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ICOM-Cardio > Cardio-pharm-Antihyperlipidemics-Lynch > Flashcards

Cardio-pharm-Antihyperlipidemics-Lynch Flashcards

1
Q

What are triglycerides as a dietary lipid?

A

Neutral fat • Energy source • Account for 90% of total lipids in body

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2
Q

What is the role of phospholipids as a dietary lipid?

A

Essential to building plasma membranes

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3
Q

What is the role of cholesterol as a dietary lipid?

A

Necessary for production of Vitamin D, Bile Acids, Cortisol, Estrogen, Testosterone

• Body makes enough cholesterol, not necessary in the diet

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4
Q

What are lipoproteins?

A

Carriers of lipid molecules

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5
Q

What do lipoproteins consist of?

A

Consist of cholesterol, triglycerides, and phospholipids with protein carrier

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6
Q

What is another name for protein carrier in lipoproteins? And what is its role?

A

Protein carrier is known as apoprotein

  • Apoproteins allow the lipoprotein to bind tissue receptors
  • Missing or defective in Familial Hypercholesterolemia
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7
Q

What are the 3 type of lipoproteins?

A

Low-density lipoprotein (LDL)

  • Very low-density lipoprotein (VLDL)
  • High-density lipoprotein (HDL)
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8
Q

What are VLDLs, where are they formed, and what do they do?

A
  • Formed by the liver
  • Major carrier of triglycerides in the blood

mainly made up of triaglycerol

• Becomes an LDL as it passes through the body

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9
Q

What are LDL’s and what do they do?

A

made up mainly of cholesterol

  • LDL transports cholesterol from liver to tissues and organs
  • Used to build plasma membranes and synthesize other steroids
  • Carries highest amount of cholesterol
  • “Bad” cholesterol
  • Contributes to plaque deposits and coronary artery disease
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10
Q

What are HDLs?

A
  • Manufactured in liver and small intestine
  • Reverse cholesterol transport • Assists in transport of cholesterol away from body tissues and back to liver
  • “Good” cholesterol • Transports cholesterol for destruction and removal from body

Vacuum cleaner

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11
Q

What is reverse cholesterol transport of HDLs?

A

Assists in transport of cholesterol away from body tissues and back to liver

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12
Q

HDLs mainly consist of which macromolecule?

A

protein

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13
Q

Which enzyme reduces HMG CoA to cholesterol?

A

HMG-CoA reductase

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14
Q

From what are bile acids made?

A

cholesterol

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15
Q

Total cholesterol lab values for high risk, moderate risk, and high risk?

A

<200 Desireable

200-240 Moderate

>240 High risk

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16
Q

LDL optimal level?

A

<100

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17
Q

HDL desireable level?

A

>60

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18
Q

triglycerides desireable level?

A

<149

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19
Q

What lifestyle changes can help control hyperlipedemia?

A
  • Monitor blood-lipid levels
  • Maintain weight; exercise
  • Reduce dietary saturated fats and cholesterol
  • Increase soluble fiber in diet
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20
Q

What are the 7 drug therapies for dyslipidemia?

A
  1. Inhibitors of HMG-CoA Reductase 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA)
  2. PCSK9 Inhibitors
  3. Bile Acid Sequestrants
  4. Niacin
  5. Fibric Acid Agents
  6. Ezetimibe
  7. Omega-3 Fatty Acids
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21
Q

What are statins?

A

Inhibitors of HMG-CoA Reductase

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22
Q

What do statins do in regards to cholesterol?

A

• Interfere with the synthesis of cholesterol

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23
Q

What are the first drugs of choice to reduce blood-lipid levels?

A

Statins (Inhibitors of HMG-CoA Reductase)

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24
Q

How do statins (Inhibitors of HMG-CoA Reductase) work?

A

Interfere with the synthesis of cholesterol

and

enhances the uptake of LDL by the liver which reduce serum LDL levels

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25
Q

How do statins uptake LDL into the liver?

A

Upregulate expression of LDL receptors which in turn takes up more LDL into the liver

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26
Q

Which two are the high-intensity statins?

A

Atorvastatin and Rosuvastatin

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27
Q

Its important to move from intensity statins to intensity statins to ensure that statins will not work with a patient with side effects.

