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Drugs: from molecules to man > Hyperlipidaemia and its treatment > Flashcards

Hyperlipidaemia and its treatment Flashcards

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Organic Chemistry 101 flashcards
1
Q

What is hyperlipidaemia a major risk factor for?

A

serious cardiovascular disorders such as heart attack, stroke and angina

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2
Q

Where does the blood supply for the heart come from?

A

The coronary blood supply?

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3
Q

What is coronary artery disease and what is heart disease?

A
  • Coronary artery disease is the build up of the fatty plaque (angina and heart attack)
  • Heart disease is the process of having the fatty plaque
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4
Q

What is angina and what is it the warning sign for?

A
  • heart is temporarily deprived of oxygen

- warning sign for a heart attack

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5
Q

What is a heart attack and what does it lead to?

A

The heart is deprived of oxygen. This compromises the heart’s ability to pump properly and leads to heart failure

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6
Q

What are dysrhythmias?

A

interrupted heart rhythm

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7
Q

What are the numbers associated with hyperlipidaemia?

A
  • 1.5 million have had a heart attack (11% die within 30 days) – (1965 70% fatal)
  • 2.3 million people have coronary heart disease
  • 2 million people have angina
  • 920, 000 people have heart failure
  • Heart attack and angina: £6.7 billion cost to UK economy
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8
Q

How do you prevent coronary heart disease?

A
  • Primary prevention: stopping it happening
  • Secondary prevention: stop it recurring or worsening (after angina, heart attack or stroke)
  • Lifestyle interventions
  • Drugs
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9
Q

What do lipoproteins do and what are they composed of?

A
  • Transport lipids in plasma
  • Composed of:
  • Lipids (triglyceride or cholesterol esters) PLUS
  • Phospholipids, cholesterol, proteins
  • Phospholipid outer layer and Apo lipid proteins
  • Cholesterol and triglycerides in core (hydrophobic core)
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10
Q

What do lipoproteins vary in?

A
  • Lipid content
  • Size and type of protein, DENSITY:
     HDL (high)
     LDL (low)
     VLDL (very low)
     Chylomicrons (lowest density)
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11
Q

Describe the production and absorption of cholesterol

A
  • Hepatocyte synthesises cholesterol
  • Cholesterol used by liver to make bile acids, these are secreted into GI tract, they act as a detergent, Bile acids recycled back to liver
  • Dietary fats taken up by GI tract into chylomicrons
  • Chylomicrons transport fats to the tissue
  • Tissue takes up fatty acid after breaking down fats using lipoprotein lipase
  • What’s left is termed chylomicron remanent, taken up by the liver where it delivers cholesterol
  • Liver then produces VLDL (releases into circulation) and HDL
  • VLDL delivers more fat to the tissues and in doing that is converted into LDL
  • LDL delivers cholesterol to the tissues (cholesterol uptake)
  • HDL takes up cholesterol from the tissues and delivers it to VLDL (cholesterol recycling)
  • LDL can be recognised by liver and taken up
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12
Q

What are LDL and BDL known as and why?

A
  • LDL and VDL known as bad cholesterol
     Involved in formation of fatty streaks
     Inhibit fibrinolysis (prevent fibrin breakdown)
     Activate platelets (increase aggregation)
     Increased risk of atherosclerosis
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13
Q

What do high levels of LDL lead to?

A 
- Stenosis (narrowing) caused by fatty plaques in the vessel wall leads to:
 Ischaemia (angina)
- Plaque ruptures, leads to: 
 Thrombosis, leads to: 
 Heart attack, stroke
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14
Q

What does HDL do?

A
  • Increases fibrinolysis (increase fibrin degradation)
  • Increase prostacyclin formation (decrease aggregation)
  • High HDL/LDL – lower risk of atherosclerosis
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15
Q

Give features of hyperlipidaemias

A
  • Number of different forms
  • High level of lipids in blood
  • Different disturbances in LDL, VLDL, cholesterol etc
  • Treated differently
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16
Q

What is familial hypercholesterolaemia, who has it and how can it be treated?

A
  • Defect in LDL receptor or ApoB protein
  • Autosomal dominant
  • 1:500 in UK heterozygous
     CVD by age 30-40
  • 1:1000000 homozygous
     Severe CVD in childhood
  • Treated using statins but other drugs may be added too
17
Q

What are the main components of an atherosclerotic plaque?

