answer all 6 questions and read below for answers please!!!! Lipid panel Results

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answer all 6 questions and read below for answers please!!!!
Lipid panel
Results

answer all 6 questions and read below for answers please!!!!
Lipid panel
Results
Optimal values
Cholesterol, total
239 mg/dL
< 200 HDL cholesterol 57 mg/dL ≥ 40 Triglycerides 128 mg/dL < 150 LDL cholesterol 156 mg/dL < 100 Cholesterol-to-HDLC ratio 4.2 calculated ≤ 3.5 Non-HDL cholesterol 182 mg/dL < 130 Lipoprotein subfractions     LDL particle number 1,722 nmol/L < 1,260 LDL small 258 nmol/L < 162 LDL medium 511 nmol/L < 201 HDL large 6,091 nmol/L > 9,386
Apolipoproteins
 
 
Apolipoprotein B
120 mg/dL
< 80 Lipoprotein (a) 33 nmol/L < 75 Inflammatory markers     HS CRP 0.5 mg/L < 1.0 Lp-PLA2 activity 93 nmol/min/mL < 75 CT cardiac scoring screen 23 (mild amount) < 99 Lp-PLA2, lipoprotein-associated phospholipase-A2. Answer the following questions based on this scenario: 1. Which of the cardiovascular diagnostic values demonstrate dyslipidemia and risk for atherogenesis? 2. Interpret and describe lipoprotein subfractions and apolipoproteins results. 3. Which of the cardiovascular diagnostic values are in the cardioprotective range? 4. What lifestyle recommendations, such as diet and exercise will be made based on these results? 5. What is his ASCVD risk score? What parameters (e.g., blood pressure) are used to calculate the risk score? 6. In addition to lifestyle recommendations, what pharmacotherapeutics are recommended? Choose all that apply. a. None b. Aspirin c. Statin d. Nicotinic acid Vascular disorders can be divided into arterial and venous disorders, and they can occur in peripheral or coronary vessels. Categorizing the disorders in this manner will help with understanding the underlying mechanisms and consequences of the vascular injury. Dyslipidemia is a common culprit, causing arterial disease and subsequent atherosclerosis. Arterial and venous abnormalities can significantly impair tissue perfusion and create an environment for thrombus formation and potential embolization. Arterial Disorders Aneurysms Walls of arteries can weaken, and areas can balloon outward, a condition known as aneurysm (FIGURE 4-24). This weakening happens much like a worn spot on a tire or a bulge in an old balloon. Just like the tire and the balloon, an aneurysm can rupture when the pressure builds inside the wall or when the wall becomes too thin. When it ruptures, blood spills out of the circulatory system, also known as exsanguination. Aneurysms may also develop slow leaks as opposed to rupturing. Aneurysms can occur in any artery, but some common locations include the aorta, particularly the abdominal and thoracic areas, and intracranial vessels. Other areas are the femoral and popliteal arteries. Intracranial aneurysms will be discussed in chapter 11. FIGURE 4-24 Aneurysm. This X-ray shows a ballooning of one of the arteries in the brain. If untreated, an aneurysm can rupture, causing a stroke. © wenht/iStock/Getty Images. The most common causes of aneurysms are atherosclerosis and hypertension. Atherosclerosis and subsequent plaque formation reduce elasticity and cause erosion. Blood traveling through narrowed arteries, like in hypertension, causes a lot of force on the arterial walls, leading to weakening and potential aneurysm development. Other factors that increase the risk of developing an aneurysm include genetic predispositions and congenital disorders (e.g., Marfan syndrome). Disorders that damage the arterial walls such as dyslipidemia and tobacco usage can lead to aneurysms. Diabetes mellitus, although associated with atherosclerosis, in epidemiologic studies has been inversely associated with the risk of aneurysm development. The reason for this inverse relation is unclear but theories include possible protective effects from antidiabetic agents (e.g., metformin). Injury (e.g., trauma) and infections (e.g., syphilis) can also cause aneurysms. The incidence of aortic aneurysms increases with age (> 65 years), and prevalence is higher in men.
