Cardiovascular Drugs Flashcards
State the primary indication for diuretics.
primarily hypertension, but also glaucoma and edema (major classes include thiazides, loop, and potassium sparing)
Describe the most common mechanism of action of diuretic agents.
Most block kidney tubular reabsorption of Na+ which is excreted with an accompanying volume of water (they increase rate of urine formation)
Discuss the mechanism of action of thiazides
Inhibition of active Na+ reabsorption in the proximal and distal tubules AND inhibition of carbonic anhydrase = decreased availability of H+ exhange with Na+
Discuss the indications for use for thiazide and loop diuretics.
First choice agents for hypertension and congestive heart failure (these are the most-commonly prescribed diuretics)
Describe oral side effects associated with diuretics.
xerostomia, lichenoid drug reaction, photosensitivity
What is a general rule for remembering which beta blockers are cardioselective?
“-olols” with a generic name that starts with a letter A-M are cardioselective (e.g. atenolol) = blocks beta1 only
What is a general rule for remembering which beta blockers are non-cardioselective?
“-olols” with a generic name that starts with a letter N-Z are non-cardioselective (e.g. propranolol = blocks both beta1 and beta2
Discuss the mechanism of action of Alpha1 receptor blocking agents
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)
What are some examples of Alpha1 receptor blockers?
“-osin” doxazosin (Cardura), prazosin (Minipress), tamsulosin (Flomax)
Discuss the mechanism of action of ACE inhibitors
Competitively inhibits angiotensin-converting enzyme (ACE) thereby preventing the conversion of angiotensin I to angiotensin II (a potent vasoconstrictor)–>vasodilation
What ending is commonly associated with ACE inhibitors?
“-pril” (e.g. lisinopril (Privnivil, Zestril)
Discuss the mechanism of action of Angiotensin Receptor Blockers (ARBs)
Block vasoconstrictor and aldosterone-secreting effects of angiotensin II thereby increasing plasma renin levels causing vasodilation, decreased sodium and water retention–>reduced blood pressure.
What ending is commonly associated with ARBs?
“-artan” (e.g. losartan (Cozaar), valsartan (Diovan)
Discuss the mechanism of action calcium channel blockers
Inhbits Ca2+ ion from entering the “slow channels”–>produces relaxation of coronary vascular smooth muscle and coronary vasodilation–>increases myocardial O2 delivery
verapamil (Calan), nifedipine (Procardia) and amlodipine (Norvasc) belong to which drug class?
Calcium channel blockers
Discuss the mechanisms of action of centrally-acting antihypertensives.
Alpha2 agonist decreases sympathetic outflow from CNS–>decreases peripheral resistance, renal vascular resistance, heart rate and BP
Describe common side effects of thiazides
hypokalemia, loss of carbonate (HCO3-), hypomagnesaemia, hyponatremia, hyperuricemia, hyperglycemia, elevated cholesterol, elevated triglycerides, weakness/fatigue, sexual dysfunciton
Describe common side effects of loop diuretics
Major loss of volume, serious electrolyte imbalance may result, ototoxicity to some degree
Describe common side effects of potassium sparing diuretics
Hyperkalemia, gynocomastia, decreased libido, menstrual irregularities
Identify at least one generic and brand name drug in the “mercurials” class (antihypertensive medications)
mercaptomerin (Thiomerin); meralluride (Mercuhydrun)
Identify at least one generic and brand name drug in the “thiazides” class (antihypertensive medications)
hydrochlorothiazide (“HCTZ”); chlorothiazide (Diuril)
Identify at least one generic and brand name drug in the “Loop (high ceiling)” class (antihypertensive medications)
furosemide (Lasix), ethacrynic acid (Edecrin)
Which two antihypertensives in particular are known for producing lichenoid drug reactions in some patients?
thazide and loop diuretics
Identify at least one generic and brand name drug in the “Carbonic anhydrase inhibitors” class (antihypertensive medications)
acetazolamide (Diamox), methazolamide (Neptazane)-primarily used for glaucoma and as an adjunctive therapy for CHF
Identify at least one generic and brand name drug in the “Potassium-sparing diuretic” class (antihypertensive medications)
spironolactone (Aldactone), triamterene (Dyrenium)
Identify at least one generic and brand name drug in the “Osmotics” class (antihypertensive medications)
urea (Ureaphil)
Identify at least one generic and brand name drug in the “Acidifying agents” class (antihypertensive medications)
Ammonium chloride
Identify at least one generic and brand name drug in the “Xanthines” class (antihypertensive medications)
caffeine
Identify the calcium channel blockers that are associated with causing gingival hyperplasia as a side effect.
