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pharm exam 2
dylipidemia
| Question | Answer |
|---|---|
| the higher the LDL, the higher the | coronary heart disease (CHD) risk |
| lipoprotein classes and inflammation | VLDL, LDL, HDL |
| VLDL | very low density lipoproteins |
| LDL | low density lipoproteins |
| HDL | high density lipoproteins - are cardio protective |
| VLDL and LDL | increase plaque formation and are potentially proinflammatory |
| cholesterol transport has two pathways | endogenous and exogenous |
| endogenous pathway | liver is responsible for clearing cholesterol from blood through the LDL receptors |
| exogenous pathway | dietary fat absorbs through gut and back to the liver |
| cholesterol transport is good for | cell membrane and hormone synthesis |
| optimal LDL cholesterol | <100 at least |
| Near or above optimal LDL cholesterol | 100-129 |
| Borderline high LDL cholesterol | 130-159 |
| High LDL cholesterol | 160-189 |
| Very high LDL cholesterol | >190 - predisposition, etc |
| ideal optimal LDL cholesterol is | 50-70 mg/dL |
| total cholesterol isn't always great because | it doesn't tell you the whole story, if its high - could be due to high LDL or HDL |
| desirable total cholesterol | <200 |
| borderline high total cholesterol | 200-239 |
| high total cholesterol | >240 |
| HDL should be | high |
| best 'tx' for low HDL | no great tx but best is exercise!!!! and diet |
| low HDL | <40 in men, <50 in women |
| high HDL | >60 |
| normal triglycerides | <150 |
| borderline triglycerides | 150-174 |
| moderate triglycerides | 175-499 |
| severe triglycerides | >500 - shifts focus to get triglycerides down because this could cause other problems like pancreatitis |
| lipid lowering agents | HMG-CoA reductase inhibitors Fibric acid derivatives (fibrates) Niacin Bile acid sequestrants/resins Selective cholesterol absorption inhibitors Omega-3 fatty acids (fish oils) PCSK9 inhibitors Small interfering RNA inhibitor Bempedoic acid |
| HMG-CoA reductase inhibitors | Atorvastatin Fluvastatin Lovastatin Pravastatin Rosuvastatin Simvastatin Pitavastatin |
| statin pharmacology | they work in the liver, inhibit the rate of cholesterol by taking up cholesterol from the blood which decreases plaque and chance of atherosclerosis |
| Pleiotropic Effects of Statins | prevent growth and unstability of plaque, stabilize plaque making it less likely to rupture - essentially 'strengthens outer cap' |
| statins are used | for the long haul and to prevent a future event |
| statin metabolization | Metabolized by liver, mostly through cytochrome P450 (CYP450) isoenzyme system |
| statin potency | Potency varies (rosuvastatin, atorvastatin most potent vs. fluvastatin, pravastatin least potent) |
| statins are best taken in | evening hours for optimal therapeutic effect because when you sleep you cholesterol increases |
| intensity of statin therapy - three levels | high, moderate, low |
| high intensity statins effectiveness | daily dose lowers LDL on average by approx >50% |
| high intensity statins examples | atorvastatin - 40-80 mg rosuvastatin - 20-40 mg |
| moderate intensity statins effectiveness | daily dose lowers LDL on average by approx 30-<50% |
| moderate intensity statins examples | atorvastatin - 10-20 mg rosuvastatin - 5-10 mg simvastatin - 20-40 mg pravastatin - 40-80 mg lovastatin - 40 mg fluvastatin XL - 80 mg fluvastatin - 40 mg BID pitavastatin - 2-4mg |
| low intensity statins effectiveness | daily dose lowers LDL on average by approx <30% |
| low intensity statins examples | simvastatin - 10 mg pravastatin - 10-20 mg lovastatin - 20 mg fluvastatin - 20-40 mg pitavastatin - 1mg |
| adverse effects of statins on the liver | Hepatic transaminase (AST/ ALT) elevations infrequent may start/ continue with therapy if < 3x normal obtain baseline AST/ ALT |
