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PHARM EXAM 2 > lipid lowering therapy > Flashcards

lipid lowering therapy Flashcards

1
Q

What are the lipoproteins produced in the liver?

A

Two types: LDL (BAD) and HDL (GOOD). LDL causes plaque on arteries, CAD, and atherosclerosis, increasing risk for MI or stroke. HDL helps get rid of LDL’s, improving cardiovascular risk.

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2
Q

How is cellular cholesterol produced?

A

HmG-COA reductase converts into cellular cholesterol, which is needed for normal brain function.

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3
Q

What are the gold standard meds for lipid lowering therapy?

A

HmG-COA reductase inhibitors, also known as statins.

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4
Q

What are the causes of hyperlipidemia?

A

Excessive dietary intake of fats, genetic alterations in fat metabolism, hypercholesterolemia, hypertriglyceridemia, and alterations in LDL and HDL concentrations.

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5
Q

Which lipoprotein do we want high/low?

A

We want HDL to be high, and LDL to be low.

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6
Q

What are the normal and high levels of total cholesterol?

A

Normal is <200, high is >240.

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7
Q

What are the optimal, normal, high, and very high levels of LDL’s?

A

Optimal is <100, normal is 100-129, high is 160-189, very high is >190.

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8
Q

What are the low and high levels of HDL’s?

A

Low is <40, high is >60.

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9
Q

What are the normal, high, and very high levels of triglycerides?

A

Normal is <150, high is 200-499, very high is >500.

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10
Q

For what patients is a LDL goal of <70?

A

Patients with diabetes, mild CAD, and history of MI or stroke.

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11
Q

If a patient has a triglyceride of >500, they are at risk for?

A

Pancreatitis.

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12
Q

What drugs are used to treat hyperlipidemia?

A

HmG-COA reductase inhibitors/statins, bile acid sequestrants, fibrates, niacin, cholesterol absorption inhibitors.

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13
Q

Which meds are used as additives/alternatives for patients who can’t reach their LDL goal with statins or can’t tolerate them?

A

Bile acid sequestrants, fibrates, niacin, cholesterol absorption inhibitors.

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14
Q

How do bile acid sequestrants work?

A

They bind bile acids in intestines, allowing excretion in feces instead of reabsorption, lowering cholesterol levels.

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15
Q

Who are bile acid sequestrants indicated for?

A

Patients with primary hypercholesterolemia and pruritus associated with partial biliary obstruction.

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16
Q

What meds are bile acid sequestrants?

A

Welchol, Questran, Prevalite.

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17
Q

How are bile acid sequestrants given?

A

Orally, in packets mixed with liquids for patients to drink.

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18
Q

What are the adverse effects of bile acid sequestrants?

A

Nausea/Constipation (common), headache, fatigue, drowsiness, and increased bleeding times.

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19
Q

What are the drug interactions of bile acid sequestrants?

A

Malabsorption of fat soluble vitamins (A,D,E,K), change in absorption of thiazide, digoxin, warfarin, thyroid hormones, and corticosteroids.

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20
Q

How do HmG-COA Reductase Inhibitors work?

A

They inhibit HmG-COA reductase, decrease cholesterol levels, LDL’s, and triglycerides, and increase HDL levels.

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21
Q

Who are HmG-COA Reductase Inhibitors indicated for?

A

Patients with hyperlipidemia or history of atherosclerosis/CAD to prevent MI or stroke.

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22
Q

What meds are HmG-COA Reductase Inhibitors?

A

Atorvastatin (Lipitor), Rosuvastatin (Crestor), Simvastatin (Zocor), Lovastatin (Mevacor), Pravastatin (Pravachol).

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23
Q

What are contraindications of HmG-COA Reductase Inhibitors?

A

Allergy, liver disease, pregnancy/lactation.

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24
Q

In what patients should we take caution when giving HmG-COA Reductase Inhibitors?

A

Patients with impaired endocrine function.

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25
Q

What are the adverse effects of HmG-COA Reductase Inhibitors?

A

Myopathy, liver failure, Rhabdomyolysis.

26
Q

What are the drug interactions of HmG-COA Reductase Inhibitors?

A

Erythromycin, cyclosporine, gemfibrozil, niacin, grapefruit juice.

27
Q

Which med is the HmG-COA Reductase Inhibitor prototype?

A

Rosuvastatin (Crestor).

28
Q

How does Rosuvastatin (Crestor) work?

A

Decreases LDL and triglycerides, inhibits HmG-COA reductase, stabilizes blood vessel lining.

