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Pharm > Lecture 11: Drugs used to treat Atherosclerosis and Dyslipidemias > Flashcards

Lecture 11: Drugs used to treat Atherosclerosis and Dyslipidemias Flashcards

1
Q

What are the three lipoprotein complexes that lipid transport in the body is mediated by?

A
  • HDL
  • LDL
  • VLDL
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2
Q

What are Lipoproteins?

A

Packages of lipids surrounded by apolipoproteins and phospholipids

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3
Q

What is considered the good cholesterol?

A

HDL is considered the good cholesterol

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4
Q

What is considered the bad cholesterol?

A

LDL

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5
Q

What is linked to adverse cardiovascular events?

A

High levels of total cholesterol especially LDL-C

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6
Q

Which cholesterol is atherosclerotic plaques associated with?

A

High levels of LDL cholesterol

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7
Q

What are the issues with Athlersclerotic plaques?

A

They can cause thinning of blood vessels and when they rupture they can cause thrombosis

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8
Q

What do Athlersclerotic plaques develop from?

A

From the accumulation of lipids in transformed macrophages called foam cells

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9
Q

What do the foam cells in the fatty acid plaques have pathways to do?

A

Both accumulate cholesterol and get rid of cholesterol

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10
Q

How does accumulation of cholesterol work?

A

By binding and uptake of LDL and VLDLs by receptors and process them and turn them into free cholesterol

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11
Q

What is the uptake of cholesterol counteracted by?

A

The packaging of cholesterol into HDL

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12
Q

What is the overall approach of cholesterol therapies?

A

To reduce the circulating LDL-C

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13
Q

What does thinning and rupture of the cap around a plaque cause?

A

Pro-thrombotic factors that can lead to formation of thrombi and total vessel occlusion

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14
Q

What do Statins do?

A

Alter the balance between HDL and LDL cholesterol

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15
Q

Where does VLDL and LDL formation occur?

A

In the liver

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16
Q

What are Apolipoproteins packaged with?

A

Cholesterol and triglycerides

17
Q

What does Lipoprotein Lipase do?

A

It causes lipoproteins to break apart and release fatty acids that can be taken up into cells and be used as fuel

18
Q

What are the two sources of cholesterol in the liver?

A
  • Extrinsic cholesterol

* Intrinsic/synthetic cholesterol

19
Q

Where is Extrinsic Cholesterol from?

A

VLDLs or chylomicrons or dietary cholesterol

20
Q

Where is intrinsic cholesterol from?

A

Precursors like acetylcholine go into biosynthetics steps that leads to formation of cholesterol that is generated synthetically

21
Q

Which enzyme contributes to intrinsic Cholesterol?

A

HMG-CoA Reductase

22
Q

What is the Mevalonate pathway?

A

The pathway for cholesterol synthesis in the liver

23
Q

What is the rate-limiting enzyme in the pathway and is targeted by statins?

A

HMG-CoA Reductase

24
Q

What does HMG-CoA reductase do?

A

It catalyzes the formation of mevalonic acid from HMG-CoA

25
Q

Where does HMG-CoA primarily reside?

A

In the ER membrane

26
Q

What does Statins inhibiting HMG-CoA do?

A

It reduces the cholesterol pool in hepatocytes. This leads to increased expression of LDL (bad cholesterol) receptors and LDL is scavenged in the blood reducing circulating LDL

27
Q

What are the steps that make Statins work?

A

Statins inhibit HMG-CoA which means that there is less cholesterol available for packaging in the hepatocyte. this is sensed by hepatocytes and they scavenge the blood for LDL (bad) cholesterol and take it from the blood meaning there is less cholesterol available in the blood

28
Q

What is the mechanism of action of statins?

A

They are competitive inhibitors of HMG-CoA

29
Q

What is the common Statin?

A

Atorvastatin

30
Q

How are Statins are processed?

A

By first pass metabolism

31
Q

What do Fibrates target?

A

Receptors called PPARs

32
Q

What do PPARs do?

A

They act as transcription factors and influence transcription of genes

33
Q

What is the mechanism of action of fibrates?

A

They are agonists of PPARs

34
Q

What do Fibrates do in the that they bind to PPARs?

A

They increase the expression levels of Lipoprotein lipase which leads to increased breakdown of triglycerides in VLDLs and the uptake of fatty acids in fuel. This causes increased LDL uptake in the liver and reduced VLDL production in the liver

Pharm (31 decks)

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