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Cert Prep > Valley: Hemostasis > Flashcards

Valley: Hemostasis Flashcards

1
Q

What are the 4 steps involved in primary hemostasis?

A
  1. Adhesion of platelets to damages vascular wall
  2. Activation of platelets
  3. Aggregation of platelets
  4. Production of fibrin
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2
Q

Adhesion of platelets to damages vascular walls (requires ———, also known as factor —)

A

Von willebrand’s factor; 8

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3
Q

Activation of platelets (requires —, which is factor —)

A

Thrombin ; 2a

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4
Q

Aggregation of platelets (requires — and ——)

A

ADP and thromboxane A2

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5
Q

Production of fibrin (requires —, —, and ——— coagulation factors)

A

Extrinsic, intrinsic, and final common pathways

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6
Q

Platelets have an average life span of — to —days

A

8-12

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7
Q

Normal platelet count is — to — cells per ml

A

150,000 to 400,000

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8
Q

Approximately — of the platelet pool is sequestered in the spleen

A

33%

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9
Q

When vascular endothelium is damages and the subendothelium of the blood vessel wall is exposed, von willebrand’s factor anchors platelets to the — layer of the subendothelium.

A

Collagen

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10
Q

Von willebrand’s factor promotes — adhesion

A

Platelet

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11
Q

Von willebrand’s factor is manufactured, and released from, ——.

A

Endothelial cells

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12
Q

What is the most common inherited coagulation defect?

A

Von willebrand’s disease

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13
Q

—, a non-pressor analogue of arginine vasopressin, causes release of endogenous stores of vWF and is the first-line treatment for von willebrand’s disease

A

D-amino-d-arginine vasopressin (desmopressin, DDAVP)

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14
Q

When DDAVP is used with von willebrand’s disease, platelet adhesion is increased within — minutes of injection and wears off at — to — hours.

A

30 minutes; 4-6 hours

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15
Q

What is a side effect that occurs in children with the use of DDAVP?

A

Hyponatremia

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16
Q

DDAVP causes — in type 2B von willebrand’s disease.

A

Thrombocytopenia

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17
Q

— is the standard treatment for von willebrand’s disease.

A

DDAVP (desmopressin)

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18
Q

Von willebrand’s factor can be increase by giving what 3 things?

A
  1. Desmopressin (DDAVP)
  2. Cryoprecipitate
  3. Purified factor VIII
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19
Q

What 3 factors do cryoprecipitate contain?

A
  1. Factor VIII
  2. Factor 1 (fibrinogen)
  3. Factor XIII
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20
Q

Patients who do not respond to desmopressin with von willebrand’s disease should receive — or —.

A

Cryoprecipitate or factor VIII concentrate

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21
Q

What is treated to inactivate HIV and hepatitis viruses?

A

Pooled factor VIII concentrate

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22
Q

— combines with the thrombin receptor on the platelet surface to activate the platelet.

A

Thrombin (factor II)

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23
Q

Among the numerous mediators released from the activated platelets, what are the 2 that promote platelet aggregation?

A
  1. ADP
  2. Thromboxane A2
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24
Q

— activates the platelet.

A

Thrombin (factor II)

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25
Q

Thromboxane A2 and ADP uncover — receptors.

A

Fibrinogen

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26
Q

When fibrinogen attaches to its receptors, thereby linking platelets to each other the clot is still — and —.

A

Water-soluble and friable

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27
Q

— aggregates platelets.

A

Fibrinogen (factor I)

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28
Q

Cyclooxygenase (COX) is rendered non-functional because the — group of aspirin causes acetylation of cyclooxygenase.

A

Acetyl

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29
Q

— is the rate-limiting enzyme in the conversion of arachidonic acid to thromboxane A2.

A

Cyclooxygenase

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30
Q

When considering aspirin, without — then platelet aggregation is impaired.

A

Thromboxane A2

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31
Q

What are the 5 most common pharmacological causes of abnormal platelet aggregation?

A
  1. Aspirin
  2. NSAIDs
  3. Plavix (clopidogrel)
  4. Ticlopidine (Ticlid)
  5. Dipyridamole (Persantine)
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32
Q

What is the main difference with aspirin and NSAIDs?

