dyslipidemia Flashcards

1
Q

5 major lipoproteins

A

VLDL, IDL, LDL, HDL, chylomicrons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

HMG CoA reductase inhibitors
patients who benefit

A
  1. Adults with DM
  2. PTs with ASCVD
  3. 10 year risk of ASCVD greater than 7.5%
  4. LDL cholesterol greater than 190 mg/dL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

HMG CoA reductase MOA

A

inhibition of HMG-COA reductase decreases cholesterol synthesis,
this results in increased LDL receptors on hepatocytes for increased uptake/degradation

↓ cholesterol → liver ↑ receptors → receptors grab more LDL → cleans the blood → ↓ circulating LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When during the day should your patient take the statin? Why?

A

Statins should be taken at night.

Spike of cholesterol is made at night duh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Results of taking a statin

A

Therapeutic Effects
1. ↓ cholesterol synthesis
2. ↑ hepatic LDL receptors
3. ↓ circulating LDL cholesterol level by 50% or more at the HIGHEST doses

also slight ↑ HDL, ↓ triglyceride, ↓ high-sensitivity CRP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What percentage do statins reduce circulating LDL?

A

High-intensity = 50%
(recent cardiac event)
Moderate-intensity = 30-49%
(if they can tolerate low-intensity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Contraindications of statins

A
  1. PREGNANCY duh
  2. severe hepatic dysfunction
  3. extreme ↑ CPK within a matter of days after starting a statin = severe muscle damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which statin intensity is the longest-acting and has the longest half-life?

A

High intensity:
- atorvastatin
- rosuvastatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Statins with _____ intensity have less side effects and work all day long on the body

A

low-intensity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the most common side effect of statins? When would you expect to see the onset?

A

Statin-associated Muscle Symptoms (SAMS)

  • muscle aches with normal serum creatine kinase levels
  • onset = within 4-6 weeks of initiation OR dose increase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

In severe cases, starting someone on a statin can lead to the development of ______

A

myositis or rhabdomyolysis

  • CPK >10 times the upper limit

DO NOT use statins moving forward

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What Increases the risk of severe adverse effects of taking statins?

A

Co-administration with CYP450 inhibitors (niacin, fibrate, erythromycin, antifungals, nefazodone, cyclosporine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Your patient started a statin and is experiencing cognitive symptoms including memory loss, forgetfulness, and confusion. What is the next step for this patient?

A

Discontinue statin

Reversible - depending on how long symptoms started

Symptoms typically resolve around 3 wks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

With statins, there is a small increased risk of ….

A

DM II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

3 statins that inhibit CYP3A4

A

simvastatin, atorvastatin, lovastatin

= higher risk of rhabdo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Adverse effects of statins

A
  1. rhabdo
  2. elevated liver enzymes
  3. cognitive symptoms
  4. DM II
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

After 4-12 wks of starting a statin, what lab should you run?

A

Fasting lipid panel (FLP)
- check FLP for anticipated clinic response (e.g. high intensity > 50% LDL decrease)
- if LESS than anticipated, verify adherence, lifestyle, secondary causes
- consider lower statin dose if 2 consecutive LDL <40 mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What class does ezetimibe (Zetia) belong to?

A

absorption inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

MOA of ezetimibe (Zetia)

A

inhibits cholesterol transporters → inhibits intestinal absorption of dietary + biliary cholesterol across intestinal wall → ↓ LDL cholesterol 15-20% when used as monotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

When is ezetimibe (Zetia) preferred?

A

best as adjunct with statins IF LDL doesn’t improve by 70 mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What should you avoid ezetimibe (Zetia) with?

A
  1. moderate-severe liver dysfunction
  2. skeletal muscle effects (when taken with statin)
  3. pregnancy
  4. CHOLELITHIASIS when taken with fibrate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

MOA of PCSK9 Inhibitors

A

prevents degradation of LDL receptors so they continue to take up LDL

increase removal of LDL in circulation by liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

PCSK9 lowers cholesterol levels by ______ %. Best for what type of pts?

