Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
pharm
lipids
| Question | Answer |
|---|---|
| relationship between low density lipid levels and risk for CHD | as LDLs increase, so does the risk for CHD |
| protentially proinflammatory lipoproteins | increase plaque formation LDLs-low density (BAD kind) chylomicrons, VLDL, and catabolic remnants |
| potentially anti-inflammatory lipoproteins | cardio-protective HDLs -high density (GOOD kind) |
| exogenous pathway of cholesterol transport | Relates to lipids absorbed from dietary intake via the intestines. |
| endogenous pathway of cholesterol transport | The liver synthesizes VLDL, which is converted in the bloodstream into LDL as it loses triglycerides. |
| LDL cholesterol- optimal level | <100 |
| LDL cholesterol- near or above optimal | 100-129 |
| LDL cholesterol- borderline high level | 130-159 |
| LDL cholesterol- high level | 160-189 |
| LDL cholesterol- very high level | >190 may have other problems or family hx or genetic disease |
| optimal LDL cholesterol | 50-70 mg/dL |
| total cholesterol- desirable level | <200 |
| total cholesterol- borderline high level | 200-239 |
| total cholesterol- high level | >240 |
| HDL cholesterol- LOW | <40 (men) or < 50 (women) |
| HDL cholesterol- high level | >60 raise by exercise and diet |
| triglycerides- normal level | <150 |
| triglycerides- borderline level | 150-174 |
| triglycerides- moderate level | 175-499 |
| triglycerides- severe level | >500 |
| lipid lowering agents | HMG-CoA reductase inhibitors, fibrates, niacin, bile acid resins, selective cholesterol absorption inhibitors, omega 3 FA (fish oils), PCSK9 i, siRNAi, bempedoic acid **look at slides |
| lipid lowering agents: HMG-CoA reductase inhibitors examples | (-statin) atorvastatin fluvastatin lovastatin pravastatin rosuvastatin simvastatin pitavastatin |
| statin pharmocology | up regulation of LDL receptors by inhibition of cholesterol synthesis. liver has less cholesterol so it takes up cholesterol from blood... good |
| pleiotropic effects of statins | as plaque builds up, it can become either stable or unstable. unstable plaque is more prone to sudden rupture...potentially life threatening. statins decrease cholesterol in blood making plaques less likely to rupture |
| unstable plaque | could rupture at any time and cause MI or stroke |
| stable plaque | we can prevent from growing or becoming unstable. |
| statin pharmacokinetics | -metabolized by the liver, mostly through cytochrome P450 (CYP450) isoenzyme -potency varies -best taken in evening hours for optimal effect because pts sleeping/fasting at night is when liver is most effective at lowering cholesterol |
| high intensity statin therapy | daily dose lowers LDL by approx. 50% atorvastatin (40) -80 mg rosuvastatin 20 (40) mg |
| adverse effects of statins - liver | hepatic transaminase (AST/ALT) increase -infrequent -may start/continue w therapy if <3x normal -obtain baseline AST/ALT |
| adverse effects of statins- muscle: myalgias | symptoms with normal creatine kinase (CK) 1-10% |
| adverse effects of statins- muscle: myositis/myopathy | symptoms with evidence of muscle injury (CK> normal) - rare |
| adverse effects of statins- muscle: rhabdomyolysis | symptoms with CK> 10x normal + renal injury - rare |
| CK | creatine kinase bi product of muscle breakdown |
| statin intolerance | -adverse effect that resolve/improve w statin dose reduction/stop -min. of 2 statins should have tried. including atleast one at lowest dose -lower dose, switch statin, change regimen (QID or biweekly), +/- addition of non-statin to keep lipid goals |
| overall statin intolerance | -overall statin intolerance (5-30%), complete intolerance |
| notable statin drug-drug potential interactions | immunosuppressants (can still use but may need lower dose), HIV protease inhib., Abx, grapefruit juice |
| course of statin effects: lowered LDLs | more likely to survive long term, less likely to have future event |
| potential time course of statin effects | LDLs lowered ->endothelium function restored -> inflam. reduced -> ischemic episodes reduces -> vulnerable plaques stabilized -> cardiac events reduced (dec. risk of MI, inc. survival) |
| fibrates: examples | fenofibrate, gemfibrozil |
| fibrates | used for hypertriglyceridemia INC breakdown of VLDL in peripheral tissue DEC VLDL from liver and INC HDL potent triglyceride lowering effect |
| fibrates: adverse effects | GI: N/V, diarrhea (take w food) myopathy transaminase elevation (AST/ALT) |
| Niacin (aka nicotinic acid) | aka vitamin B3 -Rx formulations can help with HDL-raising and TRG-lowering, plus modest effect on LDL-lowering - not well tolerated (flushing, itching, GI, can worsen gycemia and uric acid levels) |
| Niacin when used: | no longer a main modality for modification of atherogenic lipoproteins may be used in some circumstances under the care of lipid specialist |
| bile acid sequestrates: examples | cholestyramine, colesevelam, colestipol |
