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RCE MCQE 2022 > Respirology > Flashcards

Respirology Flashcards

1
Q

How do you diagnose asthma?

A
  1. History of variable respiratory symptoms (e.g. wheeze, SOB, chest tightness, cough)
  2. Variable expiratory airflow limitation:
    - Bronchodilator reversibility: improvement in FEV1 > 12% AND 200mL post BD
    - Improvement with anti-inflammatory treatment x 4 weeks: improvement in FEV1 > 12% AND 200mL
    - Excessive FEV1 variation in lung function between visits (>12% and 200 cc variation)
    - Peak Flow Variability – Average daily diurnal PEF variability >10% x 2 weeks
    - Positive Bronchial or exercise challenge test

NEED SPIROMETRY TO HAVE DIAGNOSIS OF ASTHMA

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2
Q

What are the criteria for positive asthma challenge tests?

A

Methacholine: PC20 <4mg/mL = POSITIVE
PC20 4-16 = borderline
PC20 >16 = negative

Exercise: fall in FEV1 > 10% and 200cc from baseline

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3
Q

What are the 9 criteria for adequate asthma control?

A
  1. daytime symptoms < 4 days/week
  2. nocturnal symptoms < 1 night/week
  3. No physical activity limitation
  4. No absence from school/work
  5. Mild, infrequent exacerbations
  6. Need for SABA < 4 doses/week
  7. FEV1/PEF >/= 90% personal best
  8. PEF diurnal variation < 10 - 15%
  9. Sputum eos < 2 - 3%
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4
Q

What is the preferred reliever in asthma?

A

PRN low-dose ICS-formoterol (e.g., Symbicort)

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5
Q

What is the step-up treatment regimen for asthma (up to Step 5)?

A
  1. Low-dose Symbicort PRN
  2. Low-dose ICS (daily) + SABA PRN
  3. Low-dose ICS/LABA + low-dose Symbicort PRN
  4. Med dose ICS/LABA + low-dose Symbicort PRN
  5. High dose ICS/LABA + reliever (tiotropium, omalizumab, mepolizumab)
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6
Q

When do you consider stepping down asthma therapy?

A

symptom control for 2 months + low risk exacerbations

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7
Q

List 7 non-pharmacological asthma control strategies

A
  1. Education & written asthma action plan
  2. Weight loss, exercise training
  3. Allergein/trigger avoidance & allergen immunotherpay
  4. Smoking cessation
  5. Vaccinations
  6. NSAID avoidance
  7. Comorbidity management (GERD, PNA, obesity)
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8
Q

When is LTRA acceptable as initial controller? In what three conditions is it most effective?

A
  1. Patients unwilling/intolerant to ICS
  2. Most effective in ASA-exacerbate asthma, exercise-induced symptoms or allergic rhinitis
    Less effective than ICS at preventing exacerbations
    Increases suicidality
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9
Q

Differentiate uncontrolled from severe asthma

A
  1. Uncontrolled: poor symptom control, frequent severe exacerbations (2+/year or 1+ hospitalization) or sustained airflow reduction (FEV1 <80% personal best or < LLN post-bronchodilator)
  2. Severe asthma: asthma requiring high-dose ICS + 2nd controller for past 1 year OR PO steroids for > 50% of the year
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10
Q

What is the workup and treatment for severe asthma (5)?

A
  1. Workup: total IgE, CBC (eosinophils), sputum eosinophils and FeNO (where available)
  2. Treatment:
    - tiotropium mist inhaler
    - macrolides
    - biologics
    - low-dose PO steroids
    - bronchial thermoplasty (role unclear)
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11
Q

When do you consider biologics in asthma?

A

Omalizumab: allergic asthma (IgE 30 - 700)

IL-5 agents (mepolizumab, reslizumab, benralizumab) or IL-4/IL-13 (Dupilumab) if severe eosinophilic (eos > 300) asthma

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12
Q

What is the management of the four “special populations” in asthma?

