2 reduction in extracellular ca 2 will lead to a

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2. Reduction in extracellular Ca 2+ will lead to a reduction in the acetylcholine released and a reduction in the transmission of impulses because Ca 2+ causes release of acetylcholine into the synaptic cleft. 3. ACh opens ligand-gated channels that are equally permeable to Na+ and K+. The net effect is depolarization that reaches action potential threshold in the muscle cell.
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Title of the case: Boy with tetanus Student’s Name: LEBURA EWONUBARI GRACE Roll #: 666 Medical Physiology Clinical Case SOAP Notes Subjective Observations Possible physiological explanations 4 year old General Malaise, mild fever, indolence and anorexia. Dysphagia, difficulties opening mouth and dehydration. Fever is characterized by an elevation of body temperation above the normal range due to an increase in the temperature regulatory set point which triggers muscle tone and paralysis of muscles can disrupt the normal functioning of the muscles. Objective observations Possible physiological explanations Signs of trismus and muscle rigidity. Lack of immunization and a toe nail infection. Trismus is reduced opening of the jaw caused by spasm of the muscles of mastication. This is due to tetanus infection which occurs through wound contamination. Differential diagnosis Supporting or refuting information Tetanus infection Tetanus is a neurotoxin-mediated disease characterized by excessive sweating, fever and dysphagia. The neurotoxin (tetanospasmin) is produced by the obligate anaerobic species Clostridium tetani,it disrupts neurotransmitter release in inhibitory neurons including GABA, this diminished inhibition leads to continous stimulation of the motor neuron and the Ca2+ released from sarcoplasmic reticulum remains bound to tropolin C which extends the time of cross- bridge cycling leading to peripheral muscle rigidity and spasms.
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Hypocalcemic tetany Strychnine poisoning A disease caused by an abnormally low level of calcium in the blood. It is characterized by hyperexcitability of the neuromuscular system and results in carpopedal spasms. A common cause is a deficiency of parathyroid hormone secretion. Strychnine poisoning can be fatal to humans and can occur by inhalation, swallowing or absorption through eyes or mouth. It produces some of the most dramatic and painful symptoms of any known toxic reaction. Ten to twenty minutes after exposure, the body's muscles begin to spasm, starting with the head and neck in the form of trismus. QUESTIONS 1. On which skeletal muscle filament is troponin located? 2. What is the function of the sarcoplasmic reticulum (SR)? 3. What is the molecular basis for initiation of contraction in skeletal muscle? ANSWERS 1. Troponin is located on actin filament. 2. Sarcoplasmic reticulum (SR) functions as the site for Ca2+ storage and release for excitation-contraction coupling. 3. T-tubules depolarization opens Ca2+ channels in the SR and Ca2+ is released into the intracellular fluid. The Ca2+ released binds to troponin C on the thin filament causing conformational change in the troponin that moves the tropomyosin out of the way so that myosin can bind to actin thereby initiating contraction.
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