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CVM > DSA: Drugs for Lipid Disorders > Flashcards

DSA: Drugs for Lipid Disorders Flashcards

1
Q
  • Normally, you always start a patient off w/ diet and exercise to control lipids, what is one situation that requires drug therapy from the start?
A

Familial hypercholesterolemia

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2
Q
  • VLDL is increased by what four things?
A
  • Total fat
  • sucrose
  • fructose
  • EtOH
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3
Q
  • You advise a patient to lose weight for their lipid levels, and they successfully do so. How long does their weight have to be stable in order to draw a lipid panel to see if weight loss alone was sufficient for management?
A
  • 1 month
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4
Q
  • What are some general dietary recommendations for a patient w/ hypercholesterolemia regarding the following:
    • Calories from fat
    • saturated fat
    • cholesterol
A
  • limit total calories from fat to 20-25% of daily intake
  • saturated fats should be less than 8% of daily intake
  • cholesterol intake should not exceeed 200 mg/day

*doing these things can result in a 10-20% reduction in serum cholesterol

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5
Q
  • Name 7 Statins we need to know for this exam
A
  • Atorvastatin
  • Fluvastatin
  • Lovastatin
  • Pitavastatin
  • Pravastatin
  • Rosuvastatin
  • Simvastatin
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6
Q
  • What enzyme do statins inhibit?
    • what is significant about this enzyme?
A
  • They are HMG-CoA reducatase inhibitors
  • HMG-CoA is the rate limiting enzyme in cholesterol synthesis.
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7
Q
  • What is the MOA of statin drugs?
    • how much can they reduce serum LDL?
A
  • Statins inhibit HMG-CoA reductase, which inhibits de novo cholesterol synthesis thus depleting intracellular supply of cholesterol.
    • _​_this causes the cells to increase the number of LDL receptors that bind to circulating LDL, thus decreasing serum levels by 20-55%
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8
Q
  • Most statins have half lives of 1-3 hours, however what are the half lives of:
    • Atorvastatin?
    • Pitavastatin?
    • Rosuvastatin?
A
  • Atorvastatin: 14 hours
  • Pitavastatin: 12 hours
  • Rosuvastatin: 19 hours
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9
Q
  • Which statin drugs are metabolized primarily by CYP3A4?
A
  • Lovastatin
  • Simvastatin
  • Atorvastatin
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10
Q
  • Which statin drugs are metabolized by CYP2C9?
A
  • Fluvastatin
  • Rosuvastatin
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11
Q
  • Which statin undergoes limited CYP450 biotransformation?
A
  • Pitavastatin
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12
Q
  • Which statin drug is not metabolized by CYP450s?
A
  • Pravastatin
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13
Q
  • Most statins have oral absorption anywhere from 40-75%
    • which statin is almost completely absorbed?
A

Fluvastatin

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14
Q
  • **what is the order of potency of the 7 statins we need to know?**
A
  • Atorvastatin=rosuvastatin>simvastatin>pitavastatin=lovastatin=pravastatin>fluvastatin
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15
Q
  • What are some therapeutic benefits of statin drugs?
A
  • Plaque stabilization
  • improvement of coronary endothelial fxn
  • inhibition of platelet thrombus formation
  • anti-inflammatory effects
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16
Q
  • Statins are taken at night except for which three drugs?
A
  • Longer acting drugs
    • Atorvastatin (14 hours t1/2)
    • Pitavastatin (12 hours t1/2)
    • Rosuvastatin (19 hours t1/2)
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17
Q
  • What are the adverse effect statins have on the liver?
A
  • Increased serum aminotransferase activity, which can be up to 3X normal in patient w/ liver disease or hx of EtOH abuse
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18
Q
  • What are the adverse effects statins can have on muscles?
A
  • Creatine Kinase levels may increase
  • Rhabdo, leading to myoglobinuria, may rarely lead to renal injury
  • Myopathy
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19
Q
  • Myopathy is a possible adverse effect of statin monotherapy.
    • Myopathy is more likely when statins are combined with what other drug class?
A

