CARDIO: PHARM

Question 1

What is responsible for the timing of “Monday disease”?

Answer 1

Nitrates are associated with the following adverse effects:

1. Headache
2. Hypotension
3. Flushing
4. Reflex tachycardia (which can be prevented/treated with β-blockers)

Monday disease occurs when tolerance develops to the vasodilatory effects of nitrates during the work week, which wears off during the weekend. Upon re-exposure on Monday, the vasodilation results in tachycardia, dizziness, and headache.

The compensatory vasoconstriction on weekends can result in non-atherosclerotic ischemia and possibly cardiac arrest, the most serious complication.

Question 2

What are 2 key side-effects of methyldopa?

Answer 2

Two key side-effects of methyldopa include direct Coombs-positive hemolytic anemia and a SLE-like syndrome.

Question 3

What other antiarrhythmic class properties does amiodarone have besides its role as a K+ channel blocker?

Answer 3

Amiodarone has class I, II, III and IV effects since it alters the lipid membrane.

Question 4

What are the side effects of disopyramide?

Answer 4

Disopyramide—side effects:

1. Anticholinergic symptoms (blurry vision, urinary retention, dry mouth);
2. Heart failure
3. Torsades de pointes due to increased QT interval
4. Thrombocytopenia

Question 5

What are the cardiovascular side effects of amiodarone?

Answer 5

The cardiovascular side effects of amiodarone include bradycardia, heart block, and congestive heart failure

Question 6

What is the general mechanism of action of class IV antiarrhythmics?
Name 2 examples of class IV antiarrhythmics.

Answer 6

Class IV anti-arrhythmic agents are non-dihydropiridine calcium channel blockers (e.g., diltiazem, verapamil), which exert their anti-arrhythmic effect mainly by slowing AV node conduction by inhibiting Ca2+ influx.

Question 7

Describe the mechanism of action of resins (e.g., cholestyramine) in the treatment of hyperlipidemia.

Answer 7

The mechanism of bile acid resins is as follows:

1. Positively-charged bile acid resins bind negatively-charged bile acids, forming a complex
2. These complexes are excreted in stool, depleting the pool of bile acids (> 95% of bile acids are normally reabsorbed)
3. Hepatic synthesis of bile-acids increases, depleting hepatic cholesterol (bile acids are made from cholesterol)
4. Hepatocytes increase expression of LDL receptors
5. Serum LDL is reduced due to increased hepatic LDL uptake

Side effects of bile acid resins include:

1. GI discomfort (constipation, diarrhea, and flatulence)
2. Malabsorption of fat-soluble vitamins and drugs

Question 8

What is the mechanism of action of prazosin?

Answer 8

A:

Mechanism of prazosin: selective α1 receptor blockade which leads to vasodilation.

Question 9

What is the cellular target of ranolazine?

Answer 9

Ranolazine inhibits the late inward sodium current (INa) on cardiac myocytes.

Question 10

When taken with amiodarone, what cardiac drug shows markedly elevated levels due to decreased clearance?

Answer 10

Amiodarone decreases the clearance of digoxin leading to markedly elevated levels of digoxin when taken together.

Question 11

Which electrolyte imbalances will increase digoxin toxicity? Which combination drug therapies will increase digoxin toxicity?

Answer 11

Risks of Toxicity increased by:

1. Renal failure (only in digoxin)
2. Hypokalemia from diuretics (digoxin competes with K+ for the same binding site on Na+/K+ ATPase)
3. Hypomagnesemia
4. Quinidine, Amiodarone
5. Combination therapy with calcium channel blockers (especially Verapamil)

Note: Hyperkalemia indicates a poor prognosis in patient with digoxin toxicity.

Question 12

What is/are the possible side effect(s) of ibutilide?

Answer 12

The side effect of ibutilide is torsades de pointes.

Question 13

What are 3 commonly-tested Class IA antiarrhythmic agents?

Answer 13

Mnemonic: “Double Quarter Pounder”:

Disopyramide

Quinidine

Procainamide

Question 14

What are Class IA antiarrhythmics used for?

Answer 14

Class IA antiarrhythmics: used for most atrial and ventricular arrhythmias

Question 15

What do class III antiarrhythmics do?

Answer 15

Class III antiarrhythmics (AAs) block K+ channels and thus prolong repolarization.

Question 16

What is the classic buzzword for quinidine toxicity?

Answer 16

Quinidine—side effects = 3 T’s + cardiac depression:

Thrombocytopenia, Tinnitus, Torsades

Severe hypotension with cardiac arrest

The classic “buzzword” for quinidine toxicity is cinchonism, often described as tinnitus, blurred vision, dizziness, nausea, and vomiting.