A

the nuclei of foam cells

18
Q

What did foam cells start off as and what has this led us to recognise?

A

Foam cells started off as macrophages. This has led us to recognise that atherosclerosis is a chronic inflammatory condition instead of a lipid storage disease

19
Q

How does a macrophage turn into a foam cell and then a fatty plaque?

A
  • Hyperlipidaemia: excess LDL in blood circulation enters the intima of a blood vessel
  • Immune cells enter the intima: Monocytes migrate into the intima and transform to macrophages
  • Macrophages transform into foam cells: macrophages take up oxidised LDL and transform to foam cells. Foam cells release cytokines and other growth factors that recruit smooth muscle cells
  • Formation of fatty plaque: the foam cells attach to the endothelium and form the fatty streak. Migrating smooth muscle cells thicken the streak into a stable plaque
20
Q

What is the aim with lipid lowering drugs?

A
  • Reduce LDL/VLDL

- Increase HDL

21
Q

Give an example of a statin?

A

Atorvastatin

22
Q

What do statins do?

A
  • Competitively inhibit HMG-CoA reductase, rate limiting enzyme in production of cholesterol (similar in structure)
  • Reduces liver production of cholesterol
  • Lowered cholesterol leads to more LDL receptors (increased removal of LDL from plasma)
  • Also increase HDL and lower triglycerides
23
Q

Give a summary of initial steps in the synthesis of cholesterol

A
  • Acetyl-coenzyme A leads to:
  • HMG-CoA (using HMGCoA reductase) leads to:
  • Mevalonate, leads to:
  • Cholesterol
24
Q

What are problems with statins?

A
  • Cause Myositis (muscle inflammation)
  • Rhabdomyolysis (muscle breakdown) – myoglobin released from muscles, ends up in urine and leads to kidney failure (renal failure)
  • Altered liver function tests
25
Q

What is QRISK 3?

A
  • Calculates risk that you will have a heart attack or stroke in next 10 years
  • Uses age, ethnicity, smoking status, weight, other illnesses to assess risk
  • Cut off for statin treatment for PRIMARY PREVENTION is 10% (was 20%)
  • Also used to calculate secondary prevention
26
Q

What does Ezetimibe do and what does this result in?

A
  • Inhibits intestinal cholesterol absorption
     Inhibits specific cholesterol transport in gut
  • Results in:
     Reduced LDL
     Reduced total cholesterol
27
Q

Who is ezetimibe administered to?

A
  • Can be used in patients who cannot tolerate statins
  • Co-administered with statins in resistant cases of familial hyperlipidaemia
     Gives dual inhibition of cholesterol absorption and synthesis
28
Q

What do anion exchange resins do?

A

bind to bile acids in gut and stops it from being reabsorbed and recycled (leads to increased usage of cholesterol by the liver)

29
Q

What do fibrates do?

A

agonists at a receptor called PPARa. May be used with elevated VLDL (lower LDL)

30
Q

What does nicotinic acid do?

A

Something associated with vitamin B3

31
Q

what do fish oils do?

A
  • Reduces plasma triglycerides, increase cholesterol

 Appears to reduce platelet aggregation and reduce fibrinogen

32
Q

What does NICE conclude to do with Omega 3 derivatives?

A

there is little evidence to support the use of them?

33
Q

What is Olestra?

A

• Olestra is a fatty acid derivative

  • Can’t be absorbed from GI tract
  • Behaves pretty much the same way as ordinary fats when cooked with them
34
Q

Why is Olestra not the answer to lowering cholesterol?

A
  • Fat-soluble vitamins with stay in the Olestra and you won’t be able to absorb them
  • Diarrhoea
  • Compensatory eating (end up with more calories probably)
  • Anal leakage
  • Olestra banned in EU and Canada
35
Q

What are other ways to control hyperlipidaemia?

A
  • Dietary modifications can help by blocking absorption of cholesterol
  • Stanols and sterols are plant steroids that you can take in supplemented food like Benecol margarine
  • Oat bran and other high fibre foods can help, so can soluble fibre products like Metamucil

Drugs: from molecules to man (22 decks)

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