Nifedipine (30%), verapamil (8%), diltiazem (2%), amlodipine (<1%)
Discuss drug interactions with antihypertensive medications of significance to dentistry.
xerostomia, lichenoid drug reaction, photosensitivity
Describe important precautions to take during dental procedures when treating patients with hypertension.
Prevent suddent changes in posture, decrease stress, tissue retraction w/vasopressors is contraindicated, rebound hypertension may develop if antihypertensive agents are abruptly withdrawn.
Discuss the etiology of cardiac arrhythmias.
Arrhythmias can be caused by disease, cardiac injury or drugs and produce abnormalities of the heartbeat
What is a key feature driving the automaticity of the cardiac system?
Spontaneous opening and closing of K+ channels-the net flow of these ions repolarizes the cells and then depolarizes to threshold.
Identify the indications for use of antiarrhythmic drugs.
Treatment of arryhthmias-specific examples include: paroxysmal atrial tachycardia, paroxysmal ventricular tachycardia, atrial fibrillation, ventricular ectopic arrhthmias and digoxin-induced arrhythmias
Identify four contraindications for use of antiarrhythmic drugs.
Complete A-V heart block, CHF, hypotension, known hypersensitivity to the drug.
Describe Beta blockers (Class II antiarrhythmic drugs) in terms of mechanism of action and site of action.
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.
Describe “Class IA” Na+ channel blockers (antiarrhythmic drugs) in terms of mechanism of action and site of action.
slows conduction, prolongs AP, and increases ERP in the treatment of ventricular arrhythmias.
Describe “Class IB” Na+ channel blockers (antiarrhythmic drugs) in terms of mechanism of action and site of action.
Decrease duration of AP by shortening/decreasing repolarization (ERP) = speeds up rate to overcome ventricular ectopic foci and treat ventricular arrhythmias.
Describe “Class IC” Na+ channel blockers (antiarrhythmic drugs) in terms of mechanism of action and site of action.
Acts on the ventricles (only in cases of life-threatening ventricular arrhthmias) to cause marked conduction slowing
Describe K+ channel blockers (Class III antiarrhythmic drugs) in terms of mechanism of action and site of action.
Block K+ channels thereby prolonging AP and ERP helping to slow the heart by reducing the amount of norepinephrine released
Digoxin is classified within which class of antiarrhythimc medication?
Class IV-also called a cardiac glycoside used to treat CHF, atrial fibrillation and flutter
Adenosine is classified within which class of antiarrhythimc medication?
Class IV
Describe Ca+ channel blockers (Class IV antiarrhythmic drugs) in terms of mechanism of action and site of action.
Calcium channel blockers slow conduction velocity and increase effective refractory period of the AV node causing negative chronotropic effect (also some negative inotropic effect)
Describe the clinical manifestation of cinchonism associated with quinidine.
Cinchonism is characterized by nausea/vomiting, headache, tinnitus, deafness, symptoms of cerebral congestion, vertigo, visual distrubances = quinidine (Class IA) use
Discuss common side effects associated with “Class IA” Na+ channel blockers (antiarrhythmic drugs)
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
Discuss common side effects associated with “Class IB” Na+ channel blockers (antiarrhythmic drugs)
CNS effects, may cause arrhthmias, gingival hyperplasia (phenytoin/Dilantin)
Discuss common side effects associated with “Class IC” Na+ channel blockers (antiarrhythmic drugs).
Arrhythmias because of profound effect of Na+ channels on healthy heart tissue
Discuss common side effects associated with K+ channel blockers (Class III antiarrhythmic drugs).
Blue skin, thyroid disease, assortment of severe toxic effects
Discuss common side effects associated with Ca+ channel blockers (Class IV antiarrhythmic drugs).
gingival hyperplasia and others (CNS, GI, tachycardia, hypotension, flushing, headache)
What is the mechanism of Digoxin in treating CHF?
It inhibits Na/K ATPase pump causing an increase in intracellular Na/Ca exchange thereby increasing intracellular Ca leading to increased contractility.
Describe important dental considerations for managing patients taking antiarrhythmic medications.
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)
What are some similarities between typical angina and variant angina?
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
What are some key features of variant (atypical, Prinzmetal’s angina)?
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
List several factors that may trigger an angina attack.
stress, cold, hyperventilation
Describe the mechanism of action of nitrites/nitrates, as it relates to the management of angina.
causes relaxation of all smooth muscle, results in arterial and venous vasodilation
Describe the mechanism of action of beta-blockers as it relates to the management of angina.