| bile acid sequestrates | used to help w lowering of LDL, not the best -interfere w reabsorption of bile acids in GI tract leading to less cholesterol delivery to liver (inc LDL receptors) -adjunct for LDL lowering |
| bile acid sequestrates work where? | in the gut to help breakdown dietary fat into smaller peices to help absorb better |
| bile acid sequestrates toleration | -not well tolerated long-term and bind to other meds in the gut (need to stagger administration times) -don't give w other meds, wont be absorbed well |
| bile acid sequestrates adverse effects | GI: N/V, bloating, constipation (long term use) hypertriglyceridemia |
| selective cholesterol absorption inhibitors | Ezetimibe ezetimibe/ simvastatin |
| Ezetimibe works where | in the gut to prevent absorption of cholesterol in small intestin |
| Ezetimibe | -may be used as monotherapy or for synergistic effect in combination with statins to achieve LDL goal -oral, once daily -well tolerated (GI possible) -minimal drug interactions |
| omega-3 fatty acids examples | omega-3-acid ethyl esters (fish oils) icosapent ethyl non-prescription fish oil pills |
| comparison of fish oil supplements vs Rx drugs: Rx drugs | FDA approved to treat inc triglycerides, efficacy verified, consistent content, consistent purity (no additives), well tolerated |
| comparison of fish oil supplements vs Rx drugs: supplements | not FDA approved, consistent content varies, may contain saturated fats/ oxidized fatty acids/ contaminants/ additional calories, may cause burping/fishy taste/dyspepsia |
| omega-3 fatty acids | purified ethyl ester concentrate of EPA and DHA vs EPA decreases VLDL synthesis from liver potent triglyceride-lowering effect (for TRG >500) |
| omega-3 fatty acids- adverse effects | GI; belching, dyspepsia, altered taste Rash arthralgia (pain in joints) |
| PCSK9: proprotein convertase Subtilisin/Kexin type 9 | serine protease expressed in liver, kidney, intestines regulates plasma LDL levels by binding to LDL receptor targets LDL receptor for degradation |
| PCSK9 inhibitors examples | alirocumab, evolocumab used when youre not getting goal of statins or have effects with statins |
| increased PCSK9 = | increased LDL they decrease LDL receptors which will keep LDL in blood |
| PCSK9 inhibitors | -given SubQ by monthly or bi-monthly self-injection -potent LDL lowering effect -indicated for pts with familial hyopercholesterolemia or ASCVD espcially if not acheiving LDL goal despite statin |
| ASCVD | atherosclerotic cardiovascular disease |
| small interfering RNA (siRNA) examples | inclisiran |
| siRNA inclisiran- how it works | silences the production of mRNA and stopping PCSK9 from being produced in the first place one step before PCSK9 inhibitors |
| inclisiran | given SubQ every 3-6 months by clinician potent LDL lowering effect indicated for pts with familial hyopercholesterolemia or ASCVD espcially if not acheiving LDL goal despite statin |
| ACL inhibitor: adenosine triphostphate-citrate lyase examples | bempedoic acid, bempedoic acid/ ezetimibe |
| bempedoic acid- how it works | blocks the production of cholesterol, but is one step before statins works in the liver adjunct for LDL lowering oral, once daily |
| bempedoic acid adverse effects | hyperuricemia tendon rupture/injury |
| cholesterol measurement adults 20yo or older and not on lipid-lowering therapy: | -measure fasting or non-fasting lipid profile to document baseline LDL -if TRG >400 in non-fasting, repeat lipid profile in fasting state |
| heathly lifestyle | -foundation of ASCVD risk edu -reduces risk at all ages -assessment of lifetime risk in young adults (20-39 yrs) facilitates clinician-patient discussion (tells you 10 yr risk for ASCVD) -primary intervention for metabolic syndrome |
| statin use high intensity | use high intesity stain to lower LDL by >50% for these patients (secondary prevention) higher end of doses -clinical ASCVD - consider for DM (esp w many risk factors, age 50-75) -10 yr ASCVD risk >20% -LDL >190 (primary prevention) |
| primary prevention | never had an event |
| secondary prevention | preventing another event |
| statin use moderate intesity | moderate to lower LDL by >30% -40-75 yo with DM and LDL >70 -40-75 yo without DM and LDL >70, and 10 yr ASCVD risk >7.5% -pt is indicated for high intensity statin but experiences adverse effects |
| statin use for pts >75 yo with ASCVD (secondary) | moderate or high intensity statin may be used after evaluation for potential ASCVD risk reduction, adverse effects, drug interactions, patients frailty, and patient preferences |
| non-statin therapy for very high risk | goals: >50 % LDL reduction and LDL <55 high intensity statin or maximally tolerated |
| if goals unmet | consider Ezetimibe and/or PCSK9 inhibitor may consider bempedoic acid or inclisiran |
| therapies for hypertriglyceridemia | TRG >500 rule out secondary causes, optimize life, lowfat diet, no alcohol, glycemic control, increase statin intensity consider fibrates, Rx Omega-3 fatty acids to lower risk of pancreatitis |
Created by:
ago24