The nurse administers a drug that causes vasoconstriction, contracted piloerection muscles, pupil dilation, closure of salivary sphincter, and male sexual emission. What receptor is the drug stimulating?

A) Central nervous system (CNS), memory, and cognition: Myasthenia gravis (MG) primarily affects the neuromuscular junction, causing muscle weakness, not directly the central nervous system. While cognitive function may be affected in some patients due to fatigue or medication side effects, it is not the main system affected by MG.

B) Cardiovascular system and postural muscles: Myasthenia gravis primarily affects skeletal muscles, especially those responsible for voluntary movements like facial muscles, swallowing, and respiratory muscles. While MG can lead to general weakness, it does not typically affect the cardiovascular system directly.

C) Respiratory system and facial muscles: This is the correct answer. Myasthenia gravis primarily affects the voluntary muscles, particularly those controlling eye movements, facial expressions, swallowing, and breathing. The respiratory system is vulnerable due to weakness of the diaphragm and intercostal muscles, which can lead to respiratory distress in severe cases. Facial muscles are commonly affected, leading to symptoms like ptosis (drooping eyelids) and difficulty smiling or speaking.

D) Gastrointestinal system (GI) and lower extremity muscles: Although myasthenia gravis can cause generalized muscle weakness, it is not typically associated with the gastrointestinal system. The primary impact is on the voluntary muscles, such as those in the face, throat, and respiratory system. Lower extremity muscles can be affected, but the respiratory and facial muscles are more commonly involved.

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.