Pulmonary

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Author:
Mat
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57062
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Pulmonary
Updated:
2011-08-16 22:20:08
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Med Lungs
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Pulmonary questions
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  1. DLCO is decreased in:
    • "P-I-P-E"
    • Pulmonary fibrosis
    • ILD
    • Emphysema
    • Pulmonary hypertension
  2. DLCO is high in:
    • "A-AP"
    • Polycythemia
    • Alveolar hemorrhage
    • Asthma
  3. Medications that can increase theophylline
    • Rifampin
    • Dilantin
    • Phenobarbital
    • Carbamazepine
    • Smoking
  4. Medications that can decrease Theophylline
    • "CAM-Flouro-PAZ"
    • Acyclovir
    • Cimetidine
    • Macrolides
    • Fluoroquinolones
    • Propranolol
    • Allopurinol
    • Zafirlukast
  5. Contraindications to NPPV:
    • Medical instability-- respiratory or cardiac arrest, severe respiratory acidosis (pH <7.1), hemodynamic instbality, cardiogenic shock, UGI bleed.
    • Unable to protect airway -- excessive secretions, severe bulbar dysfunction, excessive somnolence or encephalopathy.
    • Mechanical issues -- recent facial trauma or surgery, upper airway obstruction.
  6. CXR pattern that is highly suggestive of Asbestosis:
    • Pulmonary fibrosis (reticular opacities) concentrated at the bases of the lungs.
    • Shaggy heart border
    • May have associated pleural thickening or plaques, calcification of plaques and/or diaphragm
    • "AsBasetosis" because the infiltrates are in the bases ( vs. at the upperlobes for silicosis)

    "Diaphragmatic calcification" is pathognomonic.
  7. Common presentation of malignant mesothelioma
    • chest pain and dyspnea
    • painful exudative effusion
    • pain is a dull ache
  8. CXR presentation of silicosis:
    • upper lobe distribution of fibrosis
    • egg-shell calcification in hila (10%)
  9. Coal workers pneumoconiosis, give a short summary:
    • From exposure to coal dust
    • Melanoptysis
    • Focal centrilobular emphysema
    • 1 of 3 ILDs with obstructive pattern on PFT
  10. Occupational risks for Berylliosis?
    What would the CXR look like?
    • alloy in metals or alone, seen in nuclear weapons, electronics, aerospace, ceramics, metal recycling, dental prostheses, alloy machining, defense industries, automotive.
    • CXR is difficult to differentiate from sarcoidosis other than by history
  11. Give a brief pathophysiology of Berylliosis.
    a cell-mediated immune response that can occur and persist from even a trivial exposure with a latency of 1-10 years.
  12. What percentage of workers develop berylliosis?
    2-6%
  13. How do you screen for berylliosis?
    The berylliom lymphocyte-proliferation test is a blood test that can detect beryllium sensitivity
  14. Treatment for berylliosis?
    corticosteroids
  15. Briefly discuss Lung Scleroderma.
    • Diffuse pulmonary fibrosis in 80%
    • Pulmonary involvement more severe in diffuse systemic sclerosis and less so in the CREST variant
    • Pulmonary hypertension*
  16. Pulmonary interventions in SSc?
    • A subset of patients with SSc develop rapidly progressive ILD during the first 2 years of their disease
    • Spirometry and diffusion testing should be considered mandatory for all patients at the time of diagnosis.
    • Patients with SSc should have annual lung function testing early in disease.
    • If DLCO <50% of predicted, need TTE to monitor for pulmonary HTN.
    • If pulmonary HTN present, consider warfarin therapy.
  17. When is pleural effusion transudative?
    • If none of the following is present:
    • Pleural/serum protein > 0.5
    • Pleural/serum LDH > 0.6
    • Absolute LDH value > 2/3 normal value for serum, usually > 200 IU.

    **If any one of the criteria above is met, the fluid is exudative.
  18. Most common causes of transudative pleural effusions are:
    • CHF (500,000/year)
    • Cirrhosis (50,000/year)
    • Nephrosis
    • Hypoalbuminemia
  19. If pleural fluid meets Lights criteria for exudate but looks like exudate, what do you do?
    • Check two additional tests:
    • Pleural cholesterol less than 45
    • Pleural fluid/serum albumin gradient 1.2
    • *if two above are met, then it is transudative.
  20. Two initial tests to determine if pleural fluid is transudative vs. exudative?
    LDH and protein
  21. If fluid is exudative, what following tests are recommended?
    • Description of the fluid
    • Glucose level
    • Amylase level
    • Cell count with differential
    • Cytology and microbiology
    • Pleural fluid pH
  22. What is the normal pH of pleural fluid?
    >7.6
  23. At what pleural fluid pH will antibiotic work?
    above 7.2
  24. When to drain parapneumonic effusion?
    • It is undetermined status when pH >7 but <7.2. Consider drainage if:
    • glucose <50 mg
    • LDH >1000 IU
  25. Three "T's" of bloody pleural effusion
    Tumor, Trauma, Thromboembolism
  26. Characteristics of malignant pleural effusion
    • Generally large, >50% hemithorax
    • Quick to reaccumulate
    • Generally lymphocytic WBC's
    • Often bloody
  27. How do you increase yield in malignancy workup of exudative effusion?
    • Three separate taps will improve yield to 90%.
    • If malignancy is highly suspected, VATS procedure is next step.

    *Yield is not significantly increased by blind needle biopsy so these are not done anymore.
  28. Treatment options of malignant pleural effusion:
    This is guided by the fluid pH, which reflects the metabolic activity of the tumor burden.

