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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
Q

full restoration of normal coagulation after termination of coumadin therapy requires how long?

A

at least 3-5 days

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26
Q

dose-effect relationship of coumadin varies considerably due to what?

A
  1. binding to palsma albumin
  2. variable vitamin K intake
  3. variable clearance by the liver
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27
Q

what is used to monitor effect of coumadin?

A

PT/INR

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28
Q

what is the most important side effect of coumadin treatment?

A

bleeding

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29
Q

rare coumadin-induced skin necrosis may occur and is usually associated with what?

A

protein C deficiency

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30
Q

Pradaxa (dabigatran)

A

direct thrombin inhibitor

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31
Q

factor Xa inhibitors

A
  1. Xarelto (rivaroxaban)
  2. Eliquis (apixaban)
  3. Savaysa (edoxaban)
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32
Q

why do the new oral anticoagulants (i.e. direct thrombin inhibitor and factor Xa inhibitors) not require regular lab monitoring unlike coumadin?

A

not affected by diet, liver fxn, etc

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33
Q

onset time of new oral anticoagulants (i.e. direct thrombin inhibitor and factor Xa inhibitors)

A

rapid onset of 2-3 hours

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34
Q

half life of new oral anticoagulants (i.e. direct thrombin inhibitor and factor Xa inhibitors)

A

short half-life of 8-12 hours

35
Q

T/F: new oral anticoagulants (i.e. direct thrombin inhibitor and factor Xa inhibitors) are comparable to coumadin when it comes to stroke prevention

36
Q

risk of extracranial bleeding from new oral anticoagulants (i.e. direct thrombin inhibitor and factor Xa inhibitors) when compared to coumadin is what?

A

the same (or possibly higher)

37
Q

T/F: the new oral anticoagulants (i.e. direct thrombin inhibitor and factor Xa inhibitors) have no routine testing of effect available

38
Q

T/F: little is known about safety of surgery with new oral anticoagulants (i.e. direct thrombin inhibitor and factor Xa inhibitors)

A

true, neither is benefit of local hemostatic measures

39
Q

how long should patient on new oral anticoagulants (i.e. direct thrombin inhibitor and factor Xa inhibitors) discontinue drug before oral surgery?

A

1-2 days (longer in renal patients)

40
Q

anticoagulant reversal of dabigatran (Pradaxa)

A

Idarucizamab (Praxbind)

41
Q

when is Idarucizamab (Praxbind) indicated?

A

for emergency surgery or life-threatening bleeding

42
Q

T/F: patients who used Idarucizamab (Praxbind) may remain in normal coagulation state in 24 hours

43
Q

what are the risks of using Idarucizamab (Praxbind)?

A

exposure to underlying thrombotic disease consequence

44
Q

there is a serious risk of using Idarucizamab (Praxbind) in what type of patients?

A

patients with hereditary fructose intolerance

45
Q

how is heparin given?

A

parenterally

46
Q

what is heparin?

A

a large mixture of glycosaminoglycans

47
Q

what is heparin isolated from?

A

intestines or lungs of pig, cow or other cattle

48
Q

heparin binds to what?

A

antithrombin III

49
Q

heparin potentiates inhibition of what?

A

factors IIa (thrombin) and Xa

50
Q

T/F: heparin has a dose-dependent half-life

51
Q

the anticoagulant effect of heparin may be highly variable so what is required?

A

frequent laboratory monitoring usually by PTT

52
Q

in special conditions such as during surgery, what may be used to monitor heparin?

A

activated clotting time (ACT)

53
Q

what is required when heparin is used as prophylaxis against thrombosis?

A

frequent subcutaneous injections

54
Q

how are low molecular weight heparins (LMWHs) given?

A

parenterally usually subcutaneous

55
Q

T/F: low molecular weight heparins (LMWHs) have predictable inter- and intraindividual bioavailability and clearance

A

true, it reduces the need for frequent laboratory monitoring and frequent dose adjustments

56
Q

why is it advantageous to have low molecular weight heparins (LMWHs) have much longer half-life compared to unfractionated heparin?

A

when stable anticoagulation is required over a longer period of time

57
Q

what type of drug are pentasaccharides?

A

parenteral drugs

58
Q

what is the prototype of pentasaccharides?

A

Arixtra (fondaparinux)

59
Q

when is pentasaccharides indicated?

A

for DVT (deep venous thrombosis) prophylaxis or DVT/PE (pulmonary embolism) treatment

60
Q

what are pentasaccharides?

A

synthetic compounds that exert antithrombin-dependent exclusive inhibition of factor Xa

61
Q

what is the most frequent adverse effect of heparin or heparin derivative treatment?

62
Q

heparin-induced thrombocytopenia (HIT)

A

an immunological response to heparin characterized by thrombocytopenia and thromboembolism

63
Q

when does heparin-induced thrombocytopenia (HIT) occur?

A

at 5-7 days after initial exposure to heparin but may be an immediate complication if patient has received heparin previously

64
Q

why might alternative anticoagulant therapy consist of treatment with hirudin or heparinoids but not with coumarin derivatives?

A

because it may cause skin necrosis

65
Q

long term use of heparin has been associated with what?

A

osteopenia

66
Q

what are plasminogen activators derived from?

A

exogenous sources like streptokinase

67
Q

what is the most important side effect of thrombolytic treatment?

68
Q

what are some signs that might point to a defect in the coagulation system?

A
  1. abnormal bruising
  2. petechiae
  3. splenomegaly
69
Q

preoperative screening in patients with signs or symptoms of a bleeding tendency includes what?

A
  1. platelet count
  2. PTT
  3. PT/INR
70
Q

if an abnormality in primary hemostasis is suspected, which laboratory tests are then done?

A
  1. platelet fxn is tested

2. von Willebrand factor measured

71
Q

PT/INR (prothrombin time test)

A

a mixture of calcium and thromboplastin is added to citrated blood and the time to clot formation is measured

72
Q

what does the PT value reflect?

A

the coagulation ability of the TF-VIIa coagulation pathway

73
Q

what is tissue thromboplastin a mixture of?

A

TF and phospholipid membrane fragments

74
Q

what is normal PT averages?

A

12± 2 seconds

75
Q

how is INR defined?

A

the ratio of the patient’s PT to the individual laboratory standard

76
Q

what does INR provide?

A

a standardized way to report the prothrombin time relative to control

77
Q

PT in prolonged by deficiencies in what?

A
  1. factor VII
  2. X
  3. factor V
  4. prothrombin
  5. fibrinogen
78
Q

what is PT/INR used for?

A

to monitor oral anticoagulation with coumadin-type drugs

79
Q

T/F: PT/INR is useful for NOACs

A

false, not useful

80
Q

what does aPTT (activated partial throboplastin time) measure?

A

the slower “intrinsic” pathway

81
Q

normal PTT times require presence of which coagulation factors?

A
  1. I
  2. II
  3. V
  4. VIII
  5. IX
  6. X
  7. XI
  8. XII
82
Q

deficiencies in which coagulation factors will not be detected with the PTT test?

A

factors VII or XIII

83
Q

prolonged aPTT (activated partial throboplastin time) may indicate what?

A
  1. use of heparin
  2. antiphospholipid antibody
  3. coagulation factor deficiency
  4. sepsis
  5. presence of antibodies against coagulation factors
84
Q

what is considered the gold standard for platelet function analysis?

A

platelet aggregometry (PAA)

Pharm 2 final (10 decks)

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