ASTHMA

Question 1

What is the next step if a patient with an asthma attack fails to improve after 1–2 hours of β2-agonist therapy?
A) Start intravenous corticosteroids
B) Intubate and start mechanical ventilation
C) Administer antibiotics
D) Discharge with increased inhaled corticosteroids

Answer 1

Answer:
A) Start intravenous corticosteroids

Rationale:
If a patient fails to respond to β2-agonist therapy within 1–2 hours, intravenous corticosteroids should be given to reduce airway inflammation and improve respiratory function. Intubation is reserved for severe respiratory failure, and antibiotics are only used if there is evidence of infection.

Question 2

Which of the following is a sign of impending respiratory failure in a patient with an asthma attack?
A) Hypocapnia (low Pco2)
B) Normal or near-normal Pco2
C) PEFR >80% of predicted
D) Increased inspiratory capacity

Answer 2

Answer:
B) Normal or near-normal Pco2

Rationale:
Most patients with asthma exacerbations present with hypocapnia (low Pco2) due to increased respiratory rate. If Pco2 normalizes or rises, it suggests that the patient is fatiguing and may be progressing to respiratory failure, requiring urgent intervention.

Question 3

Which treatment is considered to prevent the need for intubation in severe asthma exacerbations?
A) Noninvasive positive-pressure ventilation
B) High-dose antibiotics
C) High tidal volume mechanical ventilation
D) Beta-blockers

Answer 3

Answer:
A) Noninvasive positive-pressure ventilation

Rationale:
Noninvasive positive-pressure ventilation (NPPV) can be used in patients with severe asthma exacerbations who are experiencing respiratory exhaustion, helping to improve ventilation and prevent intubation. Antibiotics are only used if an infection is suspected, and high tidal volume ventilation is not recommended due to increased airway pressures.

Question 4

What is the recommended mechanical ventilation strategy for a patient with status asthmaticus?
A) High respiratory rates to remove CO2 quickly
B) Low respiratory rates with permissive hypercapnia
C) High tidal volumes to improve oxygenation
D) Routine bronchoscopy to remove mucus plugs

Answer 4

Answer:
B) Low respiratory rates with permissive hypercapnia

Rationale:
In mechanically ventilated patients with status asthmaticus, a low respiratory rate and low tidal volume strategy is used to avoid high airway pressures. Permissive hypercapnia (allowing CO2 to rise) helps prevent barotrauma while maintaining adequate oxygenation.

Question 5

What is a possible reason for exercise intolerance in asthma patients despite good overall control?
A) Poor inhaler technique
B) Exercise-induced bronchoconstriction
C) Excessive use of ICS
D) Overuse of antibiotics

Answer 5

Answer:
B) Exercise-induced bronchoconstriction

Rationale:
Even when asthma is well controlled, some patients experience exercise-induced bronchoconstriction (EIB), limiting their ability to exercise. This is managed with warming up, air conditioning in colder weather, and pre-treatment with a SABA.

Question 6

What is the preferred medication for preventing exercise-induced bronchoconstriction before occasional exercise?
A) Long-acting beta agonist (LABA)
B) Short-acting beta agonist (SABA)
C) Inhaled corticosteroids (ICS)
D) Oral corticosteroids (OCS)

Answer 6

Answer:
B) Short-acting beta agonist (SABA)

Rationale:
SABAs (e.g., albuterol) are the first-line choice for preventing exercise-induced bronchoconstriction when taken before exercise. While LABAs offer longer protection, their use alone is discouraged in asthma.

Question 7

Which additional intervention may help protect against exercise-induced bronchoconstriction in cold weather?
A) Using a nasal decongestant
B) Wearing a mask to warm and humidify air
C) Increasing inhaled corticosteroid doses before exercise
D) Taking an antihistamine before exercise

Answer 7

Answer:
B) Wearing a mask to warm and humidify air

Rationale:
Cold air can trigger bronchoconstriction, and wearing a mask helps condition the air before it reaches the lungs, reducing airway irritation.

Question 8

Which asthma medication has reassuring safety data for use during pregnancy?
A) Albuterol
B) PGF2-α
C) IL-5 inhibitors
D) Omalizumab

Answer 8

Answer:
A) Albuterol

Rationale:
Albuterol, along with beclomethasone, budesonide, and fluticasone, has extensive safety data in pregnancy. In contrast, PGF2-α should be avoided due to bronchoconstriction, and there is limited human data on IL-5 inhibitors and omalizumab.

