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Hem/Onc > hemostasis pharmacology and transfusion therpay > Flashcards

hemostasis pharmacology and transfusion therpay Flashcards

1
Q

major blood group systems

A

ABO
Rh

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2
Q

3 pre-transfusion testing

A
  1. typing - ensures ABO/Rh compatibility
  2. antibody screen - tests for unexpected antibodies
  3. crossmatch - tests patient’s serum against prospective unit
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3
Q

Type testing determines the ABO and Rh phenotype of ____ blood

A

recipients

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4
Q

how to perform a type and screen test?

A
  1. mix recipient’s blood with type O that contains major antigens of other blood group systems
  2. observe for agglutination
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5
Q

when do you only order a cross-match test?

A

when there is a high likelihood that patient will receive PRBCs

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6
Q

what do you use during an emergency setting with not enough time to type or match blood?

A

use O-

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7
Q

3 reasons why we use transfusion therapy

A
  1. replace acute blood loss
  2. oxygen delivery
  3. morbidity and mortality
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8
Q

who do we recommend transfusion for?

A

hgb <6 g/dL - transfusion recommended except in exceptional circumstances

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9
Q

assessment post-transfusion hgb lvl can be performed as early as ?

A

15 mins

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10
Q

1 unit of PRBCs should increase hgb ___ in avg sized adults

A

1 g/dL

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11
Q

prior to non-emergency transfusions, what must you obtain?

A

signed informed consent

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12
Q

transfusion reactions occur when?

A
  1. during transfusion
  2. within 24 hrs
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13
Q

what is the most common sign of a transfusion reaction?

A

febrile non-hemolytic reactions

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14
Q

what is the top 2 causes of death from transfusion reaction

A
  1. circulatory overload
    - CHF, renal failure more at risk
  2. transfusion related acute lung injury
    - smokers, asthma more at risk
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15
Q

5 types of transfusion products

A
  1. whole blood
  2. packed RBC (PRBC)
  3. fresh frozen plasma (FFP)
  4. cryoprecipitate
  5. platelets
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16
Q

what type of transfusion product provides O2-carrying capacity and volume expansion and commonly used during settings of massive hemorrhage

A

whole blood

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17
Q

what type of transfusion product increases the oxygen-carrying capacity in anemic pts

A

PRBC

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18
Q

3 modifications of RBCs to prevent reactions

A
  1. leukocyte reduced - reduces risk of immunologically-mediated effects
  2. irradiated - reduces graft-vs-host disease (GVHD)
  3. washed - reduces complications associated with infusion of proteins in residual plasma in red cell concentrates
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19
Q

what contains platelets and proteins (procoagulant and anticoagulant factors)

A

plasma

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20
Q

what 6 components are contained in fresh frozen plasma (FFP)

A
  1. coagulation factors
  2. fibrinogen
  3. antithrombin
  4. albumin
  5. protein C
  6. protein S
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21
Q

why is FFP the most commonly used plasma product?

A

can correct deficiencies of any of the circulating coagulation factors

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22
Q

main advantage of cryoprecipitate

A

allows vWF, factor VIII, factor XIII, and fibrinogen to be replaced using a much smaller volume

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23
Q

main advantage of factor concentrates

A

replaces specific factor deficiencies with minimal volume ONLY (no extra proteins)

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24
Q

4 indications for transfusion of PLT in critically ill pt that may be therapeutic or prophylactic

A
  1. PLT <10k - prevents hemorrhage
  2. PLT <50k
    - actively bleeding
    - scheduled for invasive procedure
    - qualitative intrinsic PLT disorder
  3. PLT <100k
    - CNS injury
    - multisystem trauma
    - neurosurgery
  4. normal PLT
    - active bleeding
    - PLT dysfunctions - congenital PLT disorder, chronic aspirin use, uremia
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25
Q

each unit of transfused PLT should increase the PLT count by ?

