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Board Review > Miscellaneous 2012 > Flashcards

Miscellaneous 2012 Flashcards

1
Q

Discuss the beta-agonist receptor polymorphism that may be relevant for asthma.

A

beta 2-adrenergic receptor genotype B16-Arg/Arg - Some early studies suggested that patients homozygous for this polymorphism may be less responsive to beta-agonist therapy. Lancet 2009 trial: randomized Arg/Arg and Gly/Gly patients to inhaled steroids or inhaled steroids plus salmeterol. No meaningful difference by genotype. 2011 JACI trial: no difference in this population between tiotropium and salmeterol, both better than placebo.

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2
Q

Discuss recent data supporting tiotropium add-on therapy for asthma.

A

JACI 2011: ~100 patients already on LABA and ICS with uncontrolled asthma, randomized to two doses of tiotropium or placebo. Tiotropium improved PFT’s but not asthma symptoms. Chest 2012: retrospective cohort analysis in Scotland; HR for all-cause mortality (vs just LABA’s and ICS’s) was 0.65.

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3
Q

What new side effect is increasingly recognized in patients on inhaled corticosteroids?

A

fracture risk (Lancet 2011, metaanalysis of ~17,000 patients, NNH 83)

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4
Q

Discuss the ultra-long-acting beta agonist.

A

Indacaterol - once daily. ERJ 2011: improved PFT response compared to twice-daily salmeterol. Chest 2011: two doses vs placebo - decreased exacerbations and albuterol use. Seems to be safe.

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5
Q

What did the NEJM 2011 study on rate of decline in FEV1 in COPD show?

A

Average ROD was 33 mL per year, but lots of variability. Higher rates in 1) smokers, 2) patients with bronchodilator reversibility, and 3) patients with emphysema.

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6
Q

Discuss emphysematous lung sealant.

A

Foam administered bronchoscopically, causes distal atelectasis, may help with hyperinflation. Respiration 2011: modest improvement in air trapping and gas exchange.

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7
Q

What happened to the omega-3 fatty acid ALI/ARDS study?

A

Stopped early: worsened ventilator-free days, ICU-free days, etc.

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8
Q

Discuss the optimal duration of a recruitment maneuver.

A

Intensive Care Medicine 2011: most alveolar recruitment occurs during the first 10 seconds of the maneuver.

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9
Q

Summarize 2011 metaanalysis of NO in ALI and ARDS.

A

14 RCT’s, 1300 patients. Improved physiology, no mortality change.

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10
Q

What is the recent update on procalcitonin in sepsis?

A

Archives of Internal Medicine 2011: review of 14 RCT’s with various algorithms for directing course of antibiotics (ICU, inpatient and outpatient settings); no change in mortality, but suggestion of shorter courses of antibiotics

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11
Q

What is the pathogenesis of LAM? Discuss the recent breakthrough in management.

A

Lymphangioleiomyomatosis (LAM) is caused by a deficiency of hamartin or tuberin, two proteins that regulate the mammalian target of rapamycin (mTOR); deficiency of either protein leads to upregulation of mTOR and promotion of cell proliferation. In a case series, 19 patients with LAM received off-label sirolimus, an mTOR inhibitor, for up to 5.4 years. Among the 11 patients with chylous effusions, 10 experienced resolution of their effusion(s) and one had a decrease in the size. In addition, several patients showed stabilization or improvement in lung function after 2 to 3 years of sirolimus therapy.

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12
Q

Give three reasons why it is important to subtype NSCLC:

A

(1) adenocarcinoma or NSCLC not otherwise specified should be tested for EGFR mutations, because the presence of these mutations is predictive of responsiveness to EGFR tyrosine kinase inhibitors, (2) adenocarcinoma histology is a strong predictor for improved outcome with pemetrexed therapy, and (3) squamous histology is a risk factor for life-threatening hemorrhage with bevacizumab therapy

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13
Q

Discuss 2011 NEJM article on intrapleural agents for empyema.

A

Intrapleural fibrinolytics hasn’t worked in the past. 210 patients, DNase vs t-PA vs both vs placebo. Individual agents: no change from placebo. Both: significant change in pleural opacity, lower surgical referral, decreased length of hospital stay.

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14
Q

What is the sensitivity and specificity for clinical impression of PE?

