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Pharm 2 final > Bleeding Disorders and Assessment part 2 > Flashcards

Bleeding Disorders and Assessment part 2 Flashcards

1
Q

clopidogrel (Plavix)

A

oral prodrug metabolized by liver

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2
Q

what percent of clopidogrel (Plavix) absorbed becomes the active form?

A

15%

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3
Q

what is the half life of clopidogrel (Plavix)?

A

8 hours

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4
Q

how long does the effect of clopidogrel (Plavix) last for?

A

platelet’s lifetime

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5
Q

what does clopidogrel (Plavix) bind irreversibly to?

A

P2Y12 ADP receptor on platelet surface

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6
Q

clopidogrel (Plavix) can be used as a secondary prophylaxis in patients with what?

A
  1. myocardial infarction
  2. stroke
  3. peripheral arterial disease
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7
Q

combo of clopidogrel (Plavix) and aspirin was shown to be superior over aspirin alone after what?

A
  1. acute coronary event
  2. percutaneous coronary interventions (PCI)
  3. coronary stent placement
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8
Q

T/F: clopidogrel (Plavix) is more expensive than aspirin

A

true

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9
Q

cons of using clopidogrel (Plavix)

A

results in more clinical bruising/bleeding than aspirin

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10
Q

T/F: like aspirin, clopidogrel (Plavix) is generally safe to continue through most oral surgery

A

true

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11
Q

other P2Y12 blockers

A
  1. ticlopidine (Ticlid)
  2. Prasugrel (Efient)
  3. direct acting, reversible inhibitors
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12
Q

T/F: ticlopidine (Ticlid) has at least 5 metabolic pathways and less variable clinical response

A

true

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13
Q

ticlopidine (Ticlid) has a more rapid onset than what?

A

clopidogrel

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14
Q

dipyramidole has antiplatelet effect by inhibition of what?

A

phosphodiesterase

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15
Q

what happens when dipyramidole inhibits phosphodiesterase?

A

results in intracellular accumulation of cyclic AMP

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16
Q

dipyramidole is a potent inhibitor of what?

A

platelet aggregation in vitro

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17
Q

what are the most potent inhibitors of platelet aggregation?

A

glycoprotein receptors IIb/IIIa inhibitors

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18
Q

glycoprotein receptors IIb/IIIa inhibitors are competitive inhibitors for what?

A

fibrinogen binding to platelet IIb/IIIa receptor

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19
Q

coumadin

A

oral vitamin K antagonist

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20
Q

what does coumadin block?

A

essential vitamin K-dependent carboxylation of coagulation factors II, VII, IX and X

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21
Q

what happens when coumadin blocks coagulation factors II, VII, IX, and X?

A
  1. results in formation of biologically inactive proteins

2. decreases the coagulant activity of these factors in plasma

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22
Q

effect of coumadin is a fxn of what and not the drug itself?

A

fxn of the decay in the concentration of the coagulation factors

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23
Q

half life of vitamin K-dependent coagulation factors

A

ranges from 6 to 60 hours

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24
Q

the full effect of coumadin is delayed for how long?

