Download Lecture 9 (Anticoags) 1. What is hemostasis? 2. What is thrombosis

Lecture 9 (Anticoags)
1. What is hemostasis?
2. What is thrombosis? What are the two forms of thrombosis? Define.
3. What is the most common form of venous thrombosis and what can it lead to?
4. Cardiogenic emboli are most commonly caused by what?
5. What are differences between red and white thrombi?
6. Anticoagulants are usually used for what type of clots? Antiplatelets?
7. What factor is the “key player” in the building of the clot? What is the rate
limiting step?
8. What is the synonym of Factor II? VII? X?
9. What is the MOA of anticoagulants?
10. What is the MOA of warfarin?
a. bind to antithrombin III and increase action of it by 1000-fold
b. inhibit epoxide reductase, thus inactivating vitamin K
c. decrease platelet formation
d. only inhibit factor X
11. What factors are indirectly inactived by warfarin?
a. X and II
b. II VII and X
c. IX and VII
d. II IX VII and X
12. If you have a patient diagnosed in the ER with DVT and you start them on
heparin, when should you start warfarin and why?
13. Where is warfarin metabolized? What enzyme?
14. What would be your treatment plan for a pregnant woman with
hypercoagulability during pregnancy? Would it change after birth?
15. What is the test you monitor in patients on warfarin? What is the goal for most
indications?
16. What drugs/disease states increase prothrombin time (PT) thus increasing INR?
17. What drugs/disease states descrease prothrombin time (PT) thus decreasing
INR?
18. What is the MOA of unfractionated heparin and LMWH?
a. bind to antithrombin III and increase action of it by 1000-fold
b. inhibit epoxide reductase, thus inactivating vitamin K
c. decrease platelet formation
d. only inhibit factor Xa
19. What do HWMH, LMWH, and fondaparinux contain that is required to bind to
ATIII?
20. What is the MOA of ATIII?
a. degrade factors II, IX, X, XI, XII
b. inhibit epoxide reductase, thus inactivating vitamin K
c. degrade factors IIa, IXa, Xa, XIa, XIIa
d. only inhibit factor X
21. Is HWMH and LWMH direct or indirect in its action? Why?
22. What is the MOA of fondaparinux?
a. bind to antithrombin III and increase action of it by 1000-fold
b. inhibit epoxide reductase, thus inactivating vitamin K
c. decrease platelet formation
d. only inhibit factor Xa
23. Which drug is safest for CKD patients?
a. enoxaparin
b. dalteparin
c. unfractionated heparin
d. fondaparinux
24. What is the difference between routes of administration for heparin vs LMWH?
25. What is the DOC for use during pregnancy?
a. warfarin
b. heparin
c. enoxaparin
d. dalteparin
e. fondaparinux
26. What is the major adverse effect of heparin to monitor for? What is the
mechanism by which it happens?
27. What are the oral, direct factor Xa inhibitors?
28. What is the major indication for direct factor Xa inhibitors?
29. What is the black box warning on direct factor Xa inhibitors? What causes this?
30. What is the major mechanism of drug interaction for rivaroxaban and apixaban?
31. Which direct thrombin inhibitor is an oral medication?
a. lepirudin
b. bivalirudin
c. desirudin
d. argatroban
e. dabigatran
32. What is the main indication for argatroban?
33. What is the major adverse effect with dabigatran? What is its black box warning?
34. What occurs to dabigatran when given simultaneously with clopidogrel?
35. What are the major indications for anticoags?
36. What patient population is high risk for DVT?
37. What is the DOC for VTE prevention following hip or knee replacement surgery?
38. How are VTEs treated?
39. What makes warfarin best choice for oral anticoagulation over direct thrombin
or factor Xa inhibitors?
40. Patient who have a mechanical valve placed must be on what drug for life?
a. clopidogrel
b. dabigatran
c. warfarin
d. rivaroxaban
Lecture 10 (Antiplatelets)
1. What is the MOA of aspirin?
2. What is aspirins major indication? Adverse effect?
3. What is the name of the oral combo drug that is a phosphodiesterase inhibitor?
4. What is the drug from the previous question MOA? Indication? Major adverse
effect?
