18-Drugs for Lipid Disorders Flashcards

1
Q

3 main types of lipids

A
  1. Triglycerides (90% of lipids, source of energy)
  2. Phospholipids (plasma membrane)
  3. Steroids (cholesterol)
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2
Q

Why is cholesterol important?

A
  • essential part of the plasma membrane

- building block for bile acids, vitamin D, cortisol, estrogen & testosterone

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3
Q

Which organ synthesizes cholesterol?

A

the liver (makes all the cholesterol we need)

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4
Q

Lipoproteins (what is it, 3 major types)

A

Complex of TGs, cholesterol and phospholipids packaged w/ an apoprotein (protein carrier) in order to be soluble in the plasma and be distributed to body tissues. 3 major types = HDL, LDL, VLDL

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5
Q

LDL functions (3)

A
  • transports cholesterol from liver to tissues
  • creates plasma membranes & other steroids
  • can be stored for later use
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6
Q

Which lipoprotein is the primary carrier of triglycerides?

A

VLDL

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7
Q

Role of VLDL

A

reduced/converted to LDL

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8
Q

HDL

A
  • “reverse cholesterol transport” –> brings cholesterol from tissues to liver (liver recycles it)
  • the cholesterol is eliminated from the body via bile in the feces
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9
Q

Hyperlipidemia

A
  • high cholesterol/LDL –> increases risk for atherosclerosis/CAD
  • associated with genetic alterations in fat metabolism and with excessive dietary intake of fats (genetics can predispose us to having high LDL levels)
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10
Q

Dyslipidemia

A
  • abnormal blood lipid levels, such as high LDL and triglycerides and low HDL. Hyperlipidemia is a type of dyslipidemia
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11
Q

When should you screen for dyslipidemia?

A

Men + women over the age of 40

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12
Q

What is the max dietary cholesterol that should be consumed?

A

300 mg/day

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13
Q

How do plant sterols/stanols help decrease cholesterol?

A
  • Sterols and stanols complete with cholesterol for absorption (prevents it from being absorbed)
  • Eat foods high in in soluble fiber such as: nuts, olive oil, corn, rye, oats, rice and wheat
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14
Q

What is the target goal for reducing LDL levels?

A

Reducing LDL by 50% (or less than 2.0 mmol/L)

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15
Q

HMG-CoA reductase

A

Synthesizes cholesterol from HMG-CoA

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16
Q

Statins

A
  • blocks HMG-CoA reductase –> no cholesterol produced
  • less cholesterol produced –> liver increases # of LDL receptors –> more LDL removed from blood
  • effects are reversible, may take up to a month to have an effect
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17
Q

What is the first-line therapy for treating lipid disorders?

A

statins

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18
Q

T or F: Statins should not be combined with other cholesterol lowering or antihypertensive meds.

A

False, they can be combined.

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19
Q

Contraindications of statins & side effects

A
  • Contraindicated in pregnancy

- Adverse effects: headache, heart burn, GI upset (take with evening meal)

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20
Q

Rhabdomyolysis:

  1. What is it
  2. What increases the risk of developing this
A
  • breakdown of muscles
  • waste products cause acute renal failure –> severe muscle pain
  • risk is increased when taken with drugs that inhibit CYP 450 enzymes (i.e. antibiotics like clarithromycin)
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21
Q

Drug-drug interactions of statins

A
  • avoid alcohol & grapefruit juice
  • increases the effects of warfarin (increased risk of bleeding)
  • increases estrogen levels in women using COCs
  • proton-pump inhibitors and H2RA antagonists increase bioavailability of some statin drugs
22
Q

Do statins increase risk of T2DM and why?

A
  • statins can increase glucose levels in some patients –> monitor blood glucose
  • longer use of statins is associated with new onset T2DM
23
Q

Ezetimibe (what does it do & side effects)

A
  • Inhibits intestinal cholesterol absorption

- Common SE = GI distress

24
Q

What drugs can ezetimibe be combined with and what can it not be co-administered with?

