module - 2 Atherosclerosis & Hyperlipidemia
Controlling Diabetes
Diabetes is known to accelerate the development of heart disease. Hyperglycemia fosters dyslipidemia, increased platelet aggregation, and altered red blood cell function, which can lead to thrombus formation. These metabolic alterations may impair endothelial cell-dependent vasodilation and smooth muscle function, promoting the development of atherosclerosis.
*Atherosclerosis*
Disease in which *plaque builds up inside arteries*. Plaque or atheromas are made up of *fat, cholesterol, calcium* Causes arteries to narrow restricting blood flow....limits flow of oxygen rich blood to tissue......effects perfusion *Major cause of Coronary Artery Disease (CAD)* Arteriosclerosis: "Hardening of the Arteries" Why is it a problem if arteries harden? Arteriosclerosis occurs when the blood vessels that carry oxygen and nutrients from your heart to the rest of your body (arteries) become thick and stiff — sometimes restricting blood flow to your organs and tissues. It is all about the effect of the vessels Your vessels need to be able to vasodilate and vasoconstrict in order to compensate and are used in the sympathetic system. It effects the whole body and perfusion if the vessels harden or are unable to expand and contract an abnormal accumulation of lipid, or fatty substances, and fibrous tissue in the lining of arterial blood vessel walls. These substances block and narrow the coronary vessels in a way that reduces blood flow to the myocardium. *Atherosclerosis involves a repetitious inflammatory response to injury of the artery wall and subsequent alteration in the structural and biochemical properties(특성) of the arterial walls*.
Pathogenesis of atherosclerosis
LDL deposits cholesterol in artery wall Macrophages sent as an immune response to engulf invading cholesterol Foam(거품) cells are macrophages full of cholesterol....forms a fatty streak(층) Fatty streak turns into fibrous plaque pushing intima(맥관 내막) into the lumen, narrowing blood flow Pathogenesis of atherosclerosis. A, Damaged endothelium. B, Fatty streak and lipid core formation. C, Fibrous plaque. Raised plaques are visible: some are yellow; others are white. D, Complicated lesion: thrombus is red; collagen is blue. Plaque is complicated by red thrombus deposition. (A, B), Atherosclerosis begins as monocytes and lipids enter the intima of an injured vessel. Smooth muscle cells proliferate within the vessel wall (C), contributing to the development of fatty accumulations and atheroma(혈관벽의 퇴행성 변화가 수반되는 동맥 경화증) (D). As the plaque enlarges, the vessel narrows and blood flow decreases (E). The plaque may rupture and a thrombus might form, obstructing blood flow.
Managing Hypertension
Long-standing elevated blood pressure may result in increased stiffness of the vessel walls, leading to vessel injury and a resulting inflammatory response within the intima. Inflammatory mediators then lead to the release of growth-promoting factors that cause vessel hypertrophy and hyperresponsiveness. These changes result in acceleration and aggravation of atherosclerosis.
Nursing management for atherosclerosis: Nutrition
Lower LDL cholesterol: decrease saturated fats and cholesterol Increase complex carbs (whole grains, fruit, veggies) Increase fiber Reduce or eliminate simple sugars and alcohol especially if have high serum triglycerides Increase Omega-3 fatty acids Substitute mono or polyunsaturated fats for sat fats Reduce Homocysteine levels by including B Vitamins in diet: - Thiamin - Riboflavin - Niacin - Folate - Vitamin B6 & B12 - Biotin - Pantothenic Acid Therapeutic Lifestyle Changes (TLC) diet: low in saturated fats and high in soluble fiber. *Mediterranean Diet: promotes veggies, fish, restricts red meat; reported to reduce mortality from cv disease*. *Omega-3 fatty acids* found in walnuts, and *fatty fish such as salmon, herring, tuna, or sardines*. Body does not make these. They contribute to *brain function; reduce inflammation, lower risk for CAD* Monounsaturated fats: olive oil, peanut oil, canola oil, avocados, nuts and seeds Polyunsaturated fats: vegetable oils, safflower oils, corn oil, sunflower oil, nuts and seeds. *Thiamin* (Pork, dark green leafy veggies, green pea, *lentils(렌즈콩)*, nuts such as almonds and pecans) *Riboflavin* (*Yogurt & Cheese*; Asparagus, spinach, chicken, fish, eggs, fortified(영양가를 높인) cereals) *Niacin* (*Chicken, turkey, salmon*, fortified cereals, legumes(콩과 식물의 총칭), peanuts) Folate(엽산의) (Leafy greens, fresh fruits, fortified cereals) *Vitamin B6* ( poultry, seafood, *bananas*, leafy green veges (spinach), *potatoes*, fortified cereals) *Vit B12*: (*soy products, shellfish such as clams, mussels, crab*, beef) Boost red cell production supports nervous system Biotin(비오틴: 비타민 B 복합체의 결정성 비타민; 간장·난황 등에 함유되어 있음, 비타민 H) : Liver, egg yolks, salmon, pork, avocado, cheeses Pantothenic Acid: Yogurt, avocado, legumes, sweet potatoes, mushrooms, broccoli.
