OSCE Resp Flashcards
A 12-year-old male with longstanding allergic asthma. He has had multiple GP visits for exacerbations in the last 6 months. They have increased his inhalers with no benefit. He is bothered by a consistent cough. He received 5 days of PO steroids and felt better. His symptoms returned after they were stopped.
Describe your approach to this case focusing on the reasons he is unresponsive to treatment. List investigations and treatment plan.
Possible reasons for uncontrolled/severe asthma:
* Noncompliant with medication
* Not using ICS, or relying on SABA
* Exposure to allergens - ie pets, HDM
* Exposure to irritants - ie smoking in the home, scents
* Improper inhaler technique
* Severe asthma requiring escalation to biologic
* Wrong diagnosis - other causes of cough (uncontrolled rhinitis, GERD, foreign body aspiration)
* Immunodef or other asthma syndrome (ABPA, EGPA)
Ix:
* CBC with eos
* Sputum analysis - including eos
* CXR or CT chest
* Full PFTs
* Repeat SPTs
* Total IgE
* Qigs, LSUBs, fungal precipitins, ANCAs
Tx
* Review Non-Pharm
* Avoiding triggers - ie allergen avoidance, smoking avoidance
* Asthma action plan
* Education around inhaler use/technique
* Medicalert
* Pharm
* Assess which stage patient is with asthma management (ie ICS/LABA, just ICS)
* Add on therapy including - LABA, LAMA, LTRA, unlikely SLIT/SCIT given severity of symptoms
Consider for biologic therapy
* Xolair
* Age >6
* Mod-severe asthma not responsive to ICS
* Perennial allergen
* IgE and weight within limits
* IgE 6-12 - 30-1300; >12 30-700
* Weight - 6-12 20-150kg, >12 30-150 kg
* Mepo
* Age >6
* Severe eos asthma not responsive to ICS and one other add-on therapy
* Eos >150 at start or 300 in the last year
* Dupi
* Age >12
* Severe asthma of Th2/Eos type or requiring steroid-dependent
You are seeing a patient who has been transferred to your care with asthma. A 19-year-old college student has just moved to your city after being followed by a respirologist for asthma. Take a focused history. You will be provided with physcial examination findings and asked to manage this patient.
a. Please take a history and describe your physical exam. What are important physical findings?
b. Investigations?
c. Management?
History:
* Symptoms consistent with asthma - cough, wheeze, SOB, CT
* Hx of variable symptoms:
* Worse at night, exercise, humidity, cold weather, infxns, allergens/outdoors, smoking
* Onset of symptoms, age of diagnosis
* Current control of asthma - daytime, nighttime, need for rescue inhaler, missing work/school, any exacerbations
* Severity - prev need for OCS, ICU admission, hospitalization, ED visits
* Current tx - what using for controller and reliever, compliance, technique
* Last testing and results
* Big 5 - FamHx, PMHx (assoc conditions, asthma, AR, GERD), Meds, SocHx, Allergies
Physical exam:
* Ht, weight, BMI
* Vitals
* CVS, Resp - any signs of work of breathing, wheezing
* Other allergic signs - dennie morgan lines, allergic shiners, evidence of eczema, urticaria
b. What investigations would you perform?
Ix:
Full PFTs
CXR
Consider Bw depending on hx and severity
SPT
c. Please outline your management.
Nonpharm
- Education about diagnosis
- Inhaler technique
- Medicalert
- Avoidance of triggers - ie if cat, close windows in summer
- Action plan
- Weight loss
Pharm:
- Need to step up therapy based on severity
- Mention AIT
Checklist
History
- Focus asthma history: age of diagnosis, hospitalizations, intubations, recent emergency visits, oral prednisone
- Current asthma status: daytime symptoms, nighttime symptoms, SABA use, physical activity level, missed school days, sleep quality, use of peak flow meter
- Associated conditions: AR, GERD, AD,
- Triggers: URI, exercise, cold, animals, pollen, cigarette smoke, known allergies
- Current management: compliance, technique, cost
- PMH
- FHX
Physical exam: BMI 31, chest sounds distant secondary to body habitus but seem clear. Otherwise normal.
