While beta blockers have no value in the treatment of an acute angina, nifedipine immediate release (oral or sublingual) can help with an acute angina attach. However, immediate release nifedipine is not recommended to treat an acute angina attach. Why?
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While beta blockers have no value in the treatment of an acute angina, nifedipine immediate release (oral or sublingual) can help with an acute angina attach. However, immediate release nifedipine is not recommended to treat an acute angina attach. Why?
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- A patient with chronic-stable angina begins taking metoprolol, and once blood levels reach the therapeutic range the frequency and severity of angina attacks and the need for sublingual nitroglycerin were reduced. Which of the following states the direct pharmacologic action by which the beta-blocker produced the desired effects? Decreased myocardial oxygen demand Dilated coronary vasculature Directly inhibited angiotensin II synthesis Reduced total peripheral resistanceA patient has frequent episodes of paroxysmal supraventricular tachycardia (PSVT). Which of the following drugs would be most suitable for outpatient prophylaxis of these events? Adenosine Lidocaine Nifedipine VerapamilAntihypertensive treatment with calcium channel blockers (CCBs) is often offered to patients with stage 2 hypertension. Please describe the intracellular signaling events, mechanisms of action on blood vessels and important adverse effects of CCBs. In addition, describe considerations such as the age of a patient when prescribing a CCB at the first stage of antihypertensive therapy according to NICE guidelines.
- A patient with chronic-stable angina is on prophylactic beta-blocker therapy, with sublingual nitroglycerin used PRN (as needed) for managing acute angina. One day he experiences particularly severe angina and takes the usually recommended dose of sublingual nitroglycerin (NTG). His discomfort is not reduced at all. Seeking relief, he repeats the usual recommended dose of NTG dose 6 times over a period of about 10 minutes, and now has taken far too much of the nitrovasodilator. An electrocardiogram taken by the paramedics, who were called for the patient’s emergency, shows changes consistent with myocardial ischemia. The patient incurs a massive infarction, goes into cardiac arrest, and cannot be resuscitated. Which of the following is the most likely cause of or contributing factor to the patient’s ultimately fatal response to the excessive dosage of NTG? Assume the patient was taking no other drugs except the NTG and a beta-blocker. Cyanide, or toxic metabolite of NTG, accumulated.…Name and explain the mechanism of action of the anticoagulants: calcium chelators (oxalate, citrate, EDTA, fluoride), warfarin, and heparin.Distinguish between arterial (white) and venous (red) clots in terms of composition and sites of formation. Know which anticoagulants would be used to treat each.Indicate and explain two of the positive effects of beta block in angina pectoris
- in stroke, how drug alters that mechanism to provide relief?why is administration of a thrombolytic agent is a first intervention for someone who has suffered a thrombotic stroke?Summarize the basic features and treatments of Angina and Arrhythmias including Antianginal and Antiarrhythmic and how they are used to treat the condition? Briefly describe how Adenosine receptor agonists works and the side effects?
