PHARM Exam 3 CH 39 Hyperlipidemia – Flashcards
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Serum lipoprotein formation
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Serum lipoproteins are formed via two pathways: dietary, or exogenous, and liver synthesis, or endogenous.
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Exogenous Pathway
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After a meal, fat and cholesterol are absorbed by the intestinal cells, esterified into TG and cholesterol, and then packaged into chylomicrons, which are transported via the lymphatic system to the thoracic duct where they enter the venous circulation. Activated endothelial lipoprotein lipase then hydrolyzes the TG into free fatty acids and glycerol, which are removed from the circulation for use by fat and muscle cells .Surface cholesterol is transferred to HDLs.
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Cholesterol function
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Makes hormones vitamin D Bile
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LDL
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Lipo-proteins that carry cholesterol LDL - Bad delivers cholesterol to cells, if too much, it can build up in artery walls forming plaques - narrowing artery - Coronary arteries is a common location for build up. The lipoproteins that contain apo B100 have been identified as the vehicles that facilitate transportof cholesterol into the arterial wall, leading to atherogenesis.LDLs, which make up 60% to 70% of the total serum cholesterol, are the major culprit in this inflammatory-mediated process. When serum LDL levels exceed a threshold of 100 mg/dL, they cross the arterial wall and become embedded in the arte-rial lumen. In the arterial lumen, LDLs undergo oxidation, aretaken up by macrophages, and form a plaque known as a fattystreak
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HDL
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HDL - Good 20% to 30% of total serum cholesterol, Helps remove excess cholesterol from cells, tissues and plaque in blood vessels. Returns excess to liver for removal of Lipo-proteins that carry cholesterol HDL suppresses the foam cell production, resulting in an anti-inflammatory response. The role of HDL may have less significance than previously believed, with the exception of when it increases after baseline values were very low, but more evidence is needed to move away from all efforts to raise serum HDL levels. Function as acceptors of free cholesterol as it passivelydiffuses from cells. This reverse transport is the mechanismby which cholesterol may be removed from atherosclerotic plaques. Apo A-I and A-IIare the major apos in HDL. The level of apos and HDLs areproposed to be inversely related to CVD risk. As serum HDLand apo levels increase, it is believed atherogenesis decreases.
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lipoproteins:
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There are four main types of lipoproteins: VLDLs, IDLs, LDLs, and HDLs.
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Atherosclerotic plaque formation (atherogenesis)
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Atherosclerotic plaques are made up of foam cells, which are transformed macrophages and smooth muscle cells filled with cholesterol. Glycation of lipoproteins in poorly controlled diabetes also contributes to foam cell generation. Arterial hypertension accelerates this process. HDL suppresses the foam cell production, resulting in an anti-inflammatory response. The second step of atherogenesis involves the formation of scar tissue over the fatty plaque in the arterial wall. This formation is called a fibrous plaque. Over time, fibrous plaques become unstable and are prone to rupture, causing potentially life-threatening luminal thromboses.
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Drugs that may raise HDL levels include:
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nicotinic acid (niacin), fibrates, and statins.
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Factors that cause low HDLs
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Cigarette smoking Drugs: beta blockers, anabolic steroids, progestational agents Elevated serum triglycerides Genetic factors (approximately 50% of cases) Overweight and obesity (probably most important) Physical inactivity Type 2 diabetes mellitus Very high carbohydrate intake (>60% of total energy intake)
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VLDLs
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are triglyceride-rich lipoproteins that contain 10%to 15% of the total serum cholesterol. The major apos ofVLDL are apo B100; apo C I, II, and III; and apo E. VLDLs are produced by the liver and are precursors of LDL. Someforms of VLDL, particularly VLDL remnants, appear to pro-mote atherosclerosis similarly to LDL. VLDL + LDL choles-terol is called non-HDL cholesterol.