Question 17

Name 3 different bile acid sequestrants.

Answer 17

Bile acid resins include:

Cholestyramine

Colestipol

Colesevelam

Question 18

What is the mechanism for methyldopa as a treatment for hypertension?

Answer 18

Mechanism of clonidine/methyldopa: Central α2 agonist. Acts in the vasomotor center of the medulla to decrease presynapstic norepinephrine release.

Question 19

What are some uses of minoxidil?

Answer 19

Minoxidil is a pro-drug that (upon sulfation by the liver) opens ATP-dependent potassium channels, causing hyperpolarization and subsequent relaxation of arteriolar smooth muscle. The net effect is arteriolar vasodilation.

Minoxidil is used in moderate to severe HTN. Because it causes hypertrichosis, or excessive hair growth, minoxidil is marketed as Rogaine.

Side effects of minoxidil and diazoxide include the following:

• Hypertrichosis (Minoxidil)
• Hyperglycemia (decrease insulin release from Diazoxide)
• Reflex tachycardia
• Edema

.

Question 20

What are the 3 components of the treatment of β-blocker toxicity?

Answer 20

The treatment for beta blocker toxicity is:

Glucagon, which increases cAMP in cardiac tissue

Saline

Atropine

Question 21

What ECG finding will be found following the administration of class II antiarrythmics (β-blockers)?

Answer 21

Class II antiarrythmics (β-blockers) decrease cAMP and Ca2+ currents, which leads to decreased SA and AV nodal activity.

Class II antiarrythmics (β-blockers) can be used to suppress abnormal pacemakers by decreasing the slope of phase 4 of the pacemaker cell action potential.

The AV node is particularly sensitive to the effects of class II antiarrythmics (β-blockers), thereby leading to an increased PR interval.

Question 22

What 2 drugs are specifically recommended for the treatment of NYHA class IV congestive heart failure?

Answer 22

Treatment for NYHA class IV or moderate to severe CHF:

Add digoxin for symptomatic relief (no improvement in mortality)

Spironolactone can also be added for treatment of NYHA class IV, as it has been shown to improve mortality in these patients.

Question 23

What are the side effects associated with dihydropyridine CCBs (calcium channel blockers)?

Answer 23

Side effects associated with dihydropyridine CCBs include:

Reflex tachycardia

Peripheral edema

Flushing

Dizziness

Constipation

Gingival hyperplasia

Question 24

Name 2 clinical uses of class IV antiarrythmics.

Answer 24

Class IV antiarrythmics are used in the prevention of nodal arrhythmias, as well as rate control during atrial fibrillation.

Question 25

Class IV antiarrythmics are used in the prevention of nodal arrhythmias, as well as rate control during atrial fibrillation.

Answer 25

Side effects associated with the prusside portion of nitroprusside include the following: ## Footnote Rebound HTN Cyanide toxicity (co-administered with nitrates and thiosulfate to decrease toxicity)

Question 26

Name the class III antiarrhythmic drugs.

Answer 26

Class III antiarrhythmics include amiodarone, ibutilide, dofetilide, andsotalol

Question 27

True or False: Digoxin binds to the intracellular subunit of the Na/K ATPase

Answer 27

Binds to extracellular α subunit of Na/K ATPase in myocytes

Question 28

Name 2 important side effects of statins.

Answer 28

Side effects of statins include: ## Footnote Myopathy/rhabdomyolysis, which is particularly common when used in combination with fibrates or niacin Hepatotoxicity which can manifest with elevated LFTs

Question 29

In the ER, a patient with coronary artery disease develops neck pain. An EKG reveals new ST depressions. In this patient, nitroglycerin administered sublingually reduces myocardial oxygen demand as a result of a reduction in which component? A Blood pressure B Intramyocardial tension C Sulfydryl bonds D Coronary vascular resistance E Heart rate

Answer 29

Intramyocardial tension Answer Explanation Nitroglycerin reduces venous tone, causing pooling of peripheral blood in the venous circulation. This both lowers peripheral arterial resistance and decreases the preload returning to the heart. As such, left ventricular end diastolic volume and therefore left ventricular end diastolic pressure are decreased. There is less stretch of the myocardial tissues, and less demand tension.

Question 30

What combination of drugs has been shown to benefit African-Americans in particular when treating congestive heart failure?

Answer 30

African American patients have also been found to benefit from hydralazine + nitrates.

