A patient comes to the clinic complaining of seasonal rhinitis. What adrenergic agonist will be prescribed for seasonal rhinitis?

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) Increased calcium: Sympathetic activation typically does not cause a direct increase in calcium levels. Calcium levels are more influenced by factors like parathyroid hormone (PTH) and vitamin D, or conditions such as bone disease or renal issues. Although some stress responses can lead to changes in calcium metabolism, an increase in calcium is not a typical response to sympathetic activation.

B) Decreased sodium: While sodium imbalances can occur in various conditions, the sympathetic nervous system does not directly cause a decrease in sodium. The body's handling of sodium is more influenced by factors like kidney function and the renin-angiotensin-aldosterone system. Stress-related changes in sodium levels are less likely to cause a significant decrease in sodium, making this an unlikely focus in monitoring.

C) Decreased potassium: During stress, the body releases catecholamines (like epinephrine) as part of the sympathetic nervous response, which stimulates the movement of potassium into cells. This can result in a transient decrease in serum potassium levels (hypokalemia). Monitoring for decreased potassium is important, as low potassium can lead to cardiac arrhythmias and muscle weakness, which are particularly concerning after surgery or trauma.

D) Increased chloride: Chloride is typically maintained in balance with sodium, and while it may shift in certain conditions, sympathetic activation does not directly lead to increased chloride levels. Most chloride imbalances are secondary to changes in sodium, acid-base disturbances, or kidney function. Therefore, an increase in chloride is less likely in this scenario.