钙拮抗剂（Calcium antagonists）

钙拮抗剂（Calcium antagonists） 钙拮抗剂(Calcium antagonists) The fifteenth chapter is calcium antagonist Section 1 Classification and drug name of calcium antagonists [assistant does not require] Selective calcium antagonists (I) Vera Pammy, paraffin. (zy2003-1-222) (two) two dihydropyridine, nifedipine, nimodipine, nitrendipine and amlodipine. (three) diltiazem and diltiazem. Two 、 non selective calcium antagonists (a) two benzene piperazine flunarizine and cinnarizine. (two) class prenylamine prenylamine. (three) other classes of methylphenidate. The following is zy2003-1-222. Phenylalkylamine calcium antagonist is the selective The A. of nifedipine The B. of verapamil Prenylamine * C. D. perhexilin " The E. of flunarizine Answer: B " The pharmacological action and clinical application of second calcium antagonists I. pharmacological effects (I) myocardium 1. the negative inotropic effect of calcium antagonists can reduce the content of Ca2+ in myocardial cells, causing negative inotropic effect, can make the myocardial oxygen consumption is reduced, and the drug induced vasodilation, the cardiac afterload decreased, the myocardial oxygen consumption decreased further. 2. negative chronotropic and dromotropic slow response cells such as sinoatrial node and atrioventricular node 0 phase and 4 phase pole automatic slow depolarization and Ca2+ influx. The 0 phase of polarization and conduction, and the 4 phase automatic depolarization and self. Calcium antagonists could inhibit the Ca2+ flow in the above cases. It can cause negative frequency and negative conduction, such as slow conduction of atrioventricular node, prolongation of refractory period, reentry and excitement. It can be used to treat paroxysmal supraventricular tachycardia. Calcium antagonists can reduce the automaticity of the sinoatrial node and slow the heart rate. 3. myocardial ischemia protection, myocardial ischemia, sodium pump and calcium pump inhibited and calcium passive transport to strengthen, can make intracellular calcium accumulation, resulting in excessive calcium overload, and ultimately lead to myocardial cell damage. Calcium antagonists can reduce intracellular calcium and protect cardiomyocytes. (two) the contraction of the vascular smooth muscle is also regulated by intracellular Ca2+, and the calcium twist can block the flow of Ca2+, which can dilate the blood vessels and increase the coronary flow. The nimodipine and flunarizine has strong dilation of cerebral blood vessels, increase blood flow to the brain function. (three) other smooth muscle can relax the bronchi, gastrointestinal tract, ureter and uterine smooth muscle. (four) improve the blood flow 1. inhibition of platelet aggregation. 2. increase the deformability of erythrocytes, reduce the blood viscosity, and improve the blood flow. (five) other functions 1., anti atherosclerosis. 2., inhibiting the role of endocrine glands, large doses of drugs can inhibit the pituitary gland secretion of oxytocin, vasopressin and inhibition of anterior pituitary secretion of ACTH, gonadotropin and thyroid stimulating hormone. It also inhibits insulin and aldosterone secretion. (XL2007-1-042) The pharmacological action of XL2007-1-042. calcium antagonist is A. atrioventricular nodal conduction is accelerated B. increases blood viscosity C. promotes platelet aggregation D. anti atherosclerosis E. increases insulin secretion Answer: D Two 、 clinical application (1) angina pectoris has different curative effects on all types of angina pectoris. 1. calcium antagonists are the first choice for variant angina pectoris. (zy2006-1-061) The preferred drug for zy2006-1-061 variant angina pectoris is A. amiodarone B.ACEI C. lidocaine D. nifedipine E. propranolol Answer: D 2. stable (exertional) angina is common in patients with coronary atherosclerosis. In fatigue, heart work increases and blood supply is insufficient, leading to angina attacks, calcium antagonists to dilate the blood vessels, heart rate slowed, contraction force decreased, blood pressure dropped, so that myocardial oxygen consumption dropped, So as to relieve angina pectoris. Vera Pammy and diltiazem are optional. 3. unstable angina is caused by the formation or rupture of atherosclerotic plaques and the increase of coronary resistance. It is more severe and can attack both day and night. Vera Pammy and diltiazem can also be selected. (two) arrhythmia is good for arrhythmia induced by supraventricular tachycardia and posterior depolarization. Commonly used Vera Pammy and diltiazem. (three) hypertension nifedipine is better for severe hypertension, while Vera Pammy and diltiazem has used for mild and moderate hypertension. (four) patients with hypertrophic cardiomyopathy often have excessive amounts of Ca2+ in myocardial cells, so calcium antagonists are commonly used for the treatment of Vera Pammy. (five) cerebral vascular disease of nimodipine and flunarizine drug has the effect of dilation of cerebral blood vessels, the cerebral blood flow increased, the formation of the treatment of cerebral thrombosis and cerebral embolism, cerebral vasospasm after subarachnoid hemorrhage effectively. (six) other patients with Raynaud's disease can be treated with nimodipine or nifedipine by cold or emotion induced vasospasm. In addition, calcium antagonists have certain effects on bronchial asthma, achalasia of the esophagus and stomach, spastic abdominal pain, premature birth, dysmenorrhea, etc.. (zy2005-4-060; zy2005-1-058; zy1999-1-078) Zy2005-4-060 has a strong effect on the expansion of cerebral vascular calcium antagonists is the The A. of verapamil The B. of nifedipine The C. of nimodipine The D. of diltiazem The E. gallopamil Answer: in the C Zy2005-1-058; zy1999-1-078. The calcium antagonists, the main drugs used for the treatment of cerebrovascular disease is the The A. of verapamil The B. of nifedipine C. diltiazem in the Prenylamine * D. The E. of nimodipine Answer: in the E in The sixteenth chapter is antiarrhythmic drugs Section 1 Classification of antiarrhythmic drugs Class I sodium channel blockers Class IA moderate block sodium channels, such as quinidine and disopyramide, procainamide etc.. Class IB slightly blocks sodium channels such as lidocaine, phenytoin, Carney, and so on. The IC class blocks sodium channels, such as fluorine, Carney, and Proba. Class II beta adrenergic receptor blocking drugs, such as propranolol. A class III drug that selectively prolongs repolarization, such as amiodarone. Class IV calcium antagonists, such as Vera Pammy. (zy2003-1-179) Anti arrhythmic drugs. Zy2003-1-179 belongs to the IC class is the The A. of quinidine The B. of lidocaine The C. of propafenone The D. of amiodarone The E. of verapamil Answer: C " Second lidocaine I. pharmacological effects Lidocaine inhibits the influx of Na + and promotes the outflow of K+, only for the general purpose system. (zy2001-1-064) (-) treatment can reduce the concentration of reducing the self-discipline of the Purkinje fiber self-discipline. (two) conduction velocity has no effect on conduction velocity, but lidocaine can slow conduction when blood K+ rises and blood tends to sour. When the blood K+ decreased or myocardial depolarization part, lidocaine by promoting K+ efflux to hyperpolarization of Purkinje fiber (resting potential downward) and accelerated velocity. High concentration lidocaine significantly inhibited the rate of 0 phase rise and slowed conduction. (three) shall not shorten the period can be shortened Purkinje fibers and ventricular muscle APD, ERP, but APD was shorter than ERP, so relatively prolonged. Two 、 clinical application For the treatment of ventricular arrhythmias such as acute myocardial infarction and ventricular contractions caused by cardiac glycosides, ventricular tachycardia and ventricular fibrillation. (zy2003-1-488) The following zy2001-1-064. of atrial fibrillation is the drug therapeutic effect A. (the cardenolide glycosides) The B. of quinidine The C. of lidocaine D. Veerappa Mi The E. of propranolol Answer: C " Third propranolol I. pharmacological effects (a) to reduce the autonomy of propranolol can reduce the sinoatrial node, self-discipline atrial conduction fibers and Purkinje fibers. (two) conduction velocity, propranolol, does not affect conduction velocity at the concentration of beta blockers. As the dose increases, a membrane stabilizing