Lipoproteins Flashcards

1
Q

what disorder is caused by ApoB truncations

A

hypobetalipoproteinemia

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2
Q

what is the consequence of truncated ApoB

A

secreted slower and cleared faster

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3
Q

what are the hypobetalipoproteinemia heterozygote LDL levels

A

25-50% of normal

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4
Q

what are the consequences of hypobetalipoproteinemia

A

tseato-hepatitis, and homozygotes get fat soluble vit deficiency and nueromuscular degeneration

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5
Q

where are VLDLs with truncated ApoB cleared?

A

renal tubule

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6
Q

abetalipoproteinemia is caused by

A

MTP definceicy

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7
Q

what does MTP do?

A

transport TG’s and cholesterol esters onto ApoB to form VLDL

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8
Q

which 2 conditions are caused by excessive ApoB synthesis in the liver?

A

Familial combined hyperlipidemia and hyperbetalipoproteinemia

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9
Q

what does Hyperapobeta look like

A

dense ApoB-100 LDL with too much apo B

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10
Q

what does FCHL look like

A

increased number of normal VLDL

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11
Q

how can there be an accumulation of normal LDL in FCHL and hyperapobeta

A

defect in LDL clearance in addition to excess VLDL production

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12
Q

Is apoB production normally constant

A

yes

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13
Q

how is more lipid normally transported

A

bigger particles

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14
Q

what happens in familial hypertriglyceridemia

A

high liver TG synthesis, TG plasma concentration, and TG/apoB ratio

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15
Q

what FHT patients tend to get CVD

A

those with a family history of CVD

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16
Q

is HDL low or high in all FHT

A

low

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17
Q

what are FHT + CAD patients likely to have

A

insulin resistance

18
Q

what things raise VLDL or TG production

A

dietary fat, visceral fat, high glucose, fructose, and alcohol

19
Q

why are visceral adipocytes bad

A

they release alot of free fatty acids

20
Q

what leads to visceral fat

A

hyperandrogenism in women, hypoandrogenism in men, and hypercortisolism

21
Q

what do saturated fatty acids do

A

stimulate cholesterol synthesis and down regulate LDL receptors

22
Q

what does LPL do

A

hydrolyzes CLDL and CM to free fatty acids is adipose cells, muscle cells, and macrophages

23
Q

what is required for LPL

A

ApoCII

24
Q

what inhibits LPL

A

ApoCIII

25
Q

what does a deficiency of LPL of ApoCII do

A

severe hypertriglyceridemia

26
Q

what does LPL biosynthesis require

A

small amount of insulin

27
Q

what is Type I HLP

A

only high chylomicrons

28
Q

what is Type V HLP

A

high VLDL and chylomicrons. clear cream and foggy plasma

29
Q

what are the only things that cause Type I HLP

A

deficiency of LPL or ApoCII

30
Q

what causes Type V HLP

A

VLDL over production and slight LPL abnormality

31
Q

when is ApoCIII elevated

A

insulin resistance

32
Q

does plasma TG correlate better with ApoCII or ApoCIII

A

ApoCIII

33
Q

where is ApoE synthesized

A

liver. macrophages, and CNS

34
Q

when is apoE secreted by macrophages

A

along with cholesterol

35
Q

what is the main function of apoE

A

clearing remnants of lipoproteins

36
Q

where is apoE kept

A

on HDL and then transferred to other particles

37
Q

what protein prevents apoE from removing CMs and VLDL too soon

A

apoCIII

38
Q

why to larger particles not bind apoE

A

the binding site is covered by lipid

39
Q

how does apoE bind

A

charge interaction

40
Q

what apoE phenotype is seen in familial dysbetalipoproteinemia

A

E2/E2

41
Q

what do E2 heterozygotes get

A

low LDL and high TG without the disease

42
Q

what do E4 people get

A

high LDL