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Pharmacology I > Atherosclerosis and Lipoprotein Metabolism > Flashcards

Atherosclerosis and Lipoprotein Metabolism Flashcards

1
Q

what is atherosclerosis

A

the build up of a waxy plaque on the inside of blood vessels

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2
Q

in greek, athere means:

A

gruel

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3
Q

in greek skleros means:

A

hard

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4
Q

what is atherogenesis

A

formation of abnormal fatty or lipid masses in arterial walls

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5
Q

main risk factor for atherosclerosis and atherogenesis is:

A

high blood cholesterol

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6
Q

what is the primary treatment to reduce cholesterol

A

statins

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7
Q

very high risk patients may need _____ to reach LDL less than 70mg/dL

A

combination therapy

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8
Q

what are the lipoproteins

A
  • chylomicrons
  • VLDL
  • LDL
  • HDL
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9
Q

which lipoprotein has the highest proportion of triglycerides

A

chylomicrons

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10
Q

what is the optimal total cholesterol level

A

less than 200 mg/dL

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11
Q

what is the optimal level for HDL

A

greater than 60 mg/dL

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12
Q

what is the optimal level for LDL

A

less than 100mg/dL

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13
Q

what is the optimal triglyceride level

A

less than 150 mg/dL

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14
Q

what is the Friedewald Formula

A

total cholesterol = LDL + HDL + TG/5

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15
Q

what are the risk factors for ASCVD

A
  • smoking
  • hypertension
  • hyperlipidemia (high LDL and TC, low HDL)
  • DM
  • Age (men greater than 45 yo, women greater than 55yo)
  • obesity
  • physical inactivity
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16
Q

what are the clinical manifestations of ASCVD

A
  • established coronary artery disease (CAD)
  • history of stroke or TIA
  • peripheral artery disease (PAD)
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17
Q

when do you need to calculate ASCVD

A

if the patient has clinical ASCVD

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18
Q

what are the steps of atherogenesis

A
  • endothelial dysfunction
  • endothelial injury
  • LDL deposits into vessel wall
  • formation of foam cells- macrophages filled with LDL
  • fatty streak
  • inflammation - smooth muscle growth
  • fibrous cap over lipid core
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19
Q

what removes cholesterol from vessel walls

A

HDL

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20
Q

what is reverse cholesterol transport

A

the process of HDL mobilizing cholesterol and transporting back to the liver

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21
Q

what are the patient symptoms for atherosclerosis

A

angina -> acute coronary syndrome -> unstable angina, NSTEMI, STEMI

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22
Q

what is the exogenous pathway of lipoprotein metabolism

A
  • cholesterol and TG absorbed from diet transported as chylomicrons to muscle and adipose tissue
  • chylomicrons metabolized by lipoprotein lipase to release TG
  • chylomicron remnants (mostly cholesterol esters) return to the liver
  • cholesterol in liver may be stored, turned into bile, enter endogenous pathway
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23
Q

what is the endogenous pathway in lipoprotein metabolism

A
  • cholesterol and TG made in liver leave as VLDL
  • VLDL metabolized by lipoprotein lipase to release TG-VLDL becomes LDL
  • LDL provides cholesterol source for cells to make cell membranes- also atherogenesis
  • cell use an LDL receptor to take up LDL
  • liver releases HDL to collect cholesterol and return to liver (reverse cholesterol transport)
  • cholesteryl ester transfer protein (CETP) facilitates the transfer of cholesterol to HDL
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24
Q

what are the lipid lowering medications

A

HMG-CoA reductase inhibitors (statins)

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25
Q

what is the mechanism of action of statins

A
  • inhibit HMG-CoA reductase
  • rate limiting step in endogenous cholesterol production
  • also induce an increase in hepatic LDL receptors
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26
Q

what are the effects of statins of lipid parameters

A
  • total cholesterol: decrease of 13-40%
  • LDL: decrease of 17-55%
  • triglycerides: decrease 2-28%
  • HDL: increase 2-10%
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27
Q

what is the definition of high and moderate intensity statin therapy

A
  • high: daily dose lowers LDL by greater than 50%
  • moderate: daily dose lowers LDL by 30-50%
28
Q

what are the high intensity statins

A

atorvastatin and rosuvastatin

29
Q

what is the primary prevention with statins

A
  • target age 40-75 YO with LDL 70-189 mg/dL
  • use ASCVD risk score to guide therapy
  • coronary calcium score helpful
  • diabetes- all patients get at least moderate intensity statin
30
Q

what is the secondary prevention for statins

A
  • all patients under 75 YO with established ASCVD
  • high intensity statin
  • very high risk consider combo therapy if LDL greater than 70 mg/dL
31
Q

what are the positive pleiotropic effects of statins

A
  • plaque stabilization
  • reduced inflammation
  • improved endothelial function
  • reduced platelet aggregability
  • increased neovascularization of ischemic tissue
32
Q

what are the negative/neutral pleiotropic effects of statins

A
  • inhibition of germ cell migration during dvelopment - pregnancy contraindication
  • immune suppression
33
Q

what are the adverse drug reactions for statins

A
  • H- hepatotoxicity
  • M- myopathy - ranging from myositis to rhabdomyloysis
  • Girls and growing children
34
Q

what are the drug-drug interactions for statins

A
  • many DDI due to hepatic metabolism
  • impaired statin metabolism -> increased risk of hepatotoxicity or myopathy
  • impaired clearance of competing drug -> increased drug of competing drug ADRs
  • pravastatin and rosuvastatin are not cleared via CYP450
  • impaired stain absorption -> decreased statin efficacy
  • increased risk of myopathy
35
Q

what are the other lipid lowering medications

A
  • fibrates
  • ACL- I
  • ezemtimibe
  • PCSK-9
  • BABA
  • niacin
36
Q

what is the mechanism of PCSK-9 inhibitors

A
  • block the action of proprotein subtilisin kexin type 9
  • PCSK-9 promotes the degradation of LDL receptors
  • inhiibition of PCSK-9 results in more active LDL receptors and lower serum LDL
37
Q

what are the names of PCSK-9 inhibitors

A
  • alirocumab
  • avolocumab
38
Q

what are PCSK-9 inhibitors effects on lipid parameters and how are they given

A
  • decrease LDL by 60%
  • most potent medication for LDL lowering
  • given by SQ injection
  • cost is $5,800/year
39
Q

what is the use, ADRs, drug interactions and dental implications for alirocumab

A
  • use: familial hyperlipidemia and high risk CV patients
  • ADRs: injection site reactions, diarrhea, decreasing LDL too low
  • drug-drug interactions: none to dentistry
  • dental implications: none
40
Q

what is the drug name of ATP- citrate lyase inhibtor and what does it do

A
  • bempedoic acid
  • inhibit cholesterol synthesis two steps ahead of statins
41
Q

what are bempedoic acid effects on lipids

A
  • decrease in LDL by 15-20%
  • synergistic LDL lowering when combined with ezetimibe therapy
42
Q

what is the use, ADRs, drug interactions and dental complications of bempedoic acid

A
  • elevated uric acid, back pain, elevated liver enzymes
  • drug interactions: none to dentistry
  • dental implications: nonee
43
Q

what are the absorption inhibitors of inhibitors of cholesterol absorption

A
  • ezetimibe
  • ezetimibe/simvastatin
44
Q

what are the bile acid binding agents in cholesterol absorption

A
  • cholestyramine
  • colesevelam
  • colestipol
45
Q

what is the MOA of ezemtimibe

A
  • blocks cholesterol absorption in the intestine
  • blocking transport protein NPC1L1 in the brush border of the enterocyte
  • does not affect absorption of fat soluble vitamins, triglycerides or bile acid
46
Q

what are ezetimibe effects on lipid parameters

A

decrease by LDL 18-20%
- synergistic LDL lowering when combined with statin therapy

