Lipids.txt

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Author:
kavinashah
ID:
25976
Filename:
Lipids.txt
Updated:
2010-07-07 19:53:49
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lipid pathbook
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lipid pathbook
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  1. What is the function of chylomicrons?
    Transport TG from gut to rest of body
  2. When should chylomicrons be present?
    After eating fat contained foods, (absent in fasting state)
  3. What are chylomicron’s main Apoprotein?
    C
  4. How do VLDL get into blood?
    Made by liver from its own fat and c/h
  5. What do VLDL do? And what is their apoprotein?
    Transport TG to peripheral tisseus. ApoC
  6. Which surgical emergency do high TG lead to?
    Acute pancreatitis
  7. Which lipoproteins are the main contributors to atherosclerosis? And how are they made?
    LDL made by VLDL metabolism
  8. What happens to excess LDL? What is their Apoprotein?
    • Taken up by liver via receptors
    • ApoB
  9. How is HDL made?
    Liver and intestines
  10. How are HDL protective?
    Reverse transport of cholesterol back to the liver
  11. What is HDL’s apoprotein?
    ApoA-1
  12. Why are raised TG levels associated with increased coagulability of blood?
    Due to increased plasma fibrinogen levels and factor VII activity
  13. What are most cases of primary hypercholesterolaemia due to?
    • Polygenic disorders which make increased susceptibility: ie overproduction of VLDL by liver which is converted to LDL leading to overloading of LDL receptor and decreased clearance from body
    • And increased dietary fat and obesity
  14. What is the commonest monogenic hyperlipidaemia? And how is it inherited?
    • Familial hypercholesterolaemia
    • Inheritance: dominant
  15. What is the problem in FH?
    • Absent or defective cell surface receptors which mediate uptake of LDL
    • Or problem with ApoB so less uptake of LDL more in circulation and so more atherosclerosis
  16. What are the features of homozygous FH? Age of athero, physical signs, chol level, age of death
    • Age of athero: childhood
    • Cutaneous xanthomata in childhood
    • Cholesterol > 15mmol/l
    • Untreated: die < 30
  17. When do heterozygous FH get coronary heart disease?
    30’s 40s
  18. What is the age of death in untreated hetero FH?
    Before 60
  19. What are the physical signs in hetero FH?
    • Corneal arcus in young
    • Xanthelasmata
    • Tendon xanthomata
  20. What are xanthelasmata?
    Lipid deposits in eyes
  21. What are eruptive xanthomata?
    Itchy nodules in crops in hypertriglyceridaemia
  22. What are tuberous xanthomata?
    Yellow plaques on elbows and knees
  23. What are planar/palmar xanthomata?
    Orange streaks in palmar creases – virtually diagnostic of remnant hyperlipidaemia
  24. What is type III disease? And what is it assoc with?
    • Combined hyperCHOL and hyperTG
    • Assoc with accelerated atherosclerosis
  25. What are physical signs of type III disease?
    • Xanthomata
    • Tubero-eruptive xanthomata
    • Palmar xanthomata
  26. What is the defect in type III disease?
    ApoE mutation
  27. What is type III disease associated with?
    • Diabetes
    • Hypothyroidism
  28. Which arteries are more susceptible to athersclerosis in type III disease than other hyperlipidaemias?
    leg
  29. what is the cause of primary hypertriglyceridaemia? (2things)
    • Increased hepatic VLDL production in association with decreased TG clearance
    • This can be familial or acquired
  30. What are the acquired causes of primary hypertriglyceridaemia?
    Diabetes, alcohol, obesity, BB, oestrogen administration
  31. What is a rare, familial but serious cause of primary hypertriglyceridaemia?
    LPL deficiency (responsible for metab of VLDL and chylomicrons)
  32. What are 4 features of familial LPL deficiency primary hypertriglyceridaemia?
    • Xanthomata
    • Hepatosplenomegaly
    • Fatty liver
    • Recurrent pancreatitis
  33. Which kidney problems can causes secondary hyperlipidaemia?
    • Nephrotic syndrome
    • Chronic renal insufficiency
  34. Which drugs cause secondary hyperlipidaemia?
    • Thiazide diuretics
    • Protease inhibitors
  35. What is the effect of oestrogen on lipids?
    • Lower LDL and Raise HDL so giving HRT post-menopausal is cardioprotective
    • But also raise TG
  36. Using other values, how do you calculate LDL cholesterol?
    Total cholesterol – HDL – TG/2.2
  37. What type of sample is needed to calculate LDL cholesterol?
    Fasting sample
  38. In patients who have had a cardiovascular event, when do they need to be treated?
    • If their total cholesterol > 5; or LDL-cholesterol > 3
    • Ie secondary prevention
  39. What are the targets for treatment for chol and LDL-chol
    • Total cholesterol < 5
    • LDL cholesterol < 3
  40. Which are the 2 main classes of lipid lowering drugs used?
    • Statins: HMG Co-A reductase inhibitors so inhibit cholesterol synthesis
    • Fibrates
  41. What are SE of statins?
    • Derangement of LFTs
    • Muscle cramps
    • Rarely rhabdomyolysis
  42. What is the action and SE of fibrates?
    Action: reduce serum TG, raise cholesterol, may cause myositis
  43. Which other diseases are associated with high cholesterol?
    • Hypothyroid
    • PBC
    • Cushings
  44. How does ezetimibe work?
    Block absorption of cholesterol from small intestine, works at brush border
  45. How does cholestyramine work?
    • Bile acid sequestrant, formed into complexes, excreted
    • So more plasma cholesterol is used to make bile acids, thereby reduced plasma cholesterol levels

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