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Pharmacology - Winter > 1 - Lipid Disorders > Flashcards

1 - Lipid Disorders Flashcards

1
Q

What causes atherosclerosis?

A

Elevated plasma cholesterol, primarily derived from LDL’s

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2
Q

What are risk factors for increased LDL?

A
  • Smoking
  • Hypertension
  • Diabetes mellitus
  • Genetics
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3
Q

Why should you control plasma cholesterol?

A

Can lead to atherosclerosis

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4
Q

Why should you control plasma triglycerides?

A

Can lead to pancreatitis

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5
Q

What causes pancreatitis?

A

Elevated triglycerides, primarily chylomicrons and VLDL’s

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6
Q

What does the body do when it needs cholesterol?

A

Liver synthesized VLDL, which are similar to chylomicrons

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7
Q

What is the function of lipoprotein lipase?

A

Hydrolyzes chylomicrons, producing free fatty acids

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8
Q

What are some possible sites to decrease cholesterol?

A
  • Decrease dietary intake
  • Decrease absorption of cholesterol or reabsorption of bile acids
  • Decrease endogenous cholesterol synthesis
  • Decrease LDL levels by decreasing VLDL or increasing LDL receptors
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9
Q

What are some non-pharm approaches to decrease cholesterol?

A
  • Increase dietary fiber (100g each day)

- Increase omega-3 fatty acids

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10
Q

What are statins?

A

HMG-CoA reductase inhibitors

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11
Q

What are some examples of statins?

A
  • Rosuvastatin
  • Atorvastatin
  • Simvastatin
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12
Q

When are statins the 1st line therapy?

A

For most px w/ risk of coronary heart disease

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13
Q

What do statins do?

A
  • Decrease LDL levels
  • Decrease triglyceride levels
  • Decrease cardiac morbidity, mortality, and reduce incidence of stroke
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14
Q

What is important about HMG-CoA reductase?

A

Rate limiting step of cholesterol synthesis

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15
Q

Statins are best given in the _____

A

Evening

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16
Q

Are statins safe in pregnancy?

A

No

17
Q

What are some adverse effects of statins?

A

Myalgia, muscle weakness

18
Q

What is contraindicated w/ statins and why?

A
  • Statins undergo first pass metabolism by CYP 3A4

- Contraindicated w/ CYP 3A4 inhibitors (grapefruit juice) because will increase bioavailability of statin

19
Q

What a flat dose response for statins mean?

A

Increasing the dose doesn’t increase effect (majority of statin LDL efficacy is w/ the starting dose)

20
Q

What drug is a cholesterol absorption inhibitors?

A

Ezetimibe

21
Q

What does ezetimibe do?

A
  • Inhibits dietary and biliary cholesterol absorption

- Inhibits cholesterol transport protein NPC1L1

22
Q

What is a side effect of ezetimibe?

A

Reflex increase in cholesterol synthesis

23
Q

Which drugs are bile acid binding resins?

A
  • Cholestyramine

- Colestipol

24
Q

When are bile acid binding resins used?

A
  • Mild to moderate elevated LDL

- Effective w/ statins or nicotinic acid in high LDL levels

25
Q

How do bile acid binding resins work?

A

Binds bile acids in intestinal lumen, preventing reabsorption

26
Q

What are some adverse effects of bile acid binding resins?

A
  • May increase VLDL levels
  • Decrease absorption of fat soluble vitamins
  • Nausea, constipation, bloating
  • Absorption of drugs altered
27
Q

Why would statins and ezetimibe be combined?

A
  • Ezetimibie decreases cholesterol uptake in gut, which causes a reflex increase in cholesterol synthesis in liver
  • Statins block this increased synthesis
28
Q

Why would statins and bile acid binding resins be combined? Are they commonly combined?

A
  • Statin inhibits synthesis of cholesterol and bile acid binding resins prevent reabsorption of bile, causing increased excretion
  • Together they decrease LDL levels
  • Not generally used b/c bile acid binding resins are poorly tolerated
29
Q

What can cause a px to fail to achieve the LDL-C target?

A
  • Poor adherence
  • High baseline LDL-C
  • High-cholesterol diet
  • High cholesterol absorption
  • Variable statin response
  • Inability to tolerate statins
30
Q

What is the newest therapy for px that can’t meet target levels of LDL? What is the name of the drug?

A
  • Target LDL receptor PCSK9 by injecting human monoclonal Ab to PCKS9 to increase LDL receptors on liver
  • Drug = evolocumab
31
Q

What are the problems w/ cholesterol lowering drugs?

A
  • Variation in px sensitivity to HMG-CoA reductase inhibitors
  • Evidence that ezetimibe plus simvastatin may be no more beneficial in plaque regression than simvastatin alone
32
Q

What are the potential ways to decrease plasma triglycerides?

A
  • Decrease dietary triglycerides
  • Increase lipoprotein lipase activity
  • Decrease VLDL secretion from liver
33
Q

What is a non-pharm to decrease dietary triglycerides? What is the problem w/ this?

A
  • Dietary fiber (soluble better than insoluble)

- Problem = need large amounts of fiber and long term effect and safety unknown

34
Q

Which drugs are fibrates?

A
  • Fenofibrate
  • Gemfibrozil
  • Clofibrate
35
Q

What do fibrates do?

A
  • Don’t change LDL levels, but decrease incidence of non-fatal MI and stroke
  • Primarily decrease triglycerides and may increase HDL
  • Increase VLDL clearance and decrease VLDL secretion
36
Q

What is important to note about clofibrate?

A
  • Increased mortality due to malignant and GI disease

- Only used in extreme unresponsive cases

37
Q

What are some adverse effects of fibrates?

A
  • Flu-like (muscle cramps, tenderness, weakness)

- Avoid in hepatic or renal dysfunction

38
Q

What does nicotinic acid do?

A
  • Increases HDL levels at low dose
  • Decreases VLDL production via inhibition of fatty acid release from adipose tissue => decreases triglycerides at higher dose
39
Q

What are some adverse effects of nicotinic acid?

A
  • Poor tolerability
  • Skin flushing and pruritus
  • Exacerbation of peptic ulcer

Pharmacology - Winter (18 decks)

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