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STEP Pharm I > Dyslipidemia Drugs > Flashcards

Dyslipidemia Drugs Flashcards

1
Q

What are some drugs used to reduce cholesterol?

A

-HMG-CoA reductuase inhibitors (STATINS)-Bile acid resins-Ezetimibe-Niacinall share a common mechanism of increasing LDL receptors on the liver

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2
Q

What do Statins do?

A

inhibit the rate-limiting step of cholesterol biosynthesis lowering LDL by 25-60%

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3
Q

What happens when Statins inhibit cholesterol synthesis?

A

a transcription factor called Sterol Regulatory Element Binding Protein 2 that normally signals HMG CoA reductase to make more cholesterol when it is low, instead binds to a sterol response element (SRE) to signal the production of more LDL receptors causing LDL to go down

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4
Q

How do bile acid resins work?

A

traps bile acids so that they cant recirculate from the ileum and cant go back to the liver to make cholesterol and then the same process occurs as with statins leading to reduced LDL

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5
Q

What does Ezetimibe do?

A

binds to the demon pick (sp?) receptor in the gut which is responsible for the dietary uptake of free cholesterol and lowers LDL

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6
Q

How does Niacin work?

A

reduces synthesis of VLDL (lowers LDL by up to 20%)

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7
Q

How do Statins work?

A

part of the molecule (open acid ring) mimics the structure of the substrate for HMG CoA reductase, mevalonate

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8
Q

What are some types of Statins?

A

Lovastatin and Simvastatin (both naturally occurring)PravastatinAtrovastatin, Rosuvastatin

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9
Q

What are Lovastatin and Simvastatin metabolized by?

A

CYP3A4 (the others are active)

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10
Q

What is one benefit of Pravastatin?

A

muscle side effects are low

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11
Q

Which statins are the most effective?

A

Atorvastatin and rosuvastatinthen Lovastatin and Simvastatin then Pravastatin

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12
Q

How is SREBP maintained with cholesterol levels are high in the body?

A

it remains quiescent by binding to sterol cleavage activating protein (SCAP)

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13
Q

What are the high intensity statins (reduce LDL by 50+%)?

A

atorvastatin (40-80mg) and rosuvastatin (20-40 mg)anyone at high risk for heart disease should be on these

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14
Q

What are the moderate intensity statins (reduce LDL by 30-50%)?

A

Atorvastatin, (10-20mg) rosuvastatin (5-10 mg)Simvastatin, (20-40mg)Pravastatin, (40-80mg)Lovastatin, (40mg)Fluvastatin, (80mg) Pitavastatin, (2-4 mg)

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15
Q

What are the low intensity statins (reduce LDL by less than 30%)?

A

Simvastatin, (10mg)Pravastatin, (10-20mg)Lovastatin, (20mg)Fluvastatin, (20-40mg) Pitavastatin, (1 mg)

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16
Q

Which statins are most susceptible to drug-drug interactions?

A

Lovastatin and Simvastatin (CYP3A4 substrates)Atorvastatin (less)

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17
Q

What is the least statin susceptible to drug-drug interactions?

A

Pravastatin

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18
Q

How are Rosuvastatin and Fluvastatin metabolized?

A

CYP2C9

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19
Q

How are most statins excreted?

A

Fecal (pravastatin is 20% renal- others are lower)

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20
Q

What would be the preferred statin for a patient with renal failure?

A

Fluvastatin (very minimal renal excretion)

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21
Q

What are some drugs that inhibit CYP3A4?

A

-Macrolides-AZOLES-SSRIs (nefazodone)-Grapefruit juice -HIV PIs-Cyclosporine-CCBs`-Gemfibrozil

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22
Q

What are some drugs that p-glycoprotein (responsible for pumping foreign toxins back into the lumen if they make it out somehow) mediated intestinal reabsorption?

A

cyclosporine, grapefruit juice P-gP is responsible for pumping a lot statin back into the lumen and is responsible for its low bioavailability in part

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23
Q

What is a side effect of statins that can be particularly bad?

A

rhabdomyolysis

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24
Q

All statins depend on what for uptake into the liver for first as?

A

OTB1- a defect in the transporter would lead to very high levels of statin and then some of it would make its way to muscle causing myocytis

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25
Q

What are some adverse effects of STATINS?

A

-generally well tolerated-GI pain -increased Liver enzymes-sleep disturbance, memory loss-myalgia, myositis, -rhabdomyolysis

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26
Q

What is the difference between myalgia and myositis?

A

In myalgia you have muscle pain/weakness without CPK rise and in myositis you see increased CPK

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27
Q

Are STATINS teratogenic?

A

Yes

28
Q

STATINS are not effective against what?

A

hemorrhagic stroke- good for MI, stroke, CHD, etc.

29
Q

Are bile acid resins systemic?

A

Nope, they just pass through the gut and bind bile acids so they cannot be recovered via enterohepatic circulationsecondary to STATINS

30
Q

How are bile acid resins given?

A

pill or powder form 2x daily with meals and LOTS of water

31
Q

Side effects of bile acid resins?

A

GI (blotting and constipation)

32
Q

Do bile acid resins decrease TAGS?

A

No, may INCREASE and only have a modest effect on HDLlower LDL by up to 25%

33
Q

What is the problem with bile acid resins?

A

they will bind the basic groups as well (e.g. warfarin, digoxin, b-blockers, thyroxine)

34
Q

Brand names of bile acid resins?

A

-Colestipol-Cholestyramine -Colesevelam

35
Q

When are bile acid resins contraindicated?

