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(C) CM 1A: Heme/Onc/Endo > Lecture 6: Hemostasis Pharmacology & Transfusion Therapy > Flashcards

Lecture 6: Hemostasis Pharmacology & Transfusion Therapy Flashcards

1
Q

What are the major blood group systems?

A

ABO
Rh

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2
Q

What antigens and antibodies does type A blood present with? O blood?

A

A blood presents with A antigens on its surface and anti-B antibodies in its plasma.

O blood presents with no antigens on its surface and anti-A and anti-B antibodies in its plasma.

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3
Q

What kind of blood can O blood receive? AB? A?

A

O blood can receive O blood.

AB blood can receive A, B, AB, and O blood.

A blood can receive A and O blood.

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4
Q

What is the difference between Rh+ and Rh-?

A

Rh+ has an antigen on its surface.
Rh- does not have an antigen on its surface.

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5
Q

When does a rhesus hemolytic transfusion reaction occur?

A

Rh+ donor blood going to Rh- person for a second time.

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6
Q

What are the pre-transfusion screenings done?

A

Type and Screen
Cross-match

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7
Q

What is typing and what is screening?

A

Typing is determine blood phenoTYPE, aka ABO and Rh.

Screening is screening for antibodies that may react against other antigens.

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8
Q

What is cross-matching?

A

Taking donor blood and mixing it with recipient blood.

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9
Q

When do you order a cross-match?

A

Only if there is a high likelihood that a patient will receive PRBCs.

DO NOT ORDER IN EMERGENCY SETTING.

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10
Q

What blood type is given in an emergency setting?

A

O- by default.

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11
Q

What is the purpose of transfusion?

A

Replace acute blood loss
O2 delivery
Morbidity and mortality

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12
Q

When is transfusion recommended barring exceptional circumstances?

A

Hgb < 6

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13
Q

What are the transfusion recommendations based on in terms of patient condition?

A

Hemodynamically stable with no active bleed.

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14
Q

How much Hb change does 1 unit of PRBCs do?

A

Increases Hb by 1g.

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15
Q

What kind of consent does a blood transfusion require?

A

SIGNED informed consent. (for non-emergency)

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16
Q

What are the most frequent reactions to being transfused?

A

Fever
Chills
Pruritis
Urticaria

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17
Q

What should I do if a transfusion reaction occurs?

A

STOP and report to blood bank.

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18
Q

What is the most common kind of transfusion reaction?

A

Febrile non-hemolytic reaction.

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19
Q

What do you get from a blood donation? (Products)

A

Whole blood
PRBCs
FFP (fresh frozen plasma)
Cryoprecipitate
Platelets

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20
Q

Why is whole blood rarely used?

A

Requires room temperature storage, which will degrade platelets and clotting factors if not used quickly.

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21
Q

When is whole blood used?

A

Massive hemorrhage. It causes the highest oxygen affinity for the Hb.

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22
Q

What is the volume of 1 unit of PRBCs?

A

200 mL usually.

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23
Q

What are some modifications I can make to PRBCs?

A

Leukocyte reduced (Now universally performed anyways)
Irradiated
Washed

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24
Q

What is the purpose of leukocyte reduced PRBCs?

A

Prevents immunologic responses or infectious transmission.

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25
Q

What is the purpose of irradiated PRBCs?

A

Avoid GVHD in immunodeficient people.

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26
Q

What is the purpose of washed PRBCs?

A

Prevent/eliminate complications associated with infusion of proteins present in residual concentrations.

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27
Q

What do you get from 1 unit of whole blood when separated?

A

1 unit of PRBCs
1 unit of platelets
1 unit of FFP

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28
Q

What blood product contains antibodies?

A

FFP

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29
Q

How does plasma transfusion differ from blood transfusion?

A

Opposite.

An AB blood person can receive donor AB plasma.

An O blood person can receive any donor plasma.

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30
Q

What is contained within FFP?