    >7.2 -- tube thoracoscopy with chemical scleroses or thoracoscopy with pleural abrasion or talc insufflation.

    <7.2 -- palliative care.
  29. What is the best way to increase yield in Tuberculous effusion?
    • AFB recovered in only 10%, but yield can be increased with up to 3 taps.
    • Culture for AFB is positive in 65%.
    • Pleural biopsy and culture together identify 85%.
    • Blind pleural biopsy may be helpful.
  30. What are we looking for in Pleural biopsy for TB?
    • Three biopsy samples will increase yield to 80%
    • shows caseating granuloma
    • if sent for TB, yield increases.
  31. What else is are important markers in tuberculous effusion to confirm the diagnosis?
    • Adenosine deaminase levels, > 50 U/L is 94% sensitive and 90% specific.
    • Levels < 45 U\L 100% sensitive and specific for nontuberculous etiology.
    • Mesothelial cells are rarely present.
  32. Interventions for undiagnosed pleural effusions (20%):
    • Follow carefully
    • CXR every 6 months
    • Approximately 80% of these will resolve, however, 20% will turn out to be cancer.
  33. Neutrophil predominance in exudative pleural effusions point toward?
    • pneumonia
    • pancreatitis
    • PE
    • peritonitis
  34. Exudative pleural effusion with lymphocyte predominance is suspicious for?
    TB or malignancy
  35. Exudative pleural effusion with glucose of <30 makes you think of?
    Rheumatoid arthritis
  36. Exudative pleural effusion with glucose of 60 makes you think of?
    Cancer or empyema
  37. Exudative pleural effusion with glucose of 80 makes you think of?
    TB
  38. Physical findings in pulmonary hypertension
    • loud 2nd heart sound
    • tricuspid regard
    • RV heave
  39. PFT findings in pulmonary hypertension
    Normal spirometry and volumes but with decreased DLCO.
  40. Most common cause of pulmonary hypertension worldwide
    schistosomiasis
  41. Workup of pulmonary hypertension:
    Echo followed by right heart cath.
  42. Definition of Pulmonary Hypertension
    • MAP -- >25 mmHg at rest, but increases to >30 mmHg during exercise.
    • Symptomatic when >45 mmHg
  43. Significance of Right Heart Catheterization in the diagnosis of Primary Pulmonary HTN
    Useful to rule out a secondary cause of pulmonary hypertension, and PCWP has to be normal.
  44. Approach to treatment of Primary Pulmonary HTN
    • Try CCB in cath lab (important to do it there due to risk of CV collapse). Only 1 in 4 will respond. If they respond, continue CCB.
    • Prostacyclin by IV infusion pump
    • Bosentan
    • Sildenafil
    • Heart-lung transplant
  45. What are the concerns of Prostacyclin treatment?
    Complications and tachyphylaxis
  46. Concerns of Bosentan therapy
    Hepatic insufficiency. Need to monitor LFTs monthly.
  47. Treatment for all pulmonary hypertension
    • Anticoagulants
    • Diuretics
    • Oxygen
  48. Patient presenting with SOB, chest pain, fixed split S2 on auscultation:
    Secondary pulmonary hypertension, probably due to ASD.
  49. Five frequent hypercoagulable states in the general population:
    • Homocysteinmia
    • Prothrombin gene mutation
    • Factor V Leident (heterozygous)
    • Factor V Ledient (homozgoust)
    • Increased factor VIII
  50. COPD patient with unexplained severe exacerbation
    What shoal you suspect?
  51. ECG signs of PE
    • Signs of RV overload
    • T wave inversion V1-V4
    • S1Q3T3
    • Transient RBBB
    • Atrial fibrillation
    • S1S2S3
  52. Treatment for "thrombus-in-transit" noted on echo during PE workup:
    thrombolytics unless contraindicated.
  53. What is the incidence of intracranial bleed from thrombolytics?
    4%
  54. Spontaneous Pneumothorax, when and what type intervention?
    • If symptomatic or if >25-40%, then chest tube
    • If chest tube is needed, then also do pleurodesis since recurrence rate is 40-50%.
    • If chest tube not needed for first PTX, most will have pleurodesis after the next recurrence.
    • No pleurodesis = no air travel, scuba
  55. A patient with bilateral spontaneous PTX suggests?
    PCP pneumonia
  56. Secondary PTX is common in what diseases?
    What is the treatment?
    • Common in COPD, ILD, CF
    • Tx is Chest tube and pleurodesis
  57. In secondary PTX, what is the significance of a chest tube with an air leak >7 days?
    • This suggests bronchopleural fistula.
    • Requires surgical consultation for stapling and pleurodesis to prevent recurrences.
  58. Define apnea
    Cessation of airflow for at least 10 seconds
  59. What is sleep apnea syndrome?
    > 10 apneic spells an hour during sleep study
  60. Differentiate between Obstructive and Central apnea
    Obstructive - continued respiratory effort during the absence of airflow

