TPS UCSD Board LDL Cholesterol Lowering Therapies Discussion
TPS UCSD Board LDL Cholesterol Lowering Therapies Discussion
For your replies, select the threads of at least 2 classmates that discuss a drug other than the class you selected and contrast the mechanism of that drug with the mode of action of PCSK-9 inhibitors (discussed in the second website). Which one seems to be better for patients?
attached 2 discussion board posts of my classmates, I need one reply for each one ( total = 2 replies)
I can also attached an example of the replies to those same post so you can get the idea and write it in your own way
Nician is my post attached
and Ezetimibe and Fibrates are for the other 2 posts that I also attached
( on the top of the post you see the Nician )
Explanation & Answer length: 500 Words Each5 attachmentsSlide 1 of 5
UNFORMATTED ATTACHMENT PREVIEW
Pathology Study Rough Draft Grading Rubric Based on 75-point maximum Criteria Content 70% Thread: Content Structure 30% Rough Draft Audio PowerPoint Submission and Currency of Article (20%) Structure: Grammar and Spelling, Levels of Achievement Advanced 90-100% Proficient 70-89% 47 to 52 points 37 to 46 points The Audio PowerPoint version of the Presentation is properly submitted with 70%89%.of topical area covered in the outline. 4 of the 5 areas of discussion (Historical Background of Pathology; Epidemiology of Illness; Signs and Symptoms of Pathology; Diagnostic Testing for Pathology; and Treatment Modalities: Past, Present and Future for Pathology. Advanced 90-100% Proficient 70-89% 13 to 15 points 10 to 12 points The Audio PowerPoint version of the presentation bibliography is missing or is not using articles published less than 5 years ago. The Audio PowerPoint version of the presentation is not initially submitted as a PDF version or is missing some publication information within the submission box. 5 to 6 points The Audio PowerPoint version of the presentation bibliography shows and uses articles published less than 5 years ago. The Audio PowerPoint version of the presentation is properly submitted. The student includes an updated bibliography. 7 to 8 points Developing 1-69% 1 to 36 points The Audio PowerPoint version of the Presentation is properly submitted with less than 70% of topical area covered in the outline. Developing 1-69% Not present 0 points Not Submitted Not present 1 to 9 points 0 points The Audio PowerPoint Not Submitted version of the presentation bibliography is missing or is not using articles published less than 5 years ago. The Audio PowerPoint version of the presentation is not initially submitted as a PDF version or is missing most of the publication information within the submission box. 1 to 4 points 0 points Not Submitted Turabian formatting (10%) Spelling and grammar are correct. Sentences are complete, clear, and concise. Paragraphs contain appropriately varied sentence structures. Where applicable, references are cited in current APA edition. Spelling and grammar has some errors. Sentences are presented as well. Paragraphs contain some varied sentence structures. Where applicable, references are cited with some current APA edition. Spelling and grammar errors distract. Sentences are incomplete or unclear. Paragraphs are poorly formed. Where applicable, references are minimally or not cited in current APA edition on both the original and reply posts. BIOM 630 PATHOLOGY STUDY ROUGH DRAFT INSTRUCTIONS Your rough draft must show that you have researched each of the 5 areas (Historical Background: Past, Present, and Future of the Pathology; Epidemiology of the Pathology; Signs and Symptoms of the Pathology; Diagnostic testing for the Pathology; and Treatment Modalities: Past, Present, and Future for the Pathology) and include: • • • At least 3 slides from each area with audio Bibliography slide Introduction slide with a picture or video introducing yourself with audio. Submit your Pathology Study Rough Draft by 11:59 p.m. (ET) on Sunday of Module/Week 5. Niacin Introduction Cholesterol is a lipid that plays a vital role in the molecular make-up of cells that make up the body. However, when there is an excess of cholesterol found in the body, it has an adverse effect on many organs. One of the main organs affected by an excess in cholesterol is the heart, high