Risk factors for CAD (Impaired perfusion)
Modifiable: - Hyperlipidemia - Tobacco use - *Hypertension* - Diabetes - *Metabolic syndrome* - Obesity - Physical Inactivity *Nonmodifiable*: - Increasing *age* (more than *45 years for men*; more than *55 years for women*) - *Gender* (men develop CAD at an earlier age than women) - *Race* (higher incidence of heart disease in African Americans than in Caucasians) - *Genetics: Family history* a cluster of metabolic abnormalities known as *metabolic syndrome* has emerged as a major risk factor for cardiovascular disease
Precursor(전조) to Drug Therapy for Atherosclerosis
*Complete lipid profile is recommended every 5 years beginning at age 20 yrs* Treatment begins with dietary caloric restriction, decreased dietary fat and cholesterol intake; increased physical activity *Reassess lipid levels after 6 weeks of diet therapy* When should most people follow up with lipid panel with primary physician? What is the recommendation?**
Factors Affecting Lipid Levels
*Cholesterol*: Sedentary lifestyle with intake of saturated fatty acids; familial hypercholesterolemia *LDL*: Excessive intake of saturated fatty acids; dietary cholesterol intake and obesity; familial hypercholesterolemia; *hypothyroidism; diabetes*. *Triglycerides*(higher): Obesity, *excessive alcohol intake, diabetes mellitus*, **beta blockers**, familial hypertriglyceridemia *HDL*(lower): Cigarette smoking, obesity, lack of regular exercise, genetic disorders of HDL metabolism, hypertriglyceridemia, and diabetes lowers HDL LIFESTYLE A Lipid Panel measures Cholesterol, triglycerides, LDL, HDL.
*Lipid* levels (KNOW THESE)
*LDL* cholesterol number is: - Optimal if it is less than 100 - Near optimal/above optimal if it is 100-129 - Borderline high if it is 130-159 - *High if it is 160-189* - *need to medication* - Very high if it is 190 or above *Triglyceride* numbers are: - Normal if they are less than *150* - Borderline high if they are 150-199 - High if they are 200-499 - Very high if they are 500 or higher Triglycerides is another fat that is with cholesterol and it can be used as energy. The problem is that if there is too much triglyceride because it is still a fat, a fatty substance. The lower the better with Triglyceride They break it down into levels to give the physician an idea of what needs to change with getting the LDL into a better level to know if they need to go LDL is the target of current therapy because of its strong association with advancing CAD. The total cholesterol level is also a clear predictor of coronary events. HDL is known as good cholesterol because it transports other lipoproteins such as LDL to the liver, where they can be degraded and excreted. Because of this, a high HDL level is a strong negative risk factor for heart disease (i.e., it protects against heart disease). Triglyceride is made up of fatty acids and is transported through the blood by a lipoprotein. Although an elevated triglyceride level (more than 200 mg/dL) may be genetic in origin, it also can be *caused by obesity, physical inactivity, excessive alcohol intake, high-carbohydrate diets, diabetes, kidney disease, and certain medications, such as oral contraceptives and corticosteroids*.
