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48 Cards in this Set
- Front
- Back
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What enzyme is used to get from acetyl coA to malonyl CoA |
Acetyl coA carboxylase |
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What is the rate limiting step of beta oxidation |
Transfer of acyl coA into mitochondria |
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What’s the rate limiting step in fatty acid synthesis |
Production of malonyl CoA |
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How does acyl-coA get across the membrane |
Carnitine shuffle (carnitine palmitoyl transferase 1) |
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What step of beta oxidation can cause SIDs |
Production of FADH2 Acyl-coA dehydrogenase |
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How is acetyl coA removed from the mitochondria |
Citrate synthase - as citrate |
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What enzyme is used to form cholesterol esters |
ACAT acyl-CoA cholesterol acyltransferase |
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Describe the pathway of cholesterol synthesis |
Acetyl CoA - HmgCoA - mevalonate - squalene - cholesterol |
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What type of fatty acids are carried by albumin in the blood |
Short chain fatty acids |
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Name 2 types of statins |
Simvastatin (natural) Atorvastatin (synthetic) |
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How do statins work |
Competitive inhibitor of HMGcoA reductase |
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What app protein is in LDl |
App-B100 |
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2 major steps of digestion of dietary TGs |
1) emulsified bile acids 2)hydrolysed by enzyme pancreatic triacylgylcerol lipase |
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What enzyme allows release of TGs at tissues |
Lipoprotein lipase |
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How does the liver recognise particles |
By ApoE |
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What causes hyper cholesterolemia |
Mutation in LDL receptor or ApoB-100 |
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What can cause LDL receptor degradation |
PCSK9 |
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How to improve lipid profile (diet) |
Reduce total fat intake Reduce transfats Exercise |
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What percentage of dietary fat intake is TAGs |
95% |
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Name 2 important polyunsaturated fats |
Linoleic acid - omega 6 Alpha linolenic acid - omega 3 |
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What is omega 6 also known as |
Linoleic acid |
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Sources of omega 6 |
Vegetable oils |
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Why is omega 6 important |
It decreases LDL cholesterol |
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Best types of omega 3 |
EPA/DHA |
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Where do you find EPA/ DHA |
Oily fish |
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Does cholesterol intake matter? |
Not really likely to make a difference in 15-25% of people |
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Where are you likely to find transfats |
Processed foods |
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Problems with transfats |
Increase LDL cholesterol Reduce HDL cholesterol Increase fasting triglyceride |
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What LDL is the most dangerous |
Small and dense |
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What forms of carbs are absorbed across the gut |
Glucose/ fructose/ galactose |
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How much should the percentage of carbs of your daily intake be |
65 or less |
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Why are carbohydrates bad |
Often a substitute for fats Can increase production of VLDL and diminish HDL |
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Why fruits and veg |
Soluble fibres in plants have been shown to decrease serum cholesterol |
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What dietary advice should you give to patients |
Reduce total fat Reduce processed food (transfats) Substitute animal fats for vegetable products/ oils/ seafood nuts and seeds Reduce sugar intake Increase fruit and veg (5 portions a day) Increase oily fish Monitor total energy intake |
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Two diets that show improvement to cholesterol |
DASH diet (fruit/veg/ low fat dairy) PREDIMED (Mediterranean |
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What type of obesity is most dangerous |
Visceral obesity (less responsive to insulin) |
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Why is exercise good |
Upregulates lipoprotein lipase activity in skeletal muscle |
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How much physical activity per week |
At least 150 mins (2 1/2 hours) moderate intensity activity |
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When is it most important to reduce salt |
When you’re hypertensive |
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What growth factors are important for turning a monocyte into a macrophage |
TNF alpha IFN gamma CM-CSF M-CSF |
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What can macrophages produce |
ROS - oxidised LDL Pro-inflammatory cytokines Scavenger receptors |
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Why is oxidised LDL bad |
Oxidised B100 binds to scavenger receptors on macrophages to generate foam cells stimulates MCP-1(monocyte chemoattractant ) and VCAM-1 Receptors for cholesterol transport are down regulated eg ABCA1 and hence reduction in HDL |
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What growth factors are produced by the endothelial cells and macrophages |
PDGF and TGF-betawhat is the effect of the growth factors released |
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What is the effect of the growth factors released? |
Migration of VSMCs into intima VSMCs produce collagen which deposits in plaque Have the ability to differentiate into macrophage like cells - foam cells |
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Define atherogenesis |
Formation of subintimal plaques in the lining of arteries |
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Difference between a vulnerable and stabilised plaque |
Stabilised - small lipid pool, high VSMC content, fewer inflammatory cells and thicker fibrous cap |
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What are the 2 hypothesis about atherogenesis |
Lipid oxidation hypothesis Response to injury hypothesis |
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Causes of endothelial injury |
high BP Raised LDL Toxins eg cigarettes Hemaodynamic stress |
