Block 9 Rx Antimuscarinic MCQ's

Atropine can most effectively counteract physostigmine-induced sweating. Atropine is an anticholinergic drug that blocks the effects of acetylcholine, the neurotransmitter responsible for stimulating sweat glands. Physostigmine, on the other hand, is a cholinesterase inhibitor that increases the levels of acetylcholine in the body, leading to excessive sweating. By blocking the effects of acetylcholine, atropine can effectively reduce or eliminate the sweating caused by physostigmine.

Antimuscarinic drugs block M3 receptors, which are involved in the synthesis of intracellular IP3. Therefore, the blockade of M3 receptors by these drugs would result in a decreased synthesis of intracellular IP3.

Glycopyrrolate is a medication commonly used to treat irritable bowel syndrome. The therapeutic effect of the drug in this patient can be explained by the blockade of M3 and Nn receptors. M3 receptors are found in the smooth muscles of the gastrointestinal tract, and blocking these receptors can help reduce the symptoms of irritable bowel syndrome such as abdominal pain and cramping. Nn receptors are nicotinic receptors found in the enteric nervous system, and blocking these receptors can also help alleviate symptoms by reducing the excessive activity in the gut. Therefore, the blockade of M3 and Nn receptors best explains the mechanism of action of glycopyrrolate in this patient.

Atropine is a medication that blocks the action of acetylcholine, a neurotransmitter that stimulates the contraction of smooth muscles. The mucociliary clearance refers to the movement of mucus and foreign particles out of the respiratory tract by the coordinated action of cilia. Atropine inhibits the activity of cilia, leading to a decrease in mucociliary clearance. Therefore, the correct answer is "Decreased mucociliary clearance."

Antimuscarinic drugs usually increase the heart rate because they can counteract the opening of K+ channels in the SA node. The SA node is responsible for initiating the electrical impulses that regulate the heart rate. Opening of K+ channels in the SA node leads to hyperpolarization, which slows down the heart rate. Antimuscarinic drugs block the effects of acetylcholine on the SA node, preventing the opening of K+ channels and allowing the heart rate to increase.

Ipratropium bromide is the only antimuscarinic drug used to treat bronchospastic disorders because it does not decrease bronchial secretions and mucociliary clearance. This is important because bronchospastic disorders, such as chronic obstructive pulmonary disease, involve excessive narrowing of the airways, leading to difficulty in breathing. By not decreasing bronchial secretions and mucociliary clearance, ipratropium allows for better clearance of mucus and maintains normal function of the cilia in the airways, helping to alleviate symptoms and improve airflow.

Nicotine is a stimulant that initially activates nicotinic receptors, leading to increased release of neurotransmitters like acetylcholine and catecholamines. However, with prolonged exposure to nicotine, desensitization of these receptors occurs, resulting in a long-lasting activation of the receptors. This leads to a ganglionic blockade, where the transmission of signals between neurons in the autonomic ganglia is inhibited. Therefore, the best explanation for the nicotine-induced ganglionic blockade is the long-lasting activation of nicotinic receptors.

A moderate dose of nicotine is most likely to stimulate the respiratory center. Nicotine is a stimulant drug that affects the central nervous system. It can increase heart rate, blood pressure, and respiration. Stimulation of the respiratory center would result in an increase in breathing rate and depth.

Antimuscarinic drugs are contraindicated in ulcerative colitis because they can worsen the symptoms of this inflammatory bowel disease. These drugs work by blocking the action of acetylcholine, a neurotransmitter that plays a role in gastrointestinal motility and secretions. In ulcerative colitis, there is already inflammation and damage to the lining of the colon, so blocking acetylcholine can further disrupt normal bowel function and exacerbate symptoms. Therefore, caution should be exercised when considering the use of antimuscarinic drugs in patients with ulcerative colitis.

The new synthetic drug X most closely resembles norepinephrine based on the changes in heart rate observed in the laboratory animals. Norepinephrine is a neurotransmitter and hormone that increases heart rate. Similarly, drug X also caused an increase in heart rate when administered to the animals. This suggests that drug X may have similar effects on the cardiovascular system as norepinephrine.

Darifenacin is an antimuscarinic drug used to treat overactive bladder. One of the common adverse effects of antimuscarinic drugs is constipation. Therefore, the statement "Darifenacin - constipation" correctly pairs the drug with its common adverse effect.

The most likely anti-muscarinic drug that the female volunteer was given is glycopyrrolate. This is because glycopyrrolate is known to block the effects of acetylcholine on the heart, leading to an increase in heart rate. In this case, the oral administration of glycopyrrolate before the injection of norepinephrine caused a significant increase in heart rate, suggesting that glycopyrrolate was able to counteract the bradycardic effects of norepinephrine. Atropine is also an anti-muscarinic drug, but it is not the most likely answer in this case as glycopyrrolate is more commonly used for this purpose.

Pretreatment with a ganglionic blocker will most effectively prevent norepinephrine-induced bradycardia. Ganglionic blockers block the transmission of signals between the pre- and post-ganglionic neurons in the autonomic nervous system. Norepinephrine acts on post-ganglionic sympathetic neurons to cause bradycardia. By blocking the ganglionic transmission, the effect of norepinephrine on the post-ganglionic neurons is prevented, resulting in the prevention of bradycardia.

Difficulty in near vision is a common side effect of quaternary ammonium antimuscarinic drugs. These drugs work by blocking the action of acetylcholine, a neurotransmitter that is involved in various bodily functions. By blocking the muscarinic receptors, these drugs can affect the muscles of the eyes, leading to difficulty in near vision. This side effect is often temporary and reversible once the drug is discontinued.