A

high, low

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28
Q

When is the absolute time to stop statins?

A

elevation in liver enzymes ( as it can cause liver damage)

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29
Q

What is another serious ADE of statins other than liver damage?

A

Myopathy (muscle pain), possibly leading to the serious condition rhabdomyolysis

this can also lead to kidney damage as myoglobin is being released in the blood and damaging kidneys

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30
Q

What are the more mild ADEs associated with statins?

A

Mild, transient GI disturbances

• Rash, Headache

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31
Q

Oral administration of statins has first-pass metabolism. This means that they metabolized most likely by which two CYPs?

A

extensive, CYP450, 3A4

32
Q

Lovastatin, simvastatin, and atorvastatin are all metabolized in the liver by which liver enzymes?

A

CYP450, CYP3A4

33
Q

Fluvastatin is metabolized in the liver by which 2 liver enzymes?

A

CYP450, 2C9

34
Q

Which 3 statins are pro-drugs?

A

Lovastatin, Atorvastatin, and Simvastatin are pro-drugs and are activated after being metabolized by CYP 3A4

35
Q

What should one monitor while using statins?

A

liver enzymes

36
Q

What is the pregnancy category of statins?

A

Pregnancy Category X

37
Q

Why are the shorter half-life statins given at night (Lovastatin)?

A

Endogenous cholesterol biosynthesis occurs mostly at night, and is where the HMG-CoA Reductase is most active. The short half-life statins can do their best work at this time.

38
Q

Lovastatin, simvastatin, and fluvastatin have a shorter half-life and can be administered at .

A

Night for the most efficacious effect

39
Q

HMG-CoA Reductase Inhibitors

• Lipid effects

  • Decrease by 22 – 55 % • Decreased endogenous cholesterol biosynthesis increases the uptake of plasma LDL by the transcription of the LDL receptor gene
  • Decrease by 10 – 30% which also decreases production
  • Increase HDL by 5 – 15% • Increase the synthesis of apoA-I
A

LDL; stimulating; triglycerides; VLDL

40
Q

What is the next step if a patient cannot tolerate the least potent statin?

A

If patient can not tolerate it then move to bile acid sequestrant ± ezetimibe

41
Q

what are the 3 gene mutations involving Familial hypercholesterolemia?

A
  1. LDL receptor gene
  2. apoB-100 gene
  3. PCSK9 gene
42
Q

Which gene mutation on chromosome 1 promotes degradation of LDL receptors on the surface of hepatocytes?

A

PCSK9 gene

43
Q

What is the result of blocking the chromosome 1 gene mutation PCSK9?

A

If you block this protein you can prevent LDL receptors from being broken down and thus more LDL cholesterol would be taken up by the liver

44
Q

What are PCSK9 inhibitors?

A

monoclonal Abs that bind to PCSK9 that inhibit them from binding to LDL receptor and degradation of that receptor.

45
Q

What are 2 important PCSK9 inhibitors?

A

Alirocumab, Evolocumab

39-62% reductions in LDL cholesterol!

46
Q

What is the route of administration of PCSK9 inhibitors?

A

By injection only.…but only 1x every 2 weeks

47
Q

What are the 3 main ADEs of PCSK9 inhibitors?

A
  • Nasopharyngitis (11%)
  • Injection site reactions (7%)
  • Influenza symptoms (5.7%)
48
Q

Bile-acid sequestrants (BAS) are ion-exchange resins and bind in the intestine to prevent recycling by the .

A

bile salts; liver

49
Q

How do bile-acid sequestrants, that bind bile salts in the intestine and prevent recycling in the liver, lower cholesterol?

A

By binding the bile salts, they cannot be recycled, and the liver has to sequester more cholesterol to synthesize more bile salts- hence, reducing cholesterol

50
Q

What are the names of the 3 bile acid sequestrants?

3 C’s

A
  • Cholestyramine
  • Colestipol
  • Colesevalam
51
Q

Bile acid sequestrants can reduce/increase LDL levels and reduce/incresse HDLs?

A

reduce; increase

52
Q

With what drug can you have a synergistic effect with Bile Acid Sequestrants (BAS) for reducing LDLs?

