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ABSITE > 02 Hematology > Flashcards

02 Hematology Flashcards

1
Q

which type of VWD is most severe?

A

III. most severe bleeding

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2
Q

where do hemophiliacs tend to bleed?

A

joints.

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3
Q

will newborns with hemophilia A bleed at circumcision?

A

No. Factor VIII crosses placenta.

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4
Q

what is the best coagulation measurement for liver synthetic function?

A

PT

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5
Q

what does prostacyclin do?

A

decreases platelet aggregation and promotes vasodilation

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6
Q

what does thromboxane do?

A

increases platelet aggregation and promotes vasoconstriction (antagonistic to prostacyclin). also triggers release of calcium from platelets –> exposes GpIIb/IIIa receptor and causes platelet to platelet binding; platelet to collagen binding via Gp1b receptor

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7
Q

what are coagulation factors?

A

cryoprecipitate, FFP, DDAVP

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8
Q

what causes type I vWD? what is the treatment?

A

reduced quantity of vWF, treat with recombinant VIII:vWF, DDAVP, cryo

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9
Q

what are PTT and PT in hemophilia A?

A

high PTT, normal PT

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10
Q

what do you need to make sure in hemophilia A people before surgery?

A

need VIII 100% pre-op, keep at 80-100% for 10-14d after surgery

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11
Q

what INR is contraindication for central line placement, percutaneous needle bx, and eye surgery?

A

INR >1.3

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12
Q

what INR is contraindication for surgical procedures?

A

INR > 1.5

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13
Q

what are the players in fibrinolysis?

A

tissue plasminogen activator, plasmin, alpha-2 antiplasmin.

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14
Q

what causes type III vWD? what is Rx?

A

complete vWF deficiency (rare). Rx is VIII:vWF, cryoppt. (DDAVP doesn’t work)

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15
Q

what is active clotting time (ACT) for routine anticoagulation and for cardiopulmonary bypass?

A

150-200 sec for routine, >460 for cardiopulm bypass

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16
Q

what does thrombin do?

A

it is the key to coagulation. converts fibrinogen to fibrin and fibrin split products, activates factors V and VIII, activates platelets

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17
Q

should you aspirate hemophiliac joint bleeds?

A

no! give ice, keep joint mobile with range of motion, give factor VIII concentrate or cryoppt

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18
Q

what test do you do to figure out VWD?

A

ristocetin test (bleeding time)

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19
Q

where does thromboxane come from?

A

platelets

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20
Q

what are the symptoms of hemophiliacs?

A

epistaxis, ICH, hematuria. treat with recombinant factor VIII or cryo

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21
Q

what should PTT be for routine anticoagulation?

A

60-90 sec

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22
Q

can PT and PTT be normal in VWD?

A

yes. can be nl or abnl

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23
Q

what is the most common cause of surgical bleeding?

A

incomplete hemostasis

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24
Q

what is the function of vWF?

A

links GpIb receptor on platelets to collagen

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25
Q

what does tissue plasminogen activator do?

A

it is released from endothelium and converts plasminogen to plasmin

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26
Q

where does prostacyclin come from?

A

endothelium

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27
Q

when does FFP take effect and how long does it last?

A

immediately, lasts 6 hrs

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28
Q

what does alpha-2 antiplasmin do?

A

it is a natural inhibitor of plasmin, released from endothelium

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29
Q

what is definition of hemophilia A?

A

VIII deficiency

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30
Q

what does ATIII do?

A

key to anticoagulation, binds and inhibits thrombin, inhibits factors IX, X, XI, heparin activates AT-III (up to 1000x normal activity)

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31
Q

which is the only factor not synthesized in liver?

A

factor VIII. it’s synthesized in the endothelium

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32
Q

what does PTT measure?

A

measures most factors except VII and XIII (does not pick up factor VII deficiency). also measures fibrinogen.

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33
Q

what do DDAVP and conjugated estrogens do?

A

cause release of VIII and vWF from endothelium. similar effect as cryoppt

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34
Q

what does plasmin do?

A

degrades factors V, VIII, fibrinogen, fibrin –> lose platelet plug

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35
Q

what does protein S do?

A

vitamin K dependent, protein C cofactor

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36
Q

what does protein C do?

A

vitamin K dependent. degrades factors V and VIII, degrades fibrinogen

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37
Q

what does PT measure?

A

II, V, VII, X, fibrinogen.

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38
Q

what is in FFP?

A

high levels of coagulation factors, protein C, S, and AT-III

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39
Q

what is the normal half life for RBCs, platelets, and PMNs?

