Coronary Artery Disease Risk Factors Flashcards

1
Q

In vivo, the subendothelium contains many types of collagen. All the following are types of subendothelial collagen except:

a. Collagen II
b. Collagen III
c. Collagen IV
d. Collagen V
e. Collagen VIII

A
  1. Answer a.

Collagen II is found largely in hyaline cartilage.

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2
Q

Endothelium secretes all the following substances in large amounts except:

a. Collagen
b. Elastin
c. Glycosaminoglycans d. Fibronectin
e. Mucopolysaccharides

A
  1. Answer e.
    Mucopolysaccharide is secreted from glandular tissue. Endothelium is a layer of thin, specialized epithelium comprised of a single layer of squamous cells in healthy tissue.
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3
Q

Which substance(s) is/are secreted by the endothelium?

a. Procoagulants
b. Anticoagulants
c. Vasoconstrictors
d. Vasodilators
e. Pro-proliferative substances

A
  1. Answers a, b, c, d, and e.
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4
Q

Which of the following is/are not true about platelets?
a. Platelet activation can occur through many biochemical pathways and receptors
b. Platelet aggregation occurs through many different surface receptors
c. Platelet adhesion occurs principally through subendothelial vWF
d. Platelet-activating factor also activates monocytes and polymorphonuclear
leukocytes
e. Removal of the endothelium exposes subendothelium and creates intense
platelet adhesion

A
  1. Answers b and c.
    While there is research dedicated to elucidating novel receptors of platelet aggrega- tion, the glycoprotein IIb/IIIa receptor is responsible for a large component of aggre- gation (as opposed to activation with thromboxane A2). In experiments of a porcine model lacking vWF, initial contact adhesion was not affected. However, activation of platelets was dependent on soluble vWF. It is thought that it is the soluble vWF that attaches to damaged and exposed subendothelium, slowing the platelets enough to allow attachment principally via the glycoprotein IIb/IIIa receptor.
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5
Q

Atherosclerosis principally affects which of the following component(s) of the vessel wall?

a. Intima
b. Adventitia
c. Media
d. Endothelium

A
  1. Answers a and c.
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6
Q

The major cell type of the normal coronary artery intima is the:

a. Macrophage
b. Smooth muscle cell
c. Lymphocyte
d. Endothelial cell
e. Foam cell

A
  1. Answer b.
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7
Q

The foam cell is a lipid-laden cell derived from:

a. Macrophage
b. Smooth muscle cell
c. Endothelial cell
d. Lymphocyte
e. Polymorphonuclear leukocyte

A
  1. Answer a and b.

Smooth muscle cells have a heterogeneity of origin including neurectoderm (neural crest) and mesoderm.

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8
Q

Which of the following is/are true about atherosclerotic plaques?
a. Studies of arteries in patients with atherosclerosis show high rates of prolifer- ation
b. Intimal cell masses found in normal young patients suggest that proliferation may have an early role in the development of the atherosclerotic lesion
c. Cells normally accumulate in the coronary arterial intima with aging
d. Evidence suggests that the fatty streak may not be an early lesion of coronary
artherosclerotic plaque
e. The cells of atherosclerotic plaques are polyclonal in origin; that is, originat-
ing from many cells

A
  1. Answers b, c, and d.
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9
Q

In the “insudation hypothesis” of atherosclerosis, which of the following is/are true?
a. Lipid accumulation in atherosclerotic plaque comes from circulating lipid
b. Smooth muscle cell proliferation is induced by lipid accumulation at physio-
logic lipid concentration
c. Fatty deposition is required for plaque growth
d. Lipids in foam cells come from synthesis by local cellular activity

A
  1. Answer a.
    Seminal work by Anitschkow in the 1920s and 1930s arrived at the hypothesis that circulating lipid accumulated and contributed to atherosclerotic “lipoids” in the plaque. This shaped the way for future investigation and research in targeting lipids in the prevention and treatment of coronary atherosclerosis.
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10
Q

Which of the following is/are true of the fatty streak?

a. It is found frequently in young children and infants
b. It is found at the same anatomical sites in young persons and adults
c. T lymphocytes may be found in many fatty streaks
d. The principal lipid of the fatty streak is unoxidized cholesteryl esters
e. The fatty streak is found principally in males at older ages

A

Answers a, b, and c.