    Central - absence of effort and airflow.
  61. When is treatment required in OSA?
    More than 15-20/hr requires treatment
  62. Treatment of OSA?
    • Weight loss for mild cases, approx. 10% of weight
    • Nasal CPAP or BiPAP for moderate/severe (if unable to lose weight.
    • Avoid sedatives, ETOH
    • If severe -- need tracheostomy
  63. Treatment for Central Sleep Apnea?
    • acidification with acetazolamide
    • supplemental O2
    • CPAP
  64. Define Narcolepsy
    • Severe daytime hypersomnolence
    • Cataplexy
    • Sleep paralysis
    • Hallucinations when drowsy
  65. How is narcolepsy diagnosed?
    Polysomnography and Multiple Sleep Latency Test (MSLT) checks hypersomnolence and frequency of REM
  66. Treatment of narcolepsy?
    Stimulants and REM suppression by tricyclic antidepressants and SSRI
  67. Treatment of Restless leg syndrome
    dopaminergic agonists and narcotics
  68. Restless leg syndrome is associated with?
    Periodic limb movement disorder -- contraction of the anterior tibialis muscle during sleep.
  69. What is the most common symptom of lung cancer?
    • Cough -- most frequent
    • Dyspnea
    • Hemoptysis
  70. What % of solitary pulmonary nodules are malignant?
    35%
  71. For solitary pulmonary nodule, when is it wise to watch and not intervene?
    • Can watch only if:
    • there is no growth in 2 years when compared to an old film
    • there is patterned calcification in the lesion.
  72. Pnemonic for approach the the Solitary Pulmonary Nodule
    • Tumor is the rumor
    • Tissue is the issue
    • Heal with steel
    • When in doubt, cut it out
  73. Approach to the solitary pulmonary nodule
    • CT scan assures that lesion is solitary and helps define if calcium is present.
    • FOB not helpful if lesion is < 3 cm in size.
    • PET scan may predict cancer probability, but it's role is not yet determined.
    • Surgery (don't bother with FNA)
  74. What stage in Lung Cancer is operable?
    Stage IIIa and under
  75. Who is inoperable in lung cancer?
    • T4 = direct invasion of mediastinum/vasculature
    • N3 = contralateral mediastinum or hilar lymph nodes or and scalene or supraclavicular nodes
    • M1 = distal mets
  76. Discuss bronchoalveolar carcinoma
    • Subclass of adenocarcinoma
    • 1/3 never smokers
    • 2:1 ratio of women to men
    • represents only 2-3% of all NSCLCs
    • may mimic pneumonia in appearance
    • -persistent pneumonia
    • Bronchorrhea is typically seen
    • -frothy sputum
    • -salty taste (due to high K+)
    • Inclined to stay within the lung and is likely to spread to other organs.
    • Has a better overall survival when matched stage for stage with other NSCLCs.
  77. Briefly discuss Pancoast tumor (Superior sulcus tumor)
    • Presents with shoulder pain (a shoulder film may be shown)
    • May have Horner syndrome
    • Most commonly squamous cell
    • Usually operable
    • Use MRI to evaluate brachial plexus and plan surgery
  78. Briefly discuss Paraneoplastic Syndromes
    • Caused mostly by primary lung tumors
    • Paraneoplastic syndrome does not indicate metastatic spread
    • Paraneoplastic syndrome does not indicate unresectability
  79. What cancer causes hypercalcemia as part of its paraneoplastic syndrome
    Squamous cell
  80. Large cell paraneoplastic manifestation?
    Hyperprolactinemia
  81. Paraneoplastic syndrome manifestation of adenocarcinoma?
    • HPO/Clubbing
    • Marantic endocarditis
  82. Paraneoplastic manifestation of Squamous cell?
    • Hypercalcemia
    • Cerebellar ataxia
  83. Manifestations of Wegener Granulomatosis
    • Diffuse alveolar hemorrhage
    • "ELKS" involvement -- ENT, Lung, Kidney, Sinusitis
    • Sinusitis
    • Cavitary lung lesions
    • Glomerulonephritis
    • Arthritis and cutaneous leukoytoclastic vasculitis
  84. Diagnosis of Wegener's Granulomatosis?
    • cANCA present 96% of the time (PR3-ANCA)
    • ANCA is 90% sensitivity and specificity

    Open lung bx or bx nasal membrane -- not kidneys
  85. In diagnosis of Wegener Granulomatosis, what tissue would you biopsy?
    Open lung or bx nasal membrane -- not kidneys.
  86. What is the early mortality for Wegener Granulomatosis?
    Early mortality is 37%
  87. In Wegener granulomatosis, what renal disease would you see?
    focal segmental necrotizing GN
  88. How do you monitor disease activity with Wegener granulomatosis?
    ESR, ANCA, serial DLCOs, urine sediment
  89. What characterizes the Pulmonary-renal syndrome of Goodpasture Syndrome?
    linear deposition of anti-glomerular basement membrane antibodies in lung and kidney (Antibody against alpha-3 chain of Type IV collagen.
  90. What part of the body is affected by Goodpasture syndrome?
    lung and kidney only, no ENT (as opposed to Wegener's)
  91. What are the hemorrhagic pulmonary-renal syndromes?
    Wegener and Goodpasture's
  92. What histology will you be looking for in a biopsy specimen for Wegener granulomatosis?
    Necrotizing granulomatous vasculitis
  93. What percentage of Goodpasture syndrome affects both lung and kidney?
    60-80%
  94. What percentage of Goodpasture syndrome affects lung only?
    5-10%
  95. Treatment for Goodpasture Syndrome?
    • High-dose corticosteroids effective for Diffuse Alveolar Hemorrhage
    • However, not effective for nephritis, so combined with cyclophosphamide and plasma exchange (usually for 2 weeks).
  96. What is the usual cause of death for Goodpasture syndrome?
    Diffuse alveolar hemorrhage (DAH)
  97. What is the 2-year survival rate for Goodpasture syndrome?
    50%
  98. What pathology result indicates best outcome, or worst outcome?
    <30% glomeruli affected, and worst with >70%
  99. Briefly discuss Loeffler syndrome:
    • Eosinophilic pneumonia
    • Eosinophils in blood and sputum
    • Migratory peripheral infiltrates on CXR
    • Minimal respiratory symptoms
    • Often idiopathic
    • Generally benign and self-limiting
  100. What do you need to rule out for Loeffler's syndrome?
    Drugs and parasites, i.e. Strongyloides
  101. Chronic Eosinophilic Pneumonia commonly occurs in? Briefly discuss
    • Most common PIE in the U.S.
    • Occurs in middle-aged females
    • Very high ESR
    • Eos in blood and sputum
    • Subacute illness: cough, wheezing, fever, night sweats, weight loss
  102. CXR presentation of Chronic Eosinophilic pneumonia?
    Radiographic negative of pulmonary edema
  103. What can cause a "radiographic negative of pulmonary edema" on CXR?
    Chronic Eosinophilic Pneumonia
  104. What entities causes "recurrent pneumothorax?"
    • Histiocytosis X
    • Eosinophilic granulomatosis
    • Langerhans cell histiocytosis

