Lipdaemias And Lipid Lowering Drugs Flashcards Preview

Cardio-respiratory Physiology And Pharmacology > Lipdaemias And Lipid Lowering Drugs > Flashcards

Flashcards in Lipdaemias And Lipid Lowering Drugs Deck (19)
0

What is hyperlipidaemia ?

Excess of lipid in plasma - especially CH and TG

1

How are lipids transported in the plasma ?

In lipoproteins

2

Explain the structure of the lipoprotein..

Central core containing cholesteryl esters and TG
Hydrophilic mono layer of polar phospholipids, free CH and apoprotein

3

What are the 4 main classes of lipoproteins ?

Chylomicrons
LDLs
VLDLs
HDLs

4

Describe chylomicrons...

High ratio of TG to CH
From GIT taken to tissues where they are hydrolysed by lipoprotein lipase to glycerol and fatty acids
The cholesteryl ester remnants from is is taken up by hepatocytes

5

What happens to cholesterol in hepatocytes ?

Stored
Converted to bile acids
Secreted unaltered in bile acids
Enters endogenous pathway

6

Describe VLDLs ...

Lower TG to CH ratio compared to chylomicrons
Transport new synthesised TG and CH to muscle and adipose
TG hydrolysed by tissue and glycerol and fatty acids used by the cells
Left over cholesteryl esters make the VLDLs turn into LDLs

7

Describe LDLs...

Highest density of CH
Some of the CH is taken up by tissues, some by liver

8

What is cholesterol used for in the body ?

Make cell membranes
Synthesis of steroids
It's a source of bile acids

9

Describe HDLs...

Similar CH levels to VLDLs - have more protein than TG
Absorbe CH produced in tissue breakdown and return it to plasma
cH is ester ivied with long chain fatty acids and then the cholesteryl esters transferred to VLDLs and LDLs in the plasma

10

What protein in the plasma is used to transfer cholesteryl esters to VLDLs and LDLs ?

Cholesteryl ester transfer protein (CETP)

11

Explain the non-specific pathway ..

LDLs taken up by endothelial cells causing monocytes/macrophages to produce free radicals that oxidise the LDLs
Produces modified LDLs that's taken up by scavenger receptors into macrophages
Activates the macrophage causing the, to release proinflammatory cytokines
Causes a build up of CH

12

What controls the pick up rate of LDLs in the plasma ?

The number of LDL receptors - can be up regulated or down regulated
- up regulation is inhibited by high LDLs levels

13

Why is LDL subtype LPa bad ?

Contains a unique apoprotein with a very similar structure to plasminogen substrate
It competes for the plasminogen receptor in endothelial wall
It prevents secretion of the plasminogen activator which means less plasminogen is produces and therefore fibrinoloysis is inhibited and thrombosis is promoted

14

What does high CH precede ?

Thrombosis
Myocardial infarction
Cerebral vascular blockade
Xanthomas

15

Who is at particular risk of high CH ?

Family history - hypercholesteremia
Smokers
Hypertensives
Diabetics

16

Explain the primary defect that causes high CH..

Genetic defect - dysfunctional LDL receptors or they are not expressed

17

What aRe the secondary aetiology for hyperlipidaemia ?

Diabetes
Hypothyroidism
Uraemia
Alcoholism
Oestrogen contraceptives

18

What does atherogenesis involve ?

1- endothelial dysfunction with altered prostaglandin biosynthesis
2- injury of dysfunctional endothelium causes expression of adhesion molecules - encourages movement of monocytes into the intima
3- LDL particles transported into vessel wall - endothelial cells and monocytes/macrophages produce free radicals which oxidise LDLs
4- oxidised LDLs taken up by macrophages by scavenger receptors which activates macrophages causing release of proinflammatory cytokines
5- sub endothelial accumulation of macrophages and t lymphocytes causes formation of fatty streaks
6-CH can be mobilised for the endothelial cell wall and transported in plasma in form of HDLS
7- more immune response causes proliferation of smooth muscle and deposition of connective tissue
Reducing a dense fibrous cal poberlying the lipid rich core fo ring an atherpmatous plaque