asthma case study mcq

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Acute asthma – Questions

Common acute asthma exam questions for medical finals, OSCEs and MRCP PACES

Question 1. presentation of asthma.

• Chest tightness

List the features that characterise a moderate asthma attack

• Worsening symptoms
• No features of acute severe asthma
• PEFR >50% of best/predicted

List the features that characterise an acute severe asthma attack

• Inability to complete sentences in a single breath
• PEFR <50% of best/predicted
• RR >/= 25
• HR >/= 110

List the features that characterise a life-threatening asthma attack

• Poor respiratory effort
• Silent chest
• Hypotension
• Reduced conscious level
• PEFR <33% of best/predicted
• SpO2 <92%
• PaO2 <8 kPa
• Normal PaCO2 = 4.6-6.0 kPa

Question 2. Management of asthma

• Sit upright.
• Salbutamol 5 mg and ipratropium bromide 0.5 mg via oxygen-driven nebuliser

Should patients display an inadequate response to initial therapy, what further treatments can be given?

• Repeat salbutamol 5 mg via oxygen-driven nebuliser if inadequate response and give prednisolone 40 mg orally (PO) or hydrocortisone 100 mg IV if unable to swallow
• Consider ‘back-to-back’ salbutamol nebulisers or continuous salbutamol nebuliser 5-10 mg/h if inadequate response
• Consider magnesium sulphate 1.2-2.0 g IV over 20 minutes in life-threatening or near-fatal asthma or in acute severe asthma with an inadequate response to initial therapy
• Consider aminophylline 5 mg/kg IV loading dose over 20 minutes followed by 0.5 mg/kg/h IV maintenance dose in life-threatening or near-fatal asthma with an inadequate response to initial therapy

What features would concern you on an ABG in acute asthma

• PaCO2 >4.6 kPa

What are the indications for requesting a CXR in acute asthma?

• Suspected pneumothorax or consolidation
• Life-threatening asthma
• Failure to respond to initial therapy
• Requirement for ventilation

What criteria would mandate admission for acute asthma?

• Near-fatal asthma
• Acute severe asthma persisting despite initial therapy

Question 3. Discharging patients with asthma

• PEFR >75% of best/predicted 1 hour after initial therapy

What would you check before discharge?

• Give prednisolone 40 mg once daily for five days
• Check inhaler technique and ensure sufficient, in-date inhaled bronchodilator
• Arrange follow up with GP in two days

[MCQ] Asthma- Part 1

I. start the exam by click the “start” button, asthma- part 1.

See all quizzes of Asthma at here:

Asthma- Part 1 | Asthma- Part 2 | Asthma- Part 3 | Asthma- Part 4 | Asthma- Part 5 | Asthma- Part 6 | Asthma- Part 7 | Asthma- Part 8

1.Which of the following statements about asthma is false ? A. 10 – 12% adults and 15% children affected by asthma B. Peak age of presentation is 3 years C. Sex ratio in adults is equal D. None of the above 2. Which of the following about asthma is false ? A. Most patients with asthma in affluent countries are atopic B. Severity of asthma varies significantly within a patient C. Onset of asthma in adulthood rarely become permanently asymptomatic D. Inflammatory disease of airways 3. Asthma is a disease of ? A. Large airway B. Medium airway C. Terminal bronchiole D. Respiratory bronchiole 4.  The term “atopy” in Greek means ? A. Inert B. Out of place C. Explosive D. Mischief 5. Allergic rhinitis is found in what percentage of asthmatic patients ? A. ~ 40 % B. ~ 60 % C. ~ 80 % D. ~ 100 % 6.  Which of the following is called ‘house-dust mite’ ? A. Dermatophagoides pteronyssinus B. Betula verrucosa C. Phleum pratense D. Ambrosia artemisiifolia 7.  Atopy is due to the genetically determined production of ? A. IgA antibody B. IgE antibody

C. IgG antibody D. IgM antibody 8.  Which of the following statements about nonatopic or intrinsic asthma is false ? A. Negative skin test to common inhalant allergens B. Normal serum IgE levels C. Have mild asthma D. Commonly have nasal polyps 9.  Novel gene associated with asthma is ? A. ADAM-33 B. DPP-10 C. GPRA D. All of the above 10.  Which of the following is strongly linked with asthma in genetic association studies ? A. TNFAIP3 B. ORMDL3 C. PTPN2 D. IL23R 11.  Airway mucosa in asthma is infiltrated with ? A. Activated eosinophils B. T lymphocytes C. Activated mucosal mast cells D. All of the above 12.  In asthma, characteristic histologic finding in airways is ? A. Normal parenchymal attachments B. Thickened airway smooth muscle C. Goblet cell metaplasia D. Thickening of basement membrane 13.  Thickening of basement membrane in airway mucosa due to subepithelial collagen deposition is a feature of ? A. Atopic asthma

