Lipid Lowering Flashcards

1
Q

PCSK9 Inhibitors

A

Alirocumab and Evolocumab

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2
Q

PCSK9 Inhibitors MOA

A

Monoclonal Antibodies stop PCSK9 proteins; proteins cant bind to LDL anymore = more free LDL to be cleared from blood

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3
Q

PCSK9 Inhibitors ADRs

A
Injection site reactions
Headache
Arthralgia
Myalgia
Limb pain
Fatigue
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4
Q

PCSK9 inhibitors target

A

targets LDL; familial hypercholesteremia

don’t use with statin

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5
Q

Fibric Acid Derivatives drugs

A

Gemfibrozil and Fenofibrate

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6
Q

Fibric Acid Derivatives MOA

A

Agonist at PPAR Alpha Receptor
Decreases VLDL synthesis in liver
Increased Lipolysis (breaks down TG)

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7
Q

Fibric Acid Derivatives ADRs

A
Myopathy (with statins)
Increased LFTs
Nausea
GI upset
Skin Rash
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8
Q

Fibric Acid Derivatives Contraindications

A

NO gemfibrizil and simvastatin because of additive myopathy effect

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9
Q

Fibric Acid Derivative Target

A

Used in patients with TG>500, very effective

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10
Q

Omega 3s

A

Fish Oil (OTC) Vascepa, Lovaza

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11
Q

Omega 3s MOA

A

Inhibition of TG secretion from the liver Promotes metabolism of TG

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12
Q

Omega 3s ADRs

A

Fishy taste, burping, Antiplatelet effects at high doses

Stop before surgery

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13
Q

HMG CoA Reductase Inhibitors

A
Rosuvastatin
Atorvastatin
Simvastatin
Lovastatin
Pravastatin
Fluvastatin
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14
Q

HMG CoA Reductase Inhibitors MOA

A

Competitive inhibition of HMG CoA reductase to stop synthesis of cholesterol
Liver will up regulate LDL receptor to result
increased LDL uptake by liver (more cholesterol clearance)

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15
Q

Intensity of statins

A

High Intensity: atorvastatin (40-80mg) and rosuvastatin (20-40mg)

Moderate intensity: Atorvastatin (10-20mg), Rosuvastatin (5-10 mg), Simvastatin (20-40mg), Pravastatin (40-80mg), Lovastatin (40mg)

low intensity: fluvastatin (20-40mg)

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16
Q

HMG CoA Inhibitor ADRs

A

Teratogenic
Hepatic dysfunction (AST/ALT monitor)
Headache

17
Q

Statins and Muscle Complications

A

Myalgia: pain (no variation in CPK)
Myopathy: weakness (slight CPK elevation)
Rhabdomyolysis: breakdown (high CPK)

18
Q

Bile Acid Sequestrants

A

Cholestyramine
Colestipol
Colesevelam

19
Q

Bile Acid Seq MOA

A

Bind to Bile acid in GI tract to increase excretion = less bile acid = use up more cholesterol to make bile acid = decrease LDL

20
Q

Bile Acid Seq ADRs

A
Poorly tolerated (only for statin intolerant)
GI effects: bloating, gas, constipation, abdominal pain, increased TG?
21
Q

Bile Acid Seq Interactions

A

binds to many medications and makes meds ineffective

Give med 1 hour before or 4 hours after

22
Q

Bile Acids and Pregnancy

A

Safe to use in pregnancy

23
Q

Niacin

A

Vitamin B3

24
Q

Niacin target

A

TGs; used in hypertriglyceridema, can possibly increase HDL and lower LDL

25
Q

Niacin MOA

A

Decrease VLDL synthesis (targets endogenous cholesterol)

HDL is a byproduct of VLDL synthesis

26
Q

Niacin ADRs

A
FLUSHING
Pruritis
Increased Uric Acid (gout) and or glucose
Nausea
Abdominal Discomfort
Pregnancy Category X
27
Q

Niacin interactions

A

For those who are potentially statin intolerant

Don’t combine with statins

28
Q

Cholesterol Absorption Inhibitor

A

Ezetimibe

29
Q

Ezetimibe target

A

LDL

30
Q

Ezetimibe MOA

A

Stops absorption of cholesterol in the intestines

Less cholesterol= less chylomicrons=less serum LDL

31
Q

Ezetimibe ADRs

A

Diarrhea
Arthralgia
Fatigue
Increased LFTs (with statins)

32
Q

Ezetimibe contraindications

A

do not combine with bile acid sequestrants

33
Q

Ezetimibe combinations

A

Use with statins

considered 2nd in line treatment (after statins)