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kardiaggeiako > farmaka > Flashcards

farmaka Flashcards

1
Q

A patient is diagnosed with essential hypertension. He wants to know his treatment options. What medication(s) can you offer him?

A

Thiazide diuretics, ACE inhibitors, angiotensin II receptor blockers, dihydropyridine Ca2+ channel blockers

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2
Q

In what circumstance is a β-blocker contraindicated in a heart failure patient?

A

In cardiogenic shock, and moreover, β-blockers must be used with caution in decompensated HF

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3
Q

A diabetic patient is also found to have essential hypertension. He takes a thiamine diuretic. Should you change him to another agent?

A

Yes, consider switching him to ACE inhibitors or ARBs, as a thiamine diuretic is protective against diabetic nephropathy

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4
Q

What are the treatment options for hypertension in diabetic patients?

A

ACE inhibitors/ARBs (both are protective against diabetic nephropathy), Ca2+ channel blockers, thiazide diuretics, β-blockers

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5
Q

A pregnant woman is found to have hypertension. What are the treatment options available for her hypertension?

A

Hydralazine, labetalol, methyldopa, nifedipine

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6
Q

You want to start a patient on a non-dihydropyridine calcium channel blocker. What adverse effects is your patient at risk for?

A

AV block and hyperprolactinemia (specific side effect of verapamil)

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7
Q

A 65-year-old man is started on nifedipine for his hypertension. What is the mechanism of action?

A

Like other calcium channel blockers, it blocks the L-type calcium channel in cardiac and smooth muscle, which reduces muscle contractility

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8
Q

A patient is started on antihypertensives. He soon returns with swollen ankles and flushing. What class of medication was he prescribed?

A

Calcium channel blockers, as peripheral edema is a possible side effect

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9
Q

What are the clinical indications for the use of non-dihydropyridine calcium channel blockers?

A

Hypertension, angina, atrial fibrillation/flutter

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10
Q

A patient suffers head trauma and develops a subarachnoid hemorrhage. Why is it beneficial to give this patient a calcium channel blocker?

A

The calcium channel blocker nimodipine can help prevent cerebral vasospasms

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11
Q

Which calcium channel blocker is used for hypertensive urgency or emergency?

A

Clevidipine

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12
Q

Rank the relative activity of the following calcium channel blockers on vascular smooth muscle: verapamil, nifedipine, amlodipine, diltiazem

A

Verapamil (verapamil = ventricle), diltiazem, amlodipine = nifedipine

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13
Q

A patient suddenly enters atrial fibrillation. Their HR is 150, RR 14, and BP 80/60. Why are you cautious about starting a diltiazem drip?

A

While Ca2+ channel blockers slow AV node conduction, they also reduce both cardiac output and blood pressure

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14
Q

Which calcium channel blockers are most selective for vascular smooth muscle? Which one agent is most cardioselective?

A

Nifedipine or amlodipine (dihydropyridines); verapamil

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15
Q

What are the clinical indications for the use of dihydropyridine calcium channel blockers, other than nimodipine and clevidipine?

A

Hypertension, angina (including Prinzmetal angina), Raynaud phenomenon

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16
Q

You want to start a patient on a dihydropyridine calcium channel blocker. What adverse effects is your patient at risk for?

A

Cardiac depression, peripheral edema, flushing, dizziness, constipation, gingival hyperplasia

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17
Q

Which does hydralazine reduce: afterload or preload? Which vessels does it dilate more: veins or arterioles?

A

Afterload; arterioles

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18
Q

Hydralazine causes smooth muscle relaxation by increasing concentrations of which substance in endothelial cells?

A

cGMP

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19
Q

A man has side effects from hydralazine. What autoimmune complication might this mimic? Is he likely to have fluid retention or excretion?

A

Systemic lupus erythematosus; fluid retention

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20
Q

A 68-year-old man with chronic hypertension recently had a cardiac stent placement. Why is hydralazine contraindicated in this patient?

A

Hydralazine is contraindicated in angina and coronary artery disease, because it causes a drop in BP that induces compensatory tachycardia

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21
Q

A 40-year-old woman with chronic hypertension has a positive pregnancy test. What is the first-line hypertensive therapy for her?

A

Hydralazine, which is safe to use during pregnancy

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22
Q

How can the reflex tachycardia that is associated with hydralazine be prevented?

A

By administering hydralazine with a β-blocker

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23
Q

What are the clinical indications for hydralazine?

A

Severe hypertension (particularly acute), heart failure (administer with organic nitrate)

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24
Q

Name some medications that can be used to treat a hypertensive emergency.

