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AA Walter Reed > Exsanguination > Flashcards

Exsanguination Flashcards

1
Q

what are the four general steps of normal hemostasis?

A
  1. capillary vasoconstriction
  2. platelet plug formation
  3. coagulation (fibrin formation)
  4. fibrinolysis (occurs simultaneously)
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2
Q

what molecule is primarily responsible for the vasoconstriction and platelet aggregation during normal hemostasis? where is it released from?

A
  • TXA2

- released from platelets

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3
Q

what molecule opposes TXA2 during normal hemostasis? where is it released from?

A
  • prostacyclin

- released from endothelium

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4
Q

what is the lifespan of megakaryocytes?

A

8d

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5
Q

1/3 of megakaryocytes are sequestered in the __________

A

spleen

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6
Q

what are the 4 steps of platelet plug formation?

A
  1. adherence
  2. activation
  3. granule release
  4. aggregation
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7
Q

platelets adhere to subendothelial collagen at site of injury mediated by _______ and _________

A

vWF and GpIb

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8
Q

platelet granule release is mediated by what two molecules? what is the result?

A
  • ADP
  • TXA2
  • result: exposure of fibrinogen receptors on platelet surface
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9
Q

what characterizes the aggregation phase of platelet plug formation?

A

fibrinogen crosslinking between platelets via GpIIb

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10
Q

all clotting factors are synthesized in the liver with the exception of:

A
  • VIII
  • vWF (cofactor VIII)

these are synthesized in the endothelium

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11
Q

what is responsible for degrading Va and VIIIa?

A

protein C (with cofactor S)

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12
Q

what is the single best test to evaluate liver function?

A

PT

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13
Q

how do the extrinsic and intrinsic pathways differ?

A
  • extrinsic: release of TF from damage OUTSIDE the blood vessel
  • intrinsic: injury to the blood vessel with release of clotting factors from circulation
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14
Q

the final common pathway results in:

A

conversion of fibrinogen to fibrin, and fibrin crosslinking

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15
Q

plasminogen is converted to ____________ by _________ / __________ / ___________

A
  • plasmin

- TPA / urokinase / streptokinase

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16
Q

what is the primary signal of fibrinolysis?

A

TPA from endothelium

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17
Q

plasmin cleaves ____________, leaving ______________

A
  • fibrin

- E and D fragments (D-dimer)

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18
Q

what are the inhibitors of fibrinolysis?

A
  • primary: a2 antiplasmin (bound to fibrin, rapid acting)

- secondary: a2 microglobulin

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19
Q

what are the anti-fibrinolysis meds?

A
  • amicar
  • aprotinin
  • TXA
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20
Q

what is the MOA of the anti-fibrinolysis drugs amicar and aprotinin?

A

block plasmin and kallikrein

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21
Q

what is the MOA of the anti-fibrinolysis drug TXA?

A

lysine analog, blocks lysine receptors on plasminogen, more powerful than amicar

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22
Q

antithrombin 3 binds and inactivates what factors?

A
  • thrombin
  • IX
  • X
  • XI
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23
Q

how does heparin work?

A

induces conformational change in antithrombin 3, increasing reaction rate 1000x (for inactivation of II, IX, X, XI)

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24
Q

what is the inheritance of antithrombin 3 deficiency?

A

AR

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25
Q

what is the clinical presentation of antithrombin 3 deficiency?

A
  • 20-50 yo
  • widespread DVT and arterial thrombosis
  • pt appears resistant to heparin
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26
Q

what is the treatment for antithrombin 3 deficiency?

A
  • FFP (replenishes AT3)

- lifelong anticoagulation

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27
Q

less than ___% normal level of protein C/S leads to hypercoagulable state

A

less than 60%

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28
Q

what is the inheritance of protein C/S deficiency?

A

AR

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29
Q

what is the pathogenesis of factor V leiden?

