Atheroma

Question 1

What is atheroma and what process develops this?

Answer 1

Atheroma is the development of plaques in the lumen wall via atherosclerosis.

Question 2

What happens to the arteries as a result of atheroma?

Answer 2

The plaques can cause narrowing of the lumen, partial or total blockage due to the formation of clots affecting blood flow.

Question 3

How is cholesterol obtained by the body?

Answer 3

Cholesterol is obtained through diet absorption and produced by the liver.

Question 4

How are cholesterol and lipids transported around the body and why?

Answer 4

They are transported as lipoprotein and they are transported this way as they are not soluble.

Question 5

What are the 4 types of lipoprotein?

Answer 5

Chylomicrons
VLDL
LDL
HDL

Question 6

What is LDL?

What is it referred to as?

Answer 6

LDL is a low density lipid rich in cholesterol and is termed bad cholesterol as high levels of LDL promotes atherosclerosis.

Question 7

What is HDL?

Answer 7

HDL, high density lipids are termed good cholesterol as the remove excess levels of cholesterol from the blood and take them to the liver to be excreted.

Question 8

How is cholesterol used by the body?

Answer 8

Cholesterol used by the body in 2 ways this includes the production of bile acids and the production of steroid hormones.

Question 9

What is the damaged at the beginning of the atherosclerosis pathway and what is affected by this damage?

Answer 9

Endothelial cells are damaged affecting the synthesis of PGI2 / NO and molecule expression.

Question 10

Once the EC is damaged what migrates into the arterial wall and what does this form?

Answer 10

Monocytes migrate into the arterial wall and form macrophages.

Question 11

What do the EC and Macrophages produce?

Answer 11

EC and Macrophages produce free radicals oxidising LDL.

Question 12

What do the oxidised LDL produce and what is released from this product?

Answer 12

Oxidised LDL produced foam cells which then release inflammatory cytokines.

Question 13

What happens to the foam cells following the release of inflammatory cytokines?

Answer 13

The foam cells coalesce producing fatty streaks.

Question 14

What is the final formation produced in the atherosclerotic pathway?

Answer 14

The final formation of the pathways is plaques produced from smooth muscle and connective tissue and if these plaques rupture thrombus occurs as a result.

Question 15

What correlation exist between cholesterol and atherosclerosis?

Answer 15

Increased levels of cholesterol specifically LDL lead to promotion of atherosclerosis.

Question 16

What causes hyperlipidaemias?

Answer 16

Increased levels of cholesterol and triglycerides lead to hyperlipidaemias.

Question 17

What treatment steps are followed in the treatment of hyperlipidaemias?

Answer 17

Initial is diet control and then drug treatment.

Question 18

What value is classed as
i) ideal cholesterol
Ii) high cholesterol

Answer 18

i) is 5mmol/L or less

ii) is 6.5 mmol/L or more

Question 19

What term is used to derived a patient experiencing hypercholestrolaemia despite having a good diet?

Answer 19

They are described as being familial hypercholestrolaemia.

Question 20

What other risk factors can cause hypercholestrolaemia?

Answer 20

High alcohol consumption

Liver/Kidney disease.

Question 21

What enzyme for the statins inhibit and what does this affect the synthesis of?

Answer 21

Statins inhibit HMG CoA reversibly which is the key enzyme in the production of mevalonic acid.

Question 22

Why is it key to affect the synthesis of mevalonic acid by lipid lowering drugs such as the statins?

Answer 22

It is key as mevalonic acids is converted into cholesterol so inhibition of the enzyme producing that will mean less cholesterol is produced.

Question 23

How else do the statins affect blood cholesterol content?

Answer 23

The increase the expression of hepatic LDL receptors and increase the clearance of cholesterol.

Question 24

Name 3 statins and explain why they are instructed to be taken in the evening?

Answer 24

Simvastatin, atrovastatin, lovastatin and they are taken in the evening to affect peak cholesterol synthesis in the morning.

Question 25

What side effects can be experienced with statin use?

Answer 25

GI problems, Muscle soreness / breakdown by affect muscular cellular systems.

Question 26

What population of patients would you not give Statins?

Answer 26

Patients who are pregnant or breastfeeding aswell as patients with liver disease.

Question 27

Give 2 examples of lipid lowering fibrates.

Answer 27

Bezafibrate and gemfibrozil.

Question 28

How do fibrates Lower triglyceride content and LDL content?

Answer 28

Fibrates stimulate lipoprotein lipase reducing VLDL / Chylomicrons content and increasing LDL receptor expression.

Question 29

Give examples of bile acid sequestrants.

Answer 29

Colestyramine, colestipol and colesevelam.

Question 30

How do bile acid sequestrants reduce cholesterol content within the blood?

Answer 30

Bile acid sequestrants bind to bile acids within the stomach stop it’s action on its corresponding receptors thus stimulating the production of bile acid from cholesterol. Increasing cholesterol demand, LDL expression and cholesterol clearance.

Question 31

What side effects are experienced when taking bile acid sequestrants?

Answer 31

Intestinal side effects such as bloating, ab discomfort and diarrhoea.

Question 32

How does nicotinic acid lower cholesterol levels?

Answer 32

Nictonic acid inhibits VLDL formation lowering triglyceride content reducing LDL production reducing cholesterol levels and increasing HDL levels.

Question 33

How does ezetimibe decrease the amount of cholesterol delivered to the liver?

Answer 33

It inhibits cholesterol absorption in the intestines.