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121 Cards in this Set
- Front
- Back
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What are the top 4 causes of death in the US and approximate values? (2009)
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#1: Heart Disease (~625k)
#2: Cancer (~550k) #3: Cerebrovascular disease (stroke) (~125k) #4: COPD and allied conditions (~125k) |
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What are the five stages of epidemiological transition?
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1) Pestilence and Famine
2) Receding Pandemics 3) Degenerative and Human-made Diseases 4) Delayed Degenerative Disease 5) Inactivity and Obesity |
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What stage is "Pestilence and Famine" and what are its characteristics, particularly CVD death%?
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1) Pestilence and Famine - malnutrition, ixns, high infant/child mortality, low mean life expectancy. CVD deaths < 10% (Rheumatic heart disease, cardiomyopathies from ixn and malnutrition)
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What stage is "Receding Pandemics" and what are its characteristics, particularly CVD death%?
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2) Receding Pandemics - better nutrition and public health, fewer ixn/malnutrition deaths, fewer children/infant mortalities. CVD deaths 10-35% (Rheumatic valvular disease, HTN, CHD, stroke [hemorrhagic])
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what stage is "Degenerative and Human-made Diseases" and what are its characteristics, particularly CVD death%?
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3) Degenerative and Human-made Diseases - increased fat/caloric intake, less physical activity - HTN and atherosclerosis emerge. Longer lives = more chronic non-IDs. CVD deaths 35-65% (CHD, stroke [ischemic and hemorrhagic])
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What stage is "Delayed Degenerative Diseases," and what are its characteristics, especially CVD death%?
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4) Delayed Degenerative Diseases - CVD and cancer are major causes of M/M - fewer deaths due to better txn and prevention, decline in age-adjusted CVD mortality rate. CVD deaths 40-50% (CHD, stroke, CHF)
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What stage is "Inactivity and Obesity," and what are its characteristics, especially CVD death%?
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5) Inactivity and Obesity - overweight/obesity increase, diabetes and HTN increase, smoking stabilizes, few people physically active. Reversal of age-adjusted declines in mortality (CHD, stroke, CHF, peripheral vascular disease)
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At what Epidemiological Stage is the US currently?
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4) Delayed Degenerative Diseases
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List a few risk factors for CVD
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Low HDL Cholesterol, High Total Cholesterol, High (untreated) Systolic BP, Smokers, Diabetes.
*Men > Women (pre-menopausal) |
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List some of the diseases of the heart and vasculature.
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Atherosclerosis (lipoproteins, dyslipidemia, metabolic syndrome, nutrition), HTN, CVD (ischemic heart disease, angina, MI, peripheral vascular diseaes), (Dys)Arrhythmias, CHF, Stroke
Less common: CHD, cardiac infections, valvular disease (congenital, ixn, CVD, HTN), cardiomyopathy, pericardial disease, shock) |
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What is the AHA goal for Cardiovascular Health by 2020?
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To improve the cardiovascular health of all Americans by 20% while reducing deaths from cardiovascular diseases and stroke by 20% by 2020
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What are behavioral risk factors for CVD?
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Tobacco use, poor diet (trans fats, simple carbohydrates), physical inactivity
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What are metabolic risk factors for CVD?
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Lipid levels, HTN, Obesity, Diabetes, Metabolic Syndrome
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What disease is the #1 killer of Americans, with 1 death every 30 seconds, that starts early, often remains silent, and usually goes undetected until a fatal or near-fatal event occurs?
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Cardiovascular Disease
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Describe the Glagov model and how it differs from the conventional model.
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In the conventional model, an atheroma develops in the wall of a vessel and protrudes out, obstructing the lumen of the vessel with relatively no change in the outer width of the vessel.
In the Glagov model, the atheroma creeps along the inside of the vessel endothelium, stretching the outer layer to the maximum and then constricting the overall diameter of the lumen. |
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What is IVUS? What is it used for? Why is it so useful?
