Term
| stroke incidence increases with age, especially after the age of ?, resulting in an increased stroke incidence due to aging of the population |
|
Definition
|
|
Term
| strokes can either be ? which acount for 88% of all strokes or ? which account for 12% of all stokes; ? stroke is the abrupt development of a focal neurologic deficit that occurs due to inadequate ? supply to an area of the brain; most often this is due to a ? or ? arterial occlusion leading to cerebral infarction |
|
Definition
| ishcemic; hemorrhagic; ischemic; blood; thrombotic or embolic |
|
|
Term
| a thrombotic occlusion occurs when a ? forms inside an artery in the brain; an ? refers to a clot originating either inside or outside of the cerebral vessels in which a piece of the clot breaks loose and is carried either futher through or into the cerebral vessels until it lodges causing occlusion; an outside source of emboli is often the heart causing ? stroke |
|
Definition
| thrombus; embolism; cardioembolic |
|
|
Term
| hemorrhagic stroke is a result of ? into the brain and other spaces within the CNS and includes ? hemorrhage, ? hemorrgage, and ? hematomas |
|
Definition
| bleeding; subarachnoid hemorrhage (SAH), intracerebral hemorrhage, subdural hematomas |
|
|
Term
| subarachnoid hemorrhages (SAH) results from sudden bleeding into the space between the inner layer and middle layer of the ?, most often due to trauma or rupture of a cerebral ? or arteriovenous malformation |
|
Definition
|
|
Term
| intracerebral hemorrhage (ICH) is bleeding directly into the brain ?, often as a result of chronic, uncontrolled ?; subdural hematomas result from bleeding under the dura which covers the ? and most ofen occur as a result of ? trauma |
|
Definition
| parenchyma; hypertension; brain; head |
|
|
Term
| there are two main classifications of cerebral ischmic events: ? and ? |
|
Definition
| transient ischemic attack (TIA) and cerebral infarction |
|
|
Term
| a TIA is a temporary reduction in perfusion to a focal region of the ? causing a short lived disturbance of function; TIAs have a ? onset of about ? minutes and ? duration usually lastin 2 to 14 minutes but up to 24 hours; they symptoms vary depending on the area of the ? affected, however, no deficit remains after the attack |
|
Definition
| brain; rapid; 5; short; brain |
|
|
Term
| the classic definition of TIA is based on symptom duration of less than ? hours, while symptoms lasting 24 hours or greater have been categorized as ?; improved brain imaging techniques have revealed that clinical symptoms lasting greater than ? hour but less than ? hours are often ?; for this reasion, it has been proposed that the definition of TIA be changed to include clinical symptoms lasting less than ? hour with no evidence of cerebral infarction |
|
Definition
| 24; cerebral infarction; 1; 24; cerebral infarctions; 1 |
|
|
Term
| a ? may be the only warning of an impeding stroke, with the greatest risk occrruing in the first ?; cerebral infarction is similar to a TIA however, symptoms last longer than ? hours, and in 90% of patients residual deficits remain after the event |
|
Definition
|
|
Term
| a sudden severe ?, ? and ?, and ? may be the first signs and symptoms of hemorrhagic stroke; a diagnosis of the type of stroke cannot be made solely on signs and symptoms, as overlap occurs between the types of stroke |
|
Definition
| headache ("worst headache of my life"), nausea and vomiting, and photophobia |
|
|
Term
| assessment of ? for ischemic stroke as well as for hemorrhagic stroke is an important component of the diagnosis and treatment of patients |
|
Definition
|
|
Term
| a major goal in the long term treatment of ischemic stroke involves the prevention of a ? stroke through the reduction and modification of risk factors |
|
Definition
|
|
Term
| ? is one of the major modifiable risk factors for both ischemic and hemorrhagic stroke especially ICH |
|
Definition
|
|
Term
| in ischemic stroke ther is an interruption of the blood supply to an area of the brain either due to ? formation or an ? which results in tissue hypoperfusion, tissue hypoxia, and cell death |
|
Definition
|
|
Term
| ? deposits in the vessel wall cause turbulent blood flow and lead to vessel injry exposing vessel collagen to blood and initiating the ? cascade |
|
Definition
|
|
Term
| hemorrhagic stroke is thoughr to be related to the presence of ? in the brain tissue and/or surrounding spaces resulting in ?; the ? that forms may continue to grow and enlarge after the initial bleed and early growth of the hematoma is associated with a poor outcome; this can lead to increased ? and herniation |
|
Definition
| blood; compression; hematoma; intracranial pressure |
|
|
Term
| all patients should have a brain ? scan or ? scan to differentiate an ischemic stroke from a hemorrhagic stroke, as the treatment will differ accordingly and ? therapy bust be avoided until a hemorrhagic stroke is ruled out |
|
Definition
|
|
Term