A

NSAIDs depression of thromboxane A2 production by platelets is temporary (~24-48hrs), not permanent

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33
Q

Which antiplatelet drug is an anti-ADP agent (life-time of the platelets)

A

Plavix (clopidogrel)

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34
Q

Which antiplatelet drug inhibits ADP-induced fibrinogen aggregation of platelets?

A

Ticlopidine (ticlid)

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35
Q

How early should you discontinue Ticlopidine (ticlid)?

A

14 days before surgery

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36
Q

Which antiplatelet drug increases cAMP in platelets?

A

Dipyridamole (persantine)

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37
Q

cAMP prevents — of platelets

A

Aggregation

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38
Q

How early do you discontinue dipyridamole (persantine)?

A

24 hours before surgery

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39
Q

How do anti-fibrinogen receptor (GPIIb/IIIa) drugs work?

A

“cap” and block the fibrinogen receptor (GPIIb/IIIa), preventing attachment of fibrinogen resulting in no linking of platelets and no aggregation

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40
Q

How early should eptifibatide (integrilin) be discontinued?

A

24 hours before surgery

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41
Q

How early should abciximab (ReoPro) be discontinued?

A

72 hours before surgery

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42
Q

How early should tirofiban (aggrastat) be discontinued?

A

24 hours before surgery

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43
Q

— activates the platelet.

A

Thrombin

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44
Q

Aspirin — inhibits cyclooxygenase

A

Irreversibly

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45
Q

Aspirin inactivates the life time of the platelet, which is about — to — days.

A

8-12

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46
Q

NSAIDs — inhibit cyclooxygenase.

A

Reversibly

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47
Q

NSAIDs inhibit the platelet for — to — hours.

A

24-48 hours

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48
Q

The most common acquired blood clotting defect is due to inhibition of — production by aspirin or NSAIDs.

A

Cyclooxygenase

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49
Q

Which clotting factors are vitamin K dependent?

A

1972 ; 10,9,7,2

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50
Q

All procoagulant clotting factors are made in the liver except for which 3?

A
  1. Von willebrand’s factor (VIII;vWF)
  2. Tissue factor (factor 3)
  3. Calcium (factor 4)
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51
Q

Factor VIII:vWF regulates the production or release of factor —.

A

VIII:C

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52
Q

Which clotting factor is the source of vascular wall and extravascular cell membranes; released from traumatized cells?

A

Tissue factor or thromboplastin (factor 3)

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53
Q

Which clotting factor is the source of diet?

A

Calcium (factor 4)

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54
Q

Which clotting factor is the source of vascular endothelial cells?

A

Von willebrand’s factor (factor VIII:vWF)

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55
Q

What 2 proteins are vitamin K dependent?

A

Protein C and protein S

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56
Q

After — aggregate, — is woven into platelets and cross-linked.

A

Platelets; fibrin

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57
Q

Cross-linked fibrin is — in water.

A

Insoluble

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58
Q

Cross-linking of fibrin strands requires coagulation factor —.

A

13

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59
Q

What 2 factors are included with the extrinsic pathway?

A

7 and 3

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60
Q

Damage outside of blood vessels triggers the release of — (factor —) from damaged cells.

A

Thromboplastin (factor 3, tissue factor)

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61
Q

Thromboplastin activates factor —.

A

7

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62
Q

Activated factor 7 activates factor —.

A

10

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63
Q

What 4 factors are involved with intrinsic pathway?

A

12, 11, 9, 8

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64
Q

What 4 factors are involved in the common pathway?

A

10, 5, 2, 1

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65
Q

What is needed for fibrin to start cross-linking?

A

Factor 13

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66
Q

Coumadin acts on the — and — pathways.

A

Extrinsic and final common

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67
Q

Coumadin is assessed by — and — blood tests.

A

PT and INR

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68
Q

Heparin acts on the — and — pathways.

A

Intrinsic and final common

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69
Q

Heparin is assessed by — and — blood tests.

A

PTT and ACT

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70
Q

The — pathway is initiated in response to damage occurring outside the blood vessel.

A

extrinsic

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71
Q

The coagulation factors of the extrinsic pathway are — and —.

A

III (also known as tissue factor or thromboplastin) and VII

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72
Q

The — pathway is initiated by damage inside the blood vessel.

A

intrinsic

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73
Q

The coagulation factors of the intrinsic pathway are —, —, —, and —.

