Drug-Induced Pulmonary Disease.txt

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    • 4 mechanisms of drug injury
    • Oxidant stress, direct cytotoxic effects, deposition of phospholipids, immune-mediated injury
  1. MOA of nitrofurantoin injury
    Oxidant stress leading to chronic fibrosis
  2. General MOA of chemotherapeutic drug injury
  3. MOA of amiodarone injury
    Phospholipidosis in alveolar macrophages and type II cells
  4. MOA of drug-induced SLE
    Autoimmune-antibodies directed against histones
  5. Presents as cough, dyspnea, fever years after discontinuation of a drug due to reactivation by radiotherapy
    Radiation recall
  6. Typicla presentation of nonproductive cough, dyspnea, fever, weight loss, no chills, nonspecific crackled, sometimes small pleural effusions. CXR initially unremarkable before showing diffuse interstitial infiltrative or diffuse mixed alveolar-interstitial pattern.
  7. Diagnostic that can be used to predict onset of chemotherapy-induced lung injury
    DLCO showing decrease preceding symptoms or CXR findings by days or weeks
  8. Typical BAL findings in chemotherapy
    Markedly atypical type II pneumocytes with relatively fewer type I cells
  9. Characteristic of Bleomycin
    Worsened toxicity with high FI02, cumulative toxicity at 450 units, radiation recall, leads to fibrosis.
  10. Monitoring for Bleomycin toxicity
    Progressive fall in DLCO, VC and pulmonary capillary blood flow may be better predictors, CT scan
  11. Microangiopathic hemolytic anemia, noncardiogenic pulmonary seems, renal failure, pulmonary HPN
    Mitomycin C
  12. Notorious for cumulative cardiotoxicity with cardiogenic pulmonary edema
  13. Symptoms very insidious, presents with a very high mortality rate, no unclear value in discontinuation of drug, CXR shows combined alveolar and interstitial process to a greater degree due to high degree of desquamation of injured epithelial cells into alveoli
  14. May present with 2 patterns: early onset pneumonitis that responds to withdrawal, and late-onset lung fibrosis and bilateral pleural thickening that does not respond to withdrawal
  15. Associated with laryngeal dysesthesia and diffuse alveolar damage in association with 5-FU
  16. Toxicity in 10%, believed to be a hypersensitive reaction due to frequent eosinophilia, lung biopsy shows weakly formed granulomas and hilar adenopathy, DLCO not decreased, drug may be reinstituted after resolution
  17. Associated with rapidly fatal noncardiac pulmonary edema with intraalveolar accumulation of proteinaceous material without cellular atypia and mononuclear infiltration
    Cytosine arabinoside
  18. Associated with intractably progressive upper lobe fibrosis, pneumothorax due to upper lobe fibrobullous changes. Synergistic with Cyclophosphamide
    BCNU or nitrosourea lung toxicity
  19. Biopsy shows alveolar edema, diffuse alveolar damage, atypical type II pneumocytes after prolonged treatment, treated by CS and withdrawal
    Etoposide and Teniposide
  20. MOA of reaction to Paclitaxel
    Type 1 hypersensitivity due to IgE antibodies
  21. CXR shows homogenous infiltrate with adenopathy or pleural effusions in 10-15%, no decrease in DLCO to pedestrian toxicity, not dose related
  22. Diffuse edema, pleuropericardial effusion, noncardiogenic pulmonary edema that may evolve to generalized capillary leak syndrome with hypotension and AKI. Due to massive release of cytokines
    Retinoic acid syndrome
  23. Associated with acute interstitial pneumonia with CT scan finding of ground glass opacities, biopsy of diffuse alveolar damage
    Gefitinib (Iressa)
  24. Associated with fatal pulmonary hemorrhage due to extensive tumor necrosis, can increase incidence of VTE twofold due to vascular injury
    Bevacizumab (VEGF antibody) designed to inhibit tumoral neoangiogenesis
  25. Severe Exacerbation of bronchospasm, granulomatous reaction with noncaseating granulomas, ILD with CD8 lymphocytic response or BOOP
    IFN α
  26. Effect of macrolide inhibitors of mTOR sirolimus
    Interstitial pneumonitis, BOOP, DAH
  27. Associated with hypertrophy of pulmonary vasculature leading to PHPN
  28. Acute: fever after 3-8 weeks which can proceed to chronic effects with vascular damage, radiation pneumonitis in the form of BOOP
  29. Fever, dyspnea, cough, leukocytosis, eosinophilia, elevated ESR, CXR if alveolar or interstitial process more prominent at bases, unilateral effusion in 1/3, due to oxidant stress
  30. 2 classes of drugs that case respiratory muscle weakness when they reach an excessive level in the blood
    Polymyxins and aminoglycosides
  31. Most common drug-induced pulmonary disease worldwide
    Heroin pulmonary edema
  32. Direct toxic effect on alveolar-capillary membrane, increased permeability, extravasation of fluid into alveoli, neurogenic response to CNS injury, allergic reaction, acute hypoxic effect
  33. Presents with acute pulmonary edema with severe hypoxemia and hypercapnia, small pupils, crackled, metabolic and respiratory acidosis, vomiting and aspiration, septic emboli
    Heroin pulmonary edema
  34. Treatment for heroin pulmonary edema
    Intubation, oxygen, IV naloxone, ABs if necessary, no need for CS
  35. Presents with left ventricular failure with CHF and edema, infection and aspiration, talcosis, particulate embolization, diffuse alveolar damage, DAH, eosinophilic infiltration
  36. Insidious onset of granulomatous interstitial fibrosis, pulmonary arterial occlusion leading to dyspnea, cough, exercise-induced sunflower and right-sided heart failure. CXR: diffuse micronodular densities 1-3 mm.
