Fitzy coag practice questions

21 terms by dejlea 

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6/4/2012

A 65-year-old man is brought to the emergency room 30 minutes after the onset of right-sided weakness and aphasia (difficulty speaking). Imaging studies ruled out cerebral hemorrhage as the cause of his acute symptoms of stroke. Prompt administration of which of the following drugs is most likely to improve this patient's clinical outcome?
1. abciximab
2. alteplase
3. factor VIII
4. streptokinase
5. vit K

2. alteplase as tPA's only one approved for stroke

abciximab: antiplatelet- anitbodythat is glycoprotien receptor antagonist, won't act to destroy clot
alteplase: tPA
facotr VIIIL coagulant
streptokinase: thrombolytic
vit K: coagulant

side notes:
have 3 hr window w/ stroke
imaging needed to rule out hemorrhagic stroke as don't want to make worse w/ thrombolytic


Controlled clinical trials have shown that alteplase improves the clinical outcome in patients with ischemic stroke if given within 3 hours after the onset of symptoms. Similar trials of streptokinase resulted in unacceptably high rates of bleeding. Glycoprotein Iib/IIIa receptor inhibitors like abciximab have not been tested in ischemic stroke. Vitamin K and factor VIII may actually worsen the patient's outcome. The answer is 2.

A 65-year-old man is brought to the emergency room 30 minutes after the onset of right-sided weakness and aphasia (difficulty speaking). Imaging studies ruled out cerebral hemorrhage as the cause of his acute symptoms of stroke. Over the next 2 days, the patient's symptoms resolved completely. To prevent a recurrence of this disease, the patient is most likely to be treated indefinitely with:
1. aminocaproic acid
2. aspirin
3. enoxaprin
4. urokinase
5. warfarin

2. aspirin

aminocaproic acid: coagulant
asprin:antiplatelet, possibility
enoxaparin: LMW herparin, probably not a possiblity
urokinase: thrombolytic, not for long term
warfarin: anticoagluant, long term treatment

key points: pt symptoms resolved completely, talking prevention of recurrence, indefinitely so should be thinking of anti-platelet drug instead of anticoagulant

Aspirin, an irreversible inhibitor of platelet cyclooxygenase, has been shown to prevent recurrence of transient ischemic attacks and ischemic stroke. The answer is 2.

A 58-year-old business executive is brought to the emergency room 2 hours after the onset of severe chest pain during a vigorous tennis game. She has a history of poorly controlled mild hypertension and elevated blood cholesterol but does not smoke. ECG changes confirm the diagnosis of myocardial infarction. The decision is made to attempt to open her occluded artery. Conversion of plasminogen to plasmin is brought about by:
1. Aminocaproic acid
2. Heparin
3. Reteplase
4. Warfarin
5. Lepirudin

reteplase

aminocarpoic acid: coagulant
heparin: acts on activated factors on coag cascade
reteplase: tPA
warfarin: works directly on coag cascade
lepirudin: direct rhombin inhibitor

Heparin and warfarin are anticoagulants that affect activation or formation of proteins in the clotting cascade. Lepirudin is an inhibitor of thrombin, and aminocaproic acid is an inhibitor, not an activator, of fibrinolysis and the conversion of plasminogen to plasmin. Reteplase is the only thrombolytic drug listed. The answer is 3.

A 58-year-old business executive is brought to the emergency room 2 hours after the onset of severe chest pain during a vigorous tennis game. She has a history of poorly controlled mild hypertension and elevated blood cholesterol but does not smoke. ECG changes confirm the diagnosis of myocardial infarction. The decision is made to attempt to open her occluded artery. If a fibrinolytic drug is used for treatment of this woman's acute myocardial infarction, the adverse drug effect that is most likely to occur is:
1. acute renal failure
2. development of antiplatelet antibodies
3. encephalitis secondary to liver dysfunction
4. hemorrhagic stroke
5. neutropenia

hemorrhagic stroke: most likely complciation- always think of! esp w/ fibrinolytic drugs

The most common serious adverse effect of the fibrinolytics is bleeding, especially in the cerebral circulation. The fibrinolytics do not usually have serious effects upon the renal, hepatic, or hematologic systems. Unlike heparin, they do not induce antiplatelet antibodies. However, streptokinase and anistreplase contain bacterial proteins and may induce formation of inactivating antibodies or even severe allergic reactions. The answer is 4.