47
Q

what are the uses, ADRs, drug interactions and dental implications of ezetimibe

A
  • use: HLD
  • ADRs: rare - maybe back pain or diarrhea
  • drug interactions: none to dentistry
  • drug: none
48
Q

what is the MOA of bile acid binding agents

A
  • bind to bile acid in the intestine
  • prevent resorption of bile acid
  • result in increase uptake of LDL by liver
49
Q

what are bile acid binding agents effects on lipid parameters

A

triglycerides increased by 2-16%

50
Q

what is an example of, use, ADRs, drug interactions of bile acid binding agents

A
  • example: colesevelam
  • use: HLD
  • ADRs: mainly Gi distress, constipation, abdominal pain, nausea, dyspepsia
  • drug interactions: none
  • dental: consider semisupine chair position for patient comfort due to GI side effects of medication
51
Q

what is the MOA of fibrates

A
  • complex mechanism of action
  • agonist of PPARalpha nuclear receptor
  • increase transcription of lipoprotein lipase: marked decrease in VLDL and triglycerides
  • also increase LDL uptake and HDL synthesis
52
Q

what are the fibrates effects on lipid parameters

A

decrease of 20-50% of triglycerides

53
Q

what is the example, use, ADRs, drug-drug interactions for fibrates

A
  • fenofibrate
  • use: HLD- specifically hypertriglyceridemia
  • ADRs: myopathy, dyspepsia, blurred vision/eye floaters, elevations in liver enzymes, GI distress
  • drug interactions: none relevant to dentistryw
54
Q

what are the dental implications for fibrates

A
  • consider semisupine chair position for patient comfort due to GI side effects of medication
  • avoid dental light in patients eyes, offer dark glasses for patient comfort due to vision SE
  • dry mouth
55
Q

what is the MOA of nicotinic acid or its derivatives

A
  • inhibits hepatic VLDL secretion
  • lowers serum triglycerides and LDL
  • increases serum HDL
56
Q

what are niacin effects on lipid parameters

A

decrease of 20-50% of triglycerides
- dose of lipid lowering effects 500-2000mg daily

57
Q

what are the ADRs of niacin

A
  • flushing: reduced by taking aspirin 30 mins before dose
  • GI distress: nausea, vomiting, diarrrhea
  • liver damage/dysfunction ( increase liver enzymes)
  • imparied glucose tolerance
  • precipitate gout flare: increased ciruclating uric acid level
58
Q

what is the use, drug interactions and dental implications of niacin

A
  • use: HLD- mainly hypertriglyceridemia
  • drug interactions: none to dentistry, increased risk when combined with statin
  • dental implications: minor- may cause dizziness- careful when standing up. may increase risk of bleeding
59
Q

what is the MOA of evinacumab

A

human monoclonal antibody that binds to and inhbits angiopoietin- like ANGPTL3. promotes VLDL processing and clearance upstream of LDL formation

60
Q

what is the use, ADRs, drug interactions, dental implaications and cost of evinacumab

A
  • use: HoFH
  • ADRs: nasopharyngitis (16%), influenza like illness (7%), dizziness (6%), rhinorrhea (5%), nausea (5%)
  • drug interactions: none relevant to dentistry
  • dental implaications: nasal adverse rxns
  • cost: $15,000/month
61
Q

what is the MOA of inclisiran

A
  • small interfering RNA targeting PCSK9
  • inhibits PCSK9 production in liver
  • thereby prolonging activity of LDL receptors
62
Q

what is the use, ADRs, drug interactions, dental implications and cost of inclisiran

A
  • use: HeFH
  • ADRs: injection site reaction (8%), arthralgia (5%), bronchitis (4%)
  • drug interactions: none signficiant to dentistry
  • dental implications: none
  • cost: $3,500/3-6 months
63
Q

what is the MOA of lomitapide

A
  • directly binds and inhibits MTP which resides in the lumen of the endoplasmic reticulum, thereby preventing the assembly of apoB- containing lipoproteins (chylomicrons and VLDL) leading to reduction in LDL
64
Q

what is the use, ADRs, drug interactions, dental implications and cost of lomitapide

A

-use: HoFH
- ADRs: chest pain (24%), diarrhea (79%), abdominal pain (34%), nasopharyngitis (17%), pharyngolaryngeal pain (14%)
- drug interactions: none of significance to dentistry
- dental implications: nasal/laryngeal adverse reactions/pain

65
Q
A

Pharmacology I (12 decks)

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