Obstructive Lung Disease Flashcards

1
Q

What is exhaled NO a measurement of in asthma patients?

A

Weakly correlated with degree of airway obstruction, specifically in regards to Th2-driven local inflammation causing upregulation of NO synthetase enzymes

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2
Q

What can cause increase exhaled NO?

A

Asthma with Th2-driven inflammation, allergic rhinitis, nonasthmatic eosinophilic bronchitis, non-CF bronchiectasis, viral URIs

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3
Q

What is the justification of the fixed 0.7 FEV1/FVC ratio for COPD diagnosis?

A

Better discrimination of COPD-related hospitalization and mortality risk vs LLN

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4
Q

For patients with moderate to severe COPD, what are the benefits of triple therapy over LABA/LAMA?

A

Improved lung function, QOL, reduces mortality and hospitalizations

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5
Q

How does obesity affect asthma?

A

Increases asthma exacerbations, and asthma is underdiagnosed in this population, and have reduced response to ICS

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6
Q

Who is a candidate for bronchial thermoplasty?

A

Severe asthma, stable on at least ICS/LABA with evidence of poor asthma control
Contraindications include under 18, more than 3 exacerbations in a year, FEV1 under 60, chronic sinus dz, active implantable device, AMI within 6 weeks, coagulopathy, incomplete prior response to BT

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7
Q

Who can be considered for roflumilast add-on therapy?

A

COPD on triple therapy with concomitant chronic bronchitis with 2 exacerbations in the last year and/or one hospitalization, avoid in Child-Pugh B or C. Watch for weight loss and psych issues. Can increase FEV1

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8
Q

What is the difference between sensitizer-induced asthma and work-exacerbated asthma?

A

Sensitizer- sputum eosinophils decrease in absence from work, airway responsiveness changes, IgE mediated
Work- exacerbated at work but persists at home. Nonspecific irritant exposure

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9
Q

How is hereditary angioedema treated?

A

With subQ icatibant (plasma-derived C1 inhibitor) or lanadelumab (monoclonal inhibitor of plasma kallikrein- a precursor to bradykinin)

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10
Q

What are the cutoffs for mannitol (indirect) challenge vs methacholine/histamine (direct) challenge?

A

Mannitol- 15+% change in FEV1 from baseline
Methacholine/histamine- 20+% change in FEV1 from baseline

Contraindicated if FEV1<1.5L

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11
Q

Who is a candidate for endobronchial valves for lung volume reduction?

A

Overinflated segments
Watch out for PTX

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12
Q

When should pulmonary rehab be started after AECOPD?

A

within 90 days of discharge to improve all-cause mortality

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13
Q

How does flu vaccination help COPD patients?

A

Reduces exacerbations and hospitalization, but not mortality benefit

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14
Q

What are the etiologies of non-CF bronchiectasis?

A

Postinfectious, iodiopathic, immunodeficiency, ABPA, primary ciliary dysfunction, CTD/RA, chronic aspiration, yellow nail syndrome. Has lower lobe predominance as opposed to CF. dornase alfa doesn’t seem to help non-CF bronchiectasis

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15
Q

What are the features of NSAID exacerbated respiratory disease

A

Hx asthma/chronic rhinosinusitis, nasal polyposis, symptoms exacerbated by NSAIDs/aspirin 30min-3hrs after ingestion

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16
Q

What are the benefits of oxygen therapy in COPD patients?

A

Mortality benefit if worn at least 16hrs, reduce exacerbations. Did not change lung function or QOL

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17
Q

What are the resistance mechanisms seen in NTMs?

A

erm(41)- macrolide resistance
rpoB- rifampin resistance in m kansasii
16S ribosomal RNA / rrs- aminoglycoside resistance in MAC
23S rRNA - macrolides in MAC and abscessus
embB- ethambutol resistance

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18
Q

What is the best way to resolve a distal central airway obstruction in an unstable patient?

A

Rigid bronchoscopy can dilate the airway, allow for debridement, tamponade bleeding while securing the airway. Heliox can be a temporizing modality, and VV ECMO can be considered in certain situations
For proximal lesions, may consider tracheostomy

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19
Q

What are the potential risks of endobronchial valves?