A
  1. Seasonal allergic asthma: start ICS with symptom onset and continue 4 weeks after pollen season ends
  2. Exercise induced: SABA pre-exercise –> LTRA pre-exercise –> regular ICS
  3. Pregnancy: continue treatment (don’t stop ICS); most evidence for budesonide (but all likely safe), give steroids for exacerbation
  4. ASA exacerbated (asthma, nasal polyps, ASA/NSAID sensitivity): avoid triggers, LTRA, desensitize to ASA if needed
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13
Q

List 5 asthma mimics or “asthma plus” syndromes:

A
  1. Bronchiectasis (including CF)
  2. EGPA: asthma, eosinophilia, granulomatous vasculitis, pANCA (30-60%)
  3. Vocal cord dysfunction: abrupt onset stridor, dx laryngoscopy, tx education, behavior modification, speech therapy, GERD treatment
  4. ABPA: frequent exacerbations, fever, brown sputum with “casts”. Dx total IgE + aspergillus specific IgE > 1000, peripheral eosinophilia + central bronchiectasis. Rx: prednisone +/- itraconazole
  5. Reactive airways dysfunction syndrome: acute irritant induced (often occupational) asthma following high dose exposure to vapors, gas or fumes lasting > 3 months. Treat like asthma exacerbation.
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14
Q

What 3 interventions improve survival in COPD?

A
  1. Smoking cessation
  2. Pulmonary rehab
  3. Supplemental oxygen (if hypoxemic)
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15
Q

What are the criteria for supplemental O2 in COPD?

A

PaO2 < 55 mm Hg
OR PaO2 < 60 + bilateral ankle edema, cor pulmonale or Hct > 56%

No benefit in moderate resting or exercise-induced moderate desaturation

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16
Q

What are the benefits of pulmonary rehab (3)?

A

Improves dyspnea, exercise capacity and health status

Reduced exacerbations if started following recent (< 4 weeks) AECOPD

Increased survival compared to usual care < 4 week post AECOPD

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17
Q

What is the recommended pharmacotherapy regimen for high risk AECOPD?

A

LAMA > LABA

–> LAMA/LABA > LABA/ICS (unless Eos > 300)

–> triple therapy

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18
Q

What are the oral therapies for high risk AECOPD on triple therapy? What non-pharm interventions reduce exacerbations?

A

Azithromycin (QTc, hearing impairment, sputum culture for NTM)

Roflumilast (diarrhea, weight loss)

NAC

NO role for theophylline

Non-pharm:

  • flu vaccine
  • pulmonary rehab < 4 weeks from AECOPD
  • education and case management
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19
Q

What are the 6 evidence based interventions for dyspnea in advanced COPD?

A
  1. oral (not nebulized) opioids
  2. NM electrical stimulation
  3. Chest wall vibration
  4. Walking aids
  5. Pursed lip breathing
  6. Continuous oxygen therapy for hypoxemic patients (reduced mortality and may reduce dyspnea, little benefit on QoL)
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20
Q

What are the management options for COPD/Asthma overlap?

A

LABA/ICS

–> triple therapy

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21
Q

What are the indications for NIV, LVR surgery and transplant in COPD?

A

NIV: severe, chronic hypercapnea (PCO2 > 51) and prior hospitalization with acute respiratory failure

LRVS: severe emphysema, upper lobe predominant disease, low post-rehab exercise capacity

Transplant: Bode score 7 - 10 and one of:

  1. hospitalization with AECOPD with pCO2 > 50
  2. Pulmonary HTN/cor pulmonale despite supplemental oxygen
  3. FEV1 < 20% with DLCO < 20%
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22
Q

When should abx be given for AECOPD?

A

Presence of three cardinal symptoms (or increasing purulence + one other)

or

Requirement of invasive or noninvasive ventilation

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23
Q

What are the indications for Bipap in AECOPD?

A

any of the following:

  1. pH = 7.35 with PCO2 >/= 45
  2. severe dyspnea (impending respiratory failure)
  3. Persistent hypoxemia despite supplemental oxygen
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24
Q

What are the pharmacological options for smoking cessation?

A
  1. Varenicline + nicotine patch
  2. Varenicline monotherapy
  3. Bupropion
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25
Q

What is bronchiectasis?

