Juxtapid In Familial Hypercholesterolemia Case Study

A higher level of fats in the body puts the patient at higher risk for Cardiovascular diseases(CAD). The patient's' family has a history of CAD. Her mom and one of her sister have CAD (Lewis et al., 2014, pp. 733-734). The patient states that she has been taking her meds for cholesterol atorvastatin regularly. Her lipase level was 8272 on 11/11/16 and 2829 on 11/12/16 U/L 1069 on 11/13/16 (Ref range 73-393 U/L). Her HDL cholesterol level was 21 ( ref range>49 mg/dl), LDL Cholesterol level 148 ( ref range: <130 mg/dL). Patient statin drug was on hold because it is contradicted on the patient with an elevated level of ALT 80, 61(Ref range 0-50 U/L) and AST 61 on 11/12/16 and 64 on 11/13/16 (ref range 0-45 U/L). The uncontrolled level of could be the cause of concern for stroke or acute myocardial

High cholesterol is a dangerous disease that can lead to many life-threatening ailments, and can be lowered by eating healthy, while maintaining a balanced diet of leveled cholesterol. Cholesterol, the sleek-fat like substance that roams in the blood of a body. It is vital to life, but when there is too much intake of cholesterol, it can cause the body to malfunction and cause problems. There are two types of cholesterol HDL and LDL, which varies in the amount of protein and cholesterol it holds Too much cholesterol in a body is dangerous, and surprisingly, has no symptoms. The two main types of cholesterol are HDL and LDL, HDL helps reduce the chances of chronic heart disease, whereas LDL is the main reason for plaque build-up in artery

MR. David likewise takes atorvastatin (Lipitor); 10 mg every day, for hypercholesterolemia (hoisted LDL cholesterol, low HDL cholesterol, and raised triglycerides). He has endured this medicine and holds fast to the day by day plan. Amid the previous 6 months, he has likewise taken chromium picolinate,

Current guidelines state that ezetimibe,is considered the best alternative for LDL reduction and tolerability in statin-intolerant patients and considered an adjuvant in this trial. The primary end point was percentage change from baseline to week 12 in LDL cholesterol. Other end points included measures of safety and tolerability of different doses of AMG145 and AMG145 plus ezetimibe. Other objectives included assessment of the safety and tolerability of 3 different doses of AMG145 and AMG145 plus ezetimibe compared with placebo plus ezetimibe. One hundred sixty patients were randomized into 5 groups, to take AMG 145 as monotherapy once a month at 280mg, 320mg and 420mg, to take AMG 145 420mg once a month with ezetimibe 10mg daily or placebo once a month with ezetimibe 10mg daily. At week 12 the AMG 145 groups had a percent change of blood levels of LDL from baseline from -40.8 % to -50.7 % dose ascending monotherapy and -63.0% with combination with ezetimibe versus -14.8% with combination of placebo and ezetimibe. Reduction in total cholesterol percentwise was from -29.8 % to -37.7 % dose ascending monotherapy and -43.3% with combination with ezetimibe versus -10.7% with combination of placebo and ezetimibe. The overall incidence of all adverse effects was similar among patients receiving

The examples of drugs in this class are atorvastatin (Lipitor), rosuvastatin (Crestor), and simvastatin (Zocor). Statins is the first line to use for lowing blood cholesterol levels. Statins works by blocking the enzyme called HMG-CoA reductase in the liver which is necessary for making cholesterol. The statins blocks the active site of the HMG-CoA reductase enzyme so that it cannot converse to mevalonate. Therefore, there is more LDL receptor available in the liver. These receptors bind to passing LDL and VLDL (very low-density lipoprotein). The LDL and VLDL then enter the liver and are digested. So that there is less LDL level in blood stream. Even though, many drugs are in the same class, but the effectiveness of each drug is different. For example, 5-40 mg of Crestor seems to work best by lowering LDL by 47-65%; whereas 10-40 mg of pravachol can lower LDL by 22-34%. Most people who take statins do not experience serious side effects. The most common minor side effects include headache, pins and needle sensations, abdominal pain, bloating, diarrhea, feeling sick, and a rash. The provider normally starts statins in a low. The dosage may be increased if this target is not reached. Statins are contradicated in patient with active liver disease and consume a large amount of alcohol. The common side effects are GI upset and