A

PTX- 27% of patients in first 45days, 34% within the first year. Mostly managed with chest tube, occasionally will need valve removed. No increase in mortality and has similar benefit to those who do not experience PTX

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20
Q

What is associated with “destroyed lung syndrome”?

A

CF, recurrent infection due to kyphoscoliosis, toxic inhalations causing cylindrical bronchiectasis, and TB. Treat with airway clearance therapies. Only treat with abx if there is objective evidence of severe infection such as fever/chills/night sweats/purulent sputum.

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21
Q

Who are candidates for lobectomy for resectable tumors?

A

Absence of cardiovascular disease, 400m walk distance, peak Vo2 above 20mL/kg/min, FEV1 above 3.0 and DLCO above 30. In emphysema patients, FEV1 may actually improve post-op due to volume reduction. Don’t delay surgery for smoking cessation

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22
Q

What is the COPD Assessment Test (CAT)?

A

COPD specific questionnaire quantifying health status. GOLD now recommends assessment and management of COPD to be based on patient’s perception of disease and risk of exacerbation along with spirometry.

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23
Q

How do cardioselective BBers affect COPD control?

A

It doesn’t! Safe to use. Don’t affect LABAs.

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24
Q

What routine testing should be done for patients with COPD?

A

Bone density scans. Routine spirometry without concern for worsening lung function is not indicated. LDCT for patients 50-80yo with 20 pack yr Hx, currently/quit within 15 years.

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25
Q

For patients with COPD and chronic hypercapnia, when should NNIV be started?

A

When patient is stable 2-4 weeks following hospital discharge for AECOPD, or pending sleep study if concern for OSA

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26
Q

What is associated with asthma deaths?

A

Uncontrolled disease with symptoms days to weeks leading up to death, pathology reveals extensive mucus plugging and eosinophilic infiltration. Previous intubation/ICU admission is associated with increased mortality along with reduced lung function, but can happen in mild disease.

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27
Q

How is chronic endobronchial Pseudomonas treated in CF patients?

A

Eradication in newly found disease with inhaled tobramycin for 28 days then surveillance of sputum every 3 months. Can achieve 60-90% eradication that can last 12-24 months.

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28
Q

What is the mechanism behind brensocatib?

A

Dipeptidyl peptidase 1 inhibitor (DPP1) to reduce neutrophil serine protein activity in patients with non-CF bronchiectasis. This prolonged time to first time exacerbation and reduced number of exacerbations. Beware in patients with dental issues.

29
Q

What are the features of premenstrual asthma?

A

Worsening asthma prior to or during the first dsays of menstruatioin, 20% of women. Follow general standard of care for asthma control. Exogenous hormones don’t seem to help and have conflicting evidence. May also be associated with NERD

30
Q

What are the features of bronchial atresia?

A

Congenital anomaly from focal obliteration of lobar/segmental/subsegmental bronchus, usually complicated by mucus impaction and/or air trapping. Seems to be apicoposterior LUL commonly. Distal alveoli have collateral ventilation routes that collapse on exhalation leading to air trapping. Neighboring bronchocele filled with mucus can look like a nodule. Treated with excision for recurrent infection/compromise of neighboring lung parenchyma

31
Q

In “pure” emphysema, what changes can be seen in FEV1 and FVC?

A

May have no change as it may involve just the small distal airways, so can have a normal ratio and otherwise normal FEV1 and FVC values

32
Q

What are the features of a tracheal bronchus?

A

Congenital abnormality, usually RUL and arises directly from the trachea. Can cause issues with atelectasis if intubated as airway is often high in the trachea and cut off via ETT

33
Q

What are the features of tracehobronchopathia osteochondroplastica?

A

Calcified submucosal nodules diffusely throughout the cartilaginous portion of the trachea. Usually males.

34
Q

What are the features of ABPA?

A

Hypersensitivity to aspergillus (asthma/CF patients), mucoid impaction of airways and can cause fibrosis. Will sometimes have fever, brown mucus plugs, rarely hemoptysis. Will see eosinophilia, IgE above 1000, positive serologic testing for aspergillus. “finger in glove” see on chest imaging, upper lobes and perihilar regions along with tubular branching opacities. Treat with steroids and often 16 weeks of antifungals. Omalizumab has been used in refractory cases

35
Q

What are the features of preserved ratio impaired spirometry (PRISm)?