Drug Therapy for Atherosclerosis: Lipid Lowering Notes
*Statins overall are the best option (at higher doses these can cause cramping in legs)* Niacin inhibits the synthesis and secretion of LDL and VLDL (has a side effect of *flushing the skin*) Omega-3 fatty acid is used in particular for patients who have triglycerides greater than 500 Cholestyramine is a bile acid sequestrate(...을 격리하다) which helps bind and remove LDL cholesterol and dumps it into the intestine to move it on to the gut to get it out Ezetimibe is a cholesterol absorption inhibitor which inhibits the intestinal absorption so that it gets taken out One side effect of all of these drugs is GI disturbance which can cause N/Diarrhea
physiology/pathophysiology
1. Central adiposity 2. Increased fasting blood glucose and production of adipokines by adipose cells. 3. metabolic syndrome: - Insulin resistance - Increased fasting blood glucose - Dyslipidemia - Hypertension - Chronic inflammation 4. Direct atherogenic effects 5. Atherosclerosis Adipokines (adipose tissue cytokines), free fatty acids, and other substances are known to modify insulin action and contribute to atherogenic changes in the cardiovascular system CRP is known to be an inflammatory marker for cardiovascular risk, including acute coronary events and stroke. The liver produces CRP in response to a stimulus such as tissue injury, and high levels of this protein may occur in people with diabetes and those who are likely to have an acute coronary event (Institute for Clinical Systems Improvement [ICSI], 2013a). To determine overall cardiovascular risk, clinicians may view high sensitivity C-reactive protein (hs-CRP) test results together with other screening tools such as measurements of lipid levels.
Drug Therapy for Atherosclerosis: Lipid lowering
1. Restricts lipoprotein production: a. Statins: atorvastatin (Lipitor) Simvastatin (Zocor) *Myalgia(근육통) and arthralgia*(관절통) are common adverse effects, Monitor liver function tests - every 6 month b. Niacin -found chicken, tuna by naturally. (Niaspan) c. Fibric Acid Derivatives: - gemfibrozil (Lopid) Adverse effects include diarrhea, flatulence(위장 내에 가스가 많이 차는 것), rash, myalgia Serious adverse effects include *pancreatitis*, hepatotoxicity, and rhabdomyolysis d. Omega-3 Fatty Acid: ↓ TGs Inhibit TG production in liver - Icosapent ethyl (Vascepa) 2. Increases lipoprotein removal: ↓ LDL Slight ↑ HDL - Bile Acid Sequestrants( can prevent the oxidation of the fats in the food) : cholestyramine (Questran) Side effects include *constipation, abdominal pain, GI bleeding* 3. Decreases cholesterol absorption: ↓ LDL Inhibits absorption of cholesterol in small intestine - Cholesterol Absorption Inhibitor: ezetimibe (Zetia)Better tolerated than bile acid sequestrants
Clinical Manifestations
CAD produces symptoms and complications according to the location and degree of narrowing of the arterial lumen, thrombus formation, and obstruction of blood flow to the myocardium. This impediment(방해) to blood flow is usually progressive, causing an inadequate blood supply that deprives the cardiac muscle cells of oxygen needed for their survival. The condition is known as ischemia. Angina pectoris refers to chest pain that is brought about by myocardial ischemia. *Angina pectoris usually is caused by significant coronary atherosclerosis*. If the decrease in blood supply is great enough, of long enough duration, or both, irreversible damage and death of myocardial cells may result. Over time, irreversibly damaged myocardium undergoes degeneration and is replaced by scar tissue, causing various degrees of myocardial dysfunction. Significant myocardial damage may result in persistently low cardiac output and heart failure where the heart cannot support the body's needs for blood. A decrease in blood supply from CAD may cause the heart to abruptly stop beating; this is known as sudden cardiac death (see Chapter 29 for further discussion on CPR). *The most common manifestation of myocardial ischemia is the onset of chest pain*. However, the classic epidemiologic study of the people in Framingham, Massachusetts, showed that nearly 15% of men and women who had coronary events, which included unstable angina, MIs, or sudden cardiac death events, were totally asymptomatic prior to the coronary event (Kannel, 1986). Patients with myocardial ischemia may present to an emergency department (ED) or clinic with a variety of symptoms other than chest pain. Some complain of *epigastric distress and pain that radiates to the jaw or left arm*. Patients who are older or have a history of diabetes or heart failure may report shortness of breath. Many women have been found to have atypical symptoms, including *indigestion, nausea, palpitations, and numbness* (Canto, Canto, & Goldberg, 2014). Prodromal symptoms may occur (i.e., angina a few hours to days before the acute episode), or a major cardiac event may be the first indication of coronary atherosclerosis.
