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Cardio > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

What is the function of cholesterol?

A

used in the synthesis of bile acid, steroid hormones, and in cell wall membrane

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2
Q

What are the sources of cholesterol?

A

diet and de Novo synthesis in the liver

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3
Q

When does synthesis occur?

A

most at night in the liver

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4
Q

What are triglycerides?

A
  • source of energy stored in adipose tissue

- made up of fatty acids and glycerol

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5
Q

What are phospholipids?

A
  • made of fatty acids
  • contain a polar head and glycerol tail
  • responsible for transport of insoluble liquids
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6
Q

What are lipoproteins?

A

vehicle for lipid transport to target tissues made up of cholesterol, triglycerides, phospholipids, and protein

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7
Q

What is the protein portion of the lipoprotein known as?

A

apolipoprotein

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8
Q

What is a chylomicron?

A

a type of lipoprotein primarily made up of TGs

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9
Q

What is the function of a chylomicron and where is made?

A
  • generated in GIT

- transports TG and cholesterol from the intestinal cells to the liver or adipose tissue

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10
Q

What is very low density lipoprotein (VLDL)?

A
  • synthesized by the liver
  • contains a core of TG (60%) and cholesterol (20%)
  • hydrolyzed by LPL to form IDL and provide surface components for HDL
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11
Q

What is intermediate density lipoprotein (IDL)?

A
  • remnants of VLDL

- cleared by the LDL receptor or remodeled into LDL by hepatic lipase

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12
Q

What is low density lipoprotein (LDL) made of?

A

cholesterol and to a less amount TG

-surface is enriched with ApoB which serves as the ligand for the LDL receptor

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13
Q

What is hepatic LDL converted to?

A

bile acids and secreted into the intestinal lumen

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14
Q

What is non-hepatic LDL used for?

A

hormone and cell membrane synthesis

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15
Q

Where is high density lipoprotein (HDL) synthesized?

A

small, immature HDL particles are synthesized in liver and intestinal cells
-acquires surface components from VLDL remnants and free cholesterol from tissue sites and other lipoproteins

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16
Q

What serves as the signal transduction protein and what is its function?

A

apolipoprotein A-1 on the surface of HDL serves as the signal transduction protein that mobilizes intracellular pools of cholesterol causing diffusion of free cholesterol. Once this cholesterol is taken up by HDL, the HDL is then fully mature and functional

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17
Q

What other function is HDL though to perform?

A
  • inhibits monocyte migration to the subintimal space
  • inhibits upregulation of ICAM-1 and VCAM-1
  • inhibits LDL oxidation
  • fibrinolytic
  • antiplatelet
  • restores endothelial function; anti-vasopastic
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18
Q

What is apoliprotein and what is its function?

A
  • aka apoproteins

- the protein portion of the lipoprotein that serves as a cofactor for enzymatic reactions and a ligand for receptors

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19
Q

What is apoA-1 and what is its function?

A
  • surface component of HDL

- stimulates mobilization of intracellular cholesterol

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20
Q

What is apoB and what is its function?

A
  • surface component of LDL (and VLDL, IDL)

- serves as the ligand for the LDL receptor

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21
Q

What is apolipoprotein a (LP(a))?

A

specialized form of LDL that contains a region that is homologous with the fibrin-binding domains of plasminogen

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22
Q

What is the function of apolipoprotein a?

A

impairs thrombolysis by interfering with fibrinolysis by competing with plasminogen binding to plasminogen receptors, fibrinogen, and fibrin

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23
Q

What is the relationship between apolipoprotein a and macrophages?

A

binds macrophages promoting foam cell formation and localization of Lp(a) at athersclerotic plaques (more easily oxidized)

24
Q

What is the primary target of the HMG CoA reductase inhibitors (aka statins)?

A

LDL

25
Q

What is the mechanism of the statins?

A
  • inhibits the HMG-CoA reducatase enzyme (rate limiting step in cholesterol synthesis)
  • decreases LDL receptor degradation in the liver
  • increases LDL receptor expression in the liver
26
Q

What are some additional beneficial effects of statins?

