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IC 1.0 > Treating Hyperlipidemias > Flashcards

Treating Hyperlipidemias Flashcards

1
Q

What is the difference between a hyperlipidemia and a hyperlipemia?

A
  • hyperlipidemia: elevations in any lipoprotein species

- hyperlipemia: elevation in triglycerides

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2
Q

What are lipoproteins?

A

high molecular weight complexes of specific proteins and lipids (e.g. VLDL, LDL, HDL) used to transport triglycerides and cholesterol in the blood

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3
Q

Why are hyperlipidemias a clinical problem?

A

because they can lead to acute pancreatitis or atherosclerosis

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4
Q

Which kind of cholesterol is shown to be beneficial and anti-atherogenic?

A

HDL

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5
Q

Which lipoproteins tend to contain more triglyceride?

A

larger, less dense ones

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6
Q

What is the role of chylomicrons?

A

they are synthesized in the enterocytes and transport dietary lipids into the circulation

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7
Q

What is the role of VLDL?

A

synthesized in hepatocytes, these transport fatty acids and cholesterol to peripheral tissues

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8
Q

What is the role of HDL?

A

transfer of cholesterol and apoliporztoeins among different lipoprotein subclasses and the liver

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9
Q

What is the role of LDL?

A

formed from remnants of depleted VLDL by the action of hepatic lipase, they are catabolized in hepatocytes via receptor-mediated endocytosis

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10
Q

Why is LDL problematic in patients?

A

because that which isn’t taken up by hepatic LDL receptors migrates into the vascular intima, to be taken up by scavenger receptors, oxidized, and accumulates in foam cells, damaging the intima via foam cell necrosis

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11
Q

Why is HDL good?

A

it decreases the amount of cholesterol available for tissue deposition by removing it from macrophages and promoting its return to the liver

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12
Q

Primary Hypertriglyceridemia

A
  • a state of high triglycerides
  • most commonly in the setting of familial hypertriglyceridemia but occasionally familial lipoprotein lipase deficiency or apoCII deficiency
  • fibrates are the drug of choice
  • treatment includes dietary change, weight reduction, exercise
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13
Q

Familial Hypercholesterolemia

A
  • presents with high cholesterol and normal triglycerides
  • due to a defect in the LDL-receptor
  • cholesterol levels are elevated from birth and require treatment
  • typically responds well to statins and other lipid lowering drugs
  • homozygotes have worse disease than heterozygotes and may have CVD in childhood
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14
Q

Familial Defective ApoB100

A
  • a mutation in ApoB100 leads to a decreased affinity for the LDL-receptor
  • present with high cholesterol and normal triglycerides (a primary hypercholesterolemia)
  • respond well to statins and niacin
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15
Q

Familial Combined

A
  • a complex lipid profile of elevated cholesterol, LDL, and triglycerides, often with reduced HDL
  • relatively common (1% prevalence)
  • often presents with obesity, hyperinsulinemia, glucose intolerance, and mild hypertension
  • requires treatment; usually statins in combination with fibrates
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16
Q

Dysbetalipoproteinemia

A
  • a mixed hyperlipidemia resulting from an poE defect
  • see an increase in chylomicrons and IDL-like particles
  • present with elevated total cholesterol, LDL, and triglycerides, often with reduced HDL
  • treatment involves decreasing fat and cholesterol intake along with niacin and fibrates
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17
Q

Risk of heart disease correlates with what lipid profiles?

A
  • correlates with increased LDL and increased triglycerides

- inverse correlation with HDL

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18
Q

Describe the protocol for measuring serum lipids.

A

measure them after a 10-hour fast

19
Q

What informs the decision of whether to treat elevated cholesterol levels?

A

risk of CVD, not genetic profile

20
Q

List five risk factors that modify target LDL.

A
  • smoking
  • hypertension
  • low HDL
  • family history of premature CHD
  • older age
21
Q

What four groups of individuals benefit from stating therapy?

A
  • those with clinical atherosclerotic cardiovascular events
  • those with an LDL-C greater than 190
  • those between 40-75 years of age with diabetes and LDL-C between 70-189
  • those 40-75 years old without atherosclerotic events, with LDL-C between 70-189, and who have an estimated 10 year ASCVD risk of 7.5% or higher
22
Q

What is the only drug category that provides acceptable ASCVD risk reduction compared to their potential for adverse effects?

A

statins

23
Q

Statins

A
  • HMG-CoA analogs that inhibit HMG-CoA reductase
  • this reduces hepatic formation of cholesterol and increases LDL receptors in hepatocytes to lower plasma LDL
  • added benefit of decreasing plasma triglycerides and increasing HDL
  • considered first-line therapy for elevated LDL; significantly reduce mortality from MI and CVD
  • best given at night when most cholesterol synthesis occurs
  • toxicity: increased creatine kinase activity indicates skeletal muscle toxicity occurring as rhabdo, exacerbated by Gemfibrozil and amiodarone
  • measure serum aminotransferase and creatine kinase before treatment
  • pleiotropic effects include reversal of endothelial dysfunction, decreased inflammation, decreased coagulation, and improved plaque stability
  • contraindicated in pregnancy as cholesterol biosynthesis is important for fetal development
  • lovastatin/ simvastatin are given as prodrugs; others in the active from
  • most have a 40-75% absorption rate, but fluvastatin is nearly 100%
  • absorption enhanced when taken with food
  • all have a high first-pass effect and are mostly excreted in the bile
24
Q

What are the pleiotropic statin effects?