A

2-3 days

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25
full restoration of normal coagulation after termination of coumadin therapy requires how long?
at least 3-5 days
26
dose-effect relationship of coumadin varies considerably due to what?
1. binding to palsma albumin 2. variable vitamin K intake 3. variable clearance by the liver
27
what is used to monitor effect of coumadin?
PT/INR
28
what is the most important side effect of coumadin treatment?
bleeding
29
rare coumadin-induced skin necrosis may occur and is usually associated with what?
protein C deficiency
30
Pradaxa (dabigatran)
direct thrombin inhibitor
31
factor Xa inhibitors
1. Xarelto (rivaroxaban) 2. Eliquis (apixaban) 3. Savaysa (edoxaban)
32
why do the new oral anticoagulants (i.e. direct thrombin inhibitor and factor Xa inhibitors) not require regular lab monitoring unlike coumadin?
not affected by diet, liver fxn, etc
33
onset time of new oral anticoagulants (i.e. direct thrombin inhibitor and factor Xa inhibitors)
rapid onset of 2-3 hours
34
half life of new oral anticoagulants (i.e. direct thrombin inhibitor and factor Xa inhibitors)
short half-life of 8-12 hours
35
T/F: new oral anticoagulants (i.e. direct thrombin inhibitor and factor Xa inhibitors) are comparable to coumadin when it comes to stroke prevention
true
36
risk of extracranial bleeding from new oral anticoagulants (i.e. direct thrombin inhibitor and factor Xa inhibitors) when compared to coumadin is what?
the same (or possibly higher)
37
T/F: the new oral anticoagulants (i.e. direct thrombin inhibitor and factor Xa inhibitors) have no routine testing of effect available
true
38
T/F: little is known about safety of surgery with new oral anticoagulants (i.e. direct thrombin inhibitor and factor Xa inhibitors)
true, neither is benefit of local hemostatic measures
39
how long should patient on new oral anticoagulants (i.e. direct thrombin inhibitor and factor Xa inhibitors) discontinue drug before oral surgery?
1-2 days (longer in renal patients)
40
anticoagulant reversal of dabigatran (Pradaxa)
Idarucizamab (Praxbind)
41
when is Idarucizamab (Praxbind) indicated?
for emergency surgery or life-threatening bleeding
42
T/F: patients who used Idarucizamab (Praxbind) may remain in normal coagulation state in 24 hours
true
43
what are the risks of using Idarucizamab (Praxbind)?
exposure to underlying thrombotic disease consequence
44
there is a serious risk of using Idarucizamab (Praxbind) in what type of patients?
patients with hereditary fructose intolerance
45
how is heparin given?
parenterally
46
what is heparin?
a large mixture of glycosaminoglycans
47
what is heparin isolated from?
intestines or lungs of pig, cow or other cattle
48
heparin binds to what?
antithrombin III
49
heparin potentiates inhibition of what?
factors IIa (thrombin) and Xa
50
T/F: heparin has a dose-dependent half-life
true
51
the anticoagulant effect of heparin may be highly variable so what is required?
frequent laboratory monitoring usually by PTT
52
in special conditions such as during surgery, what may be used to monitor heparin?
activated clotting time (ACT)
53
what is required when heparin is used as prophylaxis against thrombosis?
frequent subcutaneous injections
54
how are low molecular weight heparins (LMWHs) given?
parenterally usually subcutaneous
55
T/F: low molecular weight heparins (LMWHs) have predictable inter- and intraindividual bioavailability and clearance
true, it reduces the need for frequent laboratory monitoring and frequent dose adjustments
56
why is it advantageous to have low molecular weight heparins (LMWHs) have much longer half-life compared to unfractionated heparin?
when stable anticoagulation is required over a longer period of time
57
what type of drug are pentasaccharides?
parenteral drugs
58
what is the prototype of pentasaccharides?
Arixtra (fondaparinux)
59
when is pentasaccharides indicated?
for DVT (deep venous thrombosis) prophylaxis or DVT/PE (pulmonary embolism) treatment
60
what are pentasaccharides?
synthetic compounds that exert antithrombin-dependent exclusive inhibition of factor Xa
61
what is the most frequent adverse effect of heparin or heparin derivative treatment?
bleeding
62
heparin-induced thrombocytopenia (HIT)
an immunological response to heparin characterized by thrombocytopenia and thromboembolism
63
when does heparin-induced thrombocytopenia (HIT) occur?
at 5-7 days after initial exposure to heparin but may be an immediate complication if patient has received heparin previously
64
why might alternative anticoagulant therapy consist of treatment with hirudin or heparinoids but not with coumarin derivatives?
because it may cause skin necrosis
65
long term use of heparin has been associated with what?
osteopenia
66
what are plasminogen activators derived from?
exogenous sources like streptokinase
67
what is the most important side effect of thrombolytic treatment?
bleeding
68
what are some signs that might point to a defect in the coagulation system?
1. abnormal bruising 2. petechiae 3. splenomegaly
69
preoperative screening in patients with signs or symptoms of a bleeding tendency includes what?
1. platelet count 2. PTT 3. PT/INR
70
if an abnormality in primary hemostasis is suspected, which laboratory tests are then done?
1. platelet fxn is tested | 2. von Willebrand factor measured
71
PT/INR (prothrombin time test)
a mixture of calcium and thromboplastin is added to citrated blood and the time to clot formation is measured
72
what does the PT value reflect?
the coagulation ability of the TF-VIIa coagulation pathway
73
what is tissue thromboplastin a mixture of?
TF and phospholipid membrane fragments
74
what is normal PT averages?
12± 2 seconds
75
how is INR defined?
the ratio of the patient's PT to the individual laboratory standard
76
what does INR provide?
a standardized way to report the prothrombin time relative to control
77
PT in prolonged by deficiencies in what?
1. factor VII 2. X 3. factor V 4. prothrombin 5. fibrinogen
78
what is PT/INR used for?
to monitor oral anticoagulation with coumadin-type drugs
79
T/F: PT/INR is useful for NOACs
false, not useful
80
what does aPTT (activated partial throboplastin time) measure?
the slower "intrinsic" pathway
81
normal PTT times require presence of which coagulation factors?
1. I 2. II 3. V 4. VIII 5. IX 6. X 7. XI 8. XII
82
deficiencies in which coagulation factors will not be detected with the PTT test?
factors VII or XIII
83
prolonged aPTT (activated partial throboplastin time) may indicate what?
1. use of heparin 2. antiphospholipid antibody 3. coagulation factor deficiency 4. sepsis 5. presence of antibodies against coagulation factors
84
what is considered the gold standard for platelet function analysis?
platelet aggregometry (PAA)

Pharm 2 final (10 decks)

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