A

Ann Int Med 2011: 85%, 51%.

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15
Q

Discuss CPFE.

A

Combined pulmonary fibrosis and emphysema. Upper lobe emphysema, lower lobe fibrosis. Commonly have pHTN, ALI, lung cancer. Male smokers, high mortality. Can have normal spirometry with decreased DLCO. Slower FVC and DLCO decline than IPF, but FEV1 decline more correlated with mortality. Lousy survival.

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16
Q

Summarize PVT.

A

Pulmonary venous thrombosis. Lung cancer, lung transplant and post-lobectomy. Rare cases of systemic embolization have been described. Dx usually by autopsy vs biopsy. Ssk for delayed pulmonary venous phase on CTA, vs lack of venous flow on pulm angiography. Can sometimes see thrombus on TEE. Thrombectomy has been done in localized post-lobectomy cases. Anticoagulation.

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17
Q

Serologic test for PAP?

A

serum anti-granulocyte macrophage colony-stimulating factor (GM-CSF), elevated

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18
Q

Characteristics of BAL fluid in PAP?

A

milky, lipoproteinaceous, PAS positive, contains foamy macrophages

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19
Q

Discuss the three subtypes of PAP.

A

1) primary (autoimmune), acquired antibodies for GM-CSF, impair macrophage development; 2) congenital, germline mutations in GM-CSF receptors; 3) secondary, develops in underlying condition (hematopoetic malignancy, immunodeficiency syndromes) or inhalational exposures

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20
Q

Opportunistic infections in PAP?

A

nocardia, endemic fungi, mycobacteria

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21
Q

Novel therapy in PAP?

A

inhaled GM-CSF, effective in ~69% of patients and well-tolerated

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22
Q

Summarize LCS.

A

Langerhan Cell Sarcoma. 27 cases reported. Dendritic cell origin. Distinguished from LCH by degree of cellular atypia and clinical aggressiveness; LCS is overtly malignant. Only one case is LCH ? LCS. Often multiorgan involvement.

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23
Q

What cell markers are specific for Langerhans cells?

A

CD1a and S-100

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24
Q

Discuss the recent pulmonary concern with polymyxins.

A

Chest 2012: association with respiratory arrest. They have potent neuromuscular blocking effects. Paralysis of respiratory muscles was described in the 50’s, 60’s. Typically within 1-3 hours of administration. Renal disease may predispose.

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25
Q

Interesting fact about rapidity of CXR diagnosis.

A

A radiologist picks up 70% of abnormalities on a CXR in under .5 seconds. (Radiology.1962;78;694 - 704.)

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26
Q

An enlarging nodule doubles when its diameter increases by __%.

A

26%

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27
Q

How large need a pleural effusion be in order to blunt the costophrenic angle?

A

200 - 400 mL

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28
Q

DDx for a black pleural effusion?

A

1) infection (bacteral or fungal - aspergillus, rhizopus); 2) malignancy (melanoma); 3) hemorrhage (hemolysis)

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29
Q

Incidence of central venous hyperoxia (Scvo2 greater than 89%) in septic shock?

A

36% (Pope, Ann Emerg Med 2010;55(1):40-46,e1.)

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30
Q

Discuss Chest 2012 meta-analysis of timing of tracheotomy.

A

Seven trials, 1,044 patients. No change in short-term mortality, long-term mortality, or VAP. No significant change in length of stay, sedation, duration of ventilation.

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31
Q

Discuss 2011 Chest trial on albuterol, levalbuterol and heart rate/rhythm.

A

RCT, 70 ICU patients. Mean increase in HR was 0.89 BPM in albuterol, 0.85 BPM in levalbuterol. Arrhythmias were very uncommon (0.6%), only PVC’s and one 5-beat run of v-tach.

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32
Q

Summarize Herridge ARDS-followup article.

A

NEJM 2003. 1-year outcomes: all with decreased muscle bulks, proximal muscle weakness and fatigue. 50% unemployed. Much of post-ARDS disability is extrapulmonary.

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33
Q

Where has community-acquired C Diff become a problem?

A

Canada, England, some regions of the US

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34
Q

Discuss small-bowel enteritis with c diff.

A

Uncommon but quite toxic. Generally patients who have undergone colectomy. Generally fulminant with high mortality.

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35
Q

Rationale for oral vancomycin in severe c diff?

