Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

(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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

When does a rhesus hemolytic transfusion reaction occur?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the pre-transfusion screenings done?

A

Type and Screen
Cross-match

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is cross-matching?

A

Taking donor blood and mixing it with recipient blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What blood type is given in an emergency setting?

A

O- by default.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the purpose of transfusion?

A

Replace acute blood loss
O2 delivery
Morbidity and mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When is transfusion recommended barring exceptional circumstances?

A

Hgb < 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

Hemodynamically stable with no active bleed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How much Hb change does 1 unit of PRBCs do?

A

Increases Hb by 1g.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What kind of consent does a blood transfusion require?

A

SIGNED informed consent. (for non-emergency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the most frequent reactions to being transfused?

A

Fever
Chills
Pruritis
Urticaria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What should I do if a transfusion reaction occurs?

A

STOP and report to blood bank.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the most common kind of transfusion reaction?

A

Febrile non-hemolytic reaction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

Whole blood
PRBCs
FFP (fresh frozen plasma)
Cryoprecipitate
Platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why is whole blood rarely used?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

When is whole blood used?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the volume of 1 unit of PRBCs?

A

200 mL usually.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are some modifications I can make to PRBCs?

A

Leukocyte reduced (Now universally performed anyways)
Irradiated
Washed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the purpose of leukocyte reduced PRBCs?

A

Prevents immunologic responses or infectious transmission.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the purpose of irradiated PRBCs?

A

Avoid GVHD in immunodeficient people.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the purpose of washed PRBCs?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What blood product contains antibodies?

A

FFP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is contained within FFP?

A

Coagulation factors
Fibrinogen
Antithrombin
Albumin
Protein C & S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Why is FFP the most used plasma product?

A

Contains all factors, so it can correct any deficiency.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is cryoprecipitate?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is factor concentrate?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

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

A

5-10k.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the 4 hemostasis promoting agents?

A

Protamine sulfate
Vit K
Desmopressin
Thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the indication for protamine sulfate?

A

HEPARIN REVERSAL AGENT.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the BBW of protamine sulfate?

A

Severe hypotensive or anaphylactoid reactions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the indication and pharmaceutical name of Vitamin K?

A

Phytonadione or mephyton.

WARFARIN REVERSAL AGENT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What does vit K dosing depend on?

A

INR LEVEL
SEVERITY OF BLEEDING

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How is Vit K metabolized?

A

HEPATIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is the indication for desmopressin/DDAVP?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

When administering desmopressin, what should I monitor?

A

Fluid Restriction
Sodium levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is topical thrombin CI in?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the 3 categories of drugs that are antithrombotic?

A

AP drugs
AC drugs
Fibrinolytics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the purpose of an AC drug?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Which of the parental ACs is NOT renally cleared?

A

Unfrac heparin
Argatroban

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are the 3 general contraindications for parenteral ACs?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the parenteral ACs?

A

(Unfrac) heparin
LMWH
Bivalirudin/angiomax
Argatroban/Acova

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

How does heparin work?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How is heparin metabolized?

A

Hepatically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Is heparin preferred in pregnancy?

A

No.
LWMH is preferred.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Why does heparin need to be monitored?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How is heparin monitored?

A

aPTT or anti-F10 level.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the primary indications for heparin?

A

Prophylaxis of VT
DVT/PE
ACS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

A

Venous

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?

A

ESRD

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?

A

LWMH

81
Q

What drug is often used as bridging?

A

LWMH

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?

A

Yes

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?

A

Praxbind

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?

A

AndexXa

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?

A

AndexXa

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?

A

None.

120
Q

Which of the DOACs is primarily renally excreted?

A

Pradaxa

121
Q

Which of the DOACs has the best oral availability?

A

Xarelto

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?

A

Dyspnea

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions