Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Semester 2 Pharmacology > Cholesterol lowering drugs > Flashcards

Cholesterol lowering drugs Flashcards

1
Q

Describe the structure of a lipoprotein

A
  • Central core of hydrophobic lipid (Triglyceride or cholesterol esters)
  • Hydrophilic coat of polar substances (Phospholipids, free cholesterol and associated proteins; apoproteins or apolipidproteins)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 5 classes of lipoproteins?

A

1) High density lipoprotein (HDL)
2) Intermediate density lipoprotein (IDL)
3) Low density lipoprotein (LDL)
4) Very low density lipoprotein (VLDL)
5) Chylomicrons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Rank from smallest to largest, the classes of lipoprteins

A
  • High density lipoprotein
  • Low density lipoprotein
  • Intermediate lipoprotein
  • Very low density lipoprotein
  • Chylomicron Remnant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What varies between the different classes of lipoprotein?

A
  • Core lipids (Ratio of triglycerides to cholesterol)
  • Size
  • Density
  • Apoproteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the role of lipoprotein?

A

Transport hydrophobic substances e.g. cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the two ways that the body can get cholesterol?

A

1) Exogenous pathway: Cholesterol is taken in from the diet and absorbed in the gut
2) Endogenous pathway: Cholesterol is produced in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the exogenous pathway for cholesterol

A
  • Dietary cholesterol is taken in
  • broken down into fatty acids, glycerol and cholesterol
  • Products are absorbed (some of these require active processes)
  • Fatty acids and cholesterol are taken up into Chylomicrons (rich triglyceride centre > CE)
  • Enters into circulation
  • Interact with specific tissues (vascular endothelium of peripheral tissues) and bind to lipoprotienlipases, which generate free fatty acids from the centre
  • This reduces the triglyceride content form the centre of the chylomicrons forming chylomicron remnants (CE>TG) which are circulated to the liver
  • Interaction with surface receptors causes endocytosis and the distribution of the CE rich core
  • Some cholesterol can be requested with bile acid
  • Can strip excess cholesterol out into the GI system if there is too much
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the endogenous pathway

A
  • There is a source of Acetyl-coenzyme A which can be used to form Cholesterol (process)
  • The cholesterol level is regulated by the amount of free cholesterol in the diet
  • The cholesterol is packaged into VLDL (high content of triglycerides>CE)
  • These can be recognised by lipoproteinases which causes the release of fatty acid into tissues
  • This causes the formation of LDLs (CE) which delivers the cholesterol to the tissues requiring it
  • These are then taken back to the liver where they are endocytosed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens to cholesterol released by dying cells?

A
  • Taken up by high density lipoprotein

* HDL is repackaged to LDLs or VLDLs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the role of Chylomicrons?

A
  • Transports Triglycerides and cholesterol esters from the GI system to tissue
  • Split by lipoprotein lipase to release free fatty acids which are taken up by muscle and adipose tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the role of Chylomicron remnants?

A
  • Taken up by the liver

* Cholesterol is then stored, oxidised to bile acids or released to VLDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the role of VLDL?

A
  • Transports cholesterol and newly synthesised Triglycerides to tissues
  • Triglycerides are removed from VLDL leaving LDL with a high cholesterol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the role of HDL?

A

• Absorbs cholesterol from cell breakdown and transfers it to VLDL and LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is high plasma cholesterol associated with high LDL a risk factor for?

A 
• Coronary heart disease
• Atheromatous disease 
• May lead to:
- Atherosclerosis
- Ischaemic heart disease
- Myocardial infarction 
- Cerebral vascular accidents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is hyperlipidaemia?

A

An increase in the plasma concentration of lipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the average total cholesterol level in the UK?

A

5.7mmol/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the ideal level of cholesterol?

A

<5mmol/l

18
Q

What is a moderately high cholesterol level?

A

6.5 to 7.8mmol/l

19
Q

What is a very high cholesterol level?

A

> 7.8mmol/l

20
Q

When looking at a person’s cholesterol level, what must also be taken into account?

A
  • Ratio between ‘good’ HDL and ‘bad’ LDL cholesterol

* Other risk factors for cardiovascular disease

21
Q

Which 3 sources is cholesterol derived from?

A
  • De novo synthesis in the liver
  • Uptake from circulating LDLs
  • Uptake of chylomicron remnants
22
Q

Give the 4 mechanisms used by lipid lowering drugs

A
  • Sequester bile acids in the intestine/ decrease hepatic stores of cholesterol
  • Inhibit transport protein for cholesterol on the brush border of enterocytes in the duodenum
  • Alter the levels of plasma lipoproteins
  • Inhibit the synthesis of cholesterol in the liver
23
Q

What is Colestramine and how does it work?

A
  • Basic anion exchange resin
  • Sequesters bile acids to prevent enterohepatic recirculation
  • Increases the metabolism of endogenous cholesterol into bile acids
  • Increases LDL receptor numbers in the liver resting in the removal of LDLs from the blood
24
Q

What can be used to decrease blood cholesterol by 50%?

A

Bile sequestering drugs and inhibitors of cholesterol biosynthesis

25
Q

What are fibres and how do they work?

A
  • Activators of lipoprotein lipase which decreases the triglyceride content of VLDL
  • Decrease plasma triglycerides and to a lesser extent cholesterol
  • Particularly decrease VLDL
  • Stimulates the clearance of LDL by the liver
  • Increases HDL production and reverses cholesterol transport
26
Q

What are the clinical uses of fibrates?

A
  • Mixed dyslipidaemia (i.e. raised serum triglyceride as well as cholesterol)
  • In patients with low HDL and high risk of atheromatous disease (Type 2 diabetes)
  • Combined with other lipid-lowering drugs in patients with severe treatment resistant dyslipidaemia
27
Q

What is nicotinic acid

A
  • (Niacin)
  • Vitamin with lipid lowering properties
  • Decreases VLDL production which leads to a decrease in LDL
  • Activates lipoprotein lipase
28
Q

What is Ezetimibe?

A
  • Specifically reduces intestinal cholesterol absorption

* inhibits a sterol carrier protein in the brush border of the enterocytes

29
Q

What are statins?

A
  • Hydroxymethlglutamyl-coenxyme A reductase (HMG-CoA reductase) inhibitors
  • Stops the conversion of HMG-CoA to mevalonic acid
30
Q

What are the long lasting HMG-CoA reductase inhibitors?

A
  • Simvastatin
  • Pravastatin
  • Atorvastatin
  • Rosuvastatin
31
Q

What are the clinical uses of statins?

A
  • Secondary prevention of myocardial infarction and stroke in those who have atherosclerotic diseases
  • Primary prevention of arterial disease in patients with high serum cholesterol
  • Atorvastatin lowers serum cholesterol in familial hypercholesterolaemia
32
Q

What are the side effects of statins?

A
  • Myositis
  • Angio-oedema
  • GI disturbances
  • Insomnia
  • Rash
33
Q

What are the side effect of fibrates?

A
  • Myositis (especially in patients with renal impairments)

* GI disturbances

34
Q

What are the side effects of Colestyramine?

A

• GI symptoms (nausea, abdominal bloating, constipation, diarrhoea)

35
Q

What are the side effects of ezetimibe?

A

• GI symptoms (nausea, abdominal bloating, constipation, diarrhoea)

36
Q

What are the side effects of Nicotinic acid?

A
  • Flushing
  • Palpitations
  • GI disturbances
37
Q

What are the two routes of the mevalonate pathway?

A
  • Cholesterol synthesis

* Protein prenylation

38
Q

What is protein Prenylation?

A
  • Addition of lipid tails to small GTPase signalling molecules
  • Ensures they are localised correctly
39
Q

What are the first 3 steps of the mevalonate pathway?

A
  • Acetyl Co A
  • HMG-CoA
  • Mevalonate
40
Q

Where in the mevalonate pathway do statins act?

A

They inhibit the enzyme HMG CoA reductase to prevent HMG Co A from being converted into Mevalonate

Semester 2 Pharmacology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions