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Pharmacology > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q 
In addition to lowering LDL-C levels, statins also: 
A.  Improve endothelial function 
B.  Decrease platelet aggregation 
C.  Reduce inflammation 
D.  Reduce HDL levels 
E.  All of the above
A

A.  Improve endothelial function
B.  Decrease platelet aggregation
C.  Reduce inflammation

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2
Q

A 59-year-old man in good health with no evidence of cardiovascular disease, a BMI of 29, an HbA1c of 5.9, and an LDL-C of 167 mg/dL asks whether he should be taking a statin. You could tell him that:
A.  Statins are only approved for use in patients with documented cardiovascular disease (CVD)
B.  Statins have no demonstrated benefit in patients without CVD
C.  Statins can reduce the incidence of cardiovascular events in patients without CVD
D.  Statins may increase the risk of developing diabetes

A

C. Statins can reduce the incidence of cardiovascular events in patients without CVD
D.  Statins may increase the risk of developing diabetes, but—–that risk is outweighed by the benefits a statin may have for him

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3
Q 
According to one meta-analysis, each additional 1mmol/L reduction in LDL-C is associated with a reduction in the incidence of major vascular events of: 
A.  5%
B.  10% 
C.  20% 
D.  30%
A

C. 20%

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4
Q 
Statins have been reported to: 
A.  Increase the risk of hemorrhagic stroke 
B.  Reduce the risk of overall stroke 
C.  Reduce all-cause mortality 
D.  All of the above
A

D.  All of the above

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5
Q 
Which of the following statins is not metabolized to a clinically significant extent by CYP enzymes? 
A.  Lovastatin
B.  Pravastatin 
C.  Simvastatin 
D.  Rosuvastatin 
E.  Fluvastatin
A

B.  Pravastatin

D.  Rosuvastatin

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6
Q

Which of the following drugs has been shown to improve clinical outcomes when added to a statin?
A.  Ezetimibe (cholesterol absorption inhibitor)
B.  Alirocumab (PCSK9 inhibitor)
C.  Gemfibrozil (fibrate)
D.  Niacin

A

A.  Ezetimibe (cholesterol absorption inhibitor)

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7
Q

A74-year-old man with a long history of coronary artery
disease has been taking atorvastatin 40 mg/day for many years. Now his LDL-C is 68, but he has seen advertisements for PCSK9 inhibitors and would like to take one in addition to atorvastatin. You could tell him that:
A.  They are expensive
B.  They are only approved for patients who require
additional lowering of LDL-C
C.  They have not been shown to improve clinical outcomes
D.  They must be administered by the subcutaneous route
E.  All of the above

A

E.  All of the above

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8
Q

Consumption of alcohol is associated with which lipid

changes?

A
  1. increased HDL

2. increased triglycerides

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9
Q

__, __, and ___ are NOT water soluble

A

cholesterol
cholesterol esters
triglycerides

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10
Q

What are secondary causes of dyslipidemia

A
  1. DM
  2. excessive alcohol intake
  3. glucocorticoid excess
  4. estrogen/OCP
  5. hypothyroidism
  6. obstructive liver disease
  7. BB/Thiazide diuretics

5-7: CHOL>TG

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11
Q

What dysplipidemia classification?

  • Increased cholesterol production [familial combined]
  • Decreased LDL catabolism [familial]
  • Increases in dietary saturated fat and cholesterol can also result in increased LDL
A

hypercholesterolemia (over 85% is polygenic)

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12
Q

What dysplipidemia classification?

  • Increased VLDL production [familial]
  • Decreased triglyceride metabolism via lipoprotein lipase
A

hypertriglyceridemia

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13
Q

hypertriglyceridemia is defined as triglyceride levels of ___

A

200-500mg/dL

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14
Q

hypertriglyceridemia develops with:

A
  1. age
  2. weight gain
  3. obesity
  4. diabetes
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15
Q

HDL deficiency is defined by what levels?

A

Males: less than 40mg/dl
Females: less than 50mg/dl

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16
Q

What are causes of HDL deficiency?

A
  1. drugs: BB, diuretics, progestin, androgens, HIV protease inhibitors
  2. hypertriglyceridemic disorders
  3. sedentary lifestyle
  4. smoking
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17
Q

fatty streak is linked with ___

plaque disruption is linked with ____

A

inflammation

thrombus formation

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18
Q

antioxidants and statins proposed to prevent atherosclerosis by blocking what step?

