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Pharm II test 3 > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

Lipids are derived from dietary sources or synthesized in the body using ________ and _________.

A

Cholesterol

Triglycerides

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2
Q

What is cholesterol made?

A

liver

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3
Q

Lipids are transported to the sites of use or storage via __________ .

A

Lipoproteins - VLDL, IDL, LDL, HDL, chylomicrons

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4
Q

Where does LDL accumulate? what does this lead to?

A

subendothelial space of arteries

foam cells > fatty streaks/fibrous caps > thrombus

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5
Q

What is the drug class of the statins?

A

HMG-CoA Reductase Inhibitors

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6
Q

What is the most effective drug class for decreasing LDL cholesterol?

A

Statins

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7
Q

What is the mainstay of lipid-modifying therapy?

A

Statins

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8
Q

T or F. Statins decrease LDL and TG, increasing HDL.

A

T

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9
Q

What is the difference between the dose-related effects of statins on HDL and LDL.

A

Reduction in LDL are dose-dependent.

HDL effects are not dose dependent

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10
Q

What is the MOA of statins?

A

Reduce hepatic cholesterol synthesis by inhibiting HMG Reductase, an enzyme that catalyses the rate-limiting step in cholesterol synthesis

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11
Q

In addition to LDL/triglycerides, Statins also have the ability to decrease __________.

A

CRP - thereby decreasing inflammation

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12
Q

T or F. Statins are somewhat anti-inflammatory.

A

T - they inhibit CRP.

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13
Q

What is the middle man between HMG Co A and Cholesterol?

A

Mevalonate

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14
Q

Older statins are generally dosed ________. Newer statins can be dosed ________.

A

In the evening or at bedtime because most of the cholesterol is made at bedtime
Newer statins - amytime

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15
Q

Majority of statins (at least the older ones) undergo _________ metabolism via _____.

A

Hepatic metabolism via CYP450

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16
Q

T or F. In general, statins are extremely well tolerated.

A

Well

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17
Q

What are the most frequent effects of statins? other rarer effects? Serious ones?

A
  • Gi complaints- dyspepsia, heart burn, abdominal pain
  • Dose dependent AST/ALT elevations
  • Myalgia
  • Myositis and rhabdo are serious possible effects
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18
Q

How do you monitor statins?

When do you D/C a statin?

A
  • CK at baseline - D/C if CK = >10x NUL
  • LFTs 6-12 weeks after initiation - D/C if >3x NUL
  • Baseline lipid panels at 6 weeks and every 4-6 months after
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19
Q

Maximal statin effects of given dose usually achieved within____ weeks.

A

6

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20
Q

What are the contraindications for statins?

A
  • Active or chronic liver disease

- pregnancy category X

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21
Q

Newer statins are more “_______ lipid”.

A

Pan

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22
Q

Atorvastatin (Lipitor) is ___.

A

New

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23
Q

fluvastatin (Lescol, Lescol XL)

A

old

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24
Q

Lovastatin (Altoprev®, Mevacor®) ) is _____.

A

old - first statin

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25
Q

Pitavastatin (Livalo) is ____.

A

new

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26
Q

Pravastatin (Pravachol) is _____. How is it different from the other statins?

A

old

It does not undergo CYP450 metabolism and it is hydrophilic (renally eliminated)

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27
Q

What statin is preferred for patients with hepatic dysfunction or are on CP450 inhibitors?

A

Pravastatin

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28
Q

Pravastatin should be dose adjusted for those with ______ dysfunction.

A

Renal

29
Q

Rosuvastatin (Crestor) is _____.

A

New

30
Q

Simvastatin (Zocor) is _____.

A

old

31
Q

Newer/older agents are typically more potent.

A

Newer

32
Q

What 2 things can patients do to increase HDL?

A

exercise and red wine

33
Q

What is the second most effective class of drugs for lowering LDL and can be added to statins?

A

Bile Acid Sequestrations (BAS)

34
Q

T or F. BAS lower LDL cholesterol and triglycerides, and increase HDL.

A

F - they INCREASE triglycerides.

35
Q

What two things do not like triglycerides?

A

pancreas and CV system

36
Q

How do the BAS agents work?

A

Bind bile acids in intestine > interrupt enterohepatic circulation of bile acids > Increase fecal excretion of bile acids > depletes cholesterol content of liver cells > inrease LDL receptor expression (because LDL is used to make bile acid) >increase removal of LDL from the blood stream

37
Q

What is the AE expected with BAS agents?