B. Nonatopic asthma C. Aspirin-sensitive asthma D. All of the above 14.  Which of the following is a histopathologic feature of a small airway in fatal asthma ? A. Goblet cell aplasia B. Goblet cell dysplasia C. Goblet cell metaplasia D. Any of the above 15.  Mast cell is the key effector cell of the biologic response in ? A. Allergic rhinitis B. Urticaria C. Anaphylaxis D. All of the above 16.  Human mast cells originate from ? A. CD34+ B. CD 4+ C. CD 8+ D. All of the above 17.  In asthmatic patients, mast cells are localized to airway ? A. Epithelial cells B. Fibroblasts C. Smooth muscle D. Parenchyma 18.  Activated mast cells are found at the airway surface in ? A. Asthma patients B. Normal subjects C. Patients with eosinophilic bronchitis D. All of the above 19.  Mast cells release which of the following bronchoconstrictor  mediators ? A. Histamine B. Prostaglandin D 2

C. Cysteinyl-leukotrienes D. All of the above 20.  In “sensitization”, IgE gets attached to human mast cells and ? A. Basophils B. Eosinophils C. Monocytes D. Lymphocytes 21.  Which chain of Fc  RI is solely responsible for IgE binding ? A.  chain B.  chain C.  chain D. All of the above 22.  Bronchial asthma is associated with increased levels of ? A. Leukotrienes B. PGI 1 C. PGI 2 D. Thromboxane

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Quiz Answers

Answer Key Asthma Questions

1.) A child enters the office with the following symptoms, which symptom would NOT be associated with an asthma diagnosis?

Asthma symptoms are expiratory wheezing, chest tightness, increased heart rate, shortness of breath, anxiousness, difficulty speaking in full sentences, to name a few. Stridor is most likely associated with an upper airway obstruction or croup.

2.) What is the main function of the lungs?

b. supply adequate oxygen to the blood and remove carbon dioxide from the blood

The lungs supply oxygen to the blood and remove carbon dioxide through the processes of ventilation and perfusion.  The main function of the heart is to pump blood throughout the body via the circulatory system.  The kidneys are responsible for excreting waste through the production of urine.

3.) What is true of childhood asthma?

c. It presents more severely in smaller children due to their smaller airway diameter.

Childhood asthma is the most prevalent chronic childhood disease.  It is a type I hypersensitivity reaction.   The presentation of bronchoconstriction and airway hyperresponsiveness is reversible.

4.) Which immunoglobulin mediates the asthmatic response?

IgE is the immunoglobulin responsible for allergy-related immune responses, including asthma.  IgG protects against viral and bacterial infections.  IgM is the first responder to new infections in the body.  IgA are most commonly found in mucous membranes.

5.) True or False: The early asthmatic response is categorized by airway hyperresponsiveness and manifests 4-8 hours after introduction to antigen.

The early asthmatic response is characterized by acute bronchoconstriction that peaks at 30 minutes and lasts from 1-3 hours.  The late asthmatic response is categorized by airway hyperresponsiveness and manifests 4-8 hours after introduction to antigen.

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Case Study: Managing Severe Asthma in an Adult

—he follows his treatment plan, but this 40-year-old male athlete has asthma that is not well-controlled. what’s the next step.

By Kirstin Bass, MD, PhD Reviewed by Michael E. Wechsler, MD, MMSc

This case presents a patient with poorly controlled asthma that remains refractory to treatment despite use of standard-of-care therapeutic options. For patients such as this, one needs to embark on an extensive work-up to confirm the diagnosis, assess for comorbidities, and finally, to consider different therapeutic options.

Case presentation and patient history

Mr. T is a 40-year-old recreational athlete with a medical history significant for asthma, for which he has been using an albuterol rescue inhaler approximately 3 times per week for the past year. During this time, he has also been waking up with asthma symptoms approximately twice a month, and has had three unscheduled asthma visits for mild flares. Based on the  National Asthma Education and Prevention Program guidelines , Mr. T has asthma that is not well controlled. 1

As a result of these symptoms, spirometry was performed revealing a forced expiratory volume in the first second (FEV1) of 78% predicted. Mr. T then was prescribed treatment with a low-dose corticosteroid, fluticasone 44 mcg at two puffs twice per day. However, he remained symptomatic and continued to use his rescue inhaler 3 times per week. Therefore, he was switched to a combination inhaled steroid and long-acting beta-agonist (LABA) (fluticasone propionate 250 mcg and salmeterol 50 mcg, one puff twice a day) by his primary care doctor.

