Amer cholesterol syn
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This document discusses cholesterol metabolism and ways to lower cholesterol levels. It covers the sources of cholesterol from diet and de novo synthesis. The key enzyme in cholesterol synthesis, HMG CoA reductase, is regulated both short-term by phosphorylation and long-term by SREBP-2 which responds to cellular sterol levels. Statins are commonly used to lower cholesterol by decreasing the activity of HMG CoA reductase. Other strategies mentioned include bile sequestering agents which bind bile acids, increasing cholesterol use to make more bile acids, and niacin which inhibits VLDL excretion from the liver.
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cholesterol metabolism
This document discusses cholesterol and lipoproteins. It notes that cholesterol is manufactured by animal cells and used to construct cell membranes. Lipoproteins like LDL, VLDL, and HDL carry cholesterol in the blood, with elevated LDL and other non-HDL lipoproteins associated with increased risk of atherosclerosis and heart disease. The document discusses conditions like hypercholesterolemia and hypocholesterolemia, symptoms, causes, diagnosis, and treatment options. It also provides an overview of atherosclerosis, risk factors, diagnostic methods, clinical manifestations, and treatment strategies like lifestyle changes, medications, and procedures.
All about Cholesterol ( for undergrads)
Cholesterol performs essential functions in the body and is synthesized in the liver and intestines. The liver plays a central role in regulating blood cholesterol levels. Half of the body's cholesterol comes from synthesis, while the remainder comes from diet. Cholesterol is used to make bile acids, steroid hormones like cortisol and aldosterone, vitamin D, and is incorporated into cell membranes. Bile acids help emulsify fats and are recycled through enterohepatic circulation. Statins work by inhibiting HMG-CoA reductase, an enzyme involved in cholesterol synthesis but also the production of other important compounds.
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Cholesterol biosynthesis is a multi-step process that begins with acetyl-CoA and occurs primarily in the liver and other tissues. Key steps include the conversion of HMG-CoA to mevalonate by the rate-limiting enzyme HMG-CoA reductase. Cholesterol can then be used for membrane structure, steroid hormone synthesis, or converted to bile acids which are secreted in the bile. Cholesterol levels are regulated by feedback inhibition of HMG-CoA reductase and uptake/secretion of cholesterol and bile acids. Statins lower cholesterol by inhibiting HMG-CoA reductase.
Cholesterol biosynthesis final
1. Cholesterol is synthesized primarily in the liver at a rate of about 1g per day in adults through a series of reactions starting from acetyl-CoA.
2. The rate-limiting enzyme in cholesterol biosynthesis is HMG-CoA reductase.
3. Cholesterol biosynthesis is regulated through feedback inhibition when cholesterol levels rise, phosphorylation/dephosphorylation of HMG-CoA reductase, and hormonal and drug mechanisms that inhibit HMG-CoA reductase.
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Cholesterol performs essential functions in the body and is synthesized in the liver and intestines. The liver plays a central role in regulating blood cholesterol levels. Half of the body's cholesterol comes from synthesis, while the remainder comes from diet. Cholesterol is used to make bile acids, steroid hormones like cortisol and aldosterone, vitamin D, and is incorporated into cell membranes. Bile acids help emulsify fats and are recycled through enterohepatic circulation. Statins work by inhibiting HMG-CoA reductase, an enzyme involved in cholesterol synthesis but also the production of other important compounds.
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Cholesterol biosynthesis is a multi-step process that begins with acetyl-CoA and occurs primarily in the liver and other tissues. Key steps include the conversion of HMG-CoA to mevalonate by the rate-limiting enzyme HMG-CoA reductase. Cholesterol can then be used for membrane structure, steroid hormone synthesis, or converted to bile acids which are secreted in the bile. Cholesterol levels are regulated by feedback inhibition of HMG-CoA reductase and uptake/secretion of cholesterol and bile acids. Statins lower cholesterol by inhibiting HMG-CoA reductase.
Cholesterol biosynthesis final
1. Cholesterol is synthesized primarily in the liver at a rate of about 1g per day in adults through a series of reactions starting from acetyl-CoA.
2. The rate-limiting enzyme in cholesterol biosynthesis is HMG-CoA reductase.
3. Cholesterol biosynthesis is regulated through feedback inhibition when cholesterol levels rise, phosphorylation/dephosphorylation of HMG-CoA reductase, and hormonal and drug mechanisms that inhibit HMG-CoA reductase.