effect, the drug conduction velocity was slow atrioventricular node and Purkinje fibers. (three) the treatment period should not concentration can make APD and ERP Purkinje fiber shortened, high concentration can be prolonged. The atrioventricular node ERP has an obvious prolongation effect. Two 、 clinical effect Supraventricular arrhythmias, including sinus tachycardia, atrial fibrillation, flutter, and paroxysmal supraventricular tachycardia, are often associated with the use of cardiac glycosides to control ventricular rate. (two) ventricular arrhythmias are effective for ventricular arrhythmias induced by exercise and emotional agitation, hyperthyroidism and pheochromocytoma. (zy2001-1-063) Drug zy2001-1-063. With anti arrhythmia, anti hypertension and anti angina effect is the The A. of clonidine The B. of propranolol The C. of lidocaine The D. of nitroglycerin The E. of hydrochlorothiazide Answer: in the B Propranolol - commonly used, has many uses. Fourth section amiodarone I. pharmacological effects Amiodarone prolongs APD and ERP, blocks Na +, Ca2+ and K+ channels, and blocks the action of alpha and beta receptors. (a) reduce the self-discipline self-discipline of sinoatrial node and Purkinje fibers. Associated with the drug block of Na +, Ca2+ and channel blocker. (two) conduction velocity Purkinje fiber and atrioventricular nodal conduction velocity. With the block of Na +, Ca2+ channel. (three) refractory period can make the atrial and ventricular muscle and Purkinje fibers of APD and ERP were significantly prolonged, and blocking K+ channels and Na + channels. Two 、 clinical application For a variety of supraventricular and ventricular arrhythmias, such as for the elimination of atrial fibrillation and maintenance of sinus rhythm, paroxysmal supraventricular tachycardia, or intravenous injection for severe ventricular tachycardia and ventricular fibrillation treatment. Oral administration is also used for the prevention of ventricular tachycardia and ventricular fibrillation. (XL2007-3-022; zy2005-1-065; zy2002-1-056; zl2006-1-032; zl2007-1-032;) The major ion channel associated with the mechanism of XL2007-3-022 action with amiodarone on ventricular myocytes is ADP A.Na channel B.Ca2+ channel C.Mg2+ channel D.C1- channel E.K+ channel Answer: E Zy2005-1-065. And the major ion channels in ventricular myocytes of amiodarone prolonged APD mechanism is the The A.Na channel The B.Ca2+ channel The C.Mg2+ channel The D.Cl- channel The E.K+ channel Answer: in the E The zy2002-1-056 of amiodarone. The A. extension APD, Na + in flow block B. shortened APD, the Na + in flow block C. ERP K+ to promote the extension, outflow D. shortened APD, blocking the receptor beta E. shortened ERP, blocking the receptor alpha Answer: in the A Zl2006-1-032. amiodarone prolongs refractory period by blocking A.0 phase Na + flow B.3 phase K+ outflow C.0 phase Ca2+ internal flow D.4 phase Na + flow E.4 phase Ca2+ internal flow Answer: B Fifth quarter Vera Pammy Treatment of paroxysmal supraventricular tachycardia caused by atrioventricular nodal reentry. For patients with atrial fibrillation or flutter can reduce ventricular rate. Generally not in combination with beta blockers. (zy2003-1-489; zy2003-1-490; zy2003-1-491) (488 ~ 491 share the answers) The following drugs should be selected for the disease A. diltiazem (diltiazem) " The B. of digitalis The C. of atropine The D. of lidocaine Amiodarone in E. Zy2003-1-488. Acute anterior wall myocardial infarction and accelerated idioventricular rhythm Answer: the answer is the market popular books D Beijing Medical Training Center Dr. Zhang admitted to answer C determined by research Zy2003-1-489 preexcitation syndrome with the rapid atrial fibrillation Answer: E " Analysis: amiodarone can prolong the atrioventricular bypass refractory period, slow down the conduction pathway and slow down the ventricular rate in patients with atrial fibrillation. In Zy2003-1-490. The hypertrophic obstructive cardiomyopathy Answer: A " Analysis: diltiazem is a calcium channel blocker, which can improve cardiac diastolic function and relieve obstruction of left ventricular outflow tract. In Zy2003-1-491. The anterior wall myocardial infarction complicated with paroxysmal ventricular tachycardia and the Answer: in the D The seventeenth chapter is the treatment of congestive heart failure Cardiac glycosides Pharmacological effects and clinical application of digoxin I. pharmacological effects 1. positive inotropic effect strengthens the contractility of the myocardium, which shows the highest myocardial contraction, the increase of the tension and the maximum shortening rate, and the myocardial contraction is powerful and swift. 