Initial pulmonary assessment Even with this step up in his medication, Mr. T continued to be symptomatic and require rescue inhaler use. Therefore, he was referred to a pulmonologist, who performed the initial work-up shown here:

• Spirometry, pre-albuterol: FEV1 79%, post-albuterol: 12% improvement
• Methacholine challenge: PC 20 : 1.0 mg/mL
• Chest X-ray: Within normal limits

Continued pulmonary assessment His dose of inhaled corticosteroid (ICS) and LABA was increased to fluticasone 500 mcg/salmeterol 50 mcg, one puff twice daily. However, he continued to have symptoms and returned to the pulmonologist for further work-up, shown here:

• Chest computed tomography (CT): Normal lung parenchyma with no scarring or bronchiectasis
• Sinus CT: Mild mucosal thickening
• Complete blood count (CBC): Within normal limits, white blood cells (WBC) 10.0 K/mcL, 3% eosinophils
• Immunoglobulin E (IgE): 25 IU/mL
• Allergy-skin test: Positive for dust, trees
• Exhaled NO: Fractional exhaled nitric oxide (FeNO) 53 parts per billion (pbb)

Assessment for comorbidities contributing to asthma symptoms After this work-up, tiotropium was added to his medication regimen. However, he remained symptomatic and had two more flares over the next 3 months. He was assessed for comorbid conditions that might be affecting his symptoms, and results showed:

• Esophagram/barium swallow: Negative
• Esophageal manometry: Negative
• Esophageal impedance: Within normal limits
• ECG: Within normal limits
• Genetic testing: Negative for cystic fibrosis, alpha1 anti-trypsin deficiency

The ear, nose, and throat specialist to whom he was referred recommended only nasal inhaled steroids for his mild sinus disease and noted that he had a normal vocal cord evaluation.

Following this extensive work-up that transpired over the course of a year, Mr. T continued to have symptoms. He returned to the pulmonologist to discuss further treatment options for his refractory asthma.

Diagnosis Mr. T has refractory asthma. Work-up for this condition should include consideration of other causes for the symptoms, including allergies, gastroesophageal reflux disease, cardiac disease, sinus disease, vocal cord dysfunction, or genetic diseases, such as cystic fibrosis or alpha1 antitrypsin deficiency, as was performed for Mr. T by his pulmonary team.

Treatment options When a patient has refractory asthma, treatment options to consider include anticholinergics (tiotropium, aclidinium), leukotriene modifiers (montelukast, zafirlukast), theophylline, anti-immunoglobulin E (IgE) antibody therapy with omalizumab, antibiotics, bronchial thermoplasty, or enrollment in a clinical trial evaluating the use of agents that modulate the cell signaling and immunologic responses seen in asthma.

Treatment outcome Mr. T underwent bronchial thermoplasty for his asthma. One year after the procedure, he reports feeling great. He has not taken systemic steroids for the past year, and his asthma remains controlled on a moderate dose of ICS and a LABA. He has also been able to resume exercising on a regular basis.

Approximately 10% to 15% of asthma patients have severe asthma refractory to the commonly available medications. 2  One key aspect of care for this patient population is a careful workup to exclude other comorbidities that could be contributing to their symptoms. Following this, there are several treatment options to consider, as in recent years there have been several advances in the development of asthma therapeutics. 2

Treatment options for refractory asthma There are a number of currently approved therapies for severe, refractory asthma. In addition to therapy with ICS or combination therapies with ICS and LABAs, leukotriene antagonists have good efficacy in asthma, especially in patients with prominent allergic or exercise symptoms. 2  The anticholinergics, such as tiotropium, which was approved for asthma in 2015, enhance bronchodilation and are useful adjuncts to ICS. 3-5  Omalizumab is a monoclonal antibody against IgE recommended for use in severe treatment-refractory allergic asthma in patients with atopy. 2  A nonmedication therapeutic option to consider is bronchial thermoplasty, a bronchoscopic procedure that uses thermal energy to disrupt bronchial smooth muscle. 6,7

Personalizing treatment for each patient It is important to personalize treatment based on individual characteristics or phenotypes that predict the patient's likely response to treatment, as well as the patient's preferences and practical issues, such as adherence and cost. 8

In this case, tiotropium had already been added to Mr. T's medications and his symptoms continued. Although addition of a leukotriene modifier was an option for him, he did not wish to add another medication to his care regimen. Omalizumab was not added partly for this reason, and also because of his low IgE level. As his bronchoscopy was negative, it was determined that a course of antibiotics would not be an effective treatment option for this patient. While vitamin D insufficiency has been associated with adverse outcomes in asthma, T's vitamin D level was tested and found to be sufficient.