A 56-year-old man is admitted to the coronary care unit with myocardial infarction. You would like to attempt dissolution of the coronary occlusion with a thrombolytic agent. Recent medical history includes a streptococcal throat infection (1 month previously) and hemorrhage from a tooth socket following a difficult extraction (6 months previously). His problem list includes renal parenchymal disease. He has been taking aspirin, one 325 mg tablet daily, for the last 6 years. Which of the following is most correct?
1. d/t Hx of strep infection, alteplase carries high risk of anaphylaxis.
2 d/t Hx of bleeding, all thrombolytics are contraindicated
3. d/t Hx of strep infxn, streptokinase will be less effective than would otherwise be expected.
4. thrombolytics would be extremely hazardous in pt d/t recent consumption of aspirin.
5. urokinase shouldn't be used in pt w/ Hx of renal disease

3. d/t Hx of strep infxn, streptokinase will be less effective than would otherwise be expected.

1. streptokinase doesn't have high anaphylaxis risk
2. pt doesn't really have a significant bleeding Hx
4. pt taking aspiring 325 mg/day for past 6 yrs- not super high dose, overstates drug interaction problem, not reason not to give anti-thrombolytic
5. urokinase: derived

A previous strep infection could have led to the development of anti-streptokinase antibodies, which would make streptokinase less effective (3 is correct). The strep infection would not affect tPAs (1 is incorrect). This patient does not have a history of bleeding (a difficult extraction would be expected to result in bleeding, and it was 6 months ago; 2 is incorrect). This patient is taking aspirin to try to prevent clotting (can tell by the dosage), and it's obviously not working, so this isn't a reason not to give a thrombolytic (4 is incorrect). Urokinase is produced by the kidney, and may be lower in a patient with renal disease. This fact isn't a reason to not give urokinase as a thrombolytic (5 is incorrect).

Low molecular weight heparins (LMWH) are distinct from unfractionated heparin in several ways. Which of the following is the primary target of LMWH?
1. antihrombin III
2. factor IIa
3. factor VII
4. factor Xa
5. factor II, VII, IX, and X

1. antihrombin III

indirect thrombin inhibitor
as result of it IIa and 10 a will be decreased but not direct action as opposed to where it is in direct thrombin inhibitors

The correct answer is A. LMWHs act predominantly by activating antithrombin III.

Answer B is incorrect. Factor IIa, or thrombin, is the enzyme that catalyzes the final step of the clotting cascade, the formation of fibrin. Thrombin is a vitamin K-dependent factor that is not influenced by low-molecular-weight heparin.

Answer C is incorrect. Factor VII is part of the extrinsic pathway and is one of the vitamin K-dependent factors.

Answer D is incorrect. LMWHs act predominantly on Xa, whereas unfractionated heparin targets both Xa and IIa. A major advantage of using LMWHs over unfractionated heparin is that there is no need for monitoring of APTT.

Answer E is incorrect. Warfarin blocks the activation of vitamin K-dependent factors II, VII, IX, and X.

A patient develops severe thrombocytopenia in response to treatment with unfractionated heparin and still requires parenteral anticoagulation. The patient is most likely to be treated with:
1. abciximab
2. lepirudin
3. urokinase
4. vit K2
5. plasminogen

2. lepirudin

if pt being treated w/ anti-coagulant, make sure switch to another anti-coagulant-- so remember to know classes of drugs
1. is antiplatelet
3-5 are thrombolytics

Direct thrombin inhibitors such as lepirudin, dabigatran and argatroban provide parenteral anticoagulation similar to that achieved with heparin, but the direct thrombin inhibitors do not induce formation of antiplatelet antibodies (the cause of severe HIT). The correct answer is 2.

