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Pharmacology II > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

1
Q

State the primary indication for diuretics.

A

primarily hypertension, but also glaucoma and edema (major classes include thiazides, loop, and potassium sparing)

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2
Q

Describe the most common mechanism of action of diuretic agents.

A

Most block kidney tubular reabsorption of Na+ which is excreted with an accompanying volume of water (they increase rate of urine formation)

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3
Q

Discuss the mechanism of action of thiazides

A

Inhibition of active Na+ reabsorption in the proximal and distal tubules AND inhibition of carbonic anhydrase = decreased availability of H+ exhange with Na+

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4
Q

Discuss the indications for use for thiazide and loop diuretics.

A

First choice agents for hypertension and congestive heart failure (these are the most-commonly prescribed diuretics)

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5
Q

Describe oral side effects associated with diuretics.

A

xerostomia, lichenoid drug reaction, photosensitivity

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6
Q

What is a general rule for remembering which beta blockers are cardioselective?

A

“-olols” with a generic name that starts with a letter A-M are cardioselective (e.g. atenolol) = blocks beta1 only

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7
Q

What is a general rule for remembering which beta blockers are non-cardioselective?

A

“-olols” with a generic name that starts with a letter N-Z are non-cardioselective (e.g. propranolol = blocks both beta1 and beta2

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8
Q

Discuss the mechanism of action of Alpha1 receptor blocking agents

A

Alpha1 Blockers produce peripheral vasodilation in arterioles and venules, decreasing peripheral vascular resistance. They are more effective when used with diuretics and/or beta blockers. (Also used for BPH)

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9
Q

What are some examples of Alpha1 receptor blockers?

A

“-osin” doxazosin (Cardura), prazosin (Minipress), tamsulosin (Flomax)

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10
Q

Discuss the mechanism of action of ACE inhibitors

A

Competitively inhibits angiotensin-converting enzyme (ACE) thereby preventing the conversion of angiotensin I to angiotensin II (a potent vasoconstrictor)–>vasodilation

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11
Q

What ending is commonly associated with ACE inhibitors?

A

“-pril” (e.g. lisinopril (Privnivil, Zestril)

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12
Q

Discuss the mechanism of action of Angiotensin Receptor Blockers (ARBs)

A

Block vasoconstrictor and aldosterone-secreting effects of angiotensin II thereby increasing plasma renin levels causing vasodilation, decreased sodium and water retention–>reduced blood pressure.

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13
Q

What ending is commonly associated with ARBs?

A

“-artan” (e.g. losartan (Cozaar), valsartan (Diovan)

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14
Q

Discuss the mechanism of action calcium channel blockers

A

Inhbits Ca2+ ion from entering the “slow channels”–>produces relaxation of coronary vascular smooth muscle and coronary vasodilation–>increases myocardial O2 delivery

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15
Q

verapamil (Calan), nifedipine (Procardia) and amlodipine (Norvasc) belong to which drug class?

A

Calcium channel blockers

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16
Q

Discuss the mechanisms of action of centrally-acting antihypertensives.

A

Alpha2 agonist decreases sympathetic outflow from CNS–>decreases peripheral resistance, renal vascular resistance, heart rate and BP

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17
Q

Describe common side effects of thiazides

A

hypokalemia, loss of carbonate (HCO3-), hypomagnesaemia, hyponatremia, hyperuricemia, hyperglycemia, elevated cholesterol, elevated triglycerides, weakness/fatigue, sexual dysfunciton

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18
Q

Describe common side effects of loop diuretics

A

Major loss of volume, serious electrolyte imbalance may result, ototoxicity to some degree

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19
Q

Describe common side effects of potassium sparing diuretics

A

Hyperkalemia, gynocomastia, decreased libido, menstrual irregularities

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20
Q

Identify at least one generic and brand name drug in the “mercurials” class (antihypertensive medications)

A

mercaptomerin (Thiomerin); meralluride (Mercuhydrun)

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21
Q

Identify at least one generic and brand name drug in the “thiazides” class (antihypertensive medications)

A

hydrochlorothiazide (“HCTZ”); chlorothiazide (Diuril)

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22
Q

Identify at least one generic and brand name drug in the “Loop (high ceiling)” class (antihypertensive medications)

A

furosemide (Lasix), ethacrynic acid (Edecrin)

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23
Q

Which two antihypertensives in particular are known for producing lichenoid drug reactions in some patients?