    Lymphangiomatosis
  105. Briefly discuss Eosinophilic granuloma

    What is the typical patient?
    Chest CT or CXR will show what distinct feature?
    What clue in the history and/or current presentation should alert you to this pathology?
    • Young male, smoker
    • Proliferation of Langerhans cells from the bone marrow and mature eosinophils
    • Cystic spaces in the upper lung fields
    • 50% develop PTX in course of illness

    Clue is recurrent pneumothorax and diabetes insipidus (because the Langerhans cells go to the hypothalamus)
  106. How do you diagnose Eosinophilic Granuloma?
    • Diagnosis by FOB/BAL
    • Langerhans cells on lung biopsy or BAL (contains X-body or Birbeck granule)
  107. Treatment for Eosinophilic granuloma?
    • smoking cessation
    • supportive/trial steroids
  108. Discuss Lymphangiomyomatosis.
    • Premenopausal women
    • There is immature smooth muscle proliferation - lympatics, bronchial, alveolar, vascular
    • Honeycomb throughout
    • Cysts lead to PTX
    • Chylous pleural effusion
  109. Treatment of Lymphangiomyomatosis?
    • Hormonal manipulation
    • Exposure to estrogen is not recommended. This includes the use of contraceptive pills containing estrogen and hormone replacement therapy (HRT)
    • Rapamycin is known to inhibit the proliferation of smooth muscle cells
    • Lung transplantation
  110. Mycetoma presentation?
    • Crescent sign -- cavity in the lung after inhaling aspergillus. Pt not asthmatic. "Ball of yarn" moves when change in position.
    • Massive hemoptysis is usual presentation
  111. Intervention for Hemoptysis secondary to Mycetoma?
    • Bronchial arterial embolization (BAE) temporarily controls the bleeding
    • Does not provide definitive treatment
    • Stabilizes the patient and decreases the need for emergency surgical resection.
  112. Management of CAP for pt without comorbidities
    • treat as outpatient
    • Preferred antibiotics are:
    • Macrolides
    • Fluoquinolones
    • Doxycyline
  113. Preferred antibiotics for CAP in patient with moderate and high risk class comorbidities
    IV beta-lactam (cefotaxime or claforan) or ceftriaxone plus a macrolide level, or a fluoroquinolone alone.
  114. Discuss the British CURB-65
  115. Define "Pneumonia Treatment Failure."
    If no response to antibiotics in 72 hours. Approximately 1-15% develop treatment failure. Almost 6% manifest rapidly progressive and life-threatening pneumonia.
  116. Risk factors for infection with drug-resistant Streptococcus pneumonia:
    • age >65 years
    • previous Beta-lactam rx in last 3 months
    • previous fluoroquinone therapy
    • alcoholism
    • co-morbidities
    • immunosuppressive illness or therapy
  117. What Pneumonia organism is associated with:
    Bullous myringitis?
    Mycoplasma
  118. What Pneumonia organism is associated with:
    Herpes lip lesion
    Pneumococcus
  119. What Pneumonia organism is associated with:
    Pneumatoceles
    Staphylococcus
  120. What Pneumonia organism is associated with:
    ETOH
    Klebsiella
  121. What Pneumonia organism is associated with:
    Influenzae
    Pneumoccus/Staph
  122. What Pneumonia organism is associated with:
    Increased LDH.
    PCP
  123. What Pneumonia organism is associated with:
    steroids
    Nocardia
  124. What Pneumonia organism is associated with:
    Post transplant
    CMV
  125. Name the fungal pneumonia association:
    Birds, bats, caves
    Histoplasmosis
  126. Name the fungal pneumonia association:
    Southwest U.S.
    coccidiomycosis
  127. Name the fungal pneumonia association:
    Hunting dogs
    Blastomycosis
  128. Name the fungal pneumonia association:
    Pigeons
    Cryptococcosis
  129. Name the fungal pneumonia association:
    Thons, straw
    Sporothrichosis
  130. Name the fungal pneumonia association:
    Dental work
    Mucormycosis
  131. Name the fungal pneumonia association:
    Dental work
    Actinomysis.
  132. What are the risk factors for infections with drug-resistant Streptococcus pneumonia?
    • age >65 years
    • previous B-lactam rx in last 3 monks
    • previous fluorquinolone therapy
    • alcoholism
    • co-morbidities
    • immunosuppressive illness or therapy
  133. Fungal pneumonia associations:
    Birds, bats, caves
    Histoplasmosis
  134. Fungal pneumonia associations:
    Southwest U.S.
    Coccidiomycosis
  135. Fungal pneumonia associations:
    Hunting dogs
    Blastomycosis
  136. Fungal pneumonia associations:
    Pigeons
    Cryptococcosis
  137. Fungal pneumonia associations:
    Thorns, straw
    Sporotrichosis
  138. Fungal pneumonia associations:
    Diabetes/sinusitis
    Mucormycosis
  139. Fungal pneumonia associations:
    Dental work
