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26 Cards in this Set
- Front
- Back
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Aspirin
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Class: NSAID
MOA: Prostaglandins -precursor of thromboxane A2 (TA2) TA2 -potent inducer of platelet aggregation ASA inhibits COX irreversibly Platelets do not contain a nucleus Platelets -No TA2 -10 day lifetime Uses: Prevention of arterial thrombosis -Stroke -MI -Transient ischemic attack Low doses and infrequent intervals -81 mg po every day Higher doses (325 mg) for anticoagulation therapy |
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Clopidogrel (Plavix)
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Class: Anti-platelet agent, anticoagulant
MOA: Irreversibly inhibits platelet aggregation -Covalently modify the P2Y12 ADP receptor Inhibits sustained aggregation -Transient can still occur Inhibition last the lifetime of the platelet Need to discuss dental surgery with physician Uses: Secondary prevention -MI -Stroke -Peripheral vascular disease Coronary artery stents Coronary artery bypass grafting Adverse: inhibition lasts the lifetime of the platelet |
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Dipyridamole (Persantine)
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Class: Anti-platelet, anticoagulant
MOA: Increase in cAMP levels in platelets leads to a decrease in adhesion Inhibitors of phosphodiesterase decrease platelet aggregation by inhibiting cAMP degradation Use: With warfarin in prosthetic heart valve replacement With ASA to reduce stroke risk Adverse: Causes gingival bleeding |
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Warfarin (Coumadin)
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Class: anticoagulant
MOA: Inhibition of vitamin K epoxide reductase Vitamin K - cofactor for synthesis of many coagulation factors (VIIa, IXa, Xa, Thrombin (IIa)) Oral anticoagulation indications: Mechanical prosthetic heart valves Atrial fibrillation Treatment of venous thromboembolism Acute myocardial infarction Prevention of venous thromboembolism Episodic systemic embolism Adverse: Too much- bleeding Too little- angina, blood clots INR every 2 weeks Watch for vitamin K in diet Change of lifestyle Coumadin has t1/2 of 40 hours, with duration of action 2-5 days Factors 2,7,9,10 become under-carboxylated = less procoagulant activity Less activity = Elevates PT and INR INR = (PT patient/PT reference)ISI Normal INR = 1.0 -(Trevor Treasure, DDS, MD) Interactions: APAP, ASA, Azithromycin, Cefixime, Chloral Hydrate, Cotrimoxazole, Diflunisal, Erythromycin, Fluoro quinones, Tetracyclines, Fluvastatin, Ibuprofen, Indomethacin, Ketoprofen, Metronidazole, Miconazole, Neomycin, Salicylates, Sulfonamides |
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Heparin
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Class: anticoagulant
MOA: Serves as a catalytic surface upon which the 2 proteins bind Induces a conformational change in antithrombin III so the reactive site is more accessible Effects: Cofactor in reaction of antithrombin III - accelerates by 1000 fold (inactivates thrombin by covalently binding to serine protease and prevents it from participation in coagulation cascade Adverse/Interactions: Glycosaminoglycan |
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Lovenox
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Class: anticoagulant
MOA: Does not act as a scaffold Induces a comformational change in antithrombin III Inactivates factor Xa and leads to less efficient activation of thrombin Use: Prevention of venous thrombosis with fewer bleeding complications Longer t½ than heparin Sub-Q injection Given 1-2 times a day without monitoring |
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Lisinopril (Zestril)
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Class: ACE inhibitor
Indications: Hypertension, Heart failure, MI Pharmacological Effects: -Decrease concentrations of ATII (vasodilation) -Increase bradykinin, a vasodilator -Decrease aldosterone Adverse Effects: -Altered or reduced taste sensation -Hypotension -Bradykinin -- Cough in 20% of patients, Angioedema of the face and mouth (more common in black patients) Drug Interactions: -NSAIDS and ASA inhibit anti-HTN effects |
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Valsartan (Diovan)
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Class: Angiotensin receptor antagonist
Indications: Heart Failure, Hypertension, MI, Prevention of stroke Pharmacological Effects: - Inhibit vasoconstriction - Inhibit aldosterone secretion -Inhibit sodium retention Comparison to ACE Inhibitors: -Less adverse rxns (cough and angioedema) -Less effective vasodilation Side Effects: GI upset Drug Interactions: Increase in anti-HTN effect with fluconazole and ketoconazole Increase renal toxicity with NSAIDs |
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Spironolactone (Aldactone)