Hypertriglyceridemia
Causes: *uncontrolled diabetes mellitus*, obesity, sedentary habits. Common disorder in USA. Asymptomatic until triglycerides > 1000-2000 mg/dL S&S: - GI: Nausea, vomiting, pain in mid epigastric, chest or back - Resp: Dyspnea - Dermatologic: Xanthomas - Ophthalmologic: corneal arcus, xanthelasmas Xanthomas: Xanthomas are lesions characterized by accumulations of lipid-laden macrophages. *Xanthomas* can develop in the setting of *altered systemic lipid metabolism* or as a result of local cell dysfunction. Found most often on the *elbows, joints, tendons, knees, hands, feet, or buttocks*. *Xanthelasmas*: Cholesterol deposits in the eyelids. Little fatty areas that are deposited there *Corneal(각막의) arch is also a symptom*
Atherosclerosis-Related Diseases
Coronary Heart Disease Carotid Artery Disease Peripheral Artery Disease *Chronic Kidney Disease* Anywhere you have blood vessels you can have atherosclerosis
Contributing Risk Factors* to CAD
Diabetes Psychological States Homocysteine & C-reactive Protein Substance Abuse Metabolic syndrome (includes 3 of the following conditions): - *Insulin resistance* (fasting plasma glucose more than 100 mg/dL or abnormal glucose tolerance test) - *Central obesity* (waist circumference more than *35 inches in females*, more than *40 inches in males*) Dyslipidemia (triglycerides more than 150 mg/dL, HDL less than 50 mg/dL in females, less than 40 mg/dL in males) - *Blood pressure persistently greater than 130/85 mm Hg* - *Proinflammatory state* (high levels of C-reactive protein [CRP]) - *Prothrombotic state* (high fibrinogen level) Just having a higher level of blood glucose (*hyperglycemia*) *causes an inflammatory process* that affects the endothelial function, also *increases platelet aggregation*, can alter red blood cell function and puts people at a *higher risk of developing clots (thrombus)* Having a lot of stress has a lot of anxiety and there is a *catecholamine* released and chronically causing them flowing through the body is caustic and can *cause an inflammatory process to occur inside the vessels* *High Homocysteine* levels is an amino acid and is linked to the *development of atherosclerosis and arteriosclerosis* and can be caused if they Also *insufficient B vitamins highers the levels of Homocysteine* *C-reactive protein* is a cardiac marker for high cardiac risk and it is created in *response to chronic endothelial injury* (it is an expensive test so they do not test it very often) Substance abuse (cocaine, amphetamines) really can put people at risk for coronary artery disease (causes people to have more MIs), cocaine causes a coagulative affect and can cause more blood clots, long term use can cause coronary spasm and hypertension
Risk Factors
Epidemiologic studies point to several factors that increase the probability that a person will develop heart disease. Major risk factors are listed in Chart 27-1. Although many people with CAD have one or more risk factors, some do not have classic risk factors. Elevated low-density lipoprotein (LDL) cholesterol, also known as bad cholesterol, is a well-known risk factor and the primary target of cholesterol-lowering therapy. People at the highest risk for having a cardiac event are those with known CAD or those with diabetes, peripheral arterial disease, abdominal aortic aneurysm, or carotid artery disease. The latter diseases are referred to as CAD risk equivalents, because patients with these diseases have the same risk for a cardiac event as patients with CAD. The likelihood of having a cardiac event is also affected by factors, such as age, gender, systolic blood pressure, smoking history, level of total cholesterol, and level of high-density lipoprotein (HDL), also known as good cholesterol. The Framingham Risk Calculator is a tool commonly used to estimate the risk for having a cardiac event within the next 10 years (Goff, Lloyd-Jones, Bennett, et al., 2014). This tool is designed for adults 20 years and older. The calculation is performed using the individual's risk factor data, including age, gender, total cholesterol, HDL cholesterol, smoking status, systolic blood pressure, and need for antihypertensive medication.
