Skip to ContentGo to accessibility pageKeyboard shortcuts menu
OpenStax Logo

Case Study

c. These drugs prevent the enzyme cholinesterase from breaking down ACh, allowing more of this neurotransmitter to accumulate in the synapses and continuing to stimulate the cholinergic receptors at the NMJ. This stimulation causes increased skeletal muscle contraction.
b. MG is an autoimmune disease in which the client produces antibodies that destroy functional receptors at the NMJ, causing muscle weakness.

Review Questions

a. The drug will cross the blood–brain barrier, has a 70-hour half-life, and is unaffected by oral intake.
b. Because a decreased level of ACh is present in this disease, decreasing the action of AChE can help reduce the symptoms because less ACh will be broken down.
a. The patch needs to be changed every 24 hours, not weekly. All the other options are correct statements.
b. Memantine is an NMDA receptor antagonist. When too much calcium enters the cell, it makes it extremely excitable, interfering with cognition. Too much calcium is toxic. Normally, glutamate binds to the NMDA receptors for a brief period, allowing the calcium channel to open. Glutamate then dissociates from the receptors and magnesium binds to the NMDA receptors, closing the calcium channel and preventing further calcium from entering.
c. Propranolol is a nonselective beta blocker; therefore, one would be concerned about extremely low heart rate plus bronchoconstriction.
b. There is a potential for serious and life-threatening skin rashes when using this drug. Stevens–Johnson syndrome, a disorder of the skin and mucous membranes characterized by a painful rash that disseminates, is one example. Blisters form, and eventually the top skin layer will die and shed.
c. The drug was prescribed as a disintegrating tablet, so it must completely dissolve on the tongue. It is not to be chewed, crushed, or swallowed whole.
d. The AChE inhibitors prescribed for myasthenia gravis increase muscle strength and muscle relaxation. Since clients may have drooping of the eyes due to muscle weakness, the ability to raise the eyelids independently is evident of increased muscle strength.
c. Because the client’s dose was increased, they are at risk for cholinergic crisis. This is characterized by increased urine output, diarrhea, vomiting, excess salivation, and diaphoresis.
b. If there is cholinergic toxicity, an anticholinergic should be given to counteract the signs and symptoms. For instance, atropine will increase the heart rate and decrease intestinal motility and inhibit contraction of the detrusor muscle.

This book may not be used in the training of large language models or otherwise be ingested into large language models or generative AI offerings without OpenStax's permission.

Want to cite, share, or modify this book? This book uses the Creative Commons Attribution License and you must attribute OpenStax.

Attribution information
  • If you are redistributing all or part of this book in a print format, then you must include on every physical page the following attribution:
    Access for free at
  • If you are redistributing all or part of this book in a digital format, then you must include on every digital page view the following attribution:
    Access for free at
Citation information

© May 15, 2024 OpenStax. Textbook content produced by OpenStax is licensed under a Creative Commons Attribution License . The OpenStax name, OpenStax logo, OpenStax book covers, OpenStax CNX name, and OpenStax CNX logo are not subject to the Creative Commons license and may not be reproduced without the prior and express written consent of Rice University.