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IVUS is intravascular ultrasound - it can be inserted into a vessel lumen and it sends ultrasonic waves at the endothelium to visualize its composition - it is necessary because vessels may appear normal in an angiogram but actually contain very serious atheromas.
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What is a way to assess, educate, and form a treatment plan for a patient with high cholesterol or risk of CVD?
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National Cholesterol Education Program Adult Treatment Panel III guideline (NCEP-ATP III)
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What are some important aspects of the medical history that are associated with increased risk of CVD?
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Personal history of cardiovascular disease, cardiovascular symptoms, hypertension, diabetes, lipid disorders, smoking.
Family history is also very important (for same risk factors as listed above) |
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What are some important (vital) signs that may indicate risk of CVD?
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Typical vital signs: BP, HR, height, weight, waist circumference
Respiratory and Cardiac Exams (including auscultation of heart rate/rhythm esp S3 and S4, breathing, major arteries for bruits, peripheral pulses) Xanthomata (deposition of cholesterol at joints) Inspect eyes for a corneal arcus or retinal abnormalities |
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What are the 9 steps of the NCEP-ATP III?
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1. Determine Lipoprotein Levels
2. Identify High Risk (CHD and equivalents) 3. Determine Other Major Risk Factors 4. 2+ Risk Factors Assess 10 Year Risk 5. Determine Risk Category 6. Initiate Therapeutic Lifestyle Change 7. Consider Adding Drug if LDL Not at Goal 8. Identify Metabolic Syndrome and Treat 9. Treat Elevated Triglycerides and non-HDL |
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What are the components of determining the lipoprotein levels (step 1, NCEP-ATP III)? How do you calculate LDL?
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From a fasting specimen, you get total cholesterol (TC), high-density lipoprotein-cholesterol (HDL), and triglycerides (TG).
Calculate LDL = TC - (TG/5 + HDL) Non-HDL = TC - HDL (only when TG > 200 mg/dl and LDL at goal) |
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What are lab tests besides a cholesterol panel that would be useful in assessing CVD risk?
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Fasting glucose, TSH (thyroid stimulating hormone).
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What are some high risks for CHD and CHD equivalent?
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Clinical CHD (evidence of CVD, multiple risk factors that are poorly controlled, metabolic syndrome, acute coronary syndrome), symptomatic carotid artery disease, peripheral artery disease (ankle/brachial index <0.9), abdominal aortic aneurysm, diabetes mellitis.
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What are the risks associated with peripheral artery disease (PAD)?
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12% adults > 50 have ABI < 0.9.
> 75% are former smokers, most asymptomatic, <20% have intermittent symptoms PAD magnifies the risks of ischemic events - increases risk of MI 4x, risk of stroke 2-3x, 5 year mortality rate of 25-30%. Risk of PAD 11x higher in patients with diabetes. |
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What are differences between true claudification and pseudoclaudification?
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In true claudification, onset increases with exertion, location is the buttocks hip thigh calf and foot, character is crampy and achy, sometimes bilateral, walking distance is constant, vascular etiology, and relief from standing or rest.
Pseudoclaudification onset is with standing or movement, located in bottocks hip or thigh, character is sharp paresthetic, usually bilateral, variable walking distance, etiology is spinal stenosis, relief with sitting or leaning forward. |
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What are the recommendations regarding abdominal aortic aneurysms (AAA)?
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Screen everyone age 60-85 who has CVD risk factors.
Screen everyone over 50 who smokes or has a family history of AAA. If <3 cm, no action needed, 3-4 cm yearly ultrasound, 4-4.5 cm ultrasound q 6 months, 4.5+ cm refer to vascular specialist. |
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What are the 5 major risk factors for CHD?
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1. Age (Male > 45; Female > 55)
2. BP > 140/90 mmHg 3. HDL < 40 mg/dl in male, < 50 in females 4. Family history of premature CHD 5. Smoking history |
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Why is family history so important with regards to CHD risk?