True aneurysms are those that affect all three layers of the vessel. Two major types of true aneurysms exist—saccular and fusiform (FIGURE 4-25). The most common site of true aneurysms is the abdominal aorta. A saccular aneurysm is a bulge on the side of the vessel. A fusiform aneurysm affects the entire circumference of the vessel. A false aneurysm, in contrast to true aneurysm, does not affect all three layers of the vessel but occurs when there is vessel damage. The damaged vessel causes blood to leak into the surrounding area (e.g., hematoma) or the injury leads to blood traveling and splitting the media layer. This splitting is known as a dissection (FIGURE 4-26). The larger the aneurysm, the greater the likelihood of rupture.
FIGURE 4-25 Types of aneurysms.
FIGURE 4-26 Aortic dissection.
Courtesy of Dr. Donald Yandow, Department of Radiology, University of Wisconsin School of Medicine and Public Health.
Clinical Manifestations
Clinical manifestations of aneurysms may vary based on their location. Most aneurysms are asymptomatic until they rupture. Before rupture, thoracic aorta aneurysms can cause pressure around surrounding areas such as the lungs and esophagus. This pressure causes dysphagia, chest pain, dyspnea, and cough. Abdominal aorta aneurysms may cause a pulsating abdominal mass as well as flank and back pain. Once an aneurysm rupture occurs, symptoms intensify (e.g., severe pain, worsening dyspnea) and cardiovascular collapse can occur due to life-threatening bleeding.
Diagnosis and Treatment
Diagnosis of aneurysms often occurs incidentally during a routine physical examination or during imaging studies (e.g., X-ray) done for other purposes. If clinical manifestations are present, diagnostic procedures are necessary to confirm the diagnosis and can include an echocardiogram, CT, MRI, and arteriography (i.e., angiography). The goal of treatment is to prevent rupture or limit expansion by eliminating or treating causes (e.g., controlling blood pressure). Management of cardiovascular risk factors can include statin and antiplatelet therapy. Smoking cessation is crucial as there is a high association of rupture with continuation of smoking. The presence of symptoms with an aneurysm increases the chance of rupture and surgical repair is often indicated. Even in the absence of symptoms surgical repair may be indicated. As an example, if an aortic aneurysm has a diameter greater than 5 cm, surgery may be done to prevent rupture even in an asymptomatic patient. The larger the aortic aneurysm, the higher the risk of rupture. There is a high mortality once rupture occurs, and immediate surgery is required. Screening for abdominal aortic aneurysm is recommended for men ages 65–75 years who have smoked or have a family history.
Dyslipidemia
Dyslipidemia, or hyperlipidemia, refers to an elevated level of lipids in the blood. These lipids include cholesterol and triglycerides (fats) and phospholipids. While cholesterol and fats are different types of lipids, the term cholesterol is often used in place of lipids and/or used interchangeably with fats. High lipid levels are associated with an increased risk and severity of cardiovascular diseases such as atherosclerosis, coronary artery disease, hypertension, and stroke. In the United States from 2013 to 2016, a total of 27% of people over the age of 20 had high cholesterol levels (i.e., ≥ 240 mg/dL) or were taking a cholesterol-lowering medication (CDC, 2017). Of the 27% total, approximately 29% were males and 25% were females. The prevalence of high cholesterol among those 6–19 years of age in the United States from 2011 to 2014 was 7.4% (CDC, 2019). In the younger age group, girls had a higher incidence than boys. In both the young and old, obesity is associated with a higher cholesterol level.
Lipids are not soluble in water or plasma, and while some lipids are hydrophobic, others have a hydrophilic component (e.g., phospholipid). For the lipids to be transported around the body, they have to be bound to a carrier protein such as an apolipoprotein. The bound lipids are termed lipoproteins. Lipids are important in providing and storing energy, cellular membrane composition, steroid hormone production (e.g., testosterone, estradiol), and production of bile acids.