A

thazide and loop diuretics

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24
Q

Identify at least one generic and brand name drug in the “Carbonic anhydrase inhibitors” class (antihypertensive medications)

A

acetazolamide (Diamox), methazolamide (Neptazane)-primarily used for glaucoma and as an adjunctive therapy for CHF

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25
Q

Identify at least one generic and brand name drug in the “Potassium-sparing diuretic” class (antihypertensive medications)

A

spironolactone (Aldactone), triamterene (Dyrenium)

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26
Q

Identify at least one generic and brand name drug in the “Osmotics” class (antihypertensive medications)

A

urea (Ureaphil)

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27
Q

Identify at least one generic and brand name drug in the “Acidifying agents” class (antihypertensive medications)

A

Ammonium chloride

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28
Q

Identify at least one generic and brand name drug in the “Xanthines” class (antihypertensive medications)

A

caffeine

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29
Q

Identify the calcium channel blockers that are associated with causing gingival hyperplasia as a side effect.

A

Nifedipine (30%), verapamil (8%), diltiazem (2%), amlodipine (<1%)

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30
Q

Discuss drug interactions with antihypertensive medications of significance to dentistry.

A

xerostomia, lichenoid drug reaction, photosensitivity

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31
Q

Describe important precautions to take during dental procedures when treating patients with hypertension.

A

Prevent suddent changes in posture, decrease stress, tissue retraction w/vasopressors is contraindicated, rebound hypertension may develop if antihypertensive agents are abruptly withdrawn.

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32
Q

Discuss the etiology of cardiac arrhythmias.

A

Arrhythmias can be caused by disease, cardiac injury or drugs and produce abnormalities of the heartbeat

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33
Q

What is a key feature driving the automaticity of the cardiac system?

A

Spontaneous opening and closing of K+ channels-the net flow of these ions repolarizes the cells and then depolarizes to threshold.

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34
Q

Identify the indications for use of antiarrhythmic drugs.

A

Treatment of arryhthmias-specific examples include: paroxysmal atrial tachycardia, paroxysmal ventricular tachycardia, atrial fibrillation, ventricular ectopic arrhthmias and digoxin-induced arrhythmias

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35
Q

Identify four contraindications for use of antiarrhythmic drugs.

A

Complete A-V heart block, CHF, hypotension, known hypersensitivity to the drug.

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36
Q

Describe Beta blockers (Class II antiarrhythmic drugs) in terms of mechanism of action and site of action.

A

Blocks effect of catecholamines on pacemaker cells to prolong the refractory period thereby depressing automaticity, prolonging AV conduction, and decreasing heart rate/contractility. These also block NA+ channels.

37
Q

Describe “Class IA” Na+ channel blockers (antiarrhythmic drugs) in terms of mechanism of action and site of action.

A

slows conduction, prolongs AP, and increases ERP in the treatment of ventricular arrhythmias.

38
Q

Describe “Class IB” Na+ channel blockers (antiarrhythmic drugs) in terms of mechanism of action and site of action.

A

Decrease duration of AP by shortening/decreasing repolarization (ERP) = speeds up rate to overcome ventricular ectopic foci and treat ventricular arrhythmias.

39
Q

Describe “Class IC” Na+ channel blockers (antiarrhythmic drugs) in terms of mechanism of action and site of action.

A

Acts on the ventricles (only in cases of life-threatening ventricular arrhthmias) to cause marked conduction slowing

40
Q

Describe K+ channel blockers (Class III antiarrhythmic drugs) in terms of mechanism of action and site of action.

A

Block K+ channels thereby prolonging AP and ERP helping to slow the heart by reducing the amount of norepinephrine released

41
Q

Digoxin is classified within which class of antiarrhythimc medication?

A

Class IV-also called a cardiac glycoside used to treat CHF, atrial fibrillation and flutter

42
Q

Adenosine is classified within which class of antiarrhythimc medication?

A

Class IV

43
Q

Describe Ca+ channel blockers (Class IV antiarrhythmic drugs) in terms of mechanism of action and site of action.

A

Calcium channel blockers slow conduction velocity and increase effective refractory period of the AV node causing negative chronotropic effect (also some negative inotropic effect)

44
Q

Describe the clinical manifestation of cinchonism associated with quinidine.

