ATI RN
Chapter 11 Cardiovascular Drugs Test Questions Quizlet Questions
Question 1 of 5
Tick the drug used for malaria chemoprophylaxis and treatment:
Correct Answer: A
Rationale: Certainly! Chloroquine is the correct answer for malaria chemoprophylaxis and treatment because it is effective against Plasmodium species. It acts by accumulating in the parasite's food vacuole, interfering with heme polymerization. This prevents the parasite from utilizing hemoglobin and ultimately leads to its death. Quinidine and quinine are primarily used for severe malaria treatment. Sulfonamides are not commonly used for malaria treatment due to resistance issues and their limited efficacy against Plasmodium species.
Question 2 of 5
Which of the following would be an appropriate therapeutic adjustment for the patient with hypermagnesemia, vomiting, and heart failure?
Correct Answer: D
Rationale: Correct Answer: D Rationale: 1. Hypermagnesemia can exacerbate heart failure. 2. Vomiting may further worsen magnesium levels. 3. Digoxin toxicity is a concern in hypermagnesemia. 4. Discontinuing digoxin is crucial to avoid adverse effects. 5. Starting losartan can help manage heart failure without worsening hypermagnesemia. Summary: A: Adding potassium may worsen hypermagnesemia. B: Atropine is not indicated for hypermagnesemia or heart failure. C: Increasing furosemide may lead to electrolyte imbalances. D: Discontinuing digoxin and starting losartan is the appropriate therapeutic adjustment.
Question 3 of 5
How is plasminogen converted into active plasmin?
Correct Answer: A
Rationale: The correct answer is A: By binding to fibrin. Plasminogen is converted into active plasmin by binding to fibrin through the tissue plasminogen activator (tPA). This binding triggers the activation of plasminogen into plasmin, which then degrades fibrin clots. The other choices (B: collagen, C: heparin, D: platelets) are incorrect because plasminogen activation specifically involves binding to fibrin to initiate the fibrinolytic cascade. Collagen, heparin, and platelets do not play a direct role in the conversion of plasminogen to plasmin.
Question 4 of 5
Regarding verapamil, which one of the following statements is false?
Correct Answer: B
Rationale: Verapamil is a calcium channel blocker commonly used to treat various cardiovascular conditions. In this question, the false statement is option B - "Contraindicated in the asthmatic patient." Verapamil is not contraindicated in asthmatic patients; however, caution is advised in patients with significant left ventricular dysfunction or heart failure. Option A is correct because angina pectoris is indeed an important indication for using verapamil. Verapamil helps dilate coronary arteries, improving blood flow to the heart muscle and reducing the workload on the heart. Option C is correct as verapamil relaxes vascular smooth muscle, leading to vasodilation. This property helps lower blood pressure and improve blood flow throughout the body. Option D is correct as verapamil slows the depolarization phase of the action potential in AV nodal cells. This effect is why it is commonly used to treat certain arrhythmias by slowing down the electrical conduction in the heart. In an educational context, understanding the pharmacological actions of verapamil is crucial for healthcare providers managing patients with cardiovascular conditions. Knowing the indications, contraindications, and effects of verapamil helps ensure safe and effective medication administration. It also highlights the importance of careful consideration based on individual patient characteristics when prescribing cardiovascular drugs.
Question 5 of 5
The primary mechanism of beneficial effect of glyceryl trinitrate in classical angina pectoris is
Correct Answer: C
Rationale: In the treatment of classical angina pectoris, glyceryl trinitrate's primary beneficial effect lies in its ability to reduce cardiac preload. This means that glyceryl trinitrate works by decreasing the amount of blood returning to the heart during diastole, which in turn lowers the pressure within the heart's chambers. By reducing preload, the heart has to work less to pump blood out to the rest of the body, thus decreasing the oxygen demand on the heart muscle. In the context of angina pectoris, which is chest pain or discomfort caused by reduced blood flow to the heart muscle, reducing cardiac preload is crucial as it helps to alleviate the workload on the heart and decrease the oxygen demand. This reduction in workload can help alleviate the symptoms of angina by decreasing the heart's oxygen requirements and improving overall cardiac function. Now, let's examine why the other options are incorrect: - Option A, an increase in total coronary blood flow, is not the primary mechanism of action for glyceryl trinitrate in angina pectoris. - Option B, redistribution of coronary blood flow, is not the primary mechanism of action for glyceryl trinitrate in angina pectoris. - Option D, reduction of cardiac afterload, while important in some cardiovascular conditions, is not the primary mechanism of action for glyceryl trinitrate in angina pectoris. Understanding the mechanism of action of cardiovascular drugs like glyceryl trinitrate is crucial for healthcare professionals to provide effective patient care and manage cardiovascular conditions. By grasping the specific effects of medications, healthcare providers can tailor treatment plans to individual patient needs, ensuring optimal outcomes and symptom management.