A

XII, XI, IX, and VIII

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74
Q

The coagulation factors of the final common pathway are —, —, —, —, and —.

A

X, V, II, I and XIII

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75
Q

For 37 cents you can purchase the — pathway.

A

extrinsic

76
Q

If you cannot buy the — pathway for $12, you can get it for $11.98.

A

intrinsic

77
Q

The — pathway can be purchased at the five (V) and dime (X) for 1 (I) or 2 (II) dollars on the 13th (XIII) of the month.

A

final common

78
Q

Fibrin cross-linking occurs in the presence of factor —.

A

XIII

79
Q

Warfarin (Coumadin) interferes with the — pathway.

A

Extrinsic

80
Q

Prothrombin time (PT) and international normalized ratio (INR) assess the — pathway

A

Extrinsic

81
Q

Heparin interferes with the — pathway.

A

Intrinsic

82
Q

Partial thromboplastin time (PTT) and activated coagulation time (ACT) assess the — pathway.

A

Intrinsic

83
Q

Most common inherited bleeding disorder?

A

Von willebrand’s disease

84
Q

Sex-linked recessive genetic disorder that is carried by the female member of a kindred and affects males almost exclusively and the second most commonly inherited coagulation disorder (occurs in 1 of 10,000 male births)

A

Hemophilia A (factor VIII:C deficiency)

85
Q

3 treatment options for hemophilia A?

A

Fresh frozen plasma (FFP), cryoprecipitate, and factor 8 concentrate

86
Q

Christmas disease; factor 9 deficiency

A

Hemophilia B

87
Q

The most important clue to clinically significant bleeding disorder in an otherwise healthy patient
remains the —.

A

history

88
Q

The most common reason for coagulopathy in patients receiving massive blood transfusions is the lack of functioning —.

A

platelets

89
Q

Platelets in stored blood are nonfunctional after —to— days.

A

1-2 days

90
Q

Abnormalities of coagulation owing to dilution of factors — and — may also occur, especially if packed red blood cells are infused with a minimal volume of plasma.

A

V and VIII

91
Q

The only acceptable clinical indication for transfusion of packed red blood cells is to increase the ——— of the blood.

A

oxygen carrying capacity

92
Q

All procoagulants except — are present in fresh frozen plasma (FFP).

A

platelets

93
Q

Cryoprecipitate contains factor —, factor —, and factor —.

A

factor VIII, factor I, and factor XIII.

94
Q

— is harvested from fresh frozen plasma as it is thawing.

A

cryoprecipitate

95
Q

One unit of RBCs will increase hematocrit (Hct) —%, or —/dL.

A

3-4%, or 19/dL.

96
Q

1 cc/kg RBCs will increase Hct —%.

A

1

97
Q

One unit of platelets will increase platelet count — - —/mm3.

A

5,OOO-lO,000

98
Q

“Massive transfusion” is defined as 1 complete blood volume transfused within — hours.

A

24

99
Q

Activated antithrombin binds factor — and factor — greatly and factors —, —, and — to a lesser degree.

A

thrombin (factor IIa) and factor Xa greater ; factors IX, Xl, and XII lesser

100
Q

— works by increasing the effectiveness of antithrombin 1,000-fold or more

A

Heparin

101
Q

Antithrombin is made in the — and neutralizes — pathway factors and — pathway factors by forming complexes with them

A

liver ; final common pathway factors and intrinsic pathway factors

102
Q

— is a required cofactor for heparin

A

Antithrombin

103
Q

Heparin binds to —

A

antithrombin III

104
Q

Acquired antithrombin deficiency states are found in patients with what 2 issues?

A

Cirrhosis of the liver and Nephrotic syndrome

105
Q

An antithrombin deficiency is the most common reason a patient is unresponsive to —.

A

heparin

106
Q

A patient scheduled for CABG surgery is heparinized. The ACT is reported to be 210 seconds. After administration of more heparin, the ACT is 240 seconds. Is the patient adequately heparinized? What should you do?

A

Patient is not adequately heparinized. ACT should be greater than 400 seconds. Give the patient fresh frozen plasma (FFP). FFP contains all coagulation and anticoagulation factors made by the liver, including antithrombin. Then proceed with the case.