Question 9

What is the potential risk of chronic oral corticosteroid (OCS) use during pregnancy?
A) Increased fetal lung development
B) Reduced maternal blood pressure
C) Neonatal adrenal insufficiency and low birth weight
D) Decreased risk of preeclampsia

Answer 9

Answer:
C) Neonatal adrenal insufficiency and low birth weight

Rationale:
Chronic OCS use during pregnancy is associated with neonatal adrenal insufficiency, low birth weight, preeclampsia, and a slight increase in cleft palate risk. However, poor asthma control poses a greater risk to the fetus and mother than these side effects.

Question 10

Which of the following should be avoided during pregnancy due to its bronchoconstrictive effects?
A) Montelukast
B) Ipratropium
C) PGF2-α
D) Salmeterol

Answer 10

Answer:
C) PGF2-α

Rationale:
Prostaglandin F2-α (PGF2-α) should be avoided in pregnancy because it is associated with bronchoconstriction and may worsen asthma symptoms.

Question 11

What is a key characteristic of aspirin-exacerbated respiratory disease (AERD)?
A) Late-onset asthma with type 2 inflammation and eosinophilia
B) Childhood-onset asthma that improves over time
C) Resistance to inhaled corticosteroids
D) Exclusively triggered by acetaminophen

Answer 11

Answer:
A) Late-onset asthma with type 2 inflammation and eosinophilia

Rationale:
AERD typically presents in adulthood with severe, difficult-to-control asthma, eosinophilia, sinusitis, and nasal polyposis. It is triggered by cyclooxygenase-1 inhibitors (e.g., aspirin, NSAIDs).

Question 12

Which of the following medications should be avoided in patients with AERD?
A) Acetaminophen
B) Celecoxib
C) Ibuprofen
D) Montelukast

Answer 12

Answer:
C) Ibuprofen

Rationale:
Ibuprofen is an NSAID that inhibits cyclooxygenase-1 (COX-1) and can trigger severe asthma exacerbations in AERD. Acetaminophen and COX-2 inhibitors (e.g., celecoxib) are generally tolerated, while montelukast is part of the recommended treatment.

Question 13

What is the primary biochemical mechanism underlying AERD?
A) Excessive production of PGE2
B) Overproduction of leukotrienes due to COX-1 inhibition
C) Deficiency of eosinophils
D) Direct mast cell degranulation

Answer 13

Answer:
B) Overproduction of leukotrienes due to COX-1 inhibition

Rationale:
AERD occurs due to COX-1 inhibition, which reduces PGE2 levels and leads to overproduction of leukotrienes—potent inflammatory mediators that drive asthma exacerbations and nasal polyposis.

Question 14

Which medication class is most commonly used to treat AERD?
A) Beta-blockers
B) Antihistamines
C) Leukotriene modifiers
D) Proton pump inhibitors

Answer 14

Answer:
C) Leukotriene modifiers

Rationale:
Since AERD is driven by leukotriene overproduction, leukotriene receptor antagonists (LTRAs), such as montelukast and zileuton, are effective treatments.

Question 15

Which biologic medication is emerging as a preferred treatment for AERD, potentially reducing the need for aspirin desensitization?
A) Omalizumab
B) Dupilumab
C) Salmeterol
D) Fluticasone

Answer 15

Answer:
B) Dupilumab

Rationale:
Dupilumab (anti–IL-4Rα) and IL-5 inhibitors are showing strong efficacy in AERD and are gradually replacing aspirin desensitization, except in patients who need chronic NSAID therapy.

Question 16

Which of the following is the most common complaint among patients with asthma?
A) Hemoptysis
B) Chest pain at rest
C) Episodes of wheezing, shortness of breath, and cough
D) Persistent fever

Answer 16

Answer:
C) Episodes of wheezing, shortness of breath, and cough

Rationale:
Asthma is characterized by recurrent episodes of wheezing, dyspnea, chest tightness, mucus production, and cough, often triggered by allergens, cold air, or exercise. Fever and hemoptysis are not characteristic features.

Question 17

Which feature distinguishes exercise-induced bronchoconstriction (EIB) from cardiac-related dyspnea?
A) Symptoms develop rapidly after exercise and resolve quickly
B) Symptoms develop slowly and resolve slowly unless treated
C) Symptoms always occur at rest
D) Symptoms are unaffected by β2-agonists

Answer 17

Answer:
B) Symptoms develop slowly and resolve slowly unless treated

Rationale:
EIB symptoms develop gradually after exercise begins and persist longer after stopping exercise, unlike cardiac dyspnea, which resolves quickly with rest. β2-agonists can relieve EIB symptoms.

