A patient who is taking amitriptyline (Elavil) reports constipation and dry mouth. The nurse will give the patient which instruction?

A) They increase norepinephrine at the neuromuscular junction: Anticholinergic agents do not directly increase norepinephrine at the neuromuscular junction. Instead, they work by blocking acetylcholine receptors (specifically muscarinic receptors) in the parasympathetic nervous system, which reduces parasympathetic activity. Norepinephrine is primarily involved in the sympathetic nervous system, not the action of anticholinergics.

B) They act to block the effects of the parasympathetic nervous system: This is the correct explanation. Anticholinergic agents work by inhibiting the action of acetylcholine at muscarinic receptors, which are part of the parasympathetic nervous system. By blocking these receptors, anticholinergics reduce parasympathetic effects such as slowing of the heart rate, increased glandular secretions, and smooth muscle contraction, leading to effects like increased heart rate, dry mouth, and bronchodilation.

C) They compete with serotonin for muscarinic acetylcholine receptor sites: Anticholinergic drugs do not interact with serotonin receptors. They specifically target muscarinic acetylcholine receptors, which are involved in parasympathetic responses. Serotonin is a different neurotransmitter, and while some drugs may affect both serotonin and acetylcholine pathways, anticholinergic agents do not compete with serotonin at these receptor sites.

D) They block nicotinic receptors: Anticholinergics typically block muscarinic receptors, not nicotinic receptors. Nicotinic receptors are involved in the transmission of signals at the neuromuscular junction and in the autonomic ganglia, while muscarinic receptors are primarily involved in parasympathetic functions. Blocking nicotinic receptors would have different effects and is not the action of anticholinergic agents.

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.