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

Lecture 1 (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 2 (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 3
1. Which patient has an increased risk for hypertension?
a. 25 yo WM
b. 45 yo Asian male
c. 68 yo WF
d. 68 yo AAF
2. What is the most common form of hypertension and how do you cure it?
3. What is the most common cause of secondary hypertension?
a. unknown
b. renovascular disease
c. pulmonary disease
d. hyperlipidemia
4. What are some of the other major causes of secondary hypertension?
5. What is primarily responsible for regulating blood pressure? How?
a. SNS and liver; effects atherosclerosis
b. PNS and kidneys; effect CO and PVR
c. SNS and kidneys; effect CO and PVR
d. PNS and liver; effects atherosclerosis
6. Increments of _____ mmHg in SBP or _____ mmHg DBP ________ the risk of
cardiovascular disease.
a. 10; 20; doubles
b. 15; 10; triples
c. 20; 5; triples
d. 20; 10; doubles
7. Higher blood pressure increases the risk of what aspects of CVD?
8. In patients with Stage 1 HTN + CV risk factors, lowering SBP by how much for 10
years will prevent one death for every 11 treated?
a. 5 mmHg
b. 12 mmHg
c. 15 mmHg
d. 20 mmHg
9. A 28 yo WF presents to your clinic for a new patient visit. Her blood pressure was
130/86. According to JNC-7 what is her blood pressure classification? Would you
start drug therapy?
a. normal; no
b. prehypertension; no
c. prehypertension; yes
d. stage 1 HTN; yes
e. stage 1 HTN; no
10. A 55 yo AAM with CKD presents to your clinic with a blood pressure of 168/82.
According to JNC-8 what is the blood pressure at which you would start
pharmacotherapy on this patient?
a. >120/80
b. >140/90
c. >150/90
d. >160/100
11. A 72 yo WF presents to the clinic with a BP log of pressures averaging around
158/98. Should you start pharmacotherapy? Why or why not?
12. According to the ALLHAT study, which drug class reduced fatal/nonfatal MI in
patients with HTN plus one other CV risk as well as chlorthalidone or amlodipine?
a. ACEIs
b. ARBs
c. Beta-blockers
d. thiazide-type diuretics
13. Which drugs are first-line choice for many patients with HTN?
a. ACEIs
b. ARBs
c. Beta-blockers
d. thiazide-type diuretics
14. What is the MOA of calcium channel blockers (CCBs) and where do they
primarily act?
15. What are the two classes of CCBs and the difference between the two?
16. Which drugs are more effective at lowering BP in caucasians? Africanamericans?
17. A 55 yo AAM with CKD presents to your clinic with a blood pressure of 168/82.
What should your regimen include in this type of patient?
18. A 43 yo WF presents to the clinic for BP follow up. BP last visit was 166/86. BP
this visit is 152/99. What treatment would you start this patient on?
a. none, record a BP log at home
b. TLC
c. TLC with monotherapy
d. TLC with two drug therapy
19. A 45 yo AAF with no compelling indications follows up on her stage 1
hypertension. The TLC modifications have not reduced her BP so you decide to start
therapy. Which would be the most appropriate first line treatment?
a. ACEI or ARB
b. ACEI or CCB
c. ACEI, CCB or ARB
d. ACEI, CCB, ARB, or Thiazide diuretic
20. A 52 yo WM with diabetes is newly diagnosed with HTN. What would be the
standard pharmacotherapy for this patient?
a. ACEI
b. Diuretic
c. CCB
d. Beta-blocker
21. A 47yo WM is s/p MI and newly diagnosed with HTN. What would be standard
pharmacotherapy for him? Choose the MOST appropriate answer.
a. ACEI
b. Diuretic
c. CCB
d. Beta-blocker
22. For patients with resistant HTN what drug can be helpful if added to
pharmacotherapy regimen?