Question 31

What two pathological conditions are cardiac glycosides used to treat?

Answer 31

Cardiac glycosides: generally used to treat congestive heart failure andatrial fibrillation.

Question 32

A patient comes into the ED with chest pain that is described as "squeezing." An EKG is ordered STAT and shows S-T segment changes suspicious for myocardial infarction. The patient is given aspirin, oxygen, morphine, and a vasodilator. The most likely vasodilator used results in what changes at the cellular level? A Block the efflux of potassium B Increase intracellular cAMP C Decrease intracellular calcium levels D Increase intracellular cGMP

Answer 32

Increase intracellular cGMP Answer Explanation When a patient has a myocardial infarction (MI), or MI is suspected, remember the mnemonic MONA: Morphine Oxygen Nitroglycerin Aspirin Nitroglycerin works by increasing the levels of nitric oxide in smooth muscle cells, resulting in an increase in intracellular cGMP. The cGMP then causes smooth muscle relaxation and vasodilation. It is an important component to the initial treatment of ischemic heart disease, including MI.

Question 33

Which of the following anti-arrhythmic drugs shows no change in the phase 0 upstroke but increases the effective refractory period of the action potential? A Atenolol B Adenosine C Diltiazem D Sotalol E Quinidine

Answer 33

Sotalol Answer Explanation Sotalol is a class III antiarrhythmic that blocks K channels. Because it has no effect on Na channels, the phase 0 upstroke is unchanged. It increases action potential duration by increasing the effective refractory period.

Question 34

Describe the effect that β-blockers have on: - End-diastolic volume - Blood pressure - Contractility - Heart rate - Ejection time - Myocardial oxygen consumption

Answer 34

β blockers have the following effects on cardiac function: ## Footnote No impact or slight decrease in end diastolic volume Decreased blood pressure Decreased contractility Decreased heart rate Increased ejection time Decreased O2 consumption

Question 35

How does statin inhibition of HMG-CoA reductase decrease blood LDL levels?

Answer 35

Inhibition of HMG-CoA reductase results in: 1. Impaired hepatic cholesterol synthesis 2. Increased hepatic LDL receptor expression 1. ​(A compensatory response to the reduced intracellular hepatocyte cholesterol) 3. Serum LDL is reduced due to increased hepatic LDL uptake

Question 36

Name 4 side-effects of class IV anti-arrhythmics.

Answer 36

Calcium channel blocker toxicities include: ## Footnote Cardiovascular effects (CHF, AV block, sinus node depression) Flushing Constipation Edema

Question 37

What are the 3 Class IC antiarrhythmic agents?

Answer 37

The class IC antiarrhythmics include (mnemonic: More Fries Please): ## Footnote Moricizine Flecainide Propafenone

Question 38

What are Class IB antiarrhythmics used for?

Answer 38

Class IB antiarrhythmics: used for the termination of ventricular tachycardias and the prevention of ventricular fibrillation after cardioversion following MI (myocardial infarction)

Question 39

Describe the mechanism of action of fibrates in the treatment of hyperlipidemia.

Answer 39

Mechanism: activation of nuclear transcription factor PPARα leads to upregulation of lipoprotein lipase. This causes increased clearance of triglyceride rich lipoproteins and increased HDL synthesis

Question 40

What is the mechanism of action of Digitalis?

Answer 40

Digitalis inhibits the Na+/K+ ATPase by competing with K+ for binding to the extracellular alpha subunit.

Question 41

Why is the use of Class II antiarrythmics contraindicated in cocaine users?

Answer 41

Contraindicated in cocaine users (risk of unopposed α-adrenergic receptor agonist activity)

Question 42

Name 2 side effects of ezetimibe.

Answer 42

Side effects of ezetimibe include: ## Footnote Hepatotoxicity (rare), which manifests as increased LFTs Diarrhea

Question 43

What are the main pharmacologic treatments for mild CHF (NYHA class II)?

Answer 43

reatment for NYHA class II or mild CHF: ## Footnote Sodium restriction Loop diuretic (furosemide) to achieve volume control ACE inhibitor or ARB

Question 44

A 69-year-old patient with a history of congestive heart failure presents to the ER with increasing shortness of breath and nausea. He vomited twice earlier in the day. While in the ER, he reports seeing blurry, yellow halos. An EKG shows shortened QT intervals and prolonged PR intervals. During your examination, his heart rhythm suddenly changes to a second degree AV block. All of the following drugs should immediately be used for treatment, except? A Digitalis specific FAB antibody B Lidocaine C Potassium D Quinidine E Phenytoin

Answer 44

D Quinidine Answer Explanation The information not provided in the clinical stem is that the patient is on digoxin. However, given his CHF history and his presenting complaints, this should be suspected. Digoxin can produce various cardiac arrhythmias and cause vague abdominal and vision halo symptoms. These symptoms indicate digoxin toxicity; quinidine can actually increase the toxicity of digoxin. Quinidine slows the elimination of digoxin and simultaneously reduces digoxin's apparent volume of distribution. As a result, serum digoxin levels may double or even triple. All of the other answers are treatments in digoxin toxicity.

