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133 Cards in this Set
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Antihyperlipidemic Agents: What are 4 antihyperlipidemic agents? |
* "Statins": 3-Hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors * Niacin * Cholestyramine * Gamfibrozil
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Antihyperlipidemic Agents:
What is the first line of treatment? |
* increasing exercise and decreasing saturated fat and cholesterol from the diet
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Antihyperlipidemic Agents: What is directed at lowering the level of LDL cholesterol? |
* Drug therapy of hyperlipoproteinemia |
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Antihyperlipidemic Agents: There are two types diets/drug therapy. What are they more specific for |
* Some are more specific for cholesterol and some are more specific for triglycerides |
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Antihyperlipidemic Agents: What are foam cells more prevalent in and what do they become filled with? |
* more prevalent in uncontrolled diabetes * become filled with cholesterol |
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Antihyperlipidemic Agents: What does an accumulation of esters lead to? |
* Leads to deposition of lipids in arteries |
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Antihyperlipidemic Agents: Besides cholesterol esters, what also accumulates and what does it/they do? |
* Collagen and fibrin also accumulate, occluding the vessels |
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Antihyperlipidemic Agents: What can Atherosclerosis lead to? |
* coronary artery disease, myocardial infarction, and cerebral artery disease |
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Antihyperlipidemic Agents: What leads to formation of thrombi and clinical symptoms? |
* Endothelium over the plaques activates platelets |
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Antihyperlipidemic Agents: What are cholesterol and other plasma lipids carried in the blood as? Why? |
* Carried in the blood as protein complexes * To make them more soluble in plasma |
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Antihyperlipidemic Agents: What carries the greatest concentration of cholesterol and are considered to be most dangerous? |
* Low-Density Lipoproteins (LDLs) |
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Antihyperlipidemic Agents: What carries the least cholesterol and are considered to be beneficial? |
High-Density Lipoproteins (HDLs) |
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What are often called "statins"? |
* 3-Hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors |
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3-Hydroxy-3-Methylglutaryl Coenzyme A (HMG CoA) Reductase Inhibitors: What do they do? |
They lower cholesterol by inhibiting HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis |
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3-Hydroxy-3-Methylglutaryl Coenzyme A
(HMG CoA) Reductase Inhibitors: What are the 7 adverse reactions? |
* GI complaints, myositis, skin rash, impotence, hepatotoxicity, blurred vision, and lens opacities
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3-Hydroxy-3-Methylglutaryl Coenzyme A (HMG CoA) Reductase Inhibitors: What does the adverse reaction myositis result in? |
* Myositis results in complains of muscle pain, especially in legs |
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3-Hydroxy-3-Methylglutaryl Coenzyme A (HMG CoA) Reductase Inhibitors: What drug can the side effects increase? |
* Can increase anticoagulation effect of warfarin |
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3-Hydroxy-3-Methylglutaryl Coenzyme A (HMG CoA) Reductase Inhibitors: What does this drug class end in? |
* End with the suffix vastatins - or "statins"
e.g. atorvastatin (Lipitor), fluvastatin (Lescor), lovastatin (Mevacor), pravastatin (Pravachol), and simvastatin (Zocor) |
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Inhibitors of Intestinal Absorption of Cholesterol:
What drug works by inhibiting intestinal absorption of cholesterol? |
* ezetimibe (Zetia)
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Inhibitors of Intestinal Absorption of Cholesterol: How does ezetimibe currently come? What does this do? |
* currently comes in combination with simvastatin * treats cholesterol from two different mechanisms of action |
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Inhibitors of Intestinal Absorption of Cholesterol: What do the side effects include? |
* Side effects include fatigue, abdominal pain, and diarrhea |
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What is the B3 vitamin that, in large doses, lowers cholesterol levels by inhibiting the secretion of VLDLs without accumulation of triglycerides in the liver? |
* Niacin |
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Niacin: At larger doses, what does it commonly produce? |
* commonly produces cutaneous flushing and a sensation of warmth after each dose |
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Niacin: How do you block the cutaneous flushing and sensation of warmth that niacin commonly produces? |
* by pretreatment with aspirin or ibuprofen |
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Niacin: What are four adverse reactions that have been reported? |
* Hyperuricemia, alergic reactions, cholestasis, and hepatotoxicity have been reported |
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Niacin: What may occur due to the vasodilation that niacin produces? |
* Hypotension may occur due to vasodilation |
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Bile Acid Sequestrants: How do bile acid-binding resins lower cholesterol? |
* because cholesterol is a precursor required for the synthesis of bile acids |
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Bile Acid Sequestrants: When the resins bind with the bile acids, what do they produce? |
* they produce and insoluble product lost through the GI tract |
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Bile Acid Sequestrants: When the bile acids use up cholesterol, what does it reduce? |
* reduces cholesterol levels |
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Bile Acid Sequestrants: What do the adverse reactions relate to and what do they include? |
* Relates to the GI tract and includes constipation and bloating |
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Bile Acid Sequestrants: Because of the adverse reactions, what do patients often do? |
* abandon their use |
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Bile Acid Sequestrants: What are two examples of bile acid sequestrants? |
* Cholestyramine (Questran, Prevalite) and colestipol (Colestid) |
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gemfibrozil (Lopid):
What is gemfibrozil used to treat? |
* hyperlipidemias, especially when triglycerides are elevated
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gemfibrozil ( Lopid):
What is the MOA of gemfibrozil? |
* increases lipolysis of triglycerides, decreasing lipolysis in adipose tissue and inhibiting secreation of VLDLs from the liver
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gemfibrozil ( Lopid): What can gemfibrozil promote the formation of and what two adverse reactions have been reported? |
* Can promote gallstone formation * Taste preversion and Hyperglycemia have been reported |
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Dental Implacations of Andtihyperlipidemic Agents: What are patients taking antihyperlipidemic agents at a higher risk of? |
* At a higher risk of artherosclerosis |
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Dental Implacations of Andtihyperlipidemic Agents: What emergencies are patients taking antihyperlipidemic agents at a higher risk of? Why? |
* At a higher risk of cardiovascular emergencies * Not because of the drug, but because of the condition the drug is prescribed for |
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Dental Implacations of Andtihyperlipidemic Agents: What are side effects associated with many of these drugs? |
* GI and liver abnormalities |
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Drugs that Affect Blood Coagulation: What are the two type of drugs that affect blood coagulation? |
* Anticoagulants and drugs that increase blood clotting ( coagulants) |
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Drugs that Affect Blood Coagulation: What are 8 drugs that are anticoagulants? |
* Vitamin K antagonists * Heparin / LMWH * Direct Thrombin Inhibitors * Factor Xa Inhibitors * Antiplatelet Agents * Dipyridamole * Thrombocytice * Pentoxifylline
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Hemostasis: What is hemostasis designed to prevent? |
* Designed to prevent loss of blood after injury to a blood vessel |
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Hemostasis: What form prothrombin, thrombin, fibinogen and fibrin? |
* Thromboplastin, factors V, VII, and X; and calcium ions form prothrombin, thrombin, and finally fibrogen and fibrin |
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Hemostasis: What quickly forms the blood clot? |
* Fibrin, along with vascular spasms, platelets, and red blood cells quickly forms the clot |
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Hemostasis: What happens if the vessel's interior remains smooth? |
* circulating blood does not clot |
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Hemostasis: What happens if internal injury to the vessel occurs and a roughened surface develops? |
* intravascular clotting will take place |
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Hemostasis: Where are many factors required in the clotting process synthesized? |
* Many factors required in the clotting process are synthesized in the liver |
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Hemostasis: What does the synthesis of prothrombin (II) and factors VII, IX and X require? |
* Vitamin K |
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Hemostasis: How does Warfarin produce and anticoagulant effect? |
* Warfarin antagonizes vitamin K and interferes with the synthesis of four clotting factors to produce an anticoagulant effect |
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Hemostasis: What can form in certain diseases? |
* Intravascular clots |
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Hemostasis: What is formed by clots or thrombi breaking off of the cell walls? What can this result in? |
* Clots or thrombi may break off, forming emboli Emboli can lodge in the smaller vessels of major organs such as the heart, brain or lungs |
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Hemostasis: What does anticoagulant therapy attempt to do? |
* attempts to reduce intravascular clotting |
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Hemostasis: What happens if the dose of the anticoagulant therapy is too large? |
* Hemorrhage may occure |
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Hemostasis: What happens if the dose of the anticoagulant therapy is too small? |
The danger of embolisms remains |
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Vitamin K Antagonists: What is the MOA of Vitamin K Antagonists? |
* Causes synthesis of inactive forms of factors II, VII, IX and X, protein C and S * Prevents metabolism of inactive VKOR complex back to active form |
