Drugs do not metabolize the same way in all people. For what patient would a nurse expect to assess for an alteration in drug metabolism?

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.

A) Inhibit cyclooxygenase that is necessary for prostaglandin synthesis:
NSAIDs primarily work by inhibiting the enzyme cyclooxygenase (COX), which plays a crucial role in the conversion of arachidonic acid into prostaglandins. Prostaglandins are chemicals that promote inflammation, pain, and fever in response to injury or infection. By blocking COX, NSAIDs reduce the production of prostaglandins, thereby decreasing inflammation and alleviating pain and fever.

B) Exert direct actions to cause relaxation of smooth muscle:
NSAIDs do not directly cause the relaxation of smooth muscle. While some other classes of drugs (e.g., bronchodilators) target smooth muscle relaxation, NSAIDs primarily work by reducing the production of prostaglandins, which in turn alleviates inflammation and pain. They do not have a significant effect on smooth muscle tone itself.

C) Suppress prostaglandin activity by blocking tissue receptor sites:
NSAIDs do not block the receptor sites for prostaglandins; rather, they inhibit the cyclooxygenase enzyme, which is responsible for the synthesis of prostaglandins. This reduces the overall production of prostaglandins, rather than blocking their activity at the receptor level.

D) Interfere with neuronal pathways associated with prostaglandin action:
While NSAIDs reduce prostaglandin production, they do not directly interfere with neuronal pathways associated with prostaglandin action. They act primarily by inhibiting the cyclooxygenase enzyme to reduce the synthesis of prostaglandins at the site of injury or inflammation, rather than by modulating specific neural pathways.