Familial Hypercholesterolemia
Genetic disorder Familial: Heterozygous or Homozygous Body unable to remove LDL from blood (begins at birth) Increases risk of atherosclerosis, MI's, heart disease even in childhood, stroke, peripheral vascular disease S&S: - Xanthomas/Xanthelasmas - *Angina* - *Cramping(경련) of calves when walking* - *Sores on toes that do not heal* - *Stroke like symptoms* (loss of balance, facial drooping, weakness of arm or leg, trouble speaking) Tests to diagnose: - Lipid panel (will be positive for high total cholesterol, high LDL, normal triglycerides levels, HDL) - Genetic testing: affects 1 in 500 individuals; FH one of the most common genetic diseases Treatment: - Lifestyle changes: Diet, exercise, weight loss - Medications: *statins are commonly used*. May be combined with other meds to lower cholesterol, LDL - *Apheresis(Plasmapheresis)*: Blood or plasma is removed from the body. Special filters remove the extra LDL, cholesterol, and the blood plasma is then returned to the body. - Apheresis is a medical procedure that involves removing whole blood from a donor or patient and separating the blood into individual components so that one particular component can be removed. The remaining blood components then are re-introduced back into the bloodstream of the patient or donor. *NOT DIALIYSIS*
*Heterozygous familial hypercholesterolemia*
Heterozygous inherits mutation/alteration from 1 affected parent. FH is characterized by very high levels of LDL-C (usually > *160 mg/dL in children; >190mg/dL in adults*) as well as of total cholesterol. The condition greatly increases the risk of hardening of the arteries (atherosclerosis), which can lead to heart attacks, strokes and other vascular conditions. Individuals with FH have a 20-fold increased risk for coronary heart disease (CHD). Untreated men have a 50% risk of a nonfatal or fatal coronary event by age 50 years; untreated women have a 30% risk by age 60 years. If one or more other risk factors for CHD are present, especially cigarette smoking or diabetes mellitus, the risk of developing symptomatic CHD is even higher. FH is treatable and the associated cardiovascular disease is largely preventable with early and intensive treatment, using *statins, additional drugs, and other means*. Family members of an affected individual found through "cascade screening" or "family tracing" who have not yet exhibited symptoms and who are appropriately treated are likely to live a normal lifespan.
*Homozygous familial hypercholesterolemia*
Homozygous inherits a causal FH mutation from *both parents*. HoFH is very rare (~ 1 in 250,000 to 1 in 1 million). LDL-C levels are usually, though not always, > *400 mg/dl*. Severe vascular disease including CHD and aortic stenosis(협착증) are often seen by the teenage years. Without very aggressive treatment including LDL-C apheresis and HoFH specific medications, mortality is common before age 30. Usually going to need to be on medication
Concept of perfusion
If we don't have enough perfusion to vessels and organs people usually experience pain It can effect bowels if there is not enough perfusion to the gut(내장) It can cause confusion if there is not enough perfusion to the brain
"Know your numbers" campaign
Includes blood pressure, cholesterol, blood sugar, and BMI (body mass index) Assesses risk for heart disease and stroke Great way to educate and get people on board to personal health awareness Health Promotion: Click on Go Red For Women Link
Nursing management for atherosclerosis: Cessation of Tobacco Use
Stop tobacco use: - Educational programs - Counseling - Consistent motivation and reinforcement - Support groups - Medications: Nicotine Patch, Varenicline (Chantix), Bupropion (Zyban) Avoid smoke exposure Tobacco: Nicotinic acid triggers release of *catecholamines which increase HR & BP*. Can cause *vasoconstriction*.....increases risk of CAD and sudden cardiac death. Smoking increases oxidation of LDL, *damaging endothelial lining*. This increases platelet adhesions; higher probability of thrombus formation. Inhalation of smoke increases blood carbon monoxide levels and decreases the supply of O2. Hgb combines more readily to carbon monoxide than w/ o2. Myocardial ischemia and reduced contractility can result.
