Ch23 Restrictive Pulmonary Disorders

Card Set Information

Author:
wvuong
ID:
298681
Filename:
Ch23 Restrictive Pulmonary Disorders
Updated:
2015-03-18 20:17:09
Tags:
PulmonaryDisorders
Folders:

Description:
restrictive pulmonary disorders
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user wvuong on FreezingBlue Flashcards. What would you like to do?


  1. restrictive pulmonary disorders
    result from decreased lung expansion
  2. Restrictive pulmonary disorders 
    [characteristics]
    • decrease in vital capacity (VC), lung capacity (FRC), residual volume (RV)
    • greater the decrease in lung volume, greater the severity of disease
  3. Fibrotic interstitial lung disease 
    [etiology]
    characterized by thickening of alveolar interstitium
  4. Diffuse Interstitial lung disease 
    [pathogenesis]
    • immune reaction
    • Inflammation 
    • Fibrosis
    • Destruction
  5. Diffuse Interstitial lung disease [pathogenesis]
    immune reaction
    • begins with injury to alveolar epithelial or capillary endothelial cells 
    • interstitial and alveolar wall thickening 
    • increased collagen bundles in interstitium 
    • lung tissue becomes infiltrated 
    • persistent alveolitis leads to obliteration of alveolar capillaries, reorganization of lung parenchyma, irreversible fibrosis 
    • lead to large air-filled sacs (cysts) with dilated terminal and respiratory bronchioles
  6. Diffuse Interstitial lung disease [pathogenesis]
    inflammation
    • occurs early, reversible 
    • triggering event leads to inflammatory response and increased inflammatory cells 
    • ---injury leads to increased membrane permeability and movement of fluid/debris into alveoli
  7. Diffuse Interstitial lung disease [pathogenesis]
    Fibrosis
    • fibroblastic proliferation and deposition of large amt of collagen 
    • caused by increased mesenchymal cells and fibroblasts in interstitium 
    • Alveolar walls become thickened w/ increased amts of fibrous tissue
  8. Diffuse Interstitial lung disease [pathogenesis]
    destruction
    • end-stage disease 
    • loss of alveolar walls
  9. Diffuse Interstitial lung disease 
    [clinical manifestations]
    • progressive dyspnea w/ exercise w/ desaturation
    • rapid-shallow breathing 
    • irritating, nonproductive cough
    • clubbing of nail beds 
    • bibasilar end-expiratory crackles (Valcro rales) 
    • Cyanosis 
    • anorexia, wt loss 
    • inability to increase cardiac output with exercise
  10. Diffuse Interstitial lung disease
    [diagnosis]
    • CXR
    • PFT 
    • open lung biopsy
    • transbronchial biopsy
    • Gallium 67 scan
    • bronchoalveolar lavage
  11. Diffuse Interstitial lung disease
    [treatment]
    • smoking cessation 
    • avoid environmental exposure to cause 
    • anti-inflammatory agents 
    • immunosuppressive agents 
    • lung transplant
  12. Sarcoidosis 
    [etiology]
    • chronic common in 3rd-4th decade of life 
    • Activation of alveolar macrophage to unknown trigger
  13. Sarcoidosis 
    [pathogenesis]
    development of multiple, uniform, noncaseating epithelioid granulomas
  14. Sarcoidosis 
    [clinical manifestations]
    • malaise, fatigue 
    • wt loss 
    • fever 
    • dyspnea of insidious onset 
    • dry, nonproductive cough
    • erythema nodosum 
    • macules, papules, hyperpigmentation, and subcutaneous nodules 
    • hepatosplenomegaly, lymphadenopathy
  15. Sarcoidosis 
    [diagnosis]
    • leukopenia, anemia
    • increased eosinophil count, elevated sedimentation rate 
    • increased Ca levels 
    • elevated liver enzymes 
    • anergy 
    • elevated angiotensin-converting enzyme in active disease