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Class: aldosterone antagonist
MOA: At the cortical collecting duct cells; -Binds to intracellular mineralocorticoid receptor -Activation of the receptor -Control of sodium channel expression Spironolactone is an aldosterone antagonist -Binds to and prevents nuclear translocation of the mineralocorticoid receptor Indications: -Hypertension -Edema states -Heart failure -Hepatic cirrhosis -Congestive Heart Failure -Hypokalemia -Male to female gender transformation Adverse: Steroid structure -Gynecomastia in men -Menstrual irregularities in women -Hyperkalemia Decreased anti-HTN effect with NSAIDS |
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Hydrochlorothiazide (HCTZ)
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Class: Thiazide Diuretic
MOA: Binds to the Na+Cl- cotransporter in the distal tubule and inhibits turnover Reduction in extracellular fluid volume K+ is exchanged for Na+ leading to more K+ loss Pharmacological Effects: -Reduction in NaCl reabsorption -Increase the reabsorption of Ca+ Indications: HTN, Edema, CHF, Hepatic cirrhosis, Renal dysfunction, Corticosteroid therapy, Adverse: Hypokalemia, Hyponatremia, Gout, Dry mouth, lichenoid rxns, orthostatic hypotension Drug Interactions: NSAIDS decreases anti-HTN effects Increase orthostatic hypotension with opiates |
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Furosemide (Lasix)
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Class: Loop Diuretic
Mechanism: Inhibition of NaCl reabsorption in the Loop of Henle by binding to the Cl- site of the cotransporter. K+ secretion occurs in response to Na+ secretion Indications: HTN, Acute pulmonary edema, Edema, CHF, Hepatic cirrhosis, Renal dysfunction, Hyperkalemia, Hypercalcemia Effects: Reduces the extracellular fluid volume and BP with a greater magnitude than with thiazides Adverse Effects: Same as those for thiazides with respect to hypokalemia and hyponatremia Same dental adverse effects Ototoxicity Drug Interactions: NSAIDS decrease anti-HTN effects |
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Organic Nitrate (Nitroglycerine)
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Class: Direct acting vasodilator
MOA: @ heart – increase myocardial oxygen supply by dilating large epicardial arteries @ arteries – decrease afterload, decrease myocardial oxygen demand @ veins – greatly decreases preload, decreases myocardial oxygen demand Indications: Short-Acting For acute episodes: -Sublingual Tablet 0.4 mg -Oral Spray Long-Acting For Prophylaxis or ischemic heart disease: -Tablets -Ointment -Patch Tablets or spray - At onset of chest pain: 1 tablet (spray) under tongue Can be repeated every 5 minutes for a total of 3 tablets (spray) in 15 minutes NTG used to expire 6 months after opening. Adverse: Development of tolerance - diminished response of peripheral tissues to nitrates after long term use Headache Orthostatic hypotension, stroke, dizziness, reflex tachycardia Opiates ↑ the effects of nitric oxide |
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Amlodipine (Norvasc)
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Class: Calcium channel blocker
MOA: Act on Myocardium and vascular smooth muscle, predominately arteriolar dilators; Block voltage dependant L-type Calcium channels, different affinities for different conformation sites of the channel, differential tissue selectivity Indications: Angina, Coronary spasm, HTN Used with β blockers in HTN Adverse: Gingival hyperplasia, Interactions: Azole antifungals decrease metabolism |
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Diltiazem (Cardizem)
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Class: Calcium channel blocker
MOA: Act on Myocardium and vascular smooth muscle, predominately arteriolar dilators; Block voltage dependant L-type Calcium channels, different affinities for different conformation sites of the channel, differential tissue selectivity Indications: HTN, Atrial fibrillation, Supraventricular tachycardia Used with NTG in HTN Adverse: Gingival hyperplasia, Interactions: Azole antifungals decrease metabolism β blockers are contraindicated |
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Verapamil (Calan)
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Class: Calcium channel blocker
MOA: Act on Myocardium and vascular smooth muscle, predominately arteriolar dilators; Block voltage dependant L-type Calcium channels, different affinities for different conformation sites of the channel, differential tissue selectivity Indications: HTN, Atrial fibrillation, Supraventricular tachycardia Used with NTG in HTN Adverse: Gingival hyperplasia, Interactions: Azole antifungals decrease metabolism β blockers are contraindicated |
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Doxazosin (Cardura)
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Class: α1 antagonist