Question 45

What conditions are class III antiarrhythmics most often used to treat?

Answer 45

Class III AAs are often used to treat Wolff-Parkinson-White syndrome,ventricular tachycardia, atrial fibrillation, and atrial flutter.

Question 46

A patient with end-stage liver disease from chronic hepatitis complains of increasing pruritus. Although you are not concerned about his lipid panel, you offer to treat his symptoms with which antihyperlipidemic drug? A Lovastatin B Gemfibrozil C Niacin D Cholestyramine E Ezetimibe

Answer 46

Cholestyramine Answer Explanation Cholestyramine is a bile acid sequestrant that is used to prevent intestinal absorption of cholesterol. It is also a first line agent in cholestatic and liver disease pruritus. In hyperbilirubinemic patients, pruritus results from deposition of bile in the skin. Cholestyramine helps to sequester bile acids within the GI tract, aiding elimination. Because of this mechanism, these drugs also decrease the absorption of fat soluble vitamins. This effect may require dietary supplementation to prevent vitamin deficiency.

Question 47

What agents are most effective at lowering triglyceride levels? Give three examples.

Answer 47

Fibrates are the most effective agents in reducing triglycerides. Four examples of fibrates are: Gemfibrozil Clofibrate Bezafibrate Fenofibrate

Question 48

What are 4 side effects of Procainamide?

Answer 48

Procainamide—side effects: ## Footnote Reversible systemic lupus-like syndrome (i.e., drug-induced lupus) Agranulocytosis Torsades de pointes Thrombocytopenia

Question 49

List 6 drugs commonly used in the treatment of CHF.

Answer 49

Basic treatment of CHF can be remembered with the mnemonic: β-SAD ## Footnote β-blockers Spironolactone ACE inhibitors or ARBs (proven to improve mortality) Diuretics (furosemide, HCTZ), Digoxin

Question 50

What ion channel do Class I antiarrhythmics preferentially act upon?

Answer 50

Class I antiarrhythmics — Are all Na+ channel blockers that slow or block conduction.

Question 51

Describe the effect that nitrates (e.g. nitroglycerin, isosorbide dinitrate) have on: - End-diastolic volume - Blood pressure - Contractility - Heart rate - Ejection time - Myocardial oxygen consumption

Answer 51

Nitrates have the following effects on cardiac function: ## Footnote Decreased end-diastolic volume (preload) Decreased blood pressure (afterload) No impact on contractility Increased heart rate (reflex response) Decreased ejection time Decreased O2 consumption

Question 52

What is the mechanism of action of minoxidil in the treatment of hypertension?

Answer 52

Minoxidil is a pro-drug that (upon sulfation by the liver) opens ATP-dependent potassium channels, causing hyperpolarization and subsequent relaxation of arteriolar smooth muscle. The net effect is arteriolar vasodilation.

Question 53

Describe the expected effect of ezetimibe therapy on LDL and triglyceride levels.

Answer 53

LDL ↓↓ (incremental ↓↓↓↓ when used with statins)

Question 54

What is the most serious complication of "Monday disease"? When does it most commonly occur?

Answer 54

The compensatory vasoconstriction on weekends can result in non-atherosclerotic ischemia and possibly cardiac arrest, the most serious complication.

Question 55

What are the side effects of ranolazine?

Answer 55

Side effects of ranolazine include: ## Footnote Dizziness Constipation Headache Nausea QT prolongation

Question 56

What effect will Class IC antiarrhythmics have on the effective refractory period? What effect do Class IC antiarrhythmics have on AP duration?

Answer 56

Effects of Class IC antiarrhythmics: ## Footnote Significantly prolongs the effective refractory period in AV node and accessory bypass tracts. Minimal effect on action potential duration

Question 57

What is the main clinical use of Class II Antiarrythmics?

Answer 57

Clinical use of Class II Antiarrythmics: Used in the treatment of ventricular rate control for atrial fibrillation and atrial flutter. Its main use is forsupraventricular tachycardias.