    • Gallium 67 scan
    • PFTs
    • Bronchoalveolar lavage 
    • transbronchial lung biopsy
    • CXR
  16. Sarcoidosis 
    [stages 1]
    normal
  17. Sarcoidosis
    [stage 1]
    • good prognosis
    • hilar adenopathy alone
  18. Sarcoidosis
    Stage 2
    hilar adenopathy and bilateral pulmonary infiltrates
  19. Sarcoidosis 
    stage 3
    pulmonary infiltrates w/o adenopathy
  20. Sarcoidosis 
    stage 4
    • advanced fibrosis w/ evidence of honeycombing,
    • dilar retraction, bullae, cysts, and emphysema
  21. Sarcoidosis 
    [treatment]
    • corticosteroids 
    • immunosuppressive agents
  22. Hypersensitivity pneumonitis 
    [etiology]
    • aka extrinsic allergic alveolitis 
    • restrictive and occupational disease 
    • predominant in nonsmokers
  23. Hypersensitivity pneumonitis 
    [pathogenesis]
    • genetic predispose
    • agent suggest by pt history
    • agent confirmed by precipitating antibodies in serum
    • antigen combines with serum antibody in alveolar walls; leads to type III hypersensitivity rxn
    • antigen-antibody complexes then elicit granulomatous inflammation leading to lung tissue injury 
    • must have delayed hypersensitivity (type IV) rxn to antigen to develop pneumonitis
  24. hypersensitivity pneumonitis
    [clinical manifestations]
    Acute
    • symptoms after 4-6 hrs and resolve in 18-24hrs 
    • general:chills, sweating, shivering 
    • myalgias 
    • nausea
    • malaise, lethargy 
    • headaches

    • Respiratory symptoms: 
    • dyspnea at rest 
    • dry cough
    • tachypnea
    • chest discomfort 

    • physical findings 
    • cyanosis
    • crackles in lung bases
  25. hypersensitivity pneumonitis 
    [clinical manifestations]
    intermediate
    • acute febrile episodes
    • progressive pulmonary fibrosis with cough
    • dyspnea, fatigue 
    • cor pulmonale (R sided heart failure due to lung disorders)
  26. hypersensitivity pneumonitis
    [clinical manifestations]
    Chronic (hallmark)
    progressive, diffuse pulmonary fibrosis in upper lobes
  27. hypersensitivity pneumonitis 
    [treatment]
    • ID ofeending agent and prevent further exposure 
    • oral corticosteroids
  28. Occupational lung diseases
    [etiology]
    • result from inhalation of toxic gases or foreign particles 
    • atmospheric pollutants have large effect on occupational respiratory diseases
  29. Occupational lung diseases 
    What particles
    • pneumoncniosis
    • anthracosis
    • silicosis
    • asbestosis
  30. occupational lung disease 
    [predisposing factors]
    • preexisting lung disease 
    • exposure to atmospheric pollutants 
    • duration of dust exposure 
    • amt of dust conc. 
    • particle size of pollutant
  31. Occupational lung disease 
    [pathogenesis]
    • pollutants interfere and paralyze cilia 
    • inference with ciliary action 
    • alveolar macrophages try to engulf and remove
    • macrophages secrete lysozymes to control foreign particles activity 
    • enzymes damage alveolar walls causing deposition of fibrous materials
  32. occupational lung disease 
    [clinical manifestations]
    • symptoms depend on predisposing factor 
    • pneumonconiosis produces no signs/symptoms in early stage 
    • usually symptom free up to 10-20 yrs with chronic exposure
  33. occupational lung disease 
    [late clinical features]
    • chronic hypoxemia
    • cor pulmonale 
    • respiratory failure
  34. Occupational lung disease 
    [treatment
    • preventive measures
    • corticosteroids 
    • bronchodilators 
    • O2 therapy
  35. ARDS - Acute respiratory distress syndrome 
    [etiology]
    occurs in assoc with other pathophysio processes
  36. ARDS
    [causes]
    • severe trauma
    • sepsis
    • aspiration of gastric acid 
    • fat emboli syndrome 
    • shock
  37. ARDS 
    [pathogenesis]
    • widespread pulmonary inflammation leads to: 
    • noncardiogenic pulmonary edema assoc with leaky pulmonary capillaries 
    • atelectasis assoc. with lack of surfactant (decrease surface tension in small alveoli and prevents from collapsing) 
    • fibrosis(hyaline membranes)
  38. ARDS 
    [characteristic abnormalities]
    • injury to alveoli fr wide variety of disorders 
    • changes in alveolar diameter 
    • injury to pulmonary circulation 
    • disruptions in O2 transport and utilization
  39. ARDS
    common findings
    severe hypoxemia caused by intrapulmonary shunting of blood
  40. ARDS 
    [clinical manifestations]
    Early and Late
    • EArly: 
    • sudden marked respiratory distress
    • slight increase in pulse rate 
    • dyspnea
    • low PaO2
    • shallow, rapid breathing

