The nurse is caring for a patient who has multiple sclerosis. The patient is experiencing an acute attack. Which drug does the nurse anticipate the provider will order?
Interferon-B (IFN-B)
Mitoxantrone
Glatiramer acetate (Copaxone)
Methylprednisolone (Solu-Medrol)
The Correct Answer is D
A) Interferon-B (IFN-B): Interferon-beta is a disease-modifying therapy (DMT) used for multiple sclerosis (MS) to reduce the frequency and severity of attacks and slow disease progression. However, it is not typically used during an acute exacerbation of MS. It is more commonly prescribed for long-term management of the disease.
B) Mitoxantrone: Mitoxantrone is an immunosuppressive agent that is used as a disease-modifying therapy for patients with more aggressive forms of MS. While it can be helpful in reducing the frequency of attacks, it is not the first-line treatment during an acute relapse. Mitoxantrone is often considered for long-term use when other therapies are not effective.
C) Glatiramer acetate (Copaxone): Glatiramer acetate is another disease-modifying therapy for MS. It works by altering the immune response to protect the myelin sheath. Like interferon-beta, it is used for long-term management, not for acute attacks. It is not typically used during an exacerbation of MS.
D) Methylprednisolone (Solu-Medrol): Methylprednisolone, a corticosteroid, is the standard treatment for acute exacerbations of multiple sclerosis. It works by reducing inflammation, which helps to decrease the severity of symptoms during an MS relapse. The nurse would anticipate this drug being prescribed to manage the acute inflammatory episode and speed recovery from the attack. This medication is often administered intravenously in high doses and then tapered as the patient stabilizes.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is C
Explanation
A) Excessive salivation: Neostigmine (Prostigmin) is a cholinesterase inhibitor, which works by increasing the levels of acetylcholine at neuromuscular junctions. If a dose is missed, excessive salivation can be a side effect of too much acetylcholine activity, but it is not the most immediate symptom in this case. Muscle weakness is a more direct consequence of a missed dose.
B) Respiratory paralysis: While respiratory weakness or paralysis can occur in myasthenia gravis, it is usually associated with a severe form of the disease or if the patient is in a myasthenic crisis. A single missed dose of neostigmine typically does not result in respiratory failure unless the patient is already in a very fragile state.
C) Muscle weakness: Neostigmine helps to improve neuromuscular transmission by inhibiting the breakdown of acetylcholine, which is crucial for muscle contraction. A missed dose would directly lead to a reduction in acetylcholine levels, exacerbating the characteristic muscle weakness of myasthenia gravis. Muscle weakness is the most anticipated symptom when neostigmine is not administered on time.
D) Muscle spasms: Muscle spasms are typically not a symptom of missed neostigmine therapy. Instead, muscle weakness occurs due to impaired neuromuscular transmission. Spasms might occur if there is significant overstimulation of the muscles, but this is more associated with electrolyte imbalances or other neuromuscular issues
Correct Answer is B
Explanation
A) Pupil constriction: Pupil constriction (miosis) is primarily mediated by the parasympathetic nervous system through muscarinic receptors, not nicotinic receptors. Nicotinic receptors, when stimulated, affect skeletal muscle contraction, not the size of the pupils.
B) Muscle contraction: Nicotinic receptors are located on skeletal muscle cells and are responsible for mediating muscle contraction when activated. When a drug stimulates nicotinic receptors, the expected outcome is muscle contraction, as these receptors play a critical role in neuromuscular transmission.
C) Increase GI motility: While nicotinic receptors are involved in muscle contraction, they are not the primary mediators of gastrointestinal motility. Muscarinic receptors, which are part of the parasympathetic nervous system, primarily control GI motility. Stimulating muscarinic receptors would lead to increased motility, but not nicotinic receptors.
D) Decrease in heart rate: A decrease in heart rate is typically associated with the stimulation of muscarinic receptors, particularly those that influence the parasympathetic nervous system (vagal tone). Nicotinic receptor activation does not directly influence heart rate; in fact, their stimulation is more related to skeletal muscle contraction.
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