A

This dose gets concentrations of vanc into the colon that are 500 to 1000 times the MIC90 of c diff in stool.

36
Q

Criteria for severe c diff?

A

WBC over 15, fever over 38.3, admission to ICU, albumin under 2.5, age over 65 (Zar, 2007)

37
Q

Kidney stones, hypercalcemia, lytic rib lesions on CXR… consider:

A

brown tumors (generalized osteitis fibrosa cystica or Von Recklinghausen disease), secondary to primary parathyroidism

38
Q

What is lymphangiomatosis?

A

Lymphangiomatosis is a developmental abnormality of the lymphatic system. Abnormal proliferation of lymphatic system with compression of adjacent structures by mature cells. Can cause chylous effusions. Progressive, no good treatment.

39
Q

Why is acute hypercapnia an uncommon presentation of pulmonary embolism?

A

Patients often hyperventilate due to stimulation of vascular receptors, increases in PA and RV pressures, behavioural factors due to dyspnea and chest discomfort. If big enough to cause significant dead space increase, would also expect some hypoxemia and BP problems.

40
Q

Bottom line on extreme obesity in the ICU?

A

After adjusting for confounders, no increase in mortality. There is an increase in duration of mechanical ventilation. Some reports have seen lower mortality. (Martino, Chest 2011)

41
Q

Risk of benzocaine and tetracaine?

A

methemoglobinemia

42
Q

What nerve blocks are options for bronchoscopy anaesthesia?

A

glossopharyngeal nerve block, which causes temporary abolition of the gag reflex and loss of tactile sensation over the posterior one-third of the tongue and the lateral and posterior wall of the oropharynx and hypopharynx, and the superior laryngeal nerve block, which results in loss of tactile sensation over the posterior surface of the epiglottis and the mucosa of the larynx and upper trachea

43
Q

Weight-based dose of midazolam for conscious sedation?

A

0.06 to 0.07 mg/kg (4-5 mg for a 70 kg patient)

44
Q

Dosage of flumazenil?

A

0.2 mg IV over 15 s, may repeat same dosage at 60-s intervals (maximum dosage: 1 mg/dose; 3 mg/h)

45
Q

Difference between SS and MS LCH?

A

Single-system and multi-system Langerhans Cell Histiocytosis. Great mortality (SS) vs 20% mortality (MS).

46
Q

The common radiographic appearance of pulmonary LCH on chest radiographs (in both pediatric and adult disease) is… CT?

A

CXR: bilateral, symmetrical, reticulonodular opacities in the middle and upper lung fields, with sparing of the costophrenic angles. CT: cysts and nodules of varying size and shape, seen more sensitively than with chest radiographs. Rarely, pleural effusion and mediastinal/hilar lymphadenopathy may be seen.

47
Q

Summarize the histology of the granulomatoses:

A

Wegener’s: necrotizing vasculitis, irregular necrotic foci surrounded by palisading epithelioid cells. Lymphomatoid granulomatosis: vasculitis, little necrosis, mononuclear infiltrate. Necrotizing sarcoid: vasculitis, well-formed noncaseating granulomas around areas of necrosis, impinge upon and destroy vessels. Bronchocentric granulomatosis: necrotizing granuloma in the bronchi or bronchioles. HP: poorly formed noncaseating granulomas near bronchioles, mononuclear infiltrate.

48
Q

Compare smoking cigarettes to hookahs.

A

the longer duration of a water-pipe smoking session leads to a much higher yield of tar, nicotine, and carcinogenic polycyclic aromatic hydrocarbons and heavy metals than does cigarette smoking. One inhales the equivalent of a pack of cigarettes in a typical 30- to 60-min session.

49
Q

Describe “Hookah lung.”

A

Presumed HP to some precipitant in hookah smoke. Nodular infiltrates, poorly formed granulomas.

50
Q

What is PSP/reg?

A

Pancreatic stone protein (PSP) and regenerating protein (reg), two names for a 16 kDa polypeptide that has unclear function (stimulates Beta cell growth and regeneration?). Increased in inflammation and infection. May be superior to procalcitonin. Chest 2011: elevated and prognostic in VAP.

51
Q

Most common triggers of secondary HLH?

A

EBV, herpes viruses. But there’s a long list.