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Those with a family history of CHD make up the majority of early onset CV events. Sibling history even stronger than parental history. 17% of people have a family history of CHD and they account for 72% of premature CHD cases.
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What are the benefits of smoking cessation within...
...20 minutes? ...24 hours? ...1 year? ...5 years? ...15 years? |
20 minutes: Decreased BP, pulse and body temperature normalize
24 hours: Decrease in MI risk 1 year: Risk of CHD 1/2 that of a smoker 5 years: Risk of CVA similar to non-smoker 15 years: Risk of CHD similar to non-smoker |
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What is the Framingham point score system, and Global Risk Assessment?
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A cumulative point score including age, systolic blood pressure, smoking, total cholesterol, HDL cholesterol - it correlates to 10 year CHD risk.
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What are the different risk categories as per NCEP-ATP III guidelines?
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- Very high/high risk CHD or CHD risk equivalents - 10-year risk >20%
- Moderate high risk - 2+ risk factors, 10-year risk 10-20% - Moderate risk - 2+ risk factors, 10-year risk <10% - Lower risk - 0-1 risk factors |
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Explain Therapeutic Lifestyle Change (TLC)
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TLC diet - diet has 25-35% calories as fat, <7% as saturated fat, and cholesterol <200 mg/day, plus increase in soluble fiber intake and plant sterols/stanols.
Weight management Increased physical activity |
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What are the 5 main classes for lipid management drugs?
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Statins, Fibrates, Niacin, Bile Acid Sequestrants, Cholesterol Absorption Inhibitors
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What drug class is most effective at optimizing overall lipids (TC, TG, HDL, LDL)?
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Statins
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Which drug classes are most effective at lowering LDL?
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Statins (TC, TG, and LDL) and Bile Acid Sequestrants (only LDL)
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Which drug class has a generally modest effect and mostly lowers triglycerides?
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Fibrates
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Which drug class is most effective at raising HDL?
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Niacin
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What are five risk factors for metabolic syndrome? How many must be present to determine the presence of metabolic syndrome?
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Abdominal obesity, triglycerides (high), HDL-C (low), BP (high), Fasting Glucose (high)
Three of these factors must be present for metabolic syndrome. |
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How would one treat metabolic syndrome?
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Treat underlying cause (physical inactivity, overweight/obesity)
Treat lipid and non-lipid risk factors if persist despite lifestyle changes (treat HTN, Aspirin for CHD patients, treat elevated TG and/or low HDL) |
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What is a Reynold's Risk score? What extra values does it include?
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This risk calculation includes CRP, an acute phase reactant produced by the liver, and family history. It produces a superior 10 year CVD/CHD prediction.
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How should one measure CRP? What are the predictive values?
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Ensure that the patient is in good health (no fever or non-CVD/CHD related factors that may raise CRP), patient may be fasting or nonfasting, and two measurements should be taken at least 2 weeks apart. If level is above 10 mg/L, repeat test 2-3 weeks later and ensure the patient does not have infection or inflammation.
CRP < 1 = Low Risk CRP 1-3 = Intermediate Risk CRP 3-10 = High Risk |
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What is a chylomicron? What is it composed of and where is it produced?
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A chylomicron a large lipoprotein made in the intestinal lumen from lipids, and contains triglycerides and cholesteryl esters. It is secreted into the lymphatic system.
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What is a very low density lipoprotein (VLDL)?
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VLDLs are made in liver hepatocytes, and contain newly made triglycerides and cholesteryl esters, and those left over from chylomicrons.
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What is an intermediate density lipoprotein (IDL)?
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IDLs are formed from VLDL once the triglyceride content falls below 50% its original content.
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What is a low density lipoprotein (LDL)?
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One fate of IDL is conversion to LDL, which involves adding more CE to the IDL and the loss of all apoproteins except for Apo B100 which is needed for endocytosis into cells that need cholesterol.
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What is a high density lipoprotein (HDL)?