67 yo woman presents w/ pain in left thigh muscle. Duplex ultrasonography indicates presence of DVT in affected limb. Decision made to treat w/ enxoaparin. Relative to regular heparin, enoxaparin
1. can be used w/o monitoring pt's aPTT
2. has shorter duration of action
3. less likely to have teratogenic effect
4. more likely to be given IV
5. more likely to cause thrombosis and thrombocytopenia

1. can be used w/o monitoring pt's aPTT

Enoxaparain is a low-molecular-weight (LMW) heparin. LMW heparins have a longer half-life than standard heparin and a more consistent relationship between dose and therapeutic effect. Enoxaparin is given subcutaneously, not intravenously. It is less—not more—likely to cause thrombosis and thrombocytopenia. Neither LMW heparins nor standard heparin are teratogenic. The aPTT is not useful for monitoring the effects of LMW heparins. The correct answer is 1.

67 yo woman presents w/ pain in left thigh muscle. Duplex ultrasonography indicates presence of DVT in affected limb. If pt has marked resistance to heparin, she is most likely to be treated with:
1. abciximab
2. antithrombin III
3. plasminogen
4. urokinase
5. vit K

2. antithrombin III

if doesn't work w/ heparin have to work indirectly w/ antithrombin III

all other options excpet plasminogen are class switching
doesn't work on plasminogen

Heparin's anticlotting effect is mediated by acceleration of the action of endogenous antithrombin III, a protease that inactivates clotting factors. Patients with genetic deficiencies in antithrombin III are resistant to heparin and prone to thrombosis. Antithrombin III isolated from pooled human plasma is available for use in such patients. The correct answer is 2.

Pt in coronary care unit has been receiving warfarin for 2 wks. As result of this Tx, the pt will probably have:
1. reduced plasma factor II activity
2. reduced plasma facotr VIII activity
3. reduced plasma plasminogen actiivty
4. increased tissue plasminogen activator
5. increased platelet adenosine stores

1. reduced plasma factor II activity

remember warfarin works on 2,7,9,10

Warfarin decreases the synthesis of vitamin K dependent clotting factor zymogens (II, VII, IX, and X). The correct answer is 1.

The graph shows plasma conc of free warfarin as fxn of time for pt treated w/ 2 other drugs on daily basis at constant dosage starting at times shown. What is the most liely eplanation for observed changes in warfarin conc?
1. B displaces warfarin from plasma proteins: C displaces warfarin from tissue biding sites
2. B inhibits hepatic metabolism of warfarin, C displaces B from tissue-binding sites
3. B stimulates hepatic metabolism of warfarin; C displaces warfarin from plasma protein
4. B increased renal clearance of warfarin; C inhibits hepatic metabolsim of B

3. B stimulates hepatic metabolism of warfarin; C displaces warfarin from plasma protein

to give warfarin the conc goes up and reaches steady state
give drug B and warfarin conc goes down

A drug that increases metabolism (clearance) of the anticoagulant lowers the steady-state plasma concentration (both free and bound forms), whereas one that displaces the anticoagulant increases the plasma level of the free form only until elimination of the drug has again lowered it to the steady-state level. The correct answer is 3.

Which of the following drugs has no effect on prothrombin but increased the likelihood of bleeding in pts who are also taking warfarin?
1. carbamazepine
2. cholestyramine
3. naproxen
4. rifampin
5. vit k

3. naproxen

what are the pharmacokinetic and pharmacodynamic interactions w/ prothrombin? Has no effect of factor II, acting in synergistic way to increase likelihood of bleeding. So what has pharmacodynamic interactions with warfarin?
1. affects metab
2. affects resorption
3. only on that's left the pharmcodynamically interacts
4. affects metab
5. vit K decreased activity

Warfarin reduces the synthesis of prothrombin and several other clotting factors. Carbamazepine and rifampin interfere with this action by increasing the metabolism of warfarin. Cholestyramine decreases the oral absorption of warfarin and other acidic drugs. Vitamin K is the antidote to excessive effects of warfarin. Antiplatelet drugs such as naproxen enhance the anticoagulant effects of warfarin. The correct answer is 3.