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11
Q

Which of the following is/are true of the “vulnerable” plaque?
a. The vulnerable plaque typically has a fibrous cap covering a lipid-rich layer
b. These plaques often rupture at the central portion of the fibrous layer, where
hydrodynamic forces are increased
c. Evidence suggests that vulnerable plaque may come from hemorrhage into
the coronary artery vessel wall at certain locations
d. Thevulnerableplaqueistypicallyassociatedwithasevereangiographicstenosis
e. There is evidence suggesting that more than 90% of deaths caused by MIs are
associated with plaque rupture or ulceration

A
  1. Answers a, b, c, and e.

Vulnerable plaques are often hemodynamically insignificant (

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12
Q

Which of the following is/are true of calcification of coronary artery plaque?

a. Coronary calcification may proceed in a biochemical fashion similar to that in bone
b. The principal component of plaque calcification is calcium carbonate and, thus, is related to vitamin D intake
c. The degree of calcification is related to the overall volume of atherosclerotic plaque in coronary arteries
d. Calcific medial sclerosis as a cause of coronary arterial calcification is associ- ated with increased probability of an ACS
e. The coronary artery develops calcification late in plaque development and nearly always is associated with large plaque burden

A
  1. Answers a and c.
    Of note, in selected young patients presenting with acute atherothrombotic MI, there is little calcification around their vulnerable plaque. Hence, lack of calcification does not completely rule out vulnerable plaque, and presence or absence of calcium is therefore only a tool for risk stratification and should not supplant clinical decision making.
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13
Q

What is the current accepted practice regarding Lp(a) risk stratification for CAD?
a. It should be followed serially every 2–4 years to assess for increased risk
b. It can be targeted by pharmacotherapy to yield reduction in morbidity above
and beyond conventional risk factors
c. An elevated level may prompt moving a patient into a higher risk category
and treating to more aggressive LDL and BP goals
d. The size of Lp(a) isoforms is directly related to its atherogenic potential

A
  1. Answer c.
    The third of the population with the highest Lp(a) levels have increased risk of future CV events. However, there are no specific therapies and it varies little over time. It may be useful to identify higher risk individuals who may benefit from more aggres- sive conventional risk factor modification.
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14
Q
  1. Which of the following is true about smoking and CV disease?
    a. Smokers have their first CV event approximately 10 years earlier than matched nonsmoking cohorts
    b. Mortality of smokers is 50% greater than nonsmokers and those who quit smoking immediately after a MI
    c. The magnitude of smoking cessation on reducing mortality if EF
A
  1. Answers a, b, c, and d.
    AHA guidelines recommend addressing smoking cessation at every follow up visit. The impact of smoking on CV disease is profound. Epidemiologic studies have found continued smoking after the first MI has a hazard ratio of 1.53 compared to nonsmokers and those who quit smoking during the index hospitalization (J Clin Epidem 2002; 55:654–664). A study of patients with LV EF
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15
Q

Response to which agent can be used to measure endothelial function?
a. Methergine b. Ergonovine c. Acetylcholine d. Endothelin

A

Acetycholine-mediated vasodilation depends on an intact and functional endothe- lium to produce NO for relaxation. Methergine is used as a provocative test for coro- nary spasm and is not used to measure the endothelial function.

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16
Q

Functional assessment of an intermediate coronary lesion can be performed by all of the following except:

a. Measurement of coronary flow reserve
b. Measurement of fractional flow reserve
c. Quantitative coronary angiography

A

Angiography only gives a visual estimate of stenosis and does not yield direct func- tional significance of an intermediate lesion.

17
Q

How do ACE inhibitors affect the bradykinin system?

a. Increase degradation of bradykinin
b. Decrease degradation of bradykinin
c. Increase production of bradykinin
d. Increase kallikrein production

A

Degradation of bradykinin relies on ACE. Inhibition with ACE inhibitor allows build-up of bradykinin, which likely mediates the “cough” found in some patients intolerant of ACE inhibitor.

