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Sophomore - Pharm test 3 > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

Three major lipids in the body?

A
  1. Cholesterol
  2. Triglycerides
  3. Phospholipids
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2
Q

How does the liver make cholesterol? (Rate-limiting step)

A

HMG-CoA is converted to mavelonate by HMG-CoA reductase (this enzyme is the target of statins)

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3
Q

What job does a lipoprotein have? Why?

A

Taxi cab for cholesterol and triglycerides bc they’re insoluble in water

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4
Q

Chylomicrons - characteristics?

A

First step of packaging digested fats

Transports TG’s, cholesterol, and phospholipids derived from diet from the gut to the liver, adipose tissue, and muscle

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5
Q

What is the most abundant component in chylomicrons?

A

TG’s (90%)

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6
Q

As chylomicrons make their way to the liver, what component is dropped off at various sites along the way? How?

A

TG’s; removed by lipoprotein lipase in various cells

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7
Q

VLDL - most abundant component?

A

TG’s (55%); less than in chylomicrons, a little more cholesterol than in chylomicrons (25%

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8
Q

LDL - most abundant component?

A

Cholesterol (55%)

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9
Q

HDL - most abundant component?

A

Proteins (50%)

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10
Q

HDL’s job?

A

Scoops up cholesterol from peripheral cells and brings it back to the liver

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11
Q

VLDL’s serve as a precursor to what?

A

LDL’s

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12
Q

Which lipoprotein is known as “bad cholesterol”?

A

LDL

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13
Q

Which lipoprotein is known as “good cholesterol”?

A

HDL

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14
Q

Desirable total cholesterol number is below…?

A

200mg/dL

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15
Q

Desirable LDL number is less than…

A

100mg/dL

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16
Q

Desirable HDL cholesterol is above…?

A

60

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17
Q

Desirable TG’s is less than…?

A

150

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18
Q

Routine initiation of statin therapy in which patient population is not recommended?

A
  1. Class II through IV HF

2. Maintenance hemodialysis

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19
Q

What do we use to determine the statin benefit group?

A

The ASCVD (athersclerotic cardiovascular disease) risk algorithm

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20
Q

What is the first major statin benefit group?

A

Pt’s with clinical ASCVD (Hx of MI, CVA, unstable angina, etc)

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21
Q

What is the second major statin benefit group?

A

LDL > 190

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22
Q

What is the third major statin benefit group?

A

DM (age 40-75) with LDL 70-189mg/dL

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23
Q

What is the fourth major statin benefit group?

A
  1. No clinical ASCVD
  2. No DM
  3. Age 40-75
  4. LDL 70-189mg/dL
  5. 10-yr ASCVD > 7.5%
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24
Q

Name the two high intensity statins:

A
  1. Atorvastatin (Lipitor) 40-80mg

2. Rosuvastatin (Crestor) 20-40mg

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25
Q

Which drug class is best for increasing HDL?

A

Niacin

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26
Q

Which drug class is best for decreasing TG’s?

A

Fibrates

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27
Q

Which drug class is best for decreasing LDL’s?

A

Statins

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28
Q

HMG-CoA Reductase Inhibitors - MOA?

A

Inhibits the first committed enzymatic step of sterol synthesis by BLOCKING HMG-CoA Reductase

Depletes intracellular cholesterol supplies

Causes up-regulation of LDL receptors

Overall decrease in circulating LDL

29
Q

What time of day are statins taken? Why?

A

At night, bc your body inherently produces more cholesterol while you sleep (high dose statins can be taken anytime of day)

30
Q

Most common statin SE’s?

A 
Muscle pain (myalgias)
Rhabdomylosis
Liver toxicity
31
Q

What is a routine blood panel (other than lipid) you should obtain prior to and after initiating statin therapy? Why?

A

LFT - liver issues are common to statins (commonly seen increase in ALT)

32
Q

Factors that can increase statin-induced myopathy?

A
  1. Age >75
  2. Female
  3. Liver dysfunction
  4. Renal insufficiency
  5. ETOH abuse
  6. Grapefruit juice (inhibits CYP enzymes)
33
Q

Absolute CI’s to statins?

A
  1. Pregnancy
  2. Nursing
  3. Acute liver disease
34
Q

Statin drug interactions?

A
  1. Amio
  2. Amlodipine
  3. Dig
  4. Cardizem
  5. Coumadin
  6. Niacin
35
Q

All statins (except pravastatin) are highly _______ bound.

