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P&T Block 1 > L23 > Flashcards

L23 Flashcards

1
Q

What are the 3 components of the outside of a lipoprotein particle? What is in the core?

A

Apo-lipoproteins + free cholesterol + phospholipids = outer

Core = TGs + cholesterol esters

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2
Q

What surface molecule is unique LDL? HDL? (remember LDL & HDL are low/high density lipoproteins)

A

LDL, IDL, VLDL, remnants = apoB (binds LDL receptor)

HDL = apoA1

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3
Q

Equation for LDL

A

LDL = TC - (TG/5) - HDL

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4
Q

Does the liver secrete VLDL, IDL, or LDL?

A

VLDL

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5
Q

What happens to VLDL in circulation?

A

VLDL –> IDL
Releases TGs –> FFAs
- By lipoprotein lipase
FFAs can be taken into tissue for use and E source or into adipocytes for storage

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6
Q

What are IDL

A

Intermediate density lipoproteins = smaller, cholesterol enriched remnants

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7
Q

What happens to IDL in circulation

A
  1. Back to liver - donates cholesterol

2. IDL –> LDL, release more TGs –> FFAs into circulation

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8
Q

What is the fxn of LDL in the blood

A

Cholesterol transporter to either liver or other tissues

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9
Q

What happens if LDL is oxidized?

A

= athrogenic form

Can be taken up by marcophages without limit –> foam cell formation –> atherosclerosis

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10
Q

Describe LDL endocytosis

A

apoB + LDL receptor
In via clatharin coated pits
LDL into lysosome
Receptor recycled to membrane

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11
Q

Fxn of PCSK9 - SEs

A

LDL receptor degradation - no separation from LDL particle into lysosome
Net increase LDL in circulation b/c no receptors to bind to on tissues

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12
Q

Potential treatment for overactive PCSK9

A

mAb

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13
Q

Describe familial hypercholesterolemia - 4 most likely causes

A

High LDL –> premature CHD

  1. Hetero or homozygous for LDL receptor
  2. Mutated apoB so can’t bind LDL
  3. Mutated PCSK9 - excess
  4. LDL RAP1 mutations - can’t make clatharin pits for endocytosis
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14
Q

Physical exam findings for FH

A

Xanthomas

  • Achilles tendon
  • Corneal arcus = young pts
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15
Q

What is phytosterolemia?

A

Clinically present like FH, but doesn’t have to do with LDL

Increased absorption of non-cholesterol plant sterols

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16
Q

What is familial combined hyperlipidemia (2b)

A

Overproduce apoB - increased VLDL production

- Increased LDL & TGs

17
Q

What is type 3 hyperlipidemia? Labs + physical exam findings

A 
"Remnant removal disease"
2 hits
- Homozygous for apoE - can't clear LDL correctly 
- Metabolic condition - T2D, etc
High cholesterol, TG, IDL
Yellow palm streaks + xanthomas
18
Q

Steps of TG digestion when eaten in food

A
  1. TG uptake - catabolized by gastric & pancreatic lipases
  2. FFAs –> chylomicrons in lymph –> venous circulation
  3. Chylomicrons anchors by GPIHBP1 - allows lipoprotein lipase to breakdown TGs –> FFAs
  4. FFAs stored in fat or muscle
19
Q

IF you have diabetes, why would you also have high TGs?

A

Increased adipocyte lipolysis
Excess VLDL secretion
VLDL –> LDL or HDL
Can undergo another TG reduction –> small, denser HDL & LDL

20
Q

What are the characteristics of smaller, denser HDL and LDL?

A 
sdHDL = less efficient at cholesterol return to liver
sdLDL = more athrogenic
21
Q

Mechanism by which sdLDL is more arthrogenic

A

Less affinity for LDL receptor - more time in circulation
Easier entry into arterial wall
More susceptible to oxidative damage

22
Q

Normal blood TG levels

A
23
Q

Physical exam findings of high TGs

A

Xanthomas
Yellow palm streaks
Form layer in plasma overnight

24
Q

What lifestyle changes can significantly decrease TGs

A

Weight loss

Low fat diet - high in omega 3s

25
Q

Fxn of HDL

A

Reverse transport
Bring cholesterol from tissues (interstitial macrophages) to liver or to tissue that use cholesterol to make steroid hormones

26
Q

LCAT fxn

A

Free cholesterol –> cholesterol esters in HDL formation

27
Q

ABCA1 fxn

A

Free cholesterol uptake into new HDL

28
Q

Tangier’s disease

A

ABCA1 defect

Lipids build up in macrophages –> swollen reticuloendothelial organs (tonsils)

29
Q

LCAT deficiency may result in…

A

Corneal opacification

30
Q

Mechanism for high saturated fat diet causing high cholesterol

A

satFAs X LDL receptor
Proinflammatory
Prothrombotic

31
Q

Which diet improves CHD survival rates?

A 
Mediterranean diet 
Specifically, foods that lower LDL are:
- Soluble fiber (oatmeal, cereals)
- Antioxidants (artichokes) 
- Cherries
- Chili peppers
32
Q 
Which of the following are TG rich vs cholesterol rich:
Chylomicrons
VLDL
LDL
HDL
A

Chylomicrons & VLDL = TG rich

LDL & HDL = cholesterol rich

P&T Block 1 (43 decks)

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