    Actinomycosis
  140. Describe how blastomycosis look under the microscope: (and other clues)
    • It has a thick refractory cell wall, broad based budding yeast that makes it look like a bowling pin, and can be associated with a skin rash (dermatitis), likes to go to the bone and the brain.
    • It's favorite reservoir is the hunting dog, i.e. the beagle.
  141. In an immunocompromised patient with pulmonary infiltrates, what would be an ideal initial intervention?
    • BAL
    • If not successful, think: CMV if post-transplant, or Aspergillus if granulocytopenic (<1000 PMNs)
  142. Pulmonary infiltrates in AIDS:
    <400 T cells
    Think TB
  143. Pulmonary infiltrates in AIDS:
    <200 T cells
    Think PCP
  144. Pulmonary infiltrates in AIDS:
    <100 T cells
    Think MAI
  145. A 5 mm or greater PPD induration is relevant for patients who have:
    • HIV infection
    • Household contact with a person who has active TB
    • NH patients with fibrotic changes on chest radiograph c/w old TB
    • Organ transplants, immunosuppressed (greater than 15 mg/day prednisone for at least 1 month)
  146. A 10 mm or greater PPD induration is relevant for the following:
    • recent (within 5 years) immigrants from high prevalence countries
    • IV drug users
    • residents or employees of high-risk settings such as jails, nursing homes, shelters, and hospitals
    • those who have conditions associated with a high risk of disease after infection
    • Persons with immunosuppressive medical conditions other than HIV infection, including diabetes, renal insufficiency, gastrectomy, silicosis, corticosteroid therapy (>15mg/day of prednisone for 2 weeks), and other immunosuppressive therapy and conditions.
  147. What is the treatment of LTBI with Isoniazid (INH)?
    • 9-month regimen (300 mg/day) considered optimal regardless of HIV status
    • Contact with INH-resistant TB: 4-months daily rifampin
  148. Diagnosis of TB
    • A positive AFB smear suggests the disease
    • Only a positive culture for M. tuberculosis confirms active disease.
  149. What is the preferred regimen for the initiation phase of treatment for TB?
    • R-I-P-E
    • Rifampin
    • Isoniazid
    • Pyrazinamide
    • Ethambutol
  150. What is the preferred continuation treatment for TB after the 8-week initiation therapy?
    Twice-weekly doses of isoniazid and rifampin
  151. What do you do in case of treatment failure in the treatment for TB?
    Consult a subspecialist
  152. What do you expect on an ABG in an asthmatic patient?
    • Hypoxemia with hypocapnia
    • Hypoxemia (V/Q mismatch) responds to low-flow oxygen
    • Increased A-a gradient
    • Respiratory alkalosis is expected
    • ABGs that look normal during an acute asthma attack signal respiratory muscle fatigue.
  153. What is the new strategy of mechanical ventilation in ARDS management:
    • Low tidal volumes
    • Enough PEEP to keep PaO2 > 60 mmHg with FiO2 < 60%.
  154. Interventions to avoid ventilator-induced injury:
    Oxygen toxicity
    Keep FiO2 < 60%
  155. Interventions to avoid ventilator-induced injury:
    Barotrauma
    • Keep Peak pressures < 45 cm
    • Keep Plateau pressures < 30 cm
  156. Interventions to avoid ventilator-induced injury:
    Volutrauma
    Use tidal volume 6 cc/kg
  157. What is the only ARDS intervention known to decrease mortality?
    Protective ventilation -- lower tidal volumes allow us to minimize the contribution of mechanical ventilation to ongoing lung injury and decrease relative mortality by 22-24% (from 40 to 32%).
  158. Hemodynamic subsets of shock-- give the PAOP, CO, SVR:
    Hypovolemia
    low, low, high
  159. Hemodynamic subsets of shock-- give the PAOP, CO, SVR:
    Cardiogenic
    High, low, high
  160. Hemodynamic subsets of shock-- give the PAOP, CO, SVR:
    Sepsis
    Normal, High, Low
  161. What is the desired PAOP?
    18
  162. What is the desired Cardiac Index?
    >2.2
  163. Large v-wave indicates?
    Severe mitral regurgitation, and in the setting of a recent MI, may indicate papillary muscle dysfunction.
  164. On a swan-ganz tracing, what would indicate pericardial tamponade?
    Equalization of the diastolic.
  165. During right heart cat (swan-ganz) with oxygen sensor, what would indicate a Ventricular Septal Defect (VSD)?
    Increase of O2 saturation from RA to RV.
  166. What do you see in a significant RV infarct/failure?
    CVP > PCWP
  167. Define Type II Respiratory Failure
    • Hypercarbia with hypoxemia
    • V/Q mismatch physiology
    • Acute exacerbation of COPD
  168. In patients with Neuromuscular disease and worsening respiratory failure, when do you intubate?
    • NIF < -20 cm
    • Vital capacity < 1 liter (have them blow out)

