Hello I need help with the below question. Part I—The Hospital At last the day h

Question

Hello I need help with the below question.

Part I—The Hospital

At last the day had come. Mr. Thompson was having his wisdom teeth removed. He was tired of the aches and pains and the sight of his puffy face in the mirror every morning. He felt helpless, lying on the gurney watching the ceiling lights whiz by as he was being wheeled to surgery. Mr. Thompson had selected this particular oral surgeon because of the sign outside his practice that read: “We cater to cowards.” But the surgeon still hadn’t seemed to understand Mr. Thompson’s fear of dental procedures; he had wanted to use a local anesthetic. Fortunately, the anesthesiologist was sympathetic to his request for a general anesthetic. As the mask came over Mr. Thompson’s face, he felt so alone. It reminded him of how he felt as a boy, in the orphanage. Then the halothane* started to take effect and he went under. As surgery was about to begin, Mr. Thompson started twitching. The anesthesiologist saw Mr. Thompson’s heart rate increase, his muscle contractions become strong and widespread throughout his body, and the patient began to sweat profusely. As Mr. Thompson’s temperature quickly increased, the anesthesiologist injected a solution into the IV drip. Then Mr. Thompson went limp and all that could be heard was the sound of oxygen rushing through the ventilator, assisting Mr. Thompson’s breathing. “Next time we do as I say and we use a local,” muttered the angry surgeon as he glared at Mr. Thompson.

*Halothane is a general inhalation anesthetic used for induction and maintenance of general anesthesia. It reduces the blood pressure and frequently decreases the pulse rate and depresses respiration. Source: https://www.drugbank.ca/drugs/DB01159

Part II—The Motor Neuron

Halothane clearly had an effect on Mr. Thompson’s voluntary motor system. During this case study you will determine the location of this effect by looking at the normal function of motor nerves, chemical synapses, and the muscles. You will determine how halothane could act to produce strong and prolonged muscle contractions.

Step 1 – An action potential enters the presynaptic terminal.

Step 2 – Voltage-gated channels open and sodium and potassium ions enter the presynaptic terminal.

Step 3 – Sodium ion cause vesicular membrane to fuse with the presynaptic membrane.

Step 4 - Neurotransmitter liberated into the synaptic cleft.

Discuss each of the four stages to whether halothane could alter motor neuron function to produce strong muscle contractions.

Explanation / Answer

Step 1 – An action potential enters the presynaptic terminal.

An action potential enters the presynaptic terminal--->Voltage-gated channels open and Sodium and Potassium ions enter the presynaptic terminal. Sodium ions cause the vesicular membrane to fuse with the presynaptic membrane.

Step 2 – Voltage-gated channels open and sodium and potassium ions enter the presynaptic terminal.

Halothane blocks the Na+ current without inducing a shift in the voltage-dependence of its steady-state inactivation and reduces voltage-activated K+ currents at least as much, if not more than Na+ current in the squid giant axon. Halothane depresses the delayed outward K+ current and slightly reduces the inward rectifier K+ current in cardiac myocytes.

Step 3 – Sodium ion causes the vesicular membrane to fuse with the presynaptic membrane.

Halothane exerts varied effects on the resting membrane potential (Vm) of excitable cells.

Step 4 - Neurotransmitter liberated into the synaptic cleft.

Acetylcholine is secreted into the cleft by the motor axon. The neurotransmitter reacts with vesicles on the muscle membrane. Channels open and the muscle membrane closes. The neurotransmitter is broken down by the presynaptic membrane in the synaptic cleft. The neurotransmitter is taken up into the presynaptic.cell.

After that, The sarcoplasmic reticulum (SR) is one of the intracellular sites of action of halothane which has been shown to increase Ca2+ release from the SR in skeletal muscle). Halothane prolonged the opening of isolated ryanodine receptor Ca2+release channels from the SR. The ryanodine receptor Ca2+ release channel or the ?1-subunit of the dihydropyridine receptor are thought to be involved in malignant hyperthermia, a pharmacogenetic disorder. The effects of halothane on muscle membrane protein regulatory Ca2+-homeostasis have shown that halothane influenced Ca2+-ATPases induced oligomerization of the terminal cisternae Ca2+-binding protein calsequestrin, the junctional ryanodine receptor Ca2+-release channel and the transverse-tubular ?1-dihydropyridine receptor of rabbit skeletal muscle

Related Questions

Navigate

• Browse (All)
• Browse H
• Subjects

Integrity-first tutoring: explanations and feedback only — we do not complete graded work. Learn more.