5. What are the two irreversible adenosine diphosphate (P2Y12) receptor
antagonists? One reversible antagonist?
6. What is the MOA of clopidogrel?
7. What enzyme is clopidogrel metabolized by?
8. What P2Y12 receptor antagonist is indicated for secondary prevention of
ischemic stroke?
a. clopidogrel
b. prasugrel
c. ticlodipine
d. ticagrelor
9. What drugs are contraindicated with clopidogrel?
10. What is the MOA of eptifibate and aggrastat?
11. What is the MOA of abciximab?
12. What is the major indication for GPIIb/IIIa inhibitors? Major adverse effect?
13. What drug is a reversible inhibitor of PAR-1 receptor, which inhibits thrombininduced platelet aggregation?
14. What is the indication for vorapaxar? Contraindication?
15. What is the MOA of IV thrombolytics?
16. What is the name of the drug that directly activates plasminogen to plasmin
through proteolytic cleavage?
17. What is the major indication for use of thrombolytics? What is the timeframe?
18. What is the major adverse effect of streptokinase use as a thrombolytic?
19. What drugs are not recommended for use in treatment during acute ischemic
stroke?
20. What is the recommended therapy for secondary prevention of ischemic stroke?
a. asprin
b. clopidogrel
c. long term aspirin and clopidogrel
d. 3 weeks of aspirin and clopidogrel then D/C one of them and continue other
21. What is the drug used to manage bleeding problems due to warfarin? What is its
MOA?
22. Due to the fact that Vitamin K response is slow (24-48 hours) what should be
used as an adjunct in an acute setting?
23. What is the major adverse effect of Vitamin K?
24. What drug is a synthetic inhibitor of plasminogen activation?
a. clopidogrel
b. protamine
c. aminocaproic acid
d. andexanet alfa
25. What are the indications for fibrinolytic inhibitors?
26. Which drug is indicated for heparin reversal?
a. clopidogrel
b. protamine
c. aminocaproic acid
d. andexanet alfa
27. Which drug is currently undergoing trials and is indicated as a factor Xa
inhibitor antidote?
a. clopidogrel
b. protamine
c. aminocaproic acid
d. andexanet alfa
LECTURE 11 & 12
1. What is the primary cause of ischemic heart disease?
2. What are the short term and long term desired outcomes of ischemic heart
disease?
3. What is the difference between stable and unstable angina?
4. What is the purpose of giving a beta blocker to a patient having a CV event or
previous CV events?
5. What is the goal of BB therapy in CV prevention?
a. lower exercise HR to 50-60 bpm
b. lower blood pressure
c. lower resting HR to 50-60 bpm
d. lower oxygen supply
6. In regards to angina, beta-blockers are first line for what type?
a. Stable
b. Unstable
c. Prinzmetal
d. Chronic exertional
7. A 27 yo WF presents to the ED with intermittent episodes of chest pain. EKG
looks normal until your nurse calls you in the room when the patient experiences
the pain again and the EKG shows ST changes. She is rushed to the cath lab and
diagnosed with Prinzmetal’s angina. What is the DOC for preventive therapy in
patient’s with this diagnosis?
a. BBs
b. CCBs
c. ACEIs
d. ARBs
e. Nitrates
8. By what mechanism do CCBs help in preventing Prinzmetal’s angina?
9. Which drugs are used to prevent and treat angina attacks by relaxing venous
smooth muscle and decreasing oxygen demand?
a. BBs
b. CCBs
c. ACEIs
d. ARBs
e. Nitrates
10. What form of nitro is used during acute MI’s?
a. IV
b. Sublingual/lingual
c. Ointment
d. Oral
11. What form of nitro is used during acute angina attacks?
a. IV
b. Sublingual/lingual
c. Ointment
d. Oral
12. What form of nitro is used during long term treatment?
a. IV
b. Sublingual/lingual
c. Ointment
d. Oral
13. How should you instruct your patient about what to do when taking NTG for
acute chest pain?
