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By Q. Brenton. The College of New Jersey.

Antiplatelet Drugs These agents decrease platelet aggregation and thereby decrease the risk for thrombus formation in coronary arteries buy generic super viagra 160mg online. In patients with stable angina discount super viagra 160mg fast delivery, low-dose aspirin produces a 33% decrease in the risk for adverse cardiovascular events generic super viagra 160mg free shipping. Benefits of clopidogrel seem equal to those of aspirin, although they are not as well documented. The guidelines recommend that all patients with stable angina take 75 to 162 mg of aspirin daily, unless there is a specific reason not to. Cholesterol-Lowering Drugs Elevated cholesterol is a major risk factor for coronary atherosclerosis. Therapies that reduce cholesterol are associated with decreased mortality from coronary heart disease. Because of the well-established benefits of cholesterol- lowering therapy, the guidelines recommend that all patients with stable angina receive a cholesterol-lowering drug. Among one subset of patients—those with diabetes—benefits were particularly striking. In addition, ramipril reduced the risk for nephropathy, retinopathy, and other microvascular complications of diabetes. Antianginal Agents: Drugs Used to Reduce Anginal Pain The goal of antianginal therapy is to achieve complete (or nearly complete) elimination of anginal pain, along with a return to normal activities. Some patients can be treated with a single long-acting drug, some require two or three, and some require revascularization. In addition to providing prophylaxis, beta blockers suppress nitrate-induced reflex tachycardia. Note that, as we proceed along the drug-selection flow plan, drugs are added to the regimen, resulting in treatment with two or more agents. Note that these invasive procedures should be considered only after more conservative treatment has been tried. However, when selecting among these drugs, we must consider the coexisting disorder as well as the angina. Reduction of Risk Factors The treatment program should reduce anginal risk factors: smokers should quit; sedentary patients should get aerobic exercise; and patients with diabetes, hypertension, or high cholesterol should receive appropriate therapy. High Cholesterol As noted, high cholesterol levels increase the risk of adverse cardiovascular events, and therapies that reduce cholesterol reduce that risk. Accordingly, all patients with high cholesterol levels should receive cholesterol-lowering therapy. Hypertension High blood pressure increases the risk for cardiovascular mortality, and lowering blood pressure reduces the risk. Diabetes Both type 1 (insulin-dependent) and type 2 (non–insulin-dependent) diabetes increase the risk for cardiovascular mortality. Although there is good evidence that tight glycemic control decreases the risk for microvascular complications of diabetes, there is little evidence to show that tight glycemic control decreases the risk for cardiovascular complications. In patients with chronic stable angina, exercise increases exercise tolerance and the sense of well-being and decreases anginal symptoms, cholesterol levels, and objective measures of ischemia. Accordingly, the guidelines recommend that patients perform 30 to 60 minutes of a moderate-intensity activity 3 to 4 times a week. Management of Variant Angina Treatment of vasospastic angina can proceed in three steps. For initial therapy, either a calcium channel blocker or a long-acting nitrate is selected. These drugs act in several ways: some suppress coagulation, some inhibit platelet aggregation, and some promote clot degradation. Coagulation: Physiology and Pathophysiology Hemostasis Hemostasis is the physiologic process by which bleeding is stopped. Hemostasis occurs in two stages: (1) formation of a platelet plug, followed by (2) reinforcement of the platelet plug with fibrin. Stage One: Formation of a Platelet Plug Platelet aggregation is initiated when platelets come in contact with collagen on the exposed surface of a damaged blood vessel. In response to contact with collagen, platelets adhere to the site of vessel injury. Adhesion initiates platelet activation, which in turn leads to massive platelet aggregation. This plug is unstable, however, and must be reinforced with fibrin if protection is to last. After aggregation occurs, the platelet plug is reinforced with