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Dyslipidemia > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

What does fasting lipid Profile includes?

A

1) LDL
2)HDL
3)TG
4)Chol

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1
Q

how to calculate LDL levels when TG < 400mg/dL?

A

LDL = Total Chol - (TG/5+HDL)

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2
Q

What does Dyslipidemia leads to?

A

Atherosclerotic Cardiovascular disease (ASCVD)
Coronary artery disease
Cerebrovascular disease
Peripheral Vascular disease

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3
Q

What is the target of Lipid lowering therapy?

A

Lower LDL

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4
Q

How is LDL removed?

A

50% of LDL is removed from blood by liver
50% of LDL is taken by peripheral cells or deposited in arteries where atherosclerotic will form

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5
Q

What is the aim of HDL?

A

Transport Chol from periphery to liver

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6
Q

how to calculate the non HDL levels? and for what aim?

A

non HDL = total Chol - HDL

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7
Q

What are the traits of Polygenic Hypercholesterolemia?

A
  • Most prevalent
  • Mild to moderate increase in LDL
  • Caused by combination of:
    o Environmental factors
    o Genetic factors
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8
Q

What is Atherogenic hypercholesterolemia

A

moderate increase in TG & LDL
decrease in HDL
patients are overweight (increase in waist circumstances) &/or diabetic

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9
Q

What are Familial hypercholesterolemia 2 types?

A

Autosomal Dominant disorder
Defective clearance –> defective receptor gene –> hi LDL
Associated with premature CAD (before age 20)
Deposition of LDL in tendons (Xanthomas) & iris & Arteries (atheromas)

Two types:
Heterozygotes: 1/2 the LDL receptor are function (LDL 250-450 mg/dL)
Homozygotes: No functional LDL receptors (LDL >500mg/dL)

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10
Q

What is Another type of Familial hypercholesterolemia?

A

Familial defective apoprotein B 100
cant distinguish clinically from Heterozygous FH
defective apolipoprotein B —> Decrease binding to LDL receptors –> decrease clearance
Definitive diagnosis require : Molecular screening

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11
Q

what are the drug induced Dyslipidemia ?

A

7 drugs!!
Transient and mild:
Thiazide diuretics (HCTZ ) + Beta blockers (olol)
Moderate- Severe:
Oral contraceptive (estradiol …)
Glucocorticoids (sone - solone)
isotretinoin
Cyclosporine
Protease inhibitors (navir)

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12
Q

What are the desired levels for Total Chol ; LDL ; HDL;TG

A

Total Chol <200 mg/dL

LDL: primary prevention: <100mg/dL
secondary prevention: <70mg/dL

HDL: Men > 40mg/dL
Female > 50 mg/dL

TG: < 150mg/dL

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13
Q

How are patients divided? (4 categories)

A
  1. Clinically evident ASCVD (history of MI , multiple major ASCVD events; stable or unstable angina ; multiple high risk conditions)
  2. Age 20-75 & LDL levels > or = 190mg/dL
  3. Age 40-75 with DM and LDL >or= 70mg/dL
  4. Age 40-75 and LDL > or = 70mg/dL
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14
Q

what are Major ASCVD events?

A
  1. Recent acute coronary syndrome (within past 12 months)
  2. History of myocardial infarction
  3. History of ischemic stroke
  4. Symptomatic peripheral arterial disease (claudication)
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15
Q

What are high risk conditions?

A
  1. Age > or = 65 years
  2. Heterozygous familial hypercholesterolemia
  3. History of prior coronary bypass surgery or PCI outside of the major ASCVD
  4. DM
  5. Hypertension
  6. CKD (eGFR 15-59 mL/min/1.73m2)
  7. Current smoking
  8. Persistently elevated LDL – C > or = 100mg/dL
  9. History of congestive Heart Failure
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16
Q

How to manage patient with clinical ASCVD?