levels of LDL result in the apoptosis of tissue in the vessels of the heart, causing coronary infarction (Michihiro & et, 2015). Genetic mutations or other factors may cause defects in the LDL-receptors, forming a resistance against statin. In patients that are statin resistant, alternative therapies such as niacin can be used Compare and Contrast Niacin vs Statin LDL-Cholesterol is synthesized in the liver; the drug, statin, targets the LDL produced in the liver and inhibits the production. The inhibition of HMG CoA reductase causes a depletion of cholesterol in the body, inducing the body to utilize the excess cholesterol in the blood. The utilization restores cholesterol homeostasis and increases HDL- cholesterol (Kotowade & et, 2013). In comparison to the statin drug, the mechanism of action in niacin is similar. Niacin inhibits HMG CoA reductase in the liver, lowering the LDL-cholesterol by forcing the body to use up the excess cholesterol in the body. The increase in HDL-cholesterol is predominant and prevents the risks of coronary disease and plaque. Taken at the correct prescribed dosage, niacin (a form of vitamin b3) has shown to be effective against lowering LDL-cholesterol levels (Kamanna & Kashyap, 2008). However, both drugs show a similar mechanism of action, but their efficacy differs in many aspects. Niacin has lower efficacy in decreasing LDL-cholesterol than statin does, but niacin increases HDL-cholesterol more than statin. The common side effects of statin include muscle ache, nausea, headache, GIT complications, and a rash. Statin shows many more adverse side effects than niacin, which shows side effects such as stomach complications and cutaneous itchiness. Statin’s efficacy lowers triglyceride levels, mainly LDL-cholesterol more effectively than niacin but the side effects are more harmful and higher than niacin. A disadvantage of niacin would be the demand to have high levels of the drug consistently through dietary and supplemental pathways, in comparison to statin (D’Andrea, Hay, Ramirez, & Kesselheim, 2019). However, niacin is a good alternative for patients that are resistant to statin or patients with cardiovascular disease, it is not recommended for patients that suffer from ulcers, irritable bowel syndrome, or other gastrointestinal issues. The endothelial effects of niacin can be lethal in patients that are compromised with these additional ailments (Kotowade & et, 2013). Although niacin can be lethal, statin has similar properties in patients with hypotonia or muscle deformities. A significant side effect of statin may cause muscle weakness and contractile inhibitions in combination with hepato- endothelial depletion. Both niacin and statin pose many similarities and differences, each connected with various complications. These drugs are patient-dependant and will display different efficacy percentages according to the patient’s needs. Fibrates Low Density Lipoproteins are major carriers of cholesterol in humans and are responsible for supplying cholesterol to tissues with sterol demands. (Clay, 2020) When cells need cholesterol for membrane synthesis it creates transmembrane receptor proteins for LDL inserting them into the plasma membrane. Once there the receptors diffuse until associated with clathrin-coated pits and an endocytosis signal in the cytoplasmic tail of LDL receptors bind to the membrane-bound adaptor protein AP2 after it is unlocked by binding to PI (4,5) P2 on the plasma membrane. These bound LDL particles are then rapidly internalized and deliver their contents to early endosomes. LDL is released from its receptor and is delivered via late endosomes to lysosomes. Cholesterol esters in LDL particles are hydrolyzed into free cholesterol, available for new membrane synthesis, though if too much free cholesterol accumulates in a cell it shuts off cholesterol and LDL synthesis in order to cease both. (Alberts, 2015) This pathway is disrupted in individuals who inherit defective genes that encode LDL receptors, resulting in high level of blood cholesterol, which predisposes these individuals to develop atherosclerosis and death at an early age due to coronary artery disease. In other individuals with elevated levels of LDL they may be lacking the receptor, have defective receptors in either the