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Pharmacology > Atherosclerosis and Lipoprotein Metabolism > Flashcards

Atherosclerosis and Lipoprotein Metabolism Flashcards

1
Q

_______= the build up of a
waxy plaque on the inside of
blood vessels.

A

Atherosclerosis

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2
Q

________= formation of
abnormal fatty or lipid masses in
arterial walls

A

Atherogensis

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3
Q

What is the main risk factor for atherosclerosis/atherogenesis?

A

High blood cholesterol

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4
Q

What lipoprotien has the highest percentage of triglycerides?

A

Chylomicrons

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5
Q

What lipoprotein has the least number of triglycerides?

A

HDl

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6
Q

What lipoprotein is the bad cholesterol?

A

LDL

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7
Q

What lipoprotein is good cholesterol?

A

HDL

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8
Q

What is the optimal cholesterol level (mg/dL) for total cholesterol?

A

< or equal to 200 mg/dL

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9
Q

What is the optimal cholesterol level (mg/dL) for HDL?

A

> or equal to 60 mg/dL

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10
Q

What is the optimal cholesterol level (mg/dL) for LDL?

A

< or equal to 100 mg/dL

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11
Q

What is the optimal cholesterol level (mg/dL) for triglycerides?

A

< or equal to 150 mg/dL

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12
Q 
Risk Factors for \_\_\_\_\_\_
• Smoking
• Hypertension
• Hyperlipidemia
•  LDL and TC
•  HDL
• Diabetes mellitus 
• Age (men ≥45 yo, women 
≥55yo)
• Obesity 
• Physical Inactivity
A

ASCVD

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13
Q

Do men or women have a higher risk for ASCVD?

A

Men

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14
Q

What are the 7 steps of artherogenesis?

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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15
Q

he process of HDL mobilizing cholesterol and transporting back
to the liver is called ______

A

‘reverse cholesterol transport’

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16
Q 
\_\_\_\_\_\_\_ pathway of lipoprotein
• 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 
cholesteryl esters) return to the liver
• Cholesterol in liver may be 1) stored,  
2) turned into bile, or 3) enter 
endogenous pathway
A

Exogenous

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17
Q

Chylomicrons metabolized by

______ to release TG

A

lipoprotein lipase

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18
Q

_______ pathway of lipoprotein metabolism
• 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

A

Endogenous

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19
Q

_________

facilitates the transfer of cholesterol to HDL

A

Cholesteryl ester transfer protein (CETP)

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20
Q

____ provides cholesterol source for cells to

make cell membranes- also atherogenesis

A

LDL

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21
Q

VLDL metabolized by ________ to

release TG- VLDL becomes LDL

A

lipoprotein lipase

22
Q 
MOA of \_\_\_\_\_:
• Inhibit HMG-CoA reductase
• Rate-limiting step in 
endogenous cholesterol 
production
• Also induce an increase in 
hepatic LDL receptors
A

Statins

23
Q 
How do statins affect lipid parameters?
TOC
LDL
Triglycerides
HDL
A

Decrease TOC
Decrease LDL
Decrease TG
Increase HDL

24
Q

____ intensity statins
Daily dose lowers
LDL by ≥ 50%

A

High

25
Q

_____ intensity statins
Daily dose lowers
LDL by 30% -<50%

A

Moderate

26
Q 
Pleiotropic effects of \_\_\_\_\_\_:
• Positive:
• Plaque stabilization 
• Reduced inflammation
• Improved endothelial function
• Reduced platelet aggregability
• Increased neovascularization of ischemic tissue
• Negative/Neutral:
• Inhibition of germ cell migration during development             
(Pregnancy contraindication) 
• Immune suppression
A

Statins

27
Q

What are the 3 adverse reactions to statins?

HMG

A

Hepatotoxicity
Myopathy
Girls (preggo) and Growing children

28
Q

______ and ______ are not significantly cleared via CYP450 and
have the least amount of DDI of this type

A

Pravastatin and Rosuvastatin

29
Q
  • MOA: HMG-CoA reductase inhibitor
  • Use: Hyperlipidemia, Prevention of ASCVD
  • ADRs: Elevated liver enzymes(hepatotoxicity), myopathy, rhabdomyolysis
  • Pregnancy category: X (contraindicated)
  • Drug-Drug interactions:• Increased risk of myopathy with erythromycin, ketoconazole, itraconazole
  • Increased effects of midazolam when used in combination
  • Dental implications: Myopathy may present as weakness with chewing or brushing teeth
A

Atorvastatin

• Brand name: Lipitor®

30
Q 
\_\_\_\_\_\_ Mechanism of Action
• Block the action of proprotein 
subtilisin kexin type 9 (PCSK9)
• PCSK-9 promotes the 
degradation of LDL receptors
• Inhibition of PCSK-9 results in 
more active LDL receptors and 
lower serum LDL
A

PCSK-9 Inhibitors

31
Q

What are the PCSK-9 inhibitors?

A

Alirocumab

Evolocumab

32
Q

What is the most potent LDL lowering med?