Question 18

What spirometry finding is most suggestive of asthma?
A) Decreased FEV1/FVC ratio with reversible airflow limitation
B) Increased total lung capacity and decreased diffusing capacity
C) Normal FEV1 and FVC with increased FEV1/FVC ratio
D) Fixed airway obstruction with no reversibility after bronchodilator use

Answer 18

Answer:
A) Decreased FEV1/FVC ratio with reversible airflow limitation

Rationale:
Asthma is characterized by obstructive airway disease with reduced FEV1/FVC ratio. A ≥12% increase in FEV1 (and ≥200 mL improvement) after bronchodilator use confirms reversibility, distinguishing it from COPD.

Question 19

What is the most commonly used test to assess airway hyperresponsiveness in suspected asthma cases with normal spirometry?
A) Hypertonic saline challenge
B) Methacholine challenge test
C) Bronchoscopy with lavage
D) Lung biopsy

Answer 19

Answer:
B) Methacholine challenge test

Rationale:
Methacholine challenge testing assesses airway hyperresponsiveness, a hallmark of asthma. A ≥20% drop in FEV1 at a methacholine dose ≤400 μg is diagnostic. Other tests like hypertonic saline challenge are less commonly used.

Question 20

What defines a positive bronchodilator response in spirometry testing for asthma?
A) ≥12% increase in FEV1 and absolute increase of ≥200 mL after β2-agonist use
B) Decrease in FEV1 after bronchodilator administration
C) A fixed FEV1/FVC ratio below 0.7
D) Increase in total lung capacity after bronchodilator use

Answer 20

Answer:
A) ≥12% increase in FEV1 and absolute increase of ≥200 mL after β2-agonist use

Rationale:
A reversible increase in FEV1 ≥12% and ≥200 mL after bronchodilator administration confirms asthma. A fixed obstruction suggests COPD.

Question 21

What eosinophil count is typically associated with asthma in patients not treated with oral or high-dose ICS?
A) ≥150 cells/μL
B) ≥300 cells/μL
C) ≥500 cells/μL
D) ≥1000 cells/μL

Answer 21

Answer:
B) ≥300 cells/μL

Rationale:
Eosinophil counts ≥300 cells/μL are common in asthma patients not on systemic corticosteroids and correlate with disease severity. Extremely high eosinophil levels may indicate eosinophilic granulomatosis with polyangiitis or primary eosinophilic disorders.

Question 22

What is the primary clinical utility of measuring fraction of exhaled nitric oxide (FeNO) in asthma patients?
A) Differentiating between COPD and asthma
B) Detecting bacterial lung infections
C) Assessing eosinophilic inflammation and corticosteroid adherence
D) Measuring lung volume changes

Answer 22

Answer:
C) Assessing eosinophilic inflammation and corticosteroid adherence

Rationale:
FeNO is a marker of eosinophilic inflammation and is suppressed by ICS therapy. Elevated FeNO in a patient on moderate- to high-dose ICS suggests poor adherence or persistent type 2 inflammation.

Question 23

What FeNO level in an untreated asthma patient is indicative of eosinophilic inflammation?
A) >10 ppb
B) >20–25 ppb
C) >35–40 ppb
D) >60 ppb

Answer 23

Answer:
C) >35–40 ppb

Rationale:
In untreated patients, FeNO levels above 35–40 ppb suggest eosinophilic airway inflammation. In patients on ICS therapy, FeNO >20–25 ppb may indicate poor adherence or persistent type 2 inflammation.

Question 24

According to the GINA guidelines, what is the preferred treatment for a patient with infrequent asthma symptoms (e.g., 1–2 days per week or less)?
A) Regular daily low-dose ICS plus SABA as needed
B) Low-dose ICS-formoterol taken as needed
C) Medium-dose ICS-formoterol maintenance therapy
D) Low-dose ICS-LABA taken daily

Answer 24

Answer: B) Low-dose ICS-formoterol taken as needed
Rationale: The preferred treatment for patients with infrequent asthma symptoms is as-needed low-dose ICS-formoterol (GINA Track 1). This approach reduces the risk of exacerbations compared to using only a SABA, which is part of the alternative approach (Track 2).