Investigations
- PFT: interpretation – (obstructive lung disease, reversibility, evidence of air trapping)
- SPT: (positive cat, trees)
- Sputum eosinophils (5%)
Management
- Need to step up the therapy: either use Symbicort 200ug as maintenance and reliever OR increase to 400 BID (medium dose ICS) OR add LRTA2
- Identify that patient is a poor-perceiver. Therefore, may benefit from self-monitoring: Consider symptom diary, peak flow meter
- Asthma action plan: yellow zone – 4x the puffer3
- Flu shot
- Weight loss
- Strongly consider moving
- Mention AIT
You’re seeing a 21 year old male with a few weeks history of progressive shortness of breath
a. Please provide a differential diagnosis and outline your investigations.
b. His chest x-ray shows patchy infiltrates and PFT shows a restrictive pattern with decreased DLCO. In his history you find out that he keeps parakeets. What is the most likely diagnosis how could you confirm this?
c. What are the consistent biopsy findings?
d. What is the management?
DDx SOB:
Resp - Asthma, AERD, OA, RADS, ILD, CF, ILO
Immune - HP
Vasc - EGPA, GPA, MPA, Pulm HTN, PE,
CV - myocarditis/pericarditis, CHF
Infx - PNA (bacterial, eos), URTI, TB, fungal infxn
AI - ILD related to AI (SLE, RA, SS), sarcoidosis
Malignancy - Lung Ca
Infectious: HIV (PCP), travel, sick contacts, TB, fungal infection
Others: Deconditioning
b. His chest x-ray shows patchy infiltrates and PFT shows a restrictive pattern with decreased DLCO. In his history you find out that he keeps parakeets. What is the most likely diagnosis how could you confirm this?
Most likely - HP
Confirm - HRCT with compatible findings, Bronch with BAL showing lymphocytosis >20%, Avian precipitins, can consider inhalational challenge, although only done in select cases
CBC N, CRP, ESR mildy elevated, CXR patchy infiltrates [Symbol] micronodules and air trapping, HIV neg, sputum gram stain, bronch lymphocytosis CD8, macrophages
PFT: restrictive, decreased DLCO
Serum for precipitating IgG for avian
High total IgG and RF
c. What are the consistent biopsy findings?
- Poorly formed noncaseating granulomas, mononuclear cell infiltrate
- histopathologic triad of HP includes:
poorly formed granulomata or multinucleated giant cells located near respiratory or terminal bronchioles
- chronic cellular bronchiolitis
- chronic cellular pneumonitis with patchy lymphoplasmacytic infiltration.
d. What is the management?
Avoid the exposure
Steroids 0.5 mg/kg x 1-2 weeks, then taper over 2-4 weeks
You are seeing a patient with a chronic cough.
a. Please provide a history and outline your physical exam.
b. What is the differential diagnosis for chronic cough?
c. What are the investigations?
d. Management?
DDx:
- UACS - GERD, AR (PND)
- Psychogenic/habitual
- Asthma, COPD
- Infection / post-infectious e.g. bronchitis, pertussis, etc
- Cardiac - e.g. CHF
- GI - reflux
- Obesity?
- meds eg ACEi
History:
- HPI –> onset, duration, exacerbating/alleviating factors, productive or dry, how has it been treated / any investigations
- OPQRSTAAA
- ROS: fever, recent travel, sick contacts; wheeze, shortness of breath, chest pain; GI symptoms
Physical exam:
- Vitals, weight
- H&N exam –> rhinitis, signs of AR, polyps, etc
- Cardiac & resp exam
Investigations:
- Chest xray, pulmonary function tests, bloodwork, sutum sample
Management:
Px:
Height/weight/BMI
CV/Resp
Look for other allergic conditions - AR, AD
Ix:
CBC + eos
Renal, LFTs
ANCAs
Sputum
Total IgE
Skin prick testing
CXR
Full PFT with DLCO
- You’re seeing a 25 year old woman with worsening asthma allergic rhinitis joint pain and foot drop.
a. Please outline the diagnosis and treatment of eosinophilic granulomatosis with polyangiitis.