extracellular binding site or the site that attaches to AP2 adaptor proteins in clathrin-coated pits. (Alberts 2015) LDL’s are most often associated with causing atherogenic plaque formation as LDL levels can be elevated in individuals who consume large amounts of saturated fat or cholesterol. The endothelium lining the artery takes up circulating LDL’s depositing and trapping them in the arterial intima. There the LDL’s undergo oxidation and other modifications stimulating atherogenisis. (Clay, 2020) There are several different forms of therapies or treatment to reduce low density lipoprotein levels, though the most common is use of statins. They work to inhibit cholesterol biosynthesis, upregulate LDL receptors, and enhance LDL clearance by inhibiting HMG CO-A reductase inhibitors. (Mason, 2016) Common side effects experienced with use of statins include headaches, nausea, muscle and joint aches, and in more serious cases increased blood sugar, muscle cell damage, liver damage, and memory problems. (Statins: Are these cholesterol-lowering drugs right for you?, 2021) Aside from statins another effective for of elevated numbers of Low-density lipoproteins are Fibrates. They activate PPARа, which increases fatty acid oxidation, increases apoAI, LPL, and apoll, while also lowering triglycerides, decreasing apoCill and raising HDL. They are commonly used in severe cases of hypertriglyceridemia and hyperlipidemia and should be avoided in patients with renal insufficiency as it can predispose these individuals to myopathy. Side effects may include gastrointestinal discomfort, rash, and pruritis, and combination of fibrates with gemfibrozil and most statins is often associated with increased risk of myopathy due to increased statin levels in the blood. Fibrates are more effective at lowering serum triglyceride/VLDL than statins, therefore they are useful for treatment of dyslipidemia associated with diabetes and metabolic syndromes. (Mason, 2016) Ezetimibe The presence of blood cholesterol comes from two sources – hepatic cholesterol excretion and dietary intake. While cholesterol from the liver makes up about 75% of blood cholesterol, intestinal absorption accounts for the remaining 25%. Because of this, my proposal includes adding an intestinal-absorption-prevention medication to a statin-resistant patient’s medication regimen. An example of this type of medication is Ezetimibe. This drug functions to reduce intestinal uptake of cholesterol, reducing blood cholesterol levels by up to 25%. Typically, the intestines absorb cholesterol through enterocyte membrane sterol influx transporters. There is a particular class of these transporters, a protein referred to as the Niemann-Pick C1-like protein, referred to as NPC1L1. NPC1L1 facilitates the transport of cholesterol-containing micelles from the intestinal lumen to the enterocyte. It works in conjunction with another protein, adaptor protein 2 (AP2), and clathrin in a complex micelle uptake system. (Phan et. Al., 2012) Ezetimibe binds to NPC1L1, specifically in the jejunal brush border, inhibiting the protein’s transporting duties. Specifically, it is thought to disrupt the NPC1L1/AP2/clathrin bond, disabling the ability of NPC1L1 to bind with micelles. (Phan et. al., 2012) The inhibition of NPC1L1 creates a cascade of events. Cholesterol absorption into enterocytes is limited, chylomicron creation and secretion are thus reduced, and hepatic pools of cholesterol are depleted in an attempt to maintain enterocytic cholesterol levels. After depletion, the result is reduced serum LDL. (Phan et. Al., 2012) When used alone (rather than in conjunction with statins as it is typically used), Ezetimibe reduces LDL by an average of 18.5%. HDL increases by an average of 3%, triglycerides reduce by 8%, and total cholesterol reduces by 13%. Therefore, an overall improvement in patient health can be expected. (Phan et. Al., 2012) Unwanted physiological effects of Ezetimibe are limited to an increase in liver enzymes, such as transaminase. Adverse events related to Ezetimibe are infrequent. Liver failure while taking this medication has been documented but in minimal quantities. Long-term side effects that may occur when taking Ezetimibe include drowsiness, and temporary side effects include diarrhea, joint