107
Q

— forms a complex with antithrombin III.

A

Heparin

108
Q

The — is prolonged by heparin. Heparin blocks the classical — and — pathways.

A

partial thromboplastin time (PTT) ; intrinsic and final common pathways

109
Q

Protamine reverses the action of heparin by —.

A

neutralization

110
Q

Warfarin (Coumadin) and other coumarin-like substances bind to the — receptor in the liver and competitively inhibit —.

A

vitamin K ; vitamin K

111
Q

— is prolonged by warfarin. Warfarin and other coumarins block the classical — and — pathways.

A

Prothrombin time (PT) ; extrinsic (factor VII) and final common (factors II and X) pathways

112
Q

Reombinant hirudin, ximelagatran, and argatroban are — inhibitors.

A

direct thrombin

113
Q

Normal value for bleeding time?

A

3-10min

114
Q

Normal value for platelet count?

A

150,000-400,000 cells/mL

115
Q

Normal value for prothrombin time (PT)?

A

12-14 sec

116
Q

Normal value for partial thromboplastin time (PTT)?

A

25-35 sec

117
Q

Normal value for thrombin time (TT)?

A

<30 sec

118
Q

Normal value for activate coagulation time (ACT)?

A

80-150 sec

119
Q

Normal value for fibrinogen?

A

> 150 mg/dl

120
Q

— and — assess heparin

A

PTT and ACT

121
Q

Heparinization is adequate if ACT — - — sec

A

> 400-450 sec

122
Q

—, the inactive form of plasmin, is synthesized in the liver, circulates in the blood, and is incorporated into a clot as the clot is formed.

A

Plasminogen

123
Q

— and — are the two agents that normally convert plasminogen to its active form, plasmin.

A

Tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA)

124
Q

Plasmin breaks down —.

A

fibrin

125
Q

— is synthesized in the liver and circulates in the blood

A

Plasminogen

126
Q

-incorporated with fibrin in the forming clot
-produced by endothelial cells and released into the circulation
-release is stimulated by thrombin and venous stasis
-by binding avidly to fibrin, converts plasminogen to plasmin within the thrombus

A

Tissue-type plasminogen activator (tPA)

127
Q

-found in limited amounts in the blood
-has little affinity for fibrin
-most widely used thrombolytic agent for intra-arterial infusion into the peripheral arterial system and grafts

A

Urokinase-type plasminogen activator (uPA)

128
Q

-produced by beta-hemolytic streptococci
-has little affinity for fibrin
-preformed antibodies to this may inactivate it

A

Streptokinase

129
Q

What are the 3 plasminogen activators?

A

Tissue-type plasminogen activator (tPA), urokinase-type plasminogen activator (uPA), and streptokinase

130
Q

Aprotinin (Trasylol) inhibits —.

A

plasmin

131
Q

Epsilon aminocaproic acid (Arnicar, EACA) and tranexamic acid prevent the breakdown of — by preventing displacing the plasmin.

A

fibrin

132
Q

Aprotinin and amicar work by inhibiting —.

A

plasmin

133
Q

What is the one increased laboratory abnormality of clotting factors and enhanced fibrinolysis of DIC?

A

Fibrin degradation products

134
Q

— is the “Most common cause of an isolated high PT”

A

Liver disease

135
Q

Treatment for coagulation abnormalities with liver disease?

A

Replace clotting factors with fresh frozen plasma, cryoprecipitate, and vitamin K as needed

136
Q

Treatment for coagulation abnormalities with renal failure?

A

Adequate dialysis and elevation of hematocrit, cryoprecipitate, and DDAVP

137
Q

Transfused blood is deficient in — and coagulation factors — and —

A

platelets ; V and VIII

138
Q

Diffuse bleeding during massive transfusion is generally caused by —.

A

thrombocytopenia

139
Q

Treatment for coagulation abnormalities with massive blood transfusion?

A

Platelet transfusion (correct thrombocytopenia), fresh frozen plasma (supplies all coagulation factors), cryoprecipitate (source of factor I, VIII, and XIII)

140
Q

When the endothelial lining of the blood vessel is damaged, platelets adhere to the subendothelial collagen. What substance anchors platelets to subendothelial collagen?

A

Von Willebrand’s factor (VlII:vWF or VIII:R)

141
Q

What clotting factor activates the platelet at the site of vascular injury?

