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Cardiovascular

Pharmacology: Cardiovascular

QuestionAnswer
1. Three calcium channel blockers 2. Which is a dihydropyridine? 1. Verapamil, diltiazem, nifedipine 2. Nifedipine
Which calcium channel blockers: 1. have greater vasodilator effects? 2. are used for arrhythmias? 1. nifedipine (dihydropyridine class) 2. Verapamil, diltiazem
1. Verapamil and diltiazem bind __ channels. 2. First line drug for hypertension in pregnancy? 1. L-type calcium channels 2. methydopa or hydralazine
Hydralazine 1. Mechanism 2. Side effects 1. ↑cGMP → vasodilation 2. tachycardia, SLE-like syndrome
Minoxidil 1. Mechanism 2. Side Effects 1. opens K+ channels causing arteriolar vasodilation 2. tachycardia, edema, hirsutism (used in Rogain), hyperglycemia (↓ insulin release)
What is the normal role of calcium in smooth muscle? calcium enters vascular smooth muscle and activates MLCK MLCK phosphorylates myosin myosin can bind actin for contraction
1. Nitroprusside overdose can lead to 2. Fenoldopam mechanism of action 1. cyanide toxicity 2. D1 agonist causing renal vascular dilation
1. Two potassium channel blockers used in hypertension? 2. Three drugs used in malignant hypertensive emergencies 1. Diazoxide, Minoxidil 2. nitroprusside, diazoxide, fenoldopam
Aliskiren mechanism of action Renin inhibitor
Why are angiotensin receptor blockers effective at treating hypertension 1. reduce aldosterone levels 2. prevent ATII from causing renal vasoconstriction
1. Adverse effects of ACE inhibitors 2. Contraindications 1. angioedema, cough, hyperkalemia, 1st dose hypotension 2. acute renal failure in renal artery stenosis
1. Two α2 selective agonists 2. How do α2 agonists decrease blood pressure? 1. clonidine and methyldopa 2. α2 receptor activation will inhibit sympathetic neurotransmitter release
Adverse effect of: 1. clonidine 2. methyldopa 1. severe rebound hypertension on discontinuation 2. hemolytic anemia
β1-Specific antagonists (BAMAB) 1. Betaxolol 2. Atenolol 3. Metoprolol 4. Acebutolol 5. Bisoprolol
Prazosin 1. Mechanism of action 2. labelled use other than hypertension 1. α1 selective anagonist 2. benign prostatic hyperplasia
Contraindication of nonspecific β-blockers 1. bronchospasm in asthmatics 2. diabetics - block glycogenolysis and gluconeogenesis causing hypoglycemia
1. First line drug for hypertension 2. Drug of choice for diabetic hypertensive patients 3. Drug of choice for CHF hypertensive patients 1. thiazide diuretic 2. ACE inhibitor or ARB 3. β-blocker
How do the following components change when taking nitrates: 1. end diastolic volume 2. blood pressure 3. contractility 4. heart rate 5. ejection time 6 MVO2 1. ↓ 2. ↓ 3. ↑(reflex) 4. ↑(reflex) 5. ↓ 6. ↓
How do the following components change when taking β-blockers: 1. end diastolic volume 2. blood pressure 3. contractility 4. heart rate 5. ejection time 6 MVO2 1. ↑ 2. ↓ 3. ↓ 4. ↓ 5. ↑ 6. ↓
Mechanism of action of digoxin 1. inhibits Na+/K+ ATPase 2. leads to inhibition of Na+/Ca2+ exchanger 3. ↑ Ca2+
1. Used to treat edema with alkalosis 2. What is the difference in effects of spironolactone and amiloride 1. Acetazolamide 2. spironolactone blocks the aldosterone receptor while amioride blocks the ENaC epithelial sodium channel in the collecting duct
Mechanism of action of: 1. Triamterene 2. Hydrochlorothiazide 3. Carvedilol 4. Reserpine 1. blocks the ENaC epithelial sodium channel in the collecting duct (like amiloride) 2. blocks Na/Cl transporter in distal convoluted tubule 3. non-specific β-block/α1-blocker 4. blocks VMAT the pump involved in CNS catecholamine reuptake
