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Block 9 Week 2 > Anti-hyperlipidemic drugs Physio- Duan > Flashcards

Anti-hyperlipidemic drugs Physio- Duan Flashcards

1
Q

What are lipoproteins?

A

protein-lipid complexes responsible for transport of plasma lipids

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2
Q

What are found on the surface of Lipoproteins?

A
  • phospholipids
  • unesterified cholesterol
  • Apolipoproteins
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3
Q

What is the core of a lipoprotein made up of?

A
  • Cholestery esters (CE)

- Triglycerides (TGs)

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4
Q

What are the lipids in lipoproteins?

A

TAGs
Phosopholipids
Cholesterol Cholesteryl esters

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5
Q

What Lipoproteins (LP) are greater than 30 nm?

A

-Chylomicrons, VLDL, and catabolic remnants

D <1.006 g/ml

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6
Q

What LPs are 20-22 nm in size?

A

LDL

D=1.019-1.063g/ml

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7
Q

What LPs are 9-15 nm in size?

A

9-15 nm

D=1.063-1.21 g/ml

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8
Q

Put the types of lipoproteins in order from LARGEST densitiy and SMALLEST diameter to least dense and largest diameter.

A

HDL>LDL>IDL>VLDL>Chylomicron

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9
Q

What are the 2 pathways for lipoprotein metabolism?

A
  • Exogenous/chylomicron pathways (dietary fat i.e you eat it)
  • Endogenous pathway (lipids synthesized by the liver)
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10
Q

How do package fats into chylomicrons?

A

Bile salts solubilize dietary TG-> TGs are hydrolyzed by pancreatic lipases-> diffuse into intestinal epithelial cells-> TGs re-synthesized in ER->packaged into chylomicrons

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11
Q

What is the composoition of a chylomicron?
What lipoproteins are associated with it?
What is the half life?

A 
TG  > 90%    
CE + cholesterol <  5%
Phospholipids 5-10 %  
Protein 1-2 %  
Fat soluble vitamins

Apo A, B-48 initially
Apo E and Apo C’s
acquired in circulation

5-30 minutes

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12
Q

How do you breakdown TAGs in chylomicrons into FFA and glycerol and what happens to these?

A

Lipoprotein lipase is activated by Apo C-II on surface of capillaries of adipose and muscle tissue

  • hydrolyzes TG to free fatty acis and glycerol
  • FFA can be reused for energy or re-esterified
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13
Q

How do you go from a chylomicron to a chylomicron remnant?

A
  • as chylomicrons lose their TAGs via LPL (activated by apo- CII) they shrink.
  • Apo E and Apo C are transferred to HDL
  • WHEN ALL APO C IS GONE you now have a chylomicron remanant with CE> TG
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14
Q

What happens to the chylomicron remnants?

Whats the half life of these?

A

Since they have lose Apo C-II, LPL is no longer activated and the remnants are taken up by liver
-about 5 minutes

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15
Q

Explain the exogenous/chylomicron pathway of metabolism

A

Step 1: Bile salts solubilize dietary TGs and hydrolyzed by pancreatic lipases-> go into intestinal -> TGs re-synthesized in ER->packaged into chylomicrons
Step 2: LPL activated by ApoC-II breaks down TAG into glycerol and FFA.
Step 3: chylomicrons become remnants via loss of all APO C and get taken up by liver

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16
Q

(blank) is responsible for endogenous TG formation and transport

A

VLDL

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17
Q

What is the composition of VLDL?

A 
(smaller than chylomicrons)
Surface Monolayer 
      - Phospholipids (12%)
      - Free Cholesterol (14%)
      - Protein (4%)
Hydrophobic Core - Triglyceride (65%) 
      - Cholesteryl Esters (8%)
      - C 8-10 %, CE 12-15 %
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18
Q

What are the lipoproteins on VLDL?

What is the half life of VLDL?

A

Apo Cs (CII from HDL)
Apo E, Apo B-100
12 hours

19
Q

How does VLDL get their Apo Cs and apo Es and CE?

A

acquired from HDL in circulation

20
Q

VLDL decrease in size to become (blank) .
What is the composition of IDL?
What are the lipoproteins in IDL?
What is the half-life?

A

IDL
TG=CE
Apo Cs, Apo E, Apo B-100
-minutes to 1 hour

21
Q

What happens to IDL?