14. What are thought to be benefits of ranolazine?
15. A patient with chronic stable angina could not tolerate a beta-blocker so the
patient was placed on ranolazine. What must you be sure to monitor on the
patient’s EKG?
a. QRS complex
b. QT interval
c. P wave
d. ST segment
e. Rhythm
16. ALL patients with IHD/Stable CAD must be on ____________ unless contraindicated.
17. What does acute coronary syndrome (ACS) primarily result from?
18. ACS is classified according to EKG changes. Which is not a classification of ACS?
a. STEMI
b. Stable angina
c. NSTEMI
d. Unstable angina
19. What is the primary desired outcome in ACS?
20. What is the protocol that should be initiated in patients with ACS? What does it
stand for?
21. Early administration of aspirin is crucial during ACS. What is the initial dose and
how does it work?
22. A patient presents to your ER with ACS. You initiate MONA protocol and there is
relief but still changes on the EKG. There is no invasive cardiologist at your hospital
or a close surrounding hospital. What drug therapy might you initiate to clear the
clogged artery by destroying the clot?
a. Heparin
b. Aspirin
c. Alteplase
d. Warfarin
23. What are the ABSOLUTE contraindications in use of thrombolytics?
24. Once you get the previous patient taken care of you talk to the cardiologist who
says to start him on clopidogrel daily. The patient has a history of HTN, GERD,
Kidney stones, HLD, and chonic back pain. You do what the cardiologist says and a
few hours later receive a call from a pharmacist wanting to discuss starting
clopidogrel when the patient is on a drug that is contraindicated with clopidogrel.
What drug would come to mind first that the pharmacist may be concerned about?
a. Simvastatin
b. Tamsulosin
c. Omeprazole
d. Ibuprofen
e. Lisinopril
25. Suppose you were able to get the previous patient cath’d and stented and the
cardiologist recommended the patient be on clopidogrel. How long must the patient
be on clopidogrel post MI and stents?
a. 6 weeks
b. 6 months
c. 12 months
d. life long therapy
26. How long must unfractionated heparin (UFH) be used during ACS? Enoxaparin?
27. What is a direct thrombin inhibitor that shows similar or greater efficacy to UFH
but better safety for primary PCI?
a. bivalrudin
b. rivaroxaban
c. prasugrel
d. dabigatran
e. eptifibatide
28. What drug is a GPIIb/IIIa inhibitor used for patients undergoing primary PCI
that decreases risk of reinfarction and need for repeat PCI.
a. bivalrudin
b. rivaroxaban
c. prasugrel
d. dabigatran
e. eptifibatide
29. J.W. is a 55-year-old man who presents to the Emergency Department via EMS
with chest tightness and shortness of breath. He describes the pain as “it feels like
an elephant is sitting on my chest”.
 He is diaphoretic and complains of nausea.
 PE: BP 160/85 mm Hg, P 90 bpm, RR 18 breaths/min.
A.
B.
C.
D.
E.
 EKG shows ST-segment elevation and cardiac enzymes are positive.
 What is the first pharmacologic intervention you will prescribe?
Amlodipine
Aspirin
Atorvastatin
Metoprolol
Ranazoline
30. What is the mechanism of action of your intervention?
A. Blocks beta-1 receptors
B. Inhibits calcium influx into smooth muscle cells
C. Inhibits HMG Co-A reductase
D. Inhibits sodium current and other cardiac ion channels and transporters
E. Inhibits TXA2 formation
31. After J.W. is stabilized, it is decided to take him to the catheterization lab for
percutaneous coronary intervention (PCI). Which drug should be added to his drug
regimen and continued for 12 months?
A. ADP inhibitor
B. Direct thrombin inhibitor
C. Glycoprotein iib/iiia inhibitor
D. Low molecular weight heparin
E. Unfractionated heparin
32. What is the most serious adverse effect of this drug?
A. Angioedema
B. Bleeding
C. Bradycardia
D. QT prolongation
E. Rhabdomyolysis
33. After J.W. successfully recovers from his MI and stent placement, which of the
following should you be sure to consider as a home medication?