A

unrelated clinical effects demonstrated only in vitro or in animal models

  • reversal of endothelial dysfunction
  • decreased infalmmation
  • decreased coagulation
  • improved plaque stability
25
Q

What is the effect of statin toxicity?

A
  • increased creatine kinase activity indicates skeletal muscle rhabdo
  • presenting with generalized skeletal muscle pain, tenderness, or weakness
26
Q

What enhances the rhabdomyolysis associated with statins?

A

Gemfibrozil

27
Q

Simvastatin toxicity is exacerbated by what other drug?

A

amiodarone

28
Q

Niacin (vitamin B3)

A
  • a water-soluble vitamin converted to the amide and incorporated into NAD
  • decreases adipose lipase activity
  • large doses improve nearly every lipid parameter, including reducing free fatty acid flux to the liver, decreasing hepatic synthesis of triglycerides and VLDL, and lowering plasma LDL and triglycerides
  • considered the drug of choice for patients with elevated LDL and lowered HDL because it is the most effective drug for elevating HDL
29
Q

What is Niacin considered the drug of choice for?

A

raising HDL, especially in the setting of low LDL

30
Q

Give the mechanism and lipid effect for each of the following:

  • statin
  • niacin
  • fabric acid
  • bile resins
  • ezetimibe
A
  • statins inhibit HMG-CoA to reduce LDL
  • niacin decreases adipose lipase activity to raise HDL
  • fabric acid activates hepatic PPAR-a, lowering triglycerides and elevating HDL
  • bile resins prevent bile acid absorption to decrease LDL
  • ezetimibe inhibits intestinal cholesterol absorption to lower LDL
31
Q

Fibric Acid Derivatives

A
  • ligands for PPAR-a (peroxisome proliferator-activated receptor-alpha) in hepatocytes
  • includes Gemfibrozil and Fenofibrate
  • activation of PPAR-a decreases plasma triglycerides, VLDL, and LDL while elevating plasma HDL
  • used in the treatment of hypertriglyceridemia and dysbetalipoproteinemia
  • toxic effects are rare but include skin rashes, GI symptoms, myopathy, arrhythmia, decreased WBC or hematocrit, and rarely rhabdo
  • risk of myopathy increases in combination with statins
  • they potentiate the effects of the anticoagulants indanedione and coumarin
  • avoid use in those with hepatic or renal dysfunction
32
Q

Which two lipid treatments should not be combined for risk of rhabdomyolysis?

A

statins and fibric acid derivatives

33
Q

Gemfibrozil

A

a fibric acid derivative

34
Q

Fenofibrate

A

a fibrin acid derivative

35
Q

How do omega-3 fatty acids improve lipid profiles?

A

they active PPARa just like the fibric acid derivatives

36
Q

What effects do omega-3 and omega-6 have on lipid profiles?

A
  • omega 3 lowers triglycerides

- omega 6 raising triglycerides

37
Q

Omega-3 Fatty ACids

A
  • found in fish oils
  • reduce triglycerides by activating PPARa
  • available OTC but it is important that they are free of mercury and other contaminants
  • also available as a prescription (Lovaza)
38
Q

Where are omega-6 fatty acids found?

A

vegetable oil

39
Q

Ezetimibe

A
  • a hypolipidemic drug that inhibits intestinal absorption of cholesterol and phytosterols
  • reduces plasma LDL but has only a minimal effect on HDL
  • effective even when there is no dietary cholesterol because it inhibits reabsorption of cholesterol excreted in the bile
  • primarily used in the treatment of primary hypercholesterolemia
  • associated with a low incidence of reversible hepatic impairment
40
Q

Under what circumstances are hypolipidemic drug combinations useful?

A
  • VLDL levels increase during resin therapy of hypercholesterolemia
  • VLDL and LDL are both elevated
  • VLDL or LDL levels are not normalized by a single drug
  • cases in which lipoprotein a is elevated or HDL is deficient in the setting of another hyperlipidemia
41
Q

Simcor

A

extended release niacin plus simvastatin

42
Q

Vytorin

A
  • ezetimibe plus simvastatin

- not shown to have an advantage over simvastatin alone for carotid intimal-media thickness

43
Q

Bile Acid-Binding Resins

A
  • a group of drugs that bind bile acids and increase excretion
  • they are all large cationic exchange resins, insoluble in water
  • the liver responds to poor bile absorption by up-regulating 7a-hydroxylase, a hepatic enzyme that synthesizes bile acids from cholesterol
  • increased bile acid synthesis means there is reduced hepatic cholesterol, which increases LDL receptors, enhancing removal of LDL from the circulation
  • used to lower plasma LDL and elevate plasma DL in the setting of primary hypercholesterolemia
  • may increase VLDL, decrease absorption of fat-soluble vitamins, cause bloating or constimation, and impair absorption of other drugs
  • also used to treat digoxin toxicity

IC 1.0 (24 decks)

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