fibrin (not shown). The two pathways converge at factor Xa, after which they employ the same final series of reactions. In both pathways, each reaction in the sequence amplifies the reaction that follows. Hence, after this sequence is initiated, it becomes self- sustaining and self-reinforcing. The tissue factor pathway is turned on by trauma to the vascular wall, which 1 triggers release of tissue factor, also known as tissue thromboplastin. Second, it catalyzes the conversion of factor V into its active form (Va), a compound that greatly increases the activity of factor Xa, even though it has no direct catalytic activity of its own. The contact activation pathway is turned on when blood makes contact with collagen that has been exposed as a result of trauma to a blood vessel wall. After this, the contact activation pathway is the same as the tissue factor pathway. The significance of the vitamin K–dependent factors will become apparent when we discuss warfarin, an oral anticoagulant. Keeping Hemostasis Under Control To protect against widespread coagulation, the body must inactivate any clotting factors that stray from the site of vessel injury. Inactivation is accomplished with antithrombin, a protein that forms a complex with clotting factors and thereby inhibits their activity. The clotting factors that can be neutralized by antithrombin appear in yellow in Fig. As we shall see, antithrombin is intimately involved in the action of heparin, an injectable anticoagulant drug. Physiologic Removal of Clots As healing of an injured vessel proceeds, removal of the clot is eventually necessary. The body accomplishes this with plasmin, an enzyme that degrades the fibrin meshwork of the clot. Thrombosis A thrombus is a blood clot formed within a blood vessel or within the heart. Thrombosis (thrombus formation) reflects pathologic functioning of hemostatic mechanisms. Arterial Thrombosis Formation of an arterial thrombus begins with adhesion of platelets to the arterial wall. As blood flow comes to a stop, the coagulation cascade is initiated, causing the original plug to undergo reinforcement with fibrin.

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Diethylcarbamazine Target Organisms Diethylcarbamazine [Hetrazan] is the drug of choice for filarial infestations order 160mg super viagra with mastercard. First generic 160 mg super viagra overnight delivery, it reduces muscular activity discount super viagra 160 mg overnight delivery, causing parasites to be dislodged from their site of attachment. Second, by altering the surface properties of the parasites, it renders the organisms more vulnerable to attack by host defenses. Pharmacokinetics Diethylcarbamazine is readily absorbed and undergoes rapid and extensive metabolism. Adverse Effects Adverse effects caused directly by diethylcarbamazine are minor (headache, weakness, dizziness, nausea, vomiting). Indirect effects, occurring secondary to death of the parasites, can be more serious. These include rashes, intense itching, encephalitis, fever, tachycardia, lymphadenitis, leukocytosis, and proteinuria. Fortunately, these reactions are transient, lasting just a few days—and can be minimized by pretreatment with glucocorticoids. Ivermectin Target Organisms Ivermectin [Stromectol] is active against many nematodes. Currently, the drug has two approved indications: onchocerciasis (a major cause of blindness worldwide) and intestinal strongyloidiasis. Ivermectin can also be used to kill mites and lice, although these parasites are not approved targets. In addition to its use in humans, ivermectin is used widely in veterinary medicine. Mechanism of Action Ivermectin disrupts nerve traffic and muscle function in target parasites. By opening chloride channels on the cell surface, which allows chloride ions to rush into nerve and muscle cells. The resultant hyperpolarization of these cells causes paralysis followed by death. Host cells are not affected because ivermectin is selective for chloride channels in parasites. Pharmacokinetics Ivermectin is administered orally and achieves peak plasma levels in 4 hours. Adverse Effect: Mazotti Reaction The Mazotti reaction occurs in patients treated for onchocerciasis. Principal symptoms are pruritus, rash, fever, lymph node tenderness, and bone and joint pain. The apparent cause is an allergic and inflammatory response to the death of microfilariae. Although the nonspecialist provider does not typically have an active role in deciding how to treat cancer, as part of the interdisciplinary team caring for the patient, it remains essential to provide preventive care and to promote optimal well-being for those patients who receive treatment. Hence it is important to have a basic understanding of cancer, drugs used to treat cancer, and the effects that anticancer drugs have on patients. In the discussion that follows, we consider properties shared by neoplastic cells as a group. However, although the discussion addresses cancers in general, be aware that the term cancer refers to a large group of disorders and not to a single disease: there are more than 100 different types of cancer, most of which have multiple subtypes. These various forms of cancer differ in clinical presentation, aggressiveness, drug sensitivity, and prognosis. Because of this diversity, treatment is individualized, based on the specific biology of the cells involved. Characteristics of Neoplastic Cells Persistent Proliferation Unlike normal cells, whose proliferation is carefully controlled, cancer cells undergo unrestrained growth and division. This capacity for persistent proliferation is the most distinguishing property of malignant cells. In the absence of intervention, cancerous tissues will continue to grow until they cause death. It was once believed that cancer cells divided more rapidly than normal cells and that this excessive rate of division was responsible for the abnormal growth patterns of cancerous tissues. The correct explanation for the relentless growth of tumors is that malignant cells are unresponsive to the feedback mechanisms that regulate cellular proliferation in healthy tissue. As a result, cancer cells are able to continue multiplying under conditions that would suppress further growth and division of normal cells. In other words, instead of dividing more rapidly, they divide more frequently than normal cells. Invasive Growth In the absence of malignancy, the various types of cells that compose a tissue remain segregated from one another; cells of one type do not invade territory that belongs to cells of a different type. In contrast, malignant cells are free of the constraints that inhibit invasive growth. As a result, cells of a solid tumor can penetrate adjacent tissues, thereby allowing the cancer to spread. Formation of Metastases Metastases are secondary tumors that appear at sites distant from the primary tumor. Metastases result from the unique ability of malignant cells to break away from their site of origin, migrate to other parts of the body (through the lymphatic and circulatory systems), and then reimplant to form a new tumor. Immortality Unlike normal cells, which are programmed to differentiate and eventually die, cancer cells can undergo endless divisions. The underlying cause for this difference is telomerase, an enzyme that is active in most cancers, and expressed only rarely in normal cells. As normal cells divide and differentiate, their telomeres become progressively shorter. When telomeres have lost a critical portion of their length, the cell is unable to keep on dividing. In cancer cells, telomerase continually adds back lost pieces of the telomere, and thereby preserves or extends telomere length. Specifically, malignant transformation results from a combination of activating oncogenes (cancer-causing genes) and inactivating tumor suppressor genes (genes that prevent replication of cells that have become cancerous). These genetic alterations are caused by chemical carcinogens, viruses, and radiation (x- rays, ultraviolet light, radioisotopes). Malignant transformation occurs in three major stages, called initiation, promotion, and progression. This accumulated genetic damage leads to dysregulation of cell division and protection against cell death. It is important to appreciate that the changes in cellular function caused by malignant transformation are primarily quantitative rather than qualitative. That is, malignant transformation simply results in the overexpression or underexpression of the same gene products made by normal cells. As a result, cancer cells employ the same metabolic machinery as normal cells, use the same signaling pathways as normal cells, and express the same surface antigens as normal cells. Nonetheless, even though these changes in cellular function are only quantitative, they are still sufficient to allow unrestrained growth and avoidance of cell death.