A
  1. Oxidation of LDL apoB by arterial cells (mediated by oxidants such as O2, O2-NO
    * statins may also act to affect plaque stability
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19
Q

describe the steps of the development of atherosclerotic plaque?

A
  1. Movement of excess LDL into subintimal space of arterial wall
  2. Oxidation of LDL apoB by arterial cells (mediated by oxidants such as O2-, O2– NO)
  3. Uptake of oxidized-LDL by macrophages → Formation of foam cells in arterial walls
  4. Foam cells accumulate → Cytokines from arterial walls → Attract monocytes and T cells
  5. Contribute to progressive early lesion → Growth factor release → Arterial smooth muscle proliferation → Lipid accumulation → Fibrosis → Atherosclerotic plaque
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20
Q

Hypercholesterolemia (increased LDL) is treated with what drugs?

A
  1. statins
  2. niacin
  3. bile acid sequestrands
  4. ezetimibe
  5. sterol.stnaol esters (in diet)
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21
Q

Hypertriglyceridemia is treated with what drugs?

A
  1. Fibric acid derivative
  2. niacin
  3. fish oil
  4. HMG CoA reductase inhbitors (Higher doses)
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22
Q

Low HDL is treated with what drugs?

A
  1. niacin
  2. fibrates
  3. HMG CoA reductase inhibitors
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23
Q

Describe the 1st step in managing cholesterol to reduce atherosclerotic CVD

A
  1. determine lipoprotien levels

LDL-C = Total Cholesterol − HDL-C − VLDL

*VLDL = Triglycerides ÷ 5 Iif TG less than 400)

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24
Q

___ is primary lipoprotein of “interest”

A

LDL-C

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25
Q

Describe the 2nd step in managing cholesterol to reduce atherosclerotic CVD

A

Determine presence of major CHD risk factors

-Estimate 10 year risk of coronary heart disease event by “Pooled Cohort Equation” (risk markers include sex, race, total cholesterol, HDL-C, BP, BP treatment status, diabetes, current smoking status)

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26
Q

What are the risk markers for CHD event by Pooled Cohort equation?

A
  1. sex (male)
  2. race (AA vs Caucasian)
  3. total cholesterol
  4. low HDL-c
  5. BP (over 140 or on meds)
  6. DM
  7. current smoking status
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27
Q

What groups benefit from a high intensity statins?

A
  1. Clinical ASCVD (ACS, MI, angina, stroke, TIA, revascularization, PAD)
  2. LDL-C 190 and over
  3. 40-75 y/o w/ DM and LD 70-189
  4. No ASCVD, LDL-C 70-189, 10 yr risk of ASCVD over 7.5%
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28
Q

High intensity statins lower LDL-C __-%

Moderate intensity statins lower LDL-C __-%

A

high: 50% or greater
moderate: 30-50%

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29
Q

A 35-year-old woman appears to have familial combined
hyperlipidemia. Her serum concentrations of total cholesterol, LDL cholesterol, and triglycerides are elevated. Her serum concentration of HDL cholesterol is somewhat reduced. Which of the following drugs is most likely to increase this patient’s triglyceride and VLDL cholesterolconcentrations if used as monotherapy?

A.  Atorvastatin 
B.  Cholestyramine
C.  Ezetimibe
D.  Gemfibrozil 
E.  Colesevelam 
F.   Niacin
A

B.  Cholestyramine

E.  Colesevelam

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30
Q 
which of the following drugs should be avoided because of a risk of causing harm to the fetus?
A. Cholestyramine 
B.  Atorvastatin 
C.  Niacin 
D.  Fenofibrate 
E.  Ezetimibe 
F.   Rosuvastatin
A

B.  Atorvastatin

F.   Rosuvastatin

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31
Q

Which of the following is a major mechanism of gemfibrozil’s action?
A. Increased secretion of bile acid salts
B.  Increased expression of high-affinity LDL receptors on
hepatocytes
C.  Increased secretion of VLDL by the liver
D.  Increased triglyceride hydrolysis by lipoprotein lipase
E.  Reduced uptake of dietary cholesterol

A

D.  Increased triglyceride hydrolysis by lipoprotein lipase

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32
Q 
Select the major toxicity associated with gemfibrozil
therapy:
A.  Bloating and constipation 
B.  Cholelithiasis 
C.  Hyperuricemia 
D.  Liver damage 
E.  Severe cardiac arrhythmia
A

B.  Cholelithiasis

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33
Q

What are the doses of high intensity statins?