A

RBC: 4 months, platelets 7d, PMNs: 1-2d

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40
Q

what is another name for factor II?

A

prothrombin

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41
Q

which factor has the shortest half life?

A

factor VII

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42
Q

what is in cryoppt? when is it used?

A

high vWF-VIII. used for vWF disease and hemophilia (factor VIII deficiency). also has high levels of fibrinogen.

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43
Q

what factor is missing in hemophilia B?

A

IX

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44
Q

how is hemophilia A transmitted?

A

sex-linked recessive

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45
Q

what causes type II vWD? what is the treatment?

A

defect in vWF molecule itself, vWF does not work well. Rx is recombinant VIII:vWF, cryoppt

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46
Q

how many hours does vitamin K take to have effect?

A

6hrs

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47
Q

what is the most common congenital bleeding disorder?

A

VWD

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48
Q

which proteins in anticoagulation cascade vitamin K dependent?

A

proteins C and S, II, VII, IX, X

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49
Q

what is the most common type of VWD?

A

Type I (70% of cases), only mild sx

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50
Q

which factor is labile, lost activity in stored blood, and who continues to have activity in FFP?

A

factors V and VIII

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51
Q

what causes glanzmann’s thrombocytopenia?

A

GpIIb/IIIa receptor deficiency on platelets (can’t bind to each other). Fibrin normally links GpIIb/IIIa receptors together. Rx is platelets.

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52
Q

what causes bernard soulier?

A

Gp1b receptor deficiency on platelets (can’t bind collagen). vWF normally links GpIb to collagen. Rx is platelets

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53
Q

when does ASA need to stop before surgery?

A

7 days

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54
Q

what are the platelet disorders?

A

acquired thrombocytopenia, glanzmann’s thrombocytopenia, bernard-soulier, uremia

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55
Q

how does uremia induce thrombocytopenia? what is the treatment?

A

inhibits platelet fxn. Rx is hemodialysis (1st), then DDAVP, platelets

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56
Q

does LMWH have a decreased risk of HIT?

A

yes

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57
Q

what is PT and PTT in factor VII deficiency?

A

prolonged PT, normal PTT.

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58
Q

what are findings in DIC?

A

decreased platelets, low fibrinogen, high fibrin split products, high D-dimer, prolonged PT and PTT

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59
Q

what are lab findings in pts taking ASA?

A

prolonged bleeding times

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60
Q

what causes acquired thrombocytopenia?

A

H2 blockers, heparin

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61
Q

how is hemophilia B transmitted?

A

sex linked recessive

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62
Q

what is treatment for DIC?

A

treat underlying cause (eg sepsis)

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63
Q

high or low doses of heparin to cause HIT?

A

can occur with low

64
Q

what is treatment for HIT?

A

stop heparin, start argatroban (direct thrombin inhibitor) to anticoagulate

65
Q

what are PT and PTT in hemophilia B pts?

A

prolonged PTT, normal PT. same as hemophilia A.

66
Q

how do you treat hemophilia B?

A

recombinant factor IX, or FFP

67
Q

what is treatment for factor VII deficiency?

A

recombinant factor VII concentrate or FFP

68
Q

how does HIT cause thrombocytopenia?

A

antiplatelet antibodies (IgG PF4 antibody) resulting in platelet destruction, platelet aggregation (thrombosis), forms a white clot.

69
Q

what levels of IX do you need in a hemophilia B pt before surgery?

A

100% preop, keep at 30-40% for 2-3d after surgery

70
Q

what are the three initial responses to vascular injury?

A

vasoconstriction, platelet adhesion, thrombin generation

71
Q

what is the extrinsic pathway?

A

exposed collagen + prekallikrein + HMW kiniogen + factor XII activate XI –> activate IX, then add VIII –> activate X, then add V –> convert prothrombin (factor II) to thrombin –> thrombin then converts fibrinogen to fibrin

72
Q

what does fibrin do?

A

links platelets together (binds GpIIb/IIIa molecules) to form platelet plug –> hemostasis

73
Q

what is the intrinsic pathway?

A

tissue factor (injured tissues) + factor VII –> activate X, then add V –> convert prothrombin to thrombin –> thrombin then converts fibrinogen to fibrin

74
Q

what does tissue factor inhibitor do?

A

inhibits factor x

75
Q

what causes warfarin induced skin necrosis?

A

when pt placed on coumadin without being heparinized first

76
Q

what causes warfarin-induced skin necrosis?

A

short half life of proteins C and S –> decrease in levels compared with the procoagulation factors; results in relative hyperthrombotic state.

77
Q

who is especially susceptible to warfarin-induced necrosis?