52
Q

What percentage of patients who die in the ICU of sepsis and MODS have histiocytic hemophagocytosis?

A

One third (Crit Care Med.2004;32(6):1316-1321)

53
Q

Initial treatment of HLH?

A

Its main components are dexamethasone, etoposide, cyclosporine, and IV immunoglobulin.

54
Q

What feature of HLH was the most helpful in separating it from simple severe septic shock?

A

Cytopenias. Should prompt discussion of BM aspiration.

55
Q

ATS standard for bronchodilator reversibility?

A

FEV1 increases by more than 12% and more than 200 mL.

56
Q

Pleural manifestations of paragonimus infection?

A

61% of paragonimus infections have pleural effusions. Typically exudates with low glucose and eosiniphilia and low pH. Pseudochylothorax, chylothorax.

57
Q

The diagnosis of a chylothorax is based on… What is a pseudochylothorax?

A

triglyceride level greater than 110 mg/dL, opaque supernatant, and the absence of cholesterol crystals. Pseudochylothorax (cholesterol pleurisy) occurs with long-standing fluid in a fibrotic pleura. The fluid has a high content of cholesterol but no triglycerides or chylomicrons. In both conditions, the pleural fluid is thick, opalescent, whitish or the colour of cafe-au-lait.

58
Q

Clinical association between TNF-alpha and asthma?

A

Chest review 2011: five cases of patients with asthma unmasked by initiation of anti-TNF-alpha agents.

59
Q

Clues to quinine toxicity?

A

Sepsis without a source. Quinine-induced aplastic or hemolytic anemia, thrombocytopenia, neutropenia, coagulopathy, hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) have been reported.

60
Q

In COPDGene, what were the clinical features of patients with Chronic Bronchitis?

A

Similar lung function but younger, greater smoking history, greater likelihood of current smoking. Higher breathlessness, more upper airway symptoms. More exacerbations.

61
Q

What are the ESKAPE bugs?

A

Top six bugs for antimicrobial resistance: Enterococcus faecium, Staphylococcus aureus, Klebsiella species, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species

62
Q

Summarize the mechanisms of therapy for our pTHN treatments.

A

target (1) increased endothelin-1 production (endothelin antagonists [ETRAs]), (2) reduced activity of nitric oxide synthase (phosphodiesterase-5 [PDE-5] inhibitors), and (3) decreased prostacyclin production and increased thromboxane A 2 (prostanoids).

63
Q

Discuss “reversed halo sign.”

A

central GGO surrounded by denser airspace consolidation of crescent or ring shapes; COP, paracoccidiomycosis; TB; zygomycosis; aspergillosis, Wegener’s; sarcoid; histo - not very specific

64
Q

What is the treatment of c. gatti lung infection?

A

Pulmonary and CNS C neoformans treatment is divided into induction, consolidation, and suppression phases. Induction treatment with amphotericin and flucytosine is usually followed by fluconazole therapy for consolidation and suppression. CNS and disseminated C gattii disease, as well as small isolated pulmonary cryptococcoma, are treated similar to C neoformans with amphotericin, flucytosine, and close radiographic and clinical follow-up. New data suggest some variability in azole susceptibility among outbreak strains; however, in vitro MIC values may not reflect in vivo efficacy and should be interpreted with caution.

65
Q

Mechanism of action of sirolimus?

A

Sirolimus (rapamycin) is an immunosuppressant for use in patients after renal transplantation. It is a macrocyclic triene antibiotic isolated from Streptomyces hygroscopicus. It acts by binding to an intracellular protein, FK-binding protein, resulting in the blockage of the mammalian target of rapamycin. This blockade causes downstream events that ultimately inhibit cell cycle progression from the G1 phase to the S phase in T lymphocytes, fibroblasts, and endothelial cells, which may explain the antifungal, immunosuppressive, and antiproliferative effects of sirolimus. It is not a calcineurin inhibitor.

66
Q

Three pulmonary toxicities of sirolimus:

A

lymphocytic interstitial pneumonitis without hemorrhage, fibrosing alveolitis, and a very few cases of DAH

67
Q

In risk stratifying patients for lung resection, what PFT’s make no further workup needed?

A

FEV1 greater than 80% or 2L

68
Q

In risk stratifying patients for lung resection, what PFT’s make no further workup needed other than for pneumonectomy?

