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Pharmacology > Exam3Lec4Antihyperlipidemics > Flashcards

Exam3Lec4Antihyperlipidemics Flashcards

1
Q

What are the 2 reasons why someone might have high cholesterol?

made a joke

A

Because of low exercise and high saturated fatty acids

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2
Q

What is CHD correlated with in terms of LDL and HDL?

A

High LDL (“bad”) and low HDL (“good”)

antihyperlipidemins taken chronically

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3
Q

What are the 5 ACC/AHA Guidelines on the Management of Blood Cholesterol?

A
  1. Healthy lifestyle
  2. Clinical ASCVD: ↓ LDL-C by > 50% with high-intensity statin with a nonstatin when LDL > 70
  3. Severe hypercholesterolemia: High-intensity statin at highest tolerated dose
  4. DM & LDL-C > 70 mg/dL, 40-75 y/o : Moderate-intensity statin
  5. 10-year ASCVD risk > 7.5%, 40-75 y/o: Consider moderate-intensity statin

high-intensitty statin: atorvastatin/ rosuvastatin
non statin: ezetimibe or cholestyramine

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4
Q

For patients who took high intensity statins Atorvastatin and Rosuvastatin daily, what happened to their LDL lvls?

A

LDL-C ↓ by > 50%

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5
Q

For patients who took moderate intensity statins (a&r, S&Prav, L&F) , daily, what happened to their LDL lvls?

A

LDL-C ↓ by 30 -50%

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6
Q

For patients who took moderate intensity statins (a&r, S&Prav, L&F) , daily, what happened to their LDL lvls?

A

LDL-C ↓ by 30 -50%

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7
Q

For patients who took low intensity statins (P and L) , daily, what happened to their LDL lvls?

A

LDL-C ↓ by < 30%

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8
Q

Which drug(s) are HMG CoA reductace inhibitors?

A
  • Atorvastatin
  • Lovastatin
  • Pravastatin
  • Rosuvastatin
  • Simvastatin
  • Fluvastatin
  • Pitavastatin

all -statins

bolded is hy

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9
Q

MOA for statins in general

A

Inhibit HMG CoA reductase which is the RLS , this inhibit de novo cholesterol synthesis therefore depleting intracellular supply of cholesterol.

Low IC cholesterol stimulates synthesis for more LDL receptors so there is more LDL uptake from blood

they are Analogs of 3-OH-3-CH3-glutaryl (a cholesterol precursor )

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10
Q

Rank order potency of LDL lowering (from Greatest to Lowest)

A

Pitavastatin, Rosuvastatin, Atorvastatin > Simvastatin, Pravastatin > Lovastatin, Fluvastatin

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11
Q

Atorvastatin
1. MOA
2. Therapeutic uses

A
  1. MOA: Blocks HMG-COA reductase. Leads to Depletion of intracellular cholesterol by incr LDL receptors and bind & internalize circulating LDL (decr LDL, incr HDL, lower TAG))
  2. Therapeutic uses: hyperlipidemia, plaque stabalization, CHD

incr in LDL receptors and block its exportation (bringing everything outside inside)

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12
Q

Is atorvastatin effective for homo familial hypercholesterolemia?

A

NO, because it lacks functional LDL receptors

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13
Q

Are statins risk reducers for CHD?

A

Yes, it doesnt necessarily solve the problem, it should be used in combination with diet and exercise

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14
Q

Atorvastatin
1. SE
2. Drug interactions

A
  1. SE: constipation, no preg, confusion/memory impairment, muscle aches, DM
  2. Drug interactions: Cyclosporine, Itraconazole, Erythromycin, Gemfibrozil, Niacin

bolded hy

rhabdo=muscles

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15
Q

A 43-year-old obese man with type 2 diabetes mellitus is prescribed atorvastatin for the treatment of hyperlipidemia. Which of the following is the mechanism of action of atorvastatin?
A. Triacylglycerol secretion inhibitor
B. HMG-CoA reductase inhibitor
C. Cholesterol absorption inhibitor
D. Cholesterol secretion inhibitor

A

B. HMG-CoA reductase inhibitor

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16
Q

Which drug(s)s are lipolysis inhibitors?