Question 58

What is the primary mechanism of action of beta blockers in reducing blood pressure?

Answer 58

Beta blockers decrease renin release by blocking β1 receptors on juxtaglomerular cells in the kidneys.

Question 59

A 75-year-old man presents to his physician with a nonproductive cough. He reports increasing dyspnea and an inability to lay flat at night without becoming short of breath. He has a past medical history of renal failure. On examination he has an S3 gallop and lower extremity edema. An echocardiogram reveals an ejection fraction of 35%. The patient is prescribed digoxin. Which side effect indicates a poor prognosis in patients with digoxin toxicity? A Hypomagnesemia B Hypermagnesemia C Hyperkalemia D Hypercalcemia E Hypokalemia

Answer 59

Hyperkalemia Answer Explanation Digoxin is a cardiac glycoside that inhibits the Na+/K+ ATPase, thereby indirectly inhibiting the Na+/Ca2+ exchanger. Inhibition of the Na+/Ca2+exchanger results in increased intracellular Ca2+ within cardiac muscle cells, which increases cardiac contractility. By inhibiting the Na+/K+ATPase, digoxin prevents the shuttling of K+ into cells, which can result in hyperkalemia. Hyperkalemia indicates a poor prognosis in patients with digoxin toxicity. Hypokalemia, renal failure (as in this patient), and drugs such as amiodarone, quinidine, and verapamil all predispose patients to digoxin toxicity.

Question 60

What is the primary clinical use of nitroprusside?

Answer 60

Nitroprusside is used in hypertensive emergencies, and given by IV infusion.

Question 61

Which enzyme do statins inhibit? What reaction does this enzyme catalyze?

Answer 61

Statins competitively and reversibly inhibit HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis. HMG-CoA reductase catalyzes theconversion of HMG-CoA to mevalonate.

Question 62

What are three clinical signs commonly found in congestive heart failure?

Answer 62

Clinical signs for heart failure include: ## Footnote Rales JVD Pitting edema

Question 63

Hydralazine is contraindicated in patients with which 2 pre-existing conditions?

Answer 63

Hydralazine is contraindicated in patients with angina and/or coronary artery disease due to its propensity to induce a reflex tachycardia, which can exacerbate these conditions.

Question 64

In addition to Monday disease, what are 4 adverse effects of nitrate therapy?

Answer 64

Nitrates are associated with the following adverse effects: ## Footnote Headache Hypotension Flushing Reflex tachycardia (which can be prevented/treated with β-blockers)

Question 65

What class of anti-lipid drugs can be used to treat pruritus associated with cirrhosis?

Answer 65

Since increased levels of bile acids can irritate skin and cause pruritis, bile acid resins can be used to treat pruritus in liver failure because they deplete bile acid reserves.

Question 66

Class II antiarrythmics (β-blockers) suppress abnormal pacemakers by decreasing the slope of which phase of the pacemaker cell action potential?

Answer 66

Class II antiarrythmics (β-blockers) can be used to suppress abnormal pacemakers by decreasing the slope of phase 4 of the pacemaker cell action potential.

Question 67

Describe the effect that class IV anti-arrhythmic agents have on: - SA/AV node automaticity - Effective refractory period - PR interval

Answer 67

Class IV antiarrythmics have the following effects: ## Footnote Decrease SA/AV node automaticity Increase effective refractory period Increase PR interval

Question 68

What is the effect of Class III antiarrhythmics on QT interval length?

Answer 68

By blocking K+ channels and slowing repolarization, Class III AAs result inslowed atrial-ventricular myocyte repolarization and the potential toprolong the QT interval.

Question 69

Which of the following antiarrythmic agents preferentially affects ischemic cardiac tissue? A Ibutilide B Procainamide C Quinidine D Esmolol E Lidocaine

Answer 69

Lidocaine Answer Explanation Lidocaine and mexiletine are class IB antiarrhythmics that decrease the duration of the cardiac action potential. Class IB antiarrhythmics preferentially affect ischemic Purkinje and ventricular tissue. Because of this effect, lidocaine was historically given prophylactically to reduce the incidence of ventricular fibrillation in patients post-myocardial infarction. The use of lidocaine has since fallen out of favor due to an increase in mortality amongst hospitalized patients treated with this agent. Quinidine and procainamide are class IA antiarrythmics, esmolol is a class II antiarrythmic, ibutilide is a class III antiarrythmic.

Question 70

What are the 4 Class IB antiarrhythmic agents?