| a ? scan is the most important diagnostic test in patients with acute stroke; acute ? stroke in a medical emergency; identification of the ? and manner of stroke onset is an important determinant in treatment; the time the patient was last seen without symptoms is used as the time of stroke onset; determining the onset time can be difficult |
|
Definition
|
|
Term
| in the acute treatment of ischemic stroke, tissue ? should be maintained acutely; the oxygen saturation should be maintained at ?% or greater; electrolytes should be corrected if necessary and blood glucose should be corrected as both ? and ? may worsen brain ischemia; when hypoglycemia is present bolus with 50% ? immediately; a blood glucose that is severely elevated should be lowered to less than ? mg/dl using subcutaneous insulin |
|
Definition
| oxygenation; 92%; hypoglycemia and hyperglycemia; dextrose; 200; |
|
|
Term
| if patien is febrile, treat with ?, as fever is associated with brain ischemia and increased morbidity and mortality after stroke; also cooling devices can be used |
|
Definition
|
|
Term
| low dose ? or low dose ? administered subcutaneously will significantly decrease the risk of developing VTE post stroke |
|
Definition
|
|
Term
| in the setting of acute ischemic stroke, many patients will have an elevated ? in the first 24 to 48 hours; BP should be optimized, however hypertension should generally not be treated initially in acute ischemic stroke patients, as this may cause ? blood flow in ischemic areas, potentially increasing the infarction size; the cautious use of antihypertensive medications may be necessary in pathients who are otherwise candicates for ? therapy, including those who have severely elevated BP with a systolic greater than ? or diastolic greater than ? |
|
Definition
| blood pressure; decreased; thrombolytic; 220; 120 |
|
|
Term
| avoid using ? calcium channel blockers as these may lower BP too rapidly; BP should be check ? times with each reading taken ? minutes apart |
|
Definition
|
|
Term
| ? is an IV thrombolytic that is approved for acute stroke treatment; alteplase is the only FDA approved drug for the treatment of acute ? stroke |
|
Definition
|
|
Term
| although alteplase is an approved medication for the treatment of acute ischemic stroke, in studies the occurrence of ? was more common in the group than in placebo |
|
Definition
| ICH (intracerebral hemorrhage) |
|
|
Term
| in carefully selected patients, altepase is effective in limiting the ? size and protecting ? tissue from ischemia and cell death by restoring blood flow; treatment should preferably be givin with ? hours and not more than ? hours after symptom onset; earlier treatment is preferred due to improved outcomes |
|
Definition
|
|
Term
| a dose of aleteplase of ? mg/kg with a max dose of ? mg is recommended; the first ?% is given as an IV bolus and the remainder is infused over ? hour |
|
Definition
|
|
Term
| antiplatlet agents, anticoagulants, and invasive procedures such as insertion of a central line or placement of a nasogastric tube should be avoided for ? hours after the infusion of alteplase to prevent bleeding complications; bladder catheterization should be avoided for ? minutes postinfusion |
|
Definition
|
|
Term
| ? is measured by the elimination of existing neurologic effects and the long term improvement in neurologic status and fuctioning based on examinations and other outcome measures |
|
Definition
|
|
Term
| the major adverse effects of thrombolytic therapy such as alteplase are ?, including ? and serious systemic bleeding; mental status changes and severe headache may indicate ? |
|
Definition
| bleeding; ICH; ICH (look for bruising, black tarry stools, hematoma formation, bleeding gums, etc.)(can also see angioedema which may cause airway obsruction) |
|
|
Term
| ? and other thrombolytics, except alteplase, are not indicated for use in acute ischemic stroke due to high indidence of ? in studies conducted |
|
Definition
| streptokinase; hemmorhage |
|
|
Term
| ? thrombolytics such as r-pro UK (which is not FDA approved) is an option for treatment of acute ischemic stroke in patients who are not eligible for alteplase therapy and should be given with ? hours of onset of symptoms |
|
Definition
|
|
Term
| full dose IV ? has been commonly used in acute stroke therapy; however, no adequately designed trials have been conducted to establish is efficacy and saftey; current acute ischemic stroke guidlines do not recommend routine, urgent, full dose anticoagulation with ? or ? due to the lack of a proven benefit in improving nurologic function and the risk of intracranial bleeding; full dose ? may prevent early recurrent stroke in patients thought to be at high risk but more study is required |
|
Definition
|
|
Term
| the major complications of heparin include evolution of ? stroke into ? stroke, ?, and ? |
|
Definition
| ischemic stroke; hemorrhagic; bleeding; thrombocytopenia |
|
|
Term
