Lipid Physio & Lipid Disorders Flashcards

1
Q

What are lipid molecules made of?

A

fats and oil

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2
Q

What is cholesterol’s imp?

A
  • back bone for steroids
  • precursor for synthesis for Vita D
  • necessary for digestion of fats
  • imp for the metabolism and transport of fat soluble vitamins
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3
Q

How does diet affect cholesterol?

A

our LIVER is always making cholesterol despite what we eat, but our equilibrium is affected when we consume TOO MUCH cholesterol at once

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4
Q

What are the categories of cholesterol carriers?

A
  • HDL (good)

- LDL (bad)

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5
Q

What are the LDL receptors?

A

increasing the LDL receptors on the TISSUE will DECREASE LDL that is floating around in the serum; DECREASING LDL tissue receptors will INCREASE the amount of LDL floating

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6
Q

How do statins work?

A

-DECREASE cholesterol synthesis (decrease HMG-CoA) and INCREASING removal of LDL lipoproteins from blood by increasing the transcriptase of LDL receptors (increase receptors = decrease of LDL in serum)

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7
Q

How does bile play a role?

A

the bile is reabsorbed in the large intestine –> gets through liver –> goes into bile –> reused via enterophepatic circulation
*hard to remove old cholesterol b/c it is being recycled

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8
Q

How does hereditary play a role?

A

diet can only help so much with cholesterol, in the end, the body is fighting with “set point” via hereditary

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9
Q

How is triglyceride derived?

A

1) from what we eat
2) left over cal in our body that we didn’t use: metabolic process will convert “excess” carbs and proteins to triglyceride –> stored in adimose)
* when we fast, our body breaks down triglycerides b/c there’s nothing else to break down - found in ADIPOSE TISSUE

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10
Q

Why is triglyceride important?

A

it is an energy source for all the cells (except nervous)

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11
Q

What does increased triglyceride mean?

A
  • increase risk of atheroscelorsis
  • pancreatitis and depression (alcoholics drink a lot b/c of depression –> cxing pancreatitis –> also see incr triglyceride b/c alcohol is empty carbs
  • ASVCD (more imp in FEMALES than in males!)
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12
Q

What are lipoproteins?

A
  • helps cholesterol and triglycerides become more soluble by attaching on to them
  • absorb cholesterol, fatty acids, fat soluble vitamins –> transports them from liver to peripheral tissues –> for cholesterol: peripheral tissue to liver
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13
Q

What are the structures of lipoproteins?

A
  • hydrophobic

- hydrophillic (apolipoproteins/apoproteins)

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14
Q

Classification of lipoproteins?

A

classified by density

1) chylomicrons: largest and least dense (less protein, more fat)
2) chylomicron remnants
3) VLDL (very low den. lipoprotein)
4) IDL (int low den. lipoprotein)
5) LDL (low den. lipoprotein)
6) HDL (high den. lipoprotein)

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15
Q

What happens if you have high LDL?

A
    • HIGH LEVELS OF LDL = #1 RISK FACTOR FOR ASVCD
  • chylomicrons - IDL are cleared out of body but LDL is small so that an INCR of small LDL can can INC or atheroscelrosis (size of LDL is not imp)
    • Lpa (lipoprotein a): genetic variation of LDL –> incr risk of atheroscelorsis; usually genetic BUT other dz can cx it to rise ie) renal dz); if pt has “good” cholesterol profile but gets CAD - INVESTIGATE Lpa!
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16
Q

What happens if you have LOW HDL?

A

–LOW LEVELS OF HDL = #2 RISK FACTOR FOR ASVCD

17
Q

What does HDL do?

A

gets into tissue, snags LDL and breaks it down OUTSIDE the tissue –> lowering LDL

18
Q

What are apolipoprotiens?

A

they are protein part of the lipoprotein

19
Q

What are the classes of apolipoproteins?

A
  • A
  • B: 100
  • C
  • D
  • E
20
Q

What is the imp of apolipoprotein B 100?

A
  • EVERY LDL has a B100 (marker for LDL)

- inc B100 = inc LDL = inc risk for ADSCVD

21
Q

What is apolipoprotein E?

A
  • may be related to schizophrenia

- related to cholesterol

22
Q

What is nicotinic acid?

A

may be used to lower LDL and triglyceride but NO ammo on whether it lowers ADSCVD risk

23
Q

What is fractionated LDL?

A

to determine the size of LDL b/c smaller LDL can get under endothelial easier –> inc risk of arthelosclrosis