Answer 70

Mnemonic: “Lettuce, Tomato, Mayo, Pickles”: Lidocaine Tocainide Mexiletine Phenytoin

Question 71

What is the mechanism of action of all Class I antiarrhythmics?

Answer 71

Class I antiarrhythmics decrease the slope of phase 0 depolarization and selectively depress tissue that is frequently depolarized (state-dependent).

Question 72

What are the side effects of β blockers?

Answer 72

Side effects of Class II Antiarrhythmics (β Blockers) include: ## Footnote Impotence Exacerbation of COPD and asthma (with non-ß1 specific blockers) Cardiovascular effects (bradycardia, AV block, CHF) CNS effects (sedation, sleep alterations) Can mask the signs of hypoglycemia

Question 73

What is the cellular mechanism by which class II antiarrythmics (β-blockers) decease SA and AV nodal activity?

Answer 73

Class II antiarrythmics (β-blockers) decrease cAMP and Ca2+ currents, which leads to decreased SA and AV nodal activity. Class II antiarrythmics (β-blockers) can be used to suppress abnormal pacemakers by decreasing the slope of phase 4 of the pacemaker cell action potential. The AV node is particularly sensitive to the effects of class II antiarrythmics (β-blockers), thereby leading to an increased PR interval.

Question 74

Nitrates are used in the treatment of which 3 conditions?

Answer 74

Nitrates are used in the treatment of: ## Footnote Angina Acute coronary syndrome Pulmonary edema

Question 75

Which enzyme is inhibited by niacin in adipose tissue? Hepatic production of which lipoprotein is most directly impaired by niacin?

Answer 75

In adipose tissue, niacin inhibits hormone-sensitive lipase, which catalyzes the the lipolysis of triglycerides. This reduces the availability of free fatty acids for hepatic triglyceride synthesis. In the liver, niacin also reduces the hepatic production of VLDL, which ultimately reduces LDL levels.

Question 76

What is the effect of nitroprusside on preload? What about afterload?

Answer 76

It is important to note that nitroprusside targets both arterioles and venules equally, therefore reducing preload and afterload

Question 77

Levels of which of the following will decrease the most after statin therapy: LDL, HDL, or Triglyceride

Answer 77

Statins have the following effects on blood lipids: LDL ↓↓↓ -- greatest decrease HDL ↑ (minimal effect) Triglycerides ↓

Question 78

In addition to flushing, what are the side effects of hydralazine?

Answer 78

Side effects associated with hydralazine include: ## Footnote Reflex tachycardia, leading to angina Fluid retention Headache Lupus-like syndrome (in slow acetylators)

Question 79

What agent can be added to the regimen of patients who are considered to have "moderate CHF?"

Answer 79

Treatment for NYHA class III or mild to moderate CHF: ## Footnote Add β-blocker

Question 80

What is another name for Class II Antiarrhythmics?

Answer 80

Class II Antiarrhythmics: ß-Blockers Examples: Metoprolol, propranolol, esmolol, atenolol, timolol, carvedilo

Question 81

What are 2 side effects of fibrates?

Answer 81

Side effects of fibrates include: ## Footnote Myopathy/rhabdomyolysis, which is particularly common when used in combination with statins Cholesterol gallstones

Question 82

What effect, if any, do Class IA antiarrhythmics have on the action potential and EKG?

Answer 82

Effect of Class IA antiarrhythmics on the action potential and EKG: Like all Class I agents, Class IA antiarrhythmics block Na channels ∴ slows the rate of depolarization → - slows the upstroke of the action potential - widens the QRS complex on EKG 2. Unlike other Class I agents, Class IA antiarrhythmics also nonspecifically block K channels ∴ slows the rate of repolarization → - ↑ action potential duration; ↑ effective refractory period - ↑ QT interval on EKG

Question 83

What are the treatments for digoxin toxicity?

Answer 83

Antidote to toxicity — use the mnemonic “LAMPP”: ## Footnote Lidocaine Anti-dig Fab fragments Magnesium for treatment of hypomagnesemia Potassium for treatment of hypokalemia before administration of digoxin Phenytoin for arrhythmias that do not respond to lidocaine

Question 84

Which type of Class I antiarrhythmics will decrease the action potential duration?

Answer 84

Effects of Class IB antiarrhythmics: ## Footnote Decreases action potential duration Decreases effective refractory period

Question 85

Name 2 side effects of bile acid resins.

Answer 85

Side effects of bile acid resins include: ## Footnote GI discomfort (constipation, diarrhea, and flatulence) Malabsorption of fat-soluble vitamins and drugs

Question 86

Which Class III antiarrhythmic is a P450 inhibitor?