| patients who received ? within 24 to 48 hours of the onset of acute stroke symptoms were less likely to suffer early recurrent stroke, death, and disability; early ? therapy with an initial dose of ? to ? mg is recommended in most patients with acute ischemic stroke with 48 hours after stroke onset; the ASA dose may then be reduced to ? to ? mg daily to reduce bleeding complications; the administration of anticoagulants and antiplatelet agents should be delayed for ? hours in those patints receiving alteplase; ? either alone or in combination with aspiring is not recommended in acute ischemic sroke |
|
Definition
| aspirin; aspirin; 150 to 325; 50 to 100; 24; clopidogrel (Plavix) |
|
|
Term
| the use of ? in patients with no history of stroke or ischemic heart disease reduced th incidence of nonfatal myocardial infartcion but not stroke; studies found that the risk of stroke, especially ? stroke, was slightly increased with aspirin use; primary prevention guidelines recommend aspirin use in older ? who are at high risk for stroke however the benefit must be weighed against the risk of major bleeding; ASA is not recommended in the primary prevention of stroke in men due to increased risk of hemorrhagic sroke |
|
Definition
| asprin; hemorrhagic; women |
|
|
Term
| ? has not previously been identified as an independent risk factor for stroke; however, recent studies have found a relationship between total cholesterol levels and stroke rate; ? therapy use may reduce the incidence of a first stroke (primary prevention) in hy risk patients including patients with ? lipid levels as well as patients with history of MI, CAD, diabetes, elevated lipid levels, and other risk factors |
|
Definition
| dyslipidemia; statin; normal |
|
|
Term
| lowering ? in patiens who are hypertensive has been shown to reduce the relative risk of both ? and ? stroke; reduction of BP is the main goal as one agent has not been clearly shwn to be more beneficial than any other for the primary prevention of stroke |
|
Definition
| blood pressure; ischemic; hemorrhagic |
|
|
Term
| the relationship between ? and both ischemic and hemorrhagic stroke is clear; patients should be assisted and encouraged in smoking cessation as the stroke risk after cessation has been shown to decline over time; effective option are available including counseling, ? replacement products, and oral agents |
|
Definition
|
|
Term
| a number of other disease states and lifestyle factors should be addressed as primary prevention of stroke; ? is an imprtant and well documented risk for stroke as well as diabetes, carotid stenosis, cardiac disease, obesity, and physical inactivity |
|
Definition
|
|
Term
| in the secondary prevention of stroke, ? has been shown to be beneficial for preventing ? stroke in patients with symptomatic carotid artery stenosis of ?% or greater and is recommended in these patients; it is also recommended in patients with stenosis of 50 to 69% and have had a recent ?; currently, recommendaions suggest considering carotid endartectomy in patients with carotid artery stenosis of ?% to ?% who are between 40 and 75 years of age if there is a ? year life expectancy and the operative risks are low |
|
Definition
| carotid endartecomy; ipsilateral; 70%; stroke; 60-99%; 5 |
|
|
Term
| ? is an option for initial therapy for secondary prevention of ischemic stroke and decreases the risk of subsequent stroke by approximately 22% in both men and women with previous TIA or stroke; the FDA has approved doses of ? to ? mg daily for secondary prevention of recurrent sroke |
|
Definition
| aspirin; 50 to 325 mg (GI intolerance, GI bleeding, and hypersensitivity reaction are the most common side effects) |
|
|
Term
| recent clinical trials have not found oral anticoagulation in those patients without ? or carotid stenosis to be better than antiplatelet therapy; in patients without atrial fibrillation, antiplatelet therapy is recommended over ?; patients with atrial fibrillation and a previous TIA or stroke have the highest risk of recurrent stroke and long term anticoagulation with ? is recommended and is effective in both the primary and secondary prevention of stroke with goal INR for this indication of ? to ? |
|
Definition
| atrial fibrillation; warfarin; warfarin; 2 to 3 |
|
|
Term
| ? is slightly more beneficial in stroke prevention than aspirin in both men and women; however it is costly and side effects include bone marrow suppression, rash, diarrhea, and an increased cholesterol level; thrombotic thrombocytopenia purpura can also occur; because of this and the requirement for frequent CBC tests ticlodipine is usually clincally avoided |
|
Definition
|
|
Term
| ? is also slightly more effective than aspirin in secondary prevention of recurrent stroke; clopidogrel has a lower incidence of diarrhea and neutropenia than ticlodipine and laboratory monitoring is not required but there is still a possibility of TTP; clopidogrel should be used as a ? for stroke prevention and is an option for initial therapy and is considered first line therapy in patients with peripheral arterial disease |
|
Definition
|
|
Term
| combination therapy of ER ? plust IR ? was more effective that either treatment alone in studies; this the only combination of antiplatlet agents that is approved |