A

5-10k

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26
Q

4 hemostasis promoting agents

A
  1. protamine sulfate
  2. vit K
  3. desmopressin
  4. thrombin
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27
Q

neutralizes heparin and could result in severe hypotensive or anaphylactoid-like reactions (BBW)

A

protamine sulfate
reverses anticoagulant effect of heparin

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28
Q

dosage of protamine sulfate

A

depends on dosage of heparin

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29
Q

what is the reversal agent for warfarin (coumadin)

A

vitamin K (phytonadione)

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30
Q

dosage and route of vit K depends on:

A
  1. severity of bleeding
  2. INR
  3. procedure planned
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31
Q

MOA of desmopressin (DDAVP)

A

increases plasma level of vWF, factor VIII, and tPA = shortened activated partial thromboplastin time (aPTT) and bleeding time

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32
Q

indication for desmopressin and what must you monitor

A

hemostasis
- restrict fluid intake
- monitor sodium levels

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33
Q

MOA of topical thrombin

A

converts fibrinogen to fibrin directly at site

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34
Q

indication for topical thrombin

A

hemostasis whenever oozing blood and minor bleeding

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35
Q

contraindications for topical thrombin

A
  1. sensitivity to components of bovine origin
  2. massive bleeding
  3. large vessels
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36
Q

3 classes of antithrombotic drugs

A
  1. antiplatelet
  2. anticoagulant
  3. fibrinolytic agents
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37
Q

general indication for anticoagulants

A

prevent or treat clots!

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38
Q

contraindications for anticoagulants (3)

A
  1. bleeding
  2. impaired renal function
  3. allergic
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39
Q

4 parenteral anticoagulants

A
  1. heparin (unfractionated)
  2. low-molecular-weight heparin (LMWH)
  3. bivalirudin (angiomax)
  4. argatroban (acova)
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40
Q

MOA of unfractionated heparin

A

binds to antithrombin (III) = no activation of factor Xa and thrombin

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41
Q

no dosage adjustment is necessary for who when taking unfractionated heparin

A

renal patients

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42
Q

when on unfractionated heparin, you must monitor:

A

activated partial thromboplastin time (aPTT)
order daily CBC, monitor signs of bleeding

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43
Q

4 SE of unfractionated heparin

A
  1. bleeding
  2. thrombocytopenia
  3. osteoporosis
  4. elevate levels of transaminases
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44
Q

7 contraindications for unfractionated heparin

A
  1. HIT
  2. hypersensitivity
  3. active bleeding
  4. hemophilia (inherited bleeding disorder in which the blood does not clot properly)
  5. significant thrombocytopenia
  6. purpura
  7. severe HTN
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45
Q

what is HIT?

A

heparin-induced thrombocytopenia
induces immune antibody response resulting in PLT clearance and may also induce hypercoagulable state

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46
Q

when can HIT occur?

A

any dose, schedule, and route
more common in females

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47
Q

what is the most common manifestation of HIT

A

thrombocytopenia
a platelet count drop of >50% of baseline is typical

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48
Q

typical onset of HIT occurs ? after the initiation of heparin

A

5-10 d
takes 5-7 d to return to baseline following withdrawal

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49
Q

what is the most common thrombi in HIT and where is it most common

A

venous
sites: leg veins, cardiac vessels, small venules of skin

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50
Q

5 signs of suspected HIT

A
  1. new onset of thrombocytopenia <150k
  2. drop in PLT of +50% from prior value
  3. venous/arterial thrombosis
  4. necrotic skin lesions at injection site
  5. acute systemic reactions
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51
Q

what is the 4Ts scoring system for assessing HIT

A

1-3 = low
4 or 5 = intermediate
6-8 = high

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52
Q

how do you manage HIT

A
  1. STOP heparin
  2. start anticoagulation with a non-heparin anticoagulant
  3. long-term oral anticoagulation (warfarin) with bridging drug (lovenox)
    (do not give platelet transfusion)
53
Q

lovenox

54
Q

enoxaparin

55
Q

MOA of LMWH

A

enhance inhibition of factor Xa by AT III = less direct inhibition of Xa and virtually no direct inhibition of thrombin

56
Q

contraindication for LMWH

A

renal impairment/ESRD
reduced dosing with CrCl <30

57
Q

monitoring for LMWH

A

not necessary most of the time
recommended in:
- pregnancy
- CrCl <30
- morbid obesity

58
Q

SE of LMWH

A

same as heparin but less common
- bleeding
- HIT
-osteoporosis

59
Q

what is recommended over heparin?

A

LMWH
LMWH is pregnancy cat. B
heparin is pregnancy cat. C

60
Q

what are the pros and cons of LMWH over heparin?