The relationship between serum albumin concentration and sarcopenia
Lower serum albumin levels are associated with greater loss of muscle mass and strength over time in older adults according to some studies. The Health ABC study found that lower serum albumin was related to greater loss of appendicular skeletal muscle mass over 5 years. The LASA study also found lower serum albumin to be associated with weaker muscle strength and greater decline in strength over 3 years. However, the MrOS study found only modest and inconsistent trends between serum albumin and loss of muscle mass and function in elderly men. Overall, the relationship between serum albumin and sarcopenia requires more research.
Estimation of serum total protein
This document summarizes serum total protein estimation. It explains that proteins are polymers of amino acids and serve many important functions in the body. Abnormal total protein levels can indicate nutritional status, kidney disease, or liver disease. Hypoproteinemia is a low total protein level caused by excessive protein loss or decreased intake/synthesis. Hyperproteinemia is an increased level caused by dehydration. The biuret method is used to quantify total proteins by developing a color change proportional to protein concentration.
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This document discusses the pros and cons of egg consumption from a nutritional perspective. While eggs are a major source of dietary cholesterol which can increase risks for heart disease, several studies have found no association between egg intake and heart disease risk. Eggs are also one of the richest sources of vitamin A, and may help prevent vitamin A deficiency. However, consuming too much vitamin A can also be toxic, so intake should be monitored to gain benefits while avoiding risks.
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Cholesterol is the major sterol in the animal tissues.
Cholesterol is present in tissues and in plasma either as free cholesterol or as a storage form, combined with a long-chain fatty acid as cholesteryl ester.
In plasma, both forms are transported in lipoproteins
removed from tissues by plasma high-density lipoprotein (HDL) and transported to the liver, where it is eliminated from the body either unchanged or after conversion to bile acids in the process known as reverse cholesterol transport
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- Symptoms of high cholesterol and how it can lead to atherosclerosis and heart disease
- Methods for estimating total cholesterol using the Zak's method or enzymatic method
- Classification and functions of lipoproteins such as LDL, HDL, VLDL
- Desirable cholesterol levels according to NCEP-ATP III guidelines
- Protocol for estimating total cholesterol and HDL cholesterol levels
Powerpoints Hypolipidemics
This document summarizes various aspects of lipoproteins, lipids, and treatments for hyperlipidemia. It discusses the main classes of lipoproteins such as chylomicrons, VLDL, LDL, HDL and their roles in transporting lipids like cholesterol and triglycerides. It also outlines drug classes used to treat hyperlipidemia, including fibrates, statins, bile acid sequestrants, and niacin. Adverse effects and guidelines for drug combinations are provided.
Powerpoints Hypolipidemics
This document summarizes various types of lipids and lipoproteins, including their functions, components, and roles in atherosclerosis and coronary heart disease. It also discusses factors that influence lipid levels and guidelines for treatment and management of dyslipidemia through lifestyle modifications and lipid-altering drugs such as statins, fibrates, bile acid sequestrants, and niacin.
CHOLESTEROL
This document summarizes key information about cholesterol. It defines cholesterol as an organic molecule derived from Greek terms meaning "bile" and "solid". The document outlines cholesterol's molecular formula, structure, production in vertebrates, functions in the body, and typical daily intake versus synthesis. Cholesterol performs essential functions as a constituent of cell membranes and lipoproteins, and as a precursor for bile salts and steroid hormones. It is required for nerve transmission and formation of the myelin sheath.
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Cholesterol Biosynthesis and catabolism for MBBS, Lab. MEd. BDS.pptx
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LARYNX.pptx
The larynx is a hollow structure located in the neck that contains the vocal cords. It functions in respiration, swallowing, and voice production. The larynx has a cartilaginous skeleton including the thyroid, cricoid, arytenoid, and epiglottic cartilages connected by membranes and ligaments. It is supplied by nerves including the recurrent laryngeal nerve which controls the vocal cords. During phonation, expired air causes the vocal cords to vibrate and resonate within the larynx and pharynx to produce voice.
Liver Tests
1. The document discusses various laboratory tests used to evaluate liver disease, including tests of liver cell injury (transaminases), cholestasis (alkaline phosphatase, bilirubin), and liver function (albumin, clotting factors).
2. Transaminases indicate recent liver cell death while tests of cholestasis show impaired bile flow. Together the pattern of abnormalities on these tests can suggest the general type of liver disease.
