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____ has the highest concentration of cholesterol esters
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___ has the highest concentration of triacyglycerol
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DAST 3 EXAM 1
| Question | Answer |
|---|---|
| ____ has the highest concentration of cholesterol esters | LDL |
| ___ has the highest concentration of triacyglycerol | Chylomicron |
| ___ has the lowest concentration of triacyglycerol | HDL |
| ____ has the highest concentration of free cholesterol | LDL |
| ____ is the largest in size of the lipoproteins | chylomicron |
| _____ is the smallest of the lipoproteins | HDL |
| ____ has the largest density of the lipoproteins | HDL |
| ____ has the smallest density of the lipoprotein | chylomicron |
| chylomicrons have ___ levels of fatty acids and ___ levels of cholesterol | high, low |
| biosynthesis of cholesterol begins with ______ which comes from _____ | acetyl CoA , carbohydrate metabolism |
| lipids are made up of ____ and ____ | fatty acid esters and glycerol |
| ____ hydrolzes fats into smaller fatty acids which are slubilized by ____ | lipase, chylomicrons |
| cholesterol is needed for the synthesis of: | 1. homone synthesis 2. cell membrane synthesis 3. synthesis of bile 4. Vitamins D synthesis |
| cholesterol is synthesized from _____ | acetyl CoA |
| What does hMG stand for? | 3-hydroxy-3-methylglutaryl |
| cholesterol is oxidatively cleaved by the enzyme ____ to form pregnenolone (which is the precursor of all other endogenous steroids) | desmolase (cleaves the side chain) |
| the initial rate limiting step in the formation of bile salts from cholesterol is by the enzyme _____ and is the key control enzyme for this pathway | 7-alpha-hydroxylase |
| bile salts are reabsorbed and returned to the liver where they have negative feedback on _____ that redulates any subsequent conversion of cholesterol | 7-alpha-hydroxyase |
| Triglycerides are formed from ___ and ___ | glycerol 3 posphate and acylated CoA |
| the main effetc of ___ is to stimulate lipoprotein lipase and increase clearance of triglycerides | fibrates |
| ____ decreases VLDL formation and therefore decreases plasma levels of triglycerides and cholesterol | Niacin |
| _____ lower plasma LDL levels by indirectly increasing the rate at which LDL is cleared from the bloodstream. | Bile acid sequestrants (cholestyramine, colestipol and colesevelam) |
| MOA for bile salt seqestrants | bind to bile acid (glcocholic acid or taurocholic acid) --> increase fecal excretion--> removes feedback inhibition of 7-alpha hydroxylase and increases the hepatic conversion of cholesterol to bile acids |
| all ____ are large, hydroscopic, water insoluble resins | bile acid sequestrants |
| normal pKa for amines in bile acid sequestrants is ____ and thus all should be ionized at intestinal pH | 9-10.5 |
| _____ lowers plasma cholesterol levels by inhibiting the absorption of cholesterol at the brush border of the small intestine, specifically by binding to a transport protein in the wall causing reduction in transport and absorption | Ezetimibe (Zetia) , a cholesterol absorption inhibitor |
| ____ decrease plasma VLDL by stimulating lipoprotein lipase (the enzyme that removes triglycerides from VLDL) thus significantly lower triglyceride levels also | Fibrates |
| ___ inhibits lipolysis of adipose tissues, lowering cholesterol and tyiglyceride levels | Nicotinic Acid |
| removing a double bond in one of the bicylic rings of HMG COA RI (Ring A) will ____ activity of the drug | decrease |
| If the ester is change to n ether on the bicyclic (ring A ) of HMG CoA RI threre is a ____ in the drugs activity | decrease |
| adding a methyl group to the bicylic ring of HMG CoA RI will ___ the drugs activity | increase |
| the Fluorine cannot be ___ with the central ring on the ring B HMG CoA RI structure because it will reduce activity | coplanar |
| the absolute stereochemistry of the 3 and 5 hydroxy groups of HMG CoA RI must be the same as that found in: | mevastatin and lovastatin |