A. ACEI
B. Beta-blocker
C. HMG Co-A Reductase inhibitor
D. All of the above
E. None of the above
LECTURES 13 & 14
1. What are the two major causes of heart failure?
2. A patient is referred to your cardiology office for what their PCP is describing as
stage C heart failure. What drugs are recommended as a MUST that this patient be
on?
a. CCB and BB
b. ACEI/ARB and CCB
c. BB and ACEI/ARB
d. BB and Nitrate
3. Why are patients with current or prior symptoms of HF and reduced LVEF
recommended to be on an ACEI?
4. When would an ARB be used instead of an ACEI?
5. True or false. When used long term, loop diuretics decrease morbidity and
mortality.
6. What population has seen a reduction in morbidity and mortality when
hydralazine/isosorbide dinitrate has been added to standard therapy with ACEI
and/or B-blocker?
a. Caucasian
b. Asian
c. African-American
d. Latino
7. A 63 yo WM follows up after having an ECHO. He is a known NYHA Class II patient
and ECHO revealed a LVEF of 30%. His creatinine is 2.1, potassium level 4.6, sodium
level 140. What type of drug is recommended for this patient to reduce death and
rehospitalization risk?
a. Loop Diuretics
b. Beta-blockers
c. ACEI
d. Aldosterone Antagonists
e. CCBs
8. What is the MOA of digoxin?
9. How is digoxin eliminated?
10. A patient had been on digoxin for 3 years. He recently developed some redgreen color perception difficulty and more than normal fatigue. What might his
digoxin level be?
a. 0.3 ng/mL
b. 0.9 ng/mL
c. 1.5 ng/mL
d. 2.1 ng/mL
11. Is Dig toxicity reversible? If so, how?
12. What must you monitor in patients on digoxin (other than digoxin level)?
13. A patient is diagnosed with heart failure and has an LVEF of 55%. What drugs
would be best in treatment of the heart failure?
a. loop diuretics
b. ACEI
c. ARBs
d. BBs
e. CCBs
14. What are the two general symptoms of acute decompensating heart failure
(ADHF)?
15. What is the most common form of ADHF?
a. warm and dry
b. warm and wet
c. cold and dry
d. cold and wet
16. What are the goals of treatment in ADHF?
17. A 73 yo AAF comes in to the ER with 3+ pitting edema. She reports she already
took her 40 of furosemide this morning but hasn’t urinated much as she usually
does when she takes her fluid pill. You order for 80 mg furosemide IV and some
blood work. Blood work comes back normal so you return to the room to inform her
and notice she hasn’t voided much urine since receiving the furosemide. What drug
might you add to try next to get the fluid off?
a. metolazone
b. spironolactone
c. torsemide
d. indapamide
18. Vasodilators are indicated in patients with dyspnea due to ADHF under what
circumstance?
19. A cardiologist rounding on one of his patients finds they are having trouble
getting over the hump and being relieved from his ADHF. He writes and order for a
drug to help stimulate natriuresis. The drug is a recombinant human BNP. What
drug did he write for?
a. Nitroprusside
b. Nesiritide
c. Indapamide
d. Spironolactone
20. Under what circumstances would you write for a patient to receive dobutamine
or milrinone (inotropes)?
21. You write for a patient to receive dobutamine for short-term parenteral. What is
the MOA?
22. What is the therapeutic limitation of dobutamine? Adverse effects?
23. What is the MOA of milrinone?
24. What is associated with long term use of milrinone?
25. Which is NOT recommended for monitoring once daily in hospitalized patients
with ADHF?
a. weight
b. fluid intake/output
c. vital signs
d. electrolytes
e. renal function
A. J. is a 58-yo male seen in the ED with a chief complaint of increasing SOB and an
8kg weight gain. He has noticed increasing DOE after one flight of stairs, orthopnea
and ankle edema. He sleeps on 3 pillows.