A

Protein /// may displace other highly bound drugs (like warfarin)

36
Q

Which two HGM-CoA Reductase Inhibitors require no dose adjustment in patients with renal insufficiency?

A

Atorvastatin

Pitavastatin

37
Q

Which drug class is most beneficial in treating high triglycerides?

A

Fibrates (Fibric Acid Derivatives)

38
Q

Fibrates - MOA?

A

Stimulates lipoprotein lipase activity - hastens the removal of chylomicrons and VLDL’s from plasma, subsequently decreasing TG’s

39
Q

What is the most effective drug for increasing HDL?

A

Niacin

40
Q

What side effect may occur when Gemfibrozil is combined with a statin?

A

Myopathy and rhabdomyolysis

41
Q

Gemfibrozil - Pregnancy category?

A

C

42
Q

Niacin (aka Nicotinic Acid) - MOA?

A

Inhibits hepatic synthesis of VLDL by inhibiting lipolysis in adipose tissues, in turn decreasing production of free fatty acids

BLUF: lowers VLDL, raises HDL

43
Q

Niacin - major clinical benefit?

A

Reduces major coronary events

44
Q

Niacin - pregnancy category?

A

C

45
Q

How to reduce Niacin flushing?

A

ASA 30 mins prior to Niacin

Take Niacin with meals

46
Q

Adverse effects of Niacin - three:

A
  1. Liver tox
  2. Hyperglycemia
  3. Hyperuricemia
47
Q

Niacin - CI’s?

A
  1. Liver disease
  2. Severe gout
  3. Uncontrolled DM
  4. Active PUD
48
Q

Monitoring with Niacin?

A

Check LFT’s at baseline and every 2-3 months

49
Q

Bile Acid Sequestrants - MOA?

A

Binds bile acids and salts in the intestine, causing them to be excreted in feces

Decreased levels cause liver to use more existing cholesterol to make bile acids / salts

Overall effect, decreased cholesterol

50
Q

Bile acid sequestrants best for which type of patient?

A

Isolated high LDL (because these drugs can increase TG’s)

51
Q

Bile acid sequestrants can cause impaired absorption of?

A

Fat-soluble vitamins (A,D,E,K)

Statins

52
Q

Which bile acid sequestrants are pregnancy category B?

A

Colistepol

Colesevelam

53
Q

Which bile acid sequestrant is pregnancy category C?

A

Cholestyramine

54
Q

Bile acid sequestrants - adverse effects?

A

Gi distress, bloating, constipation (many patients are noncompliant with medication due to these effects)

Decreased absorption of:
Warfarin, Thiazides, B-blockers, fat-soluble vitamins (A,D,E,K)

55
Q

Bile acid sequestrants - CI’s?

A

Pt’s with high TG’s

56
Q

Ezetimibe - MOA?

A

Inhibits intestinal cholesterol absorption

57
Q

Ezetimibe - clinical use?

A

Reduce LDL in primary hyperlipidemia

Adjunct to statin therapy (synergistic)

58
Q

Ezetimibe - pregnancy cat?

A

C

59
Q

PCSK9 inhibitor - MOA?

A

Human monoclonal Ab

Inhibits the PCSK9 enzyme

No PCSK9 —> no degradation of LDLR’s —> increased LDLR’s expressed on hepatocyte surface —> more clearance of LDL’s from circulation —> decreased plasma LDL

60
Q

What’s so great about PCSK9? What’s so bad?

A

HIGHLY effective at lowering LDL

CRAZY expensive

61
Q

Name two PCSK9 Inhibitors:

A

Alirocumab

Evolocumab

62
Q

Benefits of Omega-3?

A

Lowers TG’s, raises HDL

63
Q

Omega-3 can have an adverse impact on?

A

Bleeding time (platelets)

64
Q

Criteria features of high intensity statin primary prevention?

A
  1. LDL > 190mg/dL

2. Pt’s w/ LDL 70-190mg/dL AND 10-yr ASCVD > 7.5%

65
Q

Clinical features of moderate intensity statin primary prevention?

A
  1. DM pt’s w/ LDL 70-189mg/dL and 10-yr ASCVD LESS THAN 7.5%
66
Q

Best drug for lowering TG’s?

A

Fenofibrate

67
Q

What is the most common type of lipid abnormality?

A

Type IIA - familial hypercholesteremia

68
Q

Type IIA causes increased…?

A

LDL

69
Q

Which lipid abnormality is NOT associated with coronary heart disease?

A

Type I (familial hyperchylomicronemia)

Sophomore - Pharm test 3 (7 decks)

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