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cardiovascular > Drug Regulation of Serum Lipids > Flashcards

Drug Regulation of Serum Lipids Flashcards

1
Q

What is dyslipidaemia?

A

An abnormal lipid profile

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2
Q

What are the three types of dyslipidaemia?

A

hypercholesterolaemia, hypertriglyceridaemia, mixed hyperlipidaemia

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3
Q

What is the target level for total cholesterol?

A

< 4.0 mmol/L

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4
Q

What is the target level for triglycerides?

A

< 2.0 mmol/L

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5
Q

What is the target level for HDL cholesterol?

A

> 1.0 mmol/L

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6
Q

What is the target level for LDL cholesterol?

A

< 2.5 mmol/L

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7
Q

What are the non-pharmalogical interventions for dyslipidaemia?

A

treat secondary causes and manage modifiable risk factors

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8
Q

How does smoking increase risk?

A

Damages the lining of the blood vessels - this both increases the likelihood of atherosclerosis and increases clotting so a greater risk of thrombosis

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9
Q

How does alcohol increase risk?

A

Increases triglyceride levels

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10
Q

How does a Mediterranean diet decrease risk?

A

By reducing cardiovascular risk

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11
Q

How do plant sterol esters decrease risk?

A

By reducing LDL cholesterol

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12
Q

How does fish oil decrease risk?

A

reduces triglycerides and increases HDL

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13
Q

Which lipoproteins can deposit lipids into artery walls?

A

Lipoproteins containing apoB-100 - LDL, VLDL, IDL

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14
Q

What are statins?

A

HMG CoA reductase inhibitors

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15
Q

How were statins discovered?

A

By screening microbes for their ability to inhibit cholesterol - initially found penicillium citrinum and then later aspergillus terreus

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16
Q

How do statins decrease cholesterol levels?

A

Initially by inhibiting HMG CoA reductase which decreases synthesis, but this results in a compensatory increase in hepatic LDL receptors which increases clearance of LDL from the blood and also leads to increased synthesis of HDL (so that more cholesterol can be taken back to the liver and recycled)

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17
Q

What is the ceiling effect in statins?

A

Once the initial dose is given, doubling or tripling dose will have little benefit but may still increase adverse effects

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18
Q

Why do statins have poor compliance?

A

Because patients don’t feel any different when taking them and it can take 1-2 years to improve lipid profile

19
Q

What should patients taking statins avoid?

A

Excessive amounts of grapefruit juice or other drugs which will create competition for cytochrome P450 metabolism and can lead to toxicity

20
Q

What is the interaction of antibiotics, antifungals and fibrates with statins?

A

Will increase statin level

21
Q

What is the interaction of phenytoin, barbiturates and glitazones with statins?

A

Will decrease statin level

22
Q

What is the result of increased serum aminotransferase in some patients taking statins?

A

Liver toxicity

23
Q

What is the result of creatine kinase in patients taking statins?

A

can lead to muscle pain and tenderness

24
Q

What are the common mild adverse effects of statins?

A

mild GI symptoms, headache, insomnia, dizziness

25
Q

What are the serious adverse effects of statins?

A

myopathy, rhabdomyolysis, renal failure, liver failure

26
Q

Why are statins contraindicated in pregnancy?

A

Causes impaired fetal myelination

27
Q

Why are statins withheld in infection, pre surgery and post trauma?

A

Because of drug drug interactions

28
Q

What are bile acid resins?

A

A granular preparation that is taken orally to treat hypercholesterolaemia

29
Q

What is the mechanism of bile acid resins?

A

Binds to bile acids to prevent their gut absorption which causes increased demand in cholesterol for bile acid synthesis so the body will up regulate hepatic LDL receptors and remove LDL from the plasma

30
Q

What are the common mild adverse effects of bile acid resins?

A

abdominal discomfort, constipation, bloating, flatulence

31
Q

What are the rare adverse effects of bile acid resins?

A

increased triglycerides, faecal impaction, decrease absorbance of fat soluble vitamins, fatty stools

32
Q

Why must other drugs be taken at a a different time to bile acid resins?

A

Because it will decrease absorption of other drugs

33
Q

What is ezetimibe?

A

A drug which inhibits the absorption of cholesterol by acting at sterol transporters in the intestines - lowers LDL while still allowing the absorption of bile acids and fat soluble vitamins

34
Q

What are the side effects of eztetimibe?

A

diarrhea, headache, tiredness, allergic reaction, joint pain

35
Q

When are ezetimibes used?

A

In patients who are intolerant to statins or in combination with statins to lower statin dose required

36
Q

What is niacin?

A

Vitamin B3 - used to decrease secretion of VLDL from the liver, reduce plasma LDL, increase plasma HDL and also potentially lowers atherogenic lipoprotein a (a protein which stops thrombolysis)

37
Q

What is the mechanism of niacin?

A

unknown

38
Q

What are the common adverse effects of niacin?

A

flushing, nausea, hypotension, vomiting

39
Q

What are the rare adverse effects of niacin?

A

itching, glucose intolerance, uric acid retention, hepatic impairment

40
Q

What are fibrates?

A

Drugs used to treat hypertriglyceridaemia

41
Q

What is the mechanism of fibrates?

A

regulates gene expression to result in an increased synthesis of LPL to breakdown triglycerides

42
Q

What is the effect of fibrates on HDL and LDL?

A

causes a moderate increase of HDL and has a variable effect on LDL - possibility for increase

43
Q

What are the common adverse effects of fibrates?

A

nausea, dry mouth, headache, rash

44
Q

What are the rare adverse effects of fibrates?

A

arrhythmias, gall stones, photosensitivity, impotence, depression and potential for liver toxicity

cardiovascular (36 decks)

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