fibrates

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20
Q
  • Which statin is l_east likely to increase warfarin levels thus less likely to induce bleeding complications in warfarin patients?_
    • why
A
  • Pravastatin, because it is not metabolized by CYPs
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21
Q
  • Statins are not recommended for what patient populations?
A
  • Pregnant women, lactating women, or those likely to become pregnant
  • not recommended in patients w/ liver disease or skeletal muscle myopathy
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22
Q
  • When would you use a statin in a pediatric patient?
A
  • kids who have homozygous and some patients with heterozygous familial hypercholesterolemia
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23
Q
  • What is the MOA of NIAICIN (nicotinic acid, vitamin B3)?
A
  • Niacin inhibits the lipolysis of triglycerides in adipose tissue, which is the primary producer of circulating ffa’s
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24
Q
  • By reducing circulating free fatty acids, Niacin has what four subsequent effects?
A
  • liver produces less VLDL
    • LDL decreases subsequently
  • catbolic rate for HDL is decreased
  • fibrinogen levels are reduced
  • tissue plasminogen activator levels are increased (clot busting *after clot formed* by activating plasminogen, which makes plasmin, which breaks apart fibrin cross linking)
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25
Q
  • What is the most commonly experienced side effect of Niacin, and what can be done to alleviate this presentation?
A
  • an intense cutatneous flush accompanied by an uncomfortable feeling of warmth that occurs after each dose when drug is started, or when the dose is increased.
    • can take NSAID (aspirin, ibuprofen)
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26
Q
  • What side effect is likely to happen if a diabetic patient is started on Niacin?
A
  • Hyperglycermia due to niacin-inducled insulin resistance
    • _​_patients w/ insulin resistance often show signs of acanthosis nigricans due to elevated insulin levels
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27
Q
  • What is the most effective drug to increase serum HDL?
A

Niacin (sketchy)

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28
Q
  • Niacin can reduce excretion of uric acid and cause hyperuricemia
    • what drug should it be given with in patients at risk for gout?
A

allopurinol

29
Q
  • Niacin should be avoided in patients with what two diseases?
A
  • hepatic disease
  • active peptic ulcer
30
Q
  • what are the two fibric acid derivatives (fibrates)?
A
  • Gemfibrozil
  • Fenofibrate
31
Q
  • What is the half life of gemfibrozil?
  • What is the half life of fenofibrate?
A
  • gemfibrozil: 1.5 hours
  • fenobibrate: 20 hours
32
Q
  • Fibrates are well absorbed (>90%) when they are taken with?
33
Q
  • What is the MOA of fibrates?
A
  • agonists for peroxisome proliferator-activated receptor alpha (PPARa, a nuclear receptor)
34
Q
  • When PPARa is activated
    • what does it regulate?
      • what things are increased, what things are decreased?
A
  • it binds to DNA and regulates the expression of genes encoding proteins involved in lipoprotein structure and function.
    • lipoprotein lipase, apo A-1, apo A-II expression increased
    • apo C-III expression is decreased
35
Q
  • What are the major effects of fibrates?
    • six
A
  • increased oxidation of fatty acids in liver and striated muscle
  • increased lipolysis of TG via lipoprotein lipase
  • intracellular lipolysis in adipose tissue is decreased
  • VLDL levels decrease
  • LDL levels modestly decrease in most
  • HDL levels increase modestly
36
Q
  • Which lipid-lowering agent is useful for treating hypertriglyceridemia that results from treatment with viral protease inhibitors? (eg. saquinavir, indinavir, or nelfinavir)
A
  • Fibric acid derivatives
    • Gemfibrozil
    • Fenofibrate
37
Q
  • Which lipid-lowering agent is indicated for use in patients with type III familial hyperlipoproteinemia (dysbetalipoproteinemia)?
    • AKA deficiency of ApoE
A
  • Fibric acid derivatives
    • Gemfibrozil
    • Fenofibrate
38
Q
  • Which lipid-lowering agent would you use in management of a patient with hypertriclyceridemia where VLDL predominates?
A
  • Fibric acid derivatives
    • Gemfibrozil
    • Fenofibrate
39
Q
  • What medication should you be careful when prescribing it to this woman?
    • why?
A
  • Fibrates
    • They increase the risk of cholelithiasis due to an increase in the cholesterol content of bile
    • Native americans, women are already at higher risk of this, so fibrates increases this risk further
40
Q
  • What are some other contraindications for the use of fibrates?
A
  • Myopathy, especially when combined with statins
  • fibrates can potentitate anticoagulants
  • avoided in hepatic or renal dysfunction patients
    • can rase LFTs 3x normal
  • pregnancy safety has not yet been established
41
Q
  • What are they three bile acid sequestrant drugs that we need to know? (Resins)
A
  • Colestipol
  • Cholestyramine
  • Colesevelam
42
Q
  • What class of drugs is described as: large polymeric cations, insoluble in water, totally excreted in feces without alteration?
43
Q
  • What is the MOA of Resin drugs?
A
  • Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more
44
Q
  • Resins cause increased bile acid excretion, which causes the liver to enhance the conversion of cholesterol to bile acids via 7a-hydroxylation
    • ​​the decline in hepatic cholesterol stimulates which hepatic receptor?
A
  • LDL receptor, which enhances LDL clearance and lowers levels, but is partially offset by the enhanced cholesterol synthesis due to loss of bile acids bound to resins
45
Q
  • Which drug class can be prescribed as monotherapy or in combination with niacin for treatment of Type IIa and Type IIb hyperlipidemia?
A
  • Resins
    • Colestipol
    • Cholestyramine
    • Colesevelam
46
Q
  • Which drug would you use to relieve the symptoms of pruritus in patients w/ bile acid accumulation?
47
Q
  • Bile acid sequestrants (resins) can be used for primary hypercholesterolemia, and reduce levels by approximately what percentage?
A