A
  1. Atoravastatin 80mg daily

2. Rosuvastain 20-40mg daily

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34
Q

What are the doses of moderate intensity statins?

A
  1. Atorvastatin 10-20 mg daily
  2. Pravastatin 40-80 mg daily
  3. Fluvastatin 80 mg (XL) daily
  4. Rosuvastatin 5-10 mg daily
  5. Lovastatin 40 mg daily
  6. Simvastatin 20-40 mg daily
  7. Pitavastatin 2-4 mg daily
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35
Q

Describe the purpose/use of chylomicrons

A
  1. Formed in intestine and carry TG/C of dietary origin
  2. Hydrolyzed by lipoprotein lipase (LPL) in vascular endothelium–> TG for utilization by adjacent tissues
  3.   Chylomicron remnants then transfer C and residual TGs to liver
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36
Q

What is the largest lipoprotein?

A

Chylomicrons

85-95% TG, 3-6% C

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37
Q

Describe the composition of

  1. Chylomicrons
  2. VLDL
  3. LDL
  4. HDL
A
  1. Chylomicrons: 85-95% TG, 3-6% C
  2. VLDL: 50-60% TG, 20-30% C
  3. LDL: less than 10% TG, 50-60% C
  4. HDL: 5% TG, 25% C
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38
Q

Describe the physiology of VLDLs

A
  1. Secreted by liver, carriers of triglycerides / cholesterol synthesized in liver to peripheral tissues
  2.   Hydrolyzed by LPL (FFA enter muscle-adipose tissue) –> converted to IDL –> endocytosed by liver (receptor-mediated) or converted to LDL in the plasma
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39
Q

source of cholesterol for incorporation into membranes and synthesis of steroids

A

LDL

40
Q

Describe the physiology of LDL

A
  1. Derived from VLDL remnants (via IDL) by action of lipoprotein lipase
  2.   LDL carries cholesterol to liver and extra-hepatic tissues with uptake into these cells regulated by surface LDL-receptors and B-100 –> source of cholesterol for incorporation into membranes and synthesis of steroids.
41
Q

What is the function of HDL

A
  1. bring cholesterol from periphery back to the liver for metabolism–“reverse cholesterol transport”
  2. transfers cholesterol esters back to VLDL particles in exchange for TGs (via CETP), resulting in its rapid clearance and lower HDL levels
42
Q

What is HDL synthesized by

A

liver and intestines

43
Q

What is the function of apolipoproteins

A

maintain structure of lipoproteins and direct the metabolism of the particle

44
Q

ApoB-100 is the structural protein in __, __, and __

A

VLDL, IDL, LDL

45
Q

directs plasma clearance as LDL receptor ligand

A

ApoB-100

*Risk factor for atherosclerosis

46
Q

Ligand for receptors binding chylomicron and VLDL remnants (IDL)

A

ApoE

47
Q

Ligand for HDL receptor; LCAT cofactor for reverse cholesterol transport

A

ApoA-1

48
Q

Cofactor with lipoprotein lipase → converts TG of chylomicrons to FFA

A

ApoC-II

49
Q

Where is HMG-CoA reducatse inhibitors site of action?

A

inhibit acetyl-CoA –> cholesterol in the liver

50
Q

Where is ezetimibe site of action?

A

inhibits cholesterol from intestines form being taken up by liver

51
Q

Where is bile acid-binding resins site of action?

A

inhibits bile acids from intestines to the liver

52
Q

Where is niacins site of action?

A

inhibits protein and TG from leaving liver in form of VLDL

53
Q

What is the MOI of HMG CoA Reductase

A

-competitive inhibitors of rate-limiting enzyme step in
cholesterol biosynthesis

-Reduced hepatic cholesterol –> increase in LDL receptors –> increased removal of LDL from plasma

54
Q

What is the rule of 6 for HMG-CoA Reductase inhibitors

A

Each doubling of dose after starting dose –> only a 6% further LDL-lowering effect

55
Q

Only class of dyslipidemic agents that is associated with a reduction in mortality from all causes

A

HMG-CoA Reductase inhibitors

56
Q

What are examples of HMG-CoA Reductase inhibitors

A
  1. Lovastatin (Mevacor)
  2. Pravastatin (Pravachol)
  3. Fluvastatin (Lescol)
  4. Simvastatin (Zocor)
  5. Atorvastatin (Lipitor)
  6. Rosuvastatin (Crestor)
57
Q