| adverse effects of statins on muscle: frequency | muscular related in about 10% of pts |
| adverse effects of statins on muscle: types | Myalgias, Myositis/Myopathy, Rhabdomyolysis |
| adverse effects of statins on muscle: Myalgias | symptoms with normal creatine kinase (CK) -kinase (CK) -1-10% 'muscle discomfort' |
| adverse effects of statins on muscle: Myositis/Myopathy | symptoms with evidence of muscle injury (CK > normal) -muscle injury (CK > normal) - rare 'muscle damage' |
| adverse effects of statins on muscle: Rhabdomyolysis | symptoms w/ CK > 10x normal + renal injury -normal + renal injury - rare 'intensive/prolonged exercise, increases CK, kidney issues' |
| statin intolerance: adverse affects | adverse effects that resolve or improve with statin dose reduction or discontinuation |
| statin intolerance: how many should be tried before stopping | A minimum of 2 statins should have been attempted, including at least one at the lowest dose |
| overall statin intolerance | (~5-30%), yet complete intolerance is < 5% and may related to nocebo effect |
| pts will benefit from statins so | do your best to figure out a regimen that works! |
| notable statin drug-drug interaction | Immunosuppressants - may just need to decrease dose or pick a different statin so just be cautious |
| potential time course of statin effects | lower within days to weeks but long term for clinical effects |
| takes days for statins to | lower LDL |
| takes years for statins to | reduce cardiac events |
| fibrates aka | triglyceride lowering |
| fibrates are used for | hypertriglyceridemia |
| fibrate examples | fenofibrate and gemfibrozil |
| fibrates increase | breakdown of VLDL in peripheral tissues |
| fibrates decrease what and increase what | decrease VLDL from liver and increase HD |
| fibrates have a potent | triglyceride lowering effect |
| fibrate adverse effects | Gastrointestinal - have them take with food to decrease n/v/d Myopathy Transaminase elevations |
| niacin aka | nicotinic acid or vitamin B3 |
| prescription formulations of niacin | can help with HDL-raising and TRG-lowering, plus modest effect on LDL-lowering |
| niacin is | not well tolerated so not really used anymore because they cause lushing, itching, liver and GI effects, can worsen glycemic and uric acid levels |
| bile acid sequestrants help with | lowering LDL, but not useful by themselves |
| bile acid sequestrants examples | cholestyramine, colesevelam, colestipol |
| bile acid sequestrants interfere with | reabsorption of bile acids in GI tract leading to less cholesterol delivery to liver (increase LDL receptors) 'work in gut to help break down dietary fat' |
| bile acid sequestrants are an adjunct for | LDL lowering - used in addition to statin |
| bile acid sequestrants are | not well tolerated long term and bind to other medications in the gut (need to stagger administration time!!!) |
| adverse effects of bile acid sequestrants | Gastrointestinal - nausea, bloating, constipation (MAJOR BARRIER TO LONG TERM) Hypertriglyceridemia |
| Selective Cholesterol Absorption Inhibitors | ezetimibe, ezetimibe/simvastatin |
| Selective Cholesterol Absorption Inhibitors are much | better tolerated |
| ezetimibe prevents | absorption of cholesterol in small intestine |
| ezetimibe may be use as | monotherapy or for synergistic effect in combination with statins to achieve LDL goal |
| how and when is ezetimibe given | oral, once daily |
| ezetimibe is | well tolerated overall (GI effects possible) and have minimal drug interactions |
| Omega-3 Fatty Acids aka | fish oils |
| Omega-3 Fatty Acids examples | Omega-3-acid ethyl esters Icosapent ethyl Non-prescription fish oil preparations |
| Omega-3-acid ethyl esters and Icosapent ethyl are | prescription |
| Omega-3 Fatty Acids are | Purified ethyl ester concentrate of EPA and DHA |