Answer 86

Amiodarone is a P450 inhibitor.

Question 87

Name the channels or receptors blocked by the major classes of antiarrhythmics: - Class I? - Class II? - Class III? - Class IV?

Answer 87

Mnemonic: “Some Block Potassium Channels”: ## Footnote Sodium channel blockers (class I) Beta blockers (class II) Potassium channel blockers (class III) Calcium channel blockers (class IV)

Question 88

How are the side effects of hydralazine prevented?

Answer 88

Hydralazine is often administered in combination treatment with diureticsto counteract fluid retention and beta blockers to prevent reflex tachycardia.

Question 89

By what mechanism does digitalis reduce heart rate?

Answer 89

Digitalis stimulates the vagus nerve, thereby reducing heart rate. This has an anti-arrhythmic effect.

Question 90

Name 3 side effects of niacin.

Answer 90

Side effects of niacin include: 1. Flushed red face (treat with preadministration of aspirin) 2. Hyperglycemia (acanthosis nigricans) 3. Hyperuricemia (exacerbates gout)

Question 91

What EKG changes are associated with administration of digoxin?

Answer 91

EKG changes ( ST depression, T wave inversion, scooping of the ST segments, ↓ QT, and ↑ PR interval) are not a sign of toxicity, rather it is expected and called the digitalis effect

Question 92

What is the mechanism of action of reserpine?

Answer 92

Reserpine blocks the vesicular monoamine transporter (VMAT) which normally transports norepinephrine/serotonin/dopamine into presynaptic vesicles for release.

Question 93

What are three clinical symptoms of congestive heart failure?

Answer 93

Symptoms of heart failure include: Dyspnea Orthopnea Fatigue

Question 94

What is the primary clinical use for ranolazine?

Answer 94

Ranolazine is used in patients with chronic angina that is refractory to medical therapy.

Question 95

Which Class III antiarrhythmic requires periodic pulmonary, liver, and thyroid function tests?

Answer 95

Patients must have pulmonary (PFTs), liver (LFTs) and thyroid function tests (TFTs) periodically when using amiodarone.

Question 96

Which subclass of CCBs are used in the treatment of atrial flutter?

Answer 96

Calcium channel blockers (CCBs) fall into two subclasses: ## Footnote Non-dihydropyridine CCBs (e.g., verapamil, diltiazem) are more specific for the heart, used in the treatment of hypertension, angina, and atrial fibrillation/flutter Dihydropyridine CCBs (“-dipines” — e.g., amlodipine, nifedipine) are more specific for blood vessels. Used in the treatment of hypertension, angina, and Raynaud phenomenom

Question 97

What symptoms are found in digoxin toxicity?

Answer 97

Toxicities of cardiac glycosides include: ## Footnote Anorexia Nausea Cholinergic effects which include disorientation, and visual effects (halos) Cardiac arrhythmias

Question 98

How do β-blockers decrease the oxygen consumption requirement of ventricular wall tissue?

Answer 98

β blockers decrease myocardial oxygen consumption (MVO2) secondary todecreased afterload (from decreased renin release), heart rate, andcontractility.

Question 99

Nitrates (e.g. nitroglycerin, isosorbide dinitrate) preferentially dilate which type of blood vessel?

Answer 99

Nitrates (e.g., nitroglycerin, isosorbide mononitrate, dinitrate) increase nitric oxide in vascular smooth muscle. This increases cGMP, leading to smooth muscle relaxation and preferential vasodilation of veins over arteries (most nitrates have a much more potent vasodilatory effect on veins than arteries).

Question 100

What is the mechanism of action of CCBs (calcium channel blockers) in the vasculature?

Answer 100

CCBs block voltage dependent L-type calcium channels, which decreases calcium influx and inhibits vascular smooth muscle contraction. Vasodilation of systemic and coronary arteries decreases TPR (total peripheral resistance) and therefore decreases afterload.

Question 101

What is the mechanism of action for nitroprusside?

Answer 101

Nitroprusside is a short-acting drug that forms and releases nitric oxideinto circulation, which generates cGMP in smooth muscle of arteries and veins. The cGMP stimulates vasodilation.

Question 102

Which antilipid medication is most effective at raising HDL levels?

Answer 102

Niacin is the most effective antilipid for elevating serum HDL levels.

Question 103

What are the side effects of prazosin?

Answer 103

Side effects of prazosin include: ## Footnote Orthostatic hypotension (particularly after the 1st dose) Reflex tachycardia Headache Dizziness

Question 104

Which selective α1 receptor blocker is used to treat PTSD?