2. negative frequency action can slow down the sinoatrial node frequency. It is mainly related to the vagus nerve excitability induced by drugs. 3. effects on electrophysiological properties (1): to reduce the amount of self treatment of sinus node automaticity, Purkinje fibers improve self-discipline. (2) conduction: slow atrioventricular nodal conduction. (3): shortening of the atrial effective refractory period and effective refractory period of Purkinje fibers. 4., the influence of ECG treatment can cause the amplitude of T wave to decrease, depress or even reverse, S T segment hook shape decreased (bow), and then P - R interval lengthened. The shortening of Q - T interval and prolongation of P - P interval were also observed. Two 、 clinical application 1. chronic or congestive heart failure (CHF) is better for CHF with atrial fibrillation, which can increase cardiac output, decrease the pressure and volume of the end diastolic and relieve the symptoms of CHF. It is good for valvular disease, hypertension and congenital heart disease. CHF is ineffective in severe mitral stenosis and constrictive pericarditis. 2. arrhythmia for the treatment of atrial fibrillation and atrial flutter. (zy2005-1-059; zy2000-1-83; zy1999-1-079) Zy2005-1-059; zy1999-1-079. Cardiac glycosides (saponins) on chronic heart failure caused by which of the following is not the reason of the effect of good The A. of hyperthyroidism The lack of vitamin B1 B. The C. severe mitral stenosis The D. of congenital heart disease The E. of constrictive pericarditis Answer: in the D The mechanism of zy2000-1-83. cardiac glycosides for treating atrial fibrillation is the main A. the shortening of the atrial effective refractory period The B. slow atrioventricular conduction C. inhibited the sinoatrial node The D. direct inhibition of atrial fibrillation E. extended the atrial refractory period Answer: B " Second angiotensin converting enzyme inhibitors Mechanism of anti heart failure Angiotensin converting enzyme inhibitors (ACEI) have been one of the most important advances in the past 10 years. Clinical studies have shown that ACEI can not only reduce symptoms of heart failure, but also reduce the mortality of GHF patients in GHF. The mechanism of action mainly involves the following aspects: (a) the activity of ACEI inhibits angiotensin converting enzyme inhibition and angiotensin converting enzyme activity, thereby inhibiting the conversion of angiotensin I into angiotensin II, the blood and tissues of AT II level decreased. It also can reduce the metabolism of bradykinin and increase the content of bradykinin in blood, which can promote the synthesis of NO, vascular endothelial hyperpolarizing factor and PGI2. Besides, ACEI can directly or indirectly reduce catecholamine and vasopressin levels of active substances in the blood, restore the downregulation of beta 1 receptor number, Gs protein and lead to increased adenylate cyclase activity and intracellular cAMP levels increased to improve. (two) hemodynamic agents can reduce the resistance of systemic vessels in different degrees, and reduce the pulmonary wedge pressure, the right atrial pressure, and the ventricular wall tension. Compared with other vasodilators, these drugs are difficult to produce resistance for a long time. (three) inhibition of hypertrophy and hyperplasia of myocardium and vessels, hypertrophy of myocardium and vascular remodeling is the main risk factor of CHF. A small dose of ACEI can effectively prevent or reverse ventricular remodeling, hypertrophy and thickening of the fibrotic tissue and the coronary wall in the muscularis, resulting in increased myocardial and vascular compliance. In addition, ACEI