WorksheetsCardio Exam 3 - Antiplatelets Austin
Total questions: 57
Worksheet time: 29mins
Name
Class
Date
1.
What are antiplatelets used for the treatment and prevention of
a)
coronary and cerebral arteries
b)
myocardial infarction
c)
stroke
2.
What are the classes of antiplatelets
a)
cyclooxygenase (COX) inhibitors (NSAIDs)
b)
phosphodiesterase inhibitors
c)
ADP receptor pathway inhibitors
d)
glycoprotein IIb-IIIa antagonists
3.
What are examples of cyclooxygenase (COX) inhibitors that work as antiplatelets
a)
aspirin
b)
NSAIDs
c)
dipyridamole
d)
cilostazole
e)
clopidogrel
4.
What are examples of phosphodiesterase (PDE) inhibitors that work as antiplatelets
a)
prasugrel
b)
ticagrelor
c)
dipyridamole
d)
cilostazole
e)
clopidogrel
5.
What are examples of ADP receptor pathway inhibitors that work as antiplatelets
a)
prasugrel
b)
ticagrelor
c)
dipyridamole
d)
cilostazole
e)
clopidogrel
6.
What are examples of glycoprotein IIb-IIIa antagonists that work as antiplatelets
a)
abciximab
b)
eptifibatide
c)
tirofiban<br />
d)
cilostazole
e)
clopidogrel
7.
What are some characteristics of the synthesis of eicosanoids
a)
derived from arachidonic acid
b)
local action
c)
short duration
d)
systemic action
e)
long duration
8.
What is the most important eicosanoid for clotting
a)
prostaglandins
b)
prostacyclin
c)
leukotrienes
d)
thromboxane<br />
9.
What is the physiological antagonist of thromboxane
a)
prostaglandins
b)
prostacyclin
c)
leukotrienes
d)
arachidonic acid
10.
COX1 synthesizes ___ in order to form clots. It is a potent vasoconstrictor and aggregation inducer
a)
prostaglandins
b)
prostacyclin
c)
leukotrienes
d)
thromboxane<br />
11.
Inhibition of COX1 will ___ platelet function
a)
increase
b)
decrease
c)
have no effect on
12.
When aspirin covalently binds to active site of COX1 and COX2, is it reversible or irreversible
a)
reversible
b)
irreversible
13.
What is the predominant isoform in platelets
a)
COX1
b)
COX2
14.
Other NSAIDs, besides aspirin, is effective as antiplatelets
a)
true
b)
false
15.
An ____ in cAMP leads to a ____ in platelet activation and aggregation
a)
increase, decrease
b)
increase, increase
c)
decrease, decrease
d)
decrease, increase
16.
Phophodiesterase (PDE) inhibitors ____ cAMP
a)
increase
b)
decrease
c)
does not effect
17.
What are some adverse effects associated with the PDE inhibitor, Dipyridamole
a)
GI upset with oral administration
b)
hypotension
c)
dizziness
d)
headache
e)
angina
18.
Which PDE inhibitor can be used IV or orally
a)
Dipyridamole
b)
Cilostazol
19.
Cilostazole (PDE inhibitor) should be reduced if used with what type of inhibitors
a)
CYP 2C9
b)
CYP 3A4
c)
CYP 1A1
d)
CYP 1A2
e)
CYP 2C19
20.
What is the PDE inhibitor, Cilostazol, contrainciated for
a)
heart failure
b)
hypertension
c)
arrhythmias
d)
hypotension
21.
P2Y12 adenosine diphosphate (ADP) receptor leads to
a)
platelet activation
b)
Gi coupled receptors that inhibit AC
c)
inhibition of platelet activation
22.
Inhibition of P2Y using ADP receptor pathway inhibitors will ___ platelet activation
a)
increase
b)
decrease
c)
does not effect
23.
Clopidogrel ___ binds to P2Y ADP receptors
a)
reversibly
b)
irreversibly
24.
Clopidogrel requires which CYP to be activated
a)
CYP 2C9
b)
CYP 3A4
c)
CYP 1A1
d)
CYP 1A2
e)
CYP 2C19
25.
Clopidogrel has a boxed warning for patients with ____ due to the potential of increased risk of CV events
a)
2C19 polymorphisms
b)
HTN
c)
HF
d)
HLD
26.
What are some boxed warnings of P2Y inhibitors, Prasugrel and Ticagrelor
a)
bleeding risk (avoid in pts with history of TIA/stroke)
b)
active bleeding
c)
severe hepatic impairment
d)
HF
27.
Glycoprotein (GP) IIb-IIIa antagonists prevent
a)
cross-linking
b)
aggregation
c)
platelet activation
d)
2C19 polymorhpisms
28.
What are examples of glycoprotein IIb-IIIa antagonists that are used parenterally and cannot be used concurrently
a)
abciximab
b)
eptifibatide
c)
tirofiban<br />
d)
cilostazole
e)
clopidogrel
29.
Abciximab binds to GPIIb-IIIa receptors
a)
reversibly
b)
irreversibly
30.
What are some contraindications of the GPIIb-IIIa antagonist, abciximab
a)
active internal bleeding, recent bleeding
b)
thrombocytopenia
c)
history of stroke (w/in last 2 years)
d)
recent trauma/surgery, severe/uncontrolled HTN
e)
use of oral anticoagulant within 7 days
31.
