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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
Pitavastatin (Livalo) is ____.
new
26
Pravastatin (Pravachol) is _____. How is it different from the other statins?
old | It does not undergo CYP450 metabolism and it is hydrophilic (renally eliminated)
27
What statin is preferred for patients with hepatic dysfunction or are on CP450 inhibitors?
Pravastatin
28
Pravastatin should be dose adjusted for those with ______ dysfunction.
Renal
29
Rosuvastatin (Crestor) is _____.
New
30
Simvastatin (Zocor) is _____.
old
31
Newer/older agents are typically more potent.
Newer
32
What 2 things can patients do to increase HDL?
exercise and red wine
33
What is the second most effective class of drugs for lowering LDL and can be added to statins?
Bile Acid Sequestrations (BAS)
34
T or F. BAS lower LDL cholesterol and triglycerides, and increase HDL.
F - they INCREASE triglycerides.
35
What two things do not like triglycerides?
pancreas and CV system
36
How do the BAS agents work?
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
What is the AE expected with BAS agents?
GI - constipation, abdominal complaints, taste is yucky
38
Which hyperlipidemia drug comes in powder form?
BAS agents
39
A patient with already high (>400 mg/dL) triglycerides should not be prescribed ______ as monotherapy.
BAS
40
Caution should be used in patients with triglycerides >_____ when considering BAS agents
>300 mg/dL
41
What is another con for BAS other than that they increase triglycerides?
they're sticky! many drug interactions. Patients on warfarin and levothyroxine may experience subtherapeutic levels from decreased absorption.
42
What is the least sticky BAS agent?
Colesevelam (WelChos)
43
What are the two stickiest BAS agents? What is their contraindication?
Colestipol and Cholestyramine | Bowel obstruction
44
What is the oldest known lipid agent still in use?
Nicotinic acid (Niacin)
45
What is the only known agent to reduce levels of lipoprotein A?
Niacin
46
T or F. Niacin lowers LDL and triglycerides, but cannot raise HDL.
F - can also raise HDL
47
T or F. Niacin is available as an extended release (Niacor) and single dose each morning.
F - Niaspan, bedtime
48
What is the less serious AE of niacin? How can you reduce this?
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
What are the 2 serious AEs of niacin?
Hyperglycemia and hepatotoxicity are severe effects that can occur typically at doses >2 gm/day.
50
Use niacin with caution in patients with what conditions? | Do NOT use with...
Type 2 or prediabetes, peptic ulcer disease, or gout | NOT - chronic liver disease
51
What drug class can be used as monotherapy or combo therapy to decrease triglycerides?
Fibric Acid Derivatives (Fibrates)
52
What are the AEs of fibrates?
- GI complaints | - Risk of myositis and rhabdo if used with statins
53
Which fibrate has a lower incidence of drug interactions with statins?
Fenofibrate
54
G is dosed _____ and F is dosed ______.
BID | daily
55
Patients with severe renal impairment should not take ______ to lower triglycerides.
Gemfibrozil.
56
T or F. Cholesterol Absorption Inhibitors work well as monotherapy.
F- only add ons
57
Ezetimibe falls under what drug category and primarily has what affect?
``` CAI Lowers LDL (primarily) and T, increase H ```
58
Those on Ezetimibe may not be able to get thru the day with doing what? Why?
pooping themselves | these drugs block the absorption of triglycerides and they end up in your poop
59
Omega-3 Acid Ethyl Esters is another name for what?
Fish Oil (Lovaza)
60
When do you use Lovaza? Benefit?
Adjunct to reduce very high TG levels (>500 mg/dl) in adult patients). Unknown mechanism for cardiovascular benefit
61
Why is Lovaza difficult to tolerate?
Taste perversion, belching, flatulence, regurgitation, loose stools, body odor. Can try to freeze the drugs to avoid them.
62
Use Lovaza with caution in patients with...
- Fish allergy | - on anticoagulants - can prolong BT
63
Which 3 drug classes are the best for decreasing triglycerides?
- Fibrates - Niacin - Fish oil
64
Which drug class is the best at raising HDL?
Niacin | -Fibrate is second
65
Which drug class can increase LDL?
Fish oil
66
Alirocumab (Praluent) is a _______ and works by ________.
``` PCSK9 inhibitor (Ab) – preserve # of LDL receptors on the liver PCSK 9 – decreases # of receptors ```
67
Alirocumab is used as _____.
- Adjunct to diet and maximally tolerated statin therapy and still aren’t seeing drops - have familial hypercholesterolemia
68
How is Alirocumab administered? maintained?
self-administered SQ once q 2 weeks | refrigerated, then warmed to room temp
69
What is the second-in-class agent of the PCSK9 inhibitors? How is it different?
Evolocumab (Repatha) - can be given every month, but is very expensive

Pharm II test 3 (8 decks)

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