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Kaplan: Biochemistry Part I > Chapter 15: Lipid Synthesis and Storage (2) > Flashcards

Chapter 15: Lipid Synthesis and Storage (2) Flashcards

1
Q

What is the purpose of apoA-1?

A

used for cholesterol recovery from fatty streaks in the BV.

Docks LCAT

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2
Q

What does LCAT stand for?

A

lecithin-cholesterol acyltransferase

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3
Q

What is another name for LCAT?

A

PCAT phophatyidyl choline-cholesterol acyltransferase

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4
Q

What is the function of LCAT?

A

adds a fatty acid to cholesterol, producing cholesterol esters which dissolve in the core of the HDL

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5
Q

What is purpose of CETP?

A

The cholesterol esters picked up in the periphery by HDL can be distributed to other lipoprotein particles such as VLDL remnants (IDL), converting them to LDL

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6
Q

What does CETP stand for?

A

cholesterol ester transfer protein

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7
Q

HDL cholesterol picked up in the periphery can enter cells through what receptor?

A

SR-B1 scavenger receptor B1

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8
Q

SR-B1 is expressed in high levels in what tissues?

A

in hepatocytes and steroidogenic tissues, including ovaries, testes, and areas of the adrenals

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9
Q

Does SR-B1 mediate endocytosis of HDL?

A

no but rather transfers cholesterol into the cell by a mechanism not clearly known

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10
Q

Damage to the endothelium of BV may be related to what factors?

A
  • normal turbulence of the blood
  • elevated LDL
  • oxidized LDL
  • free radicals from cigarette smoking
  • homocystinemia
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11
Q

Describe how atherosclerotic plaques form.

A
  1. endothelial dyfunction causes procoagulation of cells around damaged endothelium.
  2. Local inflammation recruit monocytes and macrophages with subsequent production of ROS. LDL can become oxidized then taken up, macrophages become laden with cholesterol (foam cells)
  3. subendothelial accumulation of cholesterol-laden macrophages producing fatty streaks
  4. as fatty streaks enlarge, necrotic tissue and free lipid accumulates surrounded by epitheloid cells and eventually smooth muscle cells and an advanced plaque with a fibrous cap.
  5. Plaque eventually begins to occlude the blood vessel and could break off leading to thrombosis
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12
Q

How is HDL protective in cholesterol accumulation?

A
  1. HDL is protective by picking up accumulating cholesterol before the advanced lesion forms. ApoA-1 activates LCAT which in turn adds a fatty acid to cholesterol to produce a cholesterol ester that dissolves in the core of HDL
  2. HDL can be subsequently picked up by liver through the apoE receptor or delivered cholesterol through the scavenger receptor.
  3. The HDL may also transfer the cholesterol to an IDL, reforming a normal unoxidized LDL particle
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13
Q

How does vitamin E prevent endothelial damage?

A

protects LDL from oxidation and may prevent peroxidation of membrane lipids

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14
Q

List all the dyslipidemias and their names.

A
  • Type I: Familial Dyslipidemia (Hypertriglyceridemia) (Hyperchylomicronemia)
  • Type IIa: Familial Dyslipidemia (Familial Hypercholesterolemia)
  • Type III: Familial Dyslipidemia (Dysbetalipoproteinemia)
  • Type IV: Familial Dyslipidemia (Hypertriglyceridemia)
  • Type V: Hyperlipideia secondary to Diabetes
  • Abetalipoproteinemia (Hypobetalipoproteinemia) - a hypolipidemia
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15
Q

What is the deficiency in primary Type I hyperlipidemia?

A
  • familial lipoprotein lipase (rare) deficiency
  • apoC-II (rare) deficiency
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16
Q

Inheritance of primary Type I hyperlipidemia?

A

AR

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17
Q

Lipid elevated in blood in primary Type I hyperlipidemia?

A

triglycerides

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18
Q

Which lipoprotein is elevated in those with primary Type I hyperlipidemia?

A

chylomicrons

19
Q

What are some symptoms of primary Type I hyperlipidemia?

