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Z.Fiser > Fiser.02.Hematology > Flashcards

Fiser.02.Hematology Flashcards

1
Q

What are the three initial responses to vascular injury?

A

Vascular vasoconstriction; platelet adhesion; thrombin generation

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2
Q

Name the 5 steps of primary hemostasis

A

Platelet adhesion to exposed vWF;

Shape change;

Granule release with ADP and TXA2;

Recruitment of additional platelets;

Aggregation and formation of hemostatic plug

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3
Q

Name the four initial substrates that start the “intrinsic pathway”

A

Exposed collagen, prekallikrein, HMW kininogen, factor XII

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4
Q

Name the next 5 steps of the intrinsic pathway

A

Collagen, prekallikrein, HMW kinogen, factor XII –> activate factor XI Factor XI –> activates IX and add VIII IX + VIII –> activates factor X and add V X + V –> converts prothrombin (factor II) to thrombin Thrombin –> converts fibrinogen to fibrin

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5
Q

What are the initial components that start the “extrinsic pathway”?

A

Tissue factor (from injured cells) and factor VII

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6
Q

Name the three additional steps to the extrinsic coagulation cascade

A

Tissue factor + Factor VII –> activate X, add V X + V –> convert prothrombin (factor II) to thrombin Thrombin –> converts fibrinogen to fibrin

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7
Q

Name the five components of the “prothrombin complex”

A

Factor X, factor V, Ca, platelet factor 3, prothrombin

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8
Q

Where does the prothrombin complex form?

A

Forms on platelets

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9
Q

What does the prothrombin complex do?

A

Catalyzes the formation of thrombin

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10
Q

What is the convergence point for the intrinsic and extrinsic pathways?

A

Factor X

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11
Q

What is the convergence point for the intrinsic and extrinsic pathways?

A

Factor X is common for both parts of the pathway

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12
Q

What inhibits factor X?

A

Tissue factor pathway inhibitor

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13
Q

What does fibrin do?

A

Links platelets together by binding GpIIb/IIIa molecules to form the platelet plug

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14
Q

What does factor XIII do?

A

Helps crosslink fibrin

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15
Q

Name three functions of thrombin

A

Converts fibrinogen –> fibrin + fibrin split products Activates factors V and VIII Activates platelets

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16
Q

Which factor has the shortest half life

A

Factor VII

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17
Q

Which two factors are considered labile b/c they have activity lost in stored blood but not in FFP?

A

V and VIII

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18
Q

Which factor is the only one not synthesized in the liver? Where is it synthesized?

A

Factor VIII is synthesized in the endothelium

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19
Q

Name 6 vitamin-K dependent factors

A

Factors II, VII, IX, X, Protein C, Protein S

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20
Q

How long does it take for Vitamin K to have an effect?

A

Takes 6 hours

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21
Q

How long does it take FFP to take effect

A

Immediate effect that lasts 6 hours

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22
Q

What is the normal (in vivo) half life of RBCs?

A

120 days

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23
Q

What is the normal (in vivo) half life of platelets?

A

7 days

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24
Q

What is the normal (in vivo) half life of PMNs?

A

1-2 days

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25
Q

Where is prostacyclin (PGI2) synthesized?

A

Endothelium

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26
Q

Name 2 functions of prostacyclin (PGI2). What does it antagonize?

A

Decreases platelet aggregation; promotes vasodilation; antagonistic to TXA2 (thomboxane)

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27
Q

Where is thromboxane (TXA2) synthesized?

A

Platelets

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28
Q

Name two functions of TXA2

A

Increases platelet aggregation and promotes vasoconstriction

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29
Q

Name the underlying MOA of TXA2 function in platelet aggregation

A

TXA2 triggers release of calcium in platelets –> exposes GpIIb/IIIa receptor GpIIb/IIIa receptor causes platelet-platelet binding Allows platelet-collagen binding with GpIb receptor

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30
Q

Name four functions of antithrombin III (AT III)

A

Key to anticoagulation: binds and inhibits thrombin, factor IX, X, and XI

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31
Q

How does heparin interact with AT-III and by how much does it increase its activity?

A

Consitutively activates AT-III up to 1000x normal activity

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32
Q

Name three effects of protein C

A

Degrades factor V, VIII, and fibrinogen

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33
Q

Name one effect of protein S

A

Protein C co-factor

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34
Q

Where is tissue plasminogen activator (TPA) synthesized and released from?