A

factor V resistance to activated protein C due to single amino acid substitution of arginine to glutamine

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30
Q

what is the inheritance of factor V leiden?

A

AR

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31
Q

what is the pathogenesis of acquired hypercoagulable state?

A

liver failure can lose AT3 and have a picture like AT3 deficiency

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32
Q

what do the blood studies show in vWF disease?

A
  • normal platelet count

- slightly prolonged PTT

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33
Q

hemophilia A = factor _____ deficiency

A

VIII

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34
Q

what is the inheritance of hemophilia A?

A

X-linked

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35
Q

what are the blood labs for hemophilia A?

A
  • increased PTT

* obtain factor assay

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36
Q

what is the treatment for hemophilia A?

A
  • increase factor VIII when hemostatic challenge is anticipated
  • factor VIII concentrate treatment of choice, but can also give cryoprecipitate
  • dose BID
  • need 70-100% activity for major surgery, 40-50% for minor surgery
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37
Q

hemophilia B = factor ____ deficiency

A

IX

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38
Q

what is the inheritance of hemophilia B?

A

X-linked

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39
Q

what do blood labs show for hemophilia B?

A

increased PTT

*obtain factor assay

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40
Q

what is the treatment for hemophilia B?

A
  • cryoprecipitate, dose daily

- need 50% activity for major surgery

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41
Q

which is worse - type 1 or 2 HIT?

A

type II

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42
Q

what is the cause of type 2 HIT?

A
  • immune-mediated, results in platelet aggregation and activation, then clearance in reticuloendothelial system
  • initially predisposed to thrombosis, then thrombocytopenia and hemorrhage
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43
Q

“white clots” on pathology is indicative of:

A

HIT

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44
Q

how is HIT diagnosed?

A

14C serotonin release assay / ELISA

*look for platelet clumping in presence of therapeutic heparin dosing

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45
Q

what is the treatment for HIT?

A
  • stop heparin

- use direct thrombin inhibitor (lepirudin, argatroban, coumadin) in setting of thrombosis

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46
Q

what are some direct thrombin inhibitors?

A
  • lepirudin
  • argatroban
  • coumadin
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47
Q

what do the blood labs show with DIC?

A
  • decreased platelets
  • fibrinogen
  • increased fibrin split products
  • increased PT and PTT
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48
Q

what is the treatment for DIC?

A
  • treat underlying cause

- give platelets, FFP, cryoprecipitate

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49
Q

what is the shelf life of whole blood? what is lost after 24 hrs?

A
  • 35 with addition of citrate phosphate dextrose
  • store at 4C
  • platelets, factor V, VII lost in 24 hr
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50
Q

1 unit of pRBC should raise HCT by ___% in a 70kg person

A

2-4%

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51
Q

what is the shelf life of pRBC?

A

42 days

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52
Q

what is the best blood product option to improve O2 capacity without hypervolemia?

A

pRBC

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53
Q

how long can platelets be stored for?

A

5d

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54
Q

when is a platelet transfusion indicated?

A

platelet count under 100k or 50k in patients requiring surgery

55
Q

______thermia (hypo/hyper) makes platelets unable to produce TXA2

A

hypothermia

56
Q

_____ mL/kg FFP should replete coagulation factors to levels required for hemostasis?

A

10-15 mL/kg

57
Q

FFP is stored at what temp?

A

-18C (to protect factors V, VIII)

58
Q

does FFP require typing, crossmatch, both, or neither?

A

typing, but not crossmatch

59
Q

what are the indications for FFP?

A
  • coagulopathy of liver disease
  • vitamin K deficiency
  • coumadin therapy
  • dilutional coagulopathy
  • AT3 deficiency
60
Q

what does cryoprecipitate contain?

A
  • fibrinogen
  • factor VIII
  • vWF
  • factor XIII
61
Q

how is cryoprecipitate prepared?

A

plasma frozen to -90C, warmed slowly to 4C - precipitate which forms is separated with a small amount of plasma

62
Q

what are the indications for cryoprecipitate?