| Omega-3 Fatty Acids lower | VLDL synthesis from liver |
| Omega-3 Fatty Acids have a | Potent triglyceride-lowering effect |
| Omega-3 Fatty Acids adverse effects | GI: belching, dyspepsia, altered taste Rash Arthralgia *fairly benign SE so good for long term |
| PCSK9 | Proprotein Convertase Subtilisin/Kexin type 9 |
| PCSK9 are | injections that are serine protease expressed in the liver, kidney, and intestines |
| PCSK9 regulates | plasma LDL-C levels by binding to the LDL-receptorthe LDL-receptor |
| PCSK9 targets | LDL receptor for degredation |
| PCSK9 inhibitors | Alirocumab and Evolocumab |
| PCSK9 inhibitors are given how and when | subcutaneously by monthly or bi-monthly self-injection |
| PCSK9 inhibitors have a potent | LDL lowering effect |
| PCSK9 inhibitors are indicated for | patients with familial hypercholesterolemia or those with clinical ASCVD, hypercholesterolemia or those with clinical ASCVD, especially if not achieving LDL goal despite statin |
| Small Interfering RNA (siRNA) | Inclisiran |
| Inclisiran targets | PCSK9 |
| Inclisiran are essentially | 'reverse engineers' and are caused to produce PCSK9 copy that doesn't work |
| Inclisiran are given | subcutaneously every 3 to 6 months by a clinician |
| Inclisiran has a potent | LDL lowering effect |
| Inclisiran are indicated for patients with | patients with familial hypercholesterolemia or those with clinical ASCVD, hypercholesterolemia or those with clinical ASCVD, especially if not achieving LDL goal despite statin |
| ACL Inhibitor (Adenosine triphosphate-citrate lyase) is an | enzyme |
| ACL Inhibitor (Adenosine triphosphate-citrate lyase) examples | Bempedoic acid, Bempedoic acid/ezetimibe |
| Bempedoic acid works from | the liver, one step BEFORE statins |
| Bempedoic acid is an | adjunct for LDL lowering |
| Bempedoic acid is taken when and how | orally, once daily |
| Bempedoic acid adverse effects | Hyperuricemia - increased uric acid levels Tendon rupture/injury - because thats where the enzyme is also seen in the body |
| cholesterol management fro adults aged 20 or older and not on lipid lowering therapy | Measure fasting or non-fasting lipid profile to document baseline LDL If triglycerides > 400 mg/dL in nonfasting state, then repeat lipid profile in fasting state |
| healthy lifestyle | Foundation of ASCVD risk reduction Reduces risk at all ages Primary intervention for metabolic syndrome |
| use of high-intensity statins to lower LDL by >50% for these pts (secondary prevention) | Clinical ASCVD Consider for diabetes mellitus (DM), especially with multiple risk factors, aged 50 to 75 yrs 10-yr ASCVD risk ≥ 20% LDL ≥ 190 mg/dL (primary prevention) |
| use of moderate-intensity statins to lower LDL by <30% for these pts (primary prevention) | 40 to 75 yrs with DM and LDL ≥ 70 mg/dL 40 to 75 yrs without DM and LDL ≥ 70 mg/dL, and 10-yr ASCVD risk ≥ 7.5% based on risk discussion Patient is indicated for high-intensity statin, but experiences adverse effects |
| statin use for patients > 75 yrs of age with clinical ASCVD (secondary prevention) | Moderate or high-intensity statin may be used after evaluation for potential ASCVD risk reduction, adverse effects, drug interactions, patient frailty, and patient preferences |
| non statin therapies for very high risk: goal | ≥ 50% LDL reduction & LDL < 55 |
| non statin therapies for very high risk: if goals unmet, | Consider ezetimibe and/or PCSK9 inhibitor May consider bempedoic acid or inclisiran |
| therapies for Hypertriglyceridemia: >500 | Rule out secondary causes, optimize lifestyle, low- fat diet, alcohol abstinence, glycemic control increase statin intensity |
| best therapy for Hypertriglyceridemia: >500 | condsider fibrates, prescription omega-3 fatty acids to lower risk of pancreatitis |
Created by:
leh195