Question 25

Which of the following is the preferred therapy for a patient who experiences asthma symptoms most days and wakes up at night due to asthma at least once a week? A) Low-dose ICS-formoterol as needed B) Medium-dose ICS-formoterol MART C) Low-dose ICS-LABA plus SABA as needed D) High-dose ICS plus SABA as needed

Answer 25

Answer: B) Medium-dose ICS-formoterol MART Rationale: Patients with frequent symptoms and nighttime awakenings have more severe asthma and require maintenance-and-reliever therapy (MART) with medium-dose ICS-formoterol. This approach helps control inflammation and provides quick relief when needed.

Question 26

In patients with asthma who experience symptoms less than 3–5 days per week with normal or mildly reduced lung function, what is the recommended treatment? A) Low-dose ICS-formoterol taken as needed B) High-dose ICS plus SABA as needed C) Daily medium-dose ICS plus SABA as needed D) Daily high-dose ICS-LABA plus SABA as needed

Answer 26

Answer: A) Low-dose ICS-formoterol taken as needed Rationale: For patients with mild asthma, using low-dose ICS-formoterol as needed is preferred because it provides both symptom relief and long-term control. Regular daily ICS is an alternative, but as-needed ICS-formoterol reduces the risk of exacerbations.

Question 27

Why is GINA Track 1 (ICS-formoterol as needed) preferred over GINA Track 2 (SABA plus ICS)? A) It reduces the risk of severe exacerbations B) It eliminates the need for inhaled corticosteroids C) It allows patients to rely only on short-acting beta-agonists D) It requires fewer inhaler doses per day

Answer 27

Answer: A) It reduces the risk of severe exacerbations Rationale: GINA Track 1, which uses ICS-formoterol as needed, is preferred because studies show it reduces the risk of severe asthma exacerbations compared to using SABA alone or daily ICS with SABA as needed (Track 2). It ensures that patients receive anti-inflammatory treatment whenever they use a reliever.

Question 28

Which of the following symptom patterns is most suggestive of asthma? A) Symptoms are constant and do not vary in intensity B) Symptoms worsen during exercise, laughter, or exposure to allergens C) Symptoms only occur during bacterial infections D) Symptoms improve without any treatment intervention

Answer 28

Answer: B) Symptoms worsen during exercise, laughter, or exposure to allergens Rationale: Asthma symptoms typically vary in intensity and frequency and are often triggered by exercise, allergens, laughter, or cold air. Constant symptoms or symptoms only during infections are less characteristic of asthma.

Question 29

Which of the following findings on spirometry indicates significant bronchodilator responsiveness in an adult patient? A) FEV₁ increases by 5% after bronchodilator administration B) FEV₁ or FVC increases by ≥12% and 200 mL after bronchodilator use C) FEV₁ decreases by 10% after bronchodilator administration D) FVC remains unchanged after bronchodilator administration

Answer 29

Answer: B) FEV₁ or FVC increases by ≥12% and 200 mL after bronchodilator use Rationale: A ≥12% and 200 mL increase in FEV₁ or FVC after using a bronchodilator indicates reversible airway obstruction, a hallmark feature of asthma. A 5% increase is not significant, and a decrease suggests worsening obstruction.

Question 30

Excessive daily variability in Peak Expiratory Flow (PEF) over two weeks is considered diagnostic of asthma when it exceeds what percentage in adults? A) 5% B) 10% C) 15% D) 20%

Answer 30

Answer: B) 10% Rationale: In adults, excessive daily PEF variability over two weeks is considered significant if it is greater than 10%. In children, the threshold is higher at 13%. This reflects the day-to-day fluctuations in airway obstruction seen in asthma.

Question 31

How can a positive bronchial challenge test confirm asthma? A) A 20% drop in FEV₁ after inhaling a bronchoconstrictor B) A 20% increase in FEV₁ after inhaling a bronchodilator C) A persistent decline in FEV₁ without reversibility D) No change in FEV₁ with exposure to a bronchoconstrictor

Answer 31

Answer: A) A 20% drop in FEV₁ after inhaling a bronchoconstrictor Rationale: A bronchial challenge test involves inhaling a bronchoconstrictor (e.g., methacholine) to assess airway hyperreactivity. A ≥20% drop in FEV₁ is considered a positive test, confirming increased airway responsiveness, characteristic of asthma.