A

Endothelium

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35
Q

What does TPA do?

A

Converts plasminogen to plasmin

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36
Q

Name four effects of plasmin

A

Degrades factors V, VIII, fibrinogen, and fibrin Lose platelet plug

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37
Q

What does alpha-2 antiplasmin do and where is it released from?

A

Released from endothelium, natural inhibitor of plasmin

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38
Q

Which blood product has the highest levels of vWF-VIII?

A

Cryoprecipitate

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39
Q

Name two diseases that can be treated with cryoprecipitate and why

A

Von willebrand’s disease (for vWF) Hemophilia A (for factor VIII deficiency)

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40
Q

Does cryoprecipitate contain fibrinogen?

A

Yes, contains high levels of fibrinogen

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41
Q

What factors are in FFP?

A

All coagulation factors, protein C, protein S, and AT-III

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42
Q

How does DDAVP (desmopressin) affect the coagulation cascade?

A

Causes release of factor VIII and vWF from endothelium

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43
Q

How do conjugated estrogens affect the coagulation cascade?

A

Cause release of factor VIII and vWF from endothelium

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44
Q

What does PT measure in terms of coagulation cascade (5) and organ function?

A

Factor II, V, VII, X; fibrinogen Best for liver synthetic function

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45
Q

What does PTT measure and not measure?

A

Measures most factors + fibrinogen Does not measure factor VII and XIII – therefore cannot use for factor VII deficiency

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46
Q

What is your goal PTT for routine anticoagulation?

A

Goal PTT 60-90 seconds

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47
Q

What does ACT stand for?

A

Activated clotting time

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48
Q

What is your goal ACT for routine anticoagulation?

A

ACT 150-200 seconds

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49
Q

What is your goal ACT for cardiopulmonary bypass?

A

> 460 seconds

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50
Q

What level INR is a relative CI for surgery?

A

INR > 1.5

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51
Q

What level INR is a relative CI for CVL, percutaneous needle bx, or eye surgery?

A

INR > 1.3

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52
Q

What is the MCC of surgical bleeding?

A

Incomplete hemostasis

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53
Q

What is the most common congenital bleeding disorders?

A

Von wilibrands disease

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54
Q

Which subtypes of vWD are autosomal dominant versus autosomal recessive?

A

Types I & II are AD, Type III is AR

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55
Q

What does vWF do in terms of coagulation?

A

Links the GpIb receptor on platelets to collagen

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56
Q

What is the coagulation test profile (PT/PTT/bleeding time) with von willebrands disease

A

PT normal; PTT normal/abnormal; prolonged bleeding time

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57
Q

What is another name for the bleeding time test?

A

Risocetin test

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58
Q

Which subtype of vWD is most common? What percentage of vWD does it encompasss?

A

70% of cases are Type I – mild symptoms

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59
Q

Which subtype of vWD causes the most severe symptoms?

A

Type III causes the most severe symptoms

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60
Q

What is the pathophysiology of type I vWD?

A

Reduced quantity of vWF

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61
Q

What is the treatment of type I vWD (3)?

A

Recombinant VIII:vWF, DDAVP, cryoprecipitate

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62
Q

What is the pathophysiology of type II vWD?

A

Defect in vWF molecule itself, therefore the vWF does not work well

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63
Q

What is the treatment of type II vWD (2)?

A

Recombinant VIII:vWF; cryoprecipitate

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64
Q

What is the pathophysiology of type III vWD?

A

Complete vWF deficiency (rare)

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65
Q

What is the treatment for type III vWD?

A

Recombinant VIII:vWF; cryoprecipitate DDAVP will not work

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66
Q

What is the underlying deficiency for Hemophilia A?

A

Factor VIII deficiency

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67
Q

How is hemophilia A inherited?

A

Sex-linked recessive

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68
Q

What factor VIII levels do you need preop for hemophilia A patients?

A

100% preop

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69
Q

What factor VIII levels do you need for 10-14 days after surgery for hemophilia A patients?

A

80-100%

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70
Q

What PT/PTT measurements do you see with hemophilia A patients?

A

Prolonged PTT, normal PT

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71
Q

Why may babies with hemophilia A not bleed at circumcision?

A

Because factor VIII crosses the placenta

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72
Q

How do you treat hemophiliac joint bleeding? What treatment is contraindicated?