A

PCSK-9 inhibitors

33
Q

• MOA: Binds to proprotein subtilisin kexin type 9 (PCSK9).
Preventing PCSK9 from binding LDL receptors, thereby
promoting LDL degretation within the liver
• Use: familial hyperlipidemia and high risk CV patients
• ADRs: Injection site reactions, diarrhea, decreasing LDL too
low
• Drug-Drug interactions: None of significance to dentistry
• Dental implications: none

A

Alirocumab

• Brand name: Praluent®

34
Q 
• Bempedoic acid (Nexletol®) only 
drug in class
• Inhibit cholesterol synthesis two
-steps ahead of statins (HMG-
CoA reductase inhibitors)
• Approved by the FDA in 
February 2020
• Not addressed in clinical 
guidelines
A

ATP-citrate lyase (ACL) inhibitor

35
Q

How does ACL inhibitors affect lipid parameters?

A

Lowers LDL

36
Q

• MOA: Inhibit cholesterol synthesis two-steps ahead of statins
(HMG-CoA reductase inhibitors)
• Use: familial hyperlipidemia and established high risk CV
patients
• ADRs: Elevated uric acid, back pain, elevated liver enzymes
• Drug-Drug interactions: None of significance to dentistry
• Dental implications: none

A

Bempedoic acid

• Brand name: Nexletol®

37
Q 
\_\_\_\_\_\_ Mechanism of Action
• Blocks cholesterol 
absorption in the intestine 
(duodenum) 
• Blocking transport protein 
NPC1L1 in the brush border 
of the enterocyte
• Does not affect absorption 
of fat-soluble vitamins, 
triglycerides, or bile acid
A

Ezetimibe

38
Q

What is Ezetimibe’s effect on lipid parameters?

A

Decrease TOC, LDL, and TG
Increases HDL

Not as effective as statins

39
Q

`
• MOA: Blocks absorption of cholesterol in the intestine by
blocking the NPC1L1 transport protein
• Use: hyperlipidemia
• ADRs: Rare- maybe back pain or diarrhea
• Drug-Drug interactions: None of significance to dentistry
• Dental implications: none

A

Ezetimibe

• Brand name: Zetia®

40
Q 
\_\_\_\_\_\_\_\_\_ Mechanism of Action
• Bind to bile acid in the 
intestine
• Prevent resorption of 
bile acid
• Result in increase 
uptake of LDL by liver
A

Bile Acid Binding Agents

41
Q

What are the effects of lipid parameters of bile acid binding agents?

A

Increased HDL and TG*

Decreased LDL

42
Q

• MOA: Binds bile acid preventing resorption
• Use: hyperlipidemia
• ADRs: Mainly GI distress- constipation, abdominal pain, nausea,
dyspepsia
• Drug-Drug interactions: None of significance to dentistry
• Many others due to inhibition of absorption of medications
• Take 1 hour before or 2 hours after other medications
• Consider semisupine chair position for patient
comfort due to GI side effects of medication

A

Colesevelam

• Brand name: Welchol®

43
Q 
\_\_\_\_\_ Mechanism of Action
• Complex mechanism of action
• Agonist of PPARα nuclear receptor
• Increase transcription of 
lipoprotein lipase
• Marked decrease in VLDL and 
triglycerides 
• Also increase LDL uptake and HDL 
synthesis
A

Fibrates

44
Q

If the generic drug name has FIB in it, what type of drug in it?

A

Fibrates

45
Q

What is the main effect on lipid parameters for fibrates?

A

Greatly lowers TG

46
Q

• MOA: PPARα nuclear receptor agonist increasing lipoprotein
lipase levels
• Use: hyperlipidemia- specifically hypertriglyceridemia
• ADRs: Myopathy, dyspepsia, blurred vision/eye floaters, elevations in
liver enzymes, GI distress(abdominal pain)
• Drug-Drug interactions: None of significance to dentistry
• Increase r/o ADRs when combined with statin
• Consider semisupine chair position for patient
comfort due to GI side effects of medication
• Avoid dental light in patient’s eyes; offer
dark glasses for patient comfort due to
vision side effects
• May cause dry mouth

A

Fenofibrate

• Brand name: Tricor® and others

47
Q 
\_\_\_\_\_\_\_ Mechanism of Action
• Inhibits hepatic VLDL 
secretion
• Lowers serum 
Triglycerides and LDL
• Increases serum HDL
A

Nicotinic acid or its derivatives

48
Q

What is the main effect on lipid parameters from Niacin (nicotinic acid or its derivatives)?

A

Decreased TG

49
Q

Adverse Drug Reactions to _____
• Flushing
• Reduced by taking aspirin 30 minutes before dose
• Gastrointestinal distress
• Nausea, vomiting, or diarrhea
• Liver damage/dysfunction ( liver enzymes)
• Can occur at any time during therapy
• Impaired glucose tolerance
• Can worsen a patient’s control of diabetes
• Precipitate gout flare
•  circulating uric acid level

A

Niacin

50
Q
  • MOA: Inhibits synthesis of VLDL
  • Use: hyperlipidemia (particularly hypertriglyceridemia)
  • ADRs: flushing, GI distress, Liver dysfunction, glucose intolerance, gout flare
  • Drug-Drug interactions: None of significance to dentistry
  • Increased risk of hepatotoxicity when combined with statin
  • Dental implications:
  • Minor- may cause dizziness so be careful when standing up
  • May increase risk of bleeding
A

Niacin

• Brand name: Niaspan®

Pharmacology (12 decks)

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