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    Myasthenia Gravis Medical Slides

    Generate publication-quality myasthenia gravis lecture slides in 30 seconds. AI-powered content structured for clinical education.

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    Why teach Myasthenia Gravis?

    Myasthenia gravis is the most common disorder of neuromuscular transmission, with a prevalence of 15-25 per 100,000. The bimodal age distribution (young women, older men) and association with thymic pathology make it a clinical teaching classic. The 2021 international consensus and the pivotal REGAIN and ADAPT trials have expanded the therapeutic armamentarium to include complement and FcRn inhibitors for refractory disease.

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    01NMJ Physiology and Autoimmune Pathogenesis: AChR, MuSK, and LRP4 Antibodies
    02Clinical Patterns: Ocular vs Generalized MG and MGFA Classification
    03Diagnostic Workup: AChR/MuSK Antibodies, Repetitive Nerve Stimulation, and Single-Fiber EMG
    04Pharmacotherapy: Pyridostigmine, Corticosteroids, and Steroid-Sparing Immunosuppressants
    05Myasthenic Crisis: ICU Management, Intubation Criteria, IVIG vs PLEX, and Medication Avoidance
    06Emerging Therapies: Eculizumab (REGAIN), Efgartigimod (ADAPT), and Rozanolixizumab
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    Myasthenia Gravis Presentation FAQ

    How should myasthenic crisis management be organized in teaching slides?

    Present a structured ICU approach: (1) secure airway if FVC <1L or NIF worse than -20 cmH2O, (2) hold pyridostigmine (paradoxically worsens secretions in crisis), (3) initiate IVIG 0.4 g/kg/day for 5 days or PLEX 5 exchanges — both equally effective, (4) identify and treat triggers (infection in 40%, medication changes, surgery), (5) avoid MG-exacerbating drugs (aminoglycosides, fluoroquinolones, magnesium, beta-blockers). Emphasize that crisis mortality has decreased from 40% to <5% with modern ICU care.

    How should the difference between AChR and MuSK MG be taught?

    Create a comparison: AChR-MG (85% of generalized MG, complement-mediated, thymic hyperplasia/thymoma association, responds to cholinesterase inhibitors and thymectomy) vs MuSK-MG (5-8%, IgG4-mediated non-complement-fixing, bulbar-predominant with facial/respiratory weakness, poor response to pyridostigmine, thymectomy not beneficial, rituximab often highly effective). This distinction directly guides treatment strategy and is a frequent board-style teaching point.

    What evidence supports new complement and FcRn inhibitors in MG?

    Present eculizumab (REGAIN trial, 2017): C5 complement inhibitor approved for AChR+ refractory generalized MG, improved daily activities score. Efgartigimod (ADAPT trial, 2021): FcRn inhibitor that reduces pathogenic IgG by 80%, with 68% responder rate in AChR+ MG. These represent the first targeted therapies for MG and are indicated when conventional immunosuppression fails — frame them as precision medicine applied to neuromuscular disease.

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