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NRS 271B > Dyslipidemias > Flashcards

Dyslipidemias Flashcards

1
Q

2 Sources of Cholesterol

A
  • from food
  • synthesized by the liver
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2
Q

How are lipids transported?

A
  • lipoproteins act as shuttles that transport the lipids to be:
    • stored
    • used for energy
    • steroid hormone production
    • bile acid formation
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3
Q

Types of Lipoproteins

A
  • Chylomicrons:
    • VERY large
    • dietary lipid
  • HDL:
    • contain lower amounts of cholesterol → can extract cholesterol from the periphery and transport back to the liver
    • cholesterol esters; ApoA1
  • LDL: “Bad cholesterol”
    • mostly cholesterol esters
    • ApoB-100
  • IDL: intermediate density lipoproteins
    • cholesterol esters + triglycerides
  • VLDL: From the liver
    • endogenous triglycerides >>> Cholesterol
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4
Q

ApoB-100

A

ligand for the LDL receptor

required for VLDL assembly → without this = VLDL cannot be assembled and cannot exit liver

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5
Q

ApoB-48

A

required for chylomicron assembly

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6
Q

ApoE

A

ligand for chylomicron and VLDL remnant receptor

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7
Q

MOA of statins

A

inhibit HMG-CoA reductase which is needed for cholesterol production → no HMG-CoA reductase = reduce cholesterol production

  • targets the endogenous pathway and the VLDL levels
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8
Q

Polygenic familial hypercholesterolemia

A

common primary dyslipidemia

d/t metabolic and environmental factors

LDL-C = 160-250mg/dL

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9
Q

Efficacy of LDL reduction of Statin Drugs in order:

A
  • Rosie Ate Some Pizza Left For Paul
    • Rosuvastatin
    • Atorvastatin
    • Simvastatin
    • Pitavastatin
    • Lovastatin
    • Fluvastatin
    • Pravastatin
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10
Q

Equivalent Dose of Statins

A

Peeta Rescued A Scared, Lonely, Proper Floozy

Dosed Qday

  • Pita 2mg
  • Rosu 5mg
  • Ator 10mg
  • Simva 20 mg
  • Lova 40mg
  • Prava 40 mg
  • Fluva 80 mg
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11
Q

Which statins are not metabolized by CYP450

A
  • pitavastatin
    • contraindicated with cyclosporine (causes rhabdomyolysis)
  • Rosuvastatin
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12
Q

Side Effects and Notes of Statins

A
  • SEs:
    • Elevated LFTS (d/c if 3x wnl)
    • myopathy
  • Notes:
    • most are 3A4 inhibitors → metabolized by cyp450 (except pitavastatin, pravastatin, & rosuvastatin)
    • avoid use with gemfibrozil (worsen liver toxicity & myopathy risk)
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13
Q

Bile Acid Sequestrants

A

COLE drops the BASe

  • cholestyramine
    • More GI side effects
  • colesevelam
    • less GI side effects
  • colestipol
  • MOA:
    • loss of bile → reduced cholesterol storage → upregulation of LDL receptor in liver
  • Notes:
    • ***increase triglycerides***
    • LDL cholesterol: -15% to -30%
    • Constipation
    • impairs absorption of fat soluble vitamins (A,D,E,K)
    • prevents absorption of digoxin, warfarin, thiazides, thyroxine
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14
Q

Ezetimibe

A
  • MOA: Niemann-Pick C1 like 1 transporter blocker → inhibit cholesterol absorption
  • well tolerated
  • SEs:
    • oily diarrhea
    • bloating and distention
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15
Q

Indications for Nicotinic Acid

A

High TG

High LDL

Low HDL

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16
Q

MOA of Nicotinic Acid (Niacin, Vitamin B3)

A

inhibit fatty acid release from adipose tissue & inhibits fatty acid and triglyceride synthesis from the liver → increases intracellular degradation of Apo-B → reduce VLDL release; reduce uptake of HDL → more HDL present in blood → increase uptake of cholesterol