We discussed the possibility of Mr. T's enrollment in a clinical trial. However, because this did not guarantee placement within a treatment arm and thus there was the possibility of receiving placebo, he opted to undergo bronchial thermoplasty.

Bronchial thermoplasty  Bronchial thermoplasty is effective for many patients with severe persistent asthma, such as Mr. T. This procedure may provide additional benefits to, but does not replace, standard asthma medications. During the procedure, thermal energy is delivered to the airways via a bronchoscope to reduce excess airway smooth muscle and limit its ability to constrict the airways. It is an outpatient procedure performed over three sessions by a trained physician. 9

The effects of bronchial thermoplasty have been studied in several trials. The first large-scale multicenter randomized controlled study was  the Asthma Intervention Research (AIR) Trial , which enrolled patients with moderate to severe asthma. 10  In this trial, patients who underwent the procedure had a significant improvement in asthma symptoms as measured by symptom-free days and scores on asthma control and quality of life questionnaires, as well as reductions in mild exacerbations and increases in morning peak expiratory flow. 10  Shortly after the AIR trial, the  Research in Severe Asthma (RISA) trial  was conducted to evaluate bronchial thermoplasty in patients with more severe, symptomatic asthma. 11  In this population, bronchial thermoplasty resulted in a transient worsening of asthma symptoms, with a higher rate of hospitalizations during the treatment period. 11  Hospitalization rate equalized between the treatment and control groups in the posttreatment period, however, and the treatment group showed significant improvements in rescue medication use, prebronchodilator forced expiratory volume in the first second (FEV1) % predicted, and asthma control questionnaire scores. 11

The AIR-2  trial followed, which was a multicenter, randomized, double-blind, sham-controlled study of 288 patients with severe asthma. 6  Similar to the RISA trial, patients in the treatment arm of this trial experienced an increase in adverse respiratory effects during the treatment period, the most common being airway irritation (including wheezing, chest discomfort, cough, and chest pain) and upper respiratory tract infections. 6

The majority of adverse effects occurred within 1 day of the procedure and resolved within 7 days. 6  In this study, bronchial thermoplasty was found to significantly improve quality of life, as well as reduce the rate of severe exacerbations by 32%. 6  Patients who underwent the procedure also reported fewer adverse respiratory effects, fewer days lost from work, school, or other activities due to asthma, and an 84% risk reduction in emergency department visits. 6

Long-term (5-year) follow-up studies have been conducted for patients in both  the AIR  and  the AIR-2  trials. In patients who underwent bronchial thermoplasty in either study, the rate of adverse respiratory effects remained stable in years 2 to 5 following the procedure, with no increase in hospitalizations or emergency department visits. 7,12  Additionally, FEV1 remained stable throughout the 5-year follow-up period. 7,12  This finding was maintained in patients enrolled in the AIR-2 trial despite decreased use of daily ICS. 7

Bronchial thermoplasty is an important addition to the asthma treatment armamentarium. 7  This treatment is currently approved for individuals with severe persistent asthma who remain uncontrolled despite the use of an ICS and LABA. Several clinical trials with long-term follow-up have now demonstrated its safety and ability to improve quality of life in patients with severe asthma, such as Mr. T.

Severe asthma can be a challenge to manage. Patients with this condition require an extensive workup, but there are several treatments currently available to help manage these patients, and new treatments are continuing to emerge. Managing severe asthma thus requires knowledge of the options available as well as consideration of a patient's personal situation-both in terms of disease phenotype and individual preference. In this case, the patient expressed a strong desire to not add any additional medications to his asthma regimen, which explained the rationale for choosing to treat with bronchial thermoplasty. Personalized treatment necessitates exploring which of the available or emerging options is best for each individual patient.