Eptifibatide binds to GPIIb-IIIa receptors
a)
reversibly
b)
irreversibly
32.
Tirofiban binds to GPIIb-IIIa receptors<br />
a)
reversibly
b)
irreversibly
33.
What are some characterstics of GPIIb-IIIa Antagonists Eptifibatide and Tirofiban
a)
Eptifibatide is a cyclic heptapeptide
b)
Tirofiban is a non-peptide antagonist
c)
used with aspirin and heparin
d)
additional warning for renal function and dialysis
34.
Fibrinolysis is initiated by activation of
a)
clotting cascade
b)
platelet activation
c)
aggregation
d)
cross-linking
35.
Plasmin digests
a)
fibrin
b)
fibrinogen
c)
factor V, factor VIII
d)
prothrombin
e)
factor XII
36.
Endogenous plasminogen activators are trypsin-like serine proteases
a)
true
b)
false
37.
What are some characteristics of the plasminogen activator steptokinase
a)
a protein produced by beta-hemolytic steptococci
b)
forms a stable 1:1 complex with plasminogen and exposes its active site
c)
acts as a catalyst that activates other plasminogen molecule
d)
specific and localized activity
38.
What are some limitations of the plasminogen activator streptokinase
a)
antigenic response
b)
forms a stable 1:1 complex with plasminogen and exposes its active site
c)
non-specific
d)
specific and localized activity
e)
non-localized activity
39.
Alteplaste is a ____ that is non-antigenic and has a more localized activity
a)
recombinant t-PA
b)
plasminogen activator
c)
GPIIb-IIIa antagonists
40.
Alteplaste binds to ___ formed thrombi with high affinity
a)
newly
b)
existing
c)
all
41.
What are some adverse effects associated with Alteplaste (Recombinant t-PA)
a)
high risk of bleeding
b)
many indication-specific restrictions
c)
many contraindications
d)
localized activity
42.
What are some antifibrinolytic drugs
a)
lysine analogues
b)
aminocaproic acid
c)
tranexamic acid
d)
tenecteplase<br />
e)
reteplase
43.
What are some characteristics of lysine analogue antifibrinolytics
a)
binds to lysine receptor site on plasminogen
b)
inhibit conversion to plasmin
c)
PO or IV administration
d)
bind to lysine receptor site on plasmin
e)
inhibit conversion to plasminogen
44.
What are some adverse effects of Lysine analogues of antifibrinolytics
a)
CV
b)
GI upset
c)
headache
d)
risk of vision changes
e)
seizures
45.
What are some ADRs of Transexamic Acid of antifibrinolytics
a)
CV
b)
GI upset
c)
headache
d)
risk of vision changes
e)
seizures
46.
What does low molecular weight heparin (LMWHs) effect and is it available as an oral or IV agent
a)
Thrombin
b)
Factor Xa
c)
oral
d)
IV
47.
What does direct thrombin inhibitors effect and is it available as an oral or IV agent
a)
Thrombin
b)
Factor Xa
c)
oral
d)
IV
48.
What does Vitamin K antagonists effect and is it available as an oral or IV agent
a)
Thrombin
b)
Factor Xa
c)
oral
d)
IV
49.
What does unfractionated heparin (UFH) effect and is it available as an oral or IV agent
a)
Thrombin
b)
Factor Xa
c)
oral
d)
IV
50.
What do selective factor Xa inhibitors effect and is it available as an oral or IV agent
a)
Thrombin
b)
Factor Xa
c)
oral
d)
IV
51.
What is the reversal agent for low molecular weight heparin (LMWHs) and a PK feature associated with it
a)
protamine sulfate
b)
renal dose adjustment
c)
idarucizumab
d)
acidic environment required for absorption
e)
vitamin K
52.
What is the reversal agent for direct thrombin inhibitiors and a PK feature associated with it
a)
protamine sulfate
b)
renal dose adjustment
c)
idarucizumab
d)
acidic environment required for absorption
e)
vitamin K
53.
What is the reversal agent for Vitamin K antagonists and a PK feature associated with it
a)
delayed onset of action
b)
renal dose adjustment
c)
idarucizumab
d)
acidic environment required for absorption
e)
vitamin K
54.
What is the reversal agent for unfractionated heparin (UFH) and a PK feature associated with it
a)
protamine sulfate
b)
nonlinear elimination kinetics
c)
andexanet alfa
d)
oral agent interactions- CYP3A4 and P-glycoprotein inhibitor/inducer
55.
What is the reversal agent for selective factor Xa inhibitors and a PK feature associated with it
a)
protamine sulfate
b)
nonlinear elimination kinetics
c)
andexanet alfa
d)
oral agent interactions- CYP3A4 and P-glycoprotein inhibitor/inducer
56.
Which of the following medications reversibly inhibits platlet function
a)
aspirin
b)
clopidogrel
c)
prasugrel
d)
tirofiban
57.
Tranexamic acid was developed to have greater antifibrinolytic activity in vitro. How can the difference in activity be explained chemically
a)
electronic effects (withdrawing group on transexamic acid)
b)
electronic effects (donating group on aminocaproic acid)
c)
steric effects (aminocaproic acid and has greater steric bulk)
d)
steric effects (tranexamic acid has less conformational flexibility)
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