A

Lowers by 50-60%

Best for young pts and extremely high LDL levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How often do you inject PCSK9?

A

every 2-4 weeks

25
What drug in combo with a statin causes a 15-20% reduction in CV death, MI stroke, hospital admission for unstable angina, or coronary revasc?
Evolocumab
26
MOA for bile acid-binding resins
bind bile acid in GI → forces body to take up more cholesterol → take cholesterol from the reserves thank u for ur service
27
Dyslipidemia Rx safe for pregnancy
bile-acid binding resins
28
Adverse effects of PCSK9 inhibitors
1. flu-like symptoms 2. cognitive issues 3. local injection site rxn
29
Cut off for bile acid-binding resins is a triglyceride level of _____
>500 mg/dL
30
Drug class associated with a lot of GI side effects
Bile acid-binding resins
31
Vitamin deficiency may be a consideration with what drug class
Bile acid-binding resins
32
Fibric acid derivatives mostly do what
lower triglycerides by 40%
33
MOA of fibrates
PPAR (peroxisome proliferator-activated receptor-alpha agonists) genes or whaTeva
34
Gemfibrozil considerations
Avoid with any dose of any statin (myopathy)
35
Fenofibrate Considerations
avoid with high intensity statin
36
Fibric Acid Adverse effects
Dyspepsia, SCr increase, Cholelithiasis, Myopathy, Hepatotoxicity (increase ALT)
37
Fibric acid drug interaction potential
Resin: separate dosing Warfarin: increase INR Ezetimibe: increase cholelithiasis Colchicine: increase myopathy
38
Fibrates________ in all statin-treated patients with CVD or diabetes
have not been shown to reduce CV events
39
Niacin MOA
Reduce production of VLDL particles (LDL precursor), secondary decrease in LDL and increase in HDL cholesterol levels ↓ VLDL, ↓ LDL, ↑ HDL → ↓ cholesterol
40
Niacin adverse effects
flushing + skin shiitake ..... skin flushing dyspepsia/abdominal pain nausea, vomiting, diarrhea pruritus skin rash/hypersensitivity hyperglycemia increased uric acid dry eyes myalgia hepatotoxicity
41
Niacin considerations (how to take/ what to avoid)
avoid spicy/hot food avoid alcohol take with food aspirin 30 minutes before dose
42
Omega-3 fatty acid do what
lower triglycerides by up to 30%
43
Omega-3 fatty acid preparations
Lovaza: DHA and EPA Vascepa: EPA Epanova: DHA and EPA
44
Omega-3 fatty acid warnings
Hypersensitive to fish or shellfish Pregnancy/ lactation
45
Omega-3 fatty acid adverse effects
GI disturbances: belching, dyspepsia; taste perversion skin: pruritus, rash Arthalgia/ joint pain increased bleeding risk
46
Omega-3 fatty acid monitoring
ALT+AST LDL increase (not with EPA only ie vascepa) afib/ flutter
47
Vascepa (Icosapent ethyl) is the only preparation shown to
reduce CV death, nonfatal MI/ stroke, coronary revascularization, unstable angina 25%
48
Diet therapy goal
reduce total fat to 25-30%, saturated fat to <7% of calories, no trans fat
49
LDL-C > 190 mg/dl
high intensity statin; no risk assessment
50
DM and age 40-75
moderate statin, risk assessment for high intensity
51
age>75
clinical assessment
52
0-19y/o
lifestyle mod, familial hypercholesterolemia
53
age 20-39
lifetime risk assessment/ modification consider statin with family Hx
54
40-75y/o
LDL-C >70 and <190, PT doesn't have DM 10 year ASCVD assessment
55
low risk
<5%
56
borderline risk
5-7.5%
57
intermediate risk
>7.5 to <20%, reduce LDL-C by 30-49%
58
high risk
>20%, reduce LDL-C by >50%