Investigations:
- CBCD
- ANCAs
- CRP/ESR
- Renal function
- troponin
- CXR
UTD:
●Serum cardiac troponin
●Serum N-terminal pro-brain natriuretic peptide (NT-proBNP)
●Serology for Toxocara, Strongyloides, filaria, Trichinella, and other parasites depending on the locale
●Immunoassay for human immunodeficiency virus (HIV) infection
●Serum vitamin B12
●Serum tryptase
●Peripheral blood smear to identify blasts or dysplastic eosinophils
●Urinalysis
Diagnostic criteria (need 4/6):
1. Paranasal sinus abnormality
2. Asthma (Hx of wheezing or expiratory wheezing on exam is enough)
3. Migratory or transient pulmonary opacities on imaging
4. Mononeuropathy (including multiplex) or polyneuropathy
5. >10% eosinophils on the differential leukocyte count. Usually >1.5
6. Biopsy containing a blood vessel showing the accumulation of eosinophils in extravascular areas
Treatment:
- Generally steroids
- Depending on five factor score, if 2 and above, add on cyclophosphamide (or any cardiac features)
Assess based on the FFS
Age >65, renal involvement (Cr >150), CV involvement, GI involvement, absence of ENT symptoms
Steroids 0.5-1mg/kg/d x 6-12 weeks until remission
If FFS>2, or >1 with CNS or CV nvolvement - add on cyclophosphamide
After remission –> Tx with maintenance of AZA or MTX x 12-18 months
If no effect, can consider add on with mepolizumab
- Discuss the management of asthma in pregnancy
- DDX of SOB in pregnancy
Management of asthma in pregnancy:
- Ensure good control because of poor outcomes of uncontrolled asthma in pregnancy
- Effectively same as outside of preg - except focus on choosing meds that are cat B over cat C
- Budesonide, omalizumab = cat B
- Budesonide preferred inhaler in preg
Uncontrolled asthma in preg related to risk of maternal and fetal mortality, thought to outweigh risk of OCS use in preg
Risk of OCS on baby/pregnancy:
Congenital malformations - namely cleft palate - usually less significant risk after first trimester
Preterm birth and low birth weight
GDM
Preeclampsia
GINA 2022:
Although there is a general concern about any medication use in pregnancy, the advantages of actively treating asthma in pregnancy markedly outweigh any potential risks of usual controller and reliever medications49 (Evidence A). For this reason, using medications to achieve good symptom control and prevent exacerbations is justified even when their safety in pregnancy has not been unequivocally proven. Use of ICS, beta2-agonists, montelukast or theophylline is not associated with an increased incidence of fetal abnormalities
On balance, given the evidence in pregnancy and infancy for adverse outcomes from exacerbations during pregnancy49 (Evidence A), including due to lack of ICS or poor adherence,103 and evidence for safety of usual doses of ICS and LABA516 (Evidence A), a low priority should be placed on stepping down treatment (however guided) until after delivery (Evidence D), and ICS should not be stopped in preparation for pregnancy or during pregnancy (Evidence C).
UTD
Current guidelines emphasize the following points [9-12]:
●All patients should have access to an inhaler for quick relief of asthma symptoms. Choices include a short-acting beta-agonist (eg, albuterol) or a combination inhaler with formoterol and a low-dose inhaled glucocorticoid (eg, formoterol-budesonide).
●For patients with mild persistent or more severe asthma, inhaled glucocorticoids reduce exacerbations during pregnancy, and cessation of inhaled glucocorticoids during pregnancy increases the risk of an exacerbation. Budesonide has been the preferred inhaled glucocorticoid for use during pregnancy, as more published gestational human data are available for that medication [13,14]. However, other inhaled glucocorticoids could be continued if the patient was well-controlled on one of these medications prior to pregnancy, and more recent data for fluticasone have been reassuring regarding the risk for low birth weight (<2500 grams), small for gestational age (<10th percentile for babies of same gestational age), preterm birth (<37 weeks) [15], and major congenital malformations [16].
●Salmeterol has been recommended as the inhaled long-acting beta agonist of choice in the United States due to the longer duration of clinical experience with this agent compared with formoterol. However, retrospective cohort studies provide reassuring data for both salmeterol and formoterol [15,17]. Neither of these agents should be used in asthma without an inhaled glucocorticoid.
●Although it is not the preferred therapy, a leukotriene modifier (montelukast or zafirlukast) could be considered as an alternative for mild persistent asthma or as add-on therapy to inhaled glucocorticoids, especially for patients who have shown a uniquely favorable response to this class of agents prior to pregnancy. More pregnancy data are available for montelukast than zafirlukast. (See ‘Leukotriene modifiers’ below.)
