A patient who is taking morphine for pain asks the nurse how a pain medication can also cause constipation. What does the nurse know about morphine?
It binds to different types of receptors in the body
It can cause constipation in toxic doses
It is selective to receptors that regulate more than one body process
It causes only one type of response, and the constipation is coincidental
The Correct Answer is A
Choice A reason: Morphine, an opioid, binds to mu, kappa, and delta receptors in the brain, spinal cord, and gastrointestinal tract. Mu receptors in the gut slow peristalsis, causing constipation, while central receptors relieve pain. This multi-receptor binding explains both therapeutic and side effects, making this the correct choice.
Choice B reason: Constipation from morphine occurs at therapeutic, not just toxic, doses due to mu receptor activation in the gastrointestinal tract, which reduces motility. Toxicity may worsen side effects, but constipation is a common effect at standard doses, making this choice inaccurate for explaining morphine’s mechanism.
Choice C reason: Morphine’s receptors (e.g., mu) regulate multiple processes, but the drug itself isn’t selective to multifunctional receptors. It binds broadly to opioid receptors, causing both analgesia and side effects like constipation. This choice misrepresents morphine’s non-selective binding, making it less accurate than choice A.
Choice D reason: Morphine’s effects, including analgesia and constipation, result from specific receptor binding, not coincidental processes. It activates opioid receptors in the brain for pain relief and in the gut for reduced motility. This choice incorrectly suggests constipation is unrelated to morphine’s pharmacological action, making it incorrect.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
Choice A reason: Beta 1-adrenergic drugs, like dobutamine, stimulate beta-1 receptors in the heart, increasing cyclic AMP and calcium influx, enhancing myocardial contractility. This increases stroke volume by strengthening heart contractions, directly improving cardiac output, making this the correct choice for the drug’s mechanism of action.
Choice B reason: Cardiac afterload is the resistance the heart pumps against. Beta 1-adrenergic drugs don’t directly reduce afterload; they increase contractility. Increasing afterload would decrease stroke volume, opposing the drug’s purpose, making this choice incorrect for the drug’s effect on stroke volume.
Choice C reason: Venous return affects preload, not directly influenced by beta 1-adrenergic drugs. These drugs enhance contractility, increasing stroke volume independently of venous return. While preload impacts output, it’s not the primary mechanism of beta-1 stimulation, making this choice incorrect.
Choice D reason: Cardiac preload is the initial stretch of the heart, influenced by venous return. Beta 1-adrenergic drugs increase contractility, not preload, to boost stroke volume. Preload changes are secondary and not the primary action of these drugs, making this choice incorrect.
Correct Answer is D
Explanation
Choice A reason: Insulin does not stimulate the liver to convert glycogen to glucose; instead, it promotes glycogenesis and inhibits glycogenolysis. By facilitating glucose uptake and storage, insulin lowers blood glucose levels, counteracting the process of glycogen breakdown into glucose, which is regulated by glucagon and other hormones, making this choice incorrect.
Choice B reason: Insulin does not promote amino acid synthesis into glucose (gluconeogenesis). It inhibits gluconeogenesis in the liver, reducing glucose production from amino acids and other substrates. By enhancing glucose uptake and storage, insulin maintains glucose homeostasis, making this option incorrect as it misrepresents insulin’s role in glucose metabolism.
Choice C reason: Insulin does not stimulate the pancreas to reabsorb glucose. The pancreas produces insulin, which acts on target tissues like muscle and fat to facilitate glucose uptake. Glucose reabsorption occurs in the kidneys, regulated by sodium-glucose cotransporters, not insulin, making this choice scientifically inaccurate for insulin’s function.
Choice D reason: Insulin promotes glucose uptake into cells by facilitating GLUT4 transporter translocation to cell membranes in muscle and adipose tissue. This allows glucose to enter cells for energy production via glycolysis and the Krebs cycle. This is insulin’s primary role in maintaining blood glucose homeostasis, making it the correct choice for its action.
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