A

Proportionate decrease in FEV1 and FVC resulting in normal ratio. Have worse symptoms, exercise capacity, and increased mortality than smokers with normal lung function. Not necessarily progressive.

36
Q

What is most predictive of a patient being readmitted after acute exacerbation of COPD?

A

Depression and prior hospitalization for AECODP within the last year. Also clinically significant factors are anxiety, GERD, and hyponatremia.

37
Q

Which gene is most associated with A1AT deficiency?

A

Serpina1 on chromosome 14, M allele is normal, S or Z is associated with deficiency

38
Q

What is dysanapsis?

A

Mismatch of airway tree caliber to lung size, develops early in life and increases COPD risk

39
Q

What are the features of alpha 1 antitrypsin deficiency?

A

Features: basal pan-acinar emphysema, can have concurrent liver disease/necrotizing panniculitis/c-ANCA vasculitis
Dx: Threshold is 11 microM or 57 mg/dL for AAT serum level

40
Q

What factors increase risk of exacerbations in COPD?

A

Advanced age, severity of airflow limitation, chronic mucus hypersecretion, productive cough, duration of COPD, PH, eos above 340, comorbid conditions, GERD, h/o antibiotic use, COPD related hospitalization within a year, **history of prior exacerbations

41
Q

When should ICS be avoided in COPD patients?

A

Repeated pneumonia events, eos <100, Hx mycobacterial infection

42
Q

What is available for ciliary testing for non-CF bronchiectasis?

A

exhaled NO, genetic screening, ciliary biopsy

43
Q

How is a bronchiectasis exacerbation defined?

A

Worsening symptoms (3 or more of: cough, sputum production/purulence/consistency, SOB, fatigue/malaise, hemoptysis), symptoms for 48+hrs, change of treatment needed (ie antibiotics), alternate Dx excluded

44
Q

What is the role of ICS in non-CF bronchiectasis?

A

Limited only to those with underlying bronchospasm

45
Q

What add on medications can be considered for refractory MAC?

A

Increase from intermittent to daily, clofazamine, bedaquiline, inhaled amikacin

Think about surgery

46
Q

When testing for macrolide resistance in m. abscessus, how long must you wait to see if there is inducible resistance?

A

14 days due to erm41
23S rRNA resistance will be seen at day 3 via increased MIC

47
Q

How is exercise induced bronchospasm evaluated?

A

Indirect bronchoprovocation testing such as mannitol, exercise testing FEV1 decrease of 10%, eucapneic voluntary hyperpnea testing with 10% decrease in FEV1 within 20 minutes of challenge cessation

48
Q

When is goal directed nocturnal NIV indicated for COPD patients?

A

Hypercarbia with pCO2 above 52 two weeks post discharge and otherwise medically optimized. Titrate during the day to reduce pCO2 by 6-8

49
Q

Which flow loops are consistent with variable extrathoracic vs intrathoracic airflow obstruction?

A

Flattening of the inspiratory limb = extrathoracic
Flattening of the expiratory limb = intrathoracic

50
Q

What are the features of placental transmorgification of the lung?

A

Histo: papillary structure resembling placental villi
Features: rare benign cystic/bullous lesion of a unilateral lung, DOE, chest tightness, cough
Dx: biopsy
Tx: bronchodilators, ICS, smoking cessation, vaccinations, surgical bullectomy if not responsive

51
Q

When should COPD patients be further evaluated with hypoxia altitude simulation tests?

A

If resting SpO2 is 92-95%, get a 6MWT, and if it drops below 84%, get HAST
95%+ mMRC 3+, consider 6MWT

52
Q

How is a high altitude simulation test administered and interpreted?

A

A tight fitting mask is worn and administer 15% O2 with nitrogen to simulate oxygen concentrations at 8k ft. Compare ABG at beginning of tet and 20 min of breathing lower oxygen while monitoring sats and vitals. If sats drop below 85% or paO2 is below 50, need in-flight oxygen

53
Q

If a COPD patient is already on oxygen, how much more would they need in-flight?

A

Additional 2L than their long term prescription.