|
Definition
| dipyridamole; ASA (Aggrenox) |
|
|
Term
| the current stroke treatment guidelines recommend ?, ?, or combination therapy with ER ? and IR ? as initial antiplatelet therapy for the secondary prevention of stroke; selection of the initial antiplatelet agen for the secondary prevention of ischemic stroke should be ?; ? and the combination of ER ? and IR ? are preferred over ? monotherapy; in one therapy fails try one of the others |
|
Definition
| aspirin, clopidogrel, dipyridamole, aspirin; individualized; clopidogrel; dipyridamole and aspirin; aspirin |
|
|
Term
| it is recommended that the combination therapy of an ? and a ? be used for the secondary prevention of recurrent stroke even in patiesn who are not hypertensive |
|
Definition
|
|
Term
| the risk of ? is directly related to increasing levels of serum cholesterol; hypercholesterolemia and other abnormalities in serum lipids play a major role in ? formation leading to coronary heart disease (CHD) as well as other froms of atherosclerosis such as carotid and peripheral artery disease. |
|
Definition
|
|
Term
| ? is an essential substance manufactured by most cells in the body; cholesterol is used to maintain cell ? integrity and for the biosynthesis of ? and ?; other major lipids in our body are ? and ? |
|
Definition
| cholesterol; wall; bile acids; steroid hormones; triglycerides; phospholipids |
|
|
Term
| since cholesterol is relatively water insoluble meaning that it cannot easily travel through the blood by itself, cholesterol along with trigylcerides and phospholipids are packaged in a larger carrier protein called a ? which are water soluble and allow for the transportation of these major lipids in the blood |
|
Definition
|
|
Term
| these lipoproteins differ in both ? and ?; the major lipoproteins in descending size and ascending density are ?, ?, ?, ? and ? |
|
Definition
| size; density; chylomicrons, VLDL, IDL, LDL, and HDL |
|
|
Term
| LDL cholesterol = ?; if serum trigylcerides are greater than ?, ? are present, or the patient has type ? hyperlipidemia, this formula becomes inaccurate and LDL cholesterol must be directly measured |
|
Definition
| total cholesterol - (HDL cholesterol + triglycerides/5); 400; chylomicrons; 3; |
|
|
Term
| each lipoprotein has various proteins called ? embedded on the surface and these serve many functions; Apos A-I and A-II are major structural proteins on the surface of ? cholesterol; Apo A-I interacts with ? and ? to traffic cholesterol from extrahepatic tissue to immature or nascent HDL |
|
Definition
| apolipoproteins; HDL; ATP binding cassette A1 and G1 |
|
|
Term
| cholesterol from the diet as well as from bile enters the small intestine, where it is emulsified by bile salts into ?; these micelles interact with the duodenal and jejunal enterocyte surfaces and cholesterol is transported into these cells by the ? transporter |
|
Definition
|
|
Term
| Some cholesterol and most plant sterols are exported back from the enterocyte into the intestinal lumen by the ? transporter; cholesterol within the enterocytes is esterfied and packaged into ? along with triglycerides, phospholipids, and Apo ? as well as Apos ? and ?, when are then released into the ? ciruclation; in the circulation, chylomicrons are converted to chylomicron remnants through the loss of ?; during this process, chylomicrons also interact with HDL particles and exchange triglyeride and cholesterol content, and HDL particles acquire Apos ? and ?; chylomicron remnant particles are then taken up by ? |
|
Definition
| ABCG5/G8; chylomicrons; B48; C and E; lymphatic; triglycerides; C; E; LRP |
|
|
Term
| LDL particles are cleared from the circulation primarily by hepatic ? receptors by interaction with Apo ?; they can also be taken up by extrahepatic tissues or enter the arterial wall, contributin to athergenesis; cholesterol is transported from the arterial wall or other extrahepatic tissues back to the liver by ? |
|
Definition
|
|
Term
| a variety of genetic mutations occur during lipoprotein synthesis and metabolism that cause lipid disorders; disorders that increase serum cholesterol are genrally those that affect the number or affinity of ? receptors and is known as ? hypercholesterolemia |
|
Definition
|
|
Term
| the most widely accepted theory of the process of atherosclerosis is that it is a low grade ? response due to injury of the vascular endothelium induced by lipoprotein retention in the arteral wall; the process begins when lipoproteins migrate between the endothelial cells into the arterial wall and bind to ?; the initial lesion, known as a ?, appears to form after accumulation of lipoproteins with the ? |
|
Definition
| antiinflammatory; proteoglycans; fatty streak; intima |
|
|
Term
| in the treatment of CHD, ? cholesterol is the primary diagnostic and therapeutic target; the NCEP ATP III guidlines have set the "optimal level" for LDL cholesterol for all adults as less than ? mg/dl; ? are considered first line agents in the treatment of CHD as well as diet, exercise, and weight control and the dose of the statin should be enough to reduce the LDL cholesterol by at leaset ? to ?% |