A
  • source of vWF in vWD
  • source of factor VIII in hemophilia A
  • source of fibrinogen in DIC
63
Q

what is the presentation for febrile non-hemolytic transfusion reaction?

A
  • isolated fever 1-6h after transfusion
  • flank pain
  • red/brown urine
64
Q

what is the pathophysiology of febrile non-hemolytic transfusion reaction?

A

complement mediated destruction of transfused cell components by pre-existing antibodies

65
Q

what is the treatment for febrile non-hemolytic transfusion reaction?

A
  • acetaminophen

- use buffy coat poor RBCs in the future

66
Q

what is the presentation of hemolytic transfusion reaction?

A
  • HA
  • chest pain
  • flank pain
  • hemoglobinemia
  • hemoglobinuria
  • DIC
  • acute renal failure
67
Q

when does hemolytic transfusion reaction occur?

A

within first 50cc of blood

68
Q

what is the treatment for hemolytic transfusion reaction?

A
  • stop transfusion, recheck ABO

- hydrate to UOP > 100cc/hr (mannitol, lasix, bicarb)

69
Q

what is the pathophysiology of hemolytic transfusion reaction?

A

ABO incompatibility, personal errors

70
Q

what is the pathophysiology of delayed hemolytic transfusion reaction? how does it present?

A
  • minor blood group antigen incompatibility

- days later: fever, chills, jaundice

71
Q

what is the treatment for delayed hemolytic transfusion reaction?

A

hydrate to UOP > 100cc/hr (mannitol, lasix, bicarb)

72
Q

what is the frequency of blood products as cause for TRALI?

A

FFP > PLT > RBC

73
Q

what is the treatment for TRALI?

A
  • supportive
  • steroids
  • AVOID DIURETICS
74
Q

what does thromboelastograph (TEG) test?

A

coagulation profile

75
Q

how does the thromboelastograph (TEG) test work?

A
  • sample of whole blood placed in warmed cuvette
  • pin lowered into blood, rotated backward and forward
  • fibrin strands interact with activated platelets on the surface of the pin, rotational movement of the cuvette transmitted to pin
  • stronger the clot, the more the pin moves
  • pin movement connected to computer that displays the coagulation profile
76
Q

what does the R time indicate for the thromboelastograph (TEG) test?

A

initiation: time from initiation of test to initial pin movement / initial fibrin formation

77
Q

what does a prolonged R time mean for thromboelastograph (TEG) test? what is the treatment?

A

factor deficiency - treat with FFP

78
Q

what does the K value indicated for the thromboelastograph (TEG) test?

A

amplification: time to achieve clot strength, due to thrombin and platelet activation

79
Q

what does the alpha angle represent for the thromboelastograph (TEG) test?

A
  • measures the speed at which fibrin buildup and cross linking takes place (clot strengthening)
  • assess rate of clot formation
80
Q

what does a prolonged K / reduced alpha angle mean for the thromboelastograph (TEG) test? how is it treated?

A

fibrinogen deficiency - treat with cryoprecipitate

81
Q

what is the maximum amplitude for the thromboelastograph (TEG) test?

A
  • function of the maximum dynamic properties of fibrin and platelet bonding via GpIIb/IIIa
  • represents the strongest point of fibrin clot and correlates with platelet function
82
Q

what does a reduced maximum amplitude mean for the thromboelastograph (TEG) test? how is it treated?

A
  • thrombocytopenia
  • platelet dysfunction
  • treat with platelets or ddAVP
83
Q

what does the clot lysis index (LY30) measure for the thromboelastograph (TEG) test?

A
  • give a measure of degree of fibriniolysis

- clot stability: percentage decrease in amplitude 30 minutes post-maximum amplitude

84
Q

what does an elevated LY30 mean for the thromboelastograph (TEG) test? how is it treated?

