CME/CE Quiz

Continuing Medical Education Accreditation

AMA PRA Category 1 CME credit(s)

The University of Cincinnati College of Medicine designatesthis educational activity for a maximum of two (2)^™. Physicians shouldonly claim credit commensurate with the extent of theirparticipation in this activity.

The University of Cincinnati College of Medicine is accreditedby the Accreditation Council for Continuing MedicalEducation (ACCME) to sponsor continuing medical educationfor physicians.

Continuing Pharmacy Education Accreditation

Pharmacy Times

/Ascend Media Office of Continuing ProfessionalEducation is accredited by the AccreditationCouncil for Pharmacy Education (ACPE) as a provider ofcontinuing pharmacy education. This program is approvedfor 2 contact hours (0.2 CEUs) under the ACPE universalprogram number of 290-999-06-011-H01.

Instructions

After reading "Emerging Antithrombotic Therapies: NewDevelopments in Acute Care Medicine," complete the programevaluation and select the 1 best answer to each of thefollowing questions. A statement of continuing educationhours will be mailed to those who successfully complete(with a minimum score of 70%) the examination at the conclusionof the program.

1. Which is true concerning myocardial infarction (MI)?

1. In the United States, one third of MI patients diebefore they reach the hospital.
2. In the United States, half of MI patients have anestablished history of angina.
3. MI accounts for 75% of total cardiovascular mortalityworldwide.
4. After MI, the risk of stroke, disabling heart failure,or second MI within 6 months is higher inwomen than in men.

2. Among patients with acute coronary syndromes (ACS):

1. the median age is 48 years.
2. the inhospital mortality rate is approximately 15%.
3. the actual incidence of unstable angina (UA) isbelieved to be about twice the reported incidence.
4. total direct medical costs in the United States areapproximately $20 billion.

3. Recommended strategies for managing ACS include:

1. coronary artery bypass graft early in evolving MIfor patients who are not candidates for medicalthrombolysis or percutaneous coronary intervention(PCI).
2. PCI only if symptoms persist after 24 hours ofthrombolytic therapy.
3. antiplatelet therapy with aspirin instead ofanticoagulation with heparin products.
4. treadmill-exercise echocardiography to assesstypical angina in a middle-aged man.

4. ACS comprise:

1. UA and ST-segment elevated myocardial infarction(STEMI), but not non-ST-segment elevatedmyocardial infarction (NSTEMI).
2. UA and NSTEMI, but not STEMI.
3. STEMI and NSTEMI, but not UA.
4. UA, STEMI, and NSTEMI.

5. The event that precipitates ACS is:

1. rupture of an atherosclerotic plaque.
2. fat embolism obstructing the coronary arteries.
3. platelet abnormalities.
4. coagulation factor abnormalities.

6. The coagulation cascade includes all of the followingevents except:

1. tissue factor from the exposed vascular matrixactivates factor VII to VIIa.
2. VIIa activates X, and Xa works with Va toactivate II to IIa (thrombin).
3. IIa stimulates platelet activity and fibrinformation.
4. antithrombin III (ATIII) deactivates platelets tostop the process.

7. Unfractionated heparin (UFH):

1. neutralizes ATIII.
2. is contraindicated in patients taking aspirin.
3. can be used in conjunction with fibrin-specificagents and in ACS patients at high risk forthromboembolic complications.
4. cannot be used if cardiac catheterization isplanned.

8. In terms of safety in ACS patients receiving UFH:

1. the incidence of heparin-induced thrombocytopenia(HIT) is 5% to 10%.
2. HIT is associated with an increased risk ofthrombotic events.
3. monitoring is by prothrombin time.
4. monitoring is by bleeding time.

9. Compared with UFH, low molecular weight heparins(LMWH):

1. are more homogeneous and have more reliablepharmacokinetics.
2. carry the same risk of HIT but lower risk ofsignificant bleeding.
3. require the same type of laboratory monitoring.
4. can be more easily neutralized in case ofoverdose.

10. Fondaparinux is:

1. a synthetic replicate of endogenous heparin.
2. an inhibitor of ATIII.
3. administered orally, once daily.
4. approved for treatment of HIT.

11. In a clinical trial of fondaparinux versus the LMWHenoxaparin in high-risk patients with UA or NSTEMI, thosetreated with fondaparinux showed:

1. a significantly lower incidence of the combinedoutcome of death or MI or refractory ischemia at9 days.
2. a significantly lower incidence of MI at 30 days.
3. the same incidence of death or MI or refractoryischemia at 9 days.
4. the same incidence of death at 30 days.

12. In the same fondaparinux versus enoxaparin trial:

1. the incidence of bleeding complications was thesame for both treatment groups at all time points.
2. outcomes among patients who underwent PCIswere significantly better in the fondaparinuxgroup.
3. mortality at 180 days was nonsignificantly lowerin the enoxaparin group.
4. bleeding complications were associated withhigher rates of death, reinfarction, and strokewithin both treatment groups.

13. In a trial of STEMI patients randomized to fondaparinuxversus "usual care" (UHF or placebo), treatment withfondaparinux was associated with a significantly lowerincidence of:

1. death or reinfarction at 9 days, 30 days, and endof study.
2. severe bleeding in the subset of patients undergoingPCI.
3. guide-wire thrombosis in the subset of patientsundergoing PCI.
4. All of the above

14. In which group of ACS patients is fondaparinux leastlikely to be advantageous in comparison with UHF or LMWH?

1. Those with renal dysfunction.
2. Those in whom PCI is not feasible.
3. Those treated with early invasive strategies.
4. Those at increased risk of bleeding complications.

15. Among patients who survive acute MI:

1. approximately half will die within 1 year.
2. mortality within 1 year is higher among womenthan among men.
3. the risk of illness and death is 3 to 5 times higherthan in the general population.
4. anticoagulant therapy must be continued for life.

16. In clinical trials of enoxaparin versus UHF in patientswith ACS:

1. enoxaparin was used instead of but not in combinationwith a glycoprotein IIb/IIIa inhibitor.
2. enoxaparin was associated with a 20% lower riskof death and serious cardiac ischemic events.
3. there was no significant difference in the incidenceof death or recurrent ischemic events at30 days.
4. outcomes were better with enoxaparin at 30days, but there were no significant differencesthereafter.

17. Which statement is true concerning costs of anticoagulanttherapy in ACS?

1. Acquisition cost is higher with enoxaparin thanwith UHF, but overall costs are lower.
2. Acquisition cost is higher with enoxaparin thanwith UHF, but overall costs are the same.
3. Acquisition cost and overall costs are higherwith enoxaparin than with UHF, but the clinicaladvantages outweigh cost considerations.
4. There are no firm data on the economic impactof anticoagulation with enoxaparin versus UHF.

18. Fondaparinux works by:

1. directly activating factor Xa.
2. directly inactivating factor Xa.
3. decreasing the ability of antithrombin III toinactivate factor Xa.
4. increasing the ability of antithrombin III toinactivate factor Xa.

19. Fondaparinux:

1. undergoes hepatic excretion.
2. can be administered on a once-weekly basis.
3. is unlikely to induce thrombocytopenia.
4. is significantly more effective than enoxaparin intreating deep vein thrombosis.

20.With regard to the use of fondaparinux versusenoxaparin in ACS:

1. incidence rates of death or recurrent or refractoryischemia are similar.
2. the incidence of major bleeding is slightly worsewith fondaparinux.
3. fondaparinux offers significant advantage inpatients undergoing PCI.
4. total costs for anticoagulation are significantlylower with fondaparinux.

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