A

Nitroprusside, nicardipine, clevidipine, fenoldopam, labetalol

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25
Q

Nitroprusside is a ____ (short/long)-acting drug that increases which substance via direct release of nitric oxide?

A

Short; cGMp

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26
Q

Fenoldopam is an agonist of which receptor? What is its mechanism of action?

A

Dopamine D1 (relaxes renal vasculature, which can ↓ BP and ↑ natriuresis; also induces coronary, peripheral, and splanchnic vasodilation)

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27
Q

A man has a hypertensive emergency. You give a short-acting drug that raises cGMP levels via NO. Why do you monitor oxygenation closely?

A

Patients should be monitored closely after nitroprusside is given, as it can cause cyanide toxicity (deprives cells of ability to use O2)

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28
Q

A 55-year-old man develops severe chest pain after walking up a hill. He puts a pill under his tongue that stops the pain. How does it work?

A

Nitrates release nitric oxide in smooth muscle (↑cGMP/smooth muscle relaxation), causing vasodilation (veins &62;> arteries) and ↓preload

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29
Q

What are the three main indications for the use of nitrates (nitroglycerin, isosorbide dinitrate, isosorbide mononitrate)?

A

Angina, pulmonary edema, and acute coronary syndrome

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30
Q

Name four adverse effects of nitrates.

A

Reflex tachycardia, hypotension, flushing, and headache

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31
Q

A 35-year-old man gets a headache every Monday and jokes that he is “allergic’ to his job at an explosives factory. What may be the cause?

A

His “Monday disease” is from industrial exposure to nitroglycerin; causes tachycardia, dizziness, headache on re-exposure to nitroglycerin

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32
Q

A man on nitroglycerin presents with hypotension. Home medications are held. A day later, he is tachycardic yet normotensive. What happened?

A

He is having reflex tachycardia from stopping nitroglycerin (treat with a β-blocker)

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33
Q

What is the mechanism by which pharmacologic treatments can reduce angina?

A

Reduce myocardial oxygen consumption by decreasing one or more of end-diastolic volume, BP, HR, contractility

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34
Q

Among the calcium channel blockers, which acts similarly to a β-blocker?

A

Verapamil

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35
Q

What are the effects of β-blockers, nitrates, and both together on end-diastolic volume?

A

β-blockers either have no effect or decrease EDV, nitrates decrease EDV, a combination of both either has no effect or decreases EDV

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36
Q

What are the effects of nitrates, β-blockers, and both together on blood pressure?

A

β-blockers, nitrates, and a combination of both all decrease blood pressure

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37
Q

What are the effects of nitrates, β-blockers, and both together on contractility?

A

Nitrates have no effect, β-blockers decrease contractility, and a combination of both has little or no effect

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38
Q

What are the effects of nitrates, β-blockers, and both together on heart rate?

A

Nitrates increase HR (reflex response), β-blockers decrease heart rate, and a combination of both has no effect or decreases heart rate

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39
Q

What are the effects of nitrates, β-blockers, and both together on ejection time?

A

Nitrates decrease ejection time; β-blockers increase ejection time, and a combination of both has little or no effect on ejection time

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40
Q

What are the effects of nitrates, β-blockers, and both together on myocardial oxygen consumption?

A

Both β-blockers & nitrates decrease myocardial O2 consumption, & a combination of both decreases myocardial O2 consumption drastically

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41
Q

Your patient with angina needs a β-blocker. You offer pindolol and acebutolol, but your attending scoffs at this proposal. Why?

A

Pindolol and acebutolol, both partial β-agonists, can increase myocardial oxygen consumption and are poor choices for patients with angina

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42
Q

A 35-year-old man has a low-density lipoprotein of 200 mg/dL. Which drug class would have the most powerful LDL-lowering effect?

A

HMG-CoA reductase inhibitors (statins) have the strongest reducing effect of all of the lipid-lowering drugs

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43
Q

A patient cannot take statins due to side effects. What other drugs can lower his low-density lipoprotein levels?

A

Niacin (vitamin B3), bile acid resins, ezetimibe, fibrates (although all reduce LDL less effectively than do statins)

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44
Q

Which lipid-lowering agent causes the greatest increase in high-density lipoprotein levels? Which agents cause a more modest increase?

A

Niacin causes the greatest increase in HDL; statins and fibrates have a moderate effect on HDL (bile acid resins increase it slightly)

45
Q

Which lipid-lowering agents cause the most significant reduction in triglycerides? Which have a more modest benefit?