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HDL is synthesized in the liver as a flat discoidal phospholipid bilayer surrounded by Apo AI and collects cholesterol from vascular endothelium. It gradually loses affinity to cholesterol as it collects more and eventually returns to the liver where the cholesterol is processed.
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Define an amphipathic lipid.
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Amphipathic lipid - a lipid molecule with a hydrophobic region and a hydrophilic region.
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What is the importance of amphipathic lipids in lipoprotein formation?
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Amphipathic lipids form micelles, where the hydrophobic regions aggregate and are shielded by the hydrophilic regions. Important for the spontaneous formation of chylomicrons and such.
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What is the lipoprotein carrier for triglycerides and cholesteryl esters of dietary origin?
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Within the smooth ER and Golgi of the intestinal epithelial cell, cholesteryl esters and triglycerides are packaged into chylomicrons and distributed via the lymphatics into the circulatory system.
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What is the lipoprotein carrier for triglycerides and cholesteryl esters synthesized in the liver?
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The liver synthesizes VLDL to carry triglycerides and cholesteryl esters throughout the body where they are needed.
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Rank VLDL, LDL, HDL, and Chylomicrons in order of decreasing size
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Chylomicron > VLDL > LDL > HDL
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How are chylomicrons metabolized?
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Chylomicrons circulate and distribute triglycerides, and when they are depleted they return to the liver for disassembly and reassembly into VLDL.
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Describe the stages of chylomicrons: Nascent/Early Chylomicron, Mature Chylomicron, Chylomicron Remnant
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Nascent/Early Chylomicron - made in the smooth ER or golgi of intestine, and is packed with TG and CE.
Mature Chylomicron - it picks up apoproteins and begins releasing TGs to the body, until losing 50-90% of its original TG content. Chylomicron Remnant - depleted of its TG core, it releases its apoproteins and returns to the liver for disassembly and use to make VLDL |
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What is the role of Microsomal Lipid Transfer Protein (MLTP)?
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MLTP facilitates the transfer of newly absorbed TG and CE into the core of the nascent chylomicron lipoprotein.
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What apoprotein(s) are present in the Nascent/Early Chylomicron? From where are they produced?
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B48 is the only apoprotein present in the Nascent/Early Chylomicron. Apoproteins AI and AII are added soon after. B48 is produced in the Rough ER, and AI and AII come from HDL.
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What apoproteins are present in the Mature Chylomicrons?
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In the lymphatic vessels, the chylomicron picks up apoproteins CI, CII, CIII, and E from circulating HDL. (And Apo AI, AII)
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What are the roles of C apoproteins in chylomicrons?
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Apoprotein CII is a cofactor for lipoprotein lipase (regulated by insulin). Lipoprotein lipase and Apo CII work together to hydrolyze TG in chylomicrons to free fatty acids and glycerol for use.
Apoprotein CIII inhibits lipoprotein lipase, so the ratio of Apo CII and Apo CIII affects the level of lipoprotein lipase activity. |
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What is the role of the fibrate class of drugs?
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Fibrates stimulate lipoprotein lipase activity
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What is the role of phospholipid transfer protein (PTP)?
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PTP transfers phospholipid from the shell of a chylomicron to the shell of an HDL - usually as the chylomicron goes down in size as TG is hydrolyzed.
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What apoproteins are present in Chylomicron Remnants?
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C Apoproteins are lost to HDL in circulation
Apoprotein E recognizes receptors in the liver where it binds and the chylomicron is endocytosed. |
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What is the role of an LDL-Receptor Related Protein Receptor (LRP receptor)?
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LRP receptors bind to Apoprotein E, which induces endocytosis of the lipoprotein displaying Apoprotein E.
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What apoproteins are present in LDL?
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LDL only contains Apoprotein B100, which interacts with receptors displayed by cells that need cholesterol.
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What three things may happen to cholesterol that is brought back to the liver by HDL?