A

Niacin: nicotinic acid, Vitamin B3

hy

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17
Q

Niacin
MOA

A
  1. Inhibits TAG lipolysis in adipose tissue.
  2. decr tag syntheis, decr LDL, incr HDL
  3. incr tissue plasminogen activator, decr fibrinogen
  4. Reverse some endothelial cell dyfxn, contributing to clots w/ hypercholesterolemia & atherosclerosis

TAG lipolysis-> fatty acid (adiose to liver)-> TAG->VLDL-> LDL

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18
Q

Niacin
1. Therapeutic uses
2. Side effects
3. Pharmacokinetics
4. Drug interactions

A
  1. Therapeutic uses: hyperlipidemia, lower LDL, INCR HDL THE MOST
  2. Side effects: flushing, Hyperuricemia (gout), DM, hepatitis
  3. Pharmacokinetics: Converted into nicotinamide which has no activity
  4. Drug interactions: Statins: ↑ muscle & liver toxicity risk

you can decr flushing with ASA and IBU
you need a higher dose to decr LDL
HALLMARK IS THAT IT INCR HDL THE MOST

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19
Q

Which drug(s) are fibrates?

A

Fenofibrate, Gemfibrozil

bolded is hy

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20
Q

Gemfibrozil
MOA

A
  1. Peroxisome proliferator-activated receptor-α (PPAR-α) agonists
  2. decr TAG by incr lipoprotein lipase), incr HDL, decr LDL

PPAR-α regulates lipid metabolism
HALLMARK=DECR TAG THE MOST

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21
Q

Gemfibrozil
1. Therapeutic use
2. SE
3. Drug interactions

A
  1. Therapeutic use: hyperlipidemia
  2. SE:Hepatitis, Myositis (weakness, stiffness), Gallstones (incr biliary cholesterol excretion)
  3. Drug interactions: warfarin, statins

Statins: ↑ muscle & liver toxicity risk

22
Q

Which drug(s) are Bile acid sequestrants?

A
  1. Cholestyramine
  2. Colestipol
  3. Colesevelam

bolded is hy

23
Q

Cholestyramine
MOA

A
  1. Anion exchange resins which bind (-) charged bile acids & salts in small intestines
  2. Resin/bile acid complex excreted in feces-> inhibiting entereohepatic recycling
  3. More chol is converted to bile acids, incr LDL uptake via incr in receptors, lower splasma LDL, incr HDL

bile acids (-), seqestrants (+)

Bile acid sequestrants only stay in GI tract. It binds to bile acid and it prevents it from being recycled from SI to its excreted. The body converts more choel to bile salts in the liver and you see incr in LDL receptor formation.

24
Q

What is sodium torocholate?

A

Bile acid

25
Q

Cholestyramine
1. Therapeutic use
2. SE
3. Drug interactions

A
  1. Therapeutic use: hyperlipidemia
  2. SE: Constipation, N/V, Flatulence
  3. Drug interactions: Interfere w/ absorption of acidic drugs: Warfarin, Niacin, Digoxin & Vitamins A, D, E, K

Vitamins A, D, E, K are lipid/fat soluble it can be taken up w/ bile acid

26
Q

Which drug is Considered the safest class of lipid-modifying drugs during pregnancy?

hy

A

Cholestyramine

hy

on exam

27
Q

Which drug(s) are cholesterol absorption inhibitors?

A

Ezetimibe

28
Q

Ezetimibe
MOA

A
  • Inhibits cholesterol absorption at the brush border of the intestines & liver via NPC1L1, incr LDL-R expression
  • decr LDL, decr TAG, inr HDL
29
Q

Ezetimibe
1. Therapeutic use
2. SE
3. Pharmacokinetcs

A
  1. Therapeutic use: hyperlipidemia
  2. SE: GI upset
  3. Pharmacokinetcs: UGT
30
Q

Can you use Ezetimibe with statins?

A

YES, its weaker to decr LDL so its safe to use with statins if you need to decr LDL more

31
Q

List the effect for each drug

A
  1. Statins have the greatest effect on decr LDL compared to other drugs
  2. Fibrates have the greatest effect on decr TAG compared to other drugs
  3. Niacin has the greatest effect on Incr HDL compared to other drugs
  4. Bile acid sequestrants can reduce LDL but not as great as statins, so it can be used with statins to reduce LDL more.
  5. Bile acid sequestrants can actually incr TAG in some pts and can lead to pancreatis
  6. Cholesterol absorption inhibitors are the worst at reducing LDL, so it can be used with statins to reduce LDL more

know 1-3

32
Q

Which drug(s) are Microsomal triglyceride transfer protein inhibitors?