    This indicates inadequate respiratory muscle strength.
  169. When placing a COPD patient on Bipap, how many hours do you expect to see improvement?
    Two hours, and if no improvement, intubate.
  170. Is PEEP always needed?
    It is not always needed in Type II respiratory failure. It is only needed to improve their oxygenation to a safer FiO2.
  171. In mechanical ventilation, what do you do to ensure oxygenation?
    Change PaO2 by adjusting FiO2 or PEEP
  172. In mechanical ventilation, what do you do to ensure ventilation?
    Change PaCO2 by adjusting rate and tidal volume
  173. What is peak pressure?
    The pressure needed to overcome airway resistance and lung stiffness.
  174. What is the plateau pressure?
    The amount of pressure to keep the lung inflated. No air flow
  175. What is Airway Resistance?
    the difference between peak pressure and plateau pressure.
  176. What does it mean if the peak pressure has increased but the plateau pressure has remained the same?
    • It means that Airway Resistance has increased and the patient needs a bronchodilator, suctioning, evaluate for a mucus plug, or a kink in the ET tube.
    • The differential diagnoses are: mucus plugging, bronchospasm, airway secretions, narrow ET-tube.
  177. What do you do if both the peak pressure and the plateau pressure are elevated?
    • If the difference (Airway Resistance) is the same as before the change occurred, the patient does not need a bronchodilator but may need lasix, or check for abdominal distention.
    • Differential diagnoses are: tension pneumo, atelectasis, multilobar pneumonia, pulmonary edema, bronchial intubation
  178. When can we extubate pt?
    • Weaning Standard Criteria:
    • Able to oxygenate in FiO2 of 40%
    • Resting minute ventilation < 10 liters
    • NIF > -25 cm H2O
    • Maximal tidal volume > 10 cc/kg

    These criteria are specific but not sensitive. Failure to meet one or more does not preclude success.
  179. What is the Rapid Shallow Breathing Index?
    It is the new criteria for weaning. You put the patient on CPAP mode, convert tidal volume to liters and do the math: f/VT

    f/VT <100 breaths/L then 80% chance of weaning success

    f/VT > 100 breaths/L then 95% chance of weaning failure
  180. Discuss Ventilator Associated Pneumonia preventive strategy:
    • Effective hand washing
    • Use of protective gowns and gloves
    • Semirecumbent positioning
    • Avoidance of large gastric volumes
    • Oral (non-nasal) intubation
    • Continuous subglottic suctioning
    • Postural changes
    • Proper maintenance of ventilator circuits
    • Sedation holidat
  181. What do you worry about if your intubated, septic patient repeatedly fails to wean off the vent?
    Critical Illness Neuromuscular disease. This is a complication of sepsis and multiorgan failure, occurs in approximately 25% of patients in ICU longer than 7 days. EMG will show decreased muscle and nerve action potentials. Check the DTRs. If those are absent, your diagnosis is confirmed.
  182. Risk factors for Critical Illness Neuromuscular disease:
    • Glucocorticoids
    • Malnutrition
    • Nondepolarizing muscle agents
    • Poor glucose control
  183. What are the 3 major categories of transfusion reactions?
    • Acute hemolytic reaction (10%)
    • Febrile reactions (44%)
    • Allergic reactions (45%)
  184. What component of the blood is involved in acute hemolytic reactions?
    RBC
  185. What component of the blood is involved in Transfusion febrile reactions?
    WBC
  186. What component of the blood is involved in transfusion allergic reactions?
    antigens in the plasma
  187. Normally, transfusion allergic reactions are not life-threatening, but what group of patients can develop anaphylaxis?
    Those who are IgA deficient.
  188. TRALI (Transfusion Related Acute Lung Injury) usually occurs in what period of time after a transfusion?
    6-8 hours
  189. Interventions in Sepsis (Sepsis management bundle)
    • Drotrecogin alfa (activated) administered in accordance with a standardized hospital policy
    • Low-dose steroids administered for septic shock in accordance with a standardized hospital policy
    • Glucose control maintained greater than the lower limit of normal, but less than 150 mg/dl
    • Inspiratory plateau pressures maintained less than 30 cm H2O
  190. For classification of Asthma severity, describe the frequency of symptoms, nighttime awakenings, SABA use for symptom control, interference with normal activity, and lung function for the following:
    Intermittent
    • Symptoms -- < 2 days/week
    • Nighttime awakenings -- < 2 X /month
    • SABA use for symptom control -- <2 days/week
    • interference with normal activity -- none
    • lung function -- Normal FEV1 between exacerbation, FEV1 >80% of predicted, FEV1/FVC normal
  191. Frequency of symptoms in mild, persistent asthma
    >2 days/week but not daily
  192. Frequency of symptoms in moderate, persistent asthma
    Daily
  193. Frequency of symptoms for severe, persistent asthma
    throughout the day
  194. Nighttime awakenings for:
    Intermittent asthma
    <2x / month
  195. Nighttime awakenings for:
    mild, persistent asthma
    3-4 x / month
  196. Nighttime awakenings for:
    moderate, persistent asthma
    > 1 x / week
  197. Nighttime awakenings for:
    Severe, persistent asthma
    often 7 x / week
  198. SABA use for symptom control in:
    Mild, persistent asthma
    >2 days/week but not more than 1 x / day
  199. SABA use for symptom control in:
    moderate, persistent asthma
    daily
  200. SABA use for symptom control in:
    severe, persistent asthma
    several times a day
  201. Lung function in:
    intermittent asthma
    • normal FEV1 between exacerbations FEV1 > 80% of predicted
    • FEV1/FVC normal
  202. Lung function in:
    mild, persistent asthma
    • FEV1 >80% of predicted
    • FEV1/FVC normal
  203. Lung function in:
    Moderate, persistent asthma
    • FEV1 > 60% but < 80% of predicted
    • FEV1/FVC reduced 5%
  204. Lung function in:
    Severe, persistent asthma
    • FEV1 < 60% of predicted
    • FEV1/FVC reduced > 5%
  205. Treatment for intermittent asthma:
    SABA PRN
  206. Treatment for mild, persistent asthma
    low-dose ICS
  207. When is surgery indicated in patients with COPD?
    • Lung volume reduction surgery involves resecting parts of the lung to reduce hyperinflation. This type of surgery makes respiratory muscles more effective by improving their mechanical efficiency and improves expiratory flow rates by increasing the elastic recoil pressure of the lung. Because this procedure is expensive and high-risk, it is recommended only in carefully selected patients. The surgery is most beneficial in patients with severe, predominantly upper lobe disease and a large amount of mildly emphysematous or normal middle and lower lung.
    • Patients with severe COPD who have had maximal medical treatment, including pulmonary rehabilitation, and have FEV1 greater than 20% of predicted, DLCO greater than 20% of predicted, and predominant upper lobe emphysema are likely to benefit from lung volume reduction surgery.
  208. What are the physical findings of an elevated pulmonary artery pressure?
    • loud P2
    • fixed split S2
    • pulmonic flow murmur
    • tricuspid regurgitation