    Talc granulomatosis
  37. MOA of nonproductive cough in ACEI (5-20%)
    Accumulation of kinins and substance P
  38. MOA of angioneurotic edema in ACEI
    Bradykinins or autoantibodies and complement system activation
  39. Treatment of cough in ACEI
    Withdrawal, will abate within 4 days
  40. Most serious side effect of amiodarone
    Interstitial pneumonitis
  41. Histologic findings in amiodarone pneumonitis
    Foamy alveolar macrophages and type II pneumocytes with lamellar inclusions with increased amounts of phospholipids
  42. CT scan finding of amiodarone pneumonitis
    Lesions are denser than surrounding soft tissue because amiodarone is radio opaque
  43. Effects of protamine
    Noncardiogenic pulmonary edema associated with anaphylactic reaction and bronchospasm, increase in pulmonary artery pressure, and hypotension
  44. 2 features of b adrenergic antagonists that predict potential for bronchoprovocation
    Cardioselectivity and intrinsic sympathomimetic activity
  45. B adrenergic antagonist of choice for those of obstructive airway disease
  46. Precaution if giving b antagonists to those with OPD
    Give aerosolized b2 adrenergic agents concomitantly
  47. Can cause status asthmaticus when given as eye drops in glaucoma
  48. Aspirin-asthma triad
    Asthma, rhinitis, nasal polyposis
  49. MOA of ASA bronchospasm
    Inhibition of COX preventing generation of bronchodilator prostaglandins E2
  50. MOA of noncardiac pulmonary edema in serum salicylate levels above 40 mg/dL
    Increased capillary permeability leading to hypoxemia, hyperventilation due to respiratory center stimulation leading to hypocapnia
  51. Pseudosepsis syndrome with fever, leukocytosis, hypotension, MOD can be secondary to
    Chronic salicylate ingestion
  52. MOA of gold diffuse interstitial pneumonitis and fibrosis
    Direct toxic effect
  53. Associated with drug induced SLE, bronchilitis obliterans, Goodpasture's syndrome
  54. Infliximab (anti TNF α) or etanercept may be associated with reactivation of what infection
  55. Associated with Chief-Strauss syndrome
    Zafirlukast and LTRA
  56. Associated with mediastinal lipomatosis or deposition of mediastinal fat with mediastinal widening but no lumpiness
  57. Management of mediastinal lipomatosis
    No need to d/c corticosteroids
  58. Patients who develop antinuclear antibodies to drugs are
    Slow acetylator
  59. MOA of oxygen induced toxicity
    Oxidant stress, hyperoxia produces a direct injury to endothelial cells and type 1 epithelial cells resulting to alveolar-capillary leak
  60. Phases of oxygen toxicity
    Acute exudative phase - perivascular, interstitial and alveolar edema with atelectasis and hemorrhage (reversible), and chronic proliferative - resorption, hyperplasia of type II, deposition of colalgen and elastin in interstitium and hyaline membrane deposition (irreversible)
  61. How to avoid oxygen toxicity
    Keep p02 <80, FI02 < 0.40-0.50
  62. MOA of TRALI
    Result of donor antibodies against leukocyte antigens or donor leukocyte-specific immune cells reacting against recipient leukocytes
  63. main risk factors for TRALI
    Sepsis and history of alcohol abuse, history of transfusion from multiparous female donors
  64. Presents with dyspnea, cough, fever, hypotension, urticarial rash, decreased levels of c3 or c5, normal PAWP within a few hours after inciting event
  65. Source of TRALI reaction in multiparous women
    HLA antibodies
  66. Attributed to allergic reaction with histologic examination showing aggregates of granulocytes obstructing microscopic pulmonary capillaries, releasing professes and toxic oxygen compounds, high plasma histamine due to mast cell activation
    Radiographic contrast medium induced leukostasis
  67. MOA of tocolytic drugs
    Can cause pulmonary edema due to peripheral vasodilatation, added to increased cardiac output, and autotransfusion during labor
  68. Associated with dexfenfluramine, fenfluramine, phenteramine
  69. An anemic patient pregnant with twins on tocolytic drugs and corticosteroids, is being tocolyzed with B2 adrenergics. Blood pressure drops, so saline hydration is done. However, labor continues, and postpartum, the woman develops pulmonary edema. What signaled that too much tocolytic had been given?
  70. Role of corticosteroids in pulmonary edema due to tocolytics
    Mineralocorticoid effect inducing fluid retention
  71. Treatment of tocolytic induced pulmonary edema
    Oxygen and diuretics
  72. A female patient on intermittent diuretics for fluid retention suffers from abrupt dyspnea and a low grade fever. CXR shows diffuse bilateral alveolar-interstitial infiltrates. PCWP is normal and there is no eosinophilia or ANA. What drug is associated with this picture?
  73. A patient with Parkinson's disease develops an insidious pleural thickening and moderate lymphocytic effusion not associated with pleuritic pain. Which of his medications is associated with this effect?
    Bromocriptine or cabergoline
  74. A patient undergoes esophageal variceal sclerotherapy with sodium morrhuate. Fever, chest pain and difficulty in swallowing occurred after, but spontaneously resolved. What is the most common abnormality found on CXR in these patients?
    Pleural effusion
  75. A depressed patient on tricyclic antidepressant overdoses. He arrives hypoxemic at the ER with a widened AAG, and intubation with MV is done. What are the 2 MC pulmonary complications in this population?
    Noncardiac pulmonary edema or aspiration
  76. A patient with spastic neurological disorder is being treated with Dantrolene. What pulmonary adverse effect can be seen in these patients?
    Chronic pleural effusion or pericarditis
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Drug-Induced Pulmonary Disease.txt
2012-12-10 09:17:12
Drug Induced Pulmonary Disease

Drug-Induced Pulmonary Disease
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