    • Late: 
    • tachycardia 
    • tachypnea
    • hypotension
    • marked restlessness 
    • crackles, rhonchi on auscultation
    • use of accessory muscles 
    • intercostal and sternal retractions cyanosis
  41. ARDS 
    hallmark
    hypoxemia refractory to increased levels of supplemental O2
  42. ARDS 
    [treatments]
    • mostly supportive 
    • ID underlying cause 
    • maintain fluid and electrolyte balance 
    • block system inflammatory cells
    • adequate oxygenation
  43. IRDS 
    infant respiratory distress syndrome 
    [etiology]
    • Hyaline membrane disease 
    • syndrome of premature neonates 
    • primary cause: lack of surfactant 

    • risk factors: 
    • birth prior to 25 wks gestation 
    • birth at advanced gestational age 
    • poorly controleld diabetes in mother 
    • deliveries after antepartum hemorrhage
    • C section w/o antecedent labor 
    • perinatal asphyxia
    • 2nd twin
    • previous infant with RDS
    • Rh factor incomp.
  44. IRDS
    [clinical manifestations]
    • shallow respirations, diminished breath sounds 
    • intercostal, subcostal, sternal retractions 
    • flaring of nares 
    • hypotension, bradycardia
    • peripheral edema
    • low body temp 
    • oliguria
    • tachypnea
  45. IRDS 
    [treatment]
    • prevent
    • maintain adequate oxygen level 
    • mechanical ventilation with PEEP or continuous positive airway pressure 
    • exogenous surfactant adm
    • high freq. ventilation
    • antibiotics 
    • supportive therapy
  46. Pneumothorax 
    [etiology]
    • accumulation of air in the pleural space 
    • primary cause: also, trauma 
  47. pneumothorax 
    [pathogenesis]
    open 'sucking' chest wall wound 

    • air enters during inspiration but cannot escape during expiration 
    • --leads to shift of mediastinum 
  48. Pneumothorax 
    [clinical manifestations]
    • small pneumothoraces usually not detect on physical
    • tachycardia
    • decreased/abset breath sounds on affected side 
    • hyperresonance 
    • sudden chest pain on affected side 
    • dyspnea

    tension and large spontaneous pneumothorax = emergency situations 
  49. Pneumothorax 
    [treatment]
    • management depends on severity of problem and cause of air leak 
    • lung collapse: may or may not hospitalized/ treat symptomatically 
    • --chest tube placement with H2O seal and suction 
  50. Pleural effusion 
    [etiology]
    • collection of fluid/pus in pleural cavity as result of another disease process 
    • 5-15 ml of serous fluid contained in pleural space 
  51. Flail chest 
    [etiology]
    • results from multiple rib fractures r/t trauma to chest wall 
    • ribs fractured at 2 distant sites 
  52. pneumonia 
    why and causes
    inflammatory rnx in alveoli and interstitium caused by infectious agent 

    • causes: 
    • aspiration of oropharyngeal secretions composed of normal bacterial flora/ gastric contents
    • inhalation of contaminants 
    • contamination fr. systemic circulation 
  53. Pneumonia
    classifications
    • community acquired 
    • hospital acquired
    • bacterial (G(+)) - Staphyl & Strept
    • fungal (aspergillus) 
  54. Pneumonia 
    [clinical manifestations] 
    • severity of disease and patient age causes variation in symptoms 
    • crackles and bronchial breath sounds over affected lung tissue 
    • chills 
    • fever 
    • cough, purulent sputum 
  55. Pneumonia 
    [treatment]
    antibiotic therapy 
  56. Pulmonary tuberculosis 
    [etiology]
    • prior infection
    • malnourishment, immunosuppression
    • living overcrowded condition
    • incarcerated persons 
    • immigrants 
    • elderly 
  57. Pulmonary tuberculosis 
    [clinical manifestations]
    • history of contact with infected person 
    • low grade fever 
    • cough
    • night sweats 
    • fatigue 
    • wt loss 
    • malaise 
    • anorexia 
  58. Pulmonary tuberculosis
    [treatment]
    • administer multiple drugs (antibiotics) which org is susceptible 
    • add at least 2 agents to drug regimen when tx failure is suspected 

What would you like to do?

Home > Flashcards > Print Preview