Lipids are introduced into the bloodstream in two ways—diet and liver production (FIGURE 4-27). Dietary cholesterol is found in animal products, and dietary triglycerides are found in saturated fats (e.g., fried foods and cakes). Often the foods high in fats are also high in cholesterol. The human liver makes more cholesterol than the body could possibly use, so even though cholesterol is necessary for survival, eating it is not necessary. When dietary fats and cholesterol are ingested, they are transported around by chylomicrons (bundles of lipoproteins). These chylomicrons are found in the small intestine. The chylomicrons consist primarily of triglycerides (> 80%), and the remainder are phospholipids, cholesterol, and protein. Chylomicrons’ role, therefore, is to supply the tissues with fat from dietary ingestion. Remnants of chylomicrons are transported to the liver. In the liver, several lipoproteins are synthesized. Lipoproteins are classified according to their density. This density is based on the number of triglycerides, which are low in density, versus the number of proteins, which are highly dense (FIGURE 4-28 and FIGURE 4-29). In other words, triglyceride number and degree of density are inversely proportional. The main classes of lipoproteins are chylomicrons, very-low-density lipoproteins (VLDLs), low-density lipoproteins (LDLs), intermediate-density lipoproteins (IDLs), and high-density lipoproteins (HDLs). The highest triglyceride level (i.e., low density) starts with the chylomicrons and the level of triglyceride diminishes in the following order: VLDL, LDL, IDL, HDL. The most significant of these lipoproteins in terms of cardiovascular injury and protection are LDL and HDL.
FIGURE 4-27 Transportation of lipids in the blood.
FIGURE 4-28 Low-density lipoprotein and key protein, cholesterol, phospholipid, and triglyceride.
FIGURE 4-29 High-density lipoprotein and key protein, cholesterol, phospholipid, and triglyceride.
There are primary and acquired dyslipidemias. Acquired dyslipidemia is more common and development is usually polygenic and influenced by environmental factors (e.g., diet, obesity). Primary dyslipidemia is inherited and monogenic, and is often not related to external factors such as diet and it is not as common as acquired dyslipidemia. The primary dyslipidemias include disorders of triglycerides, apolipoproteins, cholesterol, or a combination. The most common primary dyslipidemia is hypercholesteremia, which is usually a result of LDL receptor mutation and defects in breakdown.
Learning Points
Triglycerides
Triglycerides are fats in blood. Fat is mainly stored in adipose tissue. Triglycerides are made of glycerol and three fatty acid chains. The fats can be saturated (have more hydrogen bonds) or unsaturated (have fewer hydrogen bonds). An unsaturated fat can be further divided into either monounsaturated and polyunsaturated. So what does this all mean in terms of lipids and diet? Saturated fat molecules are tightly packed, making them solid at room temperature. So think of butter, cooking lard, and cheese. Saturated fats are also high in animal products (meat and dairy) and plant-based oils such as coconut and palm kernel oil. Saturated fats have been associated with higher cholesterol levels, heart disease, stroke, and diabetes. Healthier types of fats are those that are monounsaturated or polyunsaturated. Examples of monosaturated fat sources include olive, canola, peanut, and sesame oils (nontropical oils) that are all in liquid form at room temperature. Monounsaturated fats are also found in avocados, peanut butter, and other nuts and seeds. Polyunsaturated fats are found in walnuts, soybeans, corn oil, sunflower, and tofu. Omega-3 and omega-6 fatty acids are types of polyunsaturated fats that can only come from dietary sources (i.e., essential fatty acids) and are found in sources such as salmon, chia, and flaxseed. Trans fats are actually unsaturated fats that are naturally found in small amounts in some food products (e.g., meats and dairy), and when consumed in small quantities, do not have negative health effects. However, trans fats have been produced artificially to make liquid vegetable oils more solid, resulting in a high quantity of trans fats in many food products (e.g., fried foods, doughnuts, cookies, icings, and processed snacks). Foods made with trans fats can be stored longer and are inexpensive to use, and trans fats add flavor and texture to food. Trans fats have a more negative impact on health than saturated fats, but both raise cholesterol levels as well as increase risk for heart disease, stroke, and diabetes. Trans fats are banned in cooking products in several parts of the United States. All fats, regardless of type, contain approximately 9 calories per gram. While there are many diets proposing a high fat consumption, recommendations from the American Heart Association (2014) are to reduce and replace saturated and trans fats for healthier monounsaturated and polyunsaturated fats.
