Dermatomyositis (DM) and polymyositis (PM) are idiopathic inflammatory myopathies (IIM) with distinct pathogenic mechanisms, clinical presentations, and management considerations that the NP must differentiate. Dermatomyositis involves complement-mediated microangiopathy: autoantibodies activate complement (C5b-9 membrane attack complex) on endomysial capillary endothelium, causing capillary necrosis and dropout. The resulting ischemia produces perifascicular atrophy — the histological hallmark — with inflammatory infiltrate that is perivascular and perimysial (B cells, CD4+ T-helper cells, plasmacytoid dendritic cells). DM has pathognomonic cutaneous features: heliotrope rash (violaceous periorbital discoloration with edema), Gottron papules (violaceous papules over MCP/PIP/DIP joints), V-sign (chest), shawl sign (upper back), and mechanic's hands. Polymyositis involves direct CD8+ cytotoxic T-cell attack on muscle fibers. Autoreactive T cells recognize aberrantly expressed MHC class I molecules on muscle fiber surfaces and directly invade non-necrotic fibers (endomysial inflammatory infiltrate). There are NO cutaneous manifestations in PM. The diagnosis of PM requires exclusion of other causes of myopathy including inclusion body myositis (IBM), immune-mediated necrotizing myopathy (IMNM), drug-induced myopathy (statins), and endocrine myopathy (hypothyroidism, Cushing). Critical clinical distinctions: DM has a 15-30% association with underlying malignancy in adults (paraneoplastic...