Pharmacology-Hyperlipidemic Drugs Flashcards Preview

CPR I > Pharmacology-Hyperlipidemic Drugs > Flashcards

Flashcards in Pharmacology-Hyperlipidemic Drugs Deck (25)
Loading flashcards...
1
Q

What are the cholesterol levels standards after an overnight fast?

A

*

2
Q

What are risk factors for coronary heart disease? At what point should you start treating someone aggressively for CHD?

A

You treat aggressively when your patient has two or more of these factors or just one of the red factors.

3
Q

An elevated level of what apolipoprotein is associated with decreased risk of coronary heart disease?

A

Apo A1. It is on HDL which pulls cholesterol out of plaques.

4
Q

List 4 primary hypercholesterolemias.

A

Familial hypercholesterolemia, familial ligand-defective apolipoprotein B, familial combined hyperlipoproteinemia, Lp(a) hyperlipoproteinemia.

5
Q

List 4 primary hypertriglyceridemias.

A

Primary chylomicronemia, familial hypertriglyceridemia, familial combined hyperlipoproteinemia and familial dysbetalipoproteinemia.

6
Q

What are some secondary causes of hyperlipidemia?

A

*

7
Q

How can you decrease cholesterol levels by 10-20% by just changing your diet?

A

Reduce intake of fats and cholesterol. Eat oat and rice (reduces LDL). Reduce sugar intake (sugar increases VLDL synthesis). Eat nuts (reduces LDL). Omega-3 oil in fish (increases HDL and reduces LDL).

8
Q

What drugs can you prescribe to a patient with high cholesterol that are bile-acid sequestrates (resins)? What is the mechanism by which these drugs work?

A

Cholestyramine, colestipol and colesevelam (best one). They bind bile acids and inhibit reabsorption of bile acid. This increases channeling of cholesterol to bile acid production and decreases intra-hepatic cholesterol levels. As these levels decrease, the liver upregulates LDL (apoB and E) receptors and increases clearance of LDL, IDL and VLDL.

9
Q

How effective are resins at decreasing CHD events (fatal and nonfatal)? Who are these drugs particularly good for?

A

They decrease them by 19%, decreasing LDL cholesterol levels by 15-30% and increasing HDL levels by 3-5%. These drugs are safe for pregnant women as statins are not. They are used in conjunction with statins in heterozygous familial hypercholesterolemia and combined hyperlipidemia.

10
Q

What are adverse effects and interactions you need to keep in mind with bile-acid sequestrates?

A

*

11
Q

What are the main statins you will use and how do they work?

A

Simvastatin, atorvastatin and rosuvastatin. The look like mevalonate, bind to HMG-CoA reductase, inhibit it and thus reduce cholesterol synthesis. Decreasing synthesis, results in up regulation of LDL receptors and incidentally more LDLs are taken up by the liver.

12
Q

How effective are statins?

A

Rosuvastatin might be slightly better because it increases HDL more than atorvastatin.

13
Q

What are contraindications to consider with statins?

A

Myopathy (they can cause it and possibly lead to rhabdomyolysis). Asians (don't metabolize them as well). Mild hepatotoxicity. Pregnant women (teratogenic). Memory loss. Increased blood sugar levels.

14
Q

What are drug interactions you need to consider when prescribing lovastatin, simvastatin and atorvastatin? Why is rosuvastatin not considered?

A

Drugs that interact with CYP3A4. Rosuvastatin is not metabolized by CYP3A4.

15
Q

Why are statins so good for patients that just survived an MI?

A

Induce endothelial production of NO and vasodilate. Stabilize plaques. Reduce CRP (reducing inflammation). Reduces thrombotic events.

16
Q

What other chronic conditions aside from heart disease can benefit from statin therapy?

A

Multiple sclerosis (anti-inflammatory effect). Alzheimer's. Rheumatoid arthritis.

17
Q

What groups of people should receive moderate to high intensity statin therapy?

A

*

18
Q

What apolipoprotein was found in people in Italy that significantly decreased their incidence of CHD events?

A

Apo A1-Milano

19
Q

Why is estrogen-replacement therapy a controversial topic in cholesterol management?

A

*

20
Q

What drug prevents cholesterol absorption in your GI tract? What happens when you combine it with a statin?

A

Ezetimibe. It actually increases plaque formation when combined with statins.

21
Q

What happens when your triglycerides (VLDL) get too high? What drug do you use treat this that causes the largest increase in HDL levels?

A

Pancreatitis and xanthomas. Niacin increases lipoprotein lipase activity (decreasing VLDL) and raises HDL.

22
Q

What drugs are used to lower triglyceride (VLDL) levels in patients with familial hypertriglyceridemia and familial dysbetalipoproteinemia?

A

Fenofibrate (fibrin acid derivative). This drug binds to PPAR-alpha receptors, increasing LPL activity, increasing HDL and decreasing VLDL synthesis and excretion by the liver.

23
Q

Why should you not use fenofibrate in patients with renal failure?

A

It is excreted by the kidneys

24
Q

Why should you be wary prescribing gemfibrozil when a patient is on a statin?

A

Rhabdomyolysis

25
Q

What drug is used in combination with niacin to treat Lp(a) hyperlipoproteinemia?

A

Neomycin. It is an antimicrobial that actually inhibits resorption of cholesterol and bile salts.

Decks in CPR I Class (48):