A

Coagulation factors
Fibrinogen
Antithrombin
Albumin
Protein C & S

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31
Q

What are the concerns when prepping an FFP transfusion?

A

24 hours once thawed to transfuse, otherwise F5 and F8 start to degrade.

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32
Q

Why is FFP the most used plasma product?

A

Contains all factors, so it can correct any deficiency.

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33
Q

What is cryoprecipitate?

A

Thawed FFP at 4C, collecting white precipitate rich in vWF, Factor 8, 13, and fibrinogen.

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34
Q

What is the key advantage of cryoprecipitate over FFP?

A

You can replace vWF, F8, F13, and fibrinogen using a much smaller volume than FFP.

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35
Q

What is factor concentrate?

A

A concentrate of a SPECIFIC factor made from either recombinant tech or THOUSANDS OF DONORS.

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36
Q

When do I use factor concentrate?

A

Only for very specific factor deficiencies, such as hemophilia A and B.
Minimal volume, no extraneous proteins.

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37
Q

What are the indications for platelet transfusion?

A

<10k to prevent spontaneous hemorrhage.
<50k in active bleeds, scheduled for invasive procedure, or qualitative intrinsic platelet disorder.
<100k in CNS injury, multisystem trauma, or neuro-surgery.
Normal count if ongoing active bleeding + platelet dysfunction dt congenital platelet disorder, chronic asa therapy, or uremia.

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38
Q

How much does a unit of platelets increase platelet count by?

A

5-10k.

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39
Q

What are the 4 hemostasis promoting agents?

A

Protamine sulfate
Vit K
Desmopressin
Thrombin

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40
Q

What is the indication for protamine sulfate?

A

HEPARIN REVERSAL AGENT.

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41
Q

What is the BBW of protamine sulfate?

A

Severe hypotensive or anaphylactoid reactions.

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42
Q

What is the indication and pharmaceutical name of Vitamin K?

A

Phytonadione or mephyton.

WARFARIN REVERSAL AGENT

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43
Q

What does vit K dosing depend on?

A

INR LEVEL
SEVERITY OF BLEEDING

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44
Q

How is Vit K metabolized?

A

HEPATIC

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45
Q

What is the indication for desmopressin/DDAVP?

A

Increase plasma levels of vWF, F8, and tPA, which reduces aPTT and bleeding time.

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46
Q

When administering desmopressin, what should I monitor?

A

Fluid Restriction
Sodium levels

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47
Q

What is the MOA and indication for topical thrombin?

A

MOA: Convert fibrinogen to fibrin at site of bleeding.

Indicated in surgery to aid in OOZING blood and minor bleeding only from CAPILLARIES and SMALL VENULES.

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48
Q

What is topical thrombin CI in?

A

Sensitive to things of bovine origin.
Massive bleed
NO LARGE VESSELS

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49
Q

What are the 3 categories of drugs that are antithrombotic?

A

AP drugs
AC drugs
Fibrinolytics

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50
Q

What is the purpose of an AC drug?

A

Prevent/treat clot/thrombus.
Generally indicated for venous thrombosis.

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51
Q

Which of the parental ACs is NOT renally cleared?

A

Unfrac heparin
Argatroban

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52
Q

What are the 3 general contraindications for parenteral ACs?

A

Bleeding (relative)
Renal function (except unfrac heparin)
Allergy

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53
Q

What are the parenteral ACs?

A

(Unfrac) heparin
LMWH
Bivalirudin/angiomax
Argatroban/Acova

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54
Q

How does heparin work?

A

Binds to anti-thrombin III, enhances its inactivation of F10a and thrombin.

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55
Q

How is heparin metabolized?

A

Hepatically

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56
Q

Is heparin preferred in pregnancy?

A

No.
LWMH is preferred.

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57
Q

Why does heparin need to be monitored?

A

It also binds to endothelium and plasma proteins, reducing AC effect.

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58
Q

How is heparin monitored?

A

aPTT or anti-F10 level.

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59
Q

What are the primary indications for heparin?

