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Pharmacology (Topics A) > 26. Agents used in dyslipidaemias. > Flashcards

26. Agents used in dyslipidaemias. Flashcards

1
Q

List the Statin drugs.

A
  1. Lovastatin
  2. Simvastatin
  3. Older ones: Fluvastatin, Pravastatin
  4. Most potent ones:
  • Atorvastatin: can reduce cholesterol by 50%, available doses 10-20-40-80 mg
  • Rosuvastatin: 5-10-20-40 mg
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2
Q

What is the MOA of Fibrates?

A

Fibrates are PPARα agonists. They stimulate LPL via PPARα. Fenofibrate is the most important drug, safer than previous versions of the drug (e.g. Gemfibrozil). Fibrates increase activity of lipoprotein lipase → increase clearance of VLDL. Fat mobilization is also inhibited, released fatty acid TAGS go to stores. Old fibrates also would lead to increased LDL, but fenofibrate doesn’t.

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3
Q

List the new drugs.

A
  1. Mipomersen
  2. PCSK9-inhibitors: Alirocumab, evolocumab
  3. Lomitapide
  4. Anacetrapib
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4
Q

When are fibrates indicated?

A
  1. Hypertriglyceridemia
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5
Q

What are the side effects of Mipomersen?

A

Most likely no dangerous side effects, unless some unknown effects of ApoB or is hepatotoxic.

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6
Q

What are the side effects and contraindications of Fibrates?

A
  1. Bile stone risk, unless patient had cholecystectomy
  2. Combining fenofibrate with statin: be careful, can have similar myopathy problem. Especially old fibrates (gemfibrozil) were CI in combination with statins, but fenofibrate isn’t.
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7
Q

When is Mipomersen indicated?

A

It is indicated in homozygous familial hypercholesterolemia.

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8
Q

What are the side effects of using intestinal cholesterol transporter inhibitors?

A

There are only a few side effects. Its well-tolerated.

  1. Maybe hepatotoxic when combined with statins.
  2. Can also cause diarrhea.
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9
Q

What are the side effects of Bile-acid binding resins?

A
  1. Steatorrhea
  2. Meteorism
  3. Fat digestion is impaired
  4. Gallstones
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10
Q

What is the MOA of Niacin?

A

Niacin is the same as Nicotinic acid which is also know as Vitamin B3. Niacin activates LPL → LDL /VLDL ↓, HDL ↑. It acts same way as fibrates, without causing myopathy and you can safely combine with statins.

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11
Q

What are the side effects of Niacin?

A
  1. Main problem is that it also causes vasodilation, “hot flush” w/ hypotension. Prevent with NSAIDs (inhibits the vasodilating prostaglandins).
  2. Teratogenic
  3. May cause hyperuricemia
  4. Increase stomach acid
  5. Liver toxicity
  6. Hyperglycemia
  7. Insulin resistance
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12
Q

What are statins?

A

Statins are HMG-CoA reductase inhibitors.

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13
Q

What are the indications of lomitapide?

A

It is indicated in familial hypercholesterolemia.

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14
Q

What is the MOA of Ezetimibe?

A

Ezetimibe is a NPC1L1 receptor inhibitor. It was originally indicated just as secondary prevention, but now is prescribed for many patients in combination with statins. Combo may add as much as 25% additional cholesterol drop.

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15
Q

What is the MOA of Bile-acid binding resins?

A

Bile-acid binding resins are used for isolated LDL elevation. However, can cause refractory ↑ LDL/TG. Cholestyramine and Colestipol are drugs that remain in GI and don’t absorb. They bind to bile acids strongly, and so liver is forced to use cholesterol to make more bile, but liver may try to just increase cholesterol synthesis to make more bile. To prevent that you need to combine with statins.

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16
Q

What is the MOA of Lomitapide?

A

Lomitapide is a MTP-inhibitor (microsomal triglyceride … protein). It decreases both VLDL and chylomicron concentration.

17
Q

What is the MOA of PCSK9-Inhibitors?

A

PCSK9 is necessary for internalization of LDL-R in liver, allows more LDL-R expression → less circulating LDL.

18
Q

What are the indications for PCSK9-inhibitors?

A

Indicated in hypercholesterolemia.

19
Q

What are the indications of Mipomersen?

A

It is indicated in homozygous familial hypercholesterolemia.

20
Q

What is the MOA of Mipomersen?

A

Mipomersen is a anti-sense oligonucleotide. Given s.c → liver cells internalize it, finds complementary mRNA for ApoB. It inhibits ApoB protein synthesis and reduces VLDL, IDL, LDL. It is not licensed in europe, but FDA approved probably.

21
Q

What is the MOA of Omega 3 fatty acids?

A

Omega 3 fatty acids effects are debated. Riba said that recent studies show no change in patients who take or don’t take these. They are special unsaturated fatty acids w/ a lot of double bonds. Easiest source is fish, maybe walnuts. There is are two options Eicosapentaenic acid or Docozahexaenic acid. There are 3 MOAs:

  1. They cause inhibition of fat synthesis.
  2. They inhibits acyl-CoA-1,2-diacylglycerol-acyltransferase
  3. Get higher FFA level, yet the other mechanisms help deal with that. (Promote β oxidation of fatty acids and activate LPL)
22
Q

What is the MOA of Anacetrapib?

A

Anacetrapib is a CETP inhibitor → higher HDL cholesterol. It is licensed in US, but not Europe (suspended).

23
Q

What are the side effects of Anacetrapib?

A

May be hepatotoxic.

24
Q

What can be the purpose of these drugs?

A

These drugs act somewhere in the back and hope to decrease risks of cardiovascular events - “prophylactic agents”. If someone has genetic cause for hyperlipidemia, then antihyperlipidemic drugs show clear benefit. Primary hyperlipidemias are successfully treated. Secondary hyperlipidemias are not as well treated, complicated.

25
Q

What are the benefits of Statins?

A
  1. Can influence post-translational protein modification farnesilation.
  2. Can stabilize plaques: less chance to be disrupted
  3. Peripheral circulation improves, peripheral arterial flow
  4. Might promote fibrinolysis.
26
Q

What are the indications for statin therapy?

A
  1. Hypercholesterolemia: best to take before beditme.
  2. Prevention of cardiovascular complication
27
Q

What are the side effects of statin therapy?

A

Generally most tolerate them quite well.

  1. Fraction of patients who experience muscle pain, patients start to feel pain that gets stronger and stronger. Check creatinine kinase level and stop statin, should not receive statin again due to a defect that makes statin harm skeletal muscle. if you don’t stop statin, then rhabdomyolysis can occur. Most infamous statin Lipovi, some died from ARF due to rhabdomyolysis. Lipovi had stronger binding to skeletal muscle + was highly dependent on CYP450 enzyme (so taking other drugs caused it to reach toxic level).
  2. General: hepatotoxic, nephrotoxic, GI upset, insomnia, teratogenic.
28
Q

How are statins metabolized?

A

All are metabolized in liver, except rosuvastatin which is not metabolized.

29
Q

What is the route of administration of statins?

A

Orally

Pharmacology (Topics A) (39 decks)

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