|
Definition
| LDL; 100; statins (HMG CoA reducase inhibitors); 30-40% |
|
|
Term
| it has also been recommended that in patients with established CHD it is reasonable to set an LDL cholesterol goal of less than ? mg/dl; if it is not possible to attain this LDL cholesterol level due to a high baseline LDL cholesterol level; it is generally possible to achieve LDL cholesterol reduction of greater than ?% with more intensive LDL lowering therapy, including ? drug therapy |
|
Definition
| 70 mg/dl; 50%; combination |
|
|
Term
| when taking a lipoprotein profile the patient needs to have fasted for ? to ? hours; the NCEP recommends that all adults greater than 20 years of age should be screened at least every ? years using a fasting blood sample to obtain a lipid profile which consists of total cholesterol, LDL cholesterol, HDL cholesterol, and trigylcerides |
|
Definition
|
|
Term
| certain drugs and diseases can cause abnormalities in serum lipids and should be evaluated; every effort should be made to correct or control underlying diseases such as ? and ?; concurrent medication known to induce lipid abnormalities ahould be evaluated for discontinuation prior to instituting long term lipid lowering therapy |
|
Definition
| hypothyroidism and diabetes |
|
|
Term
| in patients considered very high risk, an LDL cholesterol goal of less than ? mg/dl is a therapeutic option; these patients have established CGD or present with acute coronary syndromes |
|
Definition
|
|
Term
| HDL cholesterol of greater than or equal to ? mg/dl is considered a ? risk factor and means one risk factor can be subtracted from the total count |
|
Definition
|
|
Term
| individuals with ? or more risk factorsmay carry a risk equivalent to individuals who already have established CHD and therefore should be treated with the same intensity |
|
Definition
|
|
Term
| the Framingham score is based on what 5 things? this socre determines a patient's risk category and the intensity of treatment to lower their LDL cholesterol |
|
Definition
| age, total cholesterol, hdl cholesterol, smoking status, and systolic blood pressure |
|
|
Term
| ? should be the first approach tried in all patients; and adequate trial of TLC which stands for ? should be employed in all patients, but pharmacotherapy should be instituted concurrently in higher risk patients; this includes dietary restrictions of ? and ? as well as regular ? and ? reduction; patients can also use other therapeutic options to enhance LDL cholesterol lowering by consumption of ? and ?; TLC has been shown to reduce LDL by up to ? to ?% |
|
Definition
| TLC; therapeutic lifestyle changes; cholesterol; saturated fat; exercise; weight; plant sterols; dietary fiber; 2o-25% |
|
|
Term
| patients unable or unlikely to achieve their LDL cholesterol goals following a resonable trial of TLC (typically ? weeks for patients without CHD and sooner for those at high risk or have and LDL cholesterol of greater than ? mg/dl) are candidates for drug therapy; typically, ? are the medications of choice to treat high LDL cholesterol because of their ability to substantially reduce ? cholesterol, ability to reduce morbidity and mortality from atherosclerotic disease, convenient ? daily dosing, and low risk of ? |
|
Definition
| 12 weeks; 190 mg/dl; statins; LDL; once; side effects |
|
|
Term
| diagnosis of the metabolic syndrom is made when three or more of the following risk factors are present: waist circumference greater than or equal to ? inches in men (? inches in Asian males) or ? inches in women (? inches in Asian females), triglycerides greater than or equal to ? mg/dl or a drug treatment for elevated trigylcerides, HDL cholesterol less than ? mg/dL in men or ? mg/dl in women or on drug treatment for reduced HDL cholesterol, blood pressure greater than or equal to ? mm Hg or on drug treatment for hypertension, or fasting blood glucose greater than or equal to ? mg/dl on on drug treatment for elevated glucose |
|
Definition
| 40; 35; 35; 31; 150 mg/dl; 40 mg/dl; 50 mg/dl; 130/85; 100 |
|
|
Term
| patients with the metabolic syndrome are twice as likely to develop type ? diabetes and ? times more likely to develop CHD; these patients are usually ? resistant, ?, have ?, are in a ? state, and have dylipidemia characterized by low ? and elevated ?; treatment of the metabolic syndrome starts with increased ?, ? reduction (which increases ? resistance), and moderation of ? use and ? intake; these patients can also take ? to decrease their prothrombotic state |
|
Definition
| 2; 4; insulin; obese; hypertension, prothrombotic; HDL; triglycerides; physical activity; weight; alcohol; carbohydrate; aspirin |
|
|
Term
| patients with the metabolic syndrome have an additional lipid parameter that needs to be assessed called the non - HDL cholesterol which equals ?; the target for non - HDL cholesterol is less than the patients LDL cholesterol targer plus ? mg/dl; the non HDL cholesterol goal is ? mg/dl higher than the LDL cholesterol goal; their are two treatment approaches to consider for achieving the non HDL cholesterol goal: titrating existing ? lowering therapy or adding ? or a ? to the LDL lowering therapy |