53
Q

What is the major advantage of BAS concerning absorption?

A

they are not systemically absorbed, it acts only in the gastrointestinal system

54
Q

What are some ADEs of BAS?

A

G.I. bloating, constipation, irritation.

• May raise serum triglycerides!

may bind to other drugs in intestine

55
Q

What acid based drugs do bile acid sequestrants bind to in the intestine?

A

• Thiazides, Furosemide, Digoxin, Coumarin, levothyroxine, ….etc

(avoid this by taking them 4 hours apart)

56
Q

Which drug is used mainly to increase HDLs?

A

Niacin, B3

57
Q

What can niacin, B3, do as a hyperantilipidemic?

A

• Primary use is to reduce VLDL’s triglycerides; increase HDL levels • TG Decrease up to 45% • LDL Decrease up to 20% • HDL increase up to 30%

58
Q

Which antihyperlipidemic alters the activity of lipase enzymes that metabolize triglycerides and lipids?

A

Niacin, B3

59
Q

Niacin can decrease apoA-I which in turn increases HDLs and can inhibit lipase which decreases synthesis.

A

clearance; triglycrides

60
Q

Niacin has several side effects but the most serious is what?

A

hepatotoxicity

also

  • Flushing (blocked by aspirin, implication?)
  • Pruritus
  • GI distress
  • Rhabdomyolysis
  • Worsens gout –avoid with gout
  • Impaired glucose control – avoid with diabetes
61
Q

It is important to monitor liver function, uric acid levels, and blood gluclose levels with someone taking which antihyperlipidemic?

A

Niacin, B3

62
Q

What effect does niacin have on those with peptic ulcer disease?

A

It can worsen the condition

63
Q

What can relieve the Niacin ADE flushing?

A

take aspirin one hour prior

64
Q

Which antihyperlipidemic works to activate lipase (breaking down cholesterol), suppresses the release of free fatty acids from adipose tissue, and inhibits synthesis of triglycerides in the liver?

A

Fibric acid derivatives (fibrates)

65
Q

What are the 2 fibric acid derivatives (fibrates)?

A

Gemfibrozil, Fenofibrate

66
Q

Fibrartes or fibric acid derivatives activate which receptor?

A

PPAR- peroxisome proliferatior-activated receptor

67
Q

What does PPAR (peroxisome proliferator-activated receptor) accomplish when activated by fibrates?

A

increases HDL and decreases plasma triglycerides

68
Q

Fibrates are used mainly to treat high levels of .

A

triglycerides or hypertriglyceridemia

69
Q

Fibrates have some worrisome interactions with which two types of drugs?

A
  1. Oral anticoagulants
  2. Statins- Risk for myositis, myalgias, and rhabdomyolysis is increased
70
Q

What type of effect can fibrates have on Hbg, Hct, and WBC?

A

It can decrease all of those.

71
Q

What type of effect do fibrates have on clotting time, lactate dehydrogenase level, and bilirubin level?

A

Increases all of them

72
Q

What are the main 2 ADEs of fibrates?

A

§ Adverse Effects:

§ Abdominal discomfort, diarrhea, nausea

§ Blurred vision, headache

§ Increased risk of gallstones (Clofibrate, older drug)

§ Prolonged prothrombin time

§ Liver studies may show increased enzyme levels

73
Q

2 things to consider monitoring while taking fibrates are?

A
  1. Assess for complaints of GI distress before starting drug
  2. Monitor prothrombin time/international normalized ratio (PT/INR) if taking warfarin as it may potentiate anticoagulant effects.
74
Q

Which antihyperlipidemia is only recommneded when patients do not respond to statins?

A

Ezetimibe (Zetia)

75
Q

What is the main use for Ezetimibe?

A

• Inhibits the absorption of cholesterol from the gut, and cholesterol eventually excreted.

76
Q

EZETIMIBE can be combined with a statin called ?

77
Q

Which other antihyperlipidemic activates the PPARa receptor to decrease plasma triglycerides levels other than fibrates?

A

Omega-3 fatty acids (fish oils)

OMACOR

ICOM-Cardio (32 decks)

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