Potential additional cardioprotective effects (other than LDL lowering) of statins include:

A
  1. Reversal of endothelial cell dysfunction (also with ACEIs)
  2.   Increase in plaque stability
  3.   Anti-inflammatory action = ↓ CRP in plasma
  4. Decrease susceptibility of LDLs to oxidation (via enhanced antioxidant action of paraoxonase)
  5.   Reduction of platelet aggregation
58
Q

Statin dosing considerations

A
  1. High first-pass effect is beneficial for these hepatic-active agents
  2.   Agents should be administered in the evening (hepatic cholesterol synthesis higher at night)
59
Q

Adverse reactions with statins

A

Generally well tolerated

  1. mild GI sx (take w/ meals)
  2. Rash/pruritus
  3. HA
  4. contraindicated in pregnancy and nursing mothers (Class X)
  5. Liver function biochemical abnormalities have occurred- Risk is dose-dependent and reversed after dose reduction or discontinuation
  6. Myopathy and rhabdomyolysis
  7. small increase in HbA1c (risk reduction outweigh concerns)
60
Q

When should you check LFTs with statins

A

check ALT at baseline and only repeat if sx of hepatotoxicity occurs

61
Q

Risk of myopathy and rhabdomyolysis with statins increases with ___ or in combination with __ or ___

A

dose escalation

fibrates (esp. gemfibrozil) or niacin

*Often due to DDIs which increase plasma levels (inhibitors of CYP3A4, but not seen with pravastatin or rosuvastatin)

62
Q

Increased oral anticoagulant effects are seen with what statins

A

lovastatin
simvastatin
fluvastatin

63
Q

Someone with a hx of __, __, __ or __ has an increased risk of myopathy and rhabdomyolysis with statins

A
  1. hepatic dysfunction
  2. renal failure
  3. hypothyroidism
  4. serious infection
64
Q

What is the MOI of Ezetimibe

A

Inhibits intestinal absorption of dietary and biliary cholesterol at brush border of the small intestine

65
Q

Examples of inhibitors of cholesterol absorption

A
  1. Ezetimibe (Zetia)
  2. dietary supplements:
    - plant stanol esters (Benecol),
    - Sterol esters (Take control),
    - combo (Cholestoff)
66
Q

Cholesterol lowering effect with Ezetimibe is about __% and is additive with the “statins”

A

~15%

67
Q

avoid Ezetimibe in what patients

A

if have moderate-severe hepatic insufficiency

68
Q

Dosing considerations for Ezetimibe

A
  1. Absorption can be inhibited by bile acid sequestrants, so space dosing
  2. No interactions with administration of “statins”
  3.   Minimal systemic exposure - no significant drug interactions with CYP450 substrates
69
Q

MOI of bile acid sequestrants

A
  1. Bind bile salts (metabolites of cholesterol) in gut –>
    increase excretion by 10fold–> prevent recycling to liver
    2.  Cholesterol must be converted to bile acids –> lower hepatic cholesterol –> LDL receptor upregulation
  2.   Increased removal of LDL from plasma (to supply
    cholesterol to liver) [20-35%]
70
Q

Examples of bile acids sequestrants

A
  1. Cholestyramine (Questran)
  2. Colestipol (Colestid)
  3. Colesevelam
71
Q

What results in synergistic LDL lowering in combination with “Statins”

A

bile acids sequestrants

72
Q

adverse reactions of bile acids sequestrants

A
  1. constipation
  2. bloating
  3. abdominal pain
  4. rectal irritation
  5. may increase TG
  6. interfere w/ drug and fat soluble vitamines (A, D, E, K) absorption
73
Q

Contraindicated in patients w/ elevated TG over 400

A

bile acid sequestrants

74
Q

bile acid sequestrants can interfere with absorption with what drugs

A
  1. digoxin
  2. warfarin
  3. pravastatin
  4. fluvastatin
  5. aspirin
  6. thiazide diuertics
  7. fat soluble vitamins: A, D, E, K

*after BAS agents
Take other drugs at least 1 hour before or 4 hours

75
Q

MOI of fibrates

A
  1. Activates PPARα –> increasing transcription of various proteins involved in lipid metabolism
  2. increased activity of LPL –> increase in VLDL clearance
  3.   Moderate decreases in VLDL secretion (lowering plasma triglycerides) + increased production of HDL
76
Q