29
Q

What are side effects of Rosuvastatin (Crestor)?

A

Headache, constipation, diarrhea, myalgias.

30
Q

What are the adverse effects of Rosuvastatin (Crestor)?

A

Rhabdomyolysis, photosensitivity, hyperglycemia, elevated LFT’s.

31
Q

What are the contraindications of Rosuvastatin (Crestor)?

A

Pregnancy/lactation, liver disease.

32
Q

When should we monitor LFT’s?

A

At 6-8 weeks, 6 months in, then once yearly.

33
Q

What should we take caution with when giving Rosuvastatin (Crestor)?

A

Alcohol use, Tylenol use, and history of liver disease.

34
Q

How do Cholesterol Absorption Inhibitors work?

A

They inhibit the absorption of cholesterol in the brush border of the small intestine.

35
Q

What are the indications of Cholesterol Absorption Inhibitors?

A

Lower serum cholesterol levels, treat homozygous familial hypercholesterolemia.

36
Q

How are Cholesterol Absorption Inhibitors absorbed and excreted?

A

Absorbed in GI tract, metabolized in liver, excreted in feces and urine.

37
Q

What is an example of a Cholesterol Absorption Inhibitor?

A

Zetia (Ezetimibe).

38
Q

What are the contraindications of Cholesterol Absorption Inhibitors?

A

Allergy, pregnancy and lactation if combined with a statin.

39
Q

What are the adverse effects of Cholesterol Absorption Inhibitors?

A

Abdominal pain, diarrhea, muscle pain, fatigue, dizziness, URI, back pain.

40
Q

What are the drug interactions of Cholesterol Absorption Inhibitors?

A

Cholestyramine, fenofibrate, gemfibrozil, antacids, cyclosporine, fibrates, warfarin.

41
Q

What is Niacin?

A

A lipid lowering medication.

42
Q

How does Niacin work?

A

Vitamin B3, inhibits the release of free fatty acids from adipose tissue, increases triglyceride removal from plasma.

43
Q

What is a side effect of niacin?

A

Redness across the chest and face, this is not an allergic reaction.

44
Q

What are fenofibrates?

A

Lipid lowering medication.

45
Q

How does fenofibrate work?

A

Inhibits triglyceride synthesis in the liver, decreases LDL, increases uric acid secretion.

46
Q

What is Gemfibrozil?

A

A lipid lowering medication.

47
Q

How does Gemfibrozil work?

A

Inhibits peripheral breakdown of LDL’s, reduces production of LDL and triglycerides, increases HDL.

48
Q

What are PSK9 inhibitors?

A

Injectable lipid lowering therapy for patients who can’t tolerate statins or have not reached their goal with the highest statin dose.

49
Q

How is it injected and how often?

A

Injected every 2 weeks into the thigh, resulting in about a 50% reduction of LDL’s.

50
Q

What is the most common side effect of PSK9 inhibitors?

A

Headache.

51
Q

What medications are PSK9 Inhibitors?

A

Alirocumab (Praluent), Evolocumab (Repatha).

52
Q

How is it stored?

A

Keep in the fridge and take out 30 minutes before using.

53
Q

What are peripheral vasodilators?

A

They increase blood flow to the extremities in older adults with PAD or PVD.

54
Q

What are some peripheral vasodilator meds?

A

Cilostazol (Pletal) and Trental.

55
Q

What pregnancy category is Cilostazol (Pletal)?

A

Pregnancy category C.

56
Q

What are the contraindications of Cilostazol (Pletal)?

A

CHF class 3-4, arterial bleeding, severe hypotension, postpartum, tachycardia.

57
Q

What should you take caution in when giving Cilostazol (Pletal)?

A

Bleeding disorders and tachycardia.

58
Q

What are the drug interactions of Cilostazol (Pletal)?

A

Hypotension with antihypertensive medications.

59
Q

How is Cilostazol (Pletal) given?

A

PO.

60
Q

What are the adverse effects of Cilostazol (Pletal)?

A

Tachycardia, palpitations.

61
Q

What are the side effects of Cilostazol (Pletal)?

A

Nausea/Vomiting, dizziness, syncope, blood in eye, headache, abdominal pain, abnormal stools, peripheral edema.

62
Q

What nursing care should be done for Cilostazol (Pletal)?

A

Obtain vital signs, assess for signs and symptoms of inadequate blood flow, monitor for tachycardia and hypotension.

PHARM EXAM 2 (10 decks)

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