A

Prophylaxis of VT
DVT/PE
ACS

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60
Q

What are the adverse effects of heparin?

A

Bleeding
Thrombocytopenia
Osteoporosis
Elevated transminases

61
Q

What are the caveats to osteoporosis and elevated transaminases in heparin?

A

Osteoporosis is only long-term (>1mo therapy)

Elevated LFTs is transient with no concomitant increase in bilirubin.
Returns to normal when heparin is stopped.

62
Q

What is the #1 CI for heparin?

A

HIT!!!
Heparin induced thrombocytopenia

63
Q

What are the CIs for heparin?

A

HIT
Allergy
Active Bleed
HEMOPHILIA
Significant thrombocytopenia
Purpura
Severe HTN

64
Q

What is HIT?

A

A drug-induced thrombocytopenia.

Comes from heparin and PF4 forming neoantigen on PLT surface, causing a type 2 hypersensitivity reaction and plt clearance.

65
Q

Why is HIT dangerous?

A

It can reduce platelet counts AND put pt in hypercoagulable state.

You can end up in HITT, which is HIT and thrombosis, which requires additional AC.

66
Q

When does HIT occur?

A

ANY DOSE, ANY SCHEDULE, ANY ROUTE
Most common in UFH and females.

Most typical manifestation is thrombocytopenia.

67
Q

When does HIT generally occur?

A

5-10 days post therapy INITIATION.
Early onset seen if recent heparin exposure.

68
Q

Is venous or arterial thrombi more common in HIT?

69
Q

What would cause us to suspect HIT?

A

New onset thrombocytopenia
50%+ drop in plt count from previous
Venous/arterial thrombosis
Necrotic skin lesions at injection site
Acute systemic reactions occurring after bolus.

70
Q

How do we score HIT?

A

4Ts system. 0-2 pts per cat.

Thrombocytopenia

Timing of plt count fall

Thrombosis/other sequelae

Other causes

6 or more pts = extremely likely

71
Q

What do we do if we suspect HIT?

A

STOP HEPARIN
Order HIPA, serotonin release assay, and Heparin-PF4 Ab ELISA
Switch to argatroban/angiomax if AC needed.

72
Q

What should we always do in a patient’s chart if they had HIT?

A

HEPARIN ALLERGY IN CHART.

73
Q

What is the MOA of LWMH?

A

Enhance inhibition of F10 by AT 3 with LESS direct inhibition of F10 and no effect on thrombin.

Higher ratio of antiF10 to antiF2 compared to UFH.

74
Q

What is nice about LWMH in terms of route?

A

It is administered SC in abd wall, so you can do it OP.

75
Q

How is LWMH metabolized?

A

Renally cleared and metabolized. Adjust for renal impairment.

76
Q

What are the indications for LWMH?

A

Same as UFH.
Prophylaxis of VT
DVT/PE
ACS

77
Q

What condition CIs LWMH?

78
Q

What is the main difference in MOA between UFH and LWMH?

A

LMWH has a shorter molecule, which does NOT affect thrombin.

79
Q

How is LWMH monitored?

A

Anti-F10 levels, since little effect on aPTT.

Generally not monitored unless preggo, CrCL <= 30, or morbid obesity.

80
Q

What is preferred between LWMH and UFH?

81
Q

What drug is often used as bridging?

82
Q

What are the indications for bridging and when?

A

Bridging is done prior/post elective sx or invasive procedure for pts on warfarin:

Embolic stroke in 3 months
Previous embolic stroke or VTE during interruption of chronic AC
Mechanical valve
AFib in high stroke risk pt

83
Q

What is argatroban?

A

NON-HEPARIN thrombin inhibitor

84
Q

What is the MOA of argatroban?

A

Direct, highly-selective thrombin inhibitor.

Binds to the active thrombin site reversibly.

Inhibits fibrin formation, activation of F5, F8, and F13, protein C, and platelet aggregation.

85
Q

How is argatroban metabolized?

A

Hepatically

86
Q

How is argatroban monitored?

