Asthma: Clinical

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Asthma: Clinical

USMLE® Step 2 questions

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USMLE® Step 2 style questions USMLE

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A 12-year-old boy is brought to the clinic due to recurrent episodes of dyspnea and wheezing over the past several weeks. The patient came to the clinic 3 months ago and was diagnosed with intermittent asthma. He was prescribed an albuterol inhaler and instructed to use it as needed. The patient’s parent states the patient uses the inhaler several times per day and has found mild relief. Temperature is 37.0°C (98.6°F), pulse is 80/min, respirations are 14/min, blood pressure is 110/76 mm Hg, and oxygen saturation is 99% on room air. The patient is resting comfortably. Physical examination reveals scattered wheezes on chest auscultation. Which of the following drugs should be added to this patient’s treatment regimen?  


Content Reviewers

Asthma is an episodic, chronic respiratory disorder characterized by airway obstruction caused by inflammation and hyperresponsiveness of the bronchial smooth muscle. The two golden words in asthma are “reversible”, which means the obstruction can virtually disappear with medications like bronchodilators, and “inducible”, which means the obstruction can occur in response to a variety of stimuli; including allergens like house dust mites, pet animal dander, like cat dander, and pollen, or irritants like tobacco smoke, respiratory tract infections, like a common cold or pneumonia, cold or dry air, and even emotional stress. Now, atopy is the genetic predisposition of an individual towards developing IgE antibodies to otherwise harmless environmental antigens, making that individual strongly predisposed to developing three allergic disorders, eczema or atopic dermatitis, allergic rhinitis, and asthma, collectively coined the atopic triad. Because of this genetic component, asthma is usually diagnosed in early childhood, and may or may not carry on into adulthood.

So, let’s say a genetically predisposed child is exposed to a potential allergen for the first time. First off, dendritic cells take up the allergen and present it to a type 2 helper T-cell, or Th2 cell. In asthma, Th2 cells make the mistake of thinking this harmless antigen is an allergen, so they release cytokines that stimulate B cells to make IgE antibodies. IgE antibodies then prime mast cells, which cautiously anticipate the next event. When the child is re-exposed to the allergen, the mast cells spill out vasoactive mediators like histamine and leukotrienes, which cause bronchoconstriction and inflammation. Once the child is no longer exposed to the allergen, the immune system relaxes, and everything goes back to normal, until the next event. Now, not all asthma episodes are triggered this way by an allergen. A unique form of asthma is aspirin sensitive asthma, which is characterized by the triad of asthma, nasal polyps, and sensitivity to aspirin or NSAIDs. Aspirin opposes prostaglandin production and tips the balance between prostaglandins and leukotrienes in favor of increased leukotriene production, which promotes smooth muscle contraction of the airways.


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