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Vitamin K Antagonists: How is the effect of Warfarin monitored? |
* Monitored using the INR |
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Vitamin K Antagonists:
What is the target INR for most indications and what can it range from? |
* The target INR for most indicators is between 2-3 and can range from 1-4
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Vitamin K Antagonists: What is the most common adverse effects? |
* The most common adverse effects are various forms of bleeding |
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Vitamin K Antagonists: What should you look for on the hard palate? |
* Look for petechial hemorrhages on the hard palate |
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Warfarin - Drug Interactions: What should not be given to patients taking Warfarin? Why? |
* Aspirin or aspirin-containing products * Can result in bleeding episodes or fatal hemorrhages |
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Warfarin - Drug Interactions: What can potentiate the effects of Warfarin? |
Antibiotics can potentiate the effects of warfarin |
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Warfarin - Drug Interactions: How do antibiotics potentiate the effects of Warfarin? |
*Warfarin inhibits vitamin K-dependant factors (factors for clotting). Antibiotics increase the inhibition because they reduce bacteria that create V-K = decreased absorbed V-K |
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Warfarin - Drug Interactions: Does the Warfarin/antibiotic interaction affect dental prophylaxis? |
No, The interaction does not have a chance to develop when antibiotics are used before a dental procedure (prophylaxis) |
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Warfarin - Drug Interactions:
What 4 antibiotics can potentiate Warfarin the most? And which 1 interacts the least? |
* Most = metronidazole, erythromycin, azole antifungals and cephalosporins
* Least = Clindamycin |
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Warfarin - Drug Interactions: What are 4 other drugs that can increase warfarin levels? |
* High dose acetaminophen, cimetidine, disulfuram and acute alcohol ingestion |
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Warfarin - Drug Interactions: What should be done for a patient taking Warfarin concerning bleeding? |
* Consult with a physician regarding PT (prothrombin time) or INR (international normalized ratio) |
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Heparin: What is heparin? |
* One of the most commonly used anticoagulant agents for hospitalized patients |
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Heparin:
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* Administered by injection; not used orally |
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Heparin: When is heparin used? |
* Used after MI, stroke (embolism), or thrombophlebitis |
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Heparin: What is also usually started when heparin is started? |
* When heparin is started, warfarin is also begun (most times) |
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LMWH: What does LMWH stand for? |
* low molecular weight heparin |
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LMWH (low molecular weight heparin): What does the LMWH category include? |
* enoxeparin (Lovenox) and dalteparin (Fragmin) |
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LMWH (low molecular weight heparin): What settings is it used in? What is it used to treat and prevent? |
* Used in inpatient and outpatient settings for both treatment and prevention of thrombus |
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LMWH (low molecular weight heparin): How is LMWHs administered? |
Deep SQ (subcutaneous) injection |
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LMWH (low molecular weight heparin): What is its side effects? |
* Similar to heparin |
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LMWH (low molecular weight heparin): What are they often used as? |
* Often used as a bridge to Warfarin therapy (used while Warfarin builds up in the system) |
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Direct Thrombin Inhibitors: What do direct thrombin inhibitors do? |
* inhibits both free and fibrin-bound thrombin |
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Direct Thrombin Inhibitors: What does inhibiting free and fibrin-bound thrombin do? |
* Prevents thrombin mediated cleavage of fibrinogen to fibrin monomers and activation of factors V,VII, and XII |
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Direct Thrombin Inhibitors: What is the only oral form direct thrombin inhibitor? |
* dabigatran (Pradaxa) - A prodrug |
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Direct Thrombin Inhibitors: What are 3 things dabigatrion used for? |
* To treat and prevent DVT (deep vein thrombosis) and PE (pulmonary embolism) * To prevent stroke and systemic embolism in nonvalvular Afib * Off label for postoperative thromboprophylaxis
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Direct Thrombin Inhibitors: What are their adverse reaction? |
* Increased GI bleeding compared to warfarin |
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Direct Thrombin Inhibitors: What are 3 things direct thrombin inhibitors have a decreasee incidence of when compared to Warfarin in patients 65 and older? |
* Decreased incidence of clotrelated stroke, bleeding in the brain, and death |
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Direct Thrombin Inhibitors: What do the IV forms include? |
* argatroban and bivalirudin |
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Direct Thrombin Inhibitors: When is it used SubQ (desirudin) for DVT (deep vein thrombosis) prophylaxis? |