Generally considered drug of choice for hypertriglyceridemia

A

fibrates

77
Q

Examples of fibrates

A
  1. Gemfibrozil (Lopid)

2. Fenofibrate (Tricor)

78
Q

fibrates Will also raise HDL levels by ___%

A

10-25%

79
Q

Adverse reactions with fibrates

A
  1. Nausea/abdominal discomfort (may take with food)
  2.   Myalgia (occasionally involves myocardium); increased risk if taking reductase inhibitors
  3.   Skin rash; leukopenia (monitor)
  4.   Should not use in patients with renal or hepatic dysfunction
  5.   Both agents potentiate the actions of warfarin anticoagulants [protein-binding interaction]
  6.   Gallstones possible, but lower incidence with new agents
80
Q

Fibrates should not use in patients with __ or ___

A

renal or hepatic dysfunction

81
Q 
Which one of the following drugs causes a decrease in hepatic triglyceride synthesis by limiting availability of free fatty acid precursors? 
A.  Fenofibrate 
B.  Niacin 
C.  Cholestyramine 
D.  Lovastatin 
E.  Gemfibrozil 
F.   Ezetimibe
A

B.  Niacin

82
Q

What is the MOI of niacin

A
  1. Decreases VLDL secretion from liver
    2.  Inhibits release of free fatty acids from tissue
    stores –> decreasing availability of VLDL precursors
83
Q

Niacin results in a __% lowering of TG levels and 10-__% reduction of LDL (possibility of synergistic effects in combination with resins)

A

30-40%

15%

84
Q

Largest pharmacologic effect to increase HDL

levels

A

Niacin

85
Q

Alex is a 42-year-old who was started on niacin sustained-release tablets 2 weeks ago for elevated triglycerides and low HDL levels. He is complaining of an uncomfortable flushing and itchy feeling that he thinks is
related to the niacin. Which of the following options can help this patient?
A.  Administer aspirin 30 minutes after taking niacin
B.  Administer an antihistamine 30 minutes prior to taking niacin
C.  Increase the dose of niacin SR to 1000 mg D.  Continue the current dose
E.  Change the SR formulation to immediate-release niacin
F.   Administer aspirin 30 minutes prior to taking niacin

A

F.   Administer aspirin 30 minutes prior to taking niacin

86
Q

Adverse reactions of Niacin

A
  1. Flushing, pruruits, GI distress
  2. Dyspepsia
  3. Hepatic dysfunction**
  4. decreases uric acid secretion (avoid in gout)
  5. impaired insulin sensitvitiy
87
Q

Niacin should be avoided in what patients

A
  1. severe peptic ulcer disease

2. gout

88
Q 
Hazel is a 72-year-old female who is treated for hyperlipidemia with high dose atorvastatin for the past 6 months. She also has a history of renal insufficiency. Her most recent lipid panel shows an LDL level of 131 mg/dL, triglycerides of 510 mg/dL, and HDL of 32 mg/dL. Her PA wishes to add an additional agent for her hyperlipidemia. Which of the following choices is the best option to address Hazel’s dyslipidemia? 
A.  Fenofibrate 
B.  Niacin 
C.  Cholestyramine 
D.  Add rosuvastatin 
E.  Gemfibrozil 
F.   Ezetimibe
A

B.  Niacin

89
Q

PCSK9 inhibitors have a role in patient groups that would benefit from additional lipid-lowering options:

A
  1. familial hyperlipidemia
  2. poor response to statins
  3. statin-intolerant patients

*very expensive

90
Q

PCSK9 inhibitors produce further ___% LDL lowering in patients already taking maximally tolerated doses of a statin

A

40-60

91
Q

What effects does niacin have on LDL, HDL and TG

A

LDL: decrease 5-25%

HDL: increase 15-35%**

TG: decrease 20-50%**

92
Q

What effects do fibrates have on LDL, HDL and TG

A

LDL: may increase or decrease it

HDL: increase 10-25%

TG: decrease 20-50%**

93
Q

What effects do Bile acid sequestrants have on LDL, HDL and TG

A

LDL: decrease 15-35%** (additive w/ statin)

HDL: increase 13-5%

TG: increase** (BAD)

94
Q

What effects does Ezetimibe have on LDL and HDL

A

LDL: decrease*

HDL: increase

*effect additive w/ statins

95
Q

What effects do HMG-CoA reductase inhibitors have on LDL, HDL, and TG

A

LDL: decrease

HDL: increase

TG: decrease

Pharmacology (31 decks)

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