18
Q

NO regulates which of the following processes?

a. Vasodilation
b. Platelet aggregation
c. Matrix synthesis
d. Smooth muscle cell migration
e. All of the above

A
  1. Answer e.

All of the above

19
Q

The most potent vasoconstrictor is:

a. Bradykinin b. Endothelin c. Acetylcholine d. PAI-1

A
  1. Answer b.
    Endothelin is correct. Bradykinin is not a potent vasoconstrictor; acetylcholine medi- ates constriction if endothelium is denuded or dysfunctional (but not as potently as endothelin); PAI-1 is the main inhibitor of the serine proteases tPA and urokinase and prevents fibrinolysis.
20
Q
  1. The endothelium plays a role in which of the following?
    a. Regulation of blood flow
    b. Release of growth factors
    c. Regulation of thrombosis
    d. All of the above
A
  1. Answer d.
21
Q
  1. Which of the following substances does not directly affect the microcirculation (i.e., arterioles, capillaries, venules)?
    a. Adenosine
    b. Papaverine
    c. NTG
    d. Nitroprusside
A
  1. Answer c.
22
Q
  1. Atherosclerosis is associated with:
    a. Increase in circulating endothelin concentrations
    b. Increase in oxidative stress
    c. Decrease in NO activity
    d. All of the above
A
  1. Answer d.
23
Q
  1. Coronary endothelial dysfunction is associated with:
    a. Future cardiac events
    b. Abnormal response to intracoronary adenosine
    c. Abnormal response to intracoronary NTG
    d. Abnormal response to IV Methergine
A
  1. Answer a.
    Schachinger et al. (Circ 2000; 101:1899) found a significant relationship between endothelial dysfunction as tested by vasoconstriction upon acetylcholine administra- tion and CV events.
24
Q

Which of the following substances is not an endothelium-dependent dilator?
a. Acetylcholine b. Substance P c. Bradykinin d. NTG

A
  1. Answer d.

NO is released by administration of NTG and works directly on smooth muscle as it diffuses via the bloodstream.

25
Q

Nitroprusside is an endothelial independent vasodilator. True or false?

a. True
b. False

A
  1. Answer a.

True. Nitroprusside is a NO donor and works similar to NTG as an endothelial inde- pendent vasodilator.

26
Q

All the following are obligate coronary vasodilators except:

a. NTG
b. NO
c. Acetylcholine
d. Hypoxia
e. Hypercapnia

A
  1. Answer c.
    All are known to cause vasodilatation. Only acetylcholine can be a vasoconstrictor if the endothelium is dysfunctional or absent and NO cannot be produced. In this case, it is not an obligate vasodilator.
27
Q
  1. The risk of plaque disruption depends primarily on all of the following factors except:
    a. Severity of angiographic stenosis
    b. Plaque morphology
    c. Lipid content of the plaque
    d. Endothelial function
A
  1. Answer a.
28
Q
  1. Plasma endothelin concentrations are increased in the following states:
    a. Heart failure
    b. Atherosclerosis
    c. Pulmonary HTN
    d. All of the above
A
  1. Answer d.
29
Q

NO (endothelium-derived relaxant factor) mediates its vasorelaxation effect through:

a. Specific receptor on the endothelium
b. Specific receptors on smooth muscle cells
c. Direct effect on smooth muscle cells
d. Decrease in intracellular calcium

A
  1. Answer c.
30
Q

Endothelin exerts its vasoconstriction through:

a. Activation of cGMP
b. Direct effect on smooth muscle cells
c. Injuring the endothelium
d. Specific endothelin receptors

A
  1. Answer d.
    The endothelin receptors are G-protein coupled receptors located on smooth muscle cells. Their role in proliferation and contraction of PA smooth muscle cells is the rationale behind their targeted antagonism with bosentan in pulmonary HTN.
31
Q

Endothelial dysfunction is characterized by:

a. Vasoconstriction to endothelial-dependent vasodilator substances
b. Possible occurrence without significant CAD
c. Possible causal link to smoking
d. All of the above

A
  1. Answer d.
32
Q

Endothelial dysfunction may be reversed by:

a. Lowering cholesterol
b. Stent implantation
c. Thrombolytic therapy
d. NTG

A

Answer a.