A

chronic respiratory disease

cough, sputum production and bronchial infection

permanent radiographic dilatation of the bronchi

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26
Q

What two investigations must everyone with suspected bronchiectasis have?

A
  1. CT chest

2. PFTs

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27
Q

Name 9 causes of bronchiectasis

A
  1. CF (malabsorption, pancreatitis, male infertility, pseudomonas, staph aureus, NTM)
  2. A1AT (COPD + cirrhosis)
  3. Primary ciliary dyskinesia (chronic URTI, otitis media, male infertility; abnormal ciliary beat pattern/frequency on nasal brushings)
  4. ABPA (asthma, eos, aspergillus IgG)
  5. AI/CTD (RA, SLE)
  6. IBD
  7. Aspiration
  8. Humor immunodeficiency (CVID, HIV)
  9. Post-infectious
28
Q

What investigations are part of the standard bronchiectasis workup?

A
  1. CT chest and PFTs
  2. ABPA: CBC, total IgE, aspergillus specific IgE or skin prick)
  3. Serum immunoglobulins
  4. CF (sweat chloride) and PCD (nasal NO)
  5. Sputum cultures

Consider:

  • RF< anti-CCP, ANA, ANCA
  • A1AT
  • swallow study
  • HIV
29
Q

What are the treatment options for bronchiectasis?

A
  1. Airway clearance (techniques)
  2. Mucoactive agents (3% NS; DNAase ONLY in CF)
  3. Antimicrobials (inhaled colistin or gentamicin if pseudomonas; azithro if recurrent exacerbations after NTM excluded)
  4. BRonchodilator
  5. Pulmonary rehab
  6. Vaccines
  7. Supplemental O2 (same criteria as COPD)
30
Q

How are bronchiectasis exacerbations managed?

A
  1. Abx (14 day course)

2. For major hemoptysis: IV abx + TXA + consider embolization

31
Q

Name six causes of ILD

A
  1. CTD (SSc, RA, DM, Sjogren, MCTD)
  2. Exposure related (organic = HP; inorganic = pneumoconiosis)
  3. Drugs (MTX, macrobid, amiodarone, bleomycin)
  4. Radiation
  5. Sarcoidosis
  6. Organizing pneumonia
32
Q

What investigations should be sent to workup ILD?

A
  1. ANA, RF, anti-CCP (more if indicated)
  2. HRCT chest
  3. PFTs +/- 6MWT +/- home O2 assessment
  4. Respirology +/- rheum referral

consider antibodies for known antigens, lung biopsy

33
Q

What are the hallmarks of IPF?

A

M > F, 6 - 7th decade (rare < 50), smoking history common

Chronic, progressive, fibrotic ILD

UIP on CT: reticular changes, subpleural/basal predominant, honeycombing

Absence of inconsistent features (cysts, mosaic pattern, GGO, nodules, consolidation)

34
Q

What is the treatment for IPF?

A

Smoking cessation, O2, PPI, pulmonary rehab, vaccinations

Antifibrotics (reduce declnie in FVC):

  • nintendanib
  • pirfenidone
35
Q

How are IPF flares defined and treated?

A

Acute exacerbation:

  • worsening dyspnea/hypoxemia + new diffuse GGO
  • rule out infection/PE/HF
  • consider high dose steroids + empiric abx
  • poor prognosis: 50% mortality
36
Q

What are the mainstays of ILD treatment per the CTS 2018 guidelines?

A
  1. IPF gets anti-fibrotics; immunosuppression in non-IPF
  2. Pulmonary rehab
  3. Supplemental O2 (resting or exertional hypoxemia with improved walk distance or dyspnea on O2)
  4. Dyspnea management: non-pharm techniques + low-dose opioids (also for cough in refractory cases)
  5. Lung transplant referral (early for IPF and fibrotic NSIP)
  6. Advanced care planning
37
Q

List four categories of non-IPF ILD, the causes, imaging findings and general treatment

A
  1. HP - organic exposures (mould, birds, etc); upper lobe predominant; avoid antigen, steroids, +/- MMF/AZA
  2. Pneumoconioses - inorganic exposures (asbestos, silica, etc) yrs ago; varied imaging; supportive care/transplant
  3. CTD associated - RA, SSc, DM, Sjogren, MCTD; varied; steroids, DMARDs, ritux, cyclophosphamide
  4. Drug induced - MTX, amiodarone, macrobid, bleomycin, vaping; varied; D/C drug +/- steroids
38
Q

When do you tap a pleural effusion?