A

Fibrates reduce triglycerides most significantly; statins or niacin causes a milder reduction (bile acid resins slightly increase levels)

46
Q

A 72-year-old woman being treated for hyperlipidemia develops severe leg cramps. What are the other side effects of her medication?

A

Myopathy is a side effect of statins (especially when fibrates or niacin is used), which can also cause hepatotoxicity (↑ LFTs)

47
Q

A 55-y/o woman has an HDL level of 20 mg/dL. The most effective medication for her has what mechanism and side effects?

A

Niacin blocks lipolysis/hormone-sensitive lipase in adipose tissue →↓hepatic VLDL synthesis; facial flushing, hyperglycemia, hyperuricemia

48
Q

A 60-year-old man is taking a drug that lowers LDL and slightly increases HDL and triglycerides. What are the adverse effects of this drug?

A

Can cause GI upset as well as decreased absorption of fat-soluble vitamins and other drugs (he is taking a bile acid resin)

49
Q

A woman treated for hypertriglyceridemia has myopathy and cholesterol gallstones. What is the mechanism of the drug being taken?

A

The fibrates upregulate lipoprotein lipase & triglyceride clearance & activate PPAR-α ↑HDL synthesis (the side effects suggest fibrate use)

50
Q

Which category of lipid-lowering drugs works by inhibiting the formation of the cholesterol precursor mevalonic acid?

A

HMG-CoA reductase inhibitors (statins) inhibit conversion of HMG-CoA to mevalonate (statins ↓mortality in CAD patients)

51
Q

• Which category of lipid-lowering drugs prevents intestinal reabsorption of bile acids, causing the liver to replenish them with cholesterol?

A

Bile acid resins (cholestyramine, colestipol, colesevelam)

52
Q

Which lipid-lowering agent works by preventing cholesterol reabsorption at the small intestinal brush border? Side effects?

A

Ezetimibe; can cause diarrhea and, rarely, increased LFTs

53
Q

A 50-yo man has low vitamin A/D/E/K levels since starting a new lipid-lowering drug. Which other side effect is he likely experiencing?

A

ile acid resins decrease absorption of fat-soluble vitamins and can cause GI upset

54
Q

A patient has recently started taking lovastatin. He presents with right upper quadrant pain. Which lab test should be ordered?

A

• A LFT panel to look for hepatotoxicity, which is particularly likely to happen if he is also taking fibrates or niacin

55
Q

Because it can increase contractility, digoxin is used to treat what condition? What other condition does it treat? How?

A

Heart failure (↑contractility); atrial fibrillation; digoxin ↓atrioventricular node conduction and depresses the sinoatrial node

56
Q

A 70-year-old woman starts a new drug for atrial fibrillation and develops GI upset. What other symptoms may be present? What causes them?

A

Nausea/vomiting, blurry yellow vision, arrhythmias/AV block; the drug (digoxin) has a cholinergic effect as it stimulates vagus nerve (↓HR)

57
Q

What vision complaint can occur with digoxin use?

A

Blurry yellow vision (also from cholinergic effects of stimulating the vagus nerve)—think van Gogh

58
Q

A 65-year-old man who takes digoxin recently started quinidine for an arrhythmia. What lab value should you look out for? Why?

A

Potassium level & quinidine ↓digoxin clearance due to tissue-binding site displacement & can cause hyperkalemia (indicates a poor prognosis)

59
Q

You want to start a 65-year-old man on digoxin to treat his atrial fibrillation. What blood work should you do before starting it, and why?

A

• Measure creatinine, as kidney failure lowers drug excretion, & measure K+, as hypokalemia allows more digoxin to bind Na+/K+ ATPase

60
Q

An 80-year-old man takes digoxin and develops an increased PR interval. You suspect digoxin toxicity. What are possible treatments?

A

Slow normalization of K+ levels, a cardiac pacer, anti-digoxin antibodies (Fab fragments), and Mg2+

61
Q

How does hypokalemia increase the toxicities of digoxin?

A

Potassium competes with digoxin for same binding site on Na+/K+ ATPases, so hypokalemia increases digoxin binding and toxicity

62
Q

The attending on your internal medicine rotation asks about the mechanism of digoxin. Explain.

A

It directly inhibits the Na+/K+ ATPase, indirectly inhibiting the Na+/Ca2+ exchanger, resulting in ↑[Ca2+]i and ↑inotropy/contractility

63
Q

Name two antiarrhythmics that predispose a patient to digoxin toxicity.