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The overall goal of treating hyperlipidemia is: 1. Maintain an LDL level of less than 160 mg/dL 2. To reduce atherogenesis 3. Lowering apo B, one of the apoliproteins 4. All of the above
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2. To reduce atherogenesis
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When considering which cholesterol-lowering drug to prescribe, which factor determines the type and intensity of treatment? 1. Total LDL 2. Fasting HDL 3. Coronary artery disease risk level 4. Fasting total cholesterol
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3. Coronary artery disease risk level
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First-line therapy for hyperlipidemia is: 1. Statins 2. Niacin 3. Lifestyle changes 4. Bile acid-binding resins
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3. Lifestyle changes
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James is a 45-year-old patient with an LDL level of 120 and normal triglycerides. Appropriate first-line therapy for James may include diet counseling, increased physical activity, and: 1. A statin 2. Niacin 3. Sterols 4. A fibric acid derivative
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3. Sterols
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Joanne is a 60-year-old patient with an LDL of 132 and a family history of coronary artery disease. She has already tried diet changes (increased fiber and plant sterols) to lower her LDL and after 6 months her LDL is slightly higher. The next step in her treatment would be: 1. A statin 2. Niacin 3. Sterols 4. A fibric acid derivative
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1. A statin
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Sharlene is a 65-year-old patient who has been on a lipid-lowering diet and using plant sterol margarine daily for the past 3 months. Her LDL is 135 mg/dL. An appropriate treatment for her would be: 1. A statin 2. Niacin 3. A fibric acid derivative 4. Determined by her risk factors
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4. Determined by her risk factors
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Phil is a 54-year-old male with multiple risk factors who has been on a high-dose statin for 3 months to treat his high LDL level. His LDL is 135 mg/dL and his triglycerides are elevated. A reasonable change in therapy would be to: 1. Discontinue the statin and change to a fibric acid derivative. 2. Discontinue the statin and change to ezetimibe. 3. Continue the statin and add in ezetimibe. 4. Refer him to a specialist in managing patients with recalcitrant hyperlipidemia.
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3. Continue the statin and add in ezetimibe.
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Jamie is a 34-year-old pregnant woman with familial hyperlipidemia and elevated LDL levels. What is the appropriate treatment for a pregnant woman? 1. A statin 2. Niacin 3. Fibric acid derivative 4. Bile acid-binding resins
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4. Bile acid-binding resins
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Han is a 48-year-old diabetic with hyperlipidemia and high triglycerides. His LDL is 112 mg/dL and he has not tolerated statins. He warrants a trial of a: 1. Sterol 2. Niacin 3. Fibric acid derivative 4. Bile acid-binding resin
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3. Fibric acid derivative
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Jose is a 12-year-old overweight child with a total cholesterol of 180 mg/dL and LDL of 125 mg/dL. Along with diet education and recommending increased physical activity, a treatment plan for Jose would include ____________ with a reevaluation in 6 months. 1. Statins 2. Niacin 3. Sterols 4. Bile acid-binding resins
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3. Sterols
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Monitoring of a patient who is on a lipid-lowering drug includes: 1. Fasting total cholesterol every 6 months 2. Lipid profile with attention to serum LDL 6 to 8 weeks after starting therapy, then again in 6 weeks 3. Complete blood count, C-reactive protein, and erythrocyte sedimentation rate after 6 weeks of therapy 4. All of the above
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2. Lipid profile with attention to serum LDL 6 to 8 weeks after starting therapy, then again in 6 weeks
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Before starting therapy with a statin, the following baseline laboratory values should be evaluated: 1. Complete blood count 2. Liver function (ALT/AST) and creatine kinase 3. C-reactive protein 4. All of the above
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2. Liver function (ALT/AST) and creatine kinase
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When starting a patient on a statin, education would include: 1. If they stop the medication their lipid levels will return to pretreatment levels. 2. Medication is a supplement to diet therapy and exercise. 3. If they have any muscle aches or pain, they should contact their provider. 4. All of the above
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4. All of the above 1. If they stop the medication their lipid levels will return to pretreatment levels. 2. Medication is a supplement to diet therapy and exercise. 3. If they have any muscle aches or pain, they should contact their provider.
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Omega 3 fatty acids are best used to help treat: 1. High HDL 2. Low LDL 3. High triglycerides 4. Any high lipid value
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3. High triglycerides
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When are statins traditionally ordered to be taken? 1. At bedtime 2. At noon 3. At breakfast 4. With the evening meal
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4. With the evening meal
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Which the following persons should not have a statin medication ordered? 1. Someone with 3 first- or second-degree family members with history of muscle issues when started on statins 2. Someone with high lipids, but low BMI 3. Premenopausal woman with recent history of hysterectomy 4. Prediabetic male with known metabolic syndrome
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1. Someone with 3 first- or second-degree family members with history of muscle
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Fiber supplements are great options for elderly patients who have the concurrent problem of: 1. End-stage renal failure on fluid restriction 2. Recurrent episodes of diarrhea several times a day 3. Long-term issues of constipation 4. Needing to take multiple medications around the clock every 2 hours
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3. Long-term issues of constipation
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What is considered the order of statin strength from lowest effect to highest? 1. Lovastatin, Simvastatin, Rosuvastatin 2. Rosuvastatin, Lovastatin, Atorvastatin 3. Atorvastatin, Rosuvastatin, Simvastatin 4. Simvastatin, Atorvastatin, Lovastatin
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1. Lovastatin, Simvastatin, Rosuvastatin