A
  1. Suspected exudate
  2. Unclear cause
  3. Parapneumonic > 1cm on left lateral decubitus
39
Q

What are the follow up options to work up an exudative effusion of unclear cause?

A
  1. Repeat thora x 1
  2. CT chest
  3. Pleural biopsy (note: mesothelioma usually requires pleural biopsy)
40
Q

List a brief differential for a pleural effusion with the following characteristics:

  1. Chylothorax
  2. Eos > 10%
  3. Glucose < 3
  4. Lymphocyte predominant
A
  1. Chylothorax (TG . 1.24 or + CM): malignancy, TB, trauma, surgery, LAM
  2. Eosinophils > 10%: asbestos (BAPE), drugs (macrobid), malignancy, infection (parasitic), PE, eGPA
  3. Low glucose: < 1 mmol RA, empyema. 1 - 3: malignancy, TB, SLE
  4. Lymphocytosis: malignancy, yellow nail syndrome, sarcoid, RA. > 80%: TB or lymphoma
41
Q

Describe the management of a parapneumonic effusion

A
  1. Chest tube if:
    - positive gram stain or culture
    - pH < 7.2 or glucose < 3.4
    - frank pus or cloudy fluid
    - >50% hemithorax or loculated
  2. Abx:
    - beta lactams preferred; if s. pneumo penicillin is fine
    - empiric Rx for CAP + anaerobes
    - prolonged (3+ week) course
42
Q

What is the management of a pneumothorax?

A
  1. Primary spontaneous:
    - >2cm or symptomatic = needle aspiration +/- chest tube
    - surgery if persistent leak
  2. Secondary spontaneous (underlying lung disease):
    - admit
    - chest tube
43
Q

What is sarcoidosis, and what organs are typically involved and what is the natural history?

A

Multisystem granulomatous disease

Bx: noncaseating granulomas

Lungs: > 90%
Extra-pulmonary ~30%
-Heart, CNS, eyes need urgent treatment
Most are asymptomatic
2/3 will have remission at 10yrs
After 1yr of spontaneous remission relapse very uncommon
44
Q

Name two sarcoid syndromes that do not require biopsy.

A
  1. Lofgren’s:
    - bilateral hilar adenopathy + EN + migratory polyarthralgias +/- fever
    - high likelihood of spontaneous remission
  2. Heerfordt’s syndrome
    - anterior uveitis + parotid enlargement + facial palsy +/- fever
    - may forgo biopsy
45
Q

Describe the pulmonary manifestations of sarcoidosis and their implications for spontaneous remission

A

90% have pulmonary involvement
Usually asymptomatic hilar adenopathy
Sx: dyspnea, cough, wheeze, chest pain
PFTs: literally anything

Stage based on CXR findings:

1: bilateral adenopathy
2: LNs + parenchymal lesions
3. Parenchymal lesions - LNs
4. Fibrosis

46
Q

List 6 other organ systems involved in sarcoidosis and the common disease manifestations.

A
  1. Skin: lupus pernio, EN
  2. Liver/spleen: lesions, elevated LFTs, cholestasis, rarely ALF
  3. Neuro: CN palsy, HA, ataxia, weakness. LP: nonspecific lymphocytic inflammation (MR is test of choice)
  4. Ocular: anterior uveitis
  5. Cardiac: CM, arrhythmia, heart block. Screen with ECG +/- echo – > CMR/PET scan
  6. Hypercalcemia: common, due to increased conversion of 25 –> 1,25-D3
47
Q

List the investigations required for sarcoidosis

A
  1. CBC - cytopenias
  2. Calcium, Albumin, LFTs, creatinine
  3. CRP, ESR, RF
  4. 24h urinary calcium
  5. ECG +/- echo, holter, CMR, PET
  6. 1, 25-OH Vit D
  7. HIV, TB
  8. PFTs
  9. Tissue biopsy
  10. CXR +/- CT

Ophtho referral to r/o ocular sarcoid

48
Q

Describe the management of sarcoidosis. Why are steroids not always used? What manifestation can be treated with NSAIDs alone?