A

-hyperlipidemia-complex drug regimens-history of constipation

36
Q

How effective is Ezetimibe?

A

reduces LDL by ~20% so its secondary

37
Q

Does Ezetimibe prevent coronary heart disease?

A

marginally – if LDL is still above 70-80 on the max statin dose, probably good to add to regimen

38
Q

What are some drugs that lower TAG and increase HDL?

A

Fabric Acid Derivative (Fibrates)Nicotinic Acid (Niacin)Omega 3 Polyunsaturated fatty acids (Fish Oil)

39
Q

Does a high level of TAG increase heart disease potential irrespective of LDL levels?

A

Yes, high TAGS get into HDL and then when they are striped away you have a very low potential of HDL to carry cholesterol

40
Q

There is no evidence that TAG lowering drugs show any adjunctive benefit to lowering risk of heart disease when added to STATINS

A

However, they are extremely effective at preventing pancreatitis

41
Q

What are some types of Fibric Acid Derivatives?

A

-Gemfibrozil (generic)-Fenofibrate (Tricor)-Fenofibric Acid (Trilipix)

42
Q

How is Fenofibrate metabolized?

A

UGTA2 so it won’t have drug-drug interactions with STATINS

43
Q

What is the mechanism of action for Fibric Acid Derivatives?

A

mimic short chain fatty acids and act as a ligand for PPARa nuclear receptors which turn on a lot of processes to get rid of lipids, including: the LPL gene which has a PPARa response element on it enzymes involved in fatty acid oxidation also inhibits synthesis of TAG and ApoCIII which blocks LPL function usually increases ApoCI/II synthesis so you get more HDL

44
Q

What are the results of Fibric Acid Derivatives?

A

-reduce VLDL-increase HDL-reduce TAG by 50+%no effect on LDL

45
Q

Adverse effects of Fibric Acid Derivatives?

A

-GI reflux-diarrhea-increased liver enzymes-teratogenic (Category C)-gallstones (more lithogenic bile)

46
Q

What is a side effect of Finofibrate?

A

increases creatinine (reversible), paradoxical HDL lowering

47
Q

What is Gemfibrozil metabolized by?

A

UFT1A1 (which is responsible for biotransformation of most statins) so gemfibrozil reduces statin metabolism so that is contraindicated

48
Q

T or F. Gemfibrozil can be given to patients with renal disease

A

T.

49
Q

T or F. Finofibrate can be given to patients with advanced renal disease

A

F if GFR below 30 ml/min. Accumulates with renal insufficiency dosage reduction recommended

50
Q

How is Finofibrate metabolized?

A

hepatic metabolism to active form, fenofibric acid, which undergoes renal excretion

51
Q

Do Fibric Acid Derivatives reduce Cardiovascular disease risk when added to statins?

A

no evidence in Helsinki Heart Study or VA-HIT study BUT did well in those with high TAG and low HDL

52
Q

What is Niacin?

A

vitamin B3 carboxylic acid that are available in immediate (Niacor) and extended release (Niaspan 1 -2g daily)

53
Q

What is a major side effect o Niacor?

A

flushing due to histamine release- not used often anymore. Niaspan is better tolerated

54
Q

How does Niacin work?

A

-prevents mobilization of fatty acids from adipocytes-reduces TAG synthesis-reduces ApoB synthesis and secretion-promotes conversion of VLDL to LDL via LPL-enhances ATP cassettes transfer of cholesterol from macrophages to HDL

55
Q

What is the main effect of Niacin?

A

-increases HDL by up 35%-reduces LDL by 5-25%-reduces TAG by 20-50%-makes large LDL particles-reduces Lp(a) by 30%

56
Q

Side effects of Niacin?

A

-cutaneous flushing-elevated hepatic enzymes (hepatitis, failure)-GI irritation-gout/hyperuricemia-myositis-insulin resistance-retinal detachment, conjunctivitis -dry skin, pruritus, acanthus nigricans

57
Q

Is Niacin teratogenic?

A

yes, category C

58
Q

Does addition of Niacin to Statin further reduce risk of CV disease?

A

AIM-HIGH and HPS-THRIVE trials shows no added benefit

59
Q

What are some good dietary sources of omega 3 and omega 6 fatty acids?

A

3- walnuts, flaxseed, canola oils6- corn, sunflower, fish,

60
Q

What do fatty acids result in?

A

reduced TAG by up to 35%

61
Q

What do Alirocumab and Evolocumab do?

A

mABs reduce cholesterol by inactivating PCSK9, a protein that binds LDL and is internalized with the LDL receptor where it transports it for destruction

62
Q

How should a patient under 75 with known atherosclerotic CV disease (CHD, CVD, PAD) and no safety concerns be treated?

A

high intensity statin

63
Q

How should a patient over 75 with known atherosclerotic CV disease (CHD, CVD, PAD) or other safety concerns be treated?

A

moderate intensity statins

64
Q

How should a patient with LDL above 190 mg/dL be treated?

A

if 21+ y/o- high intensity statin and may consider adding non-statin additive drugs to help

65
Q

How should a patient with diabetes (no ASCVD) aged 40-75 with LDL 70-189 mg/dL be treated?

A

should be based on 10 yr ASCVD risk based on Pooled Cohort Equations moderate intensity stain if less than 7.5%high intensity if over 7.5%

66
Q

How should a patient without diabetes or ASCVD aged 40-75 with LDL 70-189 mg/dL be treated?

A

-estimate 10 yr ASCVD risk- if 7.5+% risk, moderate to high intensityother consider moderate intensity

STEP Pharm I (36 decks)

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