A

erapamil (calcium channel blocker) and amiodarone (potassium channel blocker)

64
Q

A patient on procainamide for an arrhythmia develops a facial rash and joint pains. She has antihistone antibodies. What is the diagnosis?

A

Reversible SLE-like syndrome

65
Q

Quinidine causes symptoms of headache and tinnitus, which are collectively known as what?

A

• Cinchonism, which can occur with all quinine derivatives

66
Q

A patient takes flecainide for supraventricular tachycardia. What effect does this class of drug have on action potential duration?

A

Class IC antiarrhythmics have minimal effect on action potential duration

67
Q

Which antiarrhythmic is indicated to prevent arrhythmias after myocardial infarction? Which antiarrhythmic is contraindicated after MI?

A

Class IB antiarrhythmics (IB is Best after MI); class IC antiarrhythmics are contraindicated (IC is Contraindicated after MI)

68
Q

What is the toxicity of class IC antiarrhythmics? When are they contraindicated?

A

Proarrhythmic, as they increase refractory period of AV node & accessory bypass tracts; post-MI & after ischemic/structural heart disease

69
Q

Name the class IB antiarrhythmic drugs.

A

Lidocaine, Mexiletine (phenytoin also can fall into the IB class [I’d Buy Liddy’s Mexican tacos])

70
Q

Which antiarrhythmics belong to class IA?

A

Quinidine, Procainamide, DisoPyramide (the Queen Proclaims Diso’s Pyramid)

71
Q

What does it mean when sodium channel blockers are described as state dependent?

A

State dependent means that the antiarrhythmics act selectively on tissue that is frequently depolarized (e.g., during tachycardia)

72
Q

A 45-year-old man takes disopyramide for an arrhythmia. What type of arrhythmia may he have?

A

Class IA antiarrhythmics treat atrial and ventricular arrhythmias, notably reentrant and ectopic supraventricular/ventricular tachycardias

73
Q

A 45-year-old patient takes mexiletine for an arrhythmia. How do drugs in this class work?

A

Class IB antiarrhythmics shorten the action potential duration and preferentially affect ischemic or depolarized Purkinje/ventricular tissue

74
Q

• A 45-year-old man starts taking lidocaine. What type of arrhythmia may he have?

A

Class IB antiarrhythmics treat acute ventricular arrhythmias (especially after myocardial infarction) and digitalis-induced arrhythmias

75
Q

A 45-year-old patient takes a class IB antiarrhythmic. What are the adverse effects of this class of drug?

A

Class IB antiarrhythmics can cause central nervous system stimulation/depression and cardiovascular depression

76
Q

A 45-year-old patient starts taking propafenone. What conditions may he have?

A

Class IC antiarrhythmics treat supraventricular tachycardias (including atrial fibrillation) & are used as a last resort in refractory VT

77
Q

Which antiarrhythmics belong to class IC?

A

Flecainide, Propafenone (Can [class IC] I have Fries, Please)

78
Q

Class I antiarrhythmics slow/block conduction and decrease the slope of ___ (phase 0/1/2/3/4) myocardial action potential depolarization.

A

Phase 0 (inward sodium current), especially in depolarized cells

79
Q

Class IC antiarrhythmics have no effect on the effective refractory period in which two types of tissues?

A

Purkinje and ventricular tissues

80
Q

Name the possible side effects of class IA antiarrhythmics.

A

Cinchonism (quinidine), SLE-like syndrome (procainamide), HF (disopyramide), thrombocytopenia, torsades de pointes (↑QT interval)

81
Q

Which β-blocker is extremely short acting?

A

Esmolol

82
Q

Which antiarrhythmics belong in class II?

A

β-blockers such as propranolol, esmolol, timolol, metoprolol, atenolol, and carvedilol

83
Q

A 70-year-old woman takes atenolol for atrial fibrillation. What is the mechanism of action of this class of antiarrhythmic?

A

β-blockers (class II) ↑SA and AV nodal activity (by ↓cAMP and Ca2+ currents) & suppress abnormal pacemakers by ↓slope of phase 4

84
Q

A 70-year-old woman takes metoprolol for atrial fibrillation. Which cardiac node is most sensitive to this class of antiarrhythmic?

A

The atrioventricular node is most sensitive to β-blockers (class II), and as a result, the PR interval is lengthened on ECG

85
Q

A 70-year-old woman takes timolol. What types of arrhythmias may she have?

A

Supraventricular tachycardias, as β-blockers treat them & provide ventricular rate control for atrial fibrillation and atrial flutter

86
Q

A 70-year-old man takes esmolol to treat atrial fibrillation. What are the toxicities of this class of antiarrhythmic?