3. The degree of elevation on tests and the specific abnormalities seen provide clues about the chronicity, severity and underlying cause of liver disease. Interpreting various test results in combination is important for diagnosis.
glucagon disorder
This document discusses glycogen storage disorders (GSDs), which are caused by defects in glycogen metabolism. It describes the various enzymes involved and the biochemical tests used to diagnose different types of GSDs. Predominantly hepatic GSDs include defects in glucose-6-phosphatase (GSD I), debranching enzyme (GSD III), branching enzyme (GSD IV) and phosphorylase (GSD VI, IX). Muscle-affecting GSDs involve acid α-glucosidase deficiency (GSD II/Pompe disease), muscle phosphorylase (GSD V), and muscle phosphofructokinase (GSD VII). Diagnosis involves tests on red blood cells
Cholesterol synthesis and breakdown
I do not have enough context to answer these review questions. The document provided is a summary of cholesterol synthesis and regulation. It does not contain answers to these specific questions.
Amer cholesterol metabolism
Cholesterol is an important animal steroid that maintains membrane fluidity and is the parent molecule for bile acids, steroid hormones, and vitamin D3. The liver plays a central role in regulating cholesterol homeostasis through synthesis and excretion. Cholesterol synthesis is regulated by the rate-limiting enzyme HMG CoA reductase, which is controlled by sterol-dependent and -independent mechanisms as well as hormones like insulin and glucagon. Excess cholesterol is excreted in bile and eliminated in feces, while hypercholesterolemia can be treated with statin drugs that inhibit HMG CoA reductase or plant sterols that block cholesterol absorption.
Amer cerrhosis of liver
Cirrhosis is a diffuse process characterized by liver fibrosis and conversion to abnormal nodules. It is most commonly caused by alcoholism and viral hepatitis. Complications include portal hypertension, ascites, bleeding, and hepatic encephalopathy. Diagnosis involves blood tests of liver function and imaging. Treatment focuses on managing complications through dietary changes, medications, procedures, and potentially transplantation. Prognosis depends on severity as assessed by scales like Child-Pugh and MELD scores.
Amer glycogen storage disease
Glycogen storage disease (GSD) occurs due to defects in enzymes involved in glycogen synthesis or breakdown, leading to excess glycogen storage. There are 11 known types classified by the affected enzyme and tissue. Symptoms vary by type but can include hypoglycemia, liver and muscle involvement, and exercise intolerance. Treatment depends on type and may include dietary changes, enzyme replacement therapy, or liver transplantation. Prenatal testing is available for some types.
3 evaluation and management of rheumatoid arthritis
This document discusses the management of rheumatoid arthritis (RA). It provides details on:
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Arthritis
This document provides information on osteoarthritis (OA) and rheumatoid arthritis (RA). It defines OA as the most common form of joint disease, affecting over 90% of adults by age 40. Risk factors include aging, obesity, and joint injury from overuse. RA is a chronic systemic inflammatory disease that affects the synovial joints, with potential extra-articular manifestations. RA is believed to have an autoimmune cause and is associated with the presence of rheumatoid factor. Both diseases can cause pain, stiffness, and loss of physical function in affected joints. Treatment involves managing symptoms, maintaining function, and may include medications, exercise, joint protection, and sometimes surgery.
Final rheumatoid arthritis
Rheumatoid arthritis is an autoimmune disease that causes inflammation of the joints, resulting in pain, swelling, stiffness and destruction of cartilage and bone. It most commonly affects small joints in the hands and feet. Conventional treatments include NSAIDs, disease-modifying anti-rheumatic drugs like methotrexate, and corticosteroids. However, these may have side effects or lose effectiveness over time. Biological therapies targeting cytokines like TNF-α have been developed as alternative treatments and include anti-TNF agents infliximab, etanercept and adalimumab, as well as the IL-6 receptor antagonist tocilizumab. These biologics provide more effective relief of symptoms for many
Final rheumatoid arthritis
Rheumatoid arthritis is an autoimmune disease that causes inflammation of the joints, resulting in pain, swelling, stiffness and destruction of cartilage and bone. It most commonly affects small joints in the hands and feet. Conventional treatments include NSAIDs, disease-modifying anti-rheumatic drugs like methotrexate, and corticosteroids. However, these may have side effects or lose effectiveness over time. Biological therapies targeting cytokines like TNF-α have significantly improved treatment outcomes, with anti-TNF agents infliximab, etanercept and adalimumab being widely used options.
