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Which there are abnormally elevated levels of fat particles in the blood restrict blood flow which in turn creates significant risk of heart attack triglycerides and phospholipids now cholesterol is necessary for the membranes triglycerides are composed of glycerol and three fatty acids which and lastly phospholipids are a major component of all cell membranes and plasma
They have to be transported throughout the body in a protein capsule cholesterol and triglycerides surrounded by hydrophilic shell made of proteins that can control enzymes in lipoprotein metabolism and serve as apolipoprotein composition as well as their density lipoproteins can be lipoprotein vldl for short low-density lipoprotein ldl for short mostly of triglycerides
And relatively small amount of cholesterol and some cholesterol in the amount relatively larger in comparison to rich triglycerides to cells throughout the body once they are secreted into the releases the fatty acids which are then taken up by the tissues as the contains relatively higher percentage of cholesterol the function of ldl is and synthesis of steroid hormones
However more than half of the synthesize bile acids and as you may already know bile acids are necessary peripheral cells is transported back to the liver by hdl hdl is composed mainly small intestine now the problem arises when we have innermost layer of the artery wall and lead to formation of atherosclerotic now hdl on the other hand prevents formation of atherosclerotic
Lesions by inflammation this is why hdl is often referred to as a good cholesterol so are several major classes of lipid lowering drugs so first we have better understand how these agents work we need to take a closer look at the liver cell this is where hmg-coa reductase enzyme converts hmg-coa into so by inhibiting this enzyme statins effectively reduce concentration of
Cholesterol production and begin to compensate by synthesizing more ldl the blood additionally low intracellular cholesterol levels lead to decreased levels lastly statins may also increase hdl levels by few different mechanisms atorvastatin fluvastatin lovastatin pravastatin rosuvastatin and simvastatin thus increase risk of liver toxicity in susceptible patients secondly
Use of skeletal muscle the mechanism behind that is still being investigated however which happens to be essential precursor to other compounds that are important to lipid lowering drugs which includes only one agent that is nicotinic acid adipose tissue where it inhibits enzyme called hormone-sensitive lipase which is triglycerides which then become important component
Of vldl so by niacin effectively decreases hepatic vldl synthesis which in turn leads to different mechanisms that are still being investigated now when it comes to prostaglandin release which results in cutaneous vasodilation next niacin can hyperuricemia and gout lastly at large enough doses niacin may also cause liver fibrates so fibrates work primarily by activating
Nuclear transcription receptor called peroxisome proliferator-activated receptor alpha or ppar-alpha for short liver and adipose tissue the binding of fibrates to ppar-alpha induces lipid metabolism one of the main effects induced by fibrates is increased triglycerides from circulation and their breakdown to fatty acids furthermore also increase expression of proteins
Apo-ai and apo-aii which are major belong to this class include fenofibrate and gemfibrozil additionally just like with statins myopathy and rhabdomyolysis have mechanism of myotoxicity is still yet to be determined however it is thought content of bile they can increase risk of gallstone formation now let’s move on as you already know bile acids are produced in the liver
Stored in the and absorption of lipids now bile acids sequestrants basically serve as an ion small intestine the formation of this insoluble complex prevents the in bile acid excretion in turn creates increased demand for their production number of ldl receptors to bring in more ldl cholesterol in order to meet this example of drugs that belong to this class are colesevelam
Colestipol and indigestion constipation and nausea are quite common additionally these agents form insoluble complexes with other drugs thus interfering with their cholesterol absorption inhibitors in order to understand how cholesterol mechanism of cholesterol absorption in small intestine protein abbreviated npc1l1 which is located in the plasma membrane of cells triggers
Endocytosis which utilizes protein complex called clathrin ap2 endocytosis the cholesterol is released and the npc1l1 returns back to the simply binds to npc1l1 and inhibits its ability to interact with clathrin ap2 delivery of intestinal cholesterol to the liver which in turn causes decrease cholesterol from the circulation currently the only drug that belongs to makes it
A good choice for patients intolerant or unresponsive to statins inhibitors so pcsk9 is an abbreviated name of enzyme circulating in the blood their degradation in other words the activity of pcsk9 reduces the removal of that bind to and inactivate pcsk9 in the absence of pcsk9 there’s more ldl decreased levels of ldl cholesterol example of drugs that belong to this group
Include evolocumab and alirocumab some of the side effects that symptoms and some neurocognitive problems now before we end i wanted to fatty acids so omega-3 fatty acids are used primarily for their triglyceride triglyceride synthesis in the liver the agents that fall into this class are the eicosapentaenoic acid dha and epa for short as well as omega-3 derivative icosapent
Ethyl the most common side effects associated with these agents are aftertaste with fish-derived omega-3s lastly at high enough doses there you for watching i hope you enjoyed this video and as always stay tuned for more
Transcribed from video
Pharmacology – DRUGS FOR HYPERLIPIDEMIA (MADE EASY) By Speed Pharmacology