A

Use high intensity statin or maximally tolerated statin therapy :
1) Atorvastatin 40-80 mg
2) Rosuvastatin: 20-40 mg

====> Ezetimibe may be added in high risk ASCVD ( if LDL > or = 70mg/dL)

====>PSCK9 inhibitor might be added to ezetimibe with Statin if LDL > or = 70

17
Q

How to manage patient with the age of 20-75 & LDL>or =190mg/dL

A

Use high intensity statin or maximally tolerated statin therapy :
1) Atorvastatin 40-80 mg
2) Rosuvastatin: 20-40 mg

====> Ezetimibe may be added if LDL > or = 100mg/dL

====>PSCK9 inhibitor might be added to ezetimibe with Statin if LDL > or = 100 + high risk ASCVD

18
Q

How to manage patient with the age of DM and Age 40-75 & LDL> or = 70mg/dL

A

Use Moderate intensity statin:
1) Atorvastatin 10-20 mg
2) Rosuvastatin: 5-10 mg
3) Simvastatin 20-40mg
4)Pravastatin 40-80mg
5)lovastatin 40mg
6)Extended release Fluvastatin 80mg
7)Fluvastatin 40mg BID
8) Pitvastatin 2-4 mg

19
Q

When do we use High intensity statin for DM patient who age btw 40-75 and LDL >or = 70

A

In patients with:

A- DM risk enhancers
- Albuminuria > or = 30mcg/mg Cr
- ABI <0.9
-GFR < 60mL/min
-Long duration of DM ( > or = 10 years for TYPE II ; > or = 20 years for type I)
- neuropathy
-Retinopathy

B- Several ASCVD risk factors
- family history
- persistent LDL>or =160
-metabolic syndrome
-CKD
- Pre-eclampsia or premature menopause + age < 40
- Chronic inflammatory disorder
- High risk ethnicity (South Asians)
- persistent TG> or = 175
- APO B > or = 130 mg/dL
- CRP > or = 2 mg/L
- ABI <0.9
-lipoprotein A > or = 50 mg/dL

20
Q

How to manage patient with the age of Age 40-75 & LDL> or = 70mg/dL

A

Calculate ASCVD 10yr risk factor
> or = 20% –> high intensity
btw 7.5 and 20 & risk enhancers ASCVD –> moderate intensity
5-7.5 & risk enhancers ASCVD –> may use moderate

21
Q

what to do if decision about statin therapy is uncertain ?

A

Consider Coronary Artery Calcium (CAC):
if CAC =0 —> withhold or delay statin except in: smoker + strong family history
if CAC = 1-99 —> statin therapy especially if age > 55
if CAC > 100 or > 75th percentile —> indicated statin therapy

22
Q

what are the brand names of each Statin?

A

Atorvastatin = lipitor
Fluvastatin = lescol
Lovastatin = Mevacor
Pravastatin = Pravachol
Rosuvastatin = crestor
Simvastatin = Zocor
Pitavastatin = Livalo

23
Q

which statins are the most efficacious? ( list 3 drugs from most to least)

A

1) Rosuvastatin
2) atorvastatin
3) Simvastatin

24
Q

When it is better to administer a Statin?
Do we have statins that can be administered anytime? (what is the reason?)

A

Atorvastatin (Lipitor)
Rosuvastatin (Crestor)
Pitavastatin (Livalo)

due to their long t1/2

25
Q

What are the SE of Statin? (Mild-Transient / Serious)

A

Mild- Transient:
- headache
-myalgia
- GI
- increase glucose

Rare but serious:
- increase LFTs
- Myopathy
- Hemorrhagic stroke

26
Q

What are the contraindications of statin?

A

Pregnancy
Active liver disease

27
Q

who are the patients that are predisposed to adverse statin effects?

A

1) impaired renal or hepatic function
2) History of statin intolerance
3) Concomitant use of drugs affecting statin metabolism
4) Age > 75
5) ALT > 3 times the upper limit of normal

28
Q

Can statin lead to myalgia?

A

Yes,
if it was:
- bilateral
- involve proximal muscles
- onset of weeks/months of statin therapy
- Improves upon statin discontinuation

29
Q

what are the serious SE of statin?