17
Q

SEs & Notes of Nicotinic Acid

A

used to decrease LDL, TGs, and increase HDL

  • SEs: flushing, pruritus
    • can pre-medicate with ASA or NSAIDs 30 min prior to prevent these SEs
    • hepatotoxicity
    • increase uric acid levels
    • increase blood sugar levels (but still okay to use with DM pts)
  • Nicotinamide (no flush) aka “no flush” formulation → has no role in treating hyperlipidemia
18
Q

Fibrates

A
  • decrease TGs, increase HDLs, decrease or increase LDLs
  • MOA: unclear, inhibits TG synthesis and stimulates breakdown of TG-rich lipoproteins; activation of peroxisome proliferator-activated receptor alpha (PPAR-alpha)
    • reduce ApoB, C-3, E
    • increase ApoA1, 2
  • Fenofibrate
    • pro-drug that gets converted to fenofibric acid
    • half life = 1 day
      • 5 half lives to eliminate from body = 5 days
  • Fenofibric Acid
  • Gemfibrozil
    • DDI: with statins = rhabdomyolysis
      *
19
Q

Fibrates SEs, Contra-Indications, Max Effect

A
  • decrease TGs, increase HDLs, but can increase or decrease LDLs
  • SEs:
    • dyspepsia
    • muscle pain (myopathy, rhabdomyolysis)
      • occurs in renal dysfunction
      • combo with statins (esp gemfibrozil → AVOID)
        • prefer: fenofibrate
  • Contra:
    • gallbladder disease; liver dysfxn
    • severe kidney dysfxn
  • Max Effect:
    • fenofibrate: 2 weeks
    • gemfibrozil: 3-4 weeks
    • takes a while to start working
20
Q

Omega-3 fatty acids

A
  • Long chain fatty acid in fish oil
  • lowers TGs up to 45%
  • modulated PPAR-alpha receptors → reduced ApoB-100 production → less VLDL
  • Notes:
    • reduces platelet aggregation
    • antiarrhythmic (reduction of MI/cardiac death)
  • SEs:
    • diarrhea
    • bleeding → DDI anticoagulant and antiplatelet
      • increased risk of hemorrhagic stroke
21
Q

Icosapent (Vascepa)

A

indication: high TG > 500mg/dL

  • MOA: icosapent ethyl → eicosapentaenoic acid (EPA: active metabolite) → reduces hepatic VLDL-TG synthesis, increases TG clearance
  • SEs:
    • arthralgias
  • Metabolism: liver only (no renal excretion)
  • Precaution: allergy to fish/shellfish, prolonged bleeding time
22
Q

PCSK9 inhibitors

A

indication: use with statin for familial hypercholesterolemia or clinical ASCVD

  • Drug names:
    • Alirocumab
    • Evolocumab
  • decreases LDL-C 40-60%
  • biologix used to prevent endocytosis of LDL receptor in liver
  • SEs:
    • injx site rxn
    • nasopharyngitis
    • influenza
    • allergic rxn
  • EXPENSIVE
23
Q

ASCVD Treatment Groups

A
  • pts with clinical ASCVD (secondary prevention)
  • pts >21 yrs with LDLD >190mg/dL
  • pts with pooled cohort 10 year risk score >7.5%
  • pts 40-75 with diabetes
24
Q

ASCVD risk score and tx

A

for age 40-75 and LDL-C ≥70- <190mg/dL:

  • <5%: low risk
    • emphasize lifestyle modification
  • 5%-7.5%: borderline risk
    • if risk enhancers present → discuss moderate intensity statin
  • ≥7.5%-<20%: intermediate risk
    • risk estimate + risk enhancers → favors moderate intensity statin to reduce LDL-C by 30-49%
  • ≥ 20%: high risk
    • high-intensity statin → reduce LDL-C by 50%
25
Q

“Risk Enhancers” in the ASCVD risk score

A
  • family hx of premature ASCVD
  • persistently elevated LDL-C ≥ 160mg/dL or elevated TGs ≥ 175mg/dL
  • CKD
  • metabolic syndrome
  • pre-eclampsia, premature menopause
  • inflammatory diseases (HIV, RA, psoriasis)
  • Ethnicity (South Asian Ancestry)
    *

NRS 271B (10 decks)

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