A

aPTT and LFTs

87
Q

When is argatroban indicated?

A

PCI
ANY PT WITH HX OF HIT

88
Q

Is argatroban safe in preggo?

89
Q

What is angiomax?

A

Literally the same as argatroban in terms of class, MOA, onset.

90
Q

How is angiomax different from argatroban?

A

RENAL CLEARANCE
Argatroban is hepatic.

(UFH and A is hepatic.)

91
Q

Is angiomax safe in preggo?

A

No, because it is unknown.

92
Q

What are the two main types of oral ACs?

A

Warfarin
DOACs

93
Q

What is the MOA of warfarin?

A

Inhibit Vit K oxide reductase complex subunit 1, aka inhibits factor 2, 7, 9, 10 (all vit K dependent)

94
Q

How is warfarin metabolized?

A

Liver
Sticks to albumin for a while.

95
Q

How long does it take PT/INR to change from warfarin?

A

36-72 hrs.

96
Q

When is warfarin absolutely CId?

A

PREGGO.

Cat D if mechanical heart valve, but still not preferred.

LWMH is preferred.

97
Q

What is warfarin indicated for?

A

Prophylaxis and treatment of DVT/PE
Embolic complications from Afib or valve replacement.

98
Q

What is the other adverse effect of warfarin besides bleeding?

A

Necrosis/gangrene, generally occurs if no initial therapy of LWMH or UFH.

99
Q

What should you always do if RXing warfarin?

A

Drug interaction check.
Warfarin interacts with 745 drugs.

100
Q

What are the main things to counsel pts about regarding warfarin use?

A

AVOID ALCOHOL
AVOID FOOD WITH LOTS OF VIT K
Vit E and cranberry juice increase warfarin effect.

Maintain a consistent diet and take it at the same time everyday.

101
Q

What happens to a chronic alcoholic’s PT/INR? Binge?

A

Chronic will have decreased PT/INR (less likely to bleed)
Binge will have increased PT/INR (more likely to bleed)

102
Q

What are the DOACs and why do we love them?

A

Dabigatran/Pradaxa = thrombin inhibitor
Rivaroxaban/Xarelto = F10 inhibitor
Apixaban/Eliquis = F10 inhibitor
Edoxaban/Savaysa = F10 inhibitor

DOACs produce predictable levels of AC without changing your whole life and constant blood tests.

103
Q

What is the indication for pradaxa?

A

Stroke prevention in non-valvular Afib, DVT/PE, DVT/PE prophylaxis post hip/knee sx.

Non-valvular means no mitral involvement.

104
Q

When is pradaxa dosing adjusted?

A

Renal Impairment

CI in ESRD or HD.

105
Q

What is the reversal agent for Pradaxa?

106
Q

What are the indications for xarelto?

A

Same as pradaxa.
Stroke prevention in non-valvular Afib
DVT/PE
DVT/PE prophylaxis post hip/knee sx.

107
Q

When is xarelto dosing adjusted?

A

CrCl < 50.

CI in ESRD/HD.

Relative CI in mod-severe hepatic impairment.

108
Q

What are some counseling concerns for Xarelto Rxing?

A

NO GRAPEFRUIT JUICE
Avoid Ca++ blockers, arrhythmics, and fluoroquinolones.

109
Q

What is the reversal agent for xarelto?

110
Q

What are the indications for eliquis?

A

Same as xarelto.

111
Q

When is eliquis dosing adjusted?

A

Renal impairment

112
Q

What are some counseling concerns for eliquis Rxing?

A

NO GRAPEFRUIT JUICE

113
Q

How is eliquis metabolized?

A

Hepatically.

114
Q

What is the reversal agent for eliquis?

115
Q

What are the indications for Savaysa?

A

Stroke prevention in non-valvular Afib
DVT/PE

116
Q

When is Savaysa dosing adjusted?

A

Either in renal impairment OR for kidneys that are way too strong (>95 CrCl)

117
Q

What is unique about Savaysa MOA?

A

Its inhibition of F10 does not require AT3.

