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Cardiology > Anti-hyperlipidemics > Flashcards

Anti-hyperlipidemics Flashcards

1
Q

What type of lipid disorder is often associated with metabolic syndrome or Type II DM?

A

atherogenic dyslipidemia - inc tri’s, dec HDL-C, small LDL particles (better at invading vessel wall)

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2
Q

What enzyme do statins inhibit?

A

HMG-CoA reductase in de novo cholesterol synthesis in liver = rate-limiting step (HMG CoA –> mevalonic acid)

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3
Q

How are statins administered? Elimination site?

A
  • oral

- hepatic

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4
Q

Composition of LDL?

A

45% chol, 9% tri’s

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5
Q

Composition of VLDL?

A

22% chol, 50% tri’s

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6
Q

Composition of HDL?

A

30% chol, 8% tri’s

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7
Q

Which two statins are pro-drugs? Activation enzyme?

A
  • simvastatin, lovastatin (lipophilic in pro-drug form)
  • esterases
  • these drugs are competitive inhibitors at HMG CoA reductase site
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8
Q

What drug class is the best at dropping total cholesterol and LDL?

A

Statins; also significantly decrease VLDL-TG, but minimal effects on HDL-C

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9
Q

What are the 3 statin prototypes and which can be used for high and medium intensity statin Tx?

A
  • atorvastatin = M and H
  • pravastatin = M
  • rosuvastatin = M and H
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10
Q

Statins major site of action?

A

hepatocytes

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11
Q

What causes the biggest drop in LDL associated with statin Tx? How?

A
  • increased hepatic uptake of LDL (cell always needs cholesterol - if it can’t make it anymore, it scavenges)
  • dec chop activates SREBP which causes increased expression of LDL receptors
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12
Q

Three pleiotropic effects of statins? What may cause them?

A
  • antioxidant (slow and stabilize plaques)
  • improved endo function (vasodilation via NO)
  • anti-inflam (slow and stabilize plaques)
  • decreased isoprenoid production and therefore decreased protein anchoring on cell membranes (less communication, signaling pathways)
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13
Q

Contraindication of statin therapy?

A

Pregnancy or nursing - skeletal defects in fetal animals = CAT X

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14
Q

Three AE’s associated with statins?

A
  • skeletal muscle toxicity
  • hepatotox
  • Type II DM: tends to elevate blood Glc a bit
  • incidence of AE’s is fairly low
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15
Q

What liver enzyme do many statins inhibit?

A

CYP3A4

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16
Q

How do many statins enter hepatocytes?

A
  • OATP1B1
  • inhibition/dysfunction of transporter results in inc blood level of statin and the likelihood of myopathy
  • OAT inhibitors have major effects on statins (gemfibrozil) = increased risk of muscle tox
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17
Q

How are the pharmacokinetics of pravastatin different? How is this useful?

A
  • eliminated by multiple metabolic pathways and some renal excretion
  • affected less than other statins by pharmacokinetic drug interactions
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18
Q

Name a bile acid sequestrant. Primary function?

A
  • colesevelam
  • decrease LDL-C modestly
  • may actually increase VLDL-TG
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19
Q

How do bile acid sequestrants work?

A
  • bind bile acids and decrease their enterohepatic recirculation – fecal elimination
  • INC bile acid synthesis from cholesterol which results in INC LDLR expression to scavenge more LDL-C from blood
20
Q

What type of patient are bile acid sequestrants indicated in?

A

patients with high cholesterol who cannot tolerate statins

21
Q

How can colsevelam be used as adjunct Tx in IIDM?

A
  • reduces HbA1C levels

- improves glycemic control

22
Q

What are 3 GI adverse effects of BA sequestrants?

A
  • bloating, constipation
  • malabsorption of fat-soluble vitamins
  • decreased absorption of some neg charged or lipid soluble drugs (warfarin, oral contraceptives, digoxin)
23
Q

What drug type is ezetimibe?