Answer 104

Prazosin is used for the treatment of PTSD.

Question 105

What effect do Class III antiarrhythmics have on the action potential (AP) duration and effective refractory period (ERP)?

Answer 105

Class III AAs increase the action potential (AP) duration and increase effective refractory period (ERP).

Question 106

How do β1-blockers decrease peripheral blood pressure?

Answer 106

β blockers inhibit β1-receptors on the renal juxtaglomerular apparatus, thereby reducing the release of renin, and ultimately angiotensin II (a potent vasoconstrictor).

Question 107

What are the uses of hydralazine?

Answer 107

Hydralazine is used in moderate to severe HTN, and as first-line therapy for HTN in pregnancy, with methyldopa.

Question 108

Describe the mechanism of action of ezetimibe.

Answer 108

Ezetimibe is an inhibitor of dietary cholesterol absorption in small intestine brush border.

Question 109

What is the net effect of ranolazine therapy on diastolic wall tension and oxygen consumption?

Answer 109

The net effect of ranolazine therapy is a reduction in both diastolic wall tension and oxygen consumption. Ranolazine has no significant impact on either heart rate or contractility.

Question 110

The goal of antianginal therapy is to manipulate which 4 physiologic variables?

Answer 110

The objective of anginal therapy is to decrease myocardial oxygen demand/consumption and/or increase coronary blood flow. This can be achieved by: ## Footnote Decreasing HR (heart rate) Decreasing contractility Decreasing end-diastolic volume Decreasing blood pressure (proportional to afterload)

Question 111

What are the possible side effects of amiodarone? | (Note: the highest-yield side effects are bolded)

Answer 111

Side effects of amiodarone include: ## Footnote Pulmonary fibrosis Hepatotoxicity Hypothyroidism/hyperthyroidism Corneal deposits Blue or gray photodermatitis Neurologic effects Constipation Cardiovascular effects (heart failure, bradycardia, heart block)

Question 112

How do vasodilators treat hypertension?

Answer 112

Vasodilators are antihypertensive drugs that decrease blood pressure byrelaxing vascular smooth muscle. This results in decreased peripheral resistance, thereby lowering blood pressure.

Question 113

What is/are the possible side effect(s) of sotalol?

Answer 113

Side effects of sotalol include torsades de pointes and excessive beta blockage.

Question 114

Does hydralazine cause greater arteriolar or venous dilation?

Answer 114

Hydralazine causes much greater arteriolar dilation than ventilation, thus reducing afterload more than pre-load.

Question 115

How does digitoxin differ from digoxin?

Answer 115

Digitoxin is eliminated in the liver, unlike digoxin.

Question 116

List 5 common side effects of non-specific beta blockers.

Answer 116

Side effects of non-specific Beta Blockers include: ## Footnote Asthma (through β2 pulmonary vasodilatation blockade) Heart problems (bradycardia, AV block, CHF) Impotence Sedation Blunting of the effects of hypoglycemia

Question 117

What is the mechanism of elimination of digoxin?

Answer 117

Eliminated by kidney, so there is a longer half-life in patients with kidney failure

Question 118

What is the effect of Class III antiarrhythmics on Na+ channels and conduction velocity? Which Class III drug is an exception to this rule?

Answer 118

Class III AAs do not interfere with the function of the Na+ channel and thus do not affect conduction velocity. Exception: Amiodarone

Question 119

What are Class IC antiarrhythmics used for?

Answer 119

Class IC antiarrhythmics: used for suppressing SVTs, including atrial fibrillation. Class IC agents are used only as a last resort in refractory VT.

Question 120

What is a key neurologic side effect of reserpine?

Answer 120

Reserpine can cause drug-induced parkinsonism.

Question 121

What is the end result in cardiac muscle tissue following administration of Digitalis?

Answer 121

Inhibition of Na-K-ATPase leads to increased intracellular Na+ in myocytes, which indirectly slows down extrusion of Ca2 via Na/Ca2 pump. This leads to intracellular Ca2+ and more stored Ca2+ in sarcoplasmic reticulum, thereby increasing the amount of Ca2+ released by each subsequent action potentialwhich increases contractility (i.e. increased force of contraction for a given preload)

Question 122

What are some side effects of minoxidil and diazoxide?

Answer 122

Side effects of minoxidil and diazoxide include the following: ## Footnote Hypertrichosis (Minoxidil) Hyperglycemia (decrease insulin release from Diazoxide) Reflex tachycardia Edema