Unit 5 Case Connection

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Jasmeet Kaur Medical Biochemistry Professor LeClair 06 August 2023 Unit 5- Case Connection In Case 2, there is a 53-year-old male with a past medical history of obesity, borderline diabetes and has abnormal liver enzymes. There is a family history of liver cirrhosis and upon physical examination it is determined that the patient has mild hepatomegaly (enlarged liver). A panel of lab tests revealed the following: aspartate aminotransferase (AST) 106 (normal range 10 – 40 U/L), alanine aminotransferase (ALT) 118 (normal range 7 – 56 U/L), with normal bilirubin. He had a liver ultrasonography that showed diffuse increase in echogenicity and vascular blurring consistent with fatty infiltration. It is suspected that the patient has nonalcoholic fatty liver disease or NAFLD. Non-alcoholic fatty liver disease is the most common cause of hepatomegaly which is accumulation of fat in the liver which occurs in people who do not drink or consume alcohol. Not only does NAFLD cause liver fat accumulation, but it also causes insulin resistance and metabolic changes. The body’s cells do not respond well to insulin, and this causes high blood sugar levels and since the liver is an important component of glucose regulation it affects glucose metabolism, as well. The patient already has a family history of cirrhosis and if the patient is not treated then it can lead to liver failure. Taking everything into consideration this patient needs to make healthy lifestyle modifications to maintain proper VLDL metabolism and cardiovascular health. VLDL stands for very-low-density lipoprotein which is produced by the liver and is important when it comes to transporting triglycerides, which is a form of fat, from the liver to
other tissues in the body. They are then utilized or stored for energy. VLDL also contains cholesterol, fatty acids and a form of protein called apolipoprotein. Triglycerides are produced in the liver from extra fatty acids or from dietary carbohydrates and fats. The VLDL particles are created from triglycerides, cholesterol, and other lipids. The assembly of the VLDL particles takes place in the endoplasmic reticulum and apolipoprotein B, that helps carry fat and cholesterol, is synthesized, and combined with triglycerides and other lipids such as apolipoprotein C1 and apolipoprotein E. Once the VLDL particles fully assemble they are transported from the Golgi Apparatus to the cell surface and then into the bloodstream. As these circulate, APO CII is also added, which is a potent activator for lipoprotein lipase, which is an enzyme found on blood vessels that releases free fatty acids and glycerol. The apolipoproteins play an important role when it comes to metabolism. As VLDL particles undergo lipolysis, they lose APO C and the particles then become smaller and modify to intermediate density lipoprotein and then thru hydrolysis they form into low-density lipoprotein which is a primary carrier of cholesterol. When VLDL metabolism is occurring and IDL is formed they also lose APO E to convert to LDL. Both APO C and APO E return to HDL. The remaining VLDL particles are cleared from the bloodstream through uptake by the liver. LDL particles are taken by receptor- mediated endocytosis and IDL and VLDL particles are taken by other receptor pathways and the remaining convert to high- density lipoprotein which is referred to as good cholesterol which pick up excess cholesterol from tissues returning it to the liver for removal. When there is a disruption in lipid metabolism and the liver is exposed by an excessive number of fatty acids from the bloodstream it leads to NAFLD development. This imbalance leads to an accumulation of triglycerides in the liver cells. NAFLD is associated with obesity, insulin resistance and metabolic syndrome. In other words, NAFLD occurs due to accumulation
of free fatty acids and triglycerides in the liver due to insulin resistance and obesity. Insulin regulates blood sugar levels and controls how the body uses and stores glucose and when it becomes resistant it releases free fatty acids which can lead to fat accumulation on the liver. Obesity also leads to NAFLD, and it affects liver metabolism and fat on the liver. An imbalance between fatty acid intake, production, and export may result from the liver being exposed to many fatty acids from the bloodstream. The buildup of triglycerides in liver cells may result from this imbalance. The patient lab work and medical conditions and family history suggest that he does have NAFLD and to maintain proper VLDL metabolism and cardiovascular health it is important that patient loses weight, adopt a healthy diet, exercise, and manage diabetes and hypertension. In Case 3, a 48-year-old female presents her conditions of worsening fatigue and chest pain. Over the past two years, she has also gained weight and currently is 253 pounds. Based on the lab results and lipid levels it is evident that the patient has diabetes and is obese. The fasting blood glucose levels are 221 and 196 mg/dl, milligrams per deciliter which are way above the normal range of 70-105 mg/dl suggesting that the patient has diabetes, most likely Type 2 because she is obese as well. This means there is insulin deficiency and resistance. Since the insulin is resistant it causes the lipid metabolism to be out of order. The LDL, triglyceride, and total cholesterol levels are high due to the insulin being absent there is more lipolysis then lipogenesis. The HGBA1C is high due to low insulin. Since she has chest pains also it means that there is inflammation and there is a cardio c-reactive protein which leads to the lipid profile lab to be high, and the blood pressure is 160/80 which shows that she is hypertensive due to diabetes. Insulin and glucagon are hormones involved in glucose or blood sugar homeostasis and based on the findings she might need treatments that reduce plasma cholesterol.