* in patients undergoing hip replacement |
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Factor Xa inhibitors: What is the MOA for Factor Xa Inhibitors? |
* MOA - Inhibits platelet activation and fibrin clot formation through direct, selective and reversible inhibition of factor XA |
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Factor Xa inhibitors: What does factor Xa Do? |
* Factor Xa converts prothrombin to thrombin |
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Factor Xa inhibitors: What does Thrombin do? |
Thrombin activates platelets and converts fibrinogen to fibrin. |
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Factor Xa inhibitors: What oral and SubQ injections does this category include? |
* Oral - Apixaban and rivaroxaban * SubQi injection - fondaparinux |
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Factor Xa inhibitors: What are they used for? |
* Uses include: -- DVT (deep vein thrombosis) prophylaxis and treatment -- PE (pulmonary embolism) treatment -- Prevention of stroke and systemic emolism in patients with nonvalvular AF (arterial fibrillation) -- Reduced risk (2 percent prevention) of DVE and/or PE |
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Antiplatelet Agents:
What are the 6 drugs/categories that antiplatelet agents includes? |
* Aspirin
* Phosphodiesterace-3 enzyme inhibitors * Thienopyridines * Cyclopentyltriazolopyrimidines * Par-1 antagonists * Other agents |
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Antiplatelet Agents - Aspirin: What is the MOA of aspirin? |
* MOA - Irreversible inhibition of thomboxane A2 which leads to platelet aggregation |
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Antiplatelet Agents - Aspirin:
What is it used for? |
* Prevention/Treatment of accute coronary syndroms (STEMI, nonSTEMI, unstable angina)
* Prevention of acute ischemic stroke and transient ischemic episodes * Adjunct therapy in revascularization procedures (CABG, PTCA (percutaneous transluminal coronary angioplasty) and carotid endarterectomy) * Stent implantation |
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Antiplatelet Agents - Aspirin: What are the Dental Implications? |
* No need to discontinue for dental surgery * Local hemostatic measures sufficient to control bleeding |
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Antiplatelet Agents - Aspirin: Why is there no need to discontinue for dental surgery? |
* No statistical differences in bleeding between patients taking 100mg aspirin daily or patients not taking aspirin for the extraction |
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Antiplatelet Agents - Phosphodiesterase-3 enzyme inhibitors: What is their MOA |
- Reversible inhibition of platelet aggregation and vasodilation |
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Antiplatelet Agents - Phosphodiesterase-3 enzyme inhibitors: What two drugs does it include? |
* cilostazol and anagrelide |
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Antiplatelet Agents - Phosphodiesterase-3 enzyme inhibitors:
What is Cilostazol used for ? |
* Used for symptomatic treatment of PVD and intermittent claudication
* unlabeled use for PCI and 2percent prevention of noncardioembolicstroke or TIA |
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Antiplatelet Agents - Phosphodiesterase-3 enzyme inhibitors: What is anagrelide used for? |
* Used for treatment of thrombocythemia (also reduces platelet production) |
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Antiplatelet Agents - Thienopyridines: What is its MOA |
* an irreversible inhibitor of adenosine diphospahte (ADP)-induced platelet aggregation |
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Antiplatelet Agents - Thienopyridines: How long are blocked platelets affected for? |
* Their lifespan (7-10 days) |
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Antiplatelet Agents - Thienopyridines: What prodrugs does it include? |
* Clopidogrel (Plavix), prasugrel (Effient) and ticlopidine (has high risk of hemotologic toxicity, reserved for those who have failed other options) |
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Antiplatelet Agents - Thienopyridines: Which patients are these indicated for?
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* Indicated for patients with recent history of MI or stroke, established peripheral arterial disease and/or coronary artery syndrome |
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Antiplatelet Agents - Thienopyridines: What do the side effects include? |
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Antiplatelet Agents - Thienopyridines: What should be avoided while taking these? |
* Avoid use of NSAIDs |
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Antiplatelet Agents - Cyclopentyltriazolopyrimidines: What is their MOA |
* Reversible and non-competative ADP inhibitor which reduces platelet aggregation |
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Antiplatelet Agents - Cyclopentyltriazolopyrimidines: What does recovery of platelet function rely on? |
* Relies on serum concentration of drug and its metabolites |
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Antiplatelet Agents - Cyclopentyltriazolopyrimidines: What drug is included in this group? |
* ticagrelor (Brilinta) |
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Antiplatelet Agents - Cyclopentyltriazolopyrimidines: What should it be used with, for what, and in who? |
* used with aspirin * for 2 percent prevention of thrombotic events * in patients with unstable angina, NSTEMI or STEMI managed with PCI and/or CABG |
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Antiplatelet Agents - PAR-1 Antagonists: What drug is a Par-1 antagonist?
