Voltage Gated Sodium Channels Case Study

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Summary
Dr. Marshall had dinner with puffer fish and rice during his trip to Indonesia. Not even an hour later, he suddenly felt numbness in his lips, tongue, face and neck. Dr. Marshal also had a feeling of nausea and acutely vomiting because of the pains in his stomach and throat. He was immediately rushed to the ED. His symptoms are diaphoresis, motor dysfunction, parethesias, nausea, ascending paralysis, cyanosis, and hypoventilation. He was prescribed with atropine due to the bradycardia. As he was assumed to be poisonous with tetrodotoxin which is a neurotoxin, intravenous hydration, gastric lavage and activated charcoal was conducted next.
Background
The extracellular fluid and intracellular fluid of neuron are different significantly
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It is a specific protein presenting on the membrane of the nerve cells and muscle cells. They are responsible for action potential initiation and propagation in excitable cells (Catterall, Goldin, & Waxman, 2015). Voltage-gated sodium channels open or close to in response to the movement of sodium concentration between inside and outside of the cells. Voltage-gated sodium channels consist of two gates which function separately. An activation gate that opens when being stimulated while an inactivation gate closes and prevents the entry of sodium ions (Martini, Nath, & Bartholomew, 2015, p. 401). Voltage gated sodium channels anticipate in depolarization, repolarization and …show more content…
Westwood experienced paralysis or motor dysfunction in his legs, the upper body, arms, face and head. There will be no muscle contraction and performance without nerve impulse (Losos, Mason, Singer, Raven, & Johnson, 2008). Again, ince no motor neuron signals are transmitted to the diaphragm, Dr. Westwood had difficulty breathing. Consequently, inadequate amount of oxygen carried to the blood makes him cyanotic. If Dr. Westwood had not been rushed to the hospital in time, he would have died from respiratory

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