A

Cinchonism is characterized by nausea/vomiting, headache, tinnitus, deafness, symptoms of cerebral congestion, vertigo, visual distrubances = quinidine (Class IA) use

45
Q

Discuss common side effects associated with “Class IA” Na+ channel blockers (antiarrhythmic drugs)

A

reversible lupus-like syndrome in 25% of patients, peripheral vasoconstriction, overdose leads to cinchonism, quinidine is toxic and may exacerbate arrhthmias and can even produce fatal arrythmias, CNS effects as well

46
Q

Discuss common side effects associated with “Class IB” Na+ channel blockers (antiarrhythmic drugs)

A

CNS effects, may cause arrhthmias, gingival hyperplasia (phenytoin/Dilantin)

47
Q

Discuss common side effects associated with “Class IC” Na+ channel blockers (antiarrhythmic drugs).

A

Arrhythmias because of profound effect of Na+ channels on healthy heart tissue

48
Q

Discuss common side effects associated with K+ channel blockers (Class III antiarrhythmic drugs).

A

Blue skin, thyroid disease, assortment of severe toxic effects

49
Q

Discuss common side effects associated with Ca+ channel blockers (Class IV antiarrhythmic drugs).

A

gingival hyperplasia and others (CNS, GI, tachycardia, hypotension, flushing, headache)

50
Q

What is the mechanism of Digoxin in treating CHF?

A

It inhibits Na/K ATPase pump causing an increase in intracellular Na/Ca exchange thereby increasing intracellular Ca leading to increased contractility.

51
Q

Describe important dental considerations for managing patients taking antiarrhythmic medications.

A

Gingival hyperplasia may be seen with Ca+ channel blockers, saliva-inhibiting drugs should not be administered to a patient who is prone to arrhythmias, as they may cause tachycardia (think anticholinergic atropine)

52
Q

What are some similarities between typical angina and variant angina?

A

pain occurs when heart becomes anoxic, O2 demand of myocardium exceeds amount of available O2, triggers include physical exertion, mechanical stress, increased contractility, pulse rate and BP

53
Q

What are some key features of variant (atypical, Prinzmetal’s angina)?

A

patients present with more alpha 1 receptors than beta 2 receptors in their coronary arteries (vasoconstriction), lack of oxygenation due to vasospasm, elevated S-T segment which is not present in normal angina

54
Q

List several factors that may trigger an angina attack.

A

stress, cold, hyperventilation

55
Q

Describe the mechanism of action of nitrites/nitrates, as it relates to the management of angina.

A

causes relaxation of all smooth muscle, results in arterial and venous vasodilation

56
Q

Describe the mechanism of action of beta-blockers as it relates to the management of angina.

A

Decrease workload of the heart by decreasing cardiac output (afterload) and arterial pressure, which decreases venous return, decreases preload and decreases oxygen demand.

57
Q

Describe the mechanism of action of calcium channel blockers as it relates to the management of angina.

A

blocking Ca+ entry into the myocardial cell means there is less Ca+ inside the cell maintaining troponin’s inhibitory effect thereby causing a negative inotropic effect (some cause vasodilation too)

58
Q

Discuss the side effects of nitrites/nitrates.

A

flush, postural hypotension and syncompe, tachycardia and increased peripheral resistance, decreased O2-carrying capabilities w/large doses

59
Q

Discuss the side effects of beta-blockers.

A

Contraindicated for variant angina and some forms of CHF, bradycardia, bronchial constriction/asthma attacks

60
Q

Discuss the side effects of calcium channel blockers.

A

Gingival hyperplasia with some Ca+ channel blockers

61
Q

Which preparation of nitrites/nitrates has the fastest onset?

A

Amyl nitrate (Vaporole)-source of nitric oxide=vasodilator. Onset < 1 min and lasts 3-15 minutes

62
Q

What is the average onset of nitroglycerine?

A

1-3 mintues (short T1/2 < 10 minutes). Photosensitive, “rescue” drug in emergency kit.

63
Q

Discuss important dental care considerations for patients taking antianginal medications.

A

Gingival enlargement (Ca+ channel blockers)). Non-selective beta blockers enhance the pressor response to epinephrine: hypertension and reflex bradycardia. NDSAIDs may reduce effects of beta blockers when used for > 3 weeks.

64
Q

Describe the antiplatelet effects of aspirin and thienopyridines (e.g. clopidogrel (Plavix)).

A

Inhibit ability of ADP to induce plately aggregation (irreversible effect for the life of the platelet)

65
Q

Discuss the dental management of patients taking combination antiplatelet therapy for percutaneous coronary intervention (stents).