A

FEV1 greater than 1.5 L, DLCO greater than 40%. For pneumonectomy, get V/Q scan, exercise test.

69
Q

What laboratory value was predictive of postoperative pulmonary complications?

A

The National Veterans Affairs Surgical Risk Study found that serum albumin level was a strong predictor of 30-day mortality and was independently associated with a 22 to 44% incidence of PPCs when it was 3.5 g/dL. The association between an increase in all-cause mortality and a decrease in serum albumin level was linear.

70
Q

What functional test predicts operative mortality in pHTN?

A

Inability to walk more than 332 m in 6 minutes is predictive of mortality.

71
Q

Discuss perioperative risk assessment in ILD.

A

1) Having grade 3 or 4 dyspnea at rest is a risk factor. 2) PaCO2/PO2 over .72 is bad. 3) Composite PFT indices are more predictive than individual measurements.

72
Q

Examples of post-op pulmonary complications prediction models?

A

Physiologic and Operative Severity Score for Enumeration of Mortality and Morbidity (POSSUM) and the Cardiopulmonary Risk Index (CPRI); not very helpful.

73
Q

Two established modifiable risk factors for post-op pulmonary complications?

A

preoperative alcohol use (increases risk of ALI) and pulmonary rehabilitation

74
Q

Name two non-lung procedures that have very high rates of post-op pulmonary complications.

A

cardiac surgery and esophagectomy

75
Q

Summarize the evidence supporting preoperative steroids and bronchodilators for patients with COPD.

A

Silvanus and colleagues found fewer instances of bronchospasm during intubation in patients with bronchial hyperreactivity who were na?ve to bronchodilators when they were pretreated daily for 5 days with albuterol and methylprednisolone. Whether this benefit extends to patients who use bronchodilators in the long term has not been assessed.

76
Q

What is the only anaesthetic that doesn’t cause intraoperative atelectasis?

A

ketamine

77
Q

What is the vector for RMSF?

A

The dog tick.

78
Q

Aerosolization of mouse excreta ?

A

hantavirus or lymphangitic choriomeningitis

79
Q

Bottom line on antibiotic resistance in CF patients receiving chronic azithromycin?

A

Increased sputum organism resistance, but no change in subsequent ability to treat infections.

80
Q

Which narcotics are rarely picked up on drug screen?

A

methadone, fentanyl, hydromorphone

81
Q

Duration of action of naloxone?

A

20 - 90 minutes

82
Q

Ladder of naloxone dosing?

A

q2m: 0.04, .5, 2, 4, 10, 15 mg

83
Q

What is the oral Xa inhibitor with a reversing agent?

A

Idrabiotaparinux is a biotinylated derivate of idraparinux, and its anticoagulant activity can be rapidly reversed with IV avidin. Xa inhibitor.

84
Q

What is eritoran?

A

Anti-TLR-4 receptor agent, didn’t work in a study of 2000 patients with sepsis.

85
Q

Summarize antisynthetase syndrome.

A

Antisynthetase syndrome is a rare, chronic autoimmune disease of unknown cause that is considered a subgroup of the idiopathic inflammatory muscle diseases. Patients with antisynthetase syndrome have a characteristic clinical picture consisting of myositis and/or ILD and/or chronic articular involvement. There are 12 described antisynthetase antibodies. Anti-PL-12 antibodies are associated with a higher prevalence of ILD (70%-100%) and a lower prevalence of biochemical and clinical myositis compared to other antibodies.

86
Q

Key points on pulmonary amyloid.

A

Can be one manifestation of systemic amyloid or can be local pulmonary amyloid. Lung involvement uncommon among familial and secondary amyloid but common among primary. Diffuse, alveolar, septal deposition of amyliod: reticular or reticulonodular infiltrates. Pleural effusions probably reflect cardiac involvement. Localized: nodules, endobronchial plaques, Other issues: mediastinal LAD, macroglossia –> OSA.

87
Q

Summarize anti-synthetase syndrome.

A

Fever, arthritis (RA-like), ILD, mechanic’s hands, myositis. Anti-synthetase antibodies, common among DM/PM. 8 of these Ab’s have been described. Most common is anti-Jo1. Much more ILD in patients with DM and PM who have the antibody. Negative ANA doesn’t help. NSIP on CT. pHTN is common. Response to immunosuppression is variable.

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