A
  • co-administer with statins when patients fail to reach their LDL target with statins alone
  • do not co-administer with bile acid resins bc they reduce the efficacy of ezetimibe
25
Q

Bile acid resins / sequestrants Function

A
  • Binds to bile acids –> prevents recirculation to the liver –> instead, bile acids & cholesterol are excreted in the feces
  • prevents less absorption of bile acids

Result: less cholesterol going to the liver

26
Q

Which drug class can statins be combined with for a higher efficacy?

A

bile acid resins

27
Q

Bile acid resins (drug-drug interactions and side effects)

A

SEs: GI upset (abdominal pain, bloating, diarrhea, steatorrhea, constipation)

Interferes with the absorption of other drugs (Thiazide diuretics, warfarin, thyroid hormones, corticosteroids)
Take other medications 1 hour before, or 4 hours after!

28
Q

Vitamin deficiency may occur with what drug class?

A

Bile acid resins, decreases fat-soluble vitamins (A, D, E, K)

29
Q

PCSK9 inhibitors (action, efficacy, route of administration)

A
  • Inhibit PCSK9 proteins that target liver LDL receptors for degradation
  • Monoclonal antibodies (the inhibitors) bind to PCSK9, preventing it from binding to LDL receptors
  • lowers LDL levels by 50-70% (greater than statins)
30
Q

Why is niacin not typically used?

A

Not routinely used due to toxicity profile; only used if client is at a very high risk for CV events with significant contraindications for statins or bile-acid sequestrants.

31
Q

Framingham Risk Score

A

Estimates a client’s 10 year cardiovascular disease risk.

Takes the following into consideration:
Age of the client
HDL level
Total cholesterol level
BP
Smoking
Diabetes
32
Q

Is LDL good or bad?

A

bad

33
Q

Is HDL good or bad?

A

good

34
Q

What allows for proteins to move through the body?

A

apoprotein

35
Q

After menopause does the risk become high or lower? and Why

A

becomes higher due to less estrogen resulting in more difficulty to maintain healthy cholesterol levels

36
Q

Is hypercholesterolemia more prominent in men or women?

A

men over non menopausal women

37
Q

What is the issue when one consumes to many fats?

A
  • body cannot control or deal with such high levels
  • stored in vasculature
  • atheroscelerosis occurs as a result
38
Q

T/F: moderate alcohol consumption increases HDL levels?

A

true

39
Q

Non pharmacological management of lipid disorders include

A
  • eliminate smoking
  • moderate alcohol consumption
  • weight maintenance
  • regular exercise and stress reduction
  • reduce dietary fats (trans and saturated)
  • increase consumption of sterols and stanols and soluble fibre
40
Q

Which Cholesterol has the most to least apoprotein?

A

VLDL- lowest
HDL- most
LDL- middle

41
Q

Which ethnic groups are at a greater risk?

A
  • south asian or first nations
42
Q

Function of bile salts

A

allows for us to digest and get nutrients from fat-soluble foods

43
Q

How is cholesterol formed

A
  • acetyl CoA
  • HGM-COA
  • Cholesterol
  • Gall Bladder
  • bile salts
  • get nutrients
  • abosorption of lipids into liver
  • HGM-COA forms cholesterol
44
Q

Do statins have a high or low efficacy?

A

High

45
Q

Do statins need short or long term therapy in order to have control?

A

Long term

46
Q

When administering statins do you want a high or lose does and with combination or no combination

A
  • high does leads to more adverse effects

- therefore we want a LOW dose with combination with other hypertensive medications

47
Q

What drug is a ezetimibe?

A

selective cholesterol absorption inhibitor

48
Q

What are the functions of selective cholesterol absorption inhibitors ?

A
  • inhibit enterophepatic circulation of bile acids
  • increase the excretion of cholesterol
  • reduce blood cholesterol levels
  • reduction in cholesterol levels induces the formation of additional LDL receptors
  • reduce risk of major cardiovascular events
49
Q

Are statins and selective cholesterol absorption inhibitors equally effective

A

no

- statins > SCAI

50
Q

How are PCSK9 inhibitors given?

A

Subc every two weeks or once a month