A

Keep patients on aspirin/antiplatelet therapy. Aspirin non-adherence/withdrawal has been associated w/3X higher risk for major adverse cardiac events (amplified by a factor of 89 in patients who had undergone stenting)

66
Q

Describe the anticoagulant effects of heparin and warfarin (Coumadin).

A

interferes w/liver synthesis of vitamin-K dependient clotting factors (II, VII, IX, X and proteins C and S)

67
Q

Identify factors that can alter the efficacy of warfarin (Coumadin).

A

Drugs that induce liver metabolism will decrease levels of warfarin (ex. Phenytoin), there is a low therapeutic index/window of safety. Also fever, flu, diarrhea/vomiting, antibiotics, changes in diet can also affect efficacy.

68
Q

State the antagonists to heparin and warfarin (Coumadin).

A

Protamine

69
Q

Discuss the indications for use for direct antithrombins (Factor Xa inhibitors).

A

Low molecular weight heparins help prevent DVT with or without PE; reduce risk for PE, acute unstable angina, non-Q-wave NI

70
Q

Describe the dangers of anticoagulant medications.

A

DDIs, bleeding

71
Q

List the tests used to assess the effects of heparin and warfarin (Coumadin).

A

Bleeding time test, Prothrombin time (PT), activated partial prothrombin time (aPTT), international normalized ration (INR).

72
Q

Name an antidote for tPA.

A

Epsilon AminoCaproid Acid (Amicar)

73
Q

Name 2 thrombolytic (clot-busting) drugs.

A

tPA (tissue plaminogen activator) = IV drug, streptokinase (Streptase), urokinase

74
Q

Describe the mechanism of action of bile acid sequestrants in lowering plasma lipids.

A

reduce cholesterol by binding bile acids in gut–>increase fecal loss of bile salt bound LDL cholesterol

75
Q

Describe the mechanism of action of fibric acid derivatives in lowering plasma lipids.

A

lower plasma triglycerides, increase HDLs, inhibit cholesteol synthesis in liver

76
Q

Describe the mechanism of action of niacin in lowering plasma lipids.

A

decreases liver triacylglycerol synthesis necessary for VLDL production, decreases plasma LDLs

77
Q

Describe the mechanism of action of HMG CoA Reductase inhibitors in lowering plasma lipids.

A

“-statin”s: HMG-CaA reductase is the rate limiting step in the synthesis of cholesterol, (1) decreases synthesis of cholesterol in liver and (2) increases LDL breakdown decreasing existing bad cholesterol

78
Q

Discuss important dental drug interactions associated with HMG CoA Reductase inhibitors (“statins”).

A

Avoid azole antifungals and macrolide antibiotics

79
Q

Define congestive heart failure.

A

Inability of the heart to provide the necessary output

80
Q

State the main effect of cardiac glycosides.

A

inhibits Na/K ATPase pump resulting in increased Ca+ inside of the cell also directly suppresses AV node conduction to increase ERP

81
Q

Describe the primary effects of cardiac glycosides on the myocardium.

A

increases contraction of the heart, positive inotropic effect and decrease conduction velocity, negative chronotropic effect

82
Q

Describe the margin of safety of cardiac glycosides (therapeutic index).

A

Low therapeutic index=therapeutic dose is about 50-60% of the toxic dose

83
Q

Identify indications for the use of cardiac glycosides.

A

CHF and atrial fibrillation/flutter

84
Q

List common side effects produced by cardiac glycosides related to the cardiac system.

A

Conduction block between SA and AV nodes–>bradycardia due to AV block, decreased cardiac output, extra beats/arrhythmias

85
Q

List common side effects produced by cardiac glycosides related to the gastrointestinal system.

A

Digoxin toxicity, GI effects (N/V, +salivation, anorexia, diarrhea, abdominal pain)

86
Q

List common side effects produced by cardiac glycosides related to the central nervous system.

A

headache, fatigue, drowsiness, visual disturbances (blurry vision), green/yellowish aura (patients often know they are reaching toxic levels of digitalis when they see this aura)

87
Q

Identify the common cardiac glycoside used to treat congestive heart failure.

A

digoxin (Digitek, Lanoxin)

88
Q

Discuss dental practice considerations when treating patients with congestive heart failure.

A

Caution w/systemic azole antifungals, macrolide antibiotics (clarithromycin, erythromycin), and caution w/use of vasoconstrictors: risk for arrhythmias

Pharmacology II (13 decks)

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