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Transcript of coagulation1-VI-qnz
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1-3. A 58-year-old business executive is brought to the
emergency department 2 h 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.
1. Conversion of plasminogen to plasmin is acceleratedby
(A) Aminocaproic acid
(B) Heparin
(C) Lepirudin
(0) Reteplase
(E) Warfarin
Al
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2. 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
(A) Acute renal failure
(B) Development of antiplatelet antibodies
(C) Encephalitis secondary to liver dysfunction
(0) Hemorrhagic stroke
(E) Neutropenia
3. If this patient undergoes a percutaneous coronary
angiography procedure and placement of a stent in
a coronary blood vessel, she may be given eptifi-
batide. The mechanism of eptifibatide anticlotting
action is
(A) Activation of antithrombin III
(B) Blockade of posttranslational modification of
clotting factors
(C) Inhibition of thromboxane production
(0) Irreversible inhibition of platelet ADP receptors
(E) Reversible inhibition of glycoprotein lIb/IlIa
receptors
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4. The following graph shows the plasma
concentration of free warfarin as a function of time
in weeks for a patient who was treated with 2 other
agents, drugs B and C, on a daily basis at constant
dosage starting at the times shown. The most
accurate explanation for the observed changes in
warfarin concentration is that
(A) Drug B displaces warfarin from plasma proteins;
drug C displaces warfarin from tissue binding sites
(B) Drug B inhibits hepatic metabolism of warfarin;
drug C displaces drug B from tissue binding sites
(C) Drug B stimulates hepatic metabolism of warfarin;
drug C displaces warfarin from plasma protein
(D) Drug B increases renal clearance of warfarin;
drug C inhibits hepatic metabolism of drug B
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5-7. A 65-year-old man is brought to the
emergency department 30 min after the onset of
right-sided weak ness and aphasia (difficulty
speaking). Imaging studies ruled out cerebral
hemorrhage as the cause of his acute symptoms of
stroke.
5. Prompt administration of which of the following
drugs is most likely to improve this patient's clinical
outcome?
(A) Abciximab
(B) Alteplase
(C) Factor VIII
(D) Streptokinase
(E) Vitamin K
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6. 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
(A) Aminocaproic acid
(B) Aspirin
(C) Enoxaparin
(D) Lepirudin
(E) Warfarin
7. If the patient is unable to tolerate the drug
identified in Question 6, he may be treated with
clopidogrel. Relative to ticlopidine, clopidogrel
(A) Has a shorter duration of action
(B) Is less likely to cause neutropenia
(C) Is more likely to induce antiplatelet antibodies
(D) Is more likely to precipitate serious bleeding
(E) Will have a greater antiplatelet effect
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or heparin b
b
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8-9. A 67-year-old woman presents with pain in her
left thigh muscle. Duplex ultrasonography indicates
the presence of deep vein thrombosis (DVT) in the
affected limb.
8. The decision was made to treat this woman with
enoxaparin. Relative to unfractionated heparin,
enoxaparin
(A) Can be used without monitoring the patient's
aPTT
(B) Has a shorter duration of action
(C) Is less likely to have a teratogenic effect
(D) Is more likely to be given intravenously
(E) Is more likely to cause thrombosis and throm-
bocytopenia
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active parrial thromboblasm time !!
a
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9. During the next week, the patient was started on
warfarin and her heparin was discontinued. Two
months later, she returned after a severe
nosebleed.Laboratory analysis revealed an INR
(international normalized ratio) of7.0 (INRvalue in
such awarfarin treated patient should be 2.5-3.5).
To prevent severe hemorrhage, the warfarin should
be discontinued and this patient should be treated
immediately with(A) Aminocaproic acid
(B) Desmopressin
(C) Factor VIII
(D) Protamine
(E) Vitamin x,K
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10. 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
(A) Abciximab
(B) Aprotinin
(C) Lepirudin
(D) Plasminogen
(E) Vitamin K2
ANSWERS
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1. Reteplase is the only thrombolytic drug listed.