A

advantages:
- better bioavailability and longer half-life
- dose-independent CL
- predictable anticoagulant response
- lower risk of heparin-induced thrombocytopenia
- lower risk of osteoporosis
consequences:
- can be given SQ 1-2x daily for both prophylaxis and treatment
- simplified dosing
- coagulation monitoring is unnecessary in most patients
- safer tan heparin for short/long term
- safer than heparin for extended administration

61
Q

what is often used as a bridging drug?

62
Q

when should bridging should be done?

A

before and after surgery or invasive procedures in a pt already on warfarin with the following circumstances:
1. embolic stroke within past 3 months
2. previous embolic stroke or VTE during interruption of chronic anticoagulation
3. mechanical heart valve
4. A Fib with high stroke risk

63
Q

MOA of argatroban

A

direct, highly-selective thrombin inhibitor
reversibly binds to active thrombin site = inhibits fibrin formation

64
Q

Dose reduction of argatroban with who? how do you adjust dosing?

A

liver impairment
measure aPTT to adjust dose

65
Q

onset of argatroban is ____

66
Q

indications for argatroban

67
Q

what is the most severe SE of argatroban

68
Q

MOA of bivalirudin

A

direct, highly-selective thrombin inhibitor
reversibly binds to the active thrombin site

69
Q

CL of bivalirudin

A

renally
must reduce dosing with renal impairment

70
Q

indications for bivalirudin

A

alternative to heparin in pt underoging percutaneous coronary intervention (PCI), esp hx of HIT

71
Q

2 oral anticoagulants

A
  1. warfarin
  2. DOACs
72
Q

what is a vitamin K antagonist

73
Q

MOA of warfarin

A

inhibits vit K oxide reductase complex subunit I = inhibits factors II, VII, IX and X

74
Q

when on warfarin, you must monitor ___ for dosage adjustments

A

PT/INR
no dosage adjustments with renal impairment

75
Q

what is the pregnancy risk factor of warfarin

A

preg cat D for those with mechanical heart valve and X for all others

76
Q

indications for warfarin

A
  1. prophylaxis and tx for thromboembolic disorders (DVT/PE)
  2. embolic complications arising from afib or cardiac valve replacement
77
Q

major SE of warfarin

78
Q

dietary interactions of warfarin

A
  1. alcohol - avoid!!
    - binge drinking - decreases metabolism of warfarin, increases PT/INR
    - chronic daily alc - increases metabolism, decreases PT/INR
  2. foods
    - rich in vit K - can decrease effects of warfarin
    - vit E - can increase
    - cranberry juice - can increase
    (maintain a consistent diet)
79
Q

dabigatran (pradaxa)

80
Q

rivaroxaban

81
Q

apixaban

82
Q

edoxaban

83
Q

MOA of dabigatran (pradaxa)

A

inhibits thrombin
direct thrombin inhibitor

84
Q

indications for DOACs

A
  1. stroke prevention in:
    - nonvalvular afib
    - DVT/PE
    - DVT/PE prophylaxis after hip/knee arthroplasty
85
Q

what is given to pts on dabigatran (pradaxa) to reverse anticoagulant effects for emergency surgery/urgent procedures or in life-threatening or uncontrolled bleeding

A

praxbind (idarucizumab)

86
Q

MOA of rivaroxaban (xarelto)

A

inhibits factor Xa

87
Q

why are DOACs more convenient to administer than warfarin

A

given in fixed doses without routine coagulation monitoring
no monitoring required for dosage adjustment

88
Q

what is given to pts on rivaroxaban (xarelto) to reverse anticoagulant effects for emergencies

89
Q

MOA of apixaban (eliquis)

A

inhibits factor Xa

90
Q

pts on apixaban (eliquis) should not take with _____

A

grapefruit juice
avoid cyp3A4 inhibitors

91
Q

what is given to pts on apixaban (eliquis) to reverse anticoagulant effects during emergencies

92
Q

MOA of edoxaban (savaysa)

A

inhibits factor Xa

93
Q

DOACs dosing are reduced with ?

A

renal impairment

94
Q

Main SE of DOACs

95
Q

MOA of aspirin

A

inhibits COX-1 production
- enzyme in biosynthesis of thromboxane A2

96
Q

what irreversibly acetylates COX enzymes

97
Q

when taking clopidogrel, what should you avoid?