Familial hypercholesterolaemia (FH) is an autosomal, dominant, inherited disorder of lipoprotein metabolism that results in elevated low-density lipoprotein cholesterol (LDL) in plasma concentration (Henderson, O’kane, McGilligan, & Waterson, 2016). FH can dramatically increased risk of atherosclerosis, which can lead to a common genetic cause of premature coronary heart disease (CHD). It is crucial for patients to know their genetic family history and genogram to have early diagnosis, treatments, and follow ups that may delay the complications of the course of FH and consequently CHD or other cardiovascular diseases (CVD). The proband is paramount in identifying other at-risk individuals; hence, enabling, and educating these patients to discuss the risk with family members is essential. Nurses need the knowledge of FH genetic standpoint to educate patients and make appropriate referrals for individuals in need of genetic counseling. The purpose of this paper is to complete a genetic family history of an individual of choice. Construct a genogram and attach it to this paper as an Appendix. Provide and explanation of the genogram

You should start on your life's work in regards to cholesterol testing at about the age of 20; while it is likely that your levels should be normal at that time of your life, it would provide a baseline for your doctor. A test can follow every five years until symptoms of high cholesterol become evident when cholesterol testing would become more frequent. The lipoprotein profile shows levels for good and bad cholesterol.

Heredity – Some people are born with a genetic pre-disposition to forming high cholesterol called familial hypercholesterolemia.

Atherosclerotic research has recently concentrated on inflammatory cytokines involved in vascular inflammation and how they stimulate the production of endothelial adhesion molecules, which could enter circulation in soluble form, and have the cytokines stimulate the production of messenger cytokine interleukin-6, which incites the liver production of acute-phase reactants such as C-reactive protein to increase. (Packard et al., 2007) In short, cytokines released into the bloodstream have a tendency to bring about an inflammatory response. Researchers have also found that that treatment with lipid-reducing agents is correlated with reduced morbidity and mortality from coronary heart disease and it seems to work near the atherosclerotic lesion, causing stabilization, slowed progression and, in some cases, regression of lesions. (Blankenhorn, 1989) In research it is well know that one human risk factor for atherosclerosis is hypercholesterolemia, which is when total cholesterol and low-density lipoprotein cholesterol are elevated. (Genis et al., 2000) There are more contributors and characteristics of hypercholesterolemia, which include inflammatory responses to oxidative stress,

Statins lower the concentration of low-density lipoprotein cholesterol and very-low-density lipoprotein cholesterol in people with elevated triglycerides. Many

What is the probable genetic causation of excessive cardiovascular disease in the Family pedigree presented? Are any lifestyle issues causing an exacerbation or alleviation of this disease?

Fluvastatin is a highly regarded drug that is involved with treating hypercholesterolemia and preventing cardiovascular disease. The drug is used to lower both high cholesterol and triglycerides levels. The drug is able to perform this task by increasing good cholesterol levels (HDL) while, at the same time, reducing bad cholesterol levels (LDL). Fluvastatin decreases the production of bad cholesterol by blocking the action of the enzyme HMG- CoA reductase in the liver. This results in a decrease in the amount of cholesterol in liver cells and subsequently leads it

And what’s worse is that the cholesterol synthesis pathway doesn’t just make LDL cholesterol; branches of this same pathway are liable for synthesizing a wide type of different important molecules along with nutrition A, nutrition E, diet ok, and Coenzyme Q. So, you could want to suppose twice before you artificially intrude with this pathway by taking a statin drug.

Joseph is a 39-year-old male who suffers from pure hypercholesterolemia (E78.0), along with hypertension, mild cardiomyopathy, non-sustained ventricular tachycardia and abnormal liver function. His most recent lab reports his cholesterol at 248, triglycerides 150, HDL 48, LDL 170. Joseph has tried and failed various treatments including liptor and zetia, with his cholesterol levels being sub-optimally controlled. Your reason for denial was due to his diagnosis. Repatha is not a statin, but works differently as a PCSK9 inhibitor that targets a protein in the liver called proprotein convertase subtilisin kexin 9, or PCSK9. By reducing the amount of PCSK9 in the body, PCSK9 inhibitors allows the body to remove cholesterol more efficiently.

Many years of scientific studies have shown a close relationship between cardiovascular disease and cholesterol levels. Your doctor may request a lipid profile—a test that shows the levels of LDL (bad cholesterol), HDL (good cholesterol), and triglycerides in your blood—to assess your risk for developing heart disease.