| altering the 2 carbon distance between C6 and C7 and the bottom ring system of HMG CoA RI will ____ activity | dimish or fail to improve |
| ____ are lipid protein particles that carry exogenous lipids | chylomicrons |
| ___ are lipid protein particles that carry endogenous lipids | VLDL |
| ____ breaks triglycerides from VLDL particles to release faty acids to tissues or for storage | lipoprotein lipase |
| one or more abnormalities of blood lipids | dyslipidemia |
| what are 4 characteristics of cholesterol? | 1. naturally occuring sterol 2. bile salts precursor 3. synthesis of steroid hormones 4. cell membrane formation |
| ___ are the energy store in adipose tissue | triglycerides |
| triglyerides are synthesized from ___ and ___ | fatty acids and glycerol |
| ___ are formed from fatty acids and phosphate group, nitrogen containing alcohol and glyceryl backbone | phospholipids |
| chylomicrons are rich in ____ | triglycerides |
| ___ removes triglycerides from chylomicrons | lipoprotein lipase |
| __ are the largest, least dense lipoproteins that carry mostly triglyceride | chylomicrons |
| ___ contain 15-20% of total blood cholesterol and most of the total blood triglycerides | VLDL |
| the cholesterol concentration in VLDL particles is ___ that of their triglyceride content | 1/5 |
| Do VLDL play a large or small role in the pathogenesis of atherosclerosis? | small |
| VLDL remnants are formed from the action of _____ and are more ___ rich | lipoprotein lipase, cholesterol |
| what hapens to the VLDL remnants after they are formed by lipoprotein lipase? | half are removed from circulation by LDL receptors on the liver surface and half is converted to LDL particles |
| VLDL transport most of ____ | triglycerides |
| ____ carries 60-70% (most) of the total blood cholesterol and is the main contributor in pathogenesis of atherosclerosis | LDL |
| What happens to LDL particles after they are formed? | half are removed from circulation by the liver and the other half are taken up by peripheral cells or deposited in the intimal spaces of arteries (atherosclerosis) |
| ____on LDL surface binds to ____ on the liver cells in order for uptake and clearing of excess blood lipids to occur. | Apo-B 100, LDL receptor |
| how is cholesterol delivered to the liver from HDL? | either by direct delivery to the liver by HDL receptor or indirectly to circulating VLDL remnant and LDL particles through choleserol ster transfer protein |
| ___ have the highest triglyceride levels | chylomicrons (VLDL is also high) |
| ___ has the highest cholesterol levels | LDL |
| ____ transports cholesterol from cells TO the liver | HDL |
| desirable value for total cholesterol | less than 200 mg/dL |
| borderline-high value for total cholesterol | 200-239 mg/dL |
| high value for total cholesterol | greater than or equal to 240 mg/dL |
| desirable value for LDL cholesterol | less than 100 mg/dL is optimal, 100-129 mg/dL is near or above optimal |
| boderline-high value for LDL | 130-159 mg/dL |
| high value for LDL | greater than 160 mg/dL |
| desirable value for HDL | greater than 40 mg/dL |
| high value for HDL | greater than or equal to 60 mg/dL |
| desirable value for triglycerides | less than 120 mg/dL is desirable and less than 150 is normal |
| borderline-high value for triglycerides | 150-199 mg/dL |
| high value for triglycerides | 200-499 mg/dL is high and greater than or equal to 500 is very high |
| ____________ is due to a decrease in LDL clearance and results in an increase in LDL-C | Polygenic Hypercholesterolemia |
| the main parameter for Polygenic Hypercholesterolemia is LDL values of ____ and TG values of _____ | 130-250, 150-500 mg/dL |
| _____ is due to an increase in VLDL synthesis, a decrease in LPL activiity and a decrease in VLDL removal and results in increased TG, increased remnant VLDL, increased small dense LDL and decreased HDL | Atherogenic dyslipidemia |
| the main parameter for Atherogenic dyslipidemia is ____ | HDL-C greater than 40 mg/dL |
| ____ the due to dysfunctional or absent LDL receptors results in increased LDL-C | familial hypercholesterolemia |
| the main parameter in familial hypercholesterolemia is ____ | LDL-C 250-450 mg/dL |