A

other drugs that inhibit CYP2C19
- omeprazole
- esomeprazole
can reduce effects of clopidogrel

98
Q

MOA of clopidogrel (plavix)

A
  1. inhibit ADP pathway of PLT
  2. irreversibly blocks ADP receptor (P2Y12)
    requires metabolic activation
99
Q

MOA of prasugel (effient)

A

irreversibly blocks ADP receptor (P2Y12)
requires metabolic activation

100
Q

contraindication for prasugrel (effient)

A

hx of TIA or CVA

101
Q

what irreversibly blocks ADP receptor (P2Y12) and triggers activation of GPIIb/IIIa receptor complex = reduces platelet aggregation

A

ticlopidine (ticlid)

102
Q

SE of ticlopidine

A

hematologic rxns:
- neutropenia
- agranulocytosis
- thrombotic thrombocytopenia purpura (TTP)
- aplastic anemia

103
Q

MOA of ticagrelor (brilinta)

A

reversibly and non-competitively binds to ADP P2Y12 receptor on platelets = prevents ADP-mediated activation of the GPIIb/IIIa receptor complex = reduces platelet aggregation
does NOT require metabolic activation

104
Q

MOA of cangrelor (kengreal)

A

reversibly and non-competitively binds to ADP P2Y12 receptor on platelets = prevents ADP-mediated activation of the GPIIb/IIIa receptor complex = reduces platelet aggregation

105
Q

what is the onset of cangrelor (kengreal)

106
Q

MOA of eptifibatide (integrilin), Abciximab (reopro)

A

GPIIb/IIa receptor inhibitor = blocks receptors = inhibiting
PLT aggregation and activation

107
Q

SE of eptifibatide (integrilin), Abciximab (reopro)

A
  1. bleeding
  2. thrombocytopenia
    - immune mediated
108
Q

major SE platelet aggregation inhibitors

109
Q

what do you use to breakdown thrombi in a life-threatening setting or massive thrombi

A

fibrinolytics

110
Q

MOA of fibrinolytics

A

converts plasminogen to plasmin = degrades fibrin matrix of thrombi = makes soluble fibrin degradation products

111
Q

alteplase (tPA)

A

fibrinolytic

112
Q

streptokinase

A

fibrinolytic

113
Q

what activates plasminogen already bound to fibrin, which confines fibrinolysis to the formed thrombus = avoiding systemic activation

A

alteplase (tPA)

114
Q

what is a protein created by streptococci that combines with proactivator plasminogen = catalyzes conversion of inactive plasminogen to active plasmin

A

streptokinase

115
Q

contraindication of streptokinase

A

ischemic stroke

116
Q

why must plasma be transfused within 24h once thawed?

A

concentrations of factor V and VIII declines

117
Q

monitoring for DOAC

118
Q

Which DOAC does not have an emergency reversal

119
Q

what inhibits COX-1 and competes with ASA at the catalytic site

120
Q

ASA should be taken at least ____ before or ____ after NSAIDs

A

60mins
8hrs

121
Q

BBW of ticagrelor (brilinta)

A

reduced effectiveness with concomitant use of ASA above 100 mg daily

122
Q

contraindications for ticagrelor (brilinta)

A

severe liver failure
active bleeding

123
Q

which platelet aggregation inhibitor requires routine monitoring

A

ticlopidine (ticlid)

124
Q

pts on rivaroxaban (xarelto) should avoiding taking ____

A

grapefruit juice
avoid CYP3A4 inhibitors

125
Q

what DOAC should you not use if CrCl > 95 mL/min

A

edoxaban (savaysa)

126
Q

what are the 3 platelet aggregation inhibitors that can be given IV

A
  1. congrelor - kengreal
  2. eptifibatide - integrilin
  3. abciximab - reopro
127
Q

why is bridging necessary when on warfarin

A

to avoid skin necrosis

128
Q

3 non-heparin anticoagulants

A
  1. argatroban
  2. fondaparinux
  3. bivalirudin
129
Q

drug interactions with dabigatran (pradaxa)

A

ketoconazole, cyclosporin, tacrolimus

Hem/Onc (13 decks)

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