Phospholipid pathophys Flashcards

1
Q

Is it true that every tissue in the body makes enough cholersterol to be self-sufficient

A

Yes

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2
Q

What is the desired direction of transport for triglycerides

A

from the gut and liver to the muscle to be utilized for energy

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3
Q

What is the desired route of transport for cholesterol

A

From the peripheral tissues back to the liver.

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4
Q

Does LDL do anything good>

A

No, its basically just an end product of VLDL metabolism and must be removed before it harms the vasculature

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5
Q

All lipoproteins contain what particles

A

cholestetrol, triglycerides, phospholipids

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6
Q

without lipoproteins

A

the fats contained inside them would coalesce into huge balls that would clog up any artery

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7
Q

Apolipoproteins

A

components of lipoproteins, serve three functions:

1) influence the structural characteristics of the lipoprotein particle
2) act as enzyme cofactors which activate or inhibit the various enzymes that control lipoprotein metabolism
3) May be ligands for cell receptors

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8
Q

What are chylomicrons and VLDLs

A

triglyceride rich lipoproteins made in the small intestine and the liver.

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9
Q

Disorders or Apo B synthesis cause problems why?

A

ApoB is the structural protein of Triglycerides and CMs. Neither the liver nor the intestine can secrete triglycerides without synthesizing Apo B.

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10
Q

Truncations of ApoB synthesis lead to ?

A

hypobetalipoproteinemia….caused by mutations which casue premature termination of ApoB transcription

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11
Q

Heterozygous hypobetalipoproteinemia

A

LDL is 25-50% of normal. May develop fatty liver.

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12
Q

Homozygous hypobetalipoproteiemia

A

very low LDL will have fat malabsorption…trouble absorbing vitamins A, E, and K. E deficiency can cause neuromuscular degeneration, k causes prothrombin deficiency

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13
Q

Abetalipoproteinemia

A

Microsomal Triglyceride Transfer Protein deficiency

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14
Q

What does MTP usually do

A

transfers triglycerides and cholesterol esters between phospholipid surfaces and controls the formation of a lipid droplet to which Apo B can attach.

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15
Q

heterozygote Abetalipoproteinemia

A

no abnormalities

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16
Q

Homozygotic abetalipoproteinemia

A

NO MTP so they cannot assemble chylomicron or VLDL particles so they are unable to transport triglycerides out of the liver or intestine

17
Q

hypo and abeta are very similar

A

Yes.

18
Q

Excess ApoB levels are associated with

A

Familial Combined Hyperlipidemia (FCHL) and hyperapobetalipoproteinemia.

19
Q

What is Apo B

A

the structural protein for CMs and VLDLs

20
Q

FCHL and hyperapoB are associated with:

A

increased risk of CV disease

21
Q

One well described genetic defect associated with FCHL is

A

heterozygous deficiency of Lipoprotein lipase

22
Q

hyperapo-B is characterized by:

A

“a cholesterol depleted apoB-100 LDL particle”

Loof for an increase in ApoB without an increase in LDL cholesterol

23
Q

Famlial hypertriglyceridemia

A

Over production of triglycerides

24
Q

What environmental factors can cause VLDL levels to increase

A

ANything that increases the amount of fatty acids or triglycerides being delivered to the liver. 1) Dietary Fat 2) Visceral Adipocytes 3) High glucose 4) Fructose and alcohoc

25
Q

Increased VLDL

A

increased risk of CVD

26
Q

Triglycerides characteristics

A

often present as xanthomas when tri’s are high. Crucial for moving energy around the body under physiologic conditions