| the number one secondary cause of hypercholesterolemia is _____ | hypothyroidism |
| dietary changes should be initiated first in patients with hyperipoproteinemia unless _____ or ____ | 1. evidence of coronary or vascular diseases 2. familial or fimial combined hypercholesterolemia |
| what 3 things can increase LDL? | cholesterol, saturated fat and trans fat |
| what 3 things can increase triglycerides? | total fat, alcohol and excess calories |
| what 2 things can increase VLDL? | sucrose and fructose |
| what can increase hepatic secretion of VLDL? | alcohol |
| patients should be advised to limi total calories from fat to ___% | 25-35 |
| patients should be advised to limit saturated fat to __% of total calories. | less than 7 |
| ----_ fats should predominate the diet for management of dyslipidemia. | cis-monounsaturated |
| pharmacothrapy should be avoided in patients who are ____ | pregnant, lactating or women likely to become pregnant |
| dose adjustments are usually required if combined with ___ or ___ | warfarin or indandione anticoagulants |
| drugs are rarely inicated for those ____ years old | younger than 16 |
| what are the pharmacological effects of statins? | 1. increase in high affinity of LDL receptors 2. increase hepatic LDL catabolim 3. decrease LDL (20-60%) 4. modst decrease in TG (7-30%) 5. small increase in DL (5-15%) |
| ___ and ___ are both ianctive pactone prodrugs that are hydrolyzed in the GIT to the active form | Lovastatin and Simvastatin |
| ___ is alsmost completely absorbed | fluvastatin |
| plasma half life of most statins is 1-3 hours except for ___ and ___ due to a fluorine atom on the ring structure | Atorvastatin (14 hrs) and Rosuvastatin (19 hrs) |
| 2 adverse effects of statins are: | 1. serum transaminases elevation 2. muscle toxicity (myalgia, myopathy, rhabdomyolysis myolobbinuria and acute tubular necrosis) |
| fenofibrate and gemfibrozil are examples of _____ | Fibric Acid Derivatives. |
| ____ is a fibric acid derivative that is tightly bound to plasma proteins, undergoes enterohepatic circulation, crosses the placenta and is 70% excreted as parent drug by the kidneys | Gemfibrozil |
| ____ is a fibric acid derivative that is hydrolyzed in the intestine and is 60% excreted in the urine as a glucronide | Fenofibrate |
| Drrugs that decrease statin metabolism: | 1. Amiodarone 2. Azole antifungals 3. CCB 4. Macrolides 5. Grapefruit juice |
| ____ can reduce renal clearance of statins by reducing glucoronidation | fibrates (except fenofibrate- making it the preferred fibrate to be added to a statin regime) |
| ____ act as ligands for the PPAR receptors work by increasing fatty acid oxidation in liver and muscle, increasing lipolysis of lipoprotein TG, modestly reducing LDL and HDL | fibric acid derivatives |
| _____ decrease TG by 50% | fibric acid derivatives |
| which patients should use fibric acid derivatives? | 1. hypertriglyceridemias 2. dysbetalipoproteinemia 3. hypercholesterolemia/mixed dyslipidemia |
| what are some adverse effects of fibric acid derivatives? | 1. GI symtpoms 2. INCREASED LFT 3. MYALGIA (especially when used with statins) 4. increased risk of cholesterol gallstones (use caution in pts with biliary tract disease) |
| the hydrophilic layer of a lipoprotein contains ____ and ____ | apolipoproteins and phospholipids |
| nascent HDL is converted to HDL3 by the enzyme _____ | Lecithin-cholesterol acyltransferace (ACAT) |
| the role of nascent HDL is to _____ | pick up free cholesterol from various extrahepatic tissues |
| the two primary components of all plaques are ____ and _____ | lipid core and fibrous cap |
| outline the atherosclerotic process in order from 1 to 5 | 1. form fatty streak 2. influx of monocytes 3. macrophage uptake of LDL particles 4. foam cell formation. intima grows and thickens 5. plauque ruptures and forms clot |
| what are 4 secondary causes of lipid disorders? | 1. diet 2. drugs 3. disorders 4. diseases |
| clinical evaluation consists of ____ and _____ | lab testing and risk factor stratification |
| ____ is the primary target for treatment and treatment strategies should be based on _____ risk | LDL, overall |
