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Question #46523
The Question
A patient with a genetic deficiency of alpha-1 antitrypsin suffers from chronic IgE-mediated respiratory allergies. During recurrent allergic episodes, mast cell degranulation triggers massive neutrophil recruitment to the lungs. Which of the following best explains the accelerated alveolar damage observed in this patient?
Options
- A.
Unchecked action of neutrophil elastase degrades the alveolar septa due to the absence of protease inhibition.
- B.
Histamine released from mast cells directly digests the elastic fibers of the alveoli, leading to emphysema.
- C.
Alpha-1 antitrypsin normally inhibits IgE binding to mast cells, and its absence causes unchecked hyper-degranulation.
- D.
Neutrophils fail to phagocytose allergens, leading to the toxic accumulation of antigen-antibody complexes in the alveoli.
Check Your Answer
Correct Answer
Step-by-Step Solution
Explanation
How the Examiner Thinks
Comparative_Analysis
Sharpen your ability to evaluate multiple scenarios and distinguish between competing potential answers.
Concepts Behind This Question
IgE|Mast_Cells|Alpha-1_Antitrypsin|Proteases
Why This Question Is Tricky
Common Mistakes
Conceptual Pivot: Integrating concepts from Biotechnology (AAT function) and Human Health (Allergy mechanism).
Students often memorize 'AAT treats emphysema' without understanding the mechanism (protease inhibition).
The trap is confusing the chemical mediator of allergy (histamine) with the actual agent of tissue destruction (neutrophil elastase) during the subsequent inflammatory response.
Quick Facts About This Question
Question Information
| Subject | Biology |
| Chapter | Human Health and Disease - Class 12 |
| Concept | Allergy Mechanism |
| Difficulty | 8 |
| Cognitive Load | 5 |
| Target Solve Time | 120 sec |
| Access | Free |