bases -mean survival 5 yrs -might respond to steroids -honeycomb |
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Discuss Systemic Sclerosis
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-Accumulation of connective tissue in skin and visceral organs
-Diffuse cutaneous vs limited cutaneous (CREST) -Diffuse think antitopoisomerase -Limited think anticentromere Ab -Pulmonary HTN predicts a poor prognosis |
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"Friends say I look younger every day" or I have trouble swallowing
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Think scleroderma
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ILD related to Scleroderma
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-Lung impairment in most patients
-Usually in base of lungs -Lung disease is most common cause of death with scleroderma -High risk of bronchogenic cancer too Teat with cyclophoshamide |
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Reddish discolored knuckles (Gottron's sign)
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Dermatolysis
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Sicca Syndrome (dry and red eyes and dry mouth)
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Sjorgens
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Drug-induced ILD
dyspnea, fever, infiltrates are the usual presentation |
Bleomycin- dose dependent
Cyclophosphamide/methotrexate- time dependent Amiodarone (anitarrythmia) -DLCO of more than 80% virtually excludes it |