| ___ participates in retrieval of cholesterol from the artery wall and inhibit the oxidation of atherogenic lipoproteins | HDL |
| atherogenic lipoproteins can aggregate ischemia by: | imparing nitric oxide on smooth muscle cells, leading to vasocontriction, oxidation resotres and endothelial function |
| lipoproteins have a hydrophobic core containing ___ and _____ | cholesterol esters and triglycerides |
| lipoproteins have a hydrophilic outer layer composed of ___,____ and ___ | unesterified cholesterol, phospholipids and apoproteins |
| HDL is formed by the addition of ___ and ___ | surface lipids and small apoproteins |
| ____ is formed from LPL an the (a) protein, linked by a disulfide bridge. | Lp(a) protein |
| tendon xanthomas are often present in ____ | familial hypercholesterolemia |
| ___ is used to reduce VLDL production | Niacin |
| ___ and ___ are inactive lactone prodrugs that are hydrolyzed in the GIT to the active beta-hydroxyl derivative | simvastatin and lovastatin |
| ____ , ___ and ___ are fluorine containing HMG CoA RI that are active as given | atorvastatin, fluvastatin and rosuvastatin |
| ____ reduce prenylation od Rho and Rab (useful in Alziemers treatment) proteins | statins |
| chemistry and PK of Niacin | it is converted in the obdy to the amide which is incorporated into niacinamide adenine dinucleotide (NAD). it is excreted in the urine unmodified and as several metabolites. |
| ____ inhibits VLDL secretion in turn decreasing the production of LDL | Niacin |
| ___ is the most effective agent for increasing HDL and is the only agent that may reduce Lp(a) | Niacin |
| ___ function as ligands for the nuclear transcription receptor PPAR-alpha, causing an increase in oxidation of fatty acids in liver and striated muscle and increased lipolysis of lipoprotein tryglyceride via LPL. | Fibrates |
| ____ is a selective inhibitor of intestinal absorption of cholesterol and phytosterols | Ezetimibe |
| Discuss the pathogenesis of atherosclerosis: | 1. formation of a fatty streak 2. influx of monocytes 3. macrophages uptake of LDL particles 4. Foam cell formation. Continued intima growth/thickening 5. plaque formation 6. clot formation |
| what are the 4 D's that are secondary causes of lipid disorders? | 1. Diet (anorexia , obesity) 2. Drugs 3. Disorders 4. Diseases |
| _____ is an acute phase reactant and a nonspecific inflammatory marker that may be a stronger predictor for CHD than LDL | high sensitivity C reactive protein |
| hs-CRP is increased by ____ and decreased by _____ | increased by inflammation, smoking and HR. decreased by weight loss, statins, fibrates, ezetimibe and ASA |
| what are 3 emerging risk markers for lipid disorders? | 1. hs-CRP 2. Lp(a) 3. Homocysteine |
| how should you measure hs-CRP? | obtain 2 measurements (if greater than 10 mg/L, repeat test) |
| how do you interperet risk levels of hs-CRP? | Low: less than 1 mg/L Mid: 1-3 mg/L High: greater than 3 mg/L |
| ____ is an LDL like particle that may be thrombogenic and is an emerging risk factor for lipid disorders | Lp(a) |
| Lp(a) levels increase with ____ and decrease with ____ | increase with inflammation and genetics. decrease with niacin, estrogen and genetics. |
| ____ is a byproduct of protein metabolism that may predispose patients to atherosclerosis and may play a role in lowering CV disease. it is an emerging risk factor. | homocysteine |
| desirable total cholesterol: | less than 200 mg/dL |
| Borderline high total cholesterol: | 200-239 mg/dL |
| High total cholesterol | greater than or equal to 240 mg/dL |
| optimal LDL: | less than 100 |
| near or above normal LDL: | 100-129 |
| borderline high LDL | 130-159 |
| high LDL | 160-189 |
| very high LDL: | greater than or equal to 190 |
| High TG: | 200-499 |
| borderline high TG: | 150-199 |
| normal TG | less than 150 |
| very high TG | greater than or equal to 500 |
| LDL should be directly obtained if TG levels are ____ | above 400 (using the equation may overestiate LDL levels) |
| if a nonfasting measureent is used for FLP, only ___ and ___ are accurate. ___ will be falsely low and ____ will be falsely high. | total cholesterol, HDL, LDL, TG |