A

Most don’t require treatment: high rates of spontaneous remission with low recurrence rates

Steroids induce faster remission but increase recurrence rates

Treat if:

  • bothersome symptoms (cough, dyspnea)
  • deteriorating lung function (PFTs)
  • pHTN
  • extrapulmonary disease: ocular, CNS, cardiac, severe skin, hyperCa, symptomatic liver disease

Mild resp symptoms + stable PFTs: inhaled steroids

Dose: 20 - 40mg daily
Duration: 1 - 3 months, slow taper (year)

Relase: MTX, HCQ, LEF, TNFa inhibitors

EN usually responds well to NSAID monotherapy

49
Q

How is OSA diagnosed?

A

Symptoms + objective findings ( > 5 apnea/hypopnea events)

  • mild: 5 - 15 events/h
  • mod: 15 - 30
  • severe > 30

Nocturnal choking/gasping LR+ 3.3

Snoring non-specific; no findings good enough to rule in or out

50
Q

What is the management of OSA?

A

Treatment indications:

  • excessive sleepiness or impaired sleep-related QOL
  • HTN
  • severe asymptomatic OSA
  • critical occupation

Management:

  1. Weight loss
  2. CPAP
  3. Oral appliances (mild-mod disease)
  4. Surgery (rare)

NEJM 2016: CPAP did not decrease CV events (significance debated)

51
Q

What are the driving considerations for OSA?

A

Restrict driving if:

  • admits to excessive sleepiness while driving
  • MVA 2’ falling asleep in past 5yrs (if therapy not started)
  • nonadherence with CPAP
52
Q

What is the typical presentation of pulmonary HTN (pHTN)? How is it diagnosed? What is the workup?

A
  1. Exertional dyspnea; may have isolated reduced DLCO
  2. Mean PAP > 20 mm Hg and PVR > 3 WU on RH cath
  3. Workup based on group:
    Group 1: PAH (RH cath, CBC, lytes, LFTs, TSH, CTD screen, viral hepatitis, HIV, abdo US)
    Group 2: CHF (BNP, echo)
    Group 3: lung disease (CXR, HRCT, 6MWT, sleep study)
    Group 4: CTEPH (HRCT, V/Q)
53
Q

How is pHTN treated (overall and by group)?

A

Everyone: diuretics for overload, physical activity/rehab, OCP/contraception, O2 if hypoxemic

PAH: if vasoreactive (test during RH cath): PDE5 inhibitors or riociguat, endothelin receptor antagonist, prostanoid

Group 4: anticoagulation; refer for endarterectomy

Group 2/3/5: treat underling cause

54
Q

Who needs screening for pHTN and how frequently is this done?

A
  1. Scleroderma: annual echo + DLCO
  2. Portal HTN awaiting transplant: echo once
  3. Residual dyspnea/exercise intolerance despite 3 months of anticoagulation for acute PE: echo + V/Q once
55
Q

What is the A-a gradient equation (simplified)? What are the causes of normal/elevated A-a gradient?

A

At sea level:

(150 - [CO2 / 0.8]) - PaO2

Normal: Age / 4 + 4

Normal A-a:

  • hypoventilation (CO2 elevated)
  • low FiO2

Elevated A-a:

  • V/Q mismatch (improves with O2)
  • Shunt (doesn’t completely resolve with O2)
  • Diffuse limitation (ILD)
56
Q

What are the indications for home O2 (Ontario)?

A 
SpO2 = 88%
PaO2 = 55
PaO2 55 - 59 plus:
-cor pulmonale
-pHTN
-erythrocytosis

Based on NOTT trial showing mortality benefit in COPD (extrapolated to all lung disease)

57
Q

List six causes of hemoptysis.