 PMH: GERD, depression, HTN
 PE: BP 160/100 mm Hg, HR 90 bpm, RR 28 breaths per minute. Neck veins
are distended. S3 gallop is heard. 3+ pitting edema of extremities. Bilateral
rales.
 Meds: HCTZ, ranitidine, citalopram
 Labs:
 Na+ 132 mEq/L (135-145 mEq/L)
 K+ 3.2 mEq/L (3.3 – 4.9 mEq/L)
 Cl- 100 mEq/L (97-110 mEq/L)
 Bicarbonate 30 mEq/L (22-26 mEq/L)
 BUN 40 mg/dL (8-25 mg/dL)
 SCr 0.8 mg/dL (0.7-1.3 mg/dL)
 Glucose 100 mg/dL (65-109 mg/dL)
 CXR: bilateral pleural effusions
26. What other tests would you order?
A. BNP
B. CMP
C. EKG
D. PTT & INR
E. Troponin
F. All the above
The labs you ordered came back.
 BNP = 650 pg/mL (< 100 pg/mL)
 ALT = 60 IU/L (7-25 IU/L)
 EKG – shows LVH
 PTT = 27 seconds (25-35 sec)
 INR = .9 (.8-1.2)
 Troponin = WNL
27. What is his NYHA Classification?
A. I
B. II
C. III
D. IV
E. V
28. What will use immediately to provide quick relief of his dyspnea?
A. Dobutamine
B. Furosemide
C. Lisinopril
D. Morphine
E. Nitroglycerin
29. What will you monitor on his therapy?
A. Dyspnea
B. Edema
C. Electrolytes
D. Renal function
E. Urine output
D.F. is a 78-yo female with fatigue, SOB & decreased exercise capacity; minimal
peripheral edema
PMH: HTN
PE: BP 165/85, HR 86 bpm
Echo: EF ≈ 50%
ECG: LVH
30. What will you treat her with first?
A. Amlodipine
B. Furosemide
C. Lisinopril
D. Metoprolol
E. Valsartan
J.M. is a 65-yo AAM who presents to the ED with worsening dyspnea on exertion. He
has had intermittent SOB for a week that abruptly worsened. He also complains of
occasional CP and nocturnal cough.
PMH: HTN, COPD, OA, CAD (MI w/stent 1 year ago), HF; angioedema w/lisinopril
SH: smoking x 40 y, occasional EtOH
Meds: atorvastatin, asa, clopidogrel, valsartan, metoprolol, furosemide, naproxen (x
1 month)
PE: BP 154/100 mm Hg, HR 88 bpm, RR 22 bpm, O2 sat 96% on room air; bilateral
rales, peripheral edema, JVD
Labs: sodium 135 mEq/L, potassium 4.5 mEq/L, BUN 15 mg/dL, SCr 2.3 mg/dL,
glucose 127 mg/dL, BNP 879 pg/mL
ECG: previous MI
CXR: interstitial edema
31. You administer 160 mg of furosemide IV and an hour later there is little change
in his clinical status. Urine Output is low. What is you next step?
A. Add metolazone
B. Dobutamine
C. Increase furosemide dose
D. Milrinone
E. Nesiritide
32. J.M. is stabilized, breathing much more easily, No JVD, CRX is clearing up. What
would you consider ADDING to his home medication regimen?
A. Carvedilol
B. Digoxin
C. Isosorbide dinitrate/hydralazine
D. Metolazone
E. Spironolactone
LECTURES 15 & 16 Arrhythmias
1. Which is NOT an effect of hyperkalemia on cardiac rhythm?
a. Reduced action potential
b. slowed conduction
c. Increased risk of digoxin toxicity
d. Decreased pacemaker rate
e. decreased pacemaker arryhthmogenesis
2. Which is NOT an effect of hypokalemia on cardiac rhythm?
a. prolonged action potential duration
b. increased pacemaker rate
c. increased pacemaker arrhythmogenesis
d. increased sensitivity to potassium channel agonists
3. What drug classes selectively block activated and inactivated channels but have
little effect on resting channels?