    Chest radiographs are usually normal in early disease but may show enlarged pulmonary arteries, right atrium, and right ventricle. Electrocardiographs in these patients may show right ventricular strain or hypertrophy.
  209. A PFT study in a pt with PAH usually reveal?
    Pulmonary function studies in patients with PAH usually reveal an isolated decreased DLCO in the setting of normal airflow and lung volumes (excluding restrictive lung disease).
  210. When is lung transplantation considered in patient with severe COPD?
    Lung transplantation should be considered in patients hospitalized with COPD exacerbation complicated by hypercapnia (PCO2 greater than 50 mm Hg) and patients with FEV1 not exceeding 20% of predicted and either homogeneous disease on high-resolution CT scan or DLCO less than 20% of predicted who are at high risk of death after lung volume reduction surgery.
  211. What is a "Multiple Sleep Latency Test?"
    • objective measure
    • can be used to assess the presence and severity of excessive daytime sleepiness.
    • A multiple sleep latency test can be performed if daytime sleepiness persists in a patient who is consistently able to use CPAP set at an optimal pressure. It will objectively confirm her complaints of sleepiness but will not aid in identifying its cause.
  212. Discuss the typical presentation of a bronchial carcinoid tumor

    What is the classic pt profile?
    Where is it typically located?
    What is a typical presentation?
    A carcinoid tumor is the most likely tumor in a young person who has never smoked and who has evidence of endobronchial obstruction. Bronchial carcinoid is a slow growing tumor that originally was classified as an adenoma but has been reclassified as a malignant neoplasm because of its ability to metastasize. Most bronchial carcinoid tumors are located in proximal airways and cause symptoms by either obstructing an airway or bleeding. Common presenting symptoms include cough or wheeze, hemoptysis, and recurrent pneumonia in the same pulmonary lobe. The carcinoid syndrome is caused by systemic release of vasoactive substances such as serotonin, and the most typical features include cutaneous flushing and diarrhea. Bronchial carcinoids are not commonly associated with the carcinoid syndrome because of their relatively small amount of serotonin production.
  213. Discuss cough variant asthma

    What presentation suggests it?
    Diagnosis is suggested by the presence of airway hyperresponsiveness and confirmed when cough resolves with a trial of inhaled albuterol.
  214. In the evaluation of pumonary nodules, when is FDG-PET done?
    • 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) is generally done after CT of the chest.
    • Lung cancers are metabolically active and take up FDG avidly, whereas benign pulmonary nodules do not.
    • FDG-PET is most helpful in patients with a nodule 1 cm or larger and an intermediate probability of malignancy.
  215. Discuss paraneoplastic syndrome associated with small cell carcinoma
    • Paraneoplastic neurologic disorders are associated with systemic malignancy but are not related to direct tumor involvement or to other toxic or metabolic, infectious, or vascular complications of cancer.
    • Paraneoplastic sensory neuropathy is commonly associated with lung carcinoma (particularly small cell carcinoma) but may develop in patients with other malignancies.
    • The neurologic syndrome precedes the diagnosis of cancer in most patients.
    • Paraneoplastic sensory neuropathy manifests with progressive paresthesias, profound sensory ataxia, and multimodality sensory loss.
    • The ANNA-1 antibody is the most common antibody present in a sensory neuropathy associated with small cell carcinoma.
  216. When do you consider NPPV in a pt with COPD exacerbation?
    should be considered if patients have persistent hypoxemia and/or hypercapnia with a pH less than 7.35 and a PCO2 greater than 45 mm Hg and a respiration rate greater than 25/min despite maximal medical therapy.
  217. How do you manage a patient with a malignant pleural effusion and lung entrapment?