Question 32

What response to a four-week inhaled corticosteroid (ICS) trial suggests asthma? A) FEV₁ decreases by 5% B) FEV₁ increases by ≥12% and 200 mL C) No change in FEV₁ D) PEF decreases by 10%

Answer 32

Answer: B) FEV₁ increases by ≥12% and 200 mL Rationale: A ≥12% and 200 mL increase in FEV₁ after 4 weeks of ICS treatment suggests asthma. This improvement reflects airway inflammation reduction, supporting the diagnosis of steroid-responsive airway disease.

Question 33

Which cytokine is primarily associated with type 2 inflammation in asthma? A) IL-1β B) IL-5 C) TNF-α D) IL-6

Answer 33

Correct Answer: B) IL-5 Rationale: IL-4, IL-5, and IL-13 are the major cytokines associated with type 2 inflammation in asthma. IL-5 plays a key role in eosinophil recruitment and activation, contributing significantly to asthma pathogenesis.

Question 34

What is the role of nitric oxide in asthma? A) It acts as a vasoconstrictor. B) It increases smooth-muscle contraction. C) It is produced primarily by epithelial cells in response to IL-13. D) It reduces mucus production.

Answer 34

Correct Answer: C) It is produced primarily by epithelial cells in response to IL-13. Rationale: Nitric oxide is produced by epithelial cells, especially in response to IL-13, and by inflammatory cells like eosinophils, mast cells, and neutrophils. Its production is increased in the presence of eosinophilic inflammation in asthma.

Question 34

Which of the following cytokines is NOT associated with type 2 inflammation in asthma? A) IL-13 B) IL-5 C) IL-9 D) TNF-α

Answer 34

Correct Answer: D) TNF-α Rationale: IL-4, IL-5, IL-13, and IL-9 are associated with type 2 inflammation. TNF-α, on the other hand, is implicated in non-type 2 inflammation.

Question 35

How do reactive oxygen species contribute to asthma pathology? A) They inhibit smooth-muscle contraction. B) They promote airway hyperresponsiveness and epithelial shedding. C) They reduce mucus secretion in the airways. D) They prevent the release of inflammatory cytokines.

Answer 35

Correct Answer: B) They promote airway hyperresponsiveness and epithelial shedding. Rationale: Reactive oxygen species, produced by inflammatory cells during a respiratory burst, contribute to oxidative stress. This leads to increased airway hyperresponsiveness, mucus secretion, and epithelial shedding, all of which are characteristic features of asthma.

Question 36

Which of the following is NOT a major contributor to airway hyperresponsiveness in asthma? A) Hyperresponsiveness of airway smooth muscle B) Stimulation of sensory nerves C) Decreased subepithelial collagen deposition D) Activation of inflammatory cells

Answer 36

Correct Answer: C) Decreased subepithelial collagen deposition Rationale: Subepithelial collagen deposition contributes to airway remodeling and hyperresponsiveness in asthma, whereas a decrease in collagen deposition would not contribute to hyperresponsiveness.

Question 37

How does airway smooth muscle contribute to asthma? A) By producing excess mucus B) By reducing airway inflammation C) By hyperresponsiveness, hypertrophy, and hyperplasia D) By inhibiting collagen deposition

Answer 37

Correct Answer: C) By hyperresponsiveness, hypertrophy, and hyperplasia Rationale: Airway smooth muscle contributes to asthma through hyperresponsiveness to stimuli, hypertrophy, and hyperplasia, leading to airway wall thickening and exacerbated hyperresponsiveness.

Question 38

What causes the thickening of the subepithelial basement membrane in asthma? A) Inflammatory cell activation B) Deposition of repair-type collagens and matrix proteins C) Smooth muscle relaxation D) Decreased mucus production

Answer 38

Correct Answer: B) Deposition of repair-type collagens and matrix proteins Rationale: Thickening of the subepithelial basement membrane occurs due to the deposition of collagens and other matrix proteins, which stiffen the airway and contribute to airway remodeling.

Question 39

What is the result of epithelial goblet cell metaplasia in asthma? A) Decreased mucus production B) Increased airway inflammation C) Increased mucus production and airway obstruction D) Reduced airway smooth muscle contraction

Answer 39

Correct Answer: C) Increased mucus production and airway obstruction Rationale: Goblet cell metaplasia leads to increased mucus production, which can obstruct airways and reduce effective airway luminal area.