| Steps in Clinical Evaluation of Lipid Disorder: | 1. FLP 2. Determine presence of atherosclerotic disease 3. determine # of risk factors (if none or 1 go to step 5, if 2+ calculate FRS) 4. calculate framingham risk score 5. determine tx |
| CHD Risk Equivalents | Peripheral Artery Disease • Carotid Artery Disease • Abdominal Artery Disease • Renal Artery Stenosis • Diabetes • ≥ 20% 10-yr risk of CHD event • Chronic Kidney Disease? |
| Clinical CHD: | Prior myocardial infarction (MI) • Silent Ischemia or MI • Chronic stable angina or unstable angina • Prior revscularization procedure: -Coronary Artery Bypass Graft -PCI -Bypass graft of lower extremity -Carotid Endarterecomy |
| Major risk factor: men ___ years old and women ____ years old | greater than or equal to 45, greater than or equal to 55 |
| Major Risk Factor: Reduced HDL of ___ in men and ___ in women | less than 40, less than 50 |
| major risk factors include: | 1. age 2. family history of premature CHD- in male les than 55 and females less than 65 3. smoker 4. HTN (BP greater/equal to 140/90) 5. Reduced HDL |
| you should calculate a 10 year framingham risk score if: | the patient has 2 or more risk factors |
| you should NOT calculate a 10 yearr framingham risk score if: | a patent has been clinically diagnosed with CHD or equivalent or has 1 or 0 risk factors |
| High risk patients have a framingham score of ___ and an LDL goal of ____ | over 20%, less than 100 |
| moderately high risk patients have a framingham score of ____, and an LAL goal of ____ | 10-20%, less than 130 |
| moderate risk patients have a framingham score of ____ and an LDL goal of _____ | less than 10%, less than 130 |
| low risk patients have a ____ and an LDL goal of ___ | 0-1- risk factors (no framingham score needed), less than 160 |
| Equation for calculating the amount of LDL lowering required | (LDL(observed) – LDL (desired)) X 100% / ( LDL (observed)) |
| basic components of therapeutic lifestyle changes include ___, ____ and _____ | nutrition, physical activity and smoking cessation |
| ____ have pleotrophic effects | statins (beneficial effects that go above and beyond LDL lowering) |
| LOL Lowering Efficacy of Statins in decreasing order | Ros> Ator> sim/Pit > Lov > Prav > Flu |
| the ___ trial assessed patients of various LDL levels accros various statin groups and concluded that as the dose of the statin increased LDL improved | Stellar |
| the Rule of 6 occurs with _____ and is defined as | statins: any additional increase (or doubling of) a dose above a standard dose will only give a 6% lowering of LDL |
| ex: a patient takes 20mg simvastatin daily and has an LDL of 205. what is his expected LDL value with this medication? If MD increases this dose to 40 mg what would you expect? | 205 * 0.38 (20 mg simvastatin shows -38% reduction from chart) = 127 mg/dL. Increasing it 40mg will lower LDL another 6% (127 * 0.06) |
| ____ is the only statin that should be given with food | lovastatin |
| when should you monitor liver function tests with statins? | 1. baseline 2. at 12 weeks then annually 3. recheck in 2-6 weeks if less than 3 times above normal limits or repeat if over 3 times UNL discontinue statin, then recheck in 2 weeks then restart statin at a lower dose or switch to another statin |
| what are the 3 statins msot likely to cause drug interactions? | Lovastatin, Simvastatin and Atorvastatin (they are all substrates of CYP3A4) |
| do not start new patients on simvastatin _____mg daily | 80 |
| what was included in the ATP III update? | 1. high risk pts (those with DM) benefit from LDL lowering 2. elderly patients benefit 3. offers optional LOL goals for high and moderately high risk patients |
| the ___ trial showed a benefit in treating high risk patients with statins | HPS |
| the ____ trial showed a benefit of statin therapy in the elderly | PROSPER |
| the ____ trial was the only negative trial AAND WAS STOPPED early because of fatal CHD and nonfatal MI | ALLHAT |
| THE ____ Trial showed that high risk patients benefited from the optional <70 recommendation if they took a statin within 10 days from taking | PROVE-IT |
Created by:
cmiglis