MSCI M131 Lecture 9(Unit 2)Outline of Past Lecture I. Muscle Disordersa. Muscular DystrophyOutline of Current lectureI. Muscle Disordersa. RhabdomyolysisII. Neuromuscular Anatomy and PhysiologyCurrent LectureI. Rhabdomyolysisa. Pathophysiologyi. Results from extreme over exertionb. Etiologyi. Extreme exercise decreases energy stores and stresses mitochondria (responsible for providing energy)ii. Mitochondria are damaged and breakdown1. Cell is destroyediii. Enzymes are released into cell, cell breaks down and releases enzymes to other surrounding cellsiv. Enzymes destroy myofibril – destroys more musclec. Signs and symptomsi. Severe pain and swelling at injury siteii. Potential nerve involvement1. Nerve pinching (tingling, pain, numbness) from contractions2. Decreased blood flow from swellingiii. Dark colored urine – digested muscle cells pass through kidneyiv. Decreased urine output from cell “chunks”v. Low back pain (kidneys inflamed)vi. Cardiac arrhythmia1. Calcium released, electrolyte imbalance, contraction of heart notas goodd. DiagnosisThese 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.i. Urinalysis1. Presence of blood or myoglobin (carries oxygen in muscle tissue) indicates muscle damage2. Blood test – CK (creatine), potassium and calcium levels 3. Radiographic – methylene diphosphate (MDP) binds to calcium and reflects on X-Ray, can see where damage is and severitye. Clinical importancei. Damaged muscle is gone foreverii. Significant risk for kidney failureiii. Can be fatal, but rareiv. Increase risk of heart attack due to calcium levels in bloodf. Risk factorsi. Exercise beyond fatigueii. Exercise in hot weather – dehydration, muscles have to work even harderiii. Poor supervision; egog. Treatmentsi. Hospitalization/ dialysis – clean out blood and urine1. External source to filter blood in place of kidneysii. Intravenous fluid – diluting toxins so kidneys can better filter themiii. Rest – prevent further damage, allow scar tissue to form, decrease swellingiv. Prevent by avoiding risk factorsh. Prognosisi. Muscle forever lostii. Potential for more strain and tear – scar tissue is a problem areaiii. Massage scar tissue out to reduce risk of damageiv. Won’t be as strong, function decreased II. Neuromuscular Anatomy and Physiologya. Control of movementi. Starts with an abstract mental image in the frontal cortex, and is translated through deconstruction in the primary motor cortex to motorneurons that enable muscle contraction. Fine-tuning of motion is done by cerebellum and basal ganglia providing feedback to the primary motor cortex. The cerebellum controls coordination and timing, while the basal ganglia is involved with force control. b. Communicating with the musclesi. Motor neurons activate muscle fibers1. More than 99% of muscle contractions are the result of a motor neuron “firing”a. Less than 1% are local effects, such as dehydration and imbalance of electrolytes2. Once there is action from the neuron, there will be a contractionc. Characteristics of the motor neuroni. Myelin is fatty sheath that wraps around the nerve to increase conduction velocity of the action potential1. Action potential an electrical signal that turns to a chemical signal in the synapse, which is then turned into an electrical signal againd. characteristics of the Neuromuscular Junctioni. axon terminal sends out action potential, which releases Acetylcholine, a neurotransmitter, into the synapse between the terminal and the muscle cellii. Ach hits receptors that cause contraction and an enzyme immediately destroys