A

Ice, mobility with ROM exercises, factor VIII concentrate or cryoprecipitate DO NOT ASPIRATE

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73
Q

What is the underlying cause of Hemophilia B?

A

Factor IX deficiency

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74
Q

What is the alternative name for Hemophilia B?

A

Christmas disease

75
Q

How is Hemophilia B inherited?

A

Sex-linked recessive

76
Q

What factor IX levels do you need preop for hemophilia B?

A

Need 100% preop

77
Q

What factor IX levels do you need 2-3 days postop for hemophilia B?

A

30-40%

78
Q

What PT/PTT levels do you see in hemophilia B?

A

Prolonged PTT, normal PT

79
Q

How do you treat hemophilia B?

A

Recombinant factor IX or FFP

80
Q

What PT/PTT levels do you see with factor VII deficiency?

A

Prolonged PT, normal PTT

81
Q

How do you treat factor VII deficiency (2)?

A

Recombinant factor VII concentrate or FFP

82
Q

What symptoms are associated with platelet disorders (5)?

A

Bruising, epistaxis, mucosal bleeding, petechiae, purpura

83
Q

Name two causes of acquired thrombocytopenia

A

H2 blockers, heparin

84
Q

What is the underlying pathophysiology of Glanzmann’s thrombocytopenia

A

Gp-IIb/IIIa receptor deficiency on platelets, so they cannot bind to each other; Gp Iib/IIIa receptors normally are cross-linked by fibrin

85
Q

What is the treatment for Glanzmann’s thrombocytopenia?

A

Platelets

86
Q

What is the underlying pathophysiology of Bernard Soulier disease

A

GpIb receptor deficiency on platelets so they cannot bind to collagen vWF normally linkds GpIb receptor on platelets to collagen

87
Q

How do you treat Bernard Soulier disease?

A

Platelets

88
Q

How does uremia affect coagulation?

A

Inhibits platelet function

89
Q

How do you treat uremia-induced platelet dysfunction?

A

First line: hemodialysis Next: DDAVP, platelets

90
Q

What is the pathophysiology of heparin-induced thrombocytopenia (HIT)?

A

Antiplatelet antibodies formed against heparin-platelet factor 4 complex which results in platelet destruction

91
Q

What type of Ab is created in HIT

A

IgG PF4 antibody

92
Q

What is the underlying pathophysiology and result of heparin-induced thrombocytopenia & thrombosis (HITT)?

A

Platelet aggregation and thrombosis resulting in a white clot

93
Q

What medications cause HIT/HITT?

A

Low doses of heparin, can occur with low molecular weight heparin

94
Q

Does LMWH have the same risk of causing HIT/HITT as heparin

A

No, LMWH has reduced risk of HIT/HITT

95
Q

What is the treatment of HIT?

A

Stop heparin, start argatroban to anticoagulate

96
Q

What is the MOA of argatroban

A

Direct thrombin inhibitor

97
Q

What initiates the cascade of disseminated intravascular coagulation (DIC)?

A

Tissue factor

98
Q

What are the lab findings with DIC (6)?

A

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

99
Q

What is the treatment of DIC?

A

Treat underlying cause (ex: sepsis)

100
Q

How many days preop should you stop aspirin?

A

Stop 7 days preop

101
Q

How does ASA affect bleeding time?

A

Prolongs bleeding time

102
Q

What is the MOA of ASA

A

Inhibits cyclooxygenase in platelets and decreases TXA2

103
Q

Why is ASA’s effects on platelets irreversible?

A

Platelets lack DNA so they cannot resynthesize COX

104
Q

How many days before surgeryshould you stop clopidogrel/Plavix?

A

Stop 7 days before surgery

105
Q

What is the MOA of Plavix?

A

ADP-receptor antagnoist

106
Q

How do you reverse Plavix?

A

Platelets

107
Q

How many days before surgery should you stop coumadin? What can you bridge with?

A

Stop 7 days before surgery, consider bridging with heparin

108
Q

What level of platelets do you want preop?

A

>50K

109
Q

What level of platelets do you want postop?

A

>20K

110
Q

How can prostate surgery affect coaguulation?

A

Releases urokinase, activates plasminogen  thrombolysis

111
Q

How do you treat this complication of prostate surgery?

A

Εaminocaproic acid (Amicar)

112
Q

What is the best way to predict bleeding risk?

A

H&P

113
Q

Why doesn’t a normal circumcision rule out bleeding disorders?