pain, and viral susceptibility. (Ezetimibe: Side effects, dosages, uses and more, 2018) In comparison, statins’ mechanism of action includes the inhibition of MHG-CoA reductase. This enzyme’s responsibility is catalyzing the step of the cholesterol synthesis pathway comprising the conversion of HMG-CoA to mevalonate. This means that in the presence of statins, the synthesis of cholesterol will be reduced. The cholesterol-lowering effects of statins are an average of 35% reduction in LDL, an average of 8% increased HDL, and 23% overall reduction in cholesterol. (Sizar et. Al., 2021) Unwanted physiological effects of statins include elevated transaminases, myopathy, rhabdomyolysis, diabetes mellitus, and hepatotoxicity. Side effects that may be experienced by a patient taking statins include muscle joint and muscle pain, inflammation, confusion, headache, drowsiness, dizziness, diarrhea, bloating, and less common symptoms include hair loss, nausea, numbness, stomach and liver pain, rashes, low sex drive, and erectile dysfunction. (Side effects of cholesterol-lowering statin drugs, 2012)(Kapur, 2008) Statins appear to be more effective in improving LDL, HDL, and overall cholesterol levels in patients with cholesterol-related pathology. However, the side effects of Ezetimibe are much less numerous and severe than those of statins. Additionally, as mentioned in the prompt, some patients do not respond as they should to statins. Therefore, Ezetimibe is an excellent alternative as it still demonstrates efficacy (though reduced) and has more minor side effects. (Ezetimibe: Side effects, dosages, uses and more, 2018) References Ezetimibe: Side effects, dosage, uses, and more. (2018). https://www.healthline.com/health/ezetimibe-oral-tablet Kapur, N. (2008). Clinical efficacy and safety of statins in managing cardiovascular risk. Vascular Health and Risk Management, 4(2), 341-353. https://10.2147/VHRM.S1653 Phan, B. A. P., Dayspring, T. D., & Toth, P. P. (2012). Ezetimibe therapy: Mechanism of action and clinical update. Vascular Health and Risk Management, 8, 415-427. https://10.2147/HRM.S33664
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TPS UCSD Board LDL Cholesterol Lowering Therapies Discussion
For your replies, select the threads of at least 2 classmates that discuss a drug other than the class you selected and contrast the mechanism of that drug with the mode of action of PCSK-9 inhibitors (discussed in the second website). Which one seems to be better for patients?
attached 2 discussion board posts of my classmates, I need one reply for each one ( total = 2 replies)
I can also attached an example of the replies to those same post so you can get the idea and write it in your own way
Nician is my post attached
and Ezetimibe and Fibrates are for the other 2 posts that I also attached
( on the top of the post you see the Nician )
Explanation & Answer length: 500 Words Each5 attachmentsSlide 1 of 5
UNFORMATTED ATTACHMENT PREVIEW
Pathology Study Rough Draft Grading Rubric Based on 75-point maximum Criteria Content 70% Thread: Content Structure 30% Rough Draft Audio PowerPoint Submission and Currency of Article (20%) Structure: Grammar and Spelling, Levels of Achievement Advanced 90-100% Proficient 70-89% 47 to 52 points 37 to 46 points The Audio PowerPoint version of the Presentation is properly submitted with 70%89%.of topical area covered in the outline. 4 of the 5 areas of discussion (Historical Background of Pathology; Epidemiology of Illness; Signs and Symptoms of Pathology; Diagnostic Testing for Pathology; and Treatment Modalities: Past, Present and Future for Pathology. Advanced 90-100% Proficient 70-89% 13 to 15 points 10 to 12 points The Audio PowerPoint version of the presentation bibliography is missing or is not using articles published less than 5 years ago. The Audio PowerPoint version of the presentation is not initially submitted as a PDF version or is missing some publication information within the submission box. 5 to 6 points The Audio PowerPoint version of the presentation bibliography shows and uses articles published less than 5 years ago. The Audio PowerPoint version of the presentation is properly submitted. The student includes an updated bibliography. 