58 yo business executive rbough to ER 2 hrs after onset of severe chest pain during vigorous tennis gamel. has Hx of poorly controlled mild hyprtension and elevated blood cholesterol loeve but doesn't smoke. ECG changes confirm the Dx of myocardial infarction. The decision is made to attempt to oepn ehr occluded artery. IF pt undergoes percutaneous coronary procedure and placement of stent in coronary blood vessel, she may be given abciximab. The mechanism of anciximab's anticlotting action is
1. Activation of antithrombin III
2. Blockade of posttranslational modification of clotting factors
3. Inhibition of thromboxane production
4. Irreversible inhibition of platelet ADP receptors
5. Inhibition of glycoprotein IIb/IIIa receptors

1. activation of antithrombin III- heparin
2. blockade of posttranslational modification of clotting
3. factors- anti-coagulant- warfarin
4. inhibition of thromboxane- aspirin
5. irreversible inhibition of platelet ADP receptors

Abciximab is an inhibitor of the glycoprotein IIb/IIIa receptor, an integrin on the surface of platelets that serves as a key regulator of platelet aggregation. Glycoprotein IIb/IIIa receptor antagonists help to prevent platelet-induced occlusion of coronary stents. The correct answer is 5.

Pt being treated w/ antiplatelet drug exhibits symptoms consistent w/ transient thrombotic thrombocypopenic purpura. Which of the following drugs is she most likely taking:
1. abciximab
2. aminocaproic acid (EACA)
3. heparin
4. ticloplidine
5. warfarin

abciximab - think hypersensitivity, confusion, infections

There are only 2 antiplatelet drugs in the list: abciximab and ticloplidine. The most unique symptom of ticloplidine is transient thrombotic thrombocytopenic purpura.

A 28-year-old woman comes to her physician concerned about an excessive amount of bleeding from her gums when she brushes her teeth. Laboratory results show an increased partial thromboplastin time and increased bleeding time, but are otherwise unremarkable. Which of the following treatments is the least risky and will most likely alleviate this patient's symptoms?
1. cryoprecipitate
2. factor VIII concentrate
3. vit K
4. LMW heparin
5. protamine sulfate

1. cryoprecipitate

vit K and protamine- antidotes to warfarin and heparin- not given as coagulants on their own, pt has von Willebrand so need to give cryoprecipitate

The correct answer is A. This woman suffers from von Willebrand's disease, the most common inherited bleeding disorder; it results from a defective form or overall deficiency of vWF. vWF has two functions: it serves as the ligand for platelet adhesion to a damaged vessel wall, and it also is the plasma carrier of factor VIII. Due to platelet dysfunction and lack of a carrier for factor VIII, the unique lab finding in this disease consists of an increased bleeding time and an increased partial thromboplastin time. Cryoprecipitate is the precipitate that remains when fresh frozen plasma is thawed. It contains sufficient normal vWF to correct the bleeding dyscrasia. In addition to prolonged bleeding from mucosal surfaces as in this patient, other symptoms include easy bleeding and skin bleeding. While some clinicians do not use cryoprecipitate because of the possible risk of virus transmission, cryoprecipitate obtained from a well-screened donor may be a viable treatment option.

Answer B is incorrect. Factor VIII concentrate is used to treat individuals with hemophilia A, an inherited condition that results in factor VIII deficiency.

Answer C is incorrect. Vitamin K can be used to reverse the effects of warfarin, a vitamin K antagonist that inhibits vitamin K-dependent clotting factors. It will not correct a vWF deficiency.

Answer D is incorrect. LMWH is an anticoagulant that acts predominantly on factor Xa. This patient is in need of a procoagulant rather than an anticoagulant. LMWH can be administered subcutaneously. One advantage of LMWH over heparin is that the partial thromboplastin time does not need to be routinely monitored with this drug.

Answer E is incorrect. Protamine sulfate is used for reversal of heparinization. It is a positively charged molecule that acts by binding to heparin, a negatively charged molecule. Protamine would have no therapeutic benefit for this patient.

A patient with von Willebrand's disease is scheduled for minor dental surgery. Which of the following drugs would be the most appropriate prophylactic treatment?
A. Aminocaproic acid
B. Aprotinin
C. Desmopressin acetate
D. Phytonadione
E. Protamine sulfate

This question tests: the treatment of bleeding disorders and agents that reverse the actions of heparin and the oral anticoagulants.

While all of these drugs are procoagulant, desmopressin acetate is the agent used to increase factor VIII activity in patients with mild hemophilia A or von Willebrand's disease who are going to undergo minor surgery (C is the correct answer). Aminocaproic acid and aprotinin are fibrinolytic inhibitors that are used for life-threatening complications and as antagonists to fibrinolytic agents (tPA and streptokinase, respectively). Phytonadione (vitamin K) is a warfarin antagonist, while protamine sulfate is a heparin antagonist.