A

Because some factors cross the placenta

114
Q

What two surgical history questions pick up 99% of patients with bleeding disorders?

A

History of excessive bleeding with tonsillectomy or wisdom tooth extraction

115
Q

What are two common bleeding disorders that present with epistaxis?

A

vWF deficiency and platelet disorders

116
Q

What gynecologic problem is common in patients with bleeding disorders?

A

Menorrhagia

117
Q

How do hypercoaguable disorders usually present?

A

Venous or arterial thrombosis or emboli (DVT/PE/CVA)

118
Q

What is the most common hypercoaguable disorder

A

Factor V Leiden mutation

119
Q

What is the most common presenting symptom of Factor V Leiden mutation and in what % of patients?

A

30% of patients p/w spontaneous venous thromboses

120
Q

What is the MOA of Factor V Ledien mutation?

A

Defect on factor V causing resistance to activated protein C

121
Q

What is the treatment for Factor V Leiden mutation?

A

Heparin / warfarin

122
Q

What is the treatment for hyperhomocysteinemia

A

Folic acid and B12

123
Q

What is the treatment for prothrombin gene defect G20210A

A

Heparin / warfarin

124
Q

What is the treatment for protein C or S deficiency?

A

Heparin / warfarin

125
Q

What is a common comorbidity with antiphospholipid antibody syndrome?

A

SLE – although not all patients have this

126
Q

What is the underlying pathophysiology of antiphospholipid antibody syndrome?

A

Antibodies to cardiolipin and lupus anticoagulant (phospholipids) This makes the patients hypercoaguable

127
Q

What are three lab findings that are seen with antiphospholipid antibody syndrome?

A

Prolonged PTT despite hypercoaguable state, not corrected with FFP Positive Russel vipor venom time False-positive RPR test for syphilis

128
Q

How do you treat antiphospholipid antibody syndrome?

A

Heparin / warfarin

129
Q

What is the MCC of acquired hypercoaguability

A

Tobacco

130
Q

Name 8 other causes of acquired hypercoaguability

A

Malignancy Inflammatory disease, IBD, rheumatoid arthritis Infections OCPs / pregnancy Myeloproliferative disorders

131
Q

How does cardiopulmonary bypass result in a hypercoaguable state?

A

Factor XII (Hageman factor) activated

132
Q

How do you prevent CPB-induced hypercoaguable state?

A

Heparin to prevent

133
Q

Which patients are at risk for warfarin-induced skin necrosis?

A

Occurs when patients placed on coumadin without heparin bridge Patients with relative protein C deficiency are susceptible

134
Q

What is the MOA of warfarin-induced skin necrosis?

A

Protein C and S decrease in levels due to their short half-lives compared to other procoagulation factors Results in hyperthrombotic state

135
Q

What is the treatment of warfarin-induced skin necrosis?

A

Heparin if it occurs Prevent by bridging to coumadin with heparin

136
Q

Name the three elements of Virchow’s triad and what it predicts

A

Key elements in development of venous thrombosis Stasis, endothelial injury, hypercoaguability

137
Q

What is the key element in development of arterial thrombosis

A

Endothelial injury

138
Q

What are the three risk factors for DVT?

A

Stasis, venous injury, and hypercoaguability (Virchow’s triad)

139
Q

What is the treatment for a patient’s first postop DVT?

A

Warfarin x 1 month

140
Q

What is the treatment for a patient’s second postop DVT?

A

Warfarin x 1 year

141
Q

What is the treatment for a patient’s third postop DVT?

A

Warfarin for life

142
Q

What is the treatment for a patient s/p PE

A

Warfarin for life

143
Q

Name four indications for Greenfield filters

A

Contraindications to anticoagulation Documented PE while on anticoagulation Free-floating IVC, iliofemoral, or deep femoral DVT Recent pulmonary embolectomy

144
Q

What is the indication for temporary IVCF placement

A

Patients at high risk for DVT (head injury or prolonged bedrest)

145
Q

What is the treatment for a hemodynamically stable patient with a PE?

A

Heparin or suction catheter-based intervention

146
Q

What is the role of thrombolytics in pulmonary embolism treatment?

A

No role, they have not shown improvement in survival

147
Q

When should you go to the OR with a patient with a PE?

A

If a patient is in shock despite massive inotropes and pressors

148
Q

What is the most common origin of a pulmonary embolism?

A

Iliofemoral DVT

149
Q

What is the MOA of Amicar (ε-aminocaproic acid)?