1. What drug is used to treat ventricular arrhythmia after an MI? 2. Which antiarrhythmic class binds only to abnormally paced cardiac cells? 3. What is the biochemical affect of group 1A antiarrhythmics? 1. lidocaine (group 1B) 2. group 1B (as in after an MI) 3. block Na+ and K+ channels, antimuscarinic
Which antiarrhythmic drugs have the side effect of torsades any drug that ↓ K+ phase 2 current involved in repolarization → prolonged QT interval. Amiodarone, 1A drugs, Dofetilide, sotalol
How do the group 1 drugs change the action potential duration? 1. 1A 2. 1B 3. 1C 1. prolong 2. shorten (by acting on slow Na+ "window" currents 3. no effect
1. What is the mechanism of action of sotalol? 2. PSVT treatment (Wolff-Parkinson White) 1. K+ channel blocker and β-blocker 2. 1A or III antiarrhythmics
1. Mechanism of action of adenosine? 2. Statin mechanism of action 1. Gi coupled decrease in cAMP opens K+ channels in SA/AV node → hyperpolarization 2. inhibit HMG-CoA reductase
1. inhibits GI uptake of cholesterol 2. mechanism of action of fibrate 1. Ezetimibe 2. PPAR-α agonist (upregulate LPL to remove triglycerides from blood)
1. lipid-lowering drug used when triglycerides are elevated 2. Primarily act to ↓ VLDL synthesis 1. Fibrate 2. niacin
What effect do bile acid resins and statins have that dramatially lower LDL levels 1. primarily act to ↓ cholesterol in the hepatic pool 2. compensatory ↑ in liver LDL receptors → ↑ removal of LDL lipoproteins from blood
1. What combination of drugs significantly increases the incidence of rhabdomyolysis? 2. Which laboratory test is used to detect increased muscle breakdown in patients taking lipid-lowering drugs? 3. Which enzyme can be taken to decreases rhabdomyolysis 1. statins and fibrates 2. creatine kinase 3. Coenzyme Q
1. Which hypertension medication is contraindicated in individuals with diabetes? 2. Treatment for symptomatic Premature Ventricular Contraction 1. K+ channel blockers 2. β-blocker
1. What drug is used to reverse peripheral vasoconstriction caused by norepinephrine 2. used to reverse acute heart failure in cardiogenic shock and cardiac surgery 1. phentolamine - blocks α receptors in periphery 2. dobutamine
Most effective HDL-raising drug niacin
How do bile-acid resins and Ezetimibe differ in action? 1. resins ↓ reabsorption of all fat 2. Ezetimibe ↓ reabsorption of cholesterol alone
1. Which antihyperlipid drug is useful for pregnant women? 2. Which two antihyperlipid drugs are hepatotoxic? 1. bile acid resin 2. niacin and statins
1. Best tolerated agent in combination with statins? 2. Drug given to reduce triglyceride count if fibrates fail. 1. Ezetimibe 2. Niacin
Treatment of Atrial fibrillation 1. Rate control: Ca2+ channel, β-blocker (group II or IV) 2. Conversion: (group IA and III) dofetilide or procainamide
Treatment of atrial flutter Same as fibrillation but may anticoagulate
1. What drug ↓ vascular events in individuals with a low LDL but high CRP? 2. How do statins gain access to the liver? 1. statin 2. organic acid transporters
Two main side effects of statins 1. mialgia/rhabdomyolis 2. hepatotoxicity
1. Which lipid lowering drug is contraindicated in patients with hypertriglyceridemia? 2. What drug is useful? 1. bile-acid resins 2. fibrates
1. Does statin + niacin decrease the risk of CVD and stroke? 2. What effect do calcium channel blockers have on preload and afterload? 1. no 2. relaxes arterial smooth muscle so ↓ afterload, no effect on preload
