ILDs

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countchocula58
ID:
297080
Filename:
ILDs
Updated:
2015-02-27 22:03:36
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Pulm ILDs
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  1. Pathogenesis of IPF
    • Repeat stimulus leading to inflammation to aberrant wound healing to fibrosis
    • There are genetic factors, some promoting a TH1 TH2 imbalance
    • Injuries can be particles, chemicals, gastric reflux, viruses
  2. Epidemiology of IPF
    • Men more than women
    • Usually over age 40
    • Smoking, farming, silica, wood dust, metal dust
  3. Diagnosis of IPF
    • Exclusion!
    • History is most important
    • CXR reticular (mostly base), surgical lung biopsy
    • UIP pattern HRCT
  4. Symptoms of IPF
    • Dry, non productive cough
    • Chronic, worsening dyspnea
  5. Physical Exam of IPF
    • Clubbing
    • Velcro inspiratory crackles
    • Absence of clues suggesting CT disease
    • Restrictive
  6. UIP
    • Lots of causes including IPF
    • Subpleural and BASAL
    • Reticular
    • Honeycombing
    • Absent of other features (ground glass, nodes, air trapping)
    • Traction bronchiectasis
  7. CT related ILD
    • UIP, but better prognosis
    • Less fibroblast foci
    • Younger age
  8. Causes of death in UIP
    • Carcinoma (10 fold risk)
    • Cor pulmonale
    • Pulmonary HTN
    • Respiratory failure
    • Infection
    • Exacerbation
  9. Histology of IPF
    • Subplural heterogenous temporal and spatial
    • Microscopic honeycombing
    • Traction bronchiectasis
    • Fibroblastic foci show young (temporal heterogeneity)
    • Central sparing lobules
    • By the way, cobblestoned on gross pathology
  10. Hypersensitivity Pneumonitis
    • Bird fanciers
    • Apical predominant consolidations
    • Ground glass
  11. Prognosis of IPF
    • 25% rapid progressive 3 year mortality
    • 25% slow until acute exacerbation, probably 10 years
    • 50% IPF with emphysema 5 years
  12. Treatment of IPF
    • Pirfenidone or Nintedanib
    • Corticosteroids unproven efficacy, often perscribed
    • Oxygenation
    • Pulm rehab
    • Lung transplantation in selective patients
    • Paliative care
  13. Sarcoidosis
    • Non caseating granuloma, which can form nodules
    • African American Women
    • Steroids or self limited
    • Trees in bud
    • Hilar shadows
    • Traction bronchiectasis
    • Bronchoscopy
    • Indistinguishable from Berylliosis (history!)
  14. Diffuse Alveolar Damage Pathogenesis
    • Acute from any insult
    • Early exudative phase: Hyaline membranes
    • Organizing phase: organization and collagen
    • Can present histologically as AIP, acute interstitial pneumonitis
  15. Determing cause of DAD
    • Look for the obvious like bacteria means bacterial cause
    • Neutrophils suggest infection
    • Eosinophils-pneumonia
    • Granulomas-anything
    • Foamy macrophages-drug (amiodarone)
    • Diffuse hemorrhage and capillaritis-vasculitis
  16. DAD prognosis
    • 80% survival
    • Worse with comorbidities
  17. Pathogenesis of organizing pneumonia
    • Sub acute from any insult
    • Can be idiopathic-cryptogenic organising pneumonia
    • Minor component of many other diseases
    • Consolidation (ie pneumonia)
    • No hyaline membranes
    • Branching appearance of granulation
  18. Prognosis of OP
    • If idiopathic 70-90%
    • Secondary dependent on cause
  19. NSIP is seen in
    • Hypersensitive pneumonitis
    • Drug induced
    • CT diseases
    • Idiopathic NSIP
  20. NSIP
    • Homogenous
    • Ground glass
    • No honeycombing
    • Fibrotic type or cellular
  21. NSIP prognosis and treatment
    • Better than UIP
    • Cellular more treatable (steroids)
    • Fibrotic not as bad as UIP
  22. Causes of Granulomatous Lung Diseases
    • Hypersensitivity pneumonitis
    • Fungal, mycobacterial
    • Aspiration
    • Berylliosis
    • Drug
    • Idiopathic is sarcoidosis
  23. Causes of hypersensitivity pneumonitis
    • Extrinsic allergic alveolitis
    • Inhaled antigen or offending agent
  24. Diagnosis of HP
    • BAL with lymphocytosis (40%+)
    • Antibodies in serum
  25. Classification of HP
    • Acute: 4-6 hours after exposure, lasts 48 hours (dyspnea)
    • Subacute: Insidious over weeks to months (mildly restrictive)
    • Crhonic: Insidious leading to fibrosis (restrictive)
  26. Histology of HP
    • Centrilobular fibrosis
    • Reticulation
    • Menimal honeycombing
    • Ground glass
    • Granulomas and giant cells around bronchioles
    • Chronic can be UIP, NSIP, centrilobular or combo
  27. Prognosis of HP
    • Avoid the antigen
    • Acute/subacute resolve
    • Chronic has poor prognosis

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