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The cholesterol may be repackaged into VLDL (then LDL) and circulate through the body, the liver may convert the cholesterol into bile acids, or a small amount of cholesterol may be directly excreted into the bile.
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Describe how dietary TG makes its way from the intestinal lumen to the chylomicron.
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Dietary Triglyceride --> [Lecithin-aided digestion] --> b-monoglyceride --> [micellar aided absorption] --> b-monoglyceride
b-monoglyceride + 2 FAs --> [Fatty Acyl Transferase] --> Triglyceride --> Chylomicron core |
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What two enzymes are necessary for intestinal digestion of dietary triglycerides?
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Pancreatic Lipase, Colipase
*Pancreatic lipase is inactive when secreted, and requires colipase to become fully active* |
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What are triglycerides broken down to in order to be absorbed by the intestines?
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b-monoglyceride
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How is dietary cholesterol absorbed in the intestines?
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Cholesterol is weakly amphipathic, and form micelles with bile acids
Cholesterol is absorbed, with the aid of transporter proteins like Niemann-Pick C1 like 1 protein (NPC1L1) |
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What drugs target Niemann-Pick C1 like 1 protein (NPC1L1)?
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Zetia and Vytorin, which aim to decrease absorption of cholesterol
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What is the role of Zetia and Vytorin? How do they work?
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These drugs inhibit NPC1L1 in order to decrease cholesterol absorption.
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How is cholesterol processed once it is absorbed into the intestinal epithelial cells?
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Absorbed cholesterol is converted to its hydrophobic form cholesteryl ester (CE) by Acyl Cholesterol Acyl Transferase (ACAT). From there it is inserted into a (nascent) chylomicron.
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What transporter protein is responsible for exporting cholesterol back into the intestinal lumen?
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ATP Binding Cassette Protein 1 (ABC-1)
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What is Orlistat and what does it do?
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Orlistat is an anti-obesity drug that inhibits pancreatic lipase.
Pancreatic lipase is necessary for the breakdown of dietary triglycerides into b-monoglyceride (absorbable by the intestines). |
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What drug inhibits pancreatic lipase?
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Orlistat
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What is the structure of apolipoprotein (a)?
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Apolipoprotein (a) resembles plasminogen, the inactive precursor to plasmin. It contains the protease domain and fibrin binding region of plasminogen, as well as 10-40 repeats of the fourth kringle domain of plasminogen. 80% of the AAs coincide with plasminogen.
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Where is apolipoprotein (a) located?
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Apolipoprotein (a) is linked in one position to Apoprotein B100 of LDL, creating a variant of LDL called Lipoprotein (a) or Lp (a).
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What is the role of Lp (a) in clotting?
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Lp (a), because it contains apolipoprotein (a) which resembles plasminogen, binds to partially degraded clots. Lp (a) binds and supports the proliferation of inflammatory cells and fibroblasts.
Lp (a) also competes with plasminogen for tissue plasminogen activators, which helps clots persist. It also competes with plasminogen for binding sites on fibrin, making it more difficult for the enzyme to find its substrate. |
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How is Lp (a) correlated with cardiovascular health? How can one affect Lp (a) levels?
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Elevated Lp (a) correlates to greatly increased risk of clotting and atherosclerosis.
Lp (a) levels are genetically determined, and unaffected by everything except in some cases very high levels of niacin (intolerable and/or ineffective in some). |
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What are the two possible fates of IDL after it loses C apoproteins?
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1. IDL may be taken up by hepatocytes, disassembled, and reassembled into VLDL
2. IDL is taken up by hepatocytes and Cholesterol Exchange Transfer Protein (CETP), which enriches it with CE and converts it to an LDL. |
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How is VLDL synthesized and what apoproteins are present?
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VLDL is synthesized from the remnants of chylomicrons, TG, and CE.
Apoprotein B100, C apoproteins, and Apoprotein E are present in mature VLDL. |
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How does Apoprotein B100 get added to VLDL, and what is its role?
