Dyslipidemia Flashcards

1
Q

what is cholesterol
- where does it come from
- how is it carried through the body?
- what is its normal purpose in the body?

A

cholesterol: a type of lipid within the body which is nonpolar – meaning it cant travel well through the blood!

Cholesterol is taken in (via metabolism) into the body
- animal products (meat, butter egg yolks)

Cholesterol is also made in the body (made in cells)

cholesterol is carried inside a lipoprotein thorughout the body –> lipoprotein is the transport protein complex which contains cholesterol, triglycerides, apolipoproteins all together (these are LDL,HDL, VLDL & chylomicrons)

majority of cholesterol is contained within LDL particles

taken up by the liver and used in
- hormone synthesis (sex)
- creation of membranes (helps the lipid bylayer of cells)
- synthesizes bile acid synthesis
- helps in vit. D synthesis

  • too much cholesterol leads to the formation of atherosclerosis
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2
Q

what is a lipoprotein
how are they characterized?

A

lipoproteins: a transporter for lipids (cholesterol and triglycerides) throughout the body
- they have apolipoproteins on their surface which are able to interact with the blood & the body

the density of the lipoprotein dermines its name!!
Chylomicrons: the least dense of them all (least apolipoprotein)
VLDL: from liver –> transport triglycerides to tissues
LDL: reabsored by liver – highest cholesterol amount
HDL: removes deposits from the vessels

  • HDL and VLDL = produced in the liver
  • LDL = formed during the breakdown of VLDL
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3
Q

pathogenesis for high cholesterol
- why is it bad?

A

high cholesterol can lead to atheroslcerosis!!!! ASCVD!!
atherosclerosis leads to…

LDL deposits and begins the atheroslecrosis process

  • thrombus formation & clot formation
  • ischemia
  • aortic anyerusm
  • CHD (MI)

ultimately –> mortality!

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4
Q

where is LDL made? what about chlyomicrons?

A

chylomicrons: carry triglycerides from the DIET through the thoracic duct to circulation to release the triglycerides to the cells for use – remains are dumped into the liver

VLDL: is made in the liver to go circulate and can come back to the liver as LDL

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5
Q

common secondary conditions which affected lipid levels?

A
  1. diabetes (insulin resistant) – increased LDL levels and low HDl
  2. thyroid disease (hypo) besucase TSH plasya role in metabolism of lipids
  3. obestiy more adipose tissue
  4. cigareete smoking insulin resistnat, and increase inflammatory response
  5. alcohol use impacts liver function
  6. medications OCPs, BB, olanzapen
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6
Q

clinical signs and symptoms of dyslipidemia?

A
  • most pts. will be asymotomatic
    if symptoms…
  • eruptive xanthomas: lipid which pops through skin at places
  • if on tendons: like achilles tendon = tendinous xanthomas
  • xanthelasma: lipid pop through on the eyelids
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7
Q

screening guidelines for dyslipidemia

A

ACC/AHA: screen ALL over age 20 for high cholesterol

USPSTF:
1. at age 20 screen those with cardiovascualr RG
2. men without RF: screen at 35
3. men and women without risk factors: no guideline for 20-35 years

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8
Q

scoring tools used to help decide treatment plan for dyslipidemia

factors which are risk enhancing

A
  1. ASCVD 10-year risk calculator
  2. cornary artery calcium score
  3. identify risk enhancing factors
  • family history of disease
  • primary hypercholesterol
  • metabolic syndrome
  • CKD (not end stage)
  • chroni inflammatory conditions
  • history of pre-eclampsia
  • high triglycerides
  • high CRP
  • high lipoprotiens and apolipoprotein
  • abi > .9
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9
Q

who will benefit from treatment for hyperlipidemia

A
  1. those with an LDL > 190
  2. those with a clinical ASCVD
  3. those ages 40-75, with DM & LDL > 70
  4. those ages 40-75 with LDL > 70 AND ascvd RISK of >7.5%
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10
Q

Non-pharmacological treatment of high cholesterol

A
  1. diet (decrease total fat < 25%)
  2. exercise & weight loss
  3. smoking cessasion
  4. HTN cntrol & DM contorl
  5. antithrombotic thearpy to reduce risk of CVD
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11
Q

Pharmacologic treatment
- what is first line treatment
- second line?
- statins should not be used in what population

A

First line treatment: statin thearpy
statins should be avoided in those of childbearing age or those who are currently pregnant
- if the pt. has CVD and is over 75 – continue statin tx.

