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Pharmacology Exam 3 > Lipid lowering drugs > Flashcards

Lipid lowering drugs Flashcards

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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?

22
Q

What are the semi-synthetic statins?

Study These Flashcards
A

simvastatin, pravastatin

23
Q

What are the synthetic statins?

Study These Flashcards
A

atorvastatin, fluvastatin, rosuvastatin

24
Q

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

25
What else do statins do?
improve plaque stability, enhance endothelial function, decrease oxidative stress, decrease vascular inflammation
26
What does zetia do?
enhances statin and decreases triglycerides
27
What is another name for statin?
HMG-CoA reductase inhibitors
28
What are the 2 MOA of statins?
inhibit cholesterol synthesis, competitively inhibit HMG-CoA reductase causing increased hepatic LDL-R: reduces LDL concentration from 20-60%, increase HDL 10%
29
Are statins sufficient in reducing tryglycerides?
no, they decrease cholesterol
30
Which 2 statins are prodrugs needing metabolism to become activated?
simvastatin and lovastatin
31
How are statins metabolized?
most hepatic P450 enzymes
32
What is the DOA for most statins?
24h
33
What is the absolute contraindication for statins?
Pregancy
34
What are the side effects of statins?
skeletal muscle issues (rhabdo rare), liver enzyme changes (plasma aminotransferase increases), drug interactions such as CYP 450 3A4 inhibitors, GI upset, fatigue, headache
35
What is the MOA of Bile Acid Resins (anionic exchange)
increase hepatic bile synthesis from cholesterol stores, increasing LDL-R and the uptake of LDL from the blood
36
What are the uses of bile acid resins?
primary increased LDL level with normal triglycerides
37
What are some examples of bile acid resins?
colesevelam, cholestyramine, colestipol
38
What is unique about administration of bile acid resins?
need to be hydrated with water, they are powders with no systemic absorption
39
What's the side effects of bile acid resins?
constipation
40
What's the MOA of niacin?
inhibits synthesis of VLDL in the liver, inhibits release of free fatty acid from adipose tissue, increases activity of lipoprotein lipase
41
What are the uses of niacin?
lowers LDL and trigylderides, | MOST EFFECTIVE DRUG AT INCREASING HDL
42
Does niacin undergo 1st pass metabolism?
yes, extensively
43
What are side effects of niacin?
flushing, pruritis, GI upset, hepatic dysfunction, hypergycemia, gout, drug interactions, worsening hypotension. Massive histamine release.
44
How should you take niacin?
start slow, NSAID/ASA 30 min before taking it, avoid alcohol
45
What is the MOA of fibrates?
increased activity of lipoprotein lipase
46
What's the use of fibrates?
MOST EFFECTIVE DRUGS AT DECREASING TRIGLYCERIDES (50%), increase LDL
47
What are examples of fibrates?
Gemfibrozil, Fenofibrate, Bezafibrate
48
What are the side effects of fibrates?
GI upset, headache, gallstones, statin interaction, prolonged PTT(coumadin protein binding)
49
What's the MOA of Ezetimibe?
selective inhibitor of cholesterol absorption leading to secondary up-regulation of LDL-R
50
What is the use of Zetia?
alone decreases LDL by 22%, potentiates the effects of statins by 17%
51
What is the use of omega-3 fatty acids (fish oil)?
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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