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Pharm2 Mod 1: > Mod 1 lecture 3: antihyperlipidemia agents > Flashcards

Mod 1 lecture 3: antihyperlipidemia agents Flashcards

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1
Q

what are lipids

A

hydrophobic molecules made from mostly hydrocarbon chains

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2
Q

what his hyperlipidemia

A

excess lipids in the blood

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3
Q

what are types of lipids

A

fats - triglycerides
sterols - cholesterol
phospholipids - emulsifiers, lipid bilayer

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4
Q

what are lipoproteins

A

serve as carriers to transport lipids (cholesterol, triglycerides) in the blood

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5
Q

what type of proteins carry lipids into the atery wall

A

Apolipoprotein (apo) B- 100

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6
Q

what is LDL

A

low density lipoprotein. - contains (apo) b100

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7
Q

what is VLDL

A

very-low density lipoprotein
secreted by liver and export triglycerides to peripheral tissues
contain (apo) b100

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8
Q

what is chylmicrons

A

formed in the intestine and carry triglycerides of dietary origin, unesterified cholesterol and cholesteryl esters
contain (apo) B100

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9
Q

what is HDL

A

produced by liver and intestine
cholesterol is primary component in core
act as scavengers to take up cholesterol from peripheral tissues and triglyceride from degradation of VLDL
DO NOT contain (apo) B-100

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10
Q

what is the decreasing order of atherogenicity

A

LCL
VLDH
Chylomicrons
HDL

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11
Q

what is cholesterol

A

lipid
responsible for proper cell membrane synthesis and formation of bile acids and steroid hormones
primarily produced in the liver
INSOLUBLE in water so must be bound to lipoproteins for transport

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12
Q

what are tyriglycerides

A

main lipid component of dietary fat and fat deposits of animals
excess stored primarily in fat cells (adipocytes)
source of energy for body
INSOLUBLE in water so must be bound to lipoproteins for transportation

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13
Q

what are the classification of hyperlipidemia

A

primary (familial;hereditary) hyperlipidemia: genetically determined - type 1, 2a,2b, 3,4,5
secondary (acquired) hyperlipidemia:
- hypercholesterolemia: hyperthyroidism, nephrotic syndrome and drugs
- hypertriglyceridemia: DM, alcohol, gout, chronic renal failure

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14
Q

what is optimal total cholesterol level

A

less than or equal to 200 mg/dL

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15
Q

what is the optimal LDL-C level

A

less than or equal to 100 mg/dL

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16
Q

what is the optimal triclyceride level

A

less than or equal to 150 mg/dL

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17
Q

what is the optimal HDL level

A

greater than or equal to 60 mg/dL

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18
Q

what is TLC diet

A

Therapeutic lifestyle change diet for hyperlipoporteinemia

vegetables, fruits, whole grains
legumes and nuts
low-fat dairy produces
low-fat poultry (without skin)
fish and seafoods
non-tropical vegetable oils

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19
Q

what are the main classes of drugs used to treat hyperlipidemia

A

HMG CoA Reductase Inhibitors
Bile Acide Sequestrates
Nicotinic Acid
Cholesterol Absoprtion Inhibitor
Fibric Acids
Omega-3 Fatty Acids

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20
Q

what are the different HMG CoA reductase inhibitors

A

Statins
Atorvastatin (lipitor)
Lovastatin (mevacor)
Pravastatin (pravachol)
Rosuvastatin (crestor)
Simvastatin (Zocor)

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21
Q

what is the MOA for HMG CoA Reductase Inhibitors

A

Inhibits hepatic HMG-CaA reductase -> decrease in cholesterol synthesis -> hepatocytes synthesis more LDL receptors, increase ability to remove LDL from blood