A

pts w relative protein C deficiency

78
Q

how do you treat warfarin-induced skin necrosis?

A

heparin if it occurs. prevent by placing pt on heparin before starting warfarin

79
Q

what are the elements in deveoping venous thromboses? what is it called?

A

virchow’s triad: stasis, endothelial injury, hypercoagulability

80
Q

what are the key elements in development of arterial thrombosis?

A

endothelial injury

81
Q

what are risk factors for developing arterial thromboses?

A

stasis, venous injury, hypercoagulability

82
Q

what is post-op DVT treatment (1st, 2nd, 3rd lines)?

A

1st: warfarin for 6 months. 2nd: warfarin for 1 yr. 3rd or significant PE: warfarin for lifetime

83
Q

when are greenfield filters given?

A
  1. contraindications to anticoagulation, 2. documented PE while on anticoagulation, 3. free-floating IVC, ilio-femoral, or deep femoral DVT, 4. recent pulm embolectomy
84
Q

when can temporary IVC filters be given?

A

for pts at high risk for DVT (head injury on prolonged bed rest)

85
Q

are thrombolyics proven for treatment of PE?

A

no

86
Q

if pt is in shock from PE despite massive inotropes and pressors, what do you do?

A

go to OR; otherwise give heparin or suction catheter-based intervention

87
Q

where do most PEs arise?

A

ilio-femoral region

88
Q

what are the procoagulant agents (anti-fibrinolytics)?

A

E-aminocaproic acid (Amicar)

89
Q

what are the anticoagulation agents?

A

(warfarin, SCDs, heparin, LMWH, argatroban, bivalirudin, hirudin, ancrod

90
Q

how does warfarin work?

A

prevents vitamin K-dependent decarboxylation of glutamic residues on vitamin K-dependent factors

91
Q

how do SCDs cause anticoagulation?

A

improves venous return, induces fibrinolysis w compression (release of tPA from endothelium)

92
Q

how is heparin reversed?

A

protamine

93
Q

how does protamine work?

A

binds heparin

94
Q

what should PTT be when treating w heparin?

A

60-90 seconds. (mnemonic is half life heparin 60-90 min)

95
Q

how is heparin cleared?

A

reticuloendothelial system

96
Q

what is the reticuloendothelial system?

A

mononuclear phagocyte system

97
Q

what are the risks of taking heparin for a long time?

A

osteoporosis, alopecia

98
Q

can heparin be used during pregnancy? warfarin?

A

heparin doesn’t cross placental barrier, warfarin does

99
Q

what does protamine cross react with?

A

NPH insulin

100
Q

what does cross reaction of protamin and NPH insulin give you?

A

protamine reaction (hypotension, brady, decreased heart function)

101
Q

what are examples of LMWH?

A

enoxaparin, fondaparinux

102
Q

how does LMWH work? what are the advantages?

A

LMWH binds and activates AT-III, increases neutralization of JUST Xa and thrombin–> NOT reversed w protamine. advantage is lower risk of HIT (compared to unfractionated heparin)

103
Q

how does argatroban work?

A

it is a reversible direct thrombin inhibitor

104
Q

how is argatroban metabolized?

A

liver

105
Q

what is argatroban half life?

A

50 minutes

106
Q

when is argatroban used?

A

in pts with HITT

107
Q

how does bivalirudin work?

A

reversible direct thrombin inhibitor.

108
Q

how is bivalirudin metabolized?

A

proteinase enzymes in blood

109
Q

what is bivalirudin’s half life?

A

25 minutes

110
Q

where does hirudin come from?

A

leeches

111
Q

how does hirudin work?

A

irreversible direct thrombin inhibitor, most potent direct inhibitor of thrombin

112
Q

what is the risk of hirudin?

A

high risk for bleeding complications

113
Q

what is ancrod and how does it work?

A

malayan pit viper venom; stimulates tPA release

114
Q

of argatroban, bivalirudin, hirudin, which ones are reversible and which are irreversible direct thrombin inhibitors?

A

argatroban and bivalirudin are reversible

115
Q

what are the thrombolytics?

A

streptokinase, urokinase, and tPA

116
Q

what do thrombolytics do?

A

activate plasminogen

117
Q

what is the treatment for thrombolytic overdose?

A

E-aminocaproic acid (Amicar)

118
Q

what are the minor contraindications for thrombolytic use?

A

minor surgery, recent CPR, AF w MV dz, bacterial endocarditis, hemostatic defects (ie renal or liver disease), diabetic hemorrhagic retinopathy, pregnancy

119
Q

what are the major contraindications for thrombolytic use?