Rheumatic diseases
Rheumatoid arthritis is an autoimmune disease that causes inflammation of the joints and surrounding tissues. It affects around 1% of adults and is more common in women. The prevalence and incidence increases with age, peaking between 40-60 years old. Symptoms include morning stiffness, arthritis in 3 or more joints including the hands, and symmetric joint involvement. Lupus is an autoimmune disease that causes inflammation in tissues throughout the body including the skin, heart, lungs, and kidneys. Seronegative spondyloarthropathies are a group of related disorders including Reiter's syndrome, ankylosing spondylitis, psoriatic arthritis, and arthritis associated with inflammatory bowel disease. They
Rheumatoid arthritis
Rheumatoid arthritis is an autoimmune disease that causes inflammation and destruction of joints, tendons and bones. It results in joint deformity and immobilization. Symptoms include morning stiffness, symmetrical joint swelling, fever and fatigue. Diagnosis involves blood tests for inflammatory markers like ESR and CRP, as well as antibody tests. Treatment includes medications like NSAIDs, DMARDs, corticosteroids and biologics to reduce inflammation and slow joint destruction. Lifestyle changes such as exercise, nutrition, braces and surgery can also help manage symptoms and improve quality of life.
Cerebral circulation
The document summarizes blood circulation to the brain. It describes how blood is supplied to the brain through two internal carotid arteries and two vertebral arteries that form a complex network called the circle of Willis. It then discusses the major arteries that branch off from this circle - the anterior, middle, and posterior cerebral arteries - and the regions of the brain each supplies. It notes that decreases in blood flow through these arteries can cause impairments or weaknesses on the opposite side of the body.
Radioactive application in medical
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Endoscopy and types of endoscopy
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Developing writing
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Kingdom of fungi
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The document discusses DNA structure and replication. It notes that DNA is composed of four nucleotide bases - adenine, thymine, guanine, and cytosine. The bases pair up in a specific way, with adenine pairing with thymine and guanine pairing with cytosine. DNA replication occurs through the action of enzymes like DNA polymerase, which adds complementary bases to the DNA strands in the 5' to 3' direction. DNA polymerase is also able to repair errors that occur during replication.
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Amer cholesterol syn
- 1. Amer GUL Sending to Sir, Bashir Ahmad karimi
- 2. CHOLESTEROL METABOLISM Sources of cholesterol Cholesterol synthesis Long and short termregulation SREBP-2 Lowering cholesterol Calculating your risk forCHD
- 3. ROLES OF CHOLESTEROL Membrane component Steroid synthesis Bile acid/saltprecursor Vitamin Dprecursor
- 5. SOURCES OF CHOLESTEROL Diet De novo synthesis Cholesterol synthesized in extrahepatic tissues Liver cholesterol pool Free cholesterol In bile Conversion to bile salts/acidsSecretion of HDL and VLDL
- 7. Dietary Cholesterol Animal products –eggs Absorb about50% Increase intake = decreasedabsorption Excrete – 1 g/day (bileacids)
- 8. DIETARY CHOLESTEROL Assume 400 mg intake /day 2 0 0 mg isabsorbed 1000 mg isexcreted 8 0 0 mg from de novosynthesis Lowering cholesterol in diet has very little effect on blood cholesterol !!!
- 9. Cholesterol Synthesis Similar to ketogenic pathway Occurs in cytosol Requires NADPH and ATP Highly regulated 80 % in liver, ~10% intestine, ~5% skin
- 11. HMG CoA Reductase : Regulation Short-term regulation Inhibited byphosphorylation AMP-dependent protein kinase When AMP is high (or ATP low!), why waste energy on cholesterol synthesis Long-term regulation Proteolysis Degradation stimulated by cholesterol and cholesterol metabolites Sterol-sensing domain
- 12. HMG COA REDUCTASE - Phosphorylation AMP-Activated Protein Kinase (low activity) phosphatase insulin (+) kinase Glucagon/epi (+) increase cAMP AMP AMP-Activated Protein Kinase (high activity) (+) HMG CoA reductase – OH (active) HMG CoA reductase – P (inactive)
- 13. HMG CoA Reductase : Regulation Transcriptional regulation SREBP-2 Responds to cellular levels of sterols
- 15. Site 1 and site 2 protease -
- 17. Free Cholesterol Pool synthesis Negative Feedback (-) LDL receptor LP Negative Feedback (-) acat CE Steroid synthesis C HDL
- 18. Lowering Cholesterol Statins – decrease HMG CoA reductase activity Muscle weakness Why?
- 19. LOWERING CHOLESTEROL Bile acids Bile sequesteringagents liver Bile acids 95 % reabsorbed NH3+ NH3+ 1. Bind bile acid 2. Utilize more cholesterol to make bile acids >51%0%inifnecfecses
- 20. LOWERING A CHOLESTEROL O a t bran Soluble fiber Bind bileacids? Niacin 3-8 grams / day (need 60mg) Inhibits VLDL excretion ? (fattyliver) Flushing and liverdamage