4. What are the 4 classes of antiarrhythmics?
5. You have a patient with an arrhythmia that you need to place on a drug that will
moderately block Na+ channels and ultimately prolong action potential duration
and increase effective refractory period. Which drug would you NOT choose?
a. Disopyramide
b. Propafenone
c. Procainamide
d. Quinidine
6. Class IA drugs also exhibit what other effects?
7. A 24 yo WF presents to the ER complaining of a “flip-flopping” feeling in her chest.
EKG reveals delta waves in the QRS complex. What would be the first drug you
would use to help resolve the symptoms?
a. Amiodarone
b. Propafenone
c. Procainamide
d. Quinidine
8. What is the active metabolite of the previously used drug and what is its function?
9. The 24 yo WF in the previous questions calls her cardiologist complaining of an
adverse effect of the drug prescribed. What would be the most likely adverse effect
associated with the prescribed drug. What other drug has this problem?
a. dry cough; lisinopril
b. myalgias; simvastatin
c. lupus-like syndrome; hydralazine
d. bradycardia; metoprolol
10. A patient was placed on a class IA agent in order to try and control his
arrhythmia. This patient called complaining of headache, dizziness, and tinnitus
(cinchonism) after he took an extra few pills when his “heart felt like it was going
crazy” the other night. What drug did this patient most likely overdose on that
cause these problems? What are other possible adverse effects of this drug?
a. Disopyramide; QT prolongation and torsades de pointe
b. Propafenone; Aggravate heart failure
c. Procainamide; Torsades de pointe
d. Quinidine; QT prolongation and torsades de pointe
11. A patient presents s/p MI in V-tach. You place him on a lidocaine drip to
hopefully control the heart rate back to normal sinus. What class is Lidocaine and
what is its MOA?
a. Class IA; moderate Na+ channel blocker
b. Class IB; Weak Na+ channel blockade and shorten AP duration
c. Class IC; Strong Na+ channel blockade and no effect on AP
d. Class ID; Complete Na+ channel blockade and no effect on AP or ventricular ERP
12. Which Class I drug is least cardiotoxic?
a. procainamide
b. flecainide
c. lidocaine
d. propafenone
13. A 25 yo WM presents to the ER with SVT. You use vagal maneuvers to get him
back in to sinus rhythm. You consult cardiology and they tell you to place him on a
Class IC agent. The patient continues that for life with minimal recurrences of SVT.
What drug would be most appropriate in this scenario?
a. procainamide
b. flecainide
c. lidocaine
d. propafenone
e. amiodarone
14. What is the MOA of the drug selected?
15. A 58 yo AAM presents to the ER with EKG that shows A-fib with rapid
ventricular response. You decide to use a Class 2 antiarrhythmic agent to control
the ventricular rate. What drug would you use?
a. esmolol
b. procainamide
c. verapamil
d. lidocaine
16. What scenario are the Class 2 agents contraindicated?
17. Which drug is NOT a class 3 agent?
a. Amiodarone
b. Dofetilide
c. Dronedarone
d. Glyburide
e. Sotalol
18. A 78 yo AAF presents to the ER with what appears to be A-fib on the EKG. You
order for a drug that has broad spectrum of activity but ultimately leads to
prolongation of QT interval. What drug did you order?
a. Amiodarone
b. Propafenone
c. Procainamide
d. Quinidine
e. Sotalol
19. Long-term use of the previously use drug can lead to what disease state?
20. What is a major contraindication in patients on the previously selected drug?
Drug interactions?