A

β-blockers cause impotence, asthma/COPD exacerbations, CV effects (bradycardia, AV block, HF), and CNS effects (sedation, sleep changes)

87
Q

A patient starts taking metoprolol. Months later, his lipid panel has worsened. Is metoprolol to blame?

A

Possibly, as dyslipidemia is a side effect of metoprolol therapy

88
Q

Why might β-blockers be dangerous for someone who takes insulin? What is the antidote for β-blocker overdose?

A

Because they may mask signs of hypoglycemia

89
Q

A patient has Prinzmetal angina. Which β-blocker should not be prescribed to treat his arrhythmia? Why?

A

Propranolol should not be given; it can exacerbate vasospasms

90
Q

Patients who have overdosed on which illicit drug should not be treated with β-blockers?

A

Cocaine, as there is a risk of unopposed α1-receptor agonist activity

91
Q

Patients with which type of endocrine tumor should not be treated with β-blockers?

A

Pheochromocytoma, as there is then a risk of unopposed α1-receptor agonist activity

92
Q

A patient on amiodarone is frustrated with monthly testing that is required. What lab(s) are being tested in this patient?

A

Pulmonary function tests, liver function tests, and thyroid function tests must be checked regularly when on amiodarone

93
Q

Which antiarrhythmics belong to class III?

A

Potassium channel blockers, such as Amiodarone, Ibutilide, Dofetilide, Sotalol (AIDS)

94
Q

Name two toxicities of sotalol.

A

Torsades de pointes and excessive β-blockade

95
Q

Name a potentially fatal adverse effect of ibutilide.

A

Torsades de pointes

96
Q

A 78-year-old man takes amiodarone for an arrhythmia. Name the toxicities of this medication.

A

Pulmonary fibrosis, hepatotoxicity, hyperthyroidism, corneal and blue/gray skin deposits, constipation, cardiovascular/neurologic effects

97
Q

Which antiarrhythmic drug is lipophilic and has classes I, II, III, and IV effects?

A

Amiodarone

98
Q

A 78-year-old man takes amiodarone for an arrhythmia. Why must his thyroid function be monitored regularly?

A

Because it is 40% iodine by weight and can cause hypo- or hyperthyroidism

99
Q

A patient taking an antiarrhythmic develops corneal/skin deposits and photodermatitis. Which arrhythmias may he have?

A

Atrial fibrillation/flutter and ventricular tachycardia (the side effects suggest that he is taking amiodarone [class III])

100
Q

How does sotalol affect the duration of the action potential, effective refractory period, and QT interval?

A

Sotalol and other class III antiarrhythmics (potassium channel blockers) increase the duration of all three

101
Q

A 64-year-old woman takes verapamil for an arrhythmia. Which cardiac myocytes does this class of medication affect?

A

Class IV antiarrhythmics (Ca2+ channel blockers) ↓AV node pacemaker cells’ conduction velocity and ↑ERP/PR interval

102
Q

Which two antiarrhythmic drugs belong to class IV?

A

Diltiazem and verapamil, which prevent nodal arrhythmias (e.g., supraventricular tachycardia) and offer rate control in atrial fibrillation

103
Q

A patient develops an adverse reaction to a calcium channel blocker. What would you expect to hear in the patient’s history?

A

Constipation, flushing, edema, signs of cardiovascular abnormalities such as heart failure, atrioventricular block, sinus node depression

104
Q

What is the mechanism of action of the first-line antiarrhythmic for diagnosing and treating supraventricular tachycardia?

A

Adenosine increases the amount of K+ flowing out of cells, leading to hyperpolarization of the cell and decreased intracellular Ca2+ (ICa)

105
Q

Which ion is infused for the treatment of torsades de pointes and digoxin toxicity?

A

Mg2+

106
Q

Adenosine is infused into a patient with supraventricular tachycardia. For how long do you expect this drug to be active in the patient?

A

Adenosine is a short-acting (about 15 seconds) drug

107
Q

You diagnose a man with supraventricular tachycardia. Name the side effects of the diagnostic/treatment drug of choice.

A

Adenosine can cause flushing, hypotension, chest pain, a sense of impending doom, bronchospasm

108
Q

A man has chest pain and bronchospasm after being treated for supraventricular tachycardia. How can you alleviate these side effects?

A

They can be blunted by caffeine or theophylline (both are adenosine receptor antagonists) (these symptoms are adverse effects of adenosine

kardiaggeiako (11 decks)

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