What is a differential diagnosis for shortness of breath in pregnancy
DDX - similar to not pregnant, extras:
Physiologic dyspnea of pregnancy
Vasc - cardiomyopathy, anemia, PE, PTX, Hemorrhage
17 year old male is admitted to the ICU with a severe asthma attack after taking NSAIDs. He’s been on pulmicort 1600 micrograms a day, ventolin PRN, Flonase, and prednisone 10 mg. Advil was not an issue in the past. He has a cat, is a non-smoker and has nasal polyps on exam. Discuss your approach.
Likely aspirin exacerbated respiratory disease (AERD)
Indications for ASA desensitization:
- poorly controlled symptoms despite medical therapy
Once patient is more stable and well, ensure he is on Singulair 10 mg daily x 3 days
then bring back for 2 day protocol for ASA desensitization - up to about 325 mg in office. Once at 325 mg, can increase at home until 325 mg BID or 650 mg BID. Keep on this for at least 3-4 months and if no improvement, d/c ASA.
Other therapy options include putting him on a biologic like Dupixent
Additional information:
HISTORY
- asthma - go through asthma hx, including asthma control questions, asthma severity questions, inhaler compliance/technique
- Hx of rhinitis/sinusitis - what are symptoms, ?CPODS, what medication used
- Hx of rxn with NSAIDs - any urticaria/angioedema, how soon after taking the medication did the resp symptoms occur, one NSAID or multiple NSAIDs, tolerate acetaminophen/celecoxib in the past
- Big 5
Px - ht/weight/bmi
HEENT, CV, Resp, signs of other allergic conditions
Ix:
CBC + eos
ANCAs
CT chest/CXR
Full PFTs with DLCO
Skin testing
Tx:
- Asthma - optimize
- Nonpharm - education, technique, medicalert, avoid triggers, action plan
- Pharm - escalate tx, should also add on LTRA
- Rhinitis/sinusitis - optimize
- Increase INS, if no effect, consider biologic/surgery
- NSAIDs - avoid all COX1 inhibitors, celecoxib/acetaminophen OK (celecoxib first dose should still be given in office)
- ASA desensitization is option if pt requires ASA down the line (ie rheum condition, cardiac condition)
- Give LTRA at least 3 days prior, continue all other meds
- Start at 30-41.5mg, double every 3 hrs until reaching 162 mg
- Can tx symptoms if they occur during process:
Bronchospasm - ventolin, nasal obstruction - decongestants, ocular sx - AH, laryngospasm - Epi
- You’re seeing a 19 year old female with shortness of breath and chronic sputum production that has been increasing for the last 6 months.
a. Please provide a history physical exam
b. Please provide a differential diagnosis and investigations.
c. Please outline your management of a patient with CF – including appropriate referrals.
DDx (SOB + Sputum production):
- Infection –> ABPA, fungal infection
- Emphysema, COPD
- UACS
- Reflux
- Asthma
- AI –> ?sarcoidosis, vasculitis
DDx SOB:
Resp - Asthma, AERD, OA, RADS, ILD, CF, ILO
Immune - HP
Vasc - EGPA, GPA, MPA, Pulm HTN, PE,
CV - myocarditis/pericarditis, CHF
Infx - PNA (bacterial, eos), URTI, TB, fungal (e.g. EGPA) infxn
AI - ILD related to AI (SLE, RA, SS), sarcoidosis
Malignancy - Lung Ca
Infectious: HIV (PCP), travel, sick contacts, TB, fungal infection
Others: Deconditioning
Invx:
Bloodwork
Imaging –> CXR +/- CT
Pulmonary function testing
Sputum samples
Management
- Referral to CF clinic/team
- Nutrition / Dietician referral - should be on pancreatic enzymes
- Glucose levels need to be monitored as they are at risk of diabetes
- Respirology referral - should be seen regularly to get sputum samples
- Physiotherapy –> should do exercises to clear mucous etc; some are on inhaled dornase
- Sometimes on inhaled tobra
- Treat asthma
Nonpharm - education/support groups, medicalert
Supportive tx - Nutritional care, vitamin supplementation
Genetic assessment to see if they qualify for CFTR modulator therapy
Resp tx:
Inhaled dornase alfa
Inhaled saline
Chest physio/resp therapy
PRN SABA
Can consider: ICS, azithromycin
Abx if exacerbation
Please provide a differential diagnosis for upper lobe ILD and lower lobe ILD. What are the mimics?