A

selective cholesterol uptake inhibitor - acts in GI tract

24
Q

What is ezetimibe target and where is it found?

A
  • NPC1L1 (Niemann-pick) = transports chop into enterocytes from the lumen
25
Q

In ezetimibe treatment, what are the consequences of decreased cholesterol absorption? Primary indication of the drug?

A
  • up regulation of hepatic LDLR and hepatic LDL uptake
  • DEC LDL-C = effective (can be combined with statins for an additive effect or can stand alone in patients who can’t take statins)
26
Q

How is ezetimibe eliminated?

A
  • glucuronidated and dumped in intestines
  • undergoes enterohepatic cycling after being deconjugated by bacteria in gut = multiple plasma drug peaks and repeated exposure to its hepatic receptor
27
Q

What two drug classes are better for triglyceride Tx?

A

fibrates and nicotinic acids

28
Q

What are two fibrate drugs? Effects?

A
  • fenofibrate
  • gemfibrozil
  • sig DEC in VLDL, mild INC in HDL-C (tri’s > chol)
29
Q

What is a pharmacokinetic problem associated with fenofibrate?

A
  • poor water solubility so decreased GI absorption
  • take with meals + make particles smaller for increased bioavailability
  • different formulations cannot be substituted for one another
30
Q

What nuclear receptor regulates protein expression in liver and muscle?

A

PPAR-alpha - activated receptor translocates into the nucleus, heterodimzerizes with the retinoid X receptor before binding DNA and altering gene transcription

31
Q

Two effects of fibrates on tri’s?

A
  • dec tri syn in liver (inc ox of FA’s before inserted into tri’s)
  • inc tri removal from VLDL (increased LPL in skeletal muscle, dec syn of apoCIII in liver = VLDL apolipoprotein that inhibits VLDL binding to LPL)
32
Q

Function of endothelial LPL?

A

removal of FA’s from VLDL triglycerides

33
Q

Major effects of nicotinic acid (form of niacin vitamin) on blood lipids?

A
  • moderate dec in VLDL
  • moderate inc in HDL-C
  • small effect on LDL-C
34
Q

Three sites of nicotinic acid effects?

A

altered lipoprotein levels through effects on liver, adipocytes, muscle

35
Q

General MOA of nicotinic acid?

A
  • dec tri syn in liver

- consequent inc metabolism of VLDL tri’s

36
Q

Primary indication for nicotinic acid treatment?

A

one of the most useful drugs for Tx hypertriglyceridemia

37
Q

What drug is the best available drug to treat low HDL levels?

A

nicotinic acid, but only a modest effect

38
Q

Major AE associated with nicotinic acid?

A

hepatotoxicity

39
Q

What two disorders can be aggravated by nicotinic acid?

A
  • gout = dec uric acid secretion

- diabetes = dec insulin sensitivity

40
Q

Two common AE’s that decrease patient tolerance with nicotinic acid regimen?

A

GI irritation, cutaneous flushing

41
Q

How do fibrates decrease triglyceride synthesis in the liver?

A

increased ox of FA’s before they are inserted into triglycerides

42
Q

How do fibrates increase removal of triglycerides from VLDL in the skeletal muscle? Liver?

A
  • increased expression/activity of LPL
  • decreased synthesis of apoCIII, which is a VLDL apolipoprotein that inhibits VLDL binding to LPL –> increased VLDL binding to LDL
43
Q

Three significant AE’s associated with fibrates?

A
  • cholelithiasis
  • venous thrombosis and PE
  • myopathy, esp w/ statins
44
Q

What is a concern with co-administering gemofibrozil, a fibrate, with statins?

A

Gemfibrozil increases plasma levels of many statins

45
Q

What are three lipid imbalances associated with Type II DM?

A
  • high TG’s
  • low HDL
  • modestly elevated total chol
46
Q

In which patient subgroup may fibrates be most useful?

A

Diabetics with retinopathy because fibrates were found to decrease nephropathy, retinopathy in the 2005 FIELD study

Cardiology (6 decks)

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