ATI RN
Peter Attia Drugs Cardiovascular PCSK9 Questions
Question 1 of 5
The prescriber has changed the patient’s medication regimen to include the leukotriene receptor antagonist montelukast (Singulair) to treat asthma. The nurse will emphasize which point about this medication?
Correct Answer: C
Rationale: Step 1: Montelukast is a leukotriene receptor antagonist used for long-term control of asthma symptoms. Step 2: It works by blocking leukotrienes, which are responsible for inflammation and bronchoconstriction in asthma. Step 3: Taking montelukast daily maintains a consistent level in the body to effectively prevent asthma symptoms. Step 4: Even if symptoms improve, discontinuing montelukast abruptly can lead to a recurrence of symptoms. Step 5: Therefore, emphasizing the need for continuous daily use is crucial for optimal asthma management. Summary: A: Inhaler technique is not relevant for montelukast as it is taken orally, not inhaled. B: Montelukast is not a rescue medication for acute asthma attacks; it is for long-term control. D: Tapering or discontinuing montelukast without consulting the prescriber can lead to worsening of symptoms.
Question 2 of 5
What is the type of drug-to-drug interaction which is connected with processes of absorption, biotransformation,distribution and excretion?
Correct Answer: D
Rationale: The correct answer is D: Pharmacokinetic interaction. This type of drug interaction involves processes like absorption, distribution, metabolism, and excretion in the body. In pharmacokinetic interactions, one drug can affect the absorption, metabolism, or elimination of another drug, leading to changes in their effectiveness or toxicity. Pharmacodynamic interactions (A) involve how drugs affect the body at the target site. Physical and chemical interactions (B) refer to how drugs interact based on their chemical properties. Pharmaceutical interactions (C) are related to drug-drug interactions that occur during formulation or administration.
Question 3 of 5
Which of the following local anesthetics is more cardiotoxic?
Correct Answer: B
Rationale: The correct answer is B: Bupivacaine. Bupivacaine is more cardiotoxic compared to the other local anesthetics listed. This is due to its higher potency in blocking cardiac sodium channels, leading to a higher risk of cardiac toxicity, including arrhythmias and cardiac arrest. Procaine, lidocaine, and mepivacaine are less cardiotoxic as they have lower affinity for cardiac sodium channels and are less likely to cause significant cardiac adverse effects. It is important to be cautious when using bupivacaine to minimize the risk of cardiotoxicity.
Question 4 of 5
The mechanism of atropine action is:
Correct Answer: B
Rationale: The correct answer is B: Competitive muscarinic blockade. Atropine is an anticholinergic drug that works by competitively blocking muscarinic receptors, leading to inhibition of parasympathetic nervous system activity. This results in effects such as increased heart rate and dilated pupils. A: Competitive ganglion blockade is incorrect as atropine does not act on ganglionic receptors. C: Competitive neuromuscular blockade is incorrect as atropine does not affect neuromuscular junctions. D: Noncompetitive neuromuscular blockade is incorrect as atropine does not act in a noncompetitive manner on neuromuscular receptors.
Question 5 of 5
Which of the following diseases can augment the neuromuscular blockade produced by nondepolarizing muscle relaxants?
Correct Answer: A
Rationale: The correct answer is A: Myasthenia gravis. In myasthenia gravis, there is a decrease in the number of available acetylcholine receptors at the neuromuscular junction, leading to muscle weakness. Nondepolarizing muscle relaxants work by blocking acetylcholine receptors, so in myasthenia gravis, there are fewer receptors available for the drug to bind to, resulting in an augmented neuromuscular blockade. Burns (B), asthma (C), and Parkinsonism (D) do not directly affect the number of acetylcholine receptors at the neuromuscular junction, so they would not enhance the blockade produced by nondepolarizing muscle relaxants.