1. Treatment for prinzmetal (variant) angina? 2. How do ACE inhibitors effect preload and afterload? 1. dihydropiridine calcium channel blockers 2. ↓ both
1. Which class of drug is amlodipine? 2. How does hypokalemia effect cardiac impulse 1. dihydropyridine calcium channel blocker (like nifedipine) 2. delays repolarization and prolongs the QT interval
1. How does hypokalemia effect the polarization of cells? 2. How does hyperkalemia effect the polarization of cells? 1. hyperpolarizes cells 2. depolarizes cells (peaked T wave)
1. Treatment of heart failure with Atrial fibrillation 2. Why 1. digoxin 2. ↑ inotropy, ↑PR interval so slower repolarization
1. Diuretic used to treat nephrolithiasis? 2. Treatment of hypertension with CHF 1. thiazide decrease calcium secretion 2. ACE inhibitor
Treatment for: 1. hypertension with diabetes 2. African Americans with hypertension 3. hypertension with benign prostatic hyperplasia 1. ACE inhibitor 2. diuretic or calcium channel blocker 3. α1-antagonist (prazosin, terazosin)
Inappropriate treatment of ventricular tachycardia with calcium channel blockers can result in __. ventricular fibrillation - Calcium channel blockers are indicated for SVT b/c they slow A/V conduction. In ventricular tachycardia, Ca2+ channel blockers can slow atrial rate to where the ventrical takes over its own rhythm
What effect do β blockers have on the RAAS system? inhibition of β1 receptors in the juxtaglomerular cells → ↓ renin release
↑ cAMP effect in: 1. Heart 2. Arteries 1. ↑ contraction (β1) 2. vasodilaton (β2)
1. Which antilipid drug causes skin flushing 2. What medication can one take to counteract this effect? 1. niacin causes skin flushing by ↑ prostaglandins 2. aspirin can prevent
Endocarditis prophylaxis for dental surgery? amoxicillin
Endocarditis Rx for: 1. Streptococcal sp. 2. Staphylococcus 3. Enterococcus 4. Fungal 1. Penicillin G 2. Nafcillin/Oxacillin 3. Ampicillin 4. Amphotericin B
Which Na+ channel conformation do the following Na+ channels blockers have the greatest effect on: 1. 1A 2. 1B 3. 1C 1. open, active state 2. inactive/refractory state 3. resting state and both other states
1. Which cardiac cells do β-blockers act on the most? 2. Which phases of the action potential are most effect by β-blockers? 1. SA, AV nodal cells 2. phase 0 and phase 4
1. Adverse effect of quinidine 2. Why are these effects seen? cinchonism - nausea/vomiting, tinitus, ocular dysfunction, headache 2. quinidine has antimuscarinic and α-blocking characteristics
Adverse effects of procainamide 1. SLE-like syndrome 2. thrombocytopenia 3. torsades
1. biochemical effect of β-blockers? 2. cardiac effect of β-blockers? 1. ↑cAMP 2. ↓SA and AV nodal activity
1. Which phase of the cardiac action potential do K+ channel blockers act on? 2. What causes the extensive side effects of amiodarone? 1. phase 3 2. extensive binding of tissues due to high iodine content
What are the side effects of amiodarone? 1. pulmonary fibrosis 2. blue pigmentation of skin 3. thyroid dysfunction 4. torsades
1. Adenosine antagonist 2. Side effect of reserpine? 1. theophylline 2. depression from lack of catecholamines; edema
1. Which antihypertensive may increase LDL? 2. Which antihypertensive may decrease LDL? 1. β blockers 2. α1 blockers
Side effects of nifedipine 1. reflex tachycardia 2. gingival hyperplasia