A
  • increase LFTs > x3 upper limit
  • myositis ( increase CPK > 10x upper limit
  • rare: rhabdomyolysis , myoglobinuria , Acute tubular necrosis
30
Q

what inhibits statin? and what induce it?

A

inhibit: Gemfibrozil
Induce: Grapefruit

31
Q

what are the monitoring used for safety?

A

-LFTs
-CPK
-Renal Function

32
Q

which statin is less likely to cause muscle toxicity?

A
  • pravastatin
  • Fluvastatin
33
Q

which statin is used during severe renal impairment?

A
  • Atorvastatin
    -Fluvastatin
34
Q

which statin aren’t metabolized by CYP3A4 ?

A
  • Pravastatin
  • Fluvastatin
  • Rosuvastatin
35
Q

How to monitor statin therapy? and when?

A
  • Adherence
  • Response to therapy —> lipid panel
  • Adverse effects

—-> first time 1-3 m after initiation or change in therapy —–> then 3-12 month

36
Q

what are other Dyslipidemia Drugs can be used?

A

1) Ezetimibe (zetia)
decrease LDL
SE: Diarrhea + arthralgia + cough + fatigue
A choice in pregnancy

2) PCSK9 I : SC q 2-4 w
a- alirocumab
b- evolocumab
60% decrease in LDL
high cost

3) Fibrates:
a- gemfibrozil (Lopid) —–> mild GI upset ====> dont use with statin
b- Fenofibrate (triCor)
c- Clofibrate (Atromid)
d- Bezafibrate (EUROPE)
e- Ciprofibrate (EUROPE)
decrease TG and LDL + increase HDL & LFTs & incidence of Chol Gallstones

4) Bile acid resins:
a- colestipol (colestid)
b- cholestyramine (Questran)
c- colesevelam (Welchol)
Decrease LDL with addition to statin & absorption of fat soluble vitamin & folic acid + increase TG (avoid TG> 300mg/dL)
SE: GI ( less in colesevelam)
Colestipol + cholestyramine –> decrease absorption of anionic drugs (beta blockers + thiazide diuretics + warfarin + thyroxine + digoxin) –> space 1 hr before or 4 hrs after resin dose

5) Niacin : VITB3
decrease LDL & TG + increase HDL
Lack efficacy in reducing ASCVD
SE: flushing , hyperglycemia , hepatotoxicity
CI: active liver disease or peptic ulcers

6) Omega 3 (PUFA)
a- Decosahexaenoic acid (DHA)
b-Eicosapentaenoic aicd (EPA)
Lovaza & Icosapent ethyl (vascepa) –> decrease risk of CV if TG> 150 & established ASCVD / DM+ >or = 2 risk factors
Decrease TG by 50% –> high dose 2-4 g/d
SE: GI + A fib + fishy aftertaste + increase risk of bleeding

7) Bempedoic Acid:
decrease Chol in liver —> decrease LDL 23%
With ezetimibe –> decrease LDL by 48%
SE: increase risk of tendon rupture & increase uric acid

8) Mipomersen ( Kynamro) & lomitapide (Juxtapid) –> added in homozygous FH
SE: hepatotoxicity

9) Inclisiran :
decrease LDL by 50% with twice yearly dosing

10) FIber: or add psyllium (metamucil) – oat bran …. —> modest decrease in LDL

37
Q

what is Hypertriglyceridemia and its causes?

A

TG> 150mg / dL
TG> 500 –> increase risk of pancreatitis
secondary causes :
- chronic renal failure
- DM
- Alcohol
- Sedentary lifestyle
- Obesity
- Drugs (beta blocker + estrogen + steroids)

38
Q

How to manage Hypertriglyceridemia?

A

Omega 3 PUFA OR fibrates 1st line
ASCVD > or = 7.5 % –> statin

39
Q

what are the causes of low HDL?

A

<40 in men
<50 in women

Causes:
- insuin resistance
- Physical inactivity
- DM
- Cigarette smoking
- hi Carbs
- Drugs

40
Q

How to manage low HDL?

A
  • weight reduction
  • increased physical activity
    -smoking cessation
    -Drug therapy as needed

Dyslipidemia (2 decks)

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