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Also buy discount super viagra 160 mg online, the prescription can be ready for the patient when the patient leaves the facility—the patient does not need to drop off the paper script and then wait for a medication fill 160mg super viagra free shipping. Limitations to e-prescribing include scheduled medications generic 160 mg super viagra overnight delivery, which still require a prescription on tamper-resistant paper. Questions you should ask yourself include the following: • Is this a newer medication for this patient? If the answer to any of these questions is “yes,” consider a shorter time between refills (1 to 3 months). These are not eligible for refills and must have a new prescription each renewal period. When changing or adding to current medication regimens, it is prudent to follow up with the patient by phone or in person to assess changes. This time can be used to discuss new or increased side effects, check vital signs, obtain laboratory work, or make further adjustments. When a medication, such as warfarin, requires frequent monitoring with drug levels, an even shorter refill allotment is reasonable. If the patient has been maintained on the current dose of a medication for some time and remains stable, it is likely acceptable to continue to refill that medication for a longer time period (e. Assistance Applications for Tablets and Phones This textbook will be paramount in your learning, but it may not be convenient to carry around in the clinical setting. Although we encourage you to use this text to the fullest extent, there are many new applications and websites available to assist providers with safe prescribing (see Table 2. It must be noted, however, that all these tools still require common sense and good judgment on the part of the prescriber. As stated previously, one must take into account the individual patient as well as multiple other factors, including cost, side effects, and medication formularies. An application can assist you with the basic suggestions in dosing and duration, but ultimately there is no substitute for sound practice. Collaboration As reflected in this chapter, writing a prescription safely can be complicated. It is strongly encouraged that you use all available resources, including your colleagues. Developing a relationship with your pharmacist can be one of the most helpful and fruitful relationships you cultivate. Because this is their specialty, pharmacists will likely have additional information on formulary and drug interactions as well as suggestions for adequate medication dosing. In some practices, pharmacists are responsible for medication initiation and titration based on standardized protocols. Choosing an appropriate antimicrobial agent for a specific infectious process is often difficult for a new practitioner. This not only provides an opportunity to explain the importance of the medication but also allows the provider to dispel rumors about medications that often lead to therapy failures. Moreover, education reduces medication errors by empowering patients with accurate information and clear guidelines. Medication Education Components There are basic components that should be included when teaching about any new medication. These are (1) medication name, (2) purpose, (3) dosing regimen, (4) administration, (5) adverse effects, (6) any special storage needs, (7) associated laboratory testing, (8) food or drug interactions, and (9) duration of therapy. Unfortunately, when taking a medication history, we still have patients who refer to medications by their understood purpose (e. This creates a challenge for the provider who needs to select appropriate therapy. Both the generic name and the brand (trade) name should be given, or at least included in written handouts. Knowing both empowers the patient to catch medication errors in the event that two different providers prescribe the same generic drug under different brand names. Purpose Patients are more likely to participate in activities when they know those activities produce positive outcomes. Knowing the reason the medication is prescribed propels the patient to follow through with the medication plan because the patient is aware that this action helps to achieve the therapeutic goal. Dosing The dosing regimen needs to be reviewed with the patient even though it is written on the prescription label. Doing this ensures that the patient understands how to take the medication and provides an opportunity for the patient to ask questions. For example, “four times a day” may be interpreted in various ways by different people. Can the medication be taken every 4 hours for four doses, or does it need to be spaced out evenly to every 6 hours? Does “once a day” mean that it can be taken at any time, or it is better to take the medication in the morning or evening hours? This is also a good time to explain why drugs should be taken exactly as prescribed. Administration A common patient concern is whether medication should be taken with or without food. Patients also need to be informed of common administration needs that many of us take for granted. For example, suspensions should be shaken (or rolled, if shaking causes foaming) to equally disperse ingredients before administration. Patients need to see how these are administered and should be able to repeat a demonstration before leaving with a prescription. Although that concern is understandable, and the consequences may well be true, patients have a right to know of potential harms that may result from therapy. Therefore providers are ethically obligated to divulge adverse effects and other risks. That said, often the approach used in discussing these can make a difference in how patients view them. You probably know patients who worry about taking drugs when the product labeling (i. Patients may not know that, for most drugs, most adverse effects occur in less than 1% to 2% of those taking the drug. Most patients are unaware that the long list of adverse effects represents all effects reported during clinical trials, regardless of whether a direct association to the drug is known. When discussing adverse effects, focus on the adverse effects that are common and avoid undue attention on rare and unanticipated effects. If complex effects such as liver injury or pancytopenia may occur, teach patients the signs and symptoms to report. Let patients know that many adverse effects – most commonly nausea and sedation – are usually temporary and go away with continued medication use. Patients are often willing to endure short term adverse effects for long term health improvement.

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