    In a pt with the problem above, when do you suggest in-flight pO2?
    • The development of severe, anterior chest pain during therapeutic thoracentesis is virtually diagnostic of an unexpandable lung with the development of significant negative intrapleural pressure. The anterior chest pain is quickly relieved by allowing air entry into the pleural space through the thoracentesis needle or catheter. In this situation, the patient is best managed with an indwelling catheter. The patient and his family are instructed to drain the pleural fluid when breathlessness ensues and to discontinue drainage immediately when anterior chest pain develops.
    • Oxygen supplementation is indicated if the estimated in-flight PO2 will be less than 55 mm Hg
  218. What is the risk of post-op complications in smokers?
    • The data suggest that there is a moderate increase in risk for postoperative pulmonary complications among current smokers.
    • There is also evidence suggesting that at least 2 months of smoking cessation reduces postoperative pulmonary risk.
    • A brief period of abstinence does not improve perioperative pulmonary outcomes, and smokers who tried to decrease cigarette use shortly before surgery are more likely to develop a postoperative pulmonary complication than those who continued smoking.
  219. What is the function of bosentan in management of pulmonary arterial hypertension?
    What is its use during pregnancy?
    Bosentan, an endothelin receptor antagonist, is effective in improving symptoms in patients with PAH; however, it is teratogenic and is contraindicated for use during pregnancy.
  220. Define medication overuse headache.
    Medication overuse headache is generally defined as a headache for more than 15 days per month and the use of acute headache medication on more than 10 days per month.
  221. What is High-altitude pulmonary edema (HAPE)?
    What is used to treat it?
    • HAPE is a form of nancardiogenic pulmonary edema due to leakage of fluid and hemorrhage into the alveolar spaces. The most effective preventive measure for HAPE is an appropriately gradual axcent to altitude (not greater than 300 to 500 m (984 to 1640 ft).
    • Nifedipine is used to prevent and to treat HAPE.
  222. Acute mountain sickness

    What is used as prophylaxis?
    What is the role of dexamethasone in the management of AMS?
    • Acetazolamide is used as prophylaxis for periodic breathing related to high altitude and acute mountain sickness (AMS) but is not indicated for HAPE.
    • Dexamethasone is used for the prevention and treatment of AMS; it is not generally considered as a prophylactic agent for HAPE.
  223. What are the complications of rewarming?
    • rhabdomylsis
    • compartment syndromes
    • DIC
    • pulmonary edema
    • ATN
  224. How do you treat severe hypothermia?
    In patients with severe hypothermia (temperature less than 30.0 °C [86.0 °F]), active internal rewarming measures using warmed intravenous fluids, warm and humid oxygen, peritoneal lavage, and extracorporeal rewarming should be considered.
  225. What is respiratory bronchiolitis interstitial lung disease?
    • Diagnosis of RB-ILD requires the clinical context of a patient with a significant smoking history. Respiratory bronchiolitis, which is also called smoker’s bronchiolitis, is common among smokers and is thought to be responsible for the reduction in air flow in young, otherwise healthy smokers.
    • Pulmonary function testing typically shows a mixed obstructive–restrictive pattern with a slightly reduced diffusing capacity for carbon monoxide but in some cases, testing may be normal or associated with only an increase in the residual volume.
    • RB-ILD is causally linked to inhalation of tobacco smoke, whereas cryptogenic organizing pneumonia, idiopathic pulmonary fibrosis, and nonspecific interstitial pneumonia are not.
  226. What is the propofol infusion syndrome?
    The propofol infusion syndrome is a rare and often fatal syndrome originally described in critically ill children undergoing long-term propofol infusion at high doses. The syndrome has recently been reported in adults, mostly in patients with acute neurologic illnesses or acute inflammatory diseases complicated by severe infections or even sepsis and who are receiving catecholamines and/or corticosteroids in addition to propofol. The main features of the syndrome consist of cardiac failure, rhabdomyolysis, severe metabolic acidosis, and renal failure associated with hyperkalemia. Central nervous system activation with production of catecholamines and corticosteroids, and systemic inflammation with cytokine production are priming factors for cardiac and peripheral muscle dysfunction. High-dose propofol, but also supportive treatments with catecholamines and corticosteroids act as triggering factors. At the subcellular level, propofol impairs free fatty acid utilization and mitochondrial activity. The syndrome can be lethal if not identified early, and caution should be exercised when using prolonged (more than 48 h) propofol sedation at doses greater than 75 µg/kg/min, particularly in patients with acute neurologic or inflammatory illnesses. In these cases, alternative sedative agents should be considered immediately, and monitoring of the plasma levels of troponin I, creatine kinase, and myoglobin should be undertaken.
  227. Management of Goodpasture syndrome?
    Corticosteroids and cyclophosphamide are indicated to induce disease remission in patients with anti-GBM antibody disease. Because relapse rarely occurs, cyclophosphamide may be discontinued after 3 to 6 months. In addition, pulmonary hemorrhage is a medical emergency requiring immediate plasmapheresis to remove the causative antibody.
  228. Management of severe Wegener granulomatosis?
    patients with severe Wegener granulomatosis who underwent plasma exchange in addition to immunosuppressive therapy with daily cyclophosphamide and high-dose oral methylprednisolone had a 24% risk reduction for progression to ESKD compared with those who received immunosuppressive therapy alone.
  229. What antibodies are usually detected in patients with Wegener's?

    What antibodies are detected in pts with microscopic polyangiitis?
    Diagnosis of Wegener granulomatosis or microscopic polyangiitis involves antibody assays and kidney biopsy. Most patients are ANCA positive. Antiproteinase-3 (anti-PR3) antibodies are usually detected in patients with Wegener granulomatosis, whereas antimyeloperoxidase (anti-MPO) antibodies are usually found in those with microscopic polyangiitis. Serial ANCA testing should not be used to monitor disease activity or to guide treatment decisions in patients with Wegener granulomatosis.
  230. How do you establish the diagnosis of Wegener granulomatosis, microscopic polyangiitis, polyarteritis nodosa, or Churg-Strauss syndrome with kidney involvement?
    To establish a diagnosis of Wegener granulomatosis, microscopic polyangiitis, polyarteritis nodosa, or Churg-Strauss syndrome with kidney involvement, kidney biopsy must reveal the presence of a necrotizing crescentic glomerulonephritis or necrotizing vasculitis of microscopic vessels such as the small arteries, arterioles, capillaries, or venules.

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