A

red-orange eruptive xanthomas
fatty liver
acute pancreatitis
abdominal pain after fatty meal

20
Q

What is the deficiency causing primary type IIa hyperlipidemia?

A

LDL receptor deficiency

21
Q

What is the inheritance pattern of primary Type IIa hyperlipidemia?

A

AD

22
Q

What is the lipid elevated in the blood of an individual with primary Type IIa hyperlipidemia?

A

cholesterol

23
Q

What is the lipoprotein elevated in the blood in a person with primary Type IIa hyperlipidemia?

A

LDL

24
Q

What are the symptoms in those with primary type IIa hyperlipidemia?

A

high risk of atherosclerosis and coronary artery disease

xanthomas of achilles tendon

tuberous xanthomas on elbows

xanthelasmas

corneal arcus

  • If patient homozygous, usually death < 20 years
25
Q

What are factors that exacerbate the symptoms associated with that Type I hypertriglyceridemia?

A
  • decreased glucose and triglyceride uptake in adipose tissue
  • overactive hormone-sensitive lipase
  • unreactive lipoprotein lipase
26
Q

What is the most common type of hyperlipidemia?

A

Type V

27
Q

Why do individuals with hyperlipidemia Type V have elevated serum triclycerides in VLDL and chylomicrons in response to a meal containing carbs and fat respectively?

A

insulin has important regulatory function in adipose tissue and promotes LPL activity by increasing transcription of its gene.

therefore in diabetes there is low activity of LPL and the inability. to degrade the serum triglycerides in lipoproteins to facilitate uptake of fatty acids into adipocytes

28
Q

Abetalipoproteinemia is a hyper or hypolipidemia?

A

hypolipidemia

29
Q

What is the pathology behind abetalipoproteinemia?

A

patients have low to absent serum apoB-100 and apoB-48.

because chylomicron levels are low, fat accumulates in intestinal enterocytes and in hepatocytes.

Essential fatty acids and vitamins A and E are not well absorbed.

30
Q

What are some symptoms of abetalipoproteinemia?

A
  • steatorrhea
  • cerebellar ataxia
  • pigmentary degeneration in the retina
  • acanthocytes (thorny appearing erythrocytes)
  • possible loss of night vision
31
Q

Cholesterol is req’d for what biosynthetic proceses?

A

membrane synthesis, steroid and vitamin D synthesis, and in the liver, bile acid synthesis

32
Q

Cholestyramine MOA.

A

increase elimination of bile salts and force the liver to increase their synthesis from cholesterol, thus lowering the internal level of cholesterol in the hepatocytes

inc. LDL receptor expression,

33
Q

MOA of HMG-CoA reductase inhibitors?

A

inhibit de novo cholesterol synthesis in the hepatocyte, which subsequently increases LDL receptor expression

34
Q

What is the importance of farnesyl PPi?

A
  • synthesis of CoQ ETC
  • synthesis of dolichol PPi for N-linked glycosylation of proteins
  • prenylation of proteins (a posttranslational modification) that needs to be held in the cell membrane by a lipid tail.
35
Q

Insulin activates HMG CoA reductase through phosphorylation or dephorylation?

A

dephosphrylation

36
Q

How does glucagon affect HMG CoA reductase?

A

inhibits it

37
Q

What should be the ideal blood level of LDL?

A

< 100 mg/dL

38
Q

What is the max time for statins to reach their full effect?

A

4-6 weeks

39
Q

When should LFTs be measured after taking statins?

A

within 2-3 months

40
Q

Explain the pathology of muscle dysfunction after taking statins.

A

lessening of downstream synthesis of CoQ req’d in the ETC so less ability to produce ATP that is req’d for muscle contraction

41
Q

Why is there red-brown urine findings after taking statin drugs?

A

breakdown of myoglobin because of damaged muscle cells

42
Q

Why could there be increase CRP after using statins? What is an associated condition with elevated CRP?

A

is a liver protein that is secreted inn inflammation. There is direct correlation between elevated CRP and atherosclerosis.

43
Q

Draw out the path in cholesterol metabolism.

A

Kaplan: Biochemistry Part I (27 decks)

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