118
Q

How is Savaysa metabolized?

A

Hepatically

119
Q

What is the reversal agent for Savaysa?

120
Q

Which of the DOACs is primarily renally excreted?

121
Q

Which of the DOACs has the best oral availability?

122
Q

What is the preferred DOAC?

A

Eliquis,
Less risk of any major bleed compared to any other DOAC.

123
Q

How is Heparin monitored and reversed?

A

aPTT
daily CBC
Protamine sulfate

124
Q

How is warfarin monitored and reversed?

A

PT/INR
Vit K

125
Q

How are DOACs monitored and reversed?

A

Kidney function.
Depends on DOAC.

126
Q

What are the AP drugs?

A

ASA
Plavix
Prasugrel/Effient
Ticlopidine/Ticlid
Ticagrelor/Brilinta
Cangrelor/Kengreal
Eptifibatide/Integrilin
Abciximab/Reopro

127
Q

What is MOA of ASA?

A

COX-1 inhibitor
IRREVERSIBLE BINDING

128
Q

What competes with ASA?

A

NSAIDs.

ASA should be taken 60 mins before or 8 hrs post NSAID.

129
Q

What are the indications for ASA?

A

Primary prophylaxis of MI
Secondary prevention with hx of vascular events or disease

130
Q

What is the MOA of plavix?

A

Inhibition of ADP pathway, irreversibly blocking P2y12.
Requires metabolic activation

131
Q

What are the indications of plavix?

A

Primary prophylaxis of MI
Standard prevention in pts with hx of vascular events.

132
Q

What are some counseling tips for plavix?

A

Drugs that are 2C19 inhibitors will reduce plavix effectiveness.
Omeprazole and Esomeprazole.

133
Q

What is the MOA of Effient/Prasugrel?

A

Irreversibly blocks P2Y12

Requires metabolic activation

Faster version of plavix

134
Q

What is the CI for effient?

A

Hx of TIA or CVA

135
Q

What is the MOA of Ticlopidine/Ticlid?

A

Irreversibly blocks P2Y12

136
Q

What are the monitoring and SE concerns with Ticlopidine?

A

Life-threatening hematologic rxns.
Neutropenia
Agranulocytosis
TTP
Aplastic anemia

CBC w/diff q2weeks

137
Q

What is the MOA of ticagrelor/brilinta?

A

REVERSIBLE and non-competitive binding of P2Y12
NO METABOLIC ACTIVATION

138
Q

What is the common SE of Brilinta?

139
Q

What is the BBW of brilinta?

A

Reduced effectiveness if concomitant use of ASA > 100mg.

140
Q

What is the MOA of Cangrelor/Kengreal?

A

REVERSIBLE and non-competitive binding of P2Y12.

141
Q

What is Cangrelor/Kengreal indicated for?

A

PCI
It is IV only.

142
Q

What is the MOA of eptifibatide/integrilin and abciximab/reopro? usage?

A

Gp 2b/2a receptor inhibitor.

Used for active PCI or high-risk pts with unstable angina.

143
Q

What do fibrinolytics do and how are they deliver?

A

Used to breakdown thrombi in life-threatening situations.

Administered systemically or via catheter.

MOA is to convert plasminogen to plasmin, which degrades fibrin matrix.

144
Q

What is the MOA of alteplase/tPA?

A

Preferential activation of bound plasminogen with fibrin.
Confines fibrinolysis to formed thrombus.

145
Q

What is tPA indicated for?

A

IV for PE with hemodynamic INSTABILITY, acute STEMI, severe DVT, and ascending thrombophlebitis.

146
Q

When can tPA be used for stroke?

A

Ischemic stroke approval if used with 3 hours of onset.

147
Q

What is the MOA of streptokinase?

A

Converts inactive plasminogen to active plasmin.

Protein made by streptococci.

148
Q

When is streptokinase CId?

A

ISCHEMIC STROKE

(C) CM 1A: Heme/Onc/Endo (28 decks)

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