A

rapid clot lysis - treat with TXA

85
Q

what parameter represents the strongest point of fibrin clot and correlates with platelet function for the thromboelastograph (TEG) test?

A

maximum amplitude

86
Q

what parameter determines the function of the maximum dynamic properties of fibrin and platelet bonding via GpIIb/IIIa for the thromboelastograph (TEG) test?

A

maximum amplitude

87
Q

what parameter of the thromboelastograph (TEG) test gives a measure of degree of fibrinolysis?

A

clot lysis index (LY30)

88
Q

if you suspect a fibrinogen deficiency what parameter(s) would you look at for the thromboelastograph (TEG) test?

A

K value and alpha angle

89
Q

if you want to assess the rate of clot formation which parameter(s) would you look at for the thromboelastograph (TEG) test?

A

alpha angle

90
Q

if you want to determine the time to achieve clot strength what parameter would you look at in the thromboelastograph (TEG) test?

A

K value

91
Q

what is the half life of heparin?

A

dose dependent (45-150 min)

92
Q

how is heparin removed from the body?

A

RES and kidneys

93
Q

how is heparin function followed?

A

PTT (want 50-80s)

94
Q

how is heparin reversed?

A
  • protamine sulfate - give 1mg/100u heparin administered in preceding 2 hrs
  • cross reacts with NPH insulin
95
Q

what is the MOA of LMWH?

A

inhibits factor X over thrombin (4:1 ratio), with greater bioavailability

96
Q

what are the advantages of LMWH?

A
  • 2-4x longer half life
  • excreted through kidney
  • more predictable response to fixed doses
97
Q

how do you measure LMWH activity?

A

anti-Xa assay

98
Q

how is LMWH (Lovenox) reversed?

A

protamine sulfate: 1mg/mg Lovenox if given within 8 hrs; 0.5mg/mg Lovenox if over 8 hrs

99
Q

what is the MOA of synthetic oligosaccharides in anticoagulation?

A
  • bind to AT3, induce conformational change
  • accelerate elimination of factor X
  • analogous to pentasaccharide sequence in heparin
100
Q

what type of drug is fondaparinux (Aristra)? what is the route?

A
  • selective Xa inhibitor

- subQ

101
Q

what are the indications for the selective factor Xa inhibitor fondaparinux (Aristra)?

A
  • DVT proph

- DVT/PE treatment

102
Q

how is the selective factor Xa inhibitor fondaparinux (Aristra) cleared?

A
  • hepatic (66%)

- renal (33%)

103
Q

how can selective factor Xa inhibitor (e.g. fondaparinux (Aristra)) activity be monitored?

A

anti-Xa activity

104
Q

what is used to reverse selective factor Xa inhibitors fondaparinux (Aristra)?

A

Novoseven 90mc/kg (recombinant factor VII)

*no HD

105
Q

what type of drugs are rivaroxaban (Xarelto) and apixaban (Eliquis)? what are the routes?

A
  • selective factor Xa inhibitors

- oral

106
Q

what are the indications for rivaroxaban (Xarelto) and apixaban (Eliquis)?

A
  • Afib
  • DVT proph
  • DVT/PE treatment
  • ACS treatment
107
Q

when are direct thrombin inhibitors used?

A

use in patients with heparin contraindications

108
Q

how do direct thrombin inhibitors affect blood labs?

A
  • all will increased PTT

- must shoot for high INR if bridging to coumadin

109
Q

what are the half lives of the direct thrombin inhibitors?

A
  • lepirudin: 90 min
  • bivalrudin: 25 min
  • argatroban: 45 min
  • dabigatran: 7-9 hr
110
Q

what are the clearance routes for the direct thrombin inhibitors?

A
  • lepirudin: renal
  • bivalrudin: renal
  • argatroban: hepatic
  • dabigatran: renal
111
Q

what are the routes for the direct thrombin inhibitors?

