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Pharmacology Exam 3 > Lipid lowering drugs > Flashcards

Lipid lowering drugs Flashcards

1
Q

Genetic defect in the metabolism of cholesterol is majority or minority of population?

A

minority

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2
Q

What are the secondary causes of lipid disorders that most of the population has?

A

increased fat intake, obesity, type II DM, advanced age, hypothyroidism, obstructive liver disease, drug induced

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3
Q

What does untreated hyperlipidemia lead to?

A

acute pancreatitis (hypertriglycerides) and atherosclerosis (hypercholesteremia–plasma cholesterol)

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4
Q

What 2 things does atherosclerosis lead to?

A

macrovascular complications, microvascular complication

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5
Q

What are examples of macrovascular complications?

A

unstable angina, MI, ischemic cerebrovascular disease, CAD

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6
Q

What are examples of microvascular complications?

A

Retinopathy, nephropathy

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7
Q

What are lipoproteins?

A

macromolecular lipid plus protein complexes that transport lipids to and from peripheral tissues

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8
Q

How are lipoproteins classified?

A

based on density

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9
Q

Are the lipid and protein portions directly related or inversely related?

A

inversely related

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10
Q

What are the 5 kinds of lipoproteins in order from least protein content to most?

A

Chylomicrons, Very-Low density lipoproteints (VLDL), Intermediate density lipoproteins (IDL), Low density lipoproteins (LDL), and High density lipoproteins (HDL)

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11
Q

How do you prevent HLD?

A

decrease triglycerides, cholesterol, and LDL, increase HDL

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12
Q

What’s the optimal value for LDL?

A

<100mg/dl

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13
Q

What’s the optimal value for cholesterol?

A

<200mg/dl

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14
Q

What’s the optimal value for triglycerides?

A

<150mg/dl

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15
Q

What’s the optimal value for HDL?

A

> 60mg/dl, 40mg/dl the low end

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16
Q

What’s exogenous lipoproteins?

A

dietary fats, cholesterol, lipid soluble vitamins

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17
Q

What’s endogenous lipoproteins?

A

hepatic cholesterol synthesis

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18
Q

Who do the currently guidelines by ACC and AHA advocate for statin use for?

A

1)clinical evidence of ASCVD, 2)LDL >190, 3) age 40-70 with DM and LDL 70-189, 3)age 40-75 without DM, LDL 70-189, and an estimated 10 year risk of ASCVD.

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19
Q

When preop should you implement a statin?

A

recommended start 30 days-1week prior to high risk surgery

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20
Q

What are statins isolated from?

A

strain of aspergillus terreus

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21
Q

What is a natural statin?

A

lovastatin

22
Q

What are the semi-synthetic statins?

A

simvastatin, pravastatin

23
Q

What are the synthetic statins?

A

atorvastatin, fluvastatin, rosuvastatin

24
Q

What is the most effective drug we have to lower LDL?

A

statins

25
Q

What else do statins do?

A

improve plaque stability, enhance endothelial function, decrease oxidative stress, decrease vascular inflammation

26
Q

What does zetia do?

A

enhances statin and decreases triglycerides

27
Q

What is another name for statin?

A

HMG-CoA reductase inhibitors

28
Q

What are the 2 MOA of statins?

A

inhibit cholesterol synthesis, competitively inhibit HMG-CoA reductase causing increased hepatic LDL-R: reduces LDL concentration from 20-60%, increase HDL 10%

29
Q

Are statins sufficient in reducing tryglycerides?

A

no, they decrease cholesterol

30
Q

Which 2 statins are prodrugs needing metabolism to become activated?

A

simvastatin and lovastatin

31
Q

How are statins metabolized?

A

most hepatic P450 enzymes

32
Q

What is the DOA for most statins?

A

24h

33
Q

What is the absolute contraindication for statins?

A

Pregancy

34
Q

What are the side effects of statins?

A

skeletal muscle issues (rhabdo rare), liver enzyme changes (plasma aminotransferase increases), drug interactions such as CYP 450 3A4 inhibitors, GI upset, fatigue, headache

35
Q

What is the MOA of Bile Acid Resins (anionic exchange)

A

increase hepatic bile synthesis from cholesterol stores, increasing LDL-R and the uptake of LDL from the blood

36
Q

What are the uses of bile acid resins?

A

primary increased LDL level with normal triglycerides

37
Q

What are some examples of bile acid resins?

A

colesevelam, cholestyramine, colestipol

38
Q

What is unique about administration of bile acid resins?

A

need to be hydrated with water, they are powders with no systemic absorption

39
Q

What’s the side effects of bile acid resins?

A

constipation

40
Q

What’s the MOA of niacin?

A

inhibits synthesis of VLDL in the liver, inhibits release of free fatty acid from adipose tissue, increases activity of lipoprotein lipase

41
Q

What are the uses of niacin?

A

lowers LDL and trigylderides,

MOST EFFECTIVE DRUG AT INCREASING HDL

42
Q

Does niacin undergo 1st pass metabolism?

A

yes, extensively

43
Q

What are side effects of niacin?

A

flushing, pruritis, GI upset, hepatic dysfunction, hypergycemia, gout, drug interactions, worsening hypotension. Massive histamine release.

44
Q

How should you take niacin?

A

start slow, NSAID/ASA 30 min before taking it, avoid alcohol

45
Q

What is the MOA of fibrates?

A

increased activity of lipoprotein lipase

46
Q

What’s the use of fibrates?

A

MOST EFFECTIVE DRUGS AT DECREASING TRIGLYCERIDES (50%), increase LDL

47
Q

What are examples of fibrates?

A

Gemfibrozil, Fenofibrate, Bezafibrate

48
Q

What are the side effects of fibrates?

A

GI upset, headache, gallstones, statin interaction, prolonged PTT(coumadin protein binding)

49
Q

What’s the MOA of Ezetimibe?

A

selective inhibitor of cholesterol absorption leading to secondary up-regulation of LDL-R

50
Q

What is the use of Zetia?

A

alone decreases LDL by 22%, potentiates the effects of statins by 17%

51
Q

What is the use of omega-3 fatty acids (fish oil)?

A

decrease triglycerides. not regulated by FDA, dose is unclear, long term safety not known, no evidence to support prevents heart disease.

Pharmacology Exam 3 (5 decks)

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