Heparin and warfarin are anticoagulants that affect
activation or formation of clotting factors. Lepirudin
is a direct inhibitor of thrombin, and aminocaproic
acid is an inhibitor, not an activator, of the conver-
sion of plasminogen to plasmin. Th e answer is D.
2. The most common serious adverse effect of the
fibrolytics is bleeding, especially in the cerebral
circulation. The fibrinolytics do not usually have
serious effects on the renal, hepat ic, or
hematologic
SKILL KEEPER ANSWERS:
TREATMENT OF ATRIAL
FIBRILLATION (SEE
CHAPTERS 13 AND 14)
t , The padrenoceptor-blocking drugs(class lI ;eg,
propranolol,acebutolol)and calciumchannel -
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blockingdrugs(class IV; eq , verapamil, diltiazem)
areusefulfor treating atrial fibrillation because
theyslowatrioventricular (AV) nodal conduction
and therebyhelpcontrol ventricularrate.Digoxin
isalsosometimes usedbecause it increases the
effective refractoryperiodin AVnodal tissue and
decreases AVnodal conductionvelocity.
2. With warfarin, one isalwaysconcernedabout
pharmacodynamic and pharmacokinetic drug
interactions.Noneof these antiarrhythmic
drugsare likely to cause a pharmacodynamic
interaction with warfarin. However, many other
drugs inhibit cytochromeP450 enzymes and
increasewarfarin'santithrombotic effect.
Patientstaking suchdrugsusuallyneed to
decrease their doseofwarfarin.
systems. Unlike heparin, they do not induce
anti platelet antib odies. The answer is D.
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3. Eprifibatide is a reversible inhibitor of
glycoprotein
lIb/lIla, a protein on the surface of platelets that
serves as a key regulator of platelet aggregation.
Glycoprotein IIb/lIla receptor antagonists help pre-vent platelet-induced occlusion of coronar y stents.
The answer is E.
4. A drug that increases metabolism (clearance) of
the
anticoagulant will lower the steady-state plasma
concentration (both free and bound forms ),
whereas one that displaces the anticoagulant will
increase the plasma level of the free form only until
elimination of the drug has again lowered it to the
steady-state level.The answer is C.
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5. Alteplase improves the clinical outcome in
patients
with ischemic stroke if given within 3 h after the
onset of symptoms, after ruling out hemorrhagic
stroke. Use of streptokinase results in unacceptably
high rates of bleeding. Glycoprotein IIb/lIla recep-
tor inhibi tors like abciximab have not been testedin
ischemic stroke. The answer is B.
6. Aspirin, an irreversible inhibitor of platelet
cyclooxygenase, prevents recurrence of TlAs and
ischemic stroke. The answer is B.
7. Ticlop idine and clopidogrel have similar mecha-
nisms of action and therapeutic efficacy. The key
difference between these 2 drugs is that clopidogrel
is less likely to cause hematologic adverse effects
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(neutropenia, TTP) and, therefore, does not require
rout ine monitoring of blood cell counts during
therapy. The answer is B.
8. Enoxapar in is an LMW heparin. LMW heparins
have a longer half-life than standard hepar in and a
more consistent relationship between dose and
therapeutic effect. Enoxaparin is given subcuta-
neously, not intravenously. It is less, not more,
likely to cause thrombosis and thrombocytopenia.
Neither LMW heparins nor stand ard heparin are
teratogenic . The aPTT is not useful for monitoring
the effects of LMW heparins. The answer is A.
9. The elevated INR indicates excessive ant
icoagula-
tion with a high risk of hemorrhage. Warfarin
should be discontinued and vitamin K1 administered
to accelerate formation of vitamin K-dependent
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factors. The answer is E.
10. Direct thrombin inhibitors such as lepirudin and
argatroban provide parenteral anticoagulation simi-
lar to that achieved with heparin , but the direct
thrombin inhibitors do not induce formation of
antiplatelet antibodies. The answer is C.