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Which of the following ion channels these electrophysiologic findings most likely indicate impaired function? A 33-year-old woman who is right-handed is brought to the physician because of a 3-day history of progressive weakness and numbness of her ARMS and legs. Neurologic examination shows proximal and distal weakness of the upper and lower extremities. There is areflexia. Sensation to vibration and joint position is decreased in the fingers and toes. Nerve conduction studies show a slow conduction velocity in the median, ulnar, peroneal, and tibial nerves.

Which of the following ion channels these electrophysiologic findings most likely indicate impaired function?

A 33-year-old woman who is right-handed is brought to the physician because of a 3-day history of progressive weakness and numbness of her ARMS and legs. Neurologic examination shows proximal and distal weakness of the upper and lower extremities. There is areflexia. Sensation to vibration and joint position is decreased in the fingers and toes. Nerve conduction studies show a slow conduction velocity in the median, ulnar, peroneal, and tibial nerves.

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A. Neurotransmitter-gated CA++ channels
B. Neurotransmitter-gated K+ channels
C. Neurotransmitter-gated Na+ channels
D. Voltage-gated CA+ + channels
E. Voltage-gated K+ channels
F. Voltage-gated Na+ channels

This question is part of nbme 13 section 2 prt 2 of 2

Asked by Chance, Last updated: Aug 07, 2020

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mango man

Mango man, here, there

Answered Sep 01, 2018

For this question they're basically wanting you to address the Salatory Nerve Conduction Pathyway (action potientiation along mylinated axons)which relies on voltage-gated Na+ channels from one node to the next node of Ranvier.

 

John Smith

John Smith

Answered Sep 09, 2016

1. voltage-gated na+ channels\n-guillainbarr syndrome, is an acute polyneuropathy, a disorder affecting the peripheral nervous system. ascending paralysis, weakness beginning in the feet and hands and migrating towards the trunk, is the most typical symptom, and some subtypes cause change in sensation or pain as well as dysfunction of the autonomic nervous system. it can cause life-threatening complications, in particular if the respiratory muscles are affected or if there is autonomic nervous system involvement. the disease is usually triggered by an infection.\nthe diagnosis is usually made by nerve conduction studies and with studies of the cerebrospinal fluid.\nthe disorder is characterized by symmetrical weakness that usually affects the lower limbs first, and rapidly progresses in an ascending fashion. patients generally notice weakness in their legs, manifesting as rubbery legs or legs that tend to buckle, with or without dysesthesias (numbness or tingling). as the weakness progresses upward, usually over periods of hours to days, the arms and facial muscles also become affected. frequently, the lower cranial nerves may be affected, leading to bulbar weakness, oropharyngeal dysphagia (drooling, or difficulty swallowing and/or maintaining an open airway) and respiratory difficulties. most patients require hospitalization and about 30% require ventilatory assistance for treatment of type ii respiratory failure. facial weakness is also common. eye movement abnormalities are not commonly seen in ascending gbs, but are a prominent feature in the miller-fisher variant.\nsensory loss, if present, usually takes the form of loss of proprioception (position sense) and areflexia (complete loss of deep tendon reflexes), an important feature of gbs. loss of pain and temperature sensation is usually mild. in fact, pain is a common symptom in gbs, presenting as deep aching pain, usually in the weakened muscles, which patients compare to the pain from overexercising. these pains are self-limited and may be treated with standard analgesics. bladder dysfunction may occur in severe cases but is usually transient.\nin severe cases of gbs, loss of autonomic function is common, manifesting as wide fluctuations in blood pressure, orthostatic hypotension (a fall in blood pressure on standing, leading to an increased risk of collapse), and cardiac arrhythmias.\nacute paralysis in guillainbarrsyndrome may be related to sodium channel blocking factor in the cerebrospinal fluid (csf). significant issues involving intravenous salt and water administration may occur unpredictably in this patient group, resulting in siadh, a cause of low sodium levels in the blood.\nabstract (pubmed)\nthe effect of csf from patients with severe gbs on voltage-dependent na+ channels of myoballs was studied. the transient na+ currents, elicited by repetitive stimulation at 1 hz, were inhibited by the csf from most of the gbs patients to 10%-40% the control value. the inhibition was complete in about 5 s and was fully reversible. such inhibition was never seen with control csf. the blocking property of the csf from gbs patients was lost after the number of cells and the protein content had been lowered by means of a clinical filtration technique for cerebrospinal fluid. the results demonstrate that in guillain-barrsyndrome , blocking factors of na+ channels are present in the csf, impairing neuron impulse conduction, and thereby causing muscular weakness and sensory disturbances in the affected patient.\n

 

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