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MLTP loads lipid onto Apoprotein B100, and Apoprotein B100 is required for organization and secretion of VLDL.
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What is the fate of VLDL?
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As the TGs in VLDL are hydrolyzed and used up, VLDL becomes IDL.
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How is LDL formed?
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LDL is formed from IDL, when it is enriched with CE via CETP-carrying HDL.
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Where does most of the cholesterol of LDL end up, and what is it used for?
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60% of cholesterol from LDL is taken up by the liver for the manufacture of bile acids.
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How is cholesteryl ester converted to free cholesterol for use by cells?
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Cholesterol ester deacylase
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Describe Familial Hypercholesterolemia, and what causes it?
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FH is a disease in which there is nonspecific deposition of cholesterol. Caused by genetic defects in Apoprotein B100, for which one may be heterozygous or homozygous (early mortality).
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What is the effect of Hepatic Lipase on IDL?
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Hepatic Lipase removes E and C apoproteins from IDL, forming LDL.
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Where is HDL synthesized?
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(Nascent) HDL is synthesized in the liver, and is also known as pre-beta HDL or "lipid free" HDL. It has the highest concentration in the extravascular space.
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Which form of HDL has the highest affinity for cholesterol?
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Nascent HDL
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What apoprotein is most significant in Nascent HDL?
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Apoprotein AI is abundant in the bilayer of HDL.
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What is the role of Apoprotein AI?
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Apo AI binds to cell membranes that signal that they have a significant cholesterol content and facilitates transfer of cholesterol from the cells to the HDL.
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What is the cause of Tangier's Disease? What is its effect?
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Tangier's disease is caused by mutations in ABC-1 transfer protein on peripheral cells and facilitates transfer of cholesterol out of the cell into HDL.
Mutations in ABC-1 result in low levels of HDL and accumulation of cholesterol in peripheral cells, promoting atherosclerosis and killing nerve cells in the body. |
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What is the role of myeloperoxidase (MPO) regarding HDL and Apoprotein AI?
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MPO targets Apo AI and adds nitro- and chloro- residues to the tyrosine group. Patients with high levels of MPO have higher cardiac risks, up to 16x more than those with normal MPO levels.
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How is pre-beta HDL converted to alpha HDL?
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pre-beta HDL picks up cholesterol and interacts with triglyceride-rich lipoproteins (TGRLP), VLDL, IDL, Chylomicrons, and Chylomicron remnants.
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What three proteins are bound by HDL?
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LCAT: Lecithin-Cholesterol Acyl Transferase
CETP: Cholesterol Exchange Transfer Protein PLTP: Phospholipid Transfer Protein |
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What is HDL3?
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HDL3 is the next HDL after pre-beta HDL - it is not as capable at picking up cholesterol as pre-beta, but is better than HDL2. The presence of Apo AII seems to interfere with cholesterol salvage.
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How is HDL3 produced?
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LCAT further enriches pre-beta HDL with CE, using lecithin and free cholesterol. It forms CE and lysolecithin (disrupts cell membranes, binds to albumin).
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How is HDL3 converted to HDL2?
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Respectively: LCAT, CETP, and PLTP result in removal of cholesterol from the outer shell, exchange of CE in core of HDL for TG in core of TGRLPs, and transference of more phospholipid to the outer shell to replace the cholesterol.
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How does HDL2 return to the liver?
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HDL2 interacts with 3 proteins in the liver: SR-B1, Hepatic Lipase, and HDL receptors.
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Describe the role of SR-B1.
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They are receptors present on liver and gland cells, and are specific for HDL. It is "Scavenge Receptor Binding protein 1". When it binds HDL, cholesterol is more easily transferred from the HDL to the liver.
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Describe the role of hepatic lipase in cholesterol salvage.
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CE-depleted HDL encounters hepatic lipase. The lipase hydrolyzes TG and PL in the HDL, destabilizing the apoproteins and all are lost except Apo AI. It has now returned to pre-beta HDL which can return to circulation to scavenge more cholesterol.