23. What is resistant HTN?
24. What are factors of pseudoresistance?
25. What is the difference between hypertensive urgency/emergency?
26. A 60 yo WM presents to the ER with a headache and blood pressure of 200/126.
How should you manage this hypertensive emergency?
a. Reduce the BP 50% the first hour.
b. Reduce the BP 25% the first hour.
c. Reduce the BP as much as possible
27. In HTN emergencies what can excessive reductions in BP precipitate?
28. Which drug is used for most types of HTN emergencies?
a. Labetalol
b. Hydralazine
c. Lisinopril
d. Metoprolol
e. Nitroglycerin
29. Which drug is used in treating HTN associated with preeclampsia?
a. Labetalol
b. Hydralazine
c. Lisinopril
d. Metoprolol
e. Nitroglycerin
30. A 45 yo AAM presents to the ER with acute coronary ischemia and BP of
186/122. What drug should you use to control both problems?
a. Labetalol
b. Hydralazine
c. Lisinopril
d. Metoprolol
e. Nitroglycerin
LECTURE 4
1. Under what 3 conditions is renin released from the RAAS system?
2. What does ACEI stand for?
3. What is the MOA of ACEIs? Clinical effects?
4. Which of these is NOT an indication for ACEIs?
a. Hypertension
b. s/p MI
c. Heart failure
d. Peripheral arterial disease
e. Diabetes with early signs of renal impairment
5. A patient has been taking an ACEI for a few months and has developed a
COMMON adverse effect of the drug. What would that be?
a. hypokalemia
b. angioedema
c. dry cough
d. hypomagnesimia
6. What populations are at a greater risk of developing angioedema from taking an
ACEI?
7. A 55 yo AAM is on 20mg lisinopril daily for maintenance of his BP. He presents to
the ER with severe swelling of the tongue and lips. You decide to bypass the
tradition treatment and go for the expensive drug that is approved for hereditary
angioedema and resolves symptoms 19 hours sooner than traditional treatment.
What drug did you decide to administer?
a. Diphenhydramine
b. Epinephrine
c. Icatibant
d. Solu-Medrol
e. Famotidine
8. A 35 yo WF is on captopril, simvastatin, OCP (oral contraceptives), and naproxen
daily. Which drug will decrease efficacy of the ACEI?
a. captopril
b. simvastatin
c. OCP
d. naproxen
9. What are the contraindications for ACEIs?
10. What does ARB stand for?
11. What is the MOA of ARBs?
12. What is the major clinical difference between ACEI and ARB?
13. When would you choose an ARB over an ACEI?
14. What does DRI stand for?
15. You place a patient on aliskiren (Tekturna) for the maintenance of his BP. What
is the MOA of aliskiren?
a. allows cleavage of angiotensinogen
b. prevents cleavage of angiotensinogen
c. allows cleavage of angiotensin
d. prevents cleavage of angiotensin
16. What is the most common adverse effect of DRIs?
a. diarrhea
b. dry cough
c. fatigue
d. hypokalemia
17. Which of the following are safe to use in pregnancy?
a. Lisinopril
b. Valsartan
c. Aliskiren
d. All of the above
e. None of the above
18. A 45-yo with Type 2 DM was recently started on monotherapy for hypertension.
He has developed a persistent cough. Which of the following drugs is most likely
responsible for this side effect?
a. Aliskiren
b. Benazepril
c. Chlorthalidone
d. HCTZ
e. Irbesartan
19. Which of the following drugs selectively blocks angiotensin II receptors,
reducing vasoconstriction, aldosterone secretion and sodium reabsorption by the
proximal tubule?
a. Aliskiren
b. Losartan
c. None of the above
d. Ramipril
e. Spironolactone
20. Which characteristic(s) increase the risk of angioedema with ACEIs?
a. African-American
b. Diabetes mellitus
c. Obesity
d. Smoking
e. All of the above
21. C.M. is a 54-yo postmenopausal female with Type 2 DM and knee osteoarthritis,
for which she takes metformin and naproxen, respectively. Her BP readings on 2
occasions were 165/90 and 168/88. Which of the following regimens would you
begin?
a. TLC; recheck BP in 1 week
b. TLC + thiazide diuretic
c. TLC + ACEI
d. TLC + aliskiren
e. TLC + thiazide/ACEI combination
22. C.M. from the previous question…What labs would you order and what drug(s)
could you try in place of naproxen?
LECTURE 5
1. What is a sympatholytic?
2. What are the effects of alpha-1 adrenergic receptor antagonists?
3. A 45 yo WM presents with HAs, palpitations, diaphoresis, and sporadic HTN. The
patient has CT done and is diagnosed with pheochromocytoma. You decide to place
the patient on a non-selective alpha-adrenergic receptor antagonist until surgery
can be performed. Which drug would you place the patient on?
a. tamsulosin
b. phentolamine
c. phenoxybenzamine
d. terazosin
4. When giving a beta blocker with a non-selective alpha-adrenergic receptor
antagonist, what is the order of administration. Why?