|
Definition
| total cholesterol - HDL cholesterol; 30; 30; LDL; niacin; fibrate |
|
|
Term
| patients with serum triglycerides exceeding ? mg/dl are at increased risk of ? especially when triglyceride levels exceed ? mg/dl; reducing ? becomes the primary target for intervention in these patients as opposed to ? cholesterol; goal should be to reduce triglycerides to less than ? mg/dl; once the triglycerides are less than 500 mg/dl and the risk of pancreatitis is reduced, the primary focus of intervention should once again be on ? cholesterol |
|
Definition
| 500; pancreatitis; 1000; triglycerides; LDL; 150; LDL |
|
|
Term
| ?, ? and ? are the most effective agents in patients with hypertriglyceridemia |
|
Definition
| niacin, fibrates, and omega 3 fatty acids |
|
|
Term
| ? is amarker of low level inflammation and appears to help in predicting CHD risk beyond LDL cholesterol and major CHD risk factos |
|
Definition
|
|
Term
| statins are very effective ? lowering medications and are proven to reduce the risk of CHD, stroke, and death and are considered the preferred LDL lowering agent by the ATP III; statins inhibit conversion of ? to L mevalonic acid and subsequently cholesterol; statins lower LDL cholesterol levels by approximately ? to ? % |
|
Definition
|
|
Term
| a substantial reduction in LDL cholesterol occurs at the usual starting dose and each doubling of the daily dose only produces an additional ?% average reduction (known as the rule of ?); this is important when considering dose escalation versus adding on an additional LDL lower drug; statins are moderately effective at reducing ? and modestly raise ? cholesterol |
|
Definition
| 6%; rule of sixes; triglycerides; HDL cholesterol |
|
|
Term
| by inhibiting the synthesis of ? statins in turn inhibit other important by products in the cholesterol biosynthetic pathway; this may explain why the statins have what are called ? effects such as reducing lipoprotein oxidation, enhancing endothelial synthesis of nitric oxide, and inhibiting thrombosis; these pleiotropic effects are throught to contribute to the rapid/earlier benefit of statins on CHD risk while the decrease in serum lipids accounts for the slower/late benefit |
|
Definition
| L mevalonic acid; pleiotropic effects |
|
|
Term
| statins are generally well tolerated; elevations in ? function tests (LFTs) and ?, including ?, are important adverse effects associated with the statins; ? toxicity, defined as LFT elevations greater than three times the upper limit of normal is a possibility with the rate being higher at higher doese but progression all the way to liver failure is rare |
|
Definition
| liver; myopathy; rhabdomyolysis; liver |
|
|
Term
| LFTs should be obtained at baseline and ? to ? weeks after starting therapy or any dose escalation; ? monitoring of LFTs is usually sufficient; ?, defined as muscle symptoms with creatinine kinase 10 times the upper limit of normal is possible as well ? defined as muscle symptoms with marked elevation in creatinine kinase 10 times the upper lmit of normal with creatinine elevation usually associated with ? and brown urine |
|
Definition
| 6 to 12; annual; myopathy, rhabdomyolisis; myoglobinuria |
|
|
Term
| baseline ? should be obtained for all patients prior to startin statin therapy; follup up CK should only be obtained in patients complaining of ?, weakness, tenderness, or ? urine; with the exception of ? which is mainly metabolized in the gut to a relatively inactive metabolie, the other statins undergo biotransformation by CYPs; the time until maximum effect on lipids for statins is generally ? to ? weeks |
|
Definition
| CK (creatinine kinase); muscle pain; brown; pravastatin; 4 to 6 weeks |
|
|
Term
| ? is the first drug in a new class of agents referred to as cholesterol absorption inhibitors; ezetimibe blocks biliary and dietary cholesterol as well as plant sterol absorption by interactin with the ? tranporter located on enterocytes; ezetimibe inhibits ?% of all intestinal cholesterol absorption on average |
|
Definition
| ezetimibe (Zetia); NPC1L1; 54% |
|
|
Term
| by reducing the cholesterol content within chylomicrons delivered to the ?, ezetimibe reduces liver cholesterol stores, inducing an upregulation of ? receptor, resulting in a decrease in serum cholesterol; as a result, ezetimibe also induces a compensatory increase in cholesterol biosynthesis; since ? inhibit cholesterol biosynthesis, the compensatory increase in cholesterol biosynthesis by ezetemibe can be blocked by using combination therapy |
|
Definition
|
|
Term
| ezetimibe alone or in combination with a statin is contraindicated in patients with active ? disease or unexplained persistent elevations in ?; the time until maximum effect on lipids for ezetimibe is generally ? weeks |
|
Definition
|
|
Term
| ?, ?, and ? are the bile acid sequestrants available in the U.S.; these resins are highly ? molecules that bind to ? which are produced from ? in the gut; the resin-bile acid complex is then excreted in the feces; the loss of bile causes a compensatory conversion of hepatic ? into bile, reducing hepatocellular stores of cholesterol resulting in an upregulation of ? receptors to replenish hepatocellular stores which then result in a decrease in serum cholesterol |
|
Definition
| cholestyramine, colestipol, colesevelam; charged; bile acids; cholesterol; cholesterol; LDL; |
|
|
Term
| these bile acid sequestrants are moderately effective in lowering LDL cholesterol but do not lower ?; moreover, in patients with elevated triglycerides, the us of a resin may ? the condition which may be due to a compensatory increease in ? acivity resulting in increased assembly and secretion of ?; this increase in HMG CoA reductase activity can be blocked with a ? resutling in increased reduction of serum lipids |
|
Definition
| triglycerides; worsen; HMG CoA reductase; VLDL; statin |
|
|
Term
| resins are most ofetn used as adjuncts to ? in patients who need additional lowering of LDL cholesterol; because these drugs are not absorbed, adverse effects are limited to the ? including constipation, bloating, and flatulence; resins should be started at the ? dose and escalated slowly over weeks to months as tolerated until the desired response is obtained |
|
Definition
| statins; GI tract; lowest |
|
|
Term
| patients should be instructed to prepare the powder formulations in ? to ? ounces of noncarbonated fluids, usually juice or water; ? intake should be increased to minimize constipation |
|
Definition
|
|
Term
| ? is better tolerated with fewr GI side effects, although it is more expensive; all resins have the potential to prevent the absortion of other drugs such as digoxin, warfarin, thyroxine, thiazides, beta blockers, fat soluble vitamins, and folic acid; to avoid this take a resin either ? hour before or ? hours after these other agents; colesevelam does this less than the others; the time until maximum effect on lipids for resins is generally ? to ? weeks |
|
Definition
| colesevelam; 1; 4; 2 to 4 weeks |
|
|
Term
| ? (vitamin B3) has broad applications in the treatment of lipid disorders when used at higher doses than those used as a nutritional supplement; niacin inhibits fatty acid release from ? tissue and inhibits fatty acid and triglyceride production in ? cells and this results in a decrease in the number of secreted VLDL particles |
|
Definition
|
|
Term
| niacin also reduces the uptake of esters by the liver, thus improving the efficiency of reverse cholesterol tranport between ? particles and vascular tissue; niacin is indicated for patients with elevated ?, low ? cholesterol and elevated ? cholesterol |
|
Definition
| HDL; triglycerides; HDL; LDL |
|
|
Term
| niacin is available in ?, ?, and ? formulations; limitations of niacin IR and SR are ? and ? respectively; niacin ? is available by prescription and as a dietary supplement which is not regulated by the FDA and niacin ? is only available as a dietary supplement |
|
Definition
| IR, SR, ER; flushing and hepatotoxicity; IR; SR |
|
|
Term
| niacin IR is usually completely absorbed in ? to ? hours and is mainly metabolized by a ? capacity ? affinity system producing metabolites associated with flushing; niacin SR is normally absorbed over a ? hour period and is primarily metabolized by a ? capacity ? affinity system resulting in the formation of metabolites associated with hepatotoxicity |
|
Definition
| 1 to 2; high; low; 12; low; high |
|
|
Term
| niacin ? (Niaspan) was developed as a ? daily dosing formulation to be taken at ?, with the goal of reducing the incidence of ? without increasing the risk of ?; niacin ER has an absorption rate of ? to ? hours, intermediate to niacin IR and SR, and therefore balances metabolism more evenly over the high affinity/ low capacity pathway and the low affinity/ high capacity pathway |
|
Definition
| ER; once; bedtime; flushing; hepatotoxicity; 8 to 12 hours |
|
|
Term
| niacin use is limited by cutaneous reactions such as ? and ? of the face and body; the us of ? or a ? 30 minutes prior to taking niacin can help alleviate these reactions, as they are mediated by an increase in prostaglandin D2; in addition, taking niacin with ? and avoiding ? liquids at the time niacin is taken is helpful in minimizing flushing and pruritus |
|
Definition
| flushing and pruritis; aspirin; NSAIDs; food; hot |
|
|
Term
| niacin can raise ? levels, and in diabetics can rase ? levels; however, several clincal trials have shown that niacin can be used safely in patients with diabetes; niacin should be instituted at the ? dose and gradually titrated to a maxium dose of ? g daily for ER and SR products and no more than ? g daily for IR products; niacin products labeled "no flush" do no contain ? and therefore have no therapeutic role in the treatment of lipid disorders; the time until maximum effect on lipids for niacins is generally ? to ? weeks |