Question 40

What role does vascular proliferation play in asthma? A) It reduces airway edema. B) It contributes to airway remodeling through angiogenesis. C) It improves oxygen delivery to the lungs. D) It prevents airway smooth muscle hypertrophy.

Answer 40

Correct Answer: B) It contributes to airway remodeling through angiogenesis. Rationale: Angiogenesis and vascular proliferation can result in leakage from postcapillary venules, contributing to airway edema and chronic airway inflammation.

Question 41

Which cells are primarily responsible for the release of histamine in asthma? A) Neutrophils B) Eosinophils C) Mast cells D) Smooth muscle cells

Answer 41

Correct Answer: C) Mast cells Rationale: Mast cells release histamine and other inflammatory mediators in response to allergens or other triggers, contributing to bronchoconstriction and inflammation in asthma.

Question 42

What is the characteristic clinical triad of aspirin-exacerbated respiratory disease (AERD)? A) Chronic cough, eosinophilia, and pulmonary fibrosis B) Nasal polyposis, asthma, and aspirin/NSAID sensitivity C) Allergic rhinitis, atopic dermatitis, and aspirin intolerance D) Recurrent pneumonia, chronic bronchitis, and aspirin sensitivity

Answer 42

Answer: B) Nasal polyposis, asthma, and aspirin/NSAID sensitivity Rationale: AERD is defined by the presence of asthma, chronic rhinosinusitis with nasal polyps, and respiratory reactions to aspirin or NSAIDs. This syndrome is associated with type 2 inflammation and eosinophilia.

Question 43

What is the primary mechanism responsible for respiratory exacerbations in AERD? A) Direct histamine release from mast cells B) Overproduction of leukotrienes due to cyclooxygenase-1 inhibition C) IgE-mediated hypersensitivity reaction D) Increased production of prostaglandin E2 (PGE2)

Answer 43

Answer: B) Overproduction of leukotrienes due to cyclooxygenase-1 inhibition Rationale: In AERD, inhibition of cyclooxygenase-1 (COX-1) leads to a reduction in PGE2, which normally suppresses leukotriene production. As a result, excess leukotrienes contribute to bronchoconstriction, inflammation, and nasal polyp formation.

Question 44

Which of the following medications should be avoided in patients with AERD? A) Acetaminophen B) Celecoxib C) Ibuprofen D) Montelukast

Answer 44

Answer: C) Ibuprofen Rationale: NSAIDs like ibuprofen inhibit COX-1 and can trigger severe asthma exacerbations in patients with AERD. Acetaminophen and COX-2 selective inhibitors (e.g., celecoxib) are generally better tolerated.

Question 45

Which class of medications is particularly effective in managing AERD? A) Beta-blockers B) Leukotriene modifiers C) Anticholinergics D) First-generation antihistamines

Answer 45

Answer: B) Leukotriene modifiers Rationale: Since AERD involves excess leukotriene production, leukotriene receptor antagonists (e.g., montelukast) and leukotriene synthesis inhibitors (e.g., zileuton) help reduce inflammation and airway reactivity.

Question 46

Which biologic therapy is increasingly being used in AERD management, particularly for patients with severe type 2 inflammation? A) Omalizumab B) Dupilumab C) Rituximab D) Infliximab

Answer 46

Answer: B) Dupilumab Rationale: Dupilumab, an IL-4 and IL-13 inhibitor, and IL-5-targeting biologics are particularly effective in controlling inflammation and reducing nasal polyps in AERD patients. These therapies are becoming more common than aspirin desensitization unless NSAID therapy is required for another condition.

Question 47

How is severe asthma defined? A) Asthma that is uncontrolled despite step 5 therapy or requires step 5 therapy for control B) Asthma that requires frequent short-acting beta-agonist (SABA) use C) Asthma that is triggered by allergens and seasonal changes D) Asthma that improves with leukotriene receptor antagonists

Answer 47

Answer: A) Asthma that is uncontrolled despite step 5 therapy or requires step 5 therapy for control Rationale: Severe asthma is classified as asthma that remains uncontrolled despite optimized therapy, including high-dose inhaled corticosteroids (ICS) with long-acting beta-agonists (LABA) and additional controller medications (step 5 therapy), or requires such treatment to remain controlled.

Question 48

What percentage of asthma cases are classified as severe or difficult-to-treat? A) 1–2% B) 5–10% C) 20–30% D) 50%

Answer 48

Answer: B) 5–10% Rationale: Severe asthma accounts for approximately 5–10% of all asthma cases, yet it disproportionately contributes to almost 50% of asthma-related healthcare costs due to frequent exacerbations and hospitalizations.