A

recent (<10d) surgery, organ biopsy, obstetric delivery, left heart thrombus, active PUD, recent major trauma, uncontrolled HTN, recent eye surgery

120
Q

what are the absolute contraindications for thrombolytic use?

A

active internal bleed, recent CVA or neurosurgery (<3 mo), intracranial pathology, recent GI bleed

121
Q

what should hct and platelets be before surgery in pts with PCV?

A

hct <400 before surgery

122
Q

which types of VWD are autosomal dominant and which are autosomal recessive?

A

I and II are autosomal dominant, III is autosomal recessive

123
Q

what are the initial events to thrombus formation?

A
  1. platelet adhesion
  2. shape change
  3. granule release
  4. recruitment
  5. hemostatic plug
  6. collagen exposure
124
Q

what do you need to follow when using thrombolytics? how high should it be?

A

fibrinogen levels should be >100. if <100, associated with risk and severity of bleeding

125
Q

how does heparin work?

A

binds and activates anti-thrombin III (1000x more activity)

126
Q

how does ASA work?

A

inhibits cyclooxygenase (COX) in platelets and decreases TXA2.

127
Q

can platelets resynthesize COX?

A

no. they dont have DNA

128
Q

what is the treatment for factor V leiden?

A

heparin, warfarin

129
Q

what is the treatment for protein C or S deficiency?

A

heparin, warfarin

130
Q

how does factor V leiden mutation cause problems?

A

causes resistance to activated protein C; the defect is on factor V.

131
Q

what is the most common congenital hypercoagulability disorder?

A

factor V leiden mutation (30% of spontaneous venous thromboses)

132
Q

how high should platelets be before and after surgery?

A

> 50,000 before, >20,000 after

133
Q

when does coumadin need to stop before surgery? what do you need to consider in pts who require coumadin during this time?

A

stop 7 days before surgery, consider bridge to heparin

134
Q

if a pt has epistaxis, what diseases are most likely?

A

vWF deficiency and platelet disorders

135
Q

what is a consider in prostate surgery in terms of bleeding?

A

can release urokinase, which activates plasminogen –> thrombolysis.

136
Q

how are most patients with bleeding disorders revealed?

A

tooth extraction or tonsillectomy

137
Q

what is treatment for plavix overdose?

A

platelets

138
Q

what ist he treatment for prothrombin gene defect G202010 A?

A

heparin, warfarin

139
Q

what is the treatment for hyperhomocysteinemia?

A

folate and b12

140
Q

what causes APLAS?

A

antibiodies to cardiolipin and lupus anticoagulant (phospholipids)

141
Q

what is the most common factor causing acquired hypercoagulability?

A

tobacco

142
Q

what is treatment for APLAS?

A

heparin, warfarin

143
Q

what are causes of acquired hypercoagulability?

A

tobacco, malignancy, inflammatory states, inflammatory bowel dz, infections, oral contraceptives, pregnancy, RA, post-op, myeloproliferative disorders

144
Q

how do you diagnose APLAS?

A

prolonged PTT (corrected with FFP), russell viper venom time, false pos RPR test for syphilis

145
Q

how does cardiopulmonary bypass cause hypercoagulation? what can you do to prevent?

A

factor XII (hageman factor) is activated. Heparin prevents it.

146
Q

what is the treatment for dysfibrinogenemia, dysplasminogenemia?

A

heparin, warfarin

147
Q

how does polycythemia vera cause cause clots? what is treatment?

A

defect in platelet fxn, can get thrombosis. Rx: phlebotomy, ASA

148
Q

what is the treatment for antithrombin III deficiency?

A

heparin does not work in these pts. Rx: recombinant AT-III concentrate or FFP (highest concentraiton of AT-III) followed by heparin, then warfarin

149
Q

what happens to coags in APLAS?

A

prolonged PTT…but they are hypercoagulable

150
Q

do all pts with APLAS have SLE?

A

no

151
Q

what is special about factor X?

A

convergence point between intrinsic and extrinsic and is common for both paths.

152
Q

what is the treatment for prostate surgery bleeding?

A

E-aminocaproic acid (amicar)

153
Q

what is the prothrombin complex?

A

tissue factor (injured tissues) + factor VII –> activate X, then add V –> convert prothrombin to thrombin –> thrombin then converts fibrinogen to fibrin

154
Q

what does XIII do?

A

helps crosslink fibrin.

155
Q

what is heparin half life?

A

60-90 minutes

156
Q

what are the thrombolytic agents?

A

streptokinase, urokinase, tPA

157
Q

when does clopidogrel (plavix) need to stop before surgery? how does it work?

A

stop 7d before surgery. it is an ADP receptor antagonist.

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