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There are three treatment plans that are recommended to the patient which are statins, PCSK9 inhibitors or bile acid sequestrants. All these treatments are cholesterol-lowering therapies. First, satins is a drug that lowers the cholesterol by blocking a substance in the body that is needed to make cholesterol. The substance that it blocks is HMG-CoA reductase, 3- hydroxy-3methylglutaryl- coenzyme A reductase, which is found in the liver and is a rate- limiting enzyme for cholesterol synthesis. By blocking it, the drug leads to the liver not producing cholesterol and reduces the production of mevalonate, which is a crucial step in cholesterol biosynthesis, leading to a decrease in the plasma cholesterol levels. Some of the side effects of this drug are muscle pain, weakness, liver enzyme elevation, nausea, bloating, diarrhea, and in rare cases sometimes it causes an allergic reaction. Second, PCSK9 inhibitors is a new class of drug that lowers low-density lipoprotein or bad cholesterol. They block the enzyme PCSK9 which stands for Proprotein Convertase Subtilisin/Kexin type 9 which is produced in the liver and regulates the number of LDL receptors and by injecting it increases the number of LDL receptors leading to the removal of LDL cholesterol from the bloodstream, lower plasma cholesterol levels. The way it works is that when injected the immune system recognizes it and it gets removed from the bloods stream and since that happens more LDL receptors remain on the cell surface, and this leads to reducing plasma LDL cholesterol levels. Some of the side effects of PCSK9 are upper respiratory tract infections, allergic reactions, and injection site reactions such as redness, swelling, and pain. Third, bile acid sequestrants is a group of drugs that binds to bile acids in the intestines. Bile acid is created in the liver from cholesterol and is important when it comes to the breakdown and absorption of lipids. Sequestrants, which are positively charged resins limit the reabsorption of bile acids by binding
them and this causes the liver to use more cholesterol and produce new bile acids. Since there is an increase demand for cholesterol in bile acid synthesis it leads to more cholesterol being drawn from the bloodstream leading to lower plasma cholesterol levels. Some of the side effects of bile acid sequestrants is constipation, bloating, gas, abdominal discomfort, decrease of fat-soluble vitamins such as A, D,E, and K and elevated triglycerides. It is important that the patient takes everything into consideration and chooses the best possible therapy to reduce plasma cholesterol.
References Jennifer Moll, P. (2023, August 1). How bile acid sequestrants work . Verywell Health. https://www.verywellhealth.com/what-are-bile-acid-sequestrants-697489 Jiang, Z. G., Robson, S. C., & Yao, Z. (2013, January). Lipoprotein metabolism in nonalcoholic fatty liver disease . Journal of biomedical research. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3596749/ Mayo Foundation for Medical Education and Research. (2021, September 22). Nonalcoholic fatty liver disease . Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/nonalcoholic-fatty-liver-disease/ symptoms-causes/syc-20354567 professional, C. C. medical. (n.d.-a). PCSK9 inhibitors: How they manage cholesterol and side effects . Cleveland Clinic. https://my.clevelandclinic.org/health/drugs/22550-pcsk9- inhibitors professional, C. C. medical. (n.d.-b). Statins: Types, uses & side effects . Cleveland Clinic. https://my.clevelandclinic.org/health/treatments/22282-statins Very low density lipoprotein . Very Low Density Lipoprotein - an overview | ScienceDirect Topics. (n.d.). https://www.sciencedirect.com/topics/neuroscience/very-low-density- lipoprotein
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