Janet case study: rhinitis, polyps and hypersensitivity

Janet's case is assembled out of atopy. The flaking erythematous rash on the flexor surfaces of both arms is atopic dermatitis; the five-week course with sneezing, watery discharge and itching every spring and autumn is seasonal allergic rhinitis rather than the run of colds she calls it; the night cough raises cough-variant asthma or postnasal drip and completes the atopic triad. The findings that deserve most attention are the bilateral medium-sized nasal polyps and the maxillary sinus tenderness, because polyps in a 20-year-old are not a throwaway detail. They explain the chronic obstruction, they justify sinusitis as a differential, and in a patient this young they are the reason cystic fibrosis and aspirin-exacerbated respiratory disease belong in your list of further history questions. Boggy red mucosa, clear postnasal drainage and clear lungs together point the primary diagnosis at allergic rhinitis with nasal polyposis rather than at the recurrent infection she has been calling a cold.

The last two questions are separate and posts routinely merge them. Question four asks you to differentiate the types of hypersensitivity, which means all four Gell and Coombs mechanisms set out against each other: type I IgE-mediated and immediate, type II antibody-mediated cytotoxicity against cell-surface antigen, type III immune-complex deposition, type IV delayed and T-cell mediated. Give each its mediator, its timing and one clinical example. Question five then applies that framework to Janet and wants type I, argued from the immediacy of her symptoms on exposure, the eosinophil and mast cell involvement, and the seasonal pattern. Her atopic dermatitis is worth a sentence here because it is often described as having a delayed type IV component alongside the IgE sensitisation, which is exactly the nuance that separates a strong answer from a merely correct one, and it costs you no more than two sentences to include.