33
Q

The LDL NCEP goal for treatment of lipids in patients with known CAD or CAD risk equivalent is:
a.

A

Answer d.

NCEP/ATP III goal

34
Q

Which of the following is not considered a CAD risk equivalent?

a. Peripheral arterial disease
b. Carotid arterial disease
c. Diabetes
d. AAA

A

Answer b.
Carotid arterial disease must be symptomatic to be considered a CAD equivalent by ATP III guidelines. The other items are considered CAD equivalents.

35
Q

The NCEP ATP-III goal for LDL in the treatment of hyperlipidemia in an asymptomatic patient with no or one risk factor is:
a.

A

Answer b.

The LDL goal is

36
Q

If two risk factors are present without CAD or equivalent, a patient can still be treated as a risk equivalent if their 10-year risk is greater than:
a.

A

Answer c.
The 10-year risk is calculated using Framingham data. However, this is not a com- prehensive model of risk. If, for example, the patient has significant risk of rapid pro- gression due to XRT, it would be reasonable to treat to more aggressive therapeutic goals.

37
Q

Which of the following drugs would be first-line therapy for a patient without documented heart disease who has the following lipid profile:
LDL: 138 mg/dL HDL: 20 mg/dL Triglycerides: 964 mg/dL
a. Atorvastatin (Lipitor)
b. Simvastatin (Zocor)
c. Lovastatin (Mevacor)
d. Gemfibrozil (Lopid)
e. Fluvastatin (Lescol)

A

Answer d.
Gemfibrozil (Lopid) is the most potent triglyceride-lowering agent among the possi- ble answers. Gemfibrozil reduces plasma triglycerides by 40% to 55%, usually within 1mo of onset of therapy. Lovastatin and fluvastatin do not appreciably alter the plasma triglyceride values. Atorvastatin will lower plasma triglyceride levels by 25% to 35%, and simvastatin will usually lower plasma triglyceride values by 19% to 25% when used at dosages of 40 mg and 80 mg, respectively.

38
Q

A 55-year-old man presents for risk evaluation. He has a history of HTN (well controlled on medication) and an AAA. He does not smoke, his HDL is 41 mg/dL, and there is no family history of premature CAD.
His target LDL is:
a.

A

Answer c.

ATP-III guidelines categorize patients with AAA as “CAD risk equivalent” so target LDL is

39
Q

A 50-year-old male lawyer is evaluated because of chest pain for the past 3 mos. His cholesterol level was “high” 1 yr ago. He is trying to follow a low-fat diet and to lose weight but has not had his cholesterol level rechecked. He has no history of DM, HTN, or tobacco use. His family history is unremarkable. He does not report any previous history of chest discomfort or MI. He describes his symptoms as a “central chest burning” that comes on when he is under stress in a courtroom or when he plays doubles tennis. The discomfort has never forced him to stop a courtroom argument or to interrupt his tennis game. In fact, he notes that it fre- quently resolved while he continued his activity. The discomfort sometimes lasts for an hour or more after he stops playing tennis. He has never taken NTG for this discomfort.
■ Physical examination findings are normal
■ BP is 130/70 mmHg
■ HR is 68 bpm and regular
■ ECG is normal
On the basis of this information, what is the probability that the patient has sig- nificant CAD?
a. 10%
b. 25%
c. 50%
d. 75%
e. 90%

A

Answer c.
The physician should estimate the probability of significant CAD in all patients pre- senting with chest pain. This patient’s chest pain is substernal and provoked by exer- cise, but it is not consistently relieved by rest. Therefore, it meets the definition of atypical angina. A 50-year-old man with atypical angina has approximately a 50/50 chance of marked CAD. The presence of multiple risk factors may increase the like- lihood. In this case, with a single risk factor, the best estimate of CAD is approxi- mately 50%.