A
  1. Infection/airway (bronchitis, TB, bronchiectasis)
  2. Cancer (carcinoid, NSCLC, SCLC)
  3. CTD (anti-GBM, GPA, SLE)
  4. Drug/toxin (cocaine, anticoagulants)
  5. Vascular (AVM, PE)
  6. Upper airway/GI bleeding
58
Q

What are features of carcinoid lung CA?

A
  1. Young, non-smoker
  2. Endobronchial lesion (lung/lobar collapse)
  3. Hemoptysis (hyper-vascular)

Get PFT + echo (assess for carcinoid heart disease)

59
Q

Define massive hemoptysis and describe its management.

A

200-600cc in 24h

  1. ABCs
  2. If you can localize, position in decubitus (good lung UP)
  3. CBC, coags, ABG
  4. Hold AC/correct coagulopathy
  5. Cross-type, IVF, O2
  6. Imaging if stable (CXR/CT); flex bronch to localize prior to IR guided embolization

Definitive managmenet:

  • IR for arterial embolization
  • Thoracic Sx (rigid bronch/resection)

Patients die of asphyxiation, not exsanguination

60
Q

List 5 common causes of chronic cough and their investigations/management.

A
  1. ACEi (D/C)
  2. UACS: antihistamine/decongestant trial; sinus imaging if no improvement
  3. Asthma (PFTs/empiric ICS)
  4. NAEB: sputum eos, +/- empiric steroids
  5. GERD: PPI –> 24h pH monitoring if persistent. Sx if refractory.

Get a CXR as part of initial workup.

61
Q

What are the indications for lung transplant?

A
  1. COPD
    - FEV1 < 25% +/- PaCO2 > 55
    - severe disease + resting hypoxemia < 55
  2. CF/bronchiectasis
    - FEV1 < 30% +/- PaCO2 > 50
  3. ILD
    - symptomatic + FVC < 60-65%
  4. pHTN
    - NYHA Class III/IV
62
Q

List the lung, cardiac, GI and metabolic causes of clubbing.

A
  1. Lung: malignancy, suppurative disease (abscess, empyema, CF, bronchiectasis), ILD
  2. Cardiac: cyanotic CHD, IE
  3. GI: IBD
  4. Metabolic: Graves, hypertrophic osteoarthropathy
63
Q

List a cause of fixed upper airway, variable extra-thoracic and variable intra-thoracic obstruction.

A
  1. Fixed upper airway
    - glotic or subglotic stenosis
  2. Variable extra-thoracic:
    - vocal cord dysfunction/paralysis
  3. Variable intra-thoracic:
    - tracheomalacia
64
Q

Describe the approach to PFTs.

A
  1. Is there obstruction (FEV1/FVC < LLN)
    - reversible?
  2. Is FVC reduced?
    - Yes: restriction or gas trapping
  3. Is there restriction?
    - TLC < LLN
    - if yes, parenchymal (reduced DLCO) or extra-parenchymal (DLCO normal)
  4. Is there gas trapping?
    - RV/TLC > ULN
  5. Is there hyperinflation?
    - TLC > ULN
65
Q

Describe three PFT “clang association” patterns?

A

Positional restrictive pattern: diaphragmatic dysfunction (get MIP)

Isolated decreased DLCO:

  • pHTN
  • early ILD/emphysema
  • anemia

Increased DLCO

  • pulmonary hemorrhage
  • polycythemia
  • LV failure
66
Q

What are the contraindications to PFTs?

A
  1. Hemoptysis
  2. PTX
  3. Unstable cardiac disease
  4. Aneurysms
  5. Recent eye, thoracic or abdo sx
  6. Acute illness

Absolute CI to methacholine challenge:

  1. Severe airflow limitation (FEV1 < 50%)
  2. Recent MI or stroke (last 3 months)
  3. Uncontrolled HTN (> 200/100)
  4. Aortic aneurysm

RCE MCQE 2022 (2 decks)

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