A 14-year-old girl presents to the nurse practitioner with complaints of papules, pustules, and nodules on her face. What is the pathogenesis of acne vulgaris?

Choice A reason: While stress and environmental factors may exacerbate acne, they are not the primary pathophysiological mechanism. Acne vulgaris is fundamentally driven by changes in the pilosebaceous unit, not psychological or allergenic triggers alone. Choice B reason: UVA/UVB exposure may contribute to skin damage and inflammation, but it is not the direct cause of acne. In fact, some UV exposure may temporarily suppress inflammation, though it is not a therapeutic strategy and does not explain the formation of acne lesions. Choice C reason: Acne vulgaris results from obstruction and inflammation of pilosebaceous units. This process begins with increased sebum production, follicular hyperkeratinization, and colonization by Cutibacterium acnes, leading to comedones and inflammatory lesions such as papules, pustules, and nodules. Choice D reason: Keratinocyte proliferation and differentiation abnormalities are more characteristic of conditions like psoriasis. While keratinization plays a role in acne, this description does not fully capture the multifactorial pathogenesis involving sebum, bacteria, and inflammation.