|
Definition
| uric acid; blood glucose; lowest; 5; 2; nicotinic acid; 3 to 5 weeks |
|
|
Term
| the predominant effects of fibrates are to decrease ? levels and increase ? cholesterol levels; in patients with high trigylcerides, ? cholesterol levels may actually increase; firbrates increase the ? and reduce the ? of LDL particles much like niacin; fibrates are the most effective ? lowering drugs and are used primarily in patients with elevated ? and low ? cholesterol |
|
Definition
| triglyceride; HDL; LDL; size; density; triglyceride; triglyceride; HDL |
|
|
Term
| fibrates work by activating ?, a nuclear receptor involved in cellular function; the fibric acid derivatives are generally well tolerated with the most common adverse effects including dyspepsia, abdominal pain, diarrhea, flatulence, rash, muscle pain, and fatigue; myopathy and rhabdomyolysis can occur, and the risk appears to increase with renal insufficiency or concurrent ? therapy; if a fibrate is used with a statin ? is the preferred agent |
|
Definition
| PPAR alpha; statin; fenofibrate |
|
|
Term
| a ? level should be checked before therapy is started and if symptoms occur with a fibrate and ? should be monitored; fibrates have caused ? and ? duct disorders such as cholelithiasis and cholecystitis and are therefore contraindicated in patients with gallbladder disease, liver dysfunction, or severe kidney dysfunction; the time until maximum effect on lipids is generally ? weeks for fenofibrate and ? to ? weeks for gemfibrozil |
|
Definition
| creatinine kinase (CK); LFTs; gallbladder; bile duct; 2 weeks; 3 to 4 weeks |
|
|
Term
| ?, the predominant fatty acids in the oil of cold water fish, lower triglycerides by as much as 35% when taken in ? amounts; fish oil supplements may be useful for patients with high triglycerides despite diet, alcohol restriction, and ? therapy; O3FAs reduce ? aggegation and have ? properties, and therefore their use has been associated with a reduction in MI and sudden cardiac death |
|
Definition
| omega 3 fatty acids; large; fibrate; platelet; antiarrythmic |
|
|
Term
| prescription O3FAs are FDA approved at a dose of ? g daily for the treatment of elevated triglycerides; O3FAs free of contaminants such as ? and organic pollutants should be encouraged when using these agents; common side effects associated with O3FAs are ? and excess ?; patients taking ? or ? agents should be monitored more closely when consuming these products because excessive amounts may lead to bleeding and may increase the risk of ? stroke |
|
Definition
| 4g; mercury; diarrhea; bleeding; antiplatelets; anticoagulants; hemorrhagic |
|
|
Term
| patiens with high triglycerides, low HDL chlesterol, and high LDL cholesterol may require ? therapy in order to normalize their lipid profile; combination durg therapy is an effective means to achieve greater reductions in LDL cholesterol (options?) as well as rasing HDL cholesterol and lowering serum triglycerides (options?) |
|
Definition
| combination; statin + ezetemibe, statin + resin, ezetemibe + resin, or a 3 drug combo; statin + niacin, statin + fibrate |
|
|
Term
| for patients who don't achieve their LDL or non - HDL cholesterol goals with statin monotherapy and lifestyle modifications including those unable to tolerate high doese due to adverse effects, ? therapy may be approriate; ? or ? combine effectively with statins to augment LDL cholesterol reduction; ? and ? are available as a combination tablet (?); the usual starting dose is ? with the maximum dose being ?; adverse events are similar to those of each product taken separately; however, the percentage of patients with ? elevations greater than three times normal is slightly higher than with a statin alone, and there appears to be a slightly higher risk of ? and ? when the two are combined; the time until maximum effect on lipids for this combination product is generally ? to ? weeks |
|
Definition
| combination; resins; ezetemibe; simvastatin and ezetemibe (Vytorin); 10/20; 10/80; LFTs; myopathy; rhabdomyolysis; 2 to 6 weeks |
|
|
Term
| a statin combined with a resin results in similar reductions in LDL cholesterol as those seen with ezetemibe; however, the magnitude of triglyceride reduction is ? with a resin compared to ezetemibe and this should be considered in patients with higher baseline triglyceride levels; ? and ? can also be combined |
|
Definition
| less; ezetemibe and a resin |
|
|
Term
| ? are the most effective triglyceride lowering agents and also raise ? cholesterol levels; ? and ? should not be used together due to increased risk of myopathy and and rhabdomyolysis; reducing LDL cholesterol while raising HDL cholesterol by using ? and ? together appears to reduce the risk of atherosclerotic disease progression to a greater degree than statin monotherapy; combination products ? and ? combine a statin and ER niacin; this combination will also aid in further lowering of ? |
|
Definition
| fibrates; HDL; statin and gebfibrozil; statin and niacin; Advicor; Simcor; triglycerides |
|
|
