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Pharmacology I > Atherosclerosis and Lipoprotein Metabolism > Flashcards

Atherosclerosis and Lipoprotein Metabolism Flashcards

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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
what is the mechanism of action of statins
- inhibit HMG-CoA reductase - rate limiting step in endogenous cholesterol production - also induce an increase in hepatic LDL receptors
26
what are the effects of statins of lipid parameters
- total cholesterol: decrease of 13-40% - LDL: decrease of 17-55% - triglycerides: decrease 2-28% - HDL: increase 2-10%
27
what is the definition of high and moderate intensity statin therapy
- high: daily dose lowers LDL by greater than 50% - moderate: daily dose lowers LDL by 30-50%
28
what are the high intensity statins
atorvastatin and rosuvastatin
29
what is the primary prevention with statins
- 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
what is the secondary prevention for statins
- 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
what are the positive pleiotropic effects of statins
- plaque stabilization - reduced inflammation - improved endothelial function - reduced platelet aggregability - increased neovascularization of ischemic tissue
32
what are the negative/neutral pleiotropic effects of statins
- inhibition of germ cell migration during dvelopment - pregnancy contraindication - immune suppression
33
what are the adverse drug reactions for statins
- H- hepatotoxicity - M- myopathy - ranging from myositis to rhabdomyloysis - Girls and growing children
34
what are the drug-drug interactions for statins
- 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
what are the other lipid lowering medications
- fibrates - ACL- I - ezemtimibe - PCSK-9 - BABA - niacin
36
what is the mechanism of PCSK-9 inhibitors
- 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
what are the names of PCSK-9 inhibitors
- alirocumab - avolocumab
38
what are PCSK-9 inhibitors effects on lipid parameters and how are they given
- decrease LDL by 60% - most potent medication for LDL lowering - given by SQ injection - cost is $5,800/year
39
what is the use, ADRs, drug interactions and dental implications for alirocumab
- 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
what is the drug name of ATP- citrate lyase inhibtor and what does it do
- bempedoic acid - inhibit cholesterol synthesis two steps ahead of statins
41
what are bempedoic acid effects on lipids
- decrease in LDL by 15-20% - synergistic LDL lowering when combined with ezetimibe therapy
42
what is the use, ADRs, drug interactions and dental complications of bempedoic acid
- elevated uric acid, back pain, elevated liver enzymes - drug interactions: none to dentistry - dental implications: nonee
43
what are the absorption inhibitors of inhibitors of cholesterol absorption
- ezetimibe - ezetimibe/simvastatin
44
what are the bile acid binding agents in cholesterol absorption
- cholestyramine - colesevelam - colestipol
45
what is the MOA of ezemtimibe
- 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
what are ezetimibe effects on lipid parameters
decrease by LDL 18-20% - synergistic LDL lowering when combined with statin therapy
47
what are the uses, ADRs, drug interactions and dental implications of ezetimibe
- use: HLD - ADRs: rare - maybe back pain or diarrhea - drug interactions: none to dentistry - drug: none
48
what is the MOA of bile acid binding agents
- bind to bile acid in the intestine - prevent resorption of bile acid - result in increase uptake of LDL by liver
49
what are bile acid binding agents effects on lipid parameters
triglycerides increased by 2-16%
50
what is an example of, use, ADRs, drug interactions of bile acid binding agents
- 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
what is the MOA of fibrates
- 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
what are the fibrates effects on lipid parameters
decrease of 20-50% of triglycerides
53
what is the example, use, ADRs, drug-drug interactions for fibrates
- 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
what are the dental implications for fibrates
- 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
what is the MOA of nicotinic acid or its derivatives
- inhibits hepatic VLDL secretion - lowers serum triglycerides and LDL - increases serum HDL
56
what are niacin effects on lipid parameters
decrease of 20-50% of triglycerides - dose of lipid lowering effects 500-2000mg daily
57
what are the ADRs of niacin
- 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
what is the use, drug interactions and dental implications of niacin
- 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
what is the MOA of evinacumab
human monoclonal antibody that binds to and inhbits angiopoietin- like ANGPTL3. promotes VLDL processing and clearance upstream of LDL formation
60
what is the use, ADRs, drug interactions, dental implaications and cost of evinacumab
- 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
what is the MOA of inclisiran
- small interfering RNA targeting PCSK9 - inhibits PCSK9 production in liver - thereby prolonging activity of LDL receptors
62
what is the use, ADRs, drug interactions, dental implications and cost of inclisiran
- 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
what is the MOA of lomitapide
- 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
what is the use, ADRs, drug interactions, dental implications and cost of lomitapide
-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

Pharmacology I (12 decks)

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