Decrease workload of the heart by decreasing cardiac output (afterload) and arterial pressure, which decreases venous return, decreases preload and decreases oxygen demand.
Describe the mechanism of action of calcium channel blockers as it relates to the management of angina.
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)
Discuss the side effects of nitrites/nitrates.
flush, postural hypotension and syncompe, tachycardia and increased peripheral resistance, decreased O2-carrying capabilities w/large doses
Discuss the side effects of beta-blockers.
Contraindicated for variant angina and some forms of CHF, bradycardia, bronchial constriction/asthma attacks
Discuss the side effects of calcium channel blockers.
Gingival hyperplasia with some Ca+ channel blockers
Which preparation of nitrites/nitrates has the fastest onset?
Amyl nitrate (Vaporole)-source of nitric oxide=vasodilator. Onset < 1 min and lasts 3-15 minutes
What is the average onset of nitroglycerine?
1-3 mintues (short T1/2 < 10 minutes). Photosensitive, “rescue” drug in emergency kit.
Discuss important dental care considerations for patients taking antianginal medications.
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.
Describe the antiplatelet effects of aspirin and thienopyridines (e.g. clopidogrel (Plavix)).
Inhibit ability of ADP to induce plately aggregation (irreversible effect for the life of the platelet)
Discuss the dental management of patients taking combination antiplatelet therapy for percutaneous coronary intervention (stents).
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)
Describe the anticoagulant effects of heparin and warfarin (Coumadin).
interferes w/liver synthesis of vitamin-K dependient clotting factors (II, VII, IX, X and proteins C and S)
Identify factors that can alter the efficacy of warfarin (Coumadin).
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.
State the antagonists to heparin and warfarin (Coumadin).
Protamine
Discuss the indications for use for direct antithrombins (Factor Xa inhibitors).
Low molecular weight heparins help prevent DVT with or without PE; reduce risk for PE, acute unstable angina, non-Q-wave NI
Describe the dangers of anticoagulant medications.
DDIs, bleeding
List the tests used to assess the effects of heparin and warfarin (Coumadin).
Bleeding time test, Prothrombin time (PT), activated partial prothrombin time (aPTT), international normalized ration (INR).
Name an antidote for tPA.
Epsilon AminoCaproid Acid (Amicar)
Name 2 thrombolytic (clot-busting) drugs.
tPA (tissue plaminogen activator) = IV drug, streptokinase (Streptase), urokinase
Describe the mechanism of action of bile acid sequestrants in lowering plasma lipids.
reduce cholesterol by binding bile acids in gut–>increase fecal loss of bile salt bound LDL cholesterol
Describe the mechanism of action of fibric acid derivatives in lowering plasma lipids.
lower plasma triglycerides, increase HDLs, inhibit cholesteol synthesis in liver
Describe the mechanism of action of niacin in lowering plasma lipids.
decreases liver triacylglycerol synthesis necessary for VLDL production, decreases plasma LDLs
Describe the mechanism of action of HMG CoA Reductase inhibitors in lowering plasma lipids.
“-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
Discuss important dental drug interactions associated with HMG CoA Reductase inhibitors (“statins”).
Avoid azole antifungals and macrolide antibiotics
Define congestive heart failure.
Inability of the heart to provide the necessary output
State the main effect of cardiac glycosides.
inhibits Na/K ATPase pump resulting in increased Ca+ inside of the cell also directly suppresses AV node conduction to increase ERP
Describe the primary effects of cardiac glycosides on the myocardium.
increases contraction of the heart, positive inotropic effect and decrease conduction velocity, negative chronotropic effect
Describe the margin of safety of cardiac glycosides (therapeutic index).
Low therapeutic index=therapeutic dose is about 50-60% of the toxic dose
Identify indications for the use of cardiac glycosides.
CHF and atrial fibrillation/flutter
List common side effects produced by cardiac glycosides related to the cardiac system.
Conduction block between SA and AV nodes–>bradycardia due to AV block, decreased cardiac output, extra beats/arrhythmias
List common side effects produced by cardiac glycosides related to the gastrointestinal system.
Digoxin toxicity, GI effects (N/V, +salivation, anorexia, diarrhea, abdominal pain)
List common side effects produced by cardiac glycosides related to the central nervous system.
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)
Identify the common cardiac glycoside used to treat congestive heart failure.
digoxin (Digitek, Lanoxin)
Discuss dental practice considerations when treating patients with congestive heart failure.
Caution w/systemic azole antifungals, macrolide antibiotics (clarithromycin, erythromycin), and caution w/use of vasoconstrictors: risk for arrhythmias
