An adolescent boy is admitted to the emergency department (ED) following a bee sting. He arrives with a body rash and 30 minutes later he becomes short of breath. The nurse obtains vital signs with a blood pressure of 90/52 mm Hg, heart rate 130 beats/minute, and respiratory rate 40 breaths/minute. The client is exhibiting clinical manifestations of which type of immune reaction?
Cell-mediated tovity
Autoimmune response
IgE response hypersensitivity
Type II hypersensitivity
The Correct Answer is C
Choice A reason: Cell-mediated hypersensitivity (Type IV) involves T-cells, causing delayed reactions like contact dermatitis, not acute symptoms like rash, hypotension, and dyspnea. Bee sting reactions are rapid, driven by IgE-mediated histamine release, making this immune mechanism incorrect for the client’s presentation.
Choice B reason: Autoimmune responses target self-antigens, as in lupus, not external allergens like bee venom. The client’s acute rash, hypotension, and respiratory distress indicate an allergic reaction, not autoimmunity, making this mechanism irrelevant to the anaphylactic response observed.
Choice C reason: IgE response hypersensitivity (Type I) causes anaphylaxis, as bee venom triggers IgE-mediated mast cell degranulation, releasing histamine. This leads to rash, hypotension, and bronchoconstriction, matching the client’s symptoms, making this the correct immune reaction for the acute, life-threatening presentation.
Choice D reason: Type II hypersensitivity involves antibody-mediated cytotoxicity, as in hemolytic anemia, not allergic reactions. Bee sting anaphylaxis results from IgE-driven histamine release, not cell destruction, making this mechanism incorrect for the client’s rapid-onset allergic symptoms.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is C
Explanation
Choice A reason: Switching to decaffeinated coffee and tea reduces acid stimulation, but it does not address the misconception about dairy coating ulcers. Dairy increases acid production, worsening ulcers, making this action less critical than correcting the client’s harmful dietary plan.
Choice B reason: Frequent small meals reduce acid load, aiding ulcer management, but the client’s dairy plan increases acid secretion, negating benefits. Correcting the dairy misconception is more urgent, as it directly worsens the ulcer, making this suggestion secondary.
Choice C reason: Reviewing the need to avoid milk and cream is best, as dairy stimulates gastric acid via gastrin release, worsening duodenal ulcers. The client’s plan to use dairy for coating is incorrect, and correcting this prevents exacerbation, aligning with evidence-based ulcer management.
Choice D reason: Reinforcing dairy use by listing snacks is harmful, as milk and cream increase acid production, aggravating ulcers. This action perpetuates the client’s misconception, worsening the condition, making it incorrect compared to correcting the dietary error.
Correct Answer is A
Explanation
Choice A reason: Daily use of tiotropium via its handihaler is correct, as this long-acting anticholinergic bronchodilator is administered once daily for COPD maintenance. It relaxes airway smooth muscles, improving airflow, and consistent use prevents exacerbations, indicating proper understanding of the medication’s administration schedule.
Choice B reason: Using tiotropium for sudden shortness of breath is incorrect, as it is not a rescue inhaler. Tiotropium provides sustained bronchodilation over 24 hours, not rapid relief. Short-acting beta-agonists like albuterol are used for acute symptoms, indicating a need for further teaching.
Choice C reason: Using another inhaler between tiotropium doses suggests misunderstanding, as tiotropium is a once-daily maintenance therapy. Additional inhalers may be prescribed, but this statement implies incorrect timing or overuse, which could lead to improper COPD management, requiring clarification.
Choice D reason: Expecting thinner sputum is incorrect, as tiotropium does not affect mucus viscosity. It dilates airways, not liquefying secretions, which is the role of mucolytics. This misunderstanding indicates a need for teaching about tiotropium’s bronchodilatory, not mucolytic, effects in COPD.
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