Second line treatment: Ezetimibe & PSK9 inhibitors
**pt. LDL >70 on statin – add ezetimibe
pt. LDL > 70 on statin & ezetimibe – add PSK9 inhibitor

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12
Q

difference between high intensity and moderate statins?

  • LDL lowering capibility by how much
  • side effects of statins

how much does ezetimibe lower LDL?

A

High Intensity Statin: lowers LDL by 50%
Moderate Intesnity: lowers LDL by 30-50%
** side effects: muscle aches**

Ezetimibe: lowers LDL by 15-20%
as additive therapy with statin

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13
Q

when are PSK9 inhibitors used?

when are omega 3 Fatty acids used?
- how much can they lower triglycerides

A

PSK9: used ass triple tx. with ezetimibe and statin
alirocumab & evolcumab

Omega-3 Fatty Acids: reduce triglycerides by 30%
icosapent ethyl: used when triglycerides are above 150 + have risk factors for a CVD

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14
Q

what are Fibric Acid Derivatives used for?
- names
- side effects

what is Niacin used for?
- side effects

A

Fibric Acids: gemfibrozil & fenofibrate
- used to increase HDL & decrease triglycerides
- side effects: heaptitis, mysoitis, cholelthiasis

Niacin: decreases LDL
- side effects: hot flases & puritius

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15
Q

what statins are used for high intesnity therapy?

A

atorvostain & rosuvastatin

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16
Q

Primary Prevention- what do you do for…
- 0-19 yrs.
- 20-39 yrs.
- 40-75 yrs. (LDL >70) (LDL >190?) (risk of ASCVD >7.5%)

A

for anyone with a familial history– statin will be needed
0-19 years: lifestyle management
20-39 years: lifestyle management
- if LDL > 160 & premature ASCVD can do statin
40-75 years:
- non-DM: LDL > 70 & ASCVD 7.5% = moderate statin
- non-DM LDL > 70 & ASCVD risk >20% = high statin
- non-DM LDL > 190 = high statin
- DM LDL > 70 = moderate statin

17
Q

what are some ASCVD risk enhancers which may want to make you put someone on a statin if they have these

A
  • family history of premature ASCVD
  • persistatntly high LDL > 160
  • CKD
  • metabolic syndrome
  • pre-eclampsia or premature menopause
  • inflammatory disease
  • south asian decent
  • evelated triglycerides > 175
18
Q

Secondary Prevention
- high risk ASCVD (within 12 months)
- lower risk ASCVD (not within 12 months) – age above 75 & below

A
  1. High risk ASCVD (within 12 months) = statin therapy max
    - if LDL > 70 — add ezetamibe
    - if still > 70? add PSK9
  2. low risk ASCVD (not within 12 months) for any age = high intensity or max. tolerated statin
    - add on therapy until LDL is < 70
19
Q

what is the treatment for high triglycerides? - nonpharm & pharm

A

high triglycerides = risk of panceratitis
1. diet changes first
- avoid alcohol, sugars, starches, and trans fats & redcue calories
2. manage any secondary causes
3. start medications if TG > 500 after diet changes
- statins
- omega-3s
- fibric acid derivitives
- icosapent ethyl

20
Q

what is familial hypercholesterolemia
- etiology
- patho.
- treatment

A

etiology: 2 abnormal genes: absent or defective LDL receptors

patho: lead to a gain of function in PSK9 –> results in high LDL levels early in life & increased risk of CVD

  • homozygotes 8x risk, heterozygote 3x risk

Treatment
- liver transplant/plasmaphoresis
- early treatment with statins

21
Q

Familial Chylomicronemia Syndrome
- etiology
- patho

A

etiology: abnormal lipoprotein lipase

patho: see hypertriglycerides and recurrent pancreatitis and hepatosplenomegaly