20% reduction

48
Q
  • High doses of resin drugs can induce a deficiency of what vitamins and why?
A
  • impairs absorption of fat soluble vitamins
    • reduced ADEK
49
Q
  • What are some of the numerous drugs that interact with bile acid sequestrants?
A
  • tetracycline
  • phenobarbital
  • digoxin
  • warfarin
  • pravastatin
  • fluvastatin
  • aspirin
  • thiazide diuretics
50
Q
  • Bile acid resins should be given at least 1 hour before, or at least 2 hours after most drugs
    • what is the exception?
A
  • can be given with niacin
51
Q
  • The use of bile acid resins should be avoided in patients with what conditions?
A
  • diverticulitis, prexisting bowel diseae, cholestatis
52
Q
  • What is the first and only approved member of the cholesterol aborption inhibitor drug class?
53
Q
  • Pharmacokinetics of Ezetimibe
    • solubility in water
    • excretion
    • half life
A
  • highly water insoluble
  • majority excreted in feces
  • 22 hour half life
54
Q
  • What is the MOA of Ezetimibe
    • which transport protein is inhibited?
A
  • Selectively inhibits intestinal absorption of cholesterol and phytosterols (plant sterols)
  • inhibits NPC1L1
55
Q
  • Which drug is effective at lowering cholesterol even in the absence of dietary intake?
    • why?
A
  • Ezetimibe
  • because it inhibits reabsorption of cholesterol excreted in bile
56
Q
  • Ezetimibe is indicated for use in various causes of elevated cholesterol levels: how is it used in the following situations
    • primary hypercholesterolemia?
    • homozygous familial hypercholesterolemia?
    • mixed hyperlipidemia?
A
  • primary–> monotherapy or in combo w/ statin (does not say which)
  • homozygous–> combo with atorvastatin or simvastatin
  • mixed–> combo with fenofibrate
57
Q
  • What is the only known contraindication for administration of ezetimibe?
A
  • don’t give with bile acid sequestrant due to impaired absorption of eszetimibe
58
Q
  • Which drug class is most effective at lowering LDL?
59
Q
  • Drug class that has the highest lowering effect on TGs?
60
Q
  • drug class that has the highest increase in HDL?
61
Q
  • Drug class w/ minimal effect on TGs?
62
Q
  • What is Lomitapide used for?
A
  • treatment of homozygous familial hypercholesterolemia
63
Q
  • What is the MOA of Lomitapide?
    • what does it inhibit
      • inhibition prevents?
A
  • Inhibits microsomal triglyceride transfer protein (MTP) in the lumen of the ER
    • prevents the assembly of apo-B containing lipoproteins in enterocytes and hepatocytes
      • results in reduced production of chylomicrons and VLDL and subsequently reduces plasma LDL [cholesterol]
64
Q
  • Lomitapide is a substrate and inhibitor of which enzyme?
65
Q
  • Adverse effects of Lomitapide
  • cost?
A
  • due to CYP3A4 metabolism, interacts with lots of drugs
  • most common adverse effects are gi symtpoms
    • increased LFTs, hepatic fat accumulation
  • ​Cost is >$250,000 a year
66
Q
  • What is Mipomersen used for?
A

homozygous familial hypercholesterolemia

67
Q
  • What is the MOA of Mipomersen?
A
  • it is an antisense oligonucleotide that targets apolipoprotein B-100 mRNA and disrupts its function.
68
Q
  • Adverse effects of Mipomersen?
  • Cost?
  • when shouldit be discontinued
A
  • pain at injection site (1 inj per week)
  • flu-like symptoms
  • ^LFTs greater/= to 3x normal limit
  • $176,000 a year
  • discontinue if elevations persist or are accompained by clinical symptoms such as hepatic steatosis
69
Q

Good review slide

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