5. What are the alpha1-selective antagonists?
6. What is the major adverse effect with giving an alpha1-selective antagonist?
7. Which is not an effect of long term use of alpha1-selective antagnoists?
a. salt retention
b. postural hypotension and syncope
c. water retention
d. cold extremities
8. What drugs should be avoided when taking an alpha1-selective antagonist and
why?
9. What is the general MOA of beta-blockers?
10. Do beta-blockers decrease BP in patients who are normotensive? What is their
effect during long-term administration to hypertensive patients?
11. When beta-blockers are given in patient with arrhythmias, what is the MOA?
a. decrease AV refractory period
b. increase AV refractory period
c. decrease SA refractory period
d. increase SA refractory period
12. How do beta-blockers affect ischemic heart disease?
13. What are two special pharmacological effects of b-blockers?
a. intrinsic stabilizing activity and membrane stabilizing activity
b. intrinsic sympathomimetic activity and membrane sympathomimetic activity
c. intrinsic stabilizing activity and membrane sympathomimetic activity
d. intrinsic sympathomimetic activity and membrane stabilizing activity
14. What is the primary use of beta-blockers?
15. What is not a CV adverse effect of beta-blockers?
a. bradycardia
b. cold extremities
c. hypotension
d. bronchoconstriction
e. exacerbate heart failure
16. What should you worry about with giving a beta blocker to a patient who has
asthma?
17. A patient presents to the ER following a syncopal episode. Blood glucose was
reported to be 35 in the field. On arrival patient is AAOx3. You ask the patient if
they felt pre-syncopal at all prior to the incident and they say no. You review the
medications and find the list provided: Naproxen-PRN, Zantac-BID, Metoprolol-QHS,
Simvastatin-QHS. Which medication could have masked the hypoglycemic
conditions and kept him from recognizing the oncoming syncopal spell?
a. Naproxen
b. Zantac
c. Metoprolol
d. Simvastatin
18. Patient who are poor _________ poor metabolizers can have significantly higher
plasma levels of metoprolol, carvedilol, and nebivolol.
a. CYP2D6
b. CYP2C19
c. CYP3A4
d. CYP2D1
19. A patient is following up for migraines. You decide to put the patient on a nonselective beta-blocker for prophylaxis. You decide to use a first generation drug.
Which is the best choice for the drug the patient was started on?
a. metoprolol
b. atenolol
c. propranolol
d. carvedilol
20. What are the adverse effects of non-selective beta-blockers?
21. A 56 yo WM is following up in your cardio clinic for his newly diagnosed CHF.
Upon discharge you decided to start him on a beta-blocker. Which is the DOC for
CHF and what generation is it?
a. carvedilol; 3rd gen
b. metoprolol succinate; 2nd gen
c. pindolol; 1st gen
d. atenolol; 2nd gen
22. A 31 yo WF presents to the ER with a BP of 176/100. What would be your best
choice of therapy in reducing the BP?
a. labetalol
b. metoprolol
c. nebivolol
d. esmolol
23. What are the MOA of nebivolol?
24. What kind of drug is clonidine? What is its MOA?
25. Which drug should NOT be used for hypertensive emergencies?
a. labetalol
b. hydralazine
c. clonidine
d. nicardipine
26. What is the previous DOC to treat HTN during pregnancy?
a. labetalol
b. hydralazine
c. metoprolol
d. methyldopa
27. What are the adverse effects of clonidine?
28. What is the major adverse effect to watch for with methyldopa?
LECTURE 6 & 7
1. Which is not one of the major lipids?
a. cholesterol
b. triglycerides
c. chylomicrons
d. phospholipids
2. J.H. is a 50 yo WM with an insignificant medical history except for smoking ½ ppd
for ~20 yrs. His father had an MI when he was 54 and his mother had an MI when
she was 72. From the information provided what is a modifiable risk factor in J.H.
history?
a. Male
b. 50 yo
c. smoking
d. father MI at 54
e. mother MI at 72
3. What is a significant secondary cause of hypertriglycermia?
a. hypothyroidism
b. diabetes mellitus
c. anorexia nervosa
d. malnutrition
4. What classification of CAD is mostly genetic?
a. LDL
b. HDL
c. Triglycerides
5. What classification of CAD is mostly affected by diet?
a. LDL
b. HDL
c. Triglycerides
6. What classification of CAD is mostly affected by exercise?
a. LDL
b. HDL
c. Triglycerides
7. A 32 yo AAM presents to the ER with “pain.” When asked to point to where it
hurts the patient continues to scream “PAAAAIN.” Once you realize you aren’t going
to get a decent history you decide to get labs and for some reason you order a
triglyceride level. Well that triglyceride level comes back at 1453 mg/dL. What
should your first thought as to diagnosis should be?