A

GI - constipation, abdominal complaints, taste is yucky

38
Q

Which hyperlipidemia drug comes in powder form?

A

BAS agents

39
Q

A patient with already high (>400 mg/dL) triglycerides should not be prescribed ______ as monotherapy.

A

BAS

40
Q

Caution should be used in patients with triglycerides >_____ when considering BAS agents

A

> 300 mg/dL

41
Q

What is another con for BAS other than that they increase triglycerides?

A

they’re sticky!
many drug interactions.
Patients on warfarin and levothyroxine may experience subtherapeutic levels from decreased absorption.

42
Q

What is the least sticky BAS agent?

A

Colesevelam (WelChos)

43
Q

What are the two stickiest BAS agents? What is their contraindication?

A

Colestipol and Cholestyramine

Bowel obstruction

44
Q

What is the oldest known lipid agent still in use?

A

Nicotinic acid (Niacin)

45
Q

What is the only known agent to reduce levels of lipoprotein A?

A

Niacin

46
Q

T or F. Niacin lowers LDL and triglycerides, but cannot raise HDL.

A

F - can also raise HDL

47
Q

T or F. Niacin is available as an extended release (Niacor) and single dose each morning.

A

F - Niaspan, bedtime

48
Q

What is the less serious AE of niacin? How can you reduce this?

A

Flushing of the face and trunk
May be reduced by giving it during/after meals, avoiding hot showers and hot liquids at least 30 mins before each dose, take ASA 325 mg 30 min before morning dose (ASA reduces PGs)

49
Q

What are the 2 serious AEs of niacin?

A

Hyperglycemia and hepatotoxicity are severe effects that can occur typically at doses >2 gm/day.

50
Q

Use niacin with caution in patients with what conditions?

Do NOT use with…

A

Type 2 or prediabetes, peptic ulcer disease, or gout

NOT - chronic liver disease

51
Q

What drug class can be used as monotherapy or combo therapy to decrease triglycerides?

A

Fibric Acid Derivatives (Fibrates)

52
Q

What are the AEs of fibrates?

A
  • GI complaints

- Risk of myositis and rhabdo if used with statins

53
Q

Which fibrate has a lower incidence of drug interactions with statins?

A

Fenofibrate

54
Q

G is dosed _____ and F is dosed ______.

A

BID

daily

55
Q

Patients with severe renal impairment should not take ______ to lower triglycerides.

A

Gemfibrozil.

56
Q

T or F. Cholesterol Absorption Inhibitors work well as monotherapy.

A

F- only add ons

57
Q

Ezetimibe falls under what drug category and primarily has what affect?

A 
CAI
Lowers LDL (primarily) and T, increase H
58
Q

Those on Ezetimibe may not be able to get thru the day with doing what? Why?

A

pooping themselves

these drugs block the absorption of triglycerides and they end up in your poop

59
Q

Omega-3 Acid Ethyl Esters is another name for what?

A

Fish Oil (Lovaza)

60
Q

When do you use Lovaza? Benefit?

A

Adjunct to reduce very high TG levels (>500 mg/dl) in adult patients).
Unknown mechanism for cardiovascular benefit

61
Q

Why is Lovaza difficult to tolerate?

A

Taste perversion, belching, flatulence, regurgitation, loose stools, body odor.
Can try to freeze the drugs to avoid them.

62
Q

Use Lovaza with caution in patients with…

A
  • Fish allergy

- on anticoagulants - can prolong BT

63
Q

Which 3 drug classes are the best for decreasing triglycerides?

A
  • Fibrates
  • Niacin
  • Fish oil
64
Q

Which drug class is the best at raising HDL?

A

Niacin

-Fibrate is second

65
Q

Which drug class can increase LDL?

A

Fish oil

66
Q

Alirocumab (Praluent) is a _______ and works by ________.

A 
PCSK9 inhibitor (Ab) – preserve # of LDL receptors on the liver
PCSK 9 – decreases # of receptors
67
Q

Alirocumab is used as _____.

A
  • Adjunct to diet and maximally tolerated statin therapy and still aren’t seeing drops
  • have familial hypercholesterolemia
68
Q

How is Alirocumab administered? maintained?

A

self-administered SQ once q 2 weeks

refrigerated, then warmed to room temp

69
Q

What is the second-in-class agent of the PCSK9 inhibitors? How is it different?

A

Evolocumab (Repatha) - can be given every month, but is very expensive

Pharm II test 3 (8 decks)

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