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Pharmacology > Lipid Lowering Agents > Flashcards

Lipid Lowering Agents Flashcards

1
Q

What does cholesterol do?

A

Composed primarily of LDLs, favours abnormal deposition to the artery walls (atherosclerotic plaque and thrombus formation).

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2
Q

What other risk factors favour coronary heart disease?

A

Current smoking, hypertension (>140/90), type 2 diabetes, age (>45 for males, >55 for females), genetic factors, family history of premature CHD, low HDL (

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3
Q

What can happen when plaque builds up?

A

Atherosclerosis may partially or completely obstruct flow in the artery, eventually it damages the endothelium, forming a thrombus, blood flow is blocked. If the thrombus ruptures, an emboli will lodge in capillaries blocking venous flow.

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4
Q

What is a chylomicron?

A

Carrier of dietary lipids in blood to liver.

Triglyceride rich, some cholesterol

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5
Q

What is a very low density lipoprotein (VLDL)?

A

Carrier of lipids from liver to periphery in blood

Triglyceride rich, some cholesterol

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6
Q

What is a low density lipoprotein (LDL)?

A 
Carrier of cholesterol from liver in blood.
Bad cholesterol (best if low)
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7
Q

What is a high density lipoprotein (HDL)?

A 
Scavenge cholesterol from the artery wall.
Good cholesterol (best if high)
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8
Q

How does the exogenous pathway work?

A

Dietary fats are absorbed in the intestine and transported as chylomicrons to the liver. Bile acids and cholesterol are excreted from the liver back into the intestine, where they could be reabsorbed.

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9
Q

What happens to chylomicrons in the capillary?

A

Lipoprotein lipase breaks down them, releasing free triglycerides while the leftovers continue to the liver.

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10
Q

How does the endogenous pathway work?

A

If the body is in need of triglycerides and cholesterol, the liver sends out VLDLs, broken down to release free fatty acids and glycerol by LP lipase, now are LDLs and can go to extraheptic tissues or liver. HDL can package up cholesterol from extrahepatic tissues and bring them back to the liver.

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11
Q

What is the aim of treatment for lipid lowering agents?

A

Decrease LDL levels and increase HDL levels (or at least don’t decrease)

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12
Q

What is niacin? What does it do?

A

The water soluble vitamin B3 (nicotinic acid) which decreases risk of CV event
Low dose increases HDL
High dose decreases VLDL, triglycerides and maybe LDL

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13
Q

What are the mechanisms of niacin?

A

Decreased VLDL production, increased VLDL clearance from increased lipoprotein lipase activity.

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14
Q

How does niacin decrease VLDL production?

A

Inhibits lipolysis in the adipose tissue so fewer fatty acids are taken into the liver and less converted back to triacylglycerol thus fewer VLDLs are needed to be produced/released due to less trigylcerides.

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15
Q

Why are LDL receptors important?

A

Allow for the reabsorption of LDLs in the liver and extrahepatic tissues. More LDL receptors, better.

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16
Q

What are the adverse effects of niacin?

A

Increased liver enzymes in the blood (hepatotoxic), hyperglycemia due to insulin resistance, 1-2 weeks of skin flushing and pruritis (treat using aspirin), dry eyes, blurred vision, fatigue, GI distress

17
Q

In which patients should niacin be used with caution?

A

Those at risk of a peptic ulcer (exacerbation) and diabetes

18
Q

What are some examples of fibrates? How do they affect patients?

A

Gemfibrozil and fenofibrate

Decreased incidence of death from CHD, nonfatal MI and stroke in men with CHD

19
Q

What is the mechanism of fibrates?

A

Increased VLDL clearance by increasing lipoprotein lipase activity.

20
Q

What are the adverse effects of fibrates?

A

Flu-like muscle cramps, tenderness, stiff, weak

Increased risk of myopathy (muscle breakdown) when combined with statins

21
Q

What are some examples of bile acid binding resins? What do they do?

A

Cholestyramine and colestipol

Used only when LDL levels are elevated. Anion exchange resin (not absorbed in gut) which prevents bile reabsorption

22
Q

What happens when bile acids in the body are decreased?

A

Need to make more bile acid and thus more cholesterol is used to make.

23
Q

How does the body make more cholesterol?

A

Liver synthesizes new LDL receptors and increases LDL uptake.

24
Q

What are the adverse effects of bile acid binding resins?

A

May increase VLDL levels by an unknown mechanism (bad)

Will also bind drugs, sandy, gritty texture

25
Q

What are HMG-CoA reductase inhibitors?

A

Statins
1st line treatment for patients with risk of coronary heart disease
Decrease morbidity, mortality and incidence of stroke in those with coronary artery disease

26
Q

How do statins work?

A

Inhibit the rate limiting step of cholesterol synthesis (HMG-CoA reductase). Which decreases hepatic cholesterol which increases LDL receptors and uptake of LDLs and cholesterol from circulation

27
Q

What are the adverse effects of statins?

A

Generally well tolerated, myopathy (severe myalgia, muscle weakness), muscle soreness
Monitor liver enzymes

28
Q

What should be avoided while taking statins?

A

Pregnancy and grapefruit juice (CYP3A4 inhibitor which will prevent breakdown of statins causing sky high levels)
Simvastatin and Lovastatin have greatest bioavailability increases.
Pravastatin and Fluvastatin do not.

29
Q

What are the secondary benefits of statins?

A

Increase bone formation, lower blood pressure, decrease risk of developing dementia, preserve renal function, asthma

30
Q

How does ezetimibe work?

A

Inhibit dietary and biliary cholesterol absorption at intestinal brush border’s specific cholesterol transport protein
Lowers cholesterol in chylomicrons causing liver to increase LDL receptors and cholesterol synthesis

31
Q

What could ezetimibe be added to ?

A

Added to a statin to allow a lower statin dose, possible greater elevation of transaminases

32
Q

What are some adverse effects of ezetimibe?

A

Myalgia, hepatitis, rhabdomyolosis (muscle breakdown) and acute pancreatitis

33
Q

What drug can interact with ezetimibe?

A

Bile acid sequestrants can interfere with the actions.

34
Q

What can cholestryamine be combined with?

A

A statin (HMG-CoA inhibitor) can be combined with the bile acid binding resin. To stop the compensatory increase in cholesterol synthesis by cholestryamine’s increased LDL removal

Pharmacology (11 decks)

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