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farmaka Flashcards

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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
Nitroprusside is a ____ (short/long)-acting drug that increases which substance via direct release of nitric oxide?
Short; cGMp
26
Fenoldopam is an agonist of which receptor? What is its mechanism of action?
Dopamine D1 (relaxes renal vasculature, which can ↓ BP and ↑ natriuresis; also induces coronary, peripheral, and splanchnic vasodilation)
27
A man has a hypertensive emergency. You give a short-acting drug that raises cGMP levels via NO. Why do you monitor oxygenation closely?
Patients should be monitored closely after nitroprusside is given, as it can cause cyanide toxicity (deprives cells of ability to use O2)
28
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?
Nitrates release nitric oxide in smooth muscle (↑cGMP/smooth muscle relaxation), causing vasodilation (veins &62;> arteries) and ↓preload
29
What are the three main indications for the use of nitrates (nitroglycerin, isosorbide dinitrate, isosorbide mononitrate)?
Angina, pulmonary edema, and acute coronary syndrome
30
Name four adverse effects of nitrates.
Reflex tachycardia, hypotension, flushing, and headache
31
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?
His "Monday disease" is from industrial exposure to nitroglycerin; causes tachycardia, dizziness, headache on re-exposure to nitroglycerin
32
A man on nitroglycerin presents with hypotension. Home medications are held. A day later, he is tachycardic yet normotensive. What happened?
He is having reflex tachycardia from stopping nitroglycerin (treat with a β-blocker)
33
What is the mechanism by which pharmacologic treatments can reduce angina?
Reduce myocardial oxygen consumption by decreasing one or more of end-diastolic volume, BP, HR, contractility
34
Among the calcium channel blockers, which acts similarly to a β-blocker?
Verapamil
35
What are the effects of β-blockers, nitrates, and both together on end-diastolic volume?
β-blockers either have no effect or decrease EDV, nitrates decrease EDV, a combination of both either has no effect or decreases EDV
36
What are the effects of nitrates, β-blockers, and both together on blood pressure?
β-blockers, nitrates, and a combination of both all decrease blood pressure
37
What are the effects of nitrates, β-blockers, and both together on contractility?
Nitrates have no effect, β-blockers decrease contractility, and a combination of both has little or no effect
38
What are the effects of nitrates, β-blockers, and both together on heart rate?
Nitrates increase HR (reflex response), β-blockers decrease heart rate, and a combination of both has no effect or decreases heart rate
39
What are the effects of nitrates, β-blockers, and both together on ejection time?
Nitrates decrease ejection time; β-blockers increase ejection time, and a combination of both has little or no effect on ejection time
40
What are the effects of nitrates, β-blockers, and both together on myocardial oxygen consumption?
Both β-blockers & nitrates decrease myocardial O2 consumption, & a combination of both decreases myocardial O2 consumption drastically
41
Your patient with angina needs a β-blocker. You offer pindolol and acebutolol, but your attending scoffs at this proposal. Why?
Pindolol and acebutolol, both partial β-agonists, can increase myocardial oxygen consumption and are poor choices for patients with angina
42
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?
HMG-CoA reductase inhibitors (statins) have the strongest reducing effect of all of the lipid-lowering drugs
43
A patient cannot take statins due to side effects. What other drugs can lower his low-density lipoprotein levels?
Niacin (vitamin B3), bile acid resins, ezetimibe, fibrates (although all reduce LDL less effectively than do statins)
44
Which lipid-lowering agent causes the greatest increase in high-density lipoprotein levels? Which agents cause a more modest increase?
Niacin causes the greatest increase in HDL; statins and fibrates have a moderate effect on HDL (bile acid resins increase it slightly)
45
Which lipid-lowering agents cause the most significant reduction in triglycerides? Which have a more modest benefit?
Fibrates reduce triglycerides most significantly; statins or niacin causes a milder reduction (bile acid resins slightly increase levels)
46
A 72-year-old woman being treated for hyperlipidemia develops severe leg cramps. What are the other side effects of her medication?
Myopathy is a side effect of statins (especially when fibrates or niacin is used), which can also cause hepatotoxicity (↑ LFTs)
47
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?
Niacin blocks lipolysis/hormone-sensitive lipase in adipose tissue →↓hepatic VLDL synthesis; facial flushing, hyperglycemia, hyperuricemia
48
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?
Can cause GI upset as well as decreased absorption of fat-soluble vitamins and other drugs (he is taking a bile acid resin)
49
A woman treated for hypertriglyceridemia has myopathy and cholesterol gallstones. What is the mechanism of the drug being taken?
The fibrates upregulate lipoprotein lipase & triglyceride clearance & activate PPAR-α ↑HDL synthesis (the side effects suggest fibrate use)
50
Which category of lipid-lowering drugs works by inhibiting the formation of the cholesterol precursor mevalonic acid?
HMG-CoA reductase inhibitors (statins) inhibit conversion of HMG-CoA to mevalonate (statins ↓mortality in CAD patients)
51
• Which category of lipid-lowering drugs prevents intestinal reabsorption of bile acids, causing the liver to replenish them with cholesterol?
Bile acid resins (cholestyramine, colestipol, colesevelam)
52
Which lipid-lowering agent works by preventing cholesterol reabsorption at the small intestinal brush border? Side effects?
Ezetimibe; can cause diarrhea and, rarely, increased LFTs
53
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?
ile acid resins decrease absorption of fat-soluble vitamins and can cause GI upset
54
A patient has recently started taking lovastatin. He presents with right upper quadrant pain. Which lab test should be ordered?
• A LFT panel to look for hepatotoxicity, which is particularly likely to happen if he is also taking fibrates or niacin
55
Because it can increase contractility, digoxin is used to treat what condition? What other condition does it treat? How?
Heart failure (↑contractility); atrial fibrillation; digoxin ↓atrioventricular node conduction and depresses the sinoatrial node
56
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?
Nausea/vomiting, blurry yellow vision, arrhythmias/AV block; the drug (digoxin) has a cholinergic effect as it stimulates vagus nerve (↓HR)
57
What vision complaint can occur with digoxin use?
Blurry yellow vision (also from cholinergic effects of stimulating the vagus nerve)—think van Gogh
58
A 65-year-old man who takes digoxin recently started quinidine for an arrhythmia. What lab value should you look out for? Why?
Potassium level & quinidine ↓digoxin clearance due to tissue-binding site displacement & can cause hyperkalemia (indicates a poor prognosis)
59
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?
• Measure creatinine, as kidney failure lowers drug excretion, & measure K+, as hypokalemia allows more digoxin to bind Na+/K+ ATPase
60
An 80-year-old man takes digoxin and develops an increased PR interval. You suspect digoxin toxicity. What are possible treatments?
Slow normalization of K+ levels, a cardiac pacer, anti-digoxin antibodies (Fab fragments), and Mg2+
61
How does hypokalemia increase the toxicities of digoxin?
Potassium competes with digoxin for same binding site on Na+/K+ ATPases, so hypokalemia increases digoxin binding and toxicity
62
The attending on your internal medicine rotation asks about the mechanism of digoxin. Explain.
It directly inhibits the Na+/K+ ATPase, indirectly inhibiting the Na+/Ca2+ exchanger, resulting in ↑[Ca2+]i and ↑inotropy/contractility
63
Name two antiarrhythmics that predispose a patient to digoxin toxicity.
erapamil (calcium channel blocker) and amiodarone (potassium channel blocker)
64
A patient on procainamide for an arrhythmia develops a facial rash and joint pains. She has antihistone antibodies. What is the diagnosis?
Reversible SLE-like syndrome
65
Quinidine causes symptoms of headache and tinnitus, which are collectively known as what?
• Cinchonism, which can occur with all quinine derivatives
66
A patient takes flecainide for supraventricular tachycardia. What effect does this class of drug have on action potential duration?
Class IC antiarrhythmics have minimal effect on action potential duration
67
Which antiarrhythmic is indicated to prevent arrhythmias after myocardial infarction? Which antiarrhythmic is contraindicated after MI?
Class IB antiarrhythmics (IB is Best after MI); class IC antiarrhythmics are contraindicated (IC is Contraindicated after MI)
68
What is the toxicity of class IC antiarrhythmics? When are they contraindicated?
Proarrhythmic, as they increase refractory period of AV node & accessory bypass tracts; post-MI & after ischemic/structural heart disease
69
Name the class IB antiarrhythmic drugs.
Lidocaine, Mexiletine (phenytoin also can fall into the IB class [I’d Buy Liddy’s Mexican tacos])
70
Which antiarrhythmics belong to class IA?
Quinidine, Procainamide, DisoPyramide (the Queen Proclaims Diso's Pyramid)
71
What does it mean when sodium channel blockers are described as state dependent?
State dependent means that the antiarrhythmics act selectively on tissue that is frequently depolarized (e.g., during tachycardia)
72
A 45-year-old man takes disopyramide for an arrhythmia. What type of arrhythmia may he have?
Class IA antiarrhythmics treat atrial and ventricular arrhythmias, notably reentrant and ectopic supraventricular/ventricular tachycardias
73
A 45-year-old patient takes mexiletine for an arrhythmia. How do drugs in this class work?
Class IB antiarrhythmics shorten the action potential duration and preferentially affect ischemic or depolarized Purkinje/ventricular tissue
74
• A 45-year-old man starts taking lidocaine. What type of arrhythmia may he have?
Class IB antiarrhythmics treat acute ventricular arrhythmias (especially after myocardial infarction) and digitalis-induced arrhythmias
75
A 45-year-old patient takes a class IB antiarrhythmic. What are the adverse effects of this class of drug?
Class IB antiarrhythmics can cause central nervous system stimulation/depression and cardiovascular depression
76
A 45-year-old patient starts taking propafenone. What conditions may he have?
Class IC antiarrhythmics treat supraventricular tachycardias (including atrial fibrillation) & are used as a last resort in refractory VT
77
Which antiarrhythmics belong to class IC?
Flecainide, Propafenone (Can [class IC] I have Fries, Please)
78
Class I antiarrhythmics slow/block conduction and decrease the slope of ___ (phase 0/1/2/3/4) myocardial action potential depolarization.
Phase 0 (inward sodium current), especially in depolarized cells
79
Class IC antiarrhythmics have no effect on the effective refractory period in which two types of tissues?
Purkinje and ventricular tissues
80
Name the possible side effects of class IA antiarrhythmics.
Cinchonism (quinidine), SLE-like syndrome (procainamide), HF (disopyramide), thrombocytopenia, torsades de pointes (↑QT interval)
81
Which β-blocker is extremely short acting?
Esmolol
82
Which antiarrhythmics belong in class II?
β-blockers such as propranolol, esmolol, timolol, metoprolol, atenolol, and carvedilol
83
A 70-year-old woman takes atenolol for atrial fibrillation. What is the mechanism of action of this class of antiarrhythmic?
β-blockers (class II) ↑SA and AV nodal activity (by ↓cAMP and Ca2+ currents) & suppress abnormal pacemakers by ↓slope of phase 4
84
A 70-year-old woman takes metoprolol for atrial fibrillation. Which cardiac node is most sensitive to this class of antiarrhythmic?
The atrioventricular node is most sensitive to β-blockers (class II), and as a result, the PR interval is lengthened on ECG
85
A 70-year-old woman takes timolol. What types of arrhythmias may she have?
Supraventricular tachycardias, as β-blockers treat them & provide ventricular rate control for atrial fibrillation and atrial flutter
86
A 70-year-old man takes esmolol to treat atrial fibrillation. What are the toxicities of this class of antiarrhythmic?
β-blockers cause impotence, asthma/COPD exacerbations, CV effects (bradycardia, AV block, HF), and CNS effects (sedation, sleep changes)
87
A patient starts taking metoprolol. Months later, his lipid panel has worsened. Is metoprolol to blame?
Possibly, as dyslipidemia is a side effect of metoprolol therapy
88
Why might β-blockers be dangerous for someone who takes insulin? What is the antidote for β-blocker overdose?
Because they may mask signs of hypoglycemia
89
A patient has Prinzmetal angina. Which β-blocker should not be prescribed to treat his arrhythmia? Why?
Propranolol should not be given; it can exacerbate vasospasms
90
Patients who have overdosed on which illicit drug should not be treated with β-blockers?
Cocaine, as there is a risk of unopposed α1-receptor agonist activity
91
Patients with which type of endocrine tumor should not be treated with β-blockers?
Pheochromocytoma, as there is then a risk of unopposed α1-receptor agonist activity
92
A patient on amiodarone is frustrated with monthly testing that is required. What lab(s) are being tested in this patient?
Pulmonary function tests, liver function tests, and thyroid function tests must be checked regularly when on amiodarone
93
Which antiarrhythmics belong to class III?
Potassium channel blockers, such as Amiodarone, Ibutilide, Dofetilide, Sotalol (AIDS)
94
Name two toxicities of sotalol.
Torsades de pointes and excessive β-blockade
95
Name a potentially fatal adverse effect of ibutilide.
Torsades de pointes
96
A 78-year-old man takes amiodarone for an arrhythmia. Name the toxicities of this medication.
Pulmonary fibrosis, hepatotoxicity, hyperthyroidism, corneal and blue/gray skin deposits, constipation, cardiovascular/neurologic effects
97
Which antiarrhythmic drug is lipophilic and has classes I, II, III, and IV effects?
Amiodarone
98
A 78-year-old man takes amiodarone for an arrhythmia. Why must his thyroid function be monitored regularly?
Because it is 40% iodine by weight and can cause hypo- or hyperthyroidism
99
A patient taking an antiarrhythmic develops corneal/skin deposits and photodermatitis. Which arrhythmias may he have?
Atrial fibrillation/flutter and ventricular tachycardia (the side effects suggest that he is taking amiodarone [class III])
100
How does sotalol affect the duration of the action potential, effective refractory period, and QT interval?
Sotalol and other class III antiarrhythmics (potassium channel blockers) increase the duration of all three
101
A 64-year-old woman takes verapamil for an arrhythmia. Which cardiac myocytes does this class of medication affect?
Class IV antiarrhythmics (Ca2+ channel blockers) ↓AV node pacemaker cells' conduction velocity and ↑ERP/PR interval
102
Which two antiarrhythmic drugs belong to class IV?
Diltiazem and verapamil, which prevent nodal arrhythmias (e.g., supraventricular tachycardia) and offer rate control in atrial fibrillation
103
A patient develops an adverse reaction to a calcium channel blocker. What would you expect to hear in the patient's history?
Constipation, flushing, edema, signs of cardiovascular abnormalities such as heart failure, atrioventricular block, sinus node depression
104
What is the mechanism of action of the first-line antiarrhythmic for diagnosing and treating supraventricular tachycardia?
Adenosine increases the amount of K+ flowing out of cells, leading to hyperpolarization of the cell and decreased intracellular Ca2+ (ICa)
105
Which ion is infused for the treatment of torsades de pointes and digoxin toxicity?
Mg2+
106
Adenosine is infused into a patient with supraventricular tachycardia. For how long do you expect this drug to be active in the patient?
Adenosine is a short-acting (about 15 seconds) drug
107
You diagnose a man with supraventricular tachycardia. Name the side effects of the diagnostic/treatment drug of choice.
Adenosine can cause flushing, hypotension, chest pain, a sense of impending doom, bronchospasm
108
A man has chest pain and bronchospasm after being treated for supraventricular tachycardia. How can you alleviate these side effects?
They can be blunted by caffeine or theophylline (both are adenosine receptor antagonists) (these symptoms are adverse effects of adenosine

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