7 to 8 points Developing 1-69% 1 to 36 points The Audio PowerPoint version of the Presentation is properly submitted with less than 70% of topical area covered in the outline. Developing 1-69% Not present 0 points Not Submitted Not present 1 to 9 points 0 points The Audio PowerPoint Not Submitted version of the presentation bibliography is missing or is not using articles published less than 5 years ago. The Audio PowerPoint version of the presentation is not initially submitted as a PDF version or is missing most of the publication information within the submission box. 1 to 4 points 0 points Not Submitted Turabian formatting (10%) Spelling and grammar are correct. Sentences are complete, clear, and concise. Paragraphs contain appropriately varied sentence structures. Where applicable, references are cited in current APA edition. Spelling and grammar has some errors. Sentences are presented as well. Paragraphs contain some varied sentence structures. Where applicable, references are cited with some current APA edition. Spelling and grammar errors distract. Sentences are incomplete or unclear. Paragraphs are poorly formed. Where applicable, references are minimally or not cited in current APA edition on both the original and reply posts. BIOM 630 PATHOLOGY STUDY ROUGH DRAFT INSTRUCTIONS Your rough draft must show that you have researched each of the 5 areas (Historical Background: Past, Present, and Future of the Pathology; Epidemiology of the Pathology; Signs and Symptoms of the Pathology; Diagnostic testing for the Pathology; and Treatment Modalities: Past, Present, and Future for the Pathology) and include: • • • At least 3 slides from each area with audio Bibliography slide Introduction slide with a picture or video introducing yourself with audio. Submit your Pathology Study Rough Draft by 11:59 p.m. (ET) on Sunday of Module/Week 5. Niacin Introduction Cholesterol is a lipid that plays a vital role in the molecular make-up of cells that make up the body. However, when there is an excess of cholesterol found in the body, it has an adverse effect on many organs. One of the main organs affected by an excess in cholesterol is the heart, high levels of LDL result in the apoptosis of tissue in the vessels of the heart, causing coronary infarction (Michihiro & et, 2015). Genetic mutations or other factors may cause defects in the LDL-receptors, forming a resistance against statin. In patients that are statin resistant, alternative therapies such as niacin can be used Compare and Contrast Niacin vs Statin LDL-Cholesterol is synthesized in the liver; the drug, statin, targets the LDL produced in the liver and inhibits the production. The inhibition of HMG CoA reductase causes a depletion of cholesterol in the body, inducing the body to utilize the excess cholesterol in the blood. The utilization restores cholesterol homeostasis and increases HDL- cholesterol (Kotowade & et, 2013). In comparison to the statin drug, the mechanism of action in niacin is similar. Niacin inhibits HMG CoA reductase in the liver, lowering the LDL-cholesterol by forcing the body to use up the excess cholesterol in the body. The increase in HDL-cholesterol is predominant and prevents the risks of coronary disease and plaque. Taken at the correct prescribed dosage, niacin (a form of vitamin b3) has shown to be effective against lowering LDL-cholesterol levels (Kamanna & Kashyap, 2008). However, both drugs show a similar mechanism of action, but their efficacy differs in many aspects. Niacin has lower efficacy in decreasing LDL-cholesterol than statin does, but niacin increases HDL-cholesterol more than statin. The common side effects of statin include muscle ache, nausea, headache, GIT complications, and a rash. Statin shows many more adverse side effects than niacin, which shows side effects such as stomach complications and cutaneous itchiness. Statin’s efficacy lowers triglyceride levels, mainly LDL-cholesterol more effectively than niacin but the side effects are more harmful and higher than niacin. A disadvantage of niacin would be the demand to have high levels of the drug consistently through dietary and supplemental pathways, in comparison to statin (D’Andrea, Hay, Ramirez, & Kesselheim, 2019). However, niacin is a good alternative for patients that are resistant to statin or patients with cardiovascular disease, it is not recommended