ly

A

Lomitapide

ly

33
Q

Lomitapide
MOA

ly

A
  1. Microsomal triglyceride transfer protein inhibitor
  2. Prevents assembly of apo-B containing lipoproteins (chylomicrons & VLDL in liver & GIT) -> decr plasma LDL concentrations

ly

34
Q

Lomitapide
1. Therapeutic use
2. SE
3. Pharmacokinetcs

A
  1. Therapeutic use: homozygous familial hypercholesterolemia
  2. SE: liver damage, no pregnancy
  3. Pharmacokinetcs: CYP3A4 substrate: DI, Hepatic dysfxn

know bolded

35
Q

Which drug(s) are PCK9 inhibitors?

hy

A

Evolocumab

hy

36
Q

Evolocumab
MOA

A
  1. Selectively binds to PCSK9 & prevents PCSK9 from degrading LDL receptors in hepatocyte lysosomes which ↑ # of recycled LDL receptors
  2. incr # of LDL receptors therefore decr LDL plasma concentrations

its a monoclonal antibody
pcsk9 degrades ldl receptors

37
Q

Evolocumab
1. Therapeutic use
2. SE

A
  1. Therapeutic use: homo or hetero hypercholesterolemia, CVD, statin therapy
  2. SE: Nasopharyngitis, UPRI, Flu, Back pain, Injection site rxns , Allergic reactions
38
Q

What are fish oils?

ly

A

Omega-3-acid ethyl esters

ly

39
Q

Omega-3-acid ethyl esters
1. MOA
2. Therapeutic use
3. SE

ly

A
  1. MOA: Activation of nuclear transcription factors ( peroxisome proliferator-activated receptor-α (PPAR-α)) this leads to liver fatty acid oxidation → ↓ TAG synthesis
  2. Therapeutic use: hyperlipidemia , decr TAG, incr HDL, incr LDL (icosapent -purest form of fish oils, incr LDL the least)
  3. SE: Thrombocytopenia, Halitosis, Dysgeusia, Dyspepsia, Infection, Back pain, Flu-like syndrome

ly

found in krill oil, cold water fish, milk products for children
made a joke abt halitosis and dysgeusia

40
Q

Which drug(s) are ATP Citrate Lyase Inhibitors?

hy

A

Bempedoic acid

hy

41
Q

Bempedoic acid
MOA

hy

A
  • Inhibitor of ATP citrate lyase, ↑ LDL-R by ↓ cholesterol synthesis
  • Prodrug: Active metabolite produced in liver not muscle

hy

has less muscle toxicty/activity than statins

42
Q

Bempedoic acid
1. Therapeutic use
2. Side effects

hy

A
  1. Therapeutic use: heterozygous familial hypercholesterolemia, CVD
  2. Side effects: Gout, Tendon rupture, Anemia, ↑ Liver enzyme, Muscle spasms

hy

43
Q

Which drug(s) are siRNAs?

hy

A

Inclisiran

hy

44
Q

Inclisiran
MOA

A

Small interfering RNA (siRNA) for PCSK9 mRNA, Thus inhibits PCSK9 synthesis

know this

45
Q

Inclisiran
1. Therapeutic use
2. SE

A
  1. Therapeutic use: Hetero hypercholesterolemia, prevent Cardiovascular events
  2. SE: antibodies, inj site rxn, arthralgia, bronchitis
46
Q

Which of the following is the most clinically important side effect of the niacin sustained release dosage form (Niaspan®)?
A. Dermatitis
B. Meningitis
C. Nephritis
D. Hepatitis

A

D. Hepatitis

47
Q

Which of the following drugs is the first line treatment for high LDL lvls?

Cholestyramin
Atorvastatin
Niacin
Evolocumab

A

Atorvastatin

48
Q

Which of teh following drugs should not be given aling side a statin due to the incr risl for muscle and liver toxicity?

Gemfibrozil
Niacin
Both
Neither

A

Both

49
Q

Which of the following drugs is a PPAR-alpha receptor agonist?

Evolocumab
Ezetimibe
Bemoedoic acid
Gemfibrozil

A

Gemfibrozil

fish oil too

50
Q

A pt is taking an antihyperlipidemic and starts to experience the side effects of nausea, vomitting, constipation, and flatulance but has other systemic effect. Which of the following antihyperlipidemics is the pt likely taking?

Bempoic acid
Cholestyraramine
Atorvastin
Evolocuman

A

Cholestyraramine

51
Q

Which of the following has the gratest effect on incr HDL?
Niacin
Bempedoic acid
Ezetimibe
Atorvastatin

A

Niacin

Pharmacology (26 decks)

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