Question 49

What is a common challenge in managing severe asthma? A) Excessive reliance on biologic therapies B) Difficulty in diagnosing asthma C) Poor adherence and incorrect inhaler technique D) Overuse of short-acting bronchodilators

Answer 49

Answer: C) Poor adherence and incorrect inhaler technique Rationale: A significant proportion of patients with severe asthma struggle with medication adherence and improper inhaler technique, leading to suboptimal disease control. These factors should be thoroughly evaluated before modifying treatment.

Question 50

Which class of medications has been found useful in a subset of severe asthma patients? A) Beta-blockers B) Macrolides C) NSAIDs D) Calcium channel blockers

Answer 50

Answer: B) Macrolides Rationale: Macrolide antibiotics, such as azithromycin, have been shown to be beneficial in a subset of severe asthma patients, potentially due to their anti-inflammatory and immunomodulatory properties.

Question 51

What is a potential novel therapeutic target being investigated for severe asthma? A) IL-6, IL-33, and mast cell pathways B) Dopamine receptors C) Histamine-1 (H1) receptors D) Serotonin pathways

Answer 51

Answer: A) IL-6, IL-33, and mast cell pathways Rationale: Ongoing research is focusing on novel inflammatory pathways, including IL-6, IL-33, and mast cell activity, as potential targets for new asthma therapies.

Question 52

Which psychosocial factor is associated with an increased risk of asthma mortality? A) High educational attainment B) Depression and severe psychosocial problems C) Regular follow-up with a pulmonologist D) No history of hospital admissions

Answer 52

Answer: B) Depression and severe psychosocial problems Rationale: Mental health conditions, including depression and psychosocial stressors, can contribute to poor asthma control, reduced medication adherence, and increased risk of fatal exacerbations.

Question 53

Which of the following is a major risk factor for asthma-related mortality? A) History of seasonal allergies B) History of intubation for asthma C) Use of short-acting beta-agonists (SABA) as needed D) Mild intermittent asthma

Answer 53

Answer: B) History of intubation for asthma Rationale: A history of intubation for asthma suggests a past life-threatening exacerbation, which significantly increases the risk of future fatal asthma attacks.

Question 54

A patient presents with multiple emergency department visits (≥2 in the past 6 months) for asthma exacerbations. What does this suggest? A) Well-controlled asthma B) Low risk of future exacerbations C) Increased risk of asthma-related mortality D) Need for only short-acting bronchodilators

Answer 54

Answer: C) Increased risk of asthma-related mortality Rationale: Frequent emergency department visits for asthma indicate poor disease control and a high risk of severe exacerbations, potentially leading to fatal outcomes.

Question 55

What parameter is commonly used to assess asthma severity in the urgent care setting? A) Peak Expiratory Flow Rate (PEFR) or Forced Expiratory Volume in 1 second (FEV1) B) Chest X-ray findings C) Serum eosinophil count D) Sputum culture results

Answer 55

Answer: A) Peak Expiratory Flow Rate (PEFR) or Forced Expiratory Volume in 1 second (FEV1) Rationale: PEFR and FEV1 are objective measures used to assess airflow limitation and response to treatment in asthma exacerbations.

Question 56

When should intravenous corticosteroids be considered during an asthma exacerbation? A) Immediately upon arrival in urgent care B) If the patient fails to respond to β2-agonists within 1–2 hours C) Only if infection is present D) Only in cases of mild asthma exacerbations

Answer 56

Answer: B) If the patient fails to respond to β2-agonists within 1–2 hours Rationale: Intravenous corticosteroids, such as methylprednisolone, should be administered if a patient does not show improvement after 1–2 hours of β2-agonist treatment.

Question 57

When should a patient with an asthma exacerbation be considered for hospital admission? A) If their PEFR is >80% of predicted after treatment B) If their PEFR remains ≤60% or they have persistent severe tachypnea for 4–6 hours C) If they respond to β2-agonists within 20 minutes D) If they have mild symptoms and normal oxygen saturation

Answer 57

Answer: B) If their PEFR remains ≤60% or they have persistent severe tachypnea for 4–6 hours Rationale: Patients who fail to achieve a PEFR >60% after treatment or who have persistent severe tachypnea over 4–6 hours should be admitted for further management.