MSCI M131 Lecture 10(Unit 2)Outline of Past Lecture I. Muscle Disordersa. RhabdomyolysisII. Neuromuscular Anatomy and PhysiologyOutline of Current lectureI. Neuromuscular disordersa. Myasthenia Gravisb. Multiple SclerosisCurrent LectureI. Myasthenia Gravisa. Pathophysiologyi. Problem in neuromuscular junction – Ach receptors are attacked by the immune systemb. Etiologyi. Seems to be related to the thymus gland1. Role in the immune system is to specialize lymphocytes B cells into killer T cellsii. Abnormal cells with Ach receptors are attacked by T cellsiii. Once T cells identify abnormal cells, they attack others like it and mistakenly target cells with normal Ach receptorsiv. T and B cells communicate and both attack healthy cellsc. Signs and symptomsi. Loss of muscle controlii. Skeletal muscle weakness (cardio/ smooth not affected)iii. Any muscle can be affected, but typically asymmetrically in face, throat, and eyesiv. Vision and speech problemsv. Muscle weakness causes faster fatiguing d. Diagnosisi. Blood tests1. Check for presence of antibodiesThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.2. EMG and nerve stimulationa. Look at electricity generated by muscles b. Check the efficiency of nerve to muscle communication3. Effect of some drugsa. Neostigmine test – prevents breakdown of Ach in synapse, allows Ach to hit the receptors multiple times, builds up a stronger response and increases the probability of transmissione. Clinical importancei. Weakness decreases performance of fine-tuned motor skillsii. Facial weakness affects self esteemiii. If weakness affects breathing muscles (diaphragm is skeletal muscle) that can lead to “myasthenic crisis”f. Treatmentsi. Improve weakness1. Prevent Ach breakdown with neostigmineii. Reduce autoimmune response1. Immunosuppressantsa. Receptors will be replaced by the body2. Plasmapheresis (not done very often)a. Filter out the antibodies from the blood3. Thymectomya. Removal of the thymus gland; won’t make any more T cellsg. Prognosisi. Very good, if treated1. Reach balance where more receptors are being made than destroyedii. Drugs do have side effects1. Dosage must be monitored to not go overboardiii. In severe cases, death could occur from not breathingII. Multiple Sclerosisa. Pathophysiologyi. Degradation of myelin sheath coating the axonii. Action potential not transmitted as efficiently, signals moving at different speeds1. Lose coordination of signals and leads to numbnessiii. Auto-immune disorder1. Signal weakened because they don’t arrive at same timeb. Etiologyi. Not sureii. Possible triggers:1. Genetics2. Environmental factors a. geographic location, more common further away from the equator (sunlight? European