increases bradykinin levels and also contributes to reversal of hypertrophy. (zy2008-1-053; zy2000-1-84) The mechanism of zy2008-1-053 captopril in the treatment of heart failure is A. increases norepinephrine secretion B. reduces prostaglandin synthesis C. antagonized the action of calcium ions D. reduces the production of angiotensin II II E. increases myocardial oxygen consumption Zy2008-1-053 answer: D Item analysis: this question is to understand the memory type questions, Kato Pury belongs to the angiotensin converting enzyme inhibitor (ACEI), its mechanism of action: (a) the activity of ACEI inhibits angiotensin converting enzyme inhibition and angiotensin converting enzyme activity, thereby inhibiting the conversion of angiotensin I into angiotensin II, the blood and tissue AT II level decreased. It also can reduce the metabolism of bradykinin and increase the content of bradykinin in blood, which can promote the synthesis of NO, vascular endothelial hyperpolarizing factor and PGI2. In addition, ACEI can directly or indirectly reduce catecholamine and vasopressin levels of active substances in the blood, restore the downregulation of beta 1 receptor number, Gs protein and lead to increased adenylate cyclase activity and intracellular cAMP levels increased to improve. (two) hemodynamic agents can reduce the resistance of systemic vessels in different degrees, and reduce the pulmonary wedge pressure, the right atrial pressure, and the ventricular wall tension. Compared with other vasodilators, these drugs are difficult to produce resistance for a long time. (three) inhibition of hypertrophy and hyperplasia of myocardium and vessels, hypertrophy of myocardium and vascular remodeling is the main risk factor of CHF. A small dose of ACEI can effectively prevent or reverse ventricular remodeling, hypertrophy and thickening of the fibrotic tissue and the coronary wall in the muscularis, resulting in increased myocardial and vascular compliance. In addition, ACEI increases bradykinin levels and also contributes to reversal of hypertrophy. Analysis of the correct answer: according to the above-mentioned mechanism of captopril against heart failure, mainly to inhibit the activity of angiotensin converting enzyme, reduce the generation of angiotensin ii. Alternative answer analysis: other options do not match the questions. Train of thought expands: by this question, we must know the question teacher's train of thought: the angiotensin converting enzyme inhibitor (ACEI) is often tests the medicine, its function mechanism must grasp emphatically. Zy2000-1-84. is a drug that treats chronic cardiac insufficiency and reverses cardiac hypertrophy and reduces mortality A. cardiac glycoside B. prazosin C. nitroglycerin D. Phentolamine E. captopril Answer: E The eighteenth chapter Kangxin colic medicine [new syllabus content] Section 1 nitroglycerin First, these drugs have the structure of nitric acid polybasic ester, fat soluble high, -O-N02 in the molecule is the key structure to play a therapeutic effect. Nitroglycerin is most commonly used in this class of drugs. Nitroglycerin is a representative drug of nitrates. It is still the most commonly used medicine for the prevention and treatment of angina pectoris because of its quick onset, positive curative effect, convenient use and economy. Pharmacological action, the basic function of nitroglycerin is to relax the smooth muscle, but the selectivity of the different tissues and organs is different, which plays the most significant role in the vascular smooth muscle. Because nitroglycerin expands the circulation of blood vessels and coronary vessels, it acts as follows: 1. reduce myocardial oxygen consumption 2. dilating the coronary artery, increasing the blood perfusion in the ischemic zone 3. decreased left ventricular filling pressure, increased endocardial blood supply, and improved left ventricular compliance 4. protection of ischemic myocardial cells, reduce ischemic injury of nitroglycerin release N0, endogenous PGl2, calcitonin gene related peptide (CGRP) substances such as the generation and release of these substances, have a direct protective effect on myocardial cells. The mechanism of