Basic and Clinical Sciences (BCSE) Practice Exam

The pathophysiology of pemphigus is primarily characterized by a Type II hypersensitivity reaction, where the immune system produces antibodies that target intercellular junctions within the epidermis, specifically desmosomes. These desmosomes are critical for cell-to-cell adhesion in the epidermal layer of the skin. In pemphigus, antibodies (usually IgG) bind to proteins such as desmogleins, which are involved in maintaining the integrity of these junctions.

When these antibodies attach to their target, they disrupt the adhesion between keratinocytes, leading to acantholysis—a process where skin cells lose their connections to one another. This results in the formation of blisters and erosions, which are hallmark features of pemphigus vulgaris and pemphigus foliaceus. The damage manifests clinically as painful blisters that can easily rupture, often leading to significant morbidity.

In contrast, the other options involve different mechanisms and conditions. Type I hypersensitivity reactions are typically associated with allergic responses mediated by IgE and mast cells, such as asthma and anaphylaxis. Type III hypersensitivity involves immune complexes and is more related to diseases like systemic lupus erythematosus, where immune complexes deposit in tissues. An autoimmune