A client primary care provider prescribed a B-adrenergic receptor blocker. Which of the following therapeutic effects do the client and care provider likely seek?

A) Norepinephrine: Norepinephrine is a neurotransmitter primarily involved in the sympathetic nervous system. It is not involved in terminating the stimulation caused by acetylcholine. Norepinephrine acts on adrenergic receptors, whereas acetylcholine primarily acts on cholinergic receptors.
B) Decarboxylase: Decarboxylase is an enzyme that plays a role in the synthesis of certain neurotransmitters, including dopamine, but it does not have a role in terminating the action of acetylcholine at the effector cell. It is unrelated to the termination of acetylcholine signaling.
C) Catecholamine: Catecholamines (such as dopamine, norepinephrine, and epinephrine) are a group of neurotransmitters involved in the sympathetic nervous system. While they play a role in synaptic transmission, they are not responsible for breaking down acetylcholine or terminating its effects. Their primary function is in adrenergic signaling.
D) Acetylcholinesterase: Acetylcholinesterase is the correct enzyme. It is responsible for breaking down acetylcholine (ACh) in the synaptic cleft after it has stimulated the effector cell. By hydrolyzing acetylcholine into acetate and choline, acetylcholinesterase effectively terminates the signal and allows the effector cell's membrane to repolarize. This action prevents continuous stimulation and ensures proper function of the cholinergic system.

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.