A
  • lepirudin: IV/SC
  • bivalrudin: IV
  • argatroban: IV
  • dabigatran: PO
112
Q

how do you monitor the activity of direct thrombin inhibitors?

A

PTT (except for dabigatran - thrombin time)

113
Q

how is coumadin reversed for life threatening bleeding?

A
  • vitamin K 10g IV over 10 min
  • 4u FFP
  • r-factor PCC (Kcentra) preferred
  • INR 1.5-3.9: 25u/kg PCC
  • INR 4.0-6.0: 35u/kg PCC
  • INR over 6.0: 50u/kg PCC
114
Q

what is the MOA of aspirin?

A

irreversibly inhibits COX; decreases prostacyclin and platelet thromboxane

115
Q

how long do the effects of aspirin last? when should it be d/c’d before surgery?

A
  • effect for 7-10d

- dc one week prior to surgery

116
Q

what is the MOA for NSAIDs?

A

reversible COX inhibitors

117
Q

what is the MOA of dipyridamole?

A

inhibits adenosine deaminase and phosphodiesterase, inhibits platelet aggregation

*dosed with ASA as aggrenox

118
Q

what are the GpIIb/IIIa inhibitors?

A
  • abciximab (Reopro)
  • eptifibatide (Integrilin)
  • tirofiban (Aggrastat)
119
Q
  • lepirudin
  • bivalrudin
  • argatroban
  • dabigatran

are what type of drugs?

A

direct thrombin inhibitors

120
Q

when are the GpIIb/IIIa agents used?

A

ACS / PCTA stenting

121
Q

what is the half life of the GpIIb/IIIa agents?

A

0.5-1 hr

122
Q

what is the MOA of ticlopidine and clopidogrel?

A

platelet aggregation inhibitors - irreversibly block binding of the ADP receptor

*stronger effect than ASA

123
Q

how are the platelet aggregation inhibitors (ticlopidine and clopidogrel) metabolized?

A

cyp450

124
Q

how long does it take for the platelet aggregation inhibitors (ticlopidine and clopidogrel) to start working?

A

3-5 days

125
Q

how long before surgery should the platelet aggregation inhibitors (ticlopidine and clopidogrel) be held?

A

5 days

126
Q

which of the platelet aggregation inhibitors (ticlopidine and clopidogrel) requires first pass liver metabolism?

A

Plavix (clopidogrel) - do not use in liver failure patients

127
Q

what are the platelet aggregation inhibitors that block the p2y12 receptor for ADP?

A
  • prasugrel (Effient)
  • cangrelor (IV)
  • ticagrelor (Brilinta, PO)
128
Q

how do cangrelor and ticagrelor differ from prasugrel?

A
  • cangrelor and ticagrelor are direct and reversible inhibitors, and do NOT have p450 activation
  • very rapid onset/offset
129
Q

how does dextran work?

A
  • thrombi undergo lysis at an increased rate

- decreased platelet adhesion and aggregation

130
Q

the platelet function assay depends on what factors?

A
  • plasma vWF level

- platelet number

131
Q

how does the platelet function assay work?

A
  • small membranes coated with collagen and EPI or collagen and ADP
  • anticoagulated whole blood passed through membranes at high shear rate to simulate in vivo hemodynamics
  • time for blood to occlude membrane is the closure time
  • col/EPI done first
  • if col/EPI is prolonged, col/ADP reflexively performed
132
Q

what are the interpretations for the col/EPI and col/ADP tests for PFA?

A
  • col/EPI done first
  • closure time under 183s excludes presence of defect
  • if col/EPI is prolonged, col/ADP reflexively performed
  • if col/ADP is NORMAL (under 122s), ASA induced platelet function is most likely
133
Q

what is indicated by prolongation of both col/EPI and col/ADP for PFA?

A
  • anemia
  • thrombocytopenia
  • significant platelet dysfunction other than aspirin

AA Walter Reed (3 decks)

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