21. Which is NOT a major drug class that leads to QT prolongation?
a. Class 3 antiarrhytmics
b. Macrolides
c. Penicillins
d. Antipsychotics
22. In a-fib patients with iodine allergy what would be the BEST available option for
rhythm control?
a. Amiodarone
b. Propafenone
c. Procainamide
d. Quinidine
e. Dronedarone
23. What is problem with the previously chosen drug?
24. A 42 yo WF patient presents to the ER in atrial flutter with HR of 132. Patient
refuses DC cardioversion, so what would be a 1st-line agent for conversion back to
sinus rhythm?
a. Ibutilide
b. Dofetilide
c. Metoprolol
d. Propafenone
e. Procainamide
25. What Class 3 drug also exhibits class 2 effects and is an alternate to amiodarone
as DOC for A-fib?
a. Dofetilide
b. Propafenone
c. Procainamide
d. Quinidine
e. Sotalol
26. A 58 yo AAM presents to the ER with EKG that shows A-fib with rapid
ventricular response. What is DOC for rate control in this patient?
a. esmolol
b. procainamide
c. verapamil
d. lidocaine
27. Class 4 drugs are contraindicated in what cardiac state?
28. 45 yo WM presents to the ER in SVT. Vagal maneuvers were unsuccessful in
converting him to sinus rhythm. What is DOC in terminating SVT?
a. Ibutilide
b. Adenosine
c. Metoprolol
d. Propafenone
e. Procainamide
29. What is the previously selected drugs MOA?
30. A patient is placed on Disopyramide and 2 months later is in the ER for V-fib that
turns into torsades de pointes. What would be the BEST treatment option?
a. Sodium Chloride
b. Magnesium
c. Amiodarone
d. Sotalol
e. Potassium
31. What is the MOA of previous selected treatment?
32. What are the major drugs that should be avoided in patients with WPW?
33. What is the 3 step process in pharmacological management of atrial fibrillation?
34. A 77 yo WF with a history of HTN and GERD presents to the ER with A-fib. What
would be the CHA2DS2-VASc score and what would be appropriate therapy?
a. 2—no therapy
b. 3—oral anticoag therapy
c. 4—oral anticoag therapy
d. 5—SQ anticoag therapy
35. What would be DOC for use in this patient for anticoagulation?
a. dabigatran
b. aspirin
c. warfarin
d. rivaroxaban
36. A patient presents to the ER in atrial fibrillation with a HR of 105. What would
be the first line of treatment?
a. DC cardioversion
b. Give amiodarone
c. Give warfarin
d. Give diltiazem
37. A patient presents with sustained V-tach. You shock the patient back into sinus
rhythm. What would be the BEST option for therapy post cardioversion?
a. ventricular rate control
b. ventricular rhythm control
c. place an ICD
d. a and b
e. b and c
f. a and c
38. What is the most effective antiarrhythmic in cardiac arrest patients?
a. epinephrine
b. atropine
c. amiodarone
d. procainamide
e. lidocaine
39. A 22 yo WF presents to the ER with “elephant sitting on her chest” pressure and
shortness of breath. Chest Xray and labs are normal. EKG shows a couple of random,
bizarre wide QRS complexes that without looking at the monitor she points out
when they occur. What would be the best therapy for this patient?
a. DC cardioversion
b. Metoprolol
c. amiodarone
d. lorazepam
e. no therapy
40. I.H. a 62 yo WM, presents to the ER with complaints of chest discomfort. Physical
exam reveals an irregularly irregular rhythm with a HR averaging around 130 bpm.
What is the most appropriate treatment for this patient at this time?
a. adenosine
b. amiodarone
c. digoxin
d. metoprolol
41. H&P of I.H. reveals a history of HTN and T2DM. Which of the following agents
would be the most appropriate addition to this patient’s therapy?
a. amiodarone
b. dabigatran
c. digoxin
d. sotalol
e. warfarin
REMEMBER!!!!!
anti-arrhythmic classes.
SoBePoCa...
Class 1 sodium channel blockers
Class 2 beta blocker
Class 3 potassium channel blockers Class 4 Calcium channel blockers
Class 1a-Double Quarter Pounder (Disopyramide,
Quinidine, Procanamide)
Class 1b-[with] Lettuce Mayo (Lidocaine,
Mexiletine)
Class 1c-[and] Fries Please (Flecainide,
Propafenone)
Class 3-A Dumb Dog Isn't Scary (Amiodarone,
Dofetilide, Dronedarone, Ibutilide, Sotalol)