A patient is being released from the hospital following a myocardial infarction, and is being transitioned to 2-6 months of warfarin therapy. He is currently taking amiodarone (an antiarrythmic drug), atorvastatin (an antihyperlipidemic) and nafcillin (to treat a Staphylococcus infection acquired in the hospital). He routinely drinks grapefruit juice for breakfast. Using the accompanying drug interaction table as a guide, which of the following interactions is MOST LIKELY to occur?
A. Atorvastatin increasing the efficacy of warfarin.
B. Amiodarone increasing the efficacy of atorvastatin.
C. Grapefruit juice increasing the efficacy of warfarin.
D. Amiodarone increasing the efficacy of nafcillin.
E. Atorvastatin increasing the efficacy of warfarin.
F. Nafcillin increasing the efficacy of atorvastatin.

This question tests: use of cytochrome P450 tables, as well as testing whether you know the active enantiomer of warfarin.

All of these drugs (+ grapefruit juice) interact with CYP3A4. Only atorvastatin and R-warfarin are substrates of CYP3A4 (eliminating D), and R-warfarin is inactive, meaning that only the efficacy of atorvastatin can be affected (eliminating A,C and E). Nafcillin is an inducer of CYP3A4, and would reduce the activity of substrates (eliminating F). Amiodarone and grapefruit juice are inhibitors of CYP3A4, and would increase the efficacy of any substrate, including atorvastatin (so the correct answer is B).

Identify the target for warfarin.
A. plasminogen
B. plasmin
C. factors II, VII, IX and X
D. factors IIa, VIIa, IXa and Xa
E. factors V and VIII
F. factors Va and VIIIa
G. factors II, IX, X and XI
H. factors IIa, IXa, Xa and Xia

This question tests: define how drugs interact with coagulant and fibrinolytic pathways.

Fibrinolytic drugs target the conversion of plasminogen to plasmin. Drotrecogin alfa targets factors Va and VIIIa. Heparin activates antithrombin III to destroy IIa, IXa, Xa and XIa. Warfarin prevents the generation of vitamin K-dependent zymogens (i.e., II, VII, IX and X NOT IIa, VIIa, IXa and Xa). The correct answer is C.

Upon infusion of an anti-platelet drug, a patient goes into anaphylactic shock. What drug is the MOST likely to have caused this?
A. Abciximab
B. Acetylsalicylic acid
C. Clopidogrel
D. Dipyridamole
E. Eptifibatide
F. Ticlopidine

This question tests: side effects of anti-platelet drugs.

Monoclonal antibodies are most likely to cause hypersensitivity reactions. The correct answer is A: Abciximab.

Compared to heparin, warfarin is MORE likely to:
A. cause a hematoma upon injection.
B. produce an immediate hypothrombic response.
C. cause a transient thrombocytopenia.
D. produce effective anticoagulation in vitro
E. have teratogenic effects.

This tests: the differences between heparin and warfarin.

Heparin is given IV; warfarin is oral. Heparin's effects are immediate; warfarin has a delayed hypothrombic response (~ 1 week). A major side effect of heparin is a transient thrombocytopenia (HIT). Heparin is the effective in vitro anticoagulant. Warfarin can cause chondrodysplasia punctata and hemorrhagic disorders in infants born to mothers taking the drug during the first trimester of pregnancy. The answer is E.

All thrombolytic drugs:
A. are recombinant forms of human enzymes.
B. have long half-lives.
C. are widely used, because they are cheap and effective.
D. are most effective when used shortly after the onset of symptoms.
E. work exclusively to degrade plasmin found within a clot.

This question tests: common and distinguishing characteristics of thrombolytics.

Despite its name, streptokinase is not an enzyme, and it is derived from bacteria (i.e., it is not human). Thrombolytics have very short half-lives, have restricted use and are expensive. They work by promoting the conversion of plasminogen to plasmin, causing the degradation of fibrin. They are most effective when used less than 6 hours after the onset of symptoms (answer D is correct).

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