a. hepatitis
b. pancreatitis
c. appendicitis
d. acute MI
e. diverticulitis
8. What are the major risk factors that modify LDL goals?
9. According to National Cholesterol Education Program (NCEP) what should the
primary target of pharmacotherapy be?
a. LDL
b. HDL
c. Triglycerides
d. Total Cholesterol
10. What lab value has evidence showing that it may be a good test in improving
CAD outcomes in patients with 2 or more risk factors but low LDL?
a. ESR
b. Troponin
c. CKMB
d. CRP
e. FANA
11. What does TLC stand for?
12. What are the major changes in AHA lipid guidelines?
13. What are the 4 statin benefit groups focused on to reduce atherosclerotic
cardiovascular disease (ASCVD)?
14. Which drugs block the conversion of 3-hydroxyl-3-methyl-glutaryl coenzyme A
(HMG-CoA) to mevalonate (rate limiting step in de novo cholesterol synthesis)?
a. Ezetimibe
b. Bile acid-binding resins
c. statins
d. niacin
e. fibrates
15. The drugs from the previous question decrease LDL by how much (percent)?
16. Which HMG-CoA inhibitor is most potent upon initial dosing?
a. lovastatin
b. pitavastatin
c. atorvastatin
d. rosuvastatin
e. simvastatin
f. pravastatin
17. What are some other pharmacologic effects of statins?
18. What is a common adverse effect with statins? Contraindication?
19. High dose statins have a Level A recommendation in use for which of the
following?
a. secondary prevention in adults 75 yo and younger
b. primary prevention in adults with LDL 190 or higher
c. primary prevention in adults 40-75 yo with LDL 70-189 and estimated 10 yr risk
of CAD of 7.5% or higher
d. all the above
20. What is the recommended treatment for a patient who cannot tolerate high dose
statin therapy?
21. When is it appropriate to try nonstatin therapy?
22. Which statin has the lowest potential for drug interactions, but because of low
potency may not reach goal LDL?
a. Simvastatin
b. Atorvastatin
c. Pravastatin
d. Rosuvastatin
e. Lovastatin
23. What is the MOA of ezetimibe? What percent does it reduce LDL?
24. What is a common side effect of ezetimibe?
25. What is the MOA of bile acid sequestrants? What are its effects on LDL and TGs?
26. Which of these drugs is NOT a bile acid sequestrant?
a. colestipol
b. cilostazol
c. cholestyramine
d. colesevelam
27. What commonly used drugs do bile acid sequestrants reduce the bioavailability
of?
28. What is the MOA of Niacin (B3)?
29. What is an absolute adverse effect of niacin?
a. dry cough
b. angioedema
c. myalgias
d. cutaneous flushing and itching
30. What is the MOA of Fibrates?
31. Fibrates are indicated for what?
a. hyperlipidemia
b. hypernatremia
c. hyperlipoproteinemia
d. hypertensionemia
32. What effect do omega-3 fatty acids have on TG?
33. Which is NOT an adverse effect of omega-3 fatty acids?
a. fishy burp
b. nausea, GI discomfort
c. fatigue
d. prolonged bleeding time
34. What are two prescription omega-3 fatty acids and how are they used?
35. Which CETP inhibitor has not yet been withdrawn or halted?
a. torcetrapib
b. dalcetrapib
c. anacetrapib
36. What are CETP inhibitors supposed to be used for?
37. What do you need to monitor/emphasize during lipid therapy?
a. baseline labs
b. rechecking lipids ~6 weeks after starting
c. adverse effects
d. TLC effects and emphasize drug therapy is life-long
e. all the above
38. What is Homozygous familial hypercholesterolemia?
39. What is the MOA of Lomitapide? How is it metabolized?
40. What levels must you absolutely monitor in patients on lomitapide?
a. LFTs
b. Renal function
c. Blood counts
d. Troponins
e. CRP
41. What are the most common adverse effects in patient on lomitapide?
42. Lomitapide is contraindicated in what patients?
43. What are the adverse effects of mipomersen? Drug interactions?
44. What should you recommend for all patients with possibility of CAD?
45. What is the DOC for LDL lowering?
a. a. Ezetimibe
b. Bile acid-binding resins
c. HMG-CoA inhibitors
d. niacin
e. fibrates