In the disease myasthenia gravis, the human body makes—by mistake— antibodies to its own acetylcholine receptor molecules. These antibodies bind to and inactivate acetylcholine receptors on the plasma membrane of muscle cells. The disease leads to a devastating progressive weakening of the people affected. early on, they may have difficulty opening their eyelids, for example, and, in an animal model of the disease, rabbits have difficulty holding their ears up. As the disease progresses, most muscles weaken, and people with myasthenia gravis have difficulty speaking and swallowing. eventually, impaired breathing can cause death. explain which step of muscle function is affected.

In the disease myasthenia gravis, the human body makes—by mistake— antibodies to its own acetylcholine receptor molecules. These antibodies bind to and inactivate acetylcholine receptors on the plasma membrane of muscle cells. The disease leads to a devastating progressive weakening of the people affected. early on, they may have difficulty opening their eyelids, for example, and, in an animal model of the disease, rabbits have difficulty holding their ears up. As the disease progresses, most muscles weaken, and people with myasthenia gravis have difficulty speaking and swallowing. eventually, impaired breathing can cause death. explain which step of muscle function is affected.

Medical Terminology for Health Professions, Spiral bound Version (MindTap Course List)

8th Edition

ISBN:9781305634350

Author:Ann Ehrlich, Carol L. Schroeder, Laura Ehrlich, Katrina A. Schroeder

Publisher:Ann Ehrlich, Carol L. Schroeder, Laura Ehrlich, Katrina A. Schroeder

ChapterCom: Comprehensive Medical Terminology Review

Section: Chapter Questions

Problem 10RS

See similar textbooks

Similar questions

A nerve conduction velocity test measures nerve conduction velocity. In this test, an electrical stimulus is applied to a peripheral nerve and the length of time it takes for the corresponding muscle to contract is measured. Because the length of the nerve from stimulus point to muscle and the time it takes for the muscle to contract are both known, NCV can be calculated. This test result is helpful in distinguishing between different types of pathologies. For example, a patient with muscle weakness is being tested by a physician. There are three possible sources of the weakness: Disease of the muscle itself such as muscular dystrophy. In this condition, normal muscle tissue is replaced by adipose tissue and the muscle becomes incapable of contraction. Disease at the neuromuscular junction (NMJ) such as myasthenia gravis. This condition is described in the Skeletal Muscle Histology exercise and results from damage to the acetylcholine receptors on the muscle end plate. Disease…
Some drugs and toxic compounds interfere with removal of neurotransmitters from the synaptic cleft once they have been released. (1) Explain the two basic mechanisms affected by Sarin nerve gas and the drug Prozac. (2) If you were investigating an autoimmune disease that appeared to interfere with removal of neurotransmitters from the synaptic cleft, and you were able to isolate the causative antibody from the patient's serum, how could you use that antibody to investigate whether it affected one of the two inactivation mechanisms?
Halle Zingiber has been granted refugee status in this country. He has had to leave his wife and two children in Ethiopia. He is severely depressed and is receiving treatment with the tricyclic depressant, nortriptyline. No effects were reported when standard doses of the drug (25 mg tds) were used. His doctor increased the dose many-fold to 200 mg/day a dose, which is inducing effects. Can you explain Halle’s unusual response to therapy?
Conotoxin is produced by marine cone snails. Among its effects is to block voltage-gated Ca2+ channels in n eurons. A. What anatomical part of a neuron would be affected by conotoxin? B. How would the neuron's action potential be affected by conotoxin? Explain, using at least TWO of the following terms: threshold, depolarization, repolarization, hyperpolarization, summation, IPSP, EPSP, exocytosis C. If conotoxin affected a somatic motor neuron, would this toxin cause muscle weakness or increased muscle tension? Explain why.
A patient has been exposed to the organophosphate pesticide malathion,which inactivates acetylcholinesterase. Which of the following symptoms would you predict: blurring of vision, excess tear formation, frequent or involuntary urination, pallor (pale skin), muscle twitching, orcramps? Would atropine be an effective drug to treat the symptoms?(See Clinical Impact 16.2 for the action of atropine.) Explain.
When the neurotransmitter acetylcholine (ACh) binds the acetylcholine receptor (a GPCR) on muscle cells, it causes them to contract. ZIGGY, a chemical analog of ACh, also binds to the same acetylcholine receptor on muscle cells, but instead causes the muscle cells to relax. For this reason, it is sometimes prescribed as a muscle relaxer. Explain in 3-4 sentences how ZIGGY could cause muscle relaxation. How can both ZIGGY and ACh bind the same GPCR? And then how can they have different effects on the cells, despite binding to the same receptor on the same cells?
Organophosphate poisoning is a result of excess acetylcholine at different nerves and receptors in the body because acetylcholinesterase is blocked. Please provide rational to explain how the binding of organophosphate with serine in the acetylcholinesterase enzyme leads to excess accumulation of acetylcholine.
Students in a veterinary school are given the following hypotheticalproblem: A dog ingests organophosphate poison, and the students areresponsible for saving the animal’s life. Organophosphate poisons bindto and inhibit acetylcholinesterase. Several substances the studentscould inject include the following: acetylcholine, curare (which blocksacetylcholine receptors), and potassium chloride. If you were a studentin the class, what would you advise to save the animal?
Denervation supersensitivityof the muscle in LMN lesions is due to : -a- increased release of neurotransmitter from the degenerating nerve terminalsb- decreased release of neurotransmitter from the degenerating nerve terminalsc- increased number of transmitter receptors in fibers of the denervated muscled- decreased number of transmitter receptors in fibers of the denervated muscle
Organophosphate poisoning is a result of excess acetylcholine at different nerves and receptors in the body because acetylcholinesterase is blocked. Please provide rational to explain how the binding of organophosphate with serine in the acetylcholinesterase enzyme leads to excess accumulation of acetylcholine.
The drug Celebrex selectively inhibits PTGS2 while aspirin and other NSAID’s inhibit both PTGS1 and PTGS2 in the same way. Why do you think researchers wanted to discover a selective inhibitor to PTGS2?
Correct the following false statement: "Any cell that has the acetylcholine receptor will have the same response as any other cell that also has the acetylcholine receptor when exposed to acetylcholine". Explain why this statement is false.