PATHOSCHEMA® Immersive Experience (PIE) | Myasthenia Gravis ⛶ Expand Experience Presynaptic Terminal Action potential triggers ACh vesicle release Postsynaptic Folds & AChR Deep folds maximize receptor density 1. Autoantibody Binding 2. Receptor Blockade 3. Membrane Destruction Anti-AChR Antibodies enter Synaptic Cleft Antibodies competitively block & cross-link Receptors Complement Activation flattens folds, destroying receptor density Ocular: Ptosis & Diplopia Bulbar: Dysarthria/Dysphagia Fatiguable Proximal Weakness Myasthenic Crisis (Resp Failure) 1. Serology (Antibodies) 2. Electrophysiology (RNS/EMG) 3. Clinical (Ice Pack Test) 4. Imaging (CT Thorax) Specific Autoantibodies Anti-AChR (85%) & Anti-MuSK Repetitive Nerve Stimulation >10% Decremental Amplitude Response ICE PACK Cold Inhibits Acetylcholinesterase Improves Ptosis CT Thorax (Mediastinum) Screening for Thymoma / Thymic Hyperplasia I. Pyridostigmine II. Immunosuppression III. Plasmapheresis / IVIg IV. Thymectomy Presynaptic Nerve Terminal Postsynaptic Muscle Membrane Pyridostigmine (Acetylcholinesterase Inhibitor) Prolongs ACh presence in synaptic cleft T-Cell B-Cell Corticosteroids / Azathioprine Suppresses autoimmune activity & antibody production Plasmapheresis (PLEX) / IVIg Rapid removal / neutralization of pathogenic antibodies Thymectomy Surgical excision removes source of autoreactive T-cell maturation Clinical Evidence Mastery Question 1 of 10 Score: 0 Loading... 1. Physiology 2. Pathophysiology 3. Symptoms 4. Investigations 5. Management 6. Mastery