A
  • coronary vasodilation
  • plaque stabilization
  • ↓ C-reactive protein concentration (↓ inflammation)
  • ↓ susceptibility of lipoproteins to oxidative modification
  • ↓platelet aggregation
  • ↓fibrinogen concentratoin
27
Q

When should statins be administered?

A

at night for max efficacy (except atorvastatin and rosuvastatin because they have longer half-lives)

28
Q

Which statins are the most tolerated and why?

A

Pravastatin and Rosuvastatin are more tolerated because they are the least lipophilic of all statins

29
Q

What statin would you recommend for a patient who is worried about myalgias?

A

rosuvastatin

30
Q

What is the primary target for the cholesterol absorption inhibitor (Zetia)?

A

LDL

31
Q

What is the MOA of Zetia?

A

blocks intestinal absorption of cholesterol by inhibiting NPC1L1 transporter

32
Q

What is the primary target for Niacin?

A

LDL/TG/HDL

33
Q

What is the MOA of Niacin in adipose tissue?

A

inhibits lipolysis of TG thus reducing FFA transport to liver for use in hepatic TG synthesis (lowers TG)

34
Q

What is the MOA of Niacin in the liver?

A
  • ↓TG synthesis and esterification (↑ apoB degradation, ↓VLDL secretion by liver- lowers LDL and TG)
  • expedites removal of TG via LDL pathway (lowers TG)
  • ↓HDL catabolism (increases HDL)
35
Q

How does Niacin decrease atherogenicity?

A
  • stimulates tissue plasminogen activator (tPA) production

- converts LDL from small dense to “fluffy puffy”

36
Q

What is the extended release of Niacin?

A

Niaspan and has a decreased rate of flushing

37
Q

“No-flush” niacin contains _____ and is a ______ product

A

inositol; OTC

38
Q

What other drug should be taking with Niacin to reduce flushing?

A

ASA 325 30 min before niacin

39
Q

AIM-HIGH Trial

A

For patients at LDL goal, using niacin has no benefit

40
Q

What is the primary target of the fibric acid derivatives?

A

TG/HDL

41
Q

What is the MOA of the fibric acid derivatives?

A
  • ↑ fatty acid oxidation
  • ↑LPL synthesis (↑clearance of TG-rich lipoproteins (VLDL, chylomicrons))
  • stimualtes apoA-1 expression (↑HDL)
42
Q

What would a patient need to use fenofibrate instead of gemfibrozil when taking a statin?

A

gemfibrozil has an increased risk of myalgias with statins

43
Q

What is the primary target for bile acid sequestrants?

A

LDL

44
Q

What is resin?

A

bile acid compound too large to be reabsorbed

45
Q

What is the MOA of bile acid sequestrants?

A

Catatonic resin binds to hepatically produced bile acids in the GIT

  • causes a 10-fold increase in amount of bile acids eliminated in stool
  • results in increased LDL receptor expression in hepatocytes
46
Q

What is the primary target for the omega-3 fatty acids?

A

TG/HDL

47
Q

What is the MOA of the omega-3 fatty acids?

A

thought to decrease VLDL and apoB production

48
Q

What is the primary target for the PCSK-9 inhibitors?

A

LDL

49
Q

What is the MOA of the PCSK-9 inhibitors?

A

PCSK-9 inhibitors are monoclonal antibodies that bind PCSK-9 therefore increasing the number of LDL receptors on the lvier and decreasing serum LDL

50
Q

What are some clinical perals of PCSK-9 inhibitors?

A
  • subcutaneous injection every other week

- only indicated in combination with statin therapy

51
Q

Which medications have shown to have reductions in ASCVD?

A
  • BAS
  • Niacin
  • Fibrates
52
Q

TNT clinical trial

A

compared Atorvastatin 10 mg and 80 mg

-supports high intensity statin for patients CHD and age

53
Q

PROSPER

A

patients given pravastatin 40 mg or placebo

-pravastatin reduced the risk of CV events and LDL reduction by 34%

54
Q

CARDS

A

patients with type 2 DM given either atorvastatin 10 mg or placebo
-reductions in CV events

55
Q

JUPITER

A

Patients with no history of HTN, DM or CVD were give rosuvastatin 20 mg or placebo

  • Rosuvastatin reduced risk of primary outcome by almost half
  • results were similar among all subgroups

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