The structure which transports lipids in the blood. It has a non-polar core where triglycerides reside and a polar coat with apoproteins for receptor binding
Lipoprotein
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This emulsifies fat into smaller droplets
Bile acids
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This enzyme breaks down fat into triglycerides and cholesterol esters
Lipase
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The enzyme which catalyses the breakdown of triglycerides into free fatty acids after the chylomicrons transport it from the lymphatic system to muscle/tissue
Lipoprotein lipase
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What is left of the chylomicron after the free fatty acids are removed at the tissue - they are then removed by hepatocytes
Chylomicron remnants
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The cells which can make TGs and cholesterol, and take up chylomicron remnants
Hepatocytes
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The lipoprotein which takes up the TGs and esters which are released from the hepatocytes in the endogenous liver pathway
VLDL
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What is left of VLDLs after they pass through muscle or tissue and their TGs are hydrolysed to free fatty acids by lipoprotein lipase and taken up by the aforementioned cells
LDL
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The endogenous pathway whose source of lipid is from cells that die and release their lipid which is taken up by HDLs
Extrahepatic
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The lipoprotein which is involved in removing lipid from plaques that are developing in the walls of blood vessels (atherosclerosis)
HDL
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A type of hyperlipidemia where LDL levels are raised
Primary iia
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A type of hyperlipidemia where both LDL and HDL levels are raised
Primary iib
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A type of hyperlipidemia caused by metabolic disorders such as diabetes, hypothyroidism, renal disease, etc.
Secondary
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This is what HMG CoA Reductase Inhibitors are also known as
Statins
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A major side effect of statins
Myositis
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An example of a PCSK9 inhibitor (PCSK9 promotes the uptake of LDL receptors in the liver, causing them to degrade so uptake of lipid is reduced). It is used as an additive as it is very expensive
Evolocumab
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A drug class which increases production of lipoprotein lipase and HDL, reduces production of VLDLs, reduces TG levels and increases LDL uptake. Examples: benzafibrate and gemfibrozil. Side effect of myositis
Fibrates
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These are drugs which are used to bind to bile acids so they cannot emulsify fats - both the fat and the bile acids are lost in the stool. There is less cholesterol absorbed and increased expression of LDL receptors. GI side effects. Not first line
Bile acid resins
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A drug which inhibits intestinal absorption of cholesterol. There is no effect on absorption of fat-soluble vitamins and it is more potent than resins
Ezetimibe
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A drug which reduces synthesis of TGs; decreases levels of LDL and VLDL; increases HDL. Used in combination with statins and resins. Common side effects are intense flush and pruritis and GI upset. Risk of jaundice with high doses
Nicotinic acid
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This can be given to make eicosanoids which are less likely to cause clotting, therefore it can be used to improve survival after MI. Impact on lipids is not relevant
Fish oil
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The drug class given in primary prevention of cardiovascular events and in all diabetics over 40 yrs old (can be combined with ezetimibe)
Statins
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Two secondary prevention drugs alongside statins
Fibrates and bile acid resins
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Other cards in this set
Card 2
Front
This emulsifies fat into smaller droplets
Back
Bile acids
Card 3
Front
This enzyme breaks down fat into triglycerides and cholesterol esters
Back
Card 4
Front
The enzyme which catalyses the breakdown of triglycerides into free fatty acids after the chylomicrons transport it from the lymphatic system to muscle/tissue
Back
Card 5
Front
What is left of the chylomicron after the free fatty acids are removed at the tissue - they are then removed by hepatocytes
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