for patients that suffer from ulcers, irritable bowel syndrome, or other gastrointestinal issues. The endothelial effects of niacin can be lethal in patients that are compromised with these additional ailments (Kotowade & et, 2013). Although niacin can be lethal, statin has similar properties in patients with hypotonia or muscle deformities. A significant side effect of statin may cause muscle weakness and contractile inhibitions in combination with hepato- endothelial depletion. Both niacin and statin pose many similarities and differences, each connected with various complications. These drugs are patient-dependant and will display different efficacy percentages according to the patient’s needs. Fibrates Low Density Lipoproteins are major carriers of cholesterol in humans and are responsible for supplying cholesterol to tissues with sterol demands. (Clay, 2020) When cells need cholesterol for membrane synthesis it creates transmembrane receptor proteins for LDL inserting them into the plasma membrane. Once there the receptors diffuse until associated with clathrin-coated pits and an endocytosis signal in the cytoplasmic tail of LDL receptors bind to the membrane-bound adaptor protein AP2 after it is unlocked by binding to PI (4,5) P2 on the plasma membrane. These bound LDL particles are then rapidly internalized and deliver their contents to early endosomes. LDL is released from its receptor and is delivered via late endosomes to lysosomes. Cholesterol esters in LDL particles are hydrolyzed into free cholesterol, available for new membrane synthesis, though if too much free cholesterol accumulates in a cell it shuts off cholesterol and LDL synthesis in order to cease both. (Alberts, 2015) This pathway is disrupted in individuals who inherit defective genes that encode LDL receptors, resulting in high level of blood cholesterol, which predisposes these individuals to develop atherosclerosis and death at an early age due to coronary artery disease. In other individuals with elevated levels of LDL they may be lacking the receptor, have defective receptors in either the extracellular binding site or the site that attaches to AP2 adaptor proteins in clathrin-coated pits. (Alberts 2015) LDL’s are most often associated with causing atherogenic plaque formation as LDL levels can be elevated in individuals who consume large amounts of saturated fat or cholesterol. The endothelium lining the artery takes up circulating LDL’s depositing and trapping them in the arterial intima. There the LDL’s undergo oxidation and other modifications stimulating atherogenisis. (Clay, 2020) There are several different forms of therapies or treatment to reduce low density lipoprotein levels, though the most common is use of statins. They work to inhibit cholesterol biosynthesis, upregulate LDL receptors, and enhance LDL clearance by inhibiting HMG CO-A reductase inhibitors. (Mason, 2016) Common side effects experienced with use of statins include headaches, nausea, muscle and joint aches, and in more serious cases increased blood sugar, muscle cell damage, liver damage, and memory problems. (Statins: Are these cholesterol-lowering drugs right for you?, 2021) Aside from statins another effective for of elevated numbers of Low-density lipoproteins are Fibrates. They activate PPARа, which increases fatty acid oxidation, increases apoAI, LPL, and apoll, while also lowering triglycerides, decreasing apoCill and raising HDL. They are commonly used in severe cases of hypertriglyceridemia and hyperlipidemia and should be avoided in patients with renal insufficiency as it can predispose these individuals to myopathy. Side effects may include gastrointestinal discomfort, rash, and pruritis, and combination of fibrates with gemfibrozil and most statins is often associated with increased risk of myopathy due to increased statin levels in the blood. Fibrates are more effective at lowering serum triglyceride/VLDL than statins, therefore they are useful for treatment of dyslipidemia associated with diabetes and metabolic syndromes. (Mason, 2016) Ezetimibe The presence of blood cholesterol comes from two sources – hepatic cholesterol excretion and dietary intake. While cholesterol from the liver makes up about 75% of blood cholesterol, intestinal absorption accounts for the