**Upper lobe ILD (“FASSTEN”) **- Farmer’s lung (HP), ankylosing spondylitis, silicosis/sarcoidosis, TB, eosinophilic granuloma, neurofibromatosis
Lower lobe ILD (“BAD RASH”) - bronchiectasis, aspiration, drugs (e.g. hydralazine, nitrofurantoin, INH, amiodarone), rheum disease (e.g. RA), asbestos, Scleroderma, harmen reich (interstitial pulmonary fibrosis)
You’re seeing a 25 year old male with uncontrolled steroid dependent asthma. Found to have migrating infiltrates on his chest x-ray and eosinophils of 1.5.
a. Please provide a history and physical exam
b. Please outline your approach including investigations, diagnosis, and management.
c. What are the diagnostic criteria for ABPA?
d. What are the stages of ABPA and what is its pathophysiology?
e. What is the management of ABPA
DDX:
- severe asthma
- Infection
- Fungal –> ABPA
- Eosinophilic pneumonia
- Vasculitis
- HES
- Bronchiectasis?
- Immunodeficiency e.g. CVID
- ?CF
Investigations:
- Chest imaging –> CXR +/- CT
- Pulmonary function testing
- Bloodwork –> CBCD, total IgE, IgE, ESR/CRP aspergillus +/- precipitans, SPT, ANCAs
ABPA diagnostic criteria:
1. CF or asthma AND
2. BOTH must be present: a) serum aspergillus IgE elevated or skin test positive b) elevated total IgE > 1000
3. At least two of: a) precipitating serum antibodies or elevated IgG to aspergillus b) radiographic pulmonary opacities consistent with ABPA c) total eos > 500 cells/microL in GC naive patients
Stages of ABPA
1. acute - elevated IgE, pulm opacities
2. remission - normal IgE, no pulm opacities
3. exacerbation - elevated IgE, pulm opacities
4. steroid dependent - elevated/normal IgE, infiltrates present intermittently
5. end stage/fibrotic - fibrotic, bullous, cavitary lung lesions, IgE may be normal
Management
Corticosteroids are the mainstay of treatment
Decreases inflammation but does not inhibit growth of aspergillus
Associated with decreased wheezing, serum total IgE levels, eosinophilia, and resolution of parenchymal opacities
associated side effects
Asthma
ICS+/-LABA may help control the underlying asthma, but ICS do not have documented efficacy in preventing acute episodes of ABPA
Acute ABPA (Stage I)
UTD recommends: Prednisone 0.5mg/kg daily (higher dose [e.g. 40-60mg daily] if acute flare) x 14 days, then reduce by half and taper until discontinuation at 3 months.
There are other protocols*
*Monitor for reduction in serum IgE, radiographic remission, and clinical improvement
One article suggested serum total IgE q8-12 wks x 1 year, then annually
Repeat CT scan in 4-8 wks to ensure resolution of pulmonary opacities
PFTs to ensure improvement
Anti-fungal
IDSA recommends using itraconazole (1st line) or voriconazole (2nd line) as part of the initial therapy for acute ABPA.
UTD recommends using antifungals only in patients unable to taper OCS.
2 RCTs showed that itraconazole x 16 weeks in addition to OCS is effective for Tx of ABPA
Voriconazole has less GI side effects and has better bioavailability than itraconazole, but only 1 case series and 1 small unblinded RCT have assessed voriconazole in ABPA
Dosing (for adults):
Itraconazole loading dose of 200mg tid x 3 days, followed by 200mg bid x 16 weeks (from UTD)
Voriconazole loading dose of 400mg bid x 2 doses, followed by maintenance dose of 200mg PO bid x 16 weeks (from UTD)
Monitor:
Liver enzymes (for evidence of hepatotoxicity)
Itraconazole serum level (to ensure appropriate absorption)
Voriconazole serum level (to ensure appropriate absorption and avoid toxicity)
Clinical response should be monitored by following IgE levels q 1-2 months, and watching for resolution of radiographic infiltrates
Remission usually accompanied by a 35% drop in IgE
May not be as great a drop in those with less significant elevations in IgE (<2500 IU/mL)
ABPA exacerbation
Treat with glucocorticoids
Some may use asthma biologics in patients with ABPA & recurrent exacerbations or inability to taper off steroids (and despite anti-fungals, optimizing asthma therapies)
E.g. Mepolizumab, benralizumab, omalizumab, dupilumab
Limited data on biologics