54
Q

What are the consequences of de-escalating triple therapy to LAMA/LABA in stable COPD patients?

A

Reduction in lung function. If patients have 300+ eos, may also have more AECOPD risk and more lung function loss. Reported increased PNA with ICS doesn’t result in increased mortality or hospitalizations

55
Q

Which patients can be considered for adjunctive medications to triple therapy to reduce exacerbations?

A

Roflumilast- for chronic bronchitis patients with FEV1 <50
Azithromycin- former smokers with FEV1 <80

56
Q

Which patients can be considered for BLVR endobronchial valves?

A

FEV <45%, TLC >100%, heterogenous emphysema.

Left usually greater than right due to intact fissure and therefore less interlobar collateral ventilation

57
Q

What are the features of bronchopulmonary sequestration?

A

Features: a portion of the lung is detached and received blood supply from a systemic artery

Intralobar sequestrations are within the normal lobe and lack their own visceral pleura. Most in the posterior segment of the left lower lobe. Focal areas of lucency or irregular cystic spaces without fluid. Prone to recurrent infection and is treated with resection

58
Q

What are the mechanisms and indications of the biologics in severe asthma?

A

Omalizumab- anti-IgE, serum IgE 30-700 with sensitivity to 1+ perennial allergen. Small risk of anaphylaxis. SubQ q2-4w

Benralizumab- IL5 receptor, eos above 300, subQ q4wx3 then q8w

Mepolizumab/reslizumab- IL5, q4w (resliz IV, mepo subQ) eos 150-300 for mepo and above 400 for resliz

Dupilumab- IL4 receptor, also for comorbid atopic dermatitis and chronic sinusitis with nasal polyps, eos above 150 and/or FeNO above 25, subQ q2w

Tezepelumab- anti-TSLP, can also help non-type 2 asthma, subQ q4w in clinic

OCS dependent- mepo, benra, and dupil

59
Q

When should you consider treatment for EDAC?

A

Airway collapse of over 90% on dynamic CT or bronch along with respiratory symptoms not otherwise explained

Treat comorbid conditions (ex GERD), supportive treatment (ex airway clearance, pulm rehab), CPAP

Stent for conservative treatment failure (not permanent, use as a trial for surgical potential response) or tracheobronchoplasty surgery. Surgery has extensive post-op morbidity

60
Q

What are some non-malignant causes of tracheal obstruction?

A

LAD, vascular compression, GPA, relapsing polychondritis, granulation tissue (from intubation, tracheostomy, foreign bodies, old stents, surgical anastomosis), idiopathic

61
Q

How small is the trachea if you can see flow loop abnormalities?

A

less than 8mm in diameter

62
Q

When are patients with BLVR valves most at risk of developing PTX?

A

In the first 3 days, due to expansion of contralateral lung

63
Q

Which radiographic finding is consistent with reactivation disease in TB (not in primary TB)?

A

Apical and posterior upper lobe segment opacities that often cavitate

64
Q

What are the features of progressive primary TB?

A

Affect areas of greatest ventilation (lower and middle lobes), LAD with necrotic centers, pleural effusion, miliary TB, obstructive atelectasis due to LAD, but somtimes a normal CXR

65
Q

What is the standard treatment algorithm for TB?

A

Start RIPE therapy and wait for sensitivities. If pan-sensitive, can stop ethambutol and continue treatment for 6 months in various combinations.

9 months if: PZA not used, sputum conversion doesn’t happen in 2 months, cavitary disease, or to decrease risk of relapse

66
Q

What are some considerations for HIV+ TB patients?

A

For HAART naive: start ART within 2 weeks when CD4 is under 50 and by 8-12w for everyone else

May have IRIS reaction 2-6w after ARVs are started (self-limited in most cases, but may need to back off ARVs)

Use rifabutin in place of rifampin

Standard LBTI therapy is fine but be vigilent for active disease

67
Q

What are the regimens for LBTI treatment?

A

Rifampin x4m
INH/Rif x3m
Rifapentine/INH weekly for 4m in HIV- patients (on hold due to recall)
INH for 6-9m

68
Q

How do you treat active TB in pregnant patients?

A

INH/rif/eth x 2m then INH/rif x 7m for total 9m
No PZA due to lack of safety data