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Is HDL disassembled?
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No, hepatic lipase hydrolyzes TG and PL, resulting in the loss of all apoproteins except Apo AI, re-creating pre-beta HDL from HDL2.
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What is the role of HDL receptors?
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HDL receptors can induce endocytosis of an entire HDL lipoprotein.
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Compare Apoprotein AI and Apoprotein AII.
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Apoprotein AI promotes salvage of cholesterol by HDL, whereas Apoprotein AII inhibits salvage. The ratio of [Apo AII:Apo AI] increases as HDL accumulates cholesterol and moves from pre-beta HDL to HDL3 to HDL2.
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How is cholesterol synthesized?
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3 acetyl-CoA --> b-hydroxy-b-methyl-glutaryl (HMG) CoA --> [HMG CoA Reductase, 2NADPH2 --> 2NADP, CoASH] --> Mevalonic Acid --> Squalene --> Lanosterol --> Cholesterol
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What step in cholesterol synthesis is most regulated, and is a target of Statins?
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HMG CoA + 2NADPH2 --> [HMG CoA Reductase] --> Mevalonic Acid + 2NADP + CoASH
HMG CoA Reductase is targeted by Statins |
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What drugs target HMG CoA Reductase? For what reason?
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Statins starget HMG CoA Reductase to prevent synthesis of cholesterol in the liver.
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How is HMG CoA Reductase regulated endogenously?
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HMG CoA Reductase is regulated at the gene level via phosphorylation
When cholesterol is in excess in the livers and/or bile acids in the intestine, HMG CoA Reductase activity is decreased |
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What constitutes a positive family history for CHD?
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A history of a male family member having CHD before age 55, or a female family member having CHD before age 65.
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What constitutes a risk from smoking?
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Having smoked at least one cigarette in the past month.
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Which of the following are considered when assessing if a patient has metabolic syndrome?
Waist circumference, BP, TC, TG, LDL, HDL, FG |
Waist circumference, BP, TG, HDL, FG
LDL and TC are NOT considered |
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What is the primary goal if a patient has elevated triglycerides? The secondary goal?
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Primary: Lower the LDL
Secondary: Lower the Non-HDL *Non-HDL = TC - HDL |
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What is the Non-HDL goal relative to the LDL goal?
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30 points higher than LDL goal
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For what disease is the initial sign an MI in 62% of men, and 46% of women?
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Coronary Artery Disease
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What can initiate a prothrombotic event in patients with atheromas?
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When the fibrous wall on the luminal side of the vessel around an atheroma breaks, it begins throwing clots from the exposed surface of the atheroma.
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Statistically, what are the most likely symptoms to precede an acute MI in women? What "common" symptom is surprisingly uncommon?
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70% Unusal fatigue
48% Sleep Disturbance 42% SOB 39% Indigestion 35% Anxiety < 30% reported chest pain or discomfort prior to MI Chest pain is a lot less common in women. |
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Statistically, what are the most common symptoms during an acute MI in women?
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58% SOB
55% Weakness 43% Unusual Fatigue 39% Cold Sweat 35% Dizziness 43% Reported NO Chest Pain |
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What can be seen in mammograms that may be an indication of CVD or CAD?
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Vascular calcifications
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What is the estimated increased risk for CVD associated with metabolic syndrome? What about with 4-5 risk factors?
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Without extra risk factors, about 1.74 or 74% higher risk
With extra risk factors, 3-5x higher risk from the metabolic syndrome alone. |
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What are two likely changes happening to the ATP III list?
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1. Adding CRP values
2. Family history of MI before age 60 (eliminating male vs female ages) |
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What are some biologically plausible drugs for plaque stabilization? (confirmed via clinical trials)
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Statins, ACE inhibitors, Beta blockers, ASA.
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Use of an ACE inhibitor, beta blocker, statin, and ASA all together reduces CVE risk by how much?
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75% reduction if all four are used.
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