1. Treatment of pulmonary hypertension? 2. Drugs mechanism of action? 1. Bosentan 2. Endothelin-A receptor antagonist → pulmonary vasodilation
1. Which hypertensive meds work better in African Americans? 2. Mechanism of action of Nesiritide 1. diuretics and calcium channel blockers 2. recombinant form of BNP → guanylyl cyclase → ↑ cGMP →vasodilation
What effect does hypokalemia have on digoxin? more digoxin can bind the Na/K exchanger, worsening digoxin toxicity
1. Nitroglycerin side effect: 2. Treatment of angina 1. headache (from meningeal artery vasodilation) 2. nitrate, CCBs, and beta blockers
Action of Nitric Oxide in angina: 1. NO stimulates guanylyl cyclase 2. guanylyl cyclase converts GTP to cGMP 3. cGMP results in arteriol relaxation
1. What role does myosin light chain kinase (MLCK) play in contraction? 2. MLCK in inactivated through which pathway? 3. MLCK is activated through which pathway? 1. MLCK phosphorylates and activates myosin light chain which combines with actin for contraction 2. β2 → cAMP → PKA → MLCK phosphorylated and inactivated 3. α1,M3 → Gq → Ca+calmodulin → active MLCK
1. Antihyperlipid drug that causes malabsorption of lipid soluble vitamins 2. Which drugs utilize the same signaling pathway as endogenous bradykinin on smooth muscle? 1. bile acid sequestrants 2. cGMP pathway of nitric oxide
Which drug should you be concerned about if the patient is a slow acetylator: 1. Sotalol 2. Clonidine 3. Nitroglycerin 4. Hydralazine 5. Prazosin 4. Hydralazine
A patient with a SVT and atrial rate of 280/ventricular rate of 140. A drug is given and the atrial rate slowed to 180 but ventricular rate rose to 180. Which drug might have caused this effect? 1. adenosine 2. digoxin 3. esmolol 4. quinidine 5. Vera 4. quinidine increased AV condution by blocking action of muscarinic receptors in the heart. This effect can be offset by prior administration of digoxin or verapamil which slow AV nodal conduction.
Treatment for: 1. Digoxin induced tachyarrhythmia 2. Digoxin induced fibrillation 3. Drug induced torsades 4. Ventricular fibrillation 5. Arrhythmia prophylaxis following an MI? 1. Digoxin-immune Fab 2. lidocain, phenytoin 3. magnesium sulfate 4. amiodarone 5. β-blocker
1. Antihypertensive that causes gingival hyperplasia 2. Indirect effect of digoxin that causes ↓ heart rate and ↑ contraction is from: 1. nifedipine 2. depolarization of nerve terminals in both parasympathetic (↓HR) and sympathetic (↑ contraction) nerves
1. Antihypertensive agent given to patients with osteoporosis 2. Which group 1 antiarrhythmic dissociates fastest from the Na+ receptor? 3. Rapidly acting anti-arrhythmic causing flushing and dyspnea 1. Hydrochlorothiazide (↑ calcium reabsorption) 2. group 1B (b/c it binds least avidly) 3. adenosine
Which antilipidemic medications may cause gall stones? bile acid resins and fibrates
Mechanism of action of Ranolazine Inhibits fatty acid oxidation
Relative recovery time of group 1 antiarrhythmics: 1. 1A 2. 1B 3. 1C 1. middle (5s) 2. shortest (1s) 3. longest (>10s)
The congenital defect known as Epstein's anomaly, in which the tricupsin valve is displaced down toward the apex of the right ventricle, is caused by taking this drug during pregnancy. Lithium (large right atrium and small left ventricle)
How can one tell the difference between β1-selective and non-selective β-blockers by name alone? 1. Those that start with letters A through M are β1-selective 2. those starting with letters after M are non-selective
Class I antiarrhythmic used post-MI Class IB (Lidocaine)
Created by: amichael87