Nursing management for atherosclerosis: Physical activity
Regular physical activity assists with: - Weight reduction - *Reduction of systolic BP* - Increases HDL cholesterol Aim for 30 minutes of moderate physical activity on most days of week Weight training can treat metabolic syndrome and improve muscle strength *FITT* formula: - *Frequency (how often)* - *Intensity (how hard)* - *Type (isotonic)* - *Time (how long)* Moderate physical activity: brisk walking, hiking, biking, and swimming FITT formula: can assess a clients physical activity by asking the questions...how often, how hard, what type of exercise, how long? This may give you an idea of what they consider exercise and what is enough. Exercise benefits: Increased insulin sensitivity, improved lipid levels (increased HDL), lower BP, weight control, improved blood glucose control, reduced risk of CVD, prevent/delay onset of DM II.
*Cholesterol* levels (KNOW THESE)
Total cholesterol goal: less than *200mg/gL* LDL cholesterol goal: Less than *100mg/dL* HDL cholesterol goal: *Males > 40mg/dl*, *females >50mg/dL*, low risk for CAD, *> 60mg/dL and higher* We need higher HDL than LDL NEED TO KNOW THIS SLIDE When you draw a lipid panel it will show you this VDL is very low density
Familial hypercholesterolemia management
Treatment: - Lifestyle changes: Diet, exercise, weight loss - Medications: statins are commonly used. May be combined with other meds to lower cholesterol, LDL - Plasmapheresis: separates blood & plasma, removing harmful components - Surgical: Partial ileal bypass, portacaval shunt, Liver transplantation Surgery: *Partial ileal bypass* eliminates the reabsorption of bile acids at the distal portions of the ileum has been show to be a viable treatment in some cases of severe dyslipidemia. *Portacaval shunt*: alters cholesterol hepatic and lipoprotein metabolism *Liver Transplant*: effective in treating severe hypercholesterolemia in homozygous familial hypercholesterolemia.
*Cholesterol*
Waxy, fat-like substance found in all cells Used to make *hormones, vitamin D, bile salts* Made in body & found in foods Travels through bloodstream via lipoproteins (small packages made of fat on inside and protein on outside) Need healthy level of High Density Lipoproteins and Low Density Lipoproteins HDL: Carries cholesterol from other parts of body back to liver. Liver then removes cholesterol from body LDL: travels through body carrying cholesterol, but can lead to cholesterol build up in arteries We make our own cholesterol, and every cell in the body can do so. *The liver is the most important organ for cholesterol production and removal*. When the liver fails to function properly, cholesterol numbers can be exceedingly high and dangerous. We also get it from food when we eat If we break down cholesterol we can break it down into either HDL or LDL (HDL is healthy, LDL is bad) LDL hangs out too long and that is where the cholesterol hangs out in the body and builds up as plaque Lipoproteins and the development of atherosclerosis. As dietary cholesterol and saturated fat are processed by the gastrointestinal tract, chylomicrons enter the blood. They are broken down into chylomicron remnants in the capillaries. The liver processes them into lipoproteins. When these are released into the circulation, excess low-density lipoproteins (LDLs) adhere to receptors on the intimal wall. Macrophages also ingest LDLs and transport them into the vessel wall, beginning the process of plaque formation. HDLs, high-density lipoproteins; VLDLs, very-low-density lipoproteins.
Perfusion and circulation
Your body was designed for movement, we start to see issues with this lack of flow when people do not move or are immobile If there is an obstruction in the vessels it can slow things down
