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Cardio Module > 3. Peters - Hyperlipidemia > Flashcards

3. Peters - Hyperlipidemia Flashcards

1
Q

Signs and Symptoms of Hyperlipidemia

A
  • Typically asymptomatic until a CV events occurs
  • Pancreatitis: directly related to high TGs, >500
  • Chest pain: clot in chest, MI or angina
  • Shortness of breath: clot moves into lungs
  • Speech or movement impaired: clot in brain (stoke)
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2
Q

What is Dyslipidemia?

A
  • A combination of elevated TC, elevated TGs, elevated LDL cholesterol, and low HDL
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3
Q

What are the risk equivalents for coronary heart disease?

Hint, there’s 5

A
  1. Diabetes
  2. PAD
  3. CAD - MI or angina
  4. Abdominal aortic aneurysm (triple A syndrome)
  5. Framingham risk >20%
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4
Q

What are some major CV risk factors?

Hint, there’s 5

A
  1. Cigarette smoking
  2. Hypertension, BP >140/90
  3. Low HDL
  4. Family history of premature CHD
  5. Age, men >45 and women >55
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5
Q

What are the target numbers based on ATP III?

A

TC: 40 mg/dL
TGs:

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6
Q

Non-Pharm Therapy for Hyperlipidemia

A
  • Diet counseling
  • Weight management
  • Increased physical activity
  • Smoking cessation
  • Hypertension treatment
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7
Q

Peters - MOA of statins

A
  • HMG-CoA Reductase inhibitor
  • Decrease cholesterol synthesis, lowers intracellular cholesterol which stimulates up regulation of LDL receptors increasing the intake of LDL, and lowering circulating LDL levels
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8
Q

Pleiotropic effects of statins

A

Help decrease plaque and clot formation

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9
Q

What are the two high intensity statins and what are their available strengths?

A
  1. Atorvastatin, 40-80mg

2. Rosuvastatin, 20-40mg

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10
Q

What are the 3 main statin drug interactions to avoid?

A
  1. CCB (nondihydropyridines)
  2. Gemfibrozil
  3. Grapefruit juice
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11
Q

What are the main adverse effects of statins?

A
  • Headache and GI intolerance
  • Myalgia, which can lead to myopathy and/or rhabdomyolysis
  • New onset diabetes
  • Potential increase in LFTs
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12
Q

Managing statin therapy - how to determine if a pt is “intolerant”

A

Try 3 statins, 3 different times, at three different strengths.
If a pt does not respond, then they are considered statin intolerant

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13
Q

Peters - Fibrates and their MOA

A

Fenofibrate and Gemfibrozil

  • Agonist of proliferator-activated receptor-alpha
  • inhibit TG synthesis, increase LPL activity, increase breakdown of VLDL and increase HDL synthesis
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14
Q

What is the net effect of statins?

A

Decreased TC

Decreased LDL

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15
Q

What is the net effect of Fibrates?

A

Significantly decreased TGs –> main effect
Decreased TC
Decreased LDL
Increased HDL

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16
Q

What are the main adverse effects of Fibrates?

A
  • GI complaints
  • Changes in LFTs
  • Hypoglycemic effects in pts on sulfonureas
  • Renal dysfunction
    MAIN: Gemfibrozil inhibits break down of statins
17
Q

Examples of Bile Acid Sequestrants and their MOA

A

Cholestyramine, colestipol, colesevelam

MOA: Block the reabsorption of bile acids back into the liver, allows for easy excretion out through feces

18
Q

What is the net effect of bile acid sequestrants?

A

Decreased TC

Decreased LDL

19
Q

What are the main adverse effects of bile acid sequestrants?

A
  • GI distress
  • Potential increase in TG, should not be taken when pt >300 mg/dL
  • Impaired fat soluble vitamin absorption
  • Reduced bioavailability of other meds, separated dosing is needed
20
Q

What is Niacin’s MOA?

A

Decreased hepatic production of VLDL and LDL

21
Q

What is Niacin’s net effect?

A

BIG EFECTS:

- Decreased TGs, decreased LDL, and increased HDL

22
Q

What are Niacin’s main adverse effects?

A
  • Flushing, but tolerance will develop over time
  • P.U.D
  • Exacerbate gout
  • Exacerbate diabetes
  • Hepatotoxicity w/ ER formulation
23
Q

How should we monitor niacin?

A

Base line labs including: liver function tests, A1C and uric acid levels
- Labs should be repeated every 6 months

24
Q

What is Ezitimibe’s MOA?

A

Block cholesterol absorption by inhibiting NPC1L1 receptor at the brush boarder

25
Q

What is Ezitimibe’s net effect?

A

Decreased TC

Decreased LDL

26
Q

What is Ezitimibe’s main adverse effects?

A

Well tolerated, but can induce statin side effects when in combo.

27
Q

What are the two main sources of omega-3 fatty acids?

A

DHA and EPA

28
Q

What is omega-3 fatty acids MOA? What is different about DHA?

A

Both lower TGs, but DHA can increase LDL levels

29
Q

What are the main side effects of omega-3 fatty acids?

A

GI disturbance, increased bleeding risk, and skin changes

30
Q

What is lomitapide’s MOA?

A

Blocks to MTP receptor and inhibits the assembly of ApoB lipoproteins, leading to a decrease in LDL production

31
Q

What is Lomitapide main adverse effects?

A

Chest pain, and hepatic distress (steatosis)

32
Q

What is the MOA of Mipomersen? What what is its black box warning?

A

MOA: Oligonucleotide inhibitor of Apo-B synthesis, decreasing LDL synthesis
Black box warning: liver function, watching for elevated LFTs

33
Q

What are mipomersen’s maid adverse effects?

A

Injection site rxn (subQ injections), flu-like reactions (fatigue, headache, fever)

34
Q

What is Evolocumabs MOA?

A

PCSK-9 inhibitor, allows for more LDL receptors to be placed on the membrane of cells, increasing LDL intake and decreasing circulating LDL levels

35
Q

What are the main changes to the ACC/AHA guidelines?

Hint, there’s 6

A
  1. 4 groups named that would benefit from statin therapy
  2. New perspective on LDL and non-HLD treatment goals
  3. Global risk assessment for primary prevention
  4. Updated safety recommendations
  5. Role of biomarkers and noninvasive tests
  6. Future updates to cholesterol guidelines
36
Q

MUST KNOW THIS!

What are the 4 statin benefit groups?

A
  1. Individuals w/ clinical ASCVD >21yrs old
  2. Individuals w/ LDL >190 mg/dL and >21 yrs old
  3. Individuals 40-75 yrs old w/ diabetes and LDL between 70-189 mg/dL
  4. Individuals 40-75 yrs old w/ LDL 70-189 mg/dL and an estimated 10 year ASCVD risk >7.5% (basically everyone else who is high needs a statin)
37
Q

What is the definition of ASCVD?

PASS to a statin

A

P: peripheral artery disease
A: acute coronary syndromes (MI, angina)
S: stent; coronary revascularization
S: stroke and TIA

38
Q

In the new global risk assessment for primary prevention what are the two event predicted and the 8 risk factors assessed?

A

Events: nonfatal/fatal MI or nonfatal/fatal stroke

Risk factors: sex, age, TC, HDL, systolic BP (Tx, Y or N), smoking (Y or N), race (white/other or AA), diabetes (Y or N)

39
Q

Epidemiology of Hyperlipidemia

A
  • TCs and LDLs increase throughout life
  • Almost half of Americans > 20 yrs have a TC >200mg/dL
  • Half of those at boarder line for high risk are unaware they have hypercholesterolemia

Cardio Module (12 decks)

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