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* vorapaxar (Zontivity) |
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Antiplatelet Agents - PAR-1 Antagonists: What is their MOA? |
* Reversible antagonist of PAR-1 (protease-activated receptor-1) on platelets, inhibits thrombin induced and thrombin receptor agonist peptide (TRAP) platelet aggregation |
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Antiplatelet Agents - PAR-1 Antagonists: Although it is a reversible agent, what does its half life make it effective for? |
* it has such a long half life that it is effectively irreversible in its effect on platelet agregation |
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Antiplatelet Agents - PAR-1 Antagonists: What is it used for? |
* Reduce thrombiotic CV events in patients with history of MI or PAD (peripheral arterial disease) |
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Antiplatelet Agents - Other Agents - dipyridamole: What is their MOA? |
* Inhibits activity of adenosine deaminase and phosphodiesterase leading to inhibition of platelet aggregation. May cause vasodilation and coronary vasodilation |
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Antiplatelet Agents - Other Agents - dipyridamole: What are they used for? |
* Use - to decrease thrombosis after artificial heart valve replacement * Unlabeled use - for stroke prevention in combination with aspirin |
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Thrombolytic Agents: What are their MOA |
* Causes fibrinolysis by binding to fibrin in a thrombus and converts the trap plasminogen to plasmin |
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Thrombolytic Agents: What is it used for? |
* managemend tof STEMI (causes lysis of thrombi in coronary arteries) * Acute ischemic stroke * Acute PE |
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Thrombolytic Agents: What settings is it used in? |
* Only used in acute setting, will not see outpatients on these medications |
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Thrombolytic Agents: What do drugs does this category end in? |
* Drugs in this category have a suffex of -teplase
e.g. alteplase, reteplase, and tenecteplase |
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Blood Viscosity Reducer Agent: What is their MOA? |
* Increases blood flow to affected microcirculation *Decreases blood viscosity * Increases erythrocyte flexibility and leukocyte deformability * Decreases neutrophil adhesion and activation.
* This increases the tissue oxygenation. |
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Blood Viscosity Reducer Agent: What drug is included in this category? |
* pentoxifylline (Trental) |
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Blood Viscosity Reducer Agent: What is it used for? |
* Treatment of intermittent claudication but is not a definitive therapy. -- Only improves function and symptoms |
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Blood Viscosity Reducer Agent: What special dental precautions does it require? |
* Does not require any special dental precautions |
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Drugs that Increase Blood Clotting: What are drugs that increase blood clotting called? |
* Hemostatic agents (fibrinolytic inhibitors) |
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Drugs that Increase Blood Clotting - Hemostatic Agents: What are aminocaproic acid (EACA) and tranexamic acid (Cyklokapron) similar to? What do they inhibit? |
* Similar to the amino acid lycine * Inhibit plasminogen activation |
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Drugs that Increase Blood Clotting - Hemostatic Agents: Adverse effects of aminocaproic acid (EACA) and tranexamic acid (Cyklokapron) include what? |
* Adverse effects include intravascular thrombosis, hypotension, and abdominal discomfort |
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Drugs that Increase Blood Clotting - Hemostatic Agents: What are aminocaproic acid (EACA) and tranexamic acid (Cyklokapron) used for? |
* Used in the treatment of hemorrhage after surgery |
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Drugs that Increase Blood Clotting - Hemostatic Agents: How is tranexamic acid (Cyklokapron) used? |
* Used intravenously, orally or topically |
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Drugs that Increase Blood Clotting - Hemostatic Agents:
When is tranexamic acid (Cyklokapron) in I V form used? |
* Used immediately prior to tooth extraction and 3-4 times daily for 2-8 days following extraction in hemophiliacs
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Drugs that Increase Blood Clotting - Hemostatic Agents: What is tranexamic acid (Cyklokapron) in oral form used for? |
* Used for treatment of menorrhagia |
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Drugs that Increase Blood Clotting - Hemostatic Agents: When is tranexamic acid (Cyklokapron) in topical form used? |
* **unlabeled** Used as a 4.8% solution used for 2 days after dental procedure in patients on oral anticoagulant therapy |
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Drugs that Increase Blood Clotting - Hemostatic Agents: How is tranexamic acid (Cyklokapron) in topical form administered? |
* Rinse 10mL for 2 minutes and spit QID (four times daily) for two days |
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Drugs that Increase Blood Clotting - Hemostatic Agents: How is Aminocapronic Acid (EACA) used? |
* as an oral rinse and in oral form |
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Drugs that Increase Blood Clotting - Hemostatic Agents: How is the Aminocapronic Acid (EACA) oral rinse used? |
* QID (four times daily) for 2 days post dental procedure |
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Drugs that Increase Blood Clotting - Hemostatic Agents: What is the Aminocapronic Acid (EACA) oral form used for? |
* to control oral bleeding in coagulation disorders |