Mechanism: α1 receptor blockade smooth muscle relaxation decrease in TPR Indications: HTN Dental Adverse Effects: Dry mouth, dizziness, orthostatic hypotension |
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Clonidine (Catapres)
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Class: α2 inverse agonist
Mechanism: Inverse Agonist— -Binds to α2 medullary receptors in the brain -Inhibits sympathetic outflow to the body -Inhibition of α receptors in blood vessels Indications: HTN Dental Adverse Effects: Dry mouth, dizziness, orthostatic hypotension, abnormal taste |
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Metoprolol (Toprol)
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Class: β blockers
Mechanism: Competitive inhibitor of epinephrine and norepi at β1 Reduce blood pressure in hypertensive patients -CO decreases -HR decreases -Peripheral resistance decreases -Reduction in plasma renin activity -Decrease CNS sympathetic outflow -Alteration in baroreceptor responsiveness ↓ the force and rate of myocardial contraction ↓ O2 consumption of the heart ↓ of blood pressure in hypertensive patients Interactions: Antibiotics- Ampicillin causes ↓ levels of atenolol Allergic rxns to PCNs more severe because ↑ mediator release from mast cells Epinephrine- ↑ BP with bradycardia because of unopposed α stimulation No epi containing retraction cord NSAIDs- ↓ antihypertensive effect Limit duration to 4 days |
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Carvedilol (Coreg)
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Class: α1/β blockers
MOA: Antagonist at β1 and α1 receptors. Effects: Decrease heart rate and contractility Decrease blood pressure through alpha blockade Use: CHF (congestive heart failure) |
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Digoxin
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Positive Inotrope
Mechanism: Inhibition of the sodium-potassium ATPase ↑ in available sodium ↓ the rate of calcium-sodium exchange More calcium is available for contraction of cardiac muscle ↑ force of contraction ↓ rate of contraction Heart pumps more efficiently Interactions: Antibiotics can kill off the bacteria in the gut that would metabolize some drug before absorption Leads to Digoxin toxicity Signs of toxicity Excessive salivation Headache Fatigue and drowsiness Abdominal pain Visual disturbances Yellow or green haze around objects |
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Amiodarone
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MOA: Alteration of the lipid membrane in which channels and receptors are located
Lengthens the refractory period by inhibiting the potassium channels Blocks sodium channels Antagonizes α and β adrenergic recpetors Calcium channel blocker |
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Atorvastatin (Lipitor)
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Class: (Statin) HMG-CoA reductase inhibitor
MOA: Competitively inhibits HMG-CoA Reductase Increase Synthesis of hepatic LDL receptors Increase Hepatic uptake of LDL and ID Effect: Lowering of LDL Adverse: Rhabdomyolysis leading to kidney failure Constipation, diarrhea, stomach pain, nausea Drug Interactions: EtOH increase levels and rhabdomyolysis Erythromycin, itraconazole, ketoconazole -contraindicated with Mevacor -used with caution in others because of increase chance of rhabdomyolysis |
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Ezetimibe (Zetia)
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Class: Cholesterol absorption inhibitor
MOA: Selectively inhibits cholesterol uptake through a brush border protein PCOL Effects: ↓cholesterol absorption by 50% ↓LDL concentration in the plasma ↓cholesterol content of chylomicrons Adverse: Abdominal pain, diarrhea Contraindicated in hepatic impairment |
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Fenofibrate (TriCor)
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MOA: Binds to a DNA transcription regulator
Control the synthesis of lipoprotein metabolizing enzymes Pharmacological Effects: ↑muscle expression of lipoprotein lipase ↑uptake of TG containing lipoproteins Increased HDL Lowered TGs Fibrates displace warfarin from albumin binding sites |
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Gemfibrozil (Lopid)
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MOA: Binds to a DNA transcription regulator
Control the synthesis of lipoprotein metabolizing enzymes Pharmacological Effects: ↑muscle expression of lipoprotein lipase ↑uptake of TG containing lipoproteins Increased HDL Lowered TGs Fibrates displace warfarin from albumin binding sites |
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Niacin (Niaspan)
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Nicotinic acid (Vitamin B3)
Large doses 1500-3000 mg/day MOA: Niacin receptor on adipocytes PCOL Effects: ↑lipase activity ↓fatty acids to liver ↓VLDL production Adverse Effects: Flushing, Itching can be pre-treated with NSAIDs Gout |