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22
Q

what is HMG CoA reductase

A

a rate of controlling enzyme of the metabolic pathway that produces cholesterol

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23
Q

when are HMG CoA reductase inhibitors usually taken

A

taken at night usually
rosuvastatin and atorvastatin CAN be taken in the morning

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24
Q

what are low intensity therapies used to lower LDL levels

A

Lovastatin
Pravastain
Simvastatin

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25
when are HMG CoA reductase inhibitors usually taken
taken at night usually rosuvastatin and atorvastatin CAN be taken in the morning
26
what are the high potent statin medications
Rosuvastatin Atorvastatin
27
what are the indications for HMG CoA reductase inhibitors
used to lower the risk of atherosclerotic cardiovascular disease events helps lower plasma cholesterol levels in all types of hyperlipidemias
28
what should be avoided when using HMG CoA reductase inhibitors
avoid grapefruit or grapefruit juice (increased bioavailability of lovastatin and atorvastatin)
29
when is HMG CoA reductase inhibitors contraindicated?
pregnancy lactation active or chronic liver disease (liver function checked prior to starting) Red yeast rice
30
what are the adverse effects of HMG CoA reductase inhibitors
elevated liver enzymes myopathy and rhabdomyolysis photosensitivity may increase affect of warfarin - check INR prior GI upset (N/V, diarrhea, pain, dyspepsia)
31
what statin is labeled by the FDA for decreasing triglycerides as well as LDL and total cholesterol
Atorvastatin (Lipitor)
32
what is lovastatin (mevacor)
low potency HMG CoA reductase inhibitor take with meals immediate release avoid grapefruit or grapefruit juice
33
what are atorvastatin (lipitor) and Rosuvastatin (crestor)
HMG CoA reductase inhibitor MOST potent LDL-C lowering statin avoid grapefruit/gf juice
34
what is simvastatin (zocor)
Medium potency HMG CoA reductase inhibitor metabolized by CYP450 inhibitors of CYP450 may cause increased risk of rhabdomyolosis labeled by the FDA to treat for triglycerides, LDL and total cholesterol
35
what is pravastatin
low potency HMG CoA Reductase inhibitor fully excreted in urine
36
what is Nicotinic acid
niacin
37
what is the MOA for Niacin
inhibits lipolysis in adipose tissues -> reduced production of FFA and TGs reduces VLDL secretion from liver -> lowers LDL
38
what are the therapeutic uses of Niacin
familial hyperlipidemia, sever hypercholesteremias often with used with other agents most effective agent for increased HDL lowers Lip-A, LDL, and TG
39
what are the adverse effects of Niacin
flush, N, abd pain, gout, impaired glucose toleracne, hepatotoxicity, hypotension
40
when is Niacin contraindicated
hepatic disease active peptic ulcer low BP severe gout be cautions when prescribing to diabetics, individuals with high uric acid levels and peptic ulcer disease
41
what are the effects of Niacin
increases HDL (most effective agent) decreases lipoprotein (a) decreases LDL lowers triglycerides
42
What are Fibric Acid medications
Gemfibrozil (lopid) Fenofibrate (tricor)
43
what is the MOA for fibric acid medications
activates peroxisome proliferator - activated receptors (PPAR) - > up regulate lipoprotein lipase, induce HDL synthesis and decrease liver production of apolipoprotein C
44
what are the therapeutic uses of fibric acids
hypertriglyceridemia treatment in type III hyperlipidemia (dysbetalipoproteinemia) low HDL
45
when are Fibric Acids contraindicated
co-administration with statin therapy increases risk for myopathy and rhabdomyolysis avoid in renal and hepatic dysfunction avoid in preexisting gallbladder disease or biliary chirrhosis
46
what are the AE of fibric acid toxicity
Gi disturbances (most common) gallstones myopathy hepatic dysfunction increase effects on warfarin - INR check prior to starting
47
what are the effects of fibric acids
decreases secretion of VLDL increases lipoprotein lipase activity increase HDL
48
what are bile acid sequestrate medications
Cholestyramine (Questran, prevalite) Colesevelam (Welchol) Colestipol (colestid)
49
what is the MOA for bile avid sequestrates
prevents resorption of bile acid salts in intestines -> increases excretion - > increase synthesis -> liver cells increase LDL receptors, increase LDL uptake and decrease circulating LDL levels
50
what are the indications for bile acid sequestrates
type IIa and type IIb hyperlipidemias elevated LDL digitalis toxicity chronic pruritis
51
when are bile acid sequestrates contraindicated
Biliary cirrhosis, biliary obstruction gallstones (cholelitheiasis) hypertriglyceridemia GI obstruction preexisting coagulopathy (hemophilia) caution in hypothyroid pateints pregnangy, lactation prolonged used caution in renal disases
52
what are the AE of bile acid sequestrates
constipation bloating nausea flatulence interferes with absorption of some drugs/fat-soluble vitamin A, d, E and K reported to increase serum triglyceride concentration
53
what are the effects of bile acid sequestrants
decrease LDL (significant but less than seen in statins)
54
What is cholestyramine (questran, prevalite)
bile acid sequestrate anonion-exhange resin that binds negatively changed bile acids and salts in small intestines resin/bile acid complex excreted in feces can relieve prurutis caused by accumulation of bile aids in patients with biliary stasis
55
What is cholesterol absorption inhibitor
Ezetimbie (zetia)
56
What is the MOA of ezetimbie (zetia)
acts on cells of the brush border of the small intestine to inhibit dietary cholesterol absorption also inhibits reabsorption of cholesterol secreted in the bile
57
What is the inidcations for ezetimbe (zetia)
used as adjunct therapy to lower LDL phytosterolemia mono or combo therapy with statin
58
what are the contraindications of zetia
severe hepatic insufficiency pregnancy/lactation
59
what are the AE of zetia
SE rare: hepatic dysfunction (low) myositis
60
what are the effects of zetia
inhibits reabsorption of cholesterol excreted in bile decreased LDL and phytosterols
61
what are the omega-3 fatty acids
alpha-linolenic acid (ALA) eicosapentaenoic avid (EPA) Docosahexaenoic acid (DHA)
62
what is the MOA for omega 3 fatty acid
inhibit VLDL and triglycerides synthesis in liver
63
what are the indications for omega 3 fatty acid
lowering triglycerides (used as an adjunct to diet and exercise
64
when is fish oil contraindicated
avoided if pt has a hx of fish hypersensitivity pts on anticoagulant, thrombolytic or anti-platelet therapy as bleeding may be increased
65
what are the AE of fish oil
GI upset - abd pain, N and diarrhea fishy aftertaste increased bleeding risk with those already on anticoags need to monitor
66
what is Vytorin
combination of Ezetimibe (zetia) and simvastatin (zocor)
67
what is Advicor
combination of lovastatin and Niacin
68
what is Caduet
combination of amlopdipine/atorvastatin
69
what are the injectable medications (monoclonal antibodies)
alirocumab (praluent) Evolocumab (repathya)

Pharm2 Mod 1: (3 decks)

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