Published: April 16, 2018

• 1. National Asthma Education and Prevention Program: Asthma Care Quick Reference.
• 2. Olin JT, Wechsler ME. Asthma: pathogenesis and novel drugs for treatment. BMJ . 2014;349:g5517.
• 3. Boehringer Ingelheim. Asthma: U.S. FDA approves new indication for SPIRIVA Respimat [press release]. September 16, 2015.
• 4. Peters SP, Kunselman SJ, Icitovic N, et al. Tiotropium bromide step-up therapy for adults with uncontrolled asthma. N Engl J Med . 2010;363:1715-1726.
• 5. Kerstjens HA, Engel M, Dahl R. Tiotropium in asthma poorly controlled with standard combination therapy. N Engl J Med . 2012;367:1198-1207.
• 6. Castro M, Rubin AS, Laviolette M, et al. Effectiveness and safety of bronchial thermoplasty in the treatment of severe asthma: a multicenter, randomized, double-blind, sham-controlled clinical trial. Am J Respir Crit Care Med . 2010;181:116-124.
• 7. Wechsler ME, Laviolette M, Rubin AS, et al. Bronchial thermoplasty: long-term safety and effectiveness in patients with severe persistent asthma. J Allergy Clin Immunol . 2013;132:1295-1302.
• 8. Global Initiative for Asthma: Pocket Guide for Asthma Management and Prevention (for Adults and Children Older than 5 Years).
• 10. Cox G, Thomson NC, Rubin AS, et al. Asthma control during the year after bronchial thermoplasty. N Engl J Med . 2007;356:1327-1337.
• 11. Pavord ID, Cox G, Thomson NC, et al. Safety and efficacy of bronchial thermoplasty in symptomatic, severe asthma. Am J Respir Crit Care Med . 2007;176:1185-1191.
• 12. Thomson NC, Rubin AS, Niven RM, et al. Long-term (5 year) safety of bronchial thermoplasty: Asthma Intervention Research (AIR) trial. BMC Pulm Med . 2011;11:8.

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Pathophysiology, epidemiology, risk factors, clinical presentation.

• DESIRED OUTCOMES
• TREATMENT: GENERAL APPROACH
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Source : Sorkness CA, Blake KV. Asthma. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach . 10th ed. New York, NY: McGraw-Hill; 2017. http://accesspharmacy.mhmedical.com/content.aspx?bookid=1861&sectionid=146058008 . Accessed April 13, 2017.

Chronic inflammatory disorder of airways that causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing.

Genetic factors.

Environmental exposures (see Risk Factors)

Major characteristics:

Airflow obstruction (related to bronchospasm, edema, and hypersecretion)

Bronchial hyperresponsiveness (BHR)

Airway inflammation.

Inhaled allergen causes activation of B lymphocytes, mast cells, and macrophages, which release proinflammatory mediators such as histamine and eicosanoids that induce contraction of airway smooth muscle, mucus secretion, vasodilation, exudation, and edema with reduced mucus clearance.

Activation of eosinophils, T lymphocytes, basophils, neutrophils, and macrophages cause further release of inflammatory mediators such as leukotrienes, interleukins, histamine, platelet-activating factor (PAF), and chemotactic factors.

Affects 25.7 million persons in the United States.

Most common chronic childhood disease, affecting approximately 7 million children.

Accounts for 1.6% of ambulatory care visits (10.6 million physician office visits and 1.2 million hospital outpatient visits).

Resulted in 479,000 hospitalizations and 2.1 million emergency department (ED) visits in 2009.

Accounts for >14.4 million missed school days per year.

Genetic predisposition.

Socioeconomic status.

Family size.

Exposure to secondhand tobacco smoke in infancy and in utero.

Allergen exposure.

Ambient air pollution.

Urbanization.

Respiratory syncytial virus (RSV) and rhinovirus infection.

Decreased exposure to common childhood infectious agents.

SIGNS AND SYMPTOMS

Chronic asthma.

Symptoms: Episodic dyspnea with wheezing, chest tightness, and coughing that may occur spontaneously, with exercise, or after exposure to known allergens.

Signs: Expiratory wheezing; dry, hacking cough; atopy (eg, allergic rhinitis, eczema)

Can vary in frequency from intermittent to chronic daily symptoms.

Severity determined by lung function, symptoms, nighttime awakenings, and interference with normal activity.

Acute severe asthma.

Symptoms: Anxiousness with acute distress and complaints of severe dyspnea, shortness of breath, and chest tightness unresponsive to usual measures.

Signs: Expiratory and inspiratory wheezing; dry, hacking cough; tachypnea; tachycardia; pallor or cyanosis; hyperinflated chest with intercostal and supraclavicular retractions.

MEANS OF CONFIRMATION AND DIAGNOSIS

History of recurrent episodes of coughing, wheezing, chest tightness, or shortness of breath and confirmatory spirometry.

May be family history of allergy or asthma, or patient symptoms of allergic rhinitis.

History of exercise or cold air precipitating symptoms during specific allergen seasons.

History of previous asthma exacerbations (eg, hospitalizations, intubations) and complicating illnesses (eg, cardiac disease, diabetes).

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