Learning Points
Cholesterol
LDL is known as the” bad” cholesterol. because the small, dense molecules of LDL are damaging. Most serum cholesterol is made up of LDL. You can remember LDL as the “lousy” cholesterol. Because it is the bad cholesterol, you want the LDL level as low as you can get it. Ways to decrease LDL through lifestyle modifications include dietary changes such as avoiding high-cholesterol, high-fat foods.
HDL is known as the good cholesterol because it assists in removing some of the cholesterol from the bloodstream. You can remember this point by considering it the happy cholesterol. Because it is the “good” cholesterol, you want the HDL level as high as you can get it. Ways to increase HDL through lifestyle modifications include tobacco cessation and exercise.
Clinical Manifestations
Dyslipidemia is often asymptomatic until it develops into other diseases (e.g., atherosclerosis, coronary artery disease, or stroke). At that point, the symptoms are related to those diseases. Cholesterol screening and lipid profiles can identify specific lipid abnormalities. Further testing (e.g., angiography, ultrasound, and nuclear scanning) can be conducted to determine the development of other diseases and complications.
Diagnosis and Treatment
Diagnosis can be made by laboratory analysis of a comprehensive lipid panel. Other diagnostic tests that can be used to aid in cardiovascular risk identification or in determining treatment options include the ankle brachial index, calcium score, and inflammatory markers such as C-reactive protein and lipoprotein-associated phospholipase-A2. The goal of treatment is to normalize lipid levels and prevent complications. The commonly used clinical guideline for cholesterol management has been developed and updated by multiple organizations such as the American College of Cardiology and the American Heart Association (Grundy et al., 2018). Treatment regimens to lower lipid levels include lifestyle modifications such as consumption of low-cholesterol, low-fat foods, routine exercise, and weight reduction. Pharmacologic treatment is predominantly based on LDL levels and other clinical criteria (e.g., cardiovascular disease or risk). Pharmacologic agents should be initiated in all patients over 21 years old with clinical atherosclerotic cardiovascular disease (ASCVD) and in those with LDL levels ≥ 190 mg/dL. Examples of ASCVD include angina, myocardial infarction, peripheral artery disease, stroke, or transient ischemic attack. For those between the ages of 40 and 75 years who have diabetes mellitus and/or atherosclerotic risk (i.e., > 5%), pharmacologic therapy may be necessary in addition to lifestyle modifications. Atherosclerotic risk can be calculated using age, sex, race, blood pressure, total cholesterol, LDL and HDL levels, history of diabetes, and hypertension. Online calculators (e.g., www.cvriskcalculator.com/) and mobile applications can be used to provide a risk calculation. In patients under 21 years old and in those over 75 years, risk of cardiovascular disease and pharmacologic versus benefits must be individually evaluated.
While a wide range of lipid-lowering pharmacologic agents exists, pharmacologic treatment primarily focuses on use of HMG-CoA reductase inhibitors (also known as statins). HMG-CoA reductase is an enzyme used by the liver during the manufacture of cholesterol and inhibition will therefore decrease production. Statins also facilitate breakdown of LDL so that cholesterol can be reabsorbed. Statin therapy is either moderate or high intensity. Moderate-intensity therapy refers to lowering LDL levels by ≥ 50% (e.g., atorvastatin 10–20 mg or rosuvastatin 5-10 mg), while high-intensity therapy refers to lowering LDL by 30–50% (e.g., atorvastatin 40–80 mg or rosuvastatin 20-40 mg). Other pharmacologic agents are not commonly prescribed but include bile acid sequestrants, cholesterol absorption inhibitors, nicotinic acid, fibrates, and omega-3 fatty acids. In 2017, the Food and Drug Administration approved a new medication, evolocumab, that works by increasing liver clearance of LDL by inhibiting the protein PCSK9. This protein usually decreases the number of receptors involved in LDL clearance, and thereby inhibition will increase the number of receptors available for LDL clearance.

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