A

Inhibits fibrinolysis by inhibiting plasmin

150
Q

Name three indications for Amicar

A

DIC; persistent bleeding following cardiopulmonary bypass; thrombolytic overdoses

151
Q

What is the MOA of warfarin?

A

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

152
Q

What is the MOA of SCDs (2)?

A

Improve venous return induce fibrinolysis and release of tPA (tissue plasminogen activator) from endothelium with compression

153
Q

What is the MOA of heparin?

A

Binds to and activates antithrombin-III to 1000x baseline activity, inactivating factor Xa and thrombin

154
Q

What is the half-life of heparin

A

60-90 minutes

155
Q

What is the goal PTT for heparin?

A

60-90seconds

156
Q

How do you reverse heparin and how does it work?

A

Protamine binds to heparin

157
Q

Which system clears heparin?

A

Reticuloendothelial system (spleen)

158
Q

Name two adverse effects of long-term heparin use

A

Osteoporosis; alopecia

159
Q

Which of these are safe/unsafe to use in pregnancy and why: heparin/warfarin?

A

Heparin does not cross placenta, safe in pregnancy. Warfarin does cross placenta = not safe in pregs

160
Q

What percent of patients get a protamine reaction and how does it present (3 Sx)?

A

1% of patients, p/w hypotension, bradycardia, decreased heart function

161
Q

What is protamine reaction & what is the MOA of protamine reaction (2)?

A

Protamine reaction is the IgG/IgE-mediated anaphylactic reaction to administration of protamine that can lead to cardiac collapse. MOA= cross reacts with NPH insulin or previous protamine exposure

162
Q

What is the MOA of LMWH (compared to heparin)

A

Binds and activates antithrombin III Increases neutralization of just Xa and thrombin (has less of an effect on thrombin compared to heparin but the same effect on Xa)

163
Q

Name two LMWHs

A

Enoxaparin, fondaparinux

164
Q

Can LMWH be reversed with protamine

A

nope

165
Q

What is the risk of HIT with LMWH compared to unfractionated heparin?

A

Lower risk of HIT with LMWH

166
Q

What is the MOA of argatroban? Is it reversible or irreversible?

A

Reversible direct thrombin inhibitor

167
Q

What is the half-life of argatroban?

A

50 minutes

168
Q

Where is argatroban metabolized?

A

In the liver

169
Q

What is the MC indication for argatroban?

A

In patients with HITT

170
Q

What is the MOA of bivalirudin (angiomax) and is it reversible?

A

Reversible direct thrombin inhibitor

171
Q

What is the half-life of bivalirudin?

A

25 minutes

172
Q

Where is bivalirudin metabolized

A

Proteinase enzymes in plasma / renal

173
Q

What is the most potent direct thrombin inhibitor?

A

Hirudin (hirulog, from leeches)

174
Q

What is the MOA of hirudin (hirulog) and is it reversible?

A

Irreversible direct thrombin inhibitor

175
Q

What is the origin and MOA of Ancrod?

A

Malyan pit viper venom; stimulates tPA release

176
Q

Name three thrombolytics

A

Streptokinase, urokinase, tPA

177
Q

What is a common problem a/w using streptokinase?

A

Has high antigenicity

178
Q

What is the MOA of these three thrombolytics? (Streptokinase, urokinase, tPA)

A

All activate plasminogen

179
Q

How do you monitor anticoagulation with thrombolytics?

A

Fibrinogen levels

180
Q

What levels of fibrinogen are a/w increased risk of bleeding?

A

Fibrinogen <100

181
Q

What is the treatment for thrombolytic overdose?

A

ε-aminocaproic acid (Amicar)

182
Q

Name five absolute contraindications to thrombolytic use

A

Active internal bleeding Recent CVA / NSGY (within 3mo) Intracranial pathology Recent GI bleeding

183
Q

Name five major contraindications to thrombolytic use

A

Recent surgery, organ biopsy, obstetric delivery, or eye surgery (within 10 days) Left heart thrombus Active peptic ulcer Recent major trauma Uncontrolled HTN

184
Q

Name 7 minor contraindications to thrombolytic use

A

Minor surgery Recent CPR Afib with mitral valve disease Bacterial endocarditis Hemostatic defects (ex: a/w renal or liver disease) Diabetic hemorrhagic retinopathy pregnancy

Z.Fiser (22 decks)

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