action is that nitroglycerin, as a donor of nitric oxide (N0), catalyzes the release of N0 from the smooth muscle cells by glutathione transferase. The N0 receptor is Fe2+. soluble guanylate cyclization enzyme active center two binding after activation of guanylate cyclase (GC), increase the content of intracellular second messenger cGMP, which can activate cGMP dependent protein kinase (cGMP), the decrease of Ca2 ten and Ca2+ - release within the flow cell in the Ca2+ to reduce the dephosphorylation of myosin light chain and vascular smooth muscle relaxation. Second beta adrenergic blockers [assistants do not require] Anti angina effect 1. reduce the myocardial oxygen consumption, the beta receptor blocker can significantly reduce the myocardial oxygen consumption by antagonizing the beta receptor, reducing myocardial contractility, shortening the rate of myocardial fiber shortening, slowing heart rate and lowering blood pressure. However, it can increase ventricular volume by inhibiting myocardial contractility. Meanwhile, ventricular oxygen consumption increases with prolongation of ventricular ejection time, but the total effect is still decreasing myocardial oxygen consumption. The clinical observation showed that the patients with heart rate decrease, diastole prolongation and contraction force decrease were the best. If the heart rate is increased by atrial pacing, propranolol loses the effect of anti angina, indicating that its anti angina action is associated with slowing the heart rate. 2. improving the vascular tension of the ischemic and ischemic areas after ischemia, and increasing the blood flow to the compensatory ischemic areas, thus increasing the blood flow in the ischemic areas. Second, because heart rate is slowing, the diastole is relatively prolonged, which facilitates the flow of blood from epicardial blood vessels to the ischemic endocardium. In addition, collateral circulation in the ischemic zone can also be increased, and blood perfusion in the ischemic zone is increased. In addition, this class of drugs by blocking beta receptor, inhibited lipolytic enzyme activity, reduce myocardial free fatty acid content; improve glucose uptake in ischemic myocardium and improve glucose metabolism, reduce the oxygen consumption; promote the oxyhemoglobin dissociation of oxygen binding and increase the oxygen supply. Third calcium antagonists [assistant does not require] The effect of anti angina and the mechanism of calcium channel blockers are to block the flow of Ca2+ through blocking Ca2+ channels: 1., reduce myocardial oxygen consumption, calcium channel blockers can reduce myocardial contractility, heart rate slowed, vascular smooth muscle relaxation, blood pressure drops, cardiac load reduction, thereby reducing myocardial oxygen consumption. 2. diastolic coronary vascular dilatation of the drug transport large and small vascular resistance and coronary blood vessels, especially has a significant effect on relieving spasm in spasticity of the blood vessels, thereby increasing blood perfusion of ischemic area. In addition, the collateral circulation can be increased, and the blood supply and oxygen supply in the ischemic areas can be improved. 3. the protection of myocardial cells in ischemia, can increase the permeability of cell membrane of Ca2+, increased calcium influx or intra cell interference Ca2+ to extracellular transport, the intracellular Ca2+ accumulation, especially in mitochondria of Ca2+ overload, and lose the ability of oxidative phosphorylation and induce cell death. Ca2+ channel blockers protect myocardial cells by inhibiting the influx of extracellular calcium and attenuate Ca2+ overload in ischemic myocardium, which can reduce infarct size in patients with acute myocardial infarction. 4. inhibition of platelet aggregation, unstable angina pectoris is associated with platelet adhesion and aggregation, reduction of coronary blood flow, and most acute myocardial infarction is also caused by atherosclerotic plaques rupture, Partial formation of thrombus; sudden occlusion of coronary artery. Calcium channel blockers block Ca2+ influx, decrease Ca2+ concentration in platelets, and inhibit platelet aggregation.