A

50% gets taken up by liver via ApoE and Apo B-100

THE other 50% loses TG and becomes LDL

22
Q

(blank) activates LPL which catalyzes the hydrolysis of TG

A

ApoC-II

23
Q

(blank) is the primary carrier of cholesterol

A

LDL

24
Q

What is the composition of LDL?

A

TGs ~ 5%
C + CE ~ 70 %
Protein ~ 20 %

25
Q

LDL is removed from its stores by (Blank). What is the half-life of LDL?

A

lipoprotein ApoB-100

2.5-3 days

26
Q

Where will you find apo B-100?

A

component of VLDL, IDL, LDL

27
Q

What is Apo B-100 positively correlated with?

A

increased cardiovascular disease

28
Q

What is one of the most common mutations in humans invoving an APO?
What causes it?
What will this substitution lead to?
What does this cause?

A
  • Familial defective Apo B (FDB)
  • Glutamine being substituted for arginine at AA 3500
  • missense mutation
  • problems with binding affinity of B-100 at its receptor (LDL receptor)
29
Q

Where do you find LDL receptors?

A

hepatic and extrahepatic tissues

30
Q

What happens when LDL particles binds to LDL receptors?

A

you get endocytosis and then cholesterol is de-esterified and released as free cholesterol in cytoplasm and can be used in membranes

31
Q

What happens to excess cholesterol that is not used in membranes?

A

it is re-esterified by ACAT

acyl-CoA-Cholestero AcylTransferase

32
Q

What is the endogenous pathway for metabolism?

A

Lipids synthesized by liver-> liver makes VLDL

33
Q

What does ACAT do in the intestine?

A

participates in th exogenous pathway and regulated dietary cholesterol absorption

34
Q

What does ACT do in the liver?

A
  • Participates in endogenous pathways and esterifies cholesterol for production and release of VLDL
  • Promotes foam cell formation and atherogenesis
35
Q

As your lipoprotein gets a bigger diameter what happens to its amount of total protein? total lipid?

A

protein goes down and lipid go up

36
Q

(blank) is a plasma lipoprotein particle whose lipid component includes cholesterol and triglycerides and is commonly referred to as “bad cholesterol” due to its role promoting atherogenic heart disease.

LDL in the plasma originates from VLDL produced by the liver with (blank).

VLDL is converted to LDL by the action of (blank) removing TAGs from the VLDL particle and releasing free fatty acids.
The removal of triglycerides from VLDL leaves a greater proportion of (blank), increasing the density of the particle and changing it to LDL.

A

LDL
ApoB-100
lipoprotein lipase (LPL)
cholesterol

37
Q

Where is HDL synthesized?
What does it do?
What is the composition of HDL?

A

syntheized in liver and small intestine.
Transports cholesterol from peripheral tissues to liver
CE and phospholipids (50%)
Lipoproteins (50%)

38
Q

What are the Lipoproteins found in HDL?

A

Apo A-I (cofactor for LCAT)
Apo A-II
Apo C-II, E

39
Q

What conversts cholesterol in to CE in HDL making it spherical shaped?

A

LCAT

40
Q

Why do HDL particles increase in size?

A

they pick up cholesterol and phospholipid molecules via transporters (ABCG1 and PLTP)

41
Q

Where does HDL transport choelsterol?

A

mostely to liver or steroidgenic organs (adrenals, ovary, testes) by direct and indirect pathways

42
Q

How is the contents of HDL removed?

A

via scavenger receptors and indirect pathways (most common in humans)

43
Q

Explain the indirect pathway of HDL content removal?

A

CETP exchanges TAGS of VLDL for CEs of HDL. VLDLs are processed to LDL which get removed. The TAGs now in the HDL ae not stable and are degraded by hepatic lipase which shrinks the HDL. It can now run around in the blood stream picking up cholesterol again :)

44
Q

Give me a summary of lipid metabolism

A

step 1:Dietary fat + bile (From liver)=chylomicron formation
step 2: chylomicron + LPL= FFA and glycerol and VLDL
step 3: VLDL goes to liver to become IDL
Step 4: LPL +IDL= FFA and LDL
Step 5: LDL goes to hepatic tissue (gets recycled back through) and extrahepatic tissue
Step 6: extrahepatic LDL becomes HDL.
Step 7: HDL + LCAT= LDL
Step 8: LDL gets cycled back into liver

Block 9 Week 2 (7 decks)

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