remaining 25%. Because of this, my proposal includes adding an intestinal-absorption-prevention medication to a statin-resistant patient’s medication regimen. An example of this type of medication is Ezetimibe. This drug functions to reduce intestinal uptake of cholesterol, reducing blood cholesterol levels by up to 25%. Typically, the intestines absorb cholesterol through enterocyte membrane sterol influx transporters. There is a particular class of these transporters, a protein referred to as the Niemann-Pick C1-like protein, referred to as NPC1L1. NPC1L1 facilitates the transport of cholesterol-containing micelles from the intestinal lumen to the enterocyte. It works in conjunction with another protein, adaptor protein 2 (AP2), and clathrin in a complex micelle uptake system. (Phan et. Al., 2012) Ezetimibe binds to NPC1L1, specifically in the jejunal brush border, inhibiting the protein’s transporting duties. Specifically, it is thought to disrupt the NPC1L1/AP2/clathrin bond, disabling the ability of NPC1L1 to bind with micelles. (Phan et. al., 2012) The inhibition of NPC1L1 creates a cascade of events. Cholesterol absorption into enterocytes is limited, chylomicron creation and secretion are thus reduced, and hepatic pools of cholesterol are depleted in an attempt to maintain enterocytic cholesterol levels. After depletion, the result is reduced serum LDL. (Phan et. Al., 2012) When used alone (rather than in conjunction with statins as it is typically used), Ezetimibe reduces LDL by an average of 18.5%. HDL increases by an average of 3%, triglycerides reduce by 8%, and total cholesterol reduces by 13%. Therefore, an overall improvement in patient health can be expected. (Phan et. Al., 2012) Unwanted physiological effects of Ezetimibe are limited to an increase in liver enzymes, such as transaminase. Adverse events related to Ezetimibe are infrequent. Liver failure while taking this medication has been documented but in minimal quantities. Long-term side effects that may occur when taking Ezetimibe include drowsiness, and temporary side effects include diarrhea, joint pain, and viral susceptibility. (Ezetimibe: Side effects, dosages, uses and more, 2018) In comparison, statins’ mechanism of action includes the inhibition of MHG-CoA reductase. This enzyme’s responsibility is catalyzing the step of the cholesterol synthesis pathway comprising the conversion of HMG-CoA to mevalonate. This means that in the presence of statins, the synthesis of cholesterol will be reduced. The cholesterol-lowering effects of statins are an average of 35% reduction in LDL, an average of 8% increased HDL, and 23% overall reduction in cholesterol. (Sizar et. Al., 2021) Unwanted physiological effects of statins include elevated transaminases, myopathy, rhabdomyolysis, diabetes mellitus, and hepatotoxicity. Side effects that may be experienced by a patient taking statins include muscle joint and muscle pain, inflammation, confusion, headache, drowsiness, dizziness, diarrhea, bloating, and less common symptoms include hair loss, nausea, numbness, stomach and liver pain, rashes, low sex drive, and erectile dysfunction. (Side effects of cholesterol-lowering statin drugs, 2012)(Kapur, 2008) Statins appear to be more effective in improving LDL, HDL, and overall cholesterol levels in patients with cholesterol-related pathology. However, the side effects of Ezetimibe are much less numerous and severe than those of statins. Additionally, as mentioned in the prompt, some patients do not respond as they should to statins. Therefore, Ezetimibe is an excellent alternative as it still demonstrates efficacy (though reduced) and has more minor side effects. (Ezetimibe: Side effects, dosages, uses and more, 2018) References Ezetimibe: Side effects, dosage, uses, and more. (2018). https://www.healthline.com/health/ezetimibe-oral-tablet Kapur, N. (2008). Clinical efficacy and safety of statins in managing cardiovascular risk. Vascular Health and Risk Management, 4(2), 341-353. https://10.2147/VHRM.S1653 Phan, B. A. P., Dayspring, T. D., & Toth, P. P. (2012). Ezetimibe therapy: Mechanism of action and clinical update. Vascular Health and Risk Management, 8, 415-427. https://10.2147/HRM.S33664
Purchase answer to see full attachment
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