Question

A woman with allergic conjunctivitis uses a drug that prevents the release of chemical mediators from mast cells. Which mechanism is responsible for this pharmacologic effect? (A) activation of beta \(a_2\)-adrenoceptors (B) decreased cytokine production (C) blockade of muscarinic receptors (D) inhibition of 5-lipoxygenase (E) blockade of calcium influx

Short answer

The mechanism is the blockade of calcium influx (option E).

Step-by-step solution

Understanding the Problem

The question asks us to identify the mechanism by which a drug prevents the release of chemical mediators from mast cells. This is relevant in allergic conjunctivitis, where mast cells play a key role in the inflammatory process.

Recognizing Relevant Mechanisms

Each option presented is a different pharmacological mechanism. We need to consider which of these mechanisms is likely to prevent the release of mediators from mast cells.

Analyzing Option A

Activation of beta-2 adrenoceptors (option A) can lead to smooth muscle relaxation and bronchodilation, but it is not directly related to preventing mast cell degranulation.

Analyzing Option B

Decreased cytokine production (option B) can reduce inflammation in general, but it doesn't specifically address the prevention of mediator release from mast cells.

Analyzing Option C

Blockade of muscarinic receptors (option C) affects parasympathetic responses, like decreasing bronchial secretions, but it is not related to mast cell mediator release.

Analyzing Option D

Inhibition of 5-lipoxygenase (option D) reduces leukotriene synthesis, which can dampen inflammation, but it does not prevent the initial release of mediators from mast cells.

Analyzing Option E

Blockade of calcium influx (option E) is directly involved in preventing the degranulation of mast cells by stopping intracellular calcium increase, which is necessary for the release of mediators.

Conclusion

The most appropriate mechanism for preventing the release of chemical mediators from mast cells is blockade of calcium influx, as calcium is critical for the degranulation process.

Key concepts

Allergic Conjunctivitis

Allergic conjunctivitis is an eye condition characterized by inflammation due to an allergic reaction. This occurs when the eyes come into contact with allergens, like pollen or dust, leading to itching, redness, and tearing. Our immune system mistakenly identifies these harmless substances as dangerous invaders, setting off an allergic response. This condition often accompanies other allergic symptoms such as rhinitis, which involves nasal congestion and sneezing. Allergic conjunctivitis is non-contagious, unlike viral or bacterial conjunctivitis.

Some common triggers include:

• Pollen
• Animal dander
• Mold spores
• Smoke

Treatment often involves avoiding triggers, using antihistamines, or eye drops designed to mitigate the symptoms and reduce inflammation.

Mast Cells

Mast cells are a type of white blood cell that play a crucial role in the body's immune response. They are found in connective tissues throughout the body, particularly in areas that are ideal for encountering external antigens such as skin, lungs, and the gastrointestinal tract.

Upon activation, mast cells release a range of chemical mediators stored in their granules, such as histamine, which can lead to allergic reactions. Think of mast cells as gatekeepers that release these molecules to recruit other immune cells to the site of infection or irritation.

Among their key roles:

• Defending tissues from pathogens
• Facilitating wound healing
• Participating in immune tolerance and allergic reactions
Understanding how mast cells function helps us grasp the basis of allergic reactions, including allergic conjunctivitis.

Calcium Influx

Calcium influx refers to the movement of calcium ions into cells, a process crucial for various cellular functions. In the context of mast cells, calcium influx is essential for the release of chemical mediators during an immune response.

When an allergen triggers an immune response, calcium ions enter the mast cells, leading to their degranulation. Degranulation is the process by which mast cells release their stored chemicals into the surrounding tissue, contributing to inflammation.

Blocking calcium influx can effectively prevent mast cells from releasing these mediators, thereby reducing the symptoms of conditions like allergic conjunctivitis. This is why certain drugs are designed to target this pathway.

Chemical Mediators

Chemical mediators are substances released by cells that trigger a physiological response. During an allergic reaction, mast cells release a range of chemical mediators that lead to the symptoms we associate with allergies.

Some key chemical mediators include:

• Histamine: Causes itching, redness, and swelling.
• Leukotrienes: Contribute to prolonged inflammation.
• Prostaglandins and Thromboxanes: Involved in widening blood vessels and affecting muscle contractions.

These mediators have different roles in prolonging or intensifying the allergic response. Because they have such potent effects, targeting their release or action is a common strategy in the treatment of allergic conditions.

Drug Mechanisms

Drug mechanisms refer to the specific processes through which drugs exert their effects on the body. In the case of preventing allergic reactions like those seen in allergic conjunctivitis, drugs may block pathways vital to the activation of mast cells or the release of chemical mediators.

In our example, a critical mechanism is the blockade of calcium influx, which stops mast cells from degranulating and releasing mediators.

Other common drug actions include:

• Inhibition of mediator synthesis (like leukotriene inhibitors)
• Blocking receptor sites (antihistamines block histamine receptors)
• Reducing immune cell activation through immunosuppressants

Understanding these mechanisms allows for targeted therapy, optimizing treatment efficacy while minimizing side effects.