Lipoproteins Flashcards

(42 cards)

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

24
Q

what inhibits LPL

25
what does a deficiency of LPL of ApoCII do
severe hypertriglyceridemia
26
what does LPL biosynthesis require
small amount of insulin
27
what is Type I HLP
only high chylomicrons
28
what is Type V HLP
high VLDL and chylomicrons. clear cream and foggy plasma
29
what are the only things that cause Type I HLP
deficiency of LPL or ApoCII
30
what causes Type V HLP
VLDL over production and slight LPL abnormality
31
when is ApoCIII elevated
insulin resistance
32
does plasma TG correlate better with ApoCII or ApoCIII
ApoCIII
33
where is ApoE synthesized
liver. macrophages, and CNS
34
when is apoE secreted by macrophages
along with cholesterol
35
what is the main function of apoE
clearing remnants of lipoproteins
36
where is apoE kept
on HDL and then transferred to other particles
37
what protein prevents apoE from removing CMs and VLDL too soon
apoCIII
38
why to larger particles not bind apoE
the binding site is covered by lipid
39
how does apoE bind
charge interaction
40
what apoE phenotype is seen in familial dysbetalipoproteinemia
E2/E2
41
what do E2 heterozygotes get
low LDL and high TG without the disease
42
what do E4 people get
high LDL