A

thrombin (factor lIa)

142
Q

What two substances, released from the activated platelet, stimulate platelet aggregation?

A

ADP and thromboxane A2

143
Q

What substance links platelets together (aggregates them)?

A

fibrinogen (factor I)

144
Q

What agents inhibit platelet aggregation by impairing cyclo-oxygenase?

A

aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs)

145
Q

What clotting factors are found in the extrinsic pathway?

A

III (also known as tissue factor or thromboplastin) and VII

146
Q

What clotting factors are found in the intrinsic pathway?

A

XII, XI, IX, and VIII

147
Q

What clotting factors are found in the final common pathway?

A

I, II, V, X, XIlI

148
Q

What clotting factor is considered the physiologic initiator of the coagulation cascade?

A

III (also known as tissue factor or thromboplastin)

149
Q

What clotting factor promotes fibrin cross-linking?

A

XIII

150
Q

Antithrombin III inhibits what five clotting factors? Which of these five is in the intrinsic pathway? What two of these five clotting factors are most profoundly inhibited?

A

II, IX, X, XI, and XII (IX, XI and XII are in the intrinsic pathway; II and X are most profoundly inhibited)

151
Q

What four clotting factors are vitamin K dependent? Which of these is in the extrinsic pathway?

A

II, VII, IX, and X (VII is in the extrinsic pathway)

152
Q

How does heparin work?

A

heparin increases the activity of (“turns on”) antithrombin III

153
Q

How does coumadin work?

A

coumadin competitively inhibits the vitamin K- dependent clotting factors

154
Q

What anticoagulant affects the extrinsic and final common pathways?

A

warfarin (coumadin)

155
Q

What anticoagulant affects the intrinsic and final common pathways?

A

heparin

156
Q

What two coagulation tests assess the extrinsic pathway?

A

prothrombin time (PT) and the international normalized ratio (INR)

157
Q

What two coagulation tests assess the intrinsic pathway?

A

partial thromboplastin time (PTT) and activated coagulation time (ACT)

158
Q

How does protamine work to reverse heparin? What kind of reaction is this?

A

protamine combines electrostatically with heparin (this is a neutralization reaction)

159
Q

What enzyme is responsible for breaking down fibrin?

A

plasmin

160
Q

What two pharmacological agents inhibit plasmin?

A

epsilon-aminocaproic acid (Amicar) and aprotinin (Trasylol)

161
Q

Name three substances that convert plasminogen to plasmin?

A

urokinase plasminogen activator (uPA), tissue plasminogen activator (tPA), and streptokinase

162
Q

When is aprotinin generally used in anesthesia? How does it work?

A

aprotinin is used for repeat sternotomies and works by inhibiting plasmin

163
Q

What is the normal activated coagulation time?

A

80-150 seconds

164
Q

What is the best test of primary hemostasis, or platelet function?

A

standardized skin bleeding time

165
Q

What is the most common reason for coagulopathy after a massive blood transfusion?

A

lack of functioning platelets (thrombocytopenia)

166
Q

What clotting factors are found in fresh frozen plasma?

A

all procoagulants

167
Q

Cryoprecipitate contains what clotting factors?

A

factor I (fibrinogen), factor VIII, and factor XIIl

168
Q

What are the typical manifestations of disseminated intravascular coagulopathy?

A

bleeding, with oozing from tubes, wounds, and vascular access sites

169
Q

Transfused blood is deficient in what two coagulation factors?

A

factors V and VIII

170
Q

What is the most common inherited coagulation defect?

A

Von Willebrand’s disease

171
Q

The patient with von Willebrand’s disease has not responded to desmopressin (DDAVP). What will
you try next?
a. Fresh frozen plasma
b. Cryoprecipitate
c. Amicar
d. Plasmin

A

Cryoprecipitate

172
Q

What antiplatelet agent prevents ADP-induced platelet aggregation?
a. Aspirin
b. Ibuprofen
c. Ketorolac
d. Ticlopidine

A

Ticlopidine

173
Q

Each of the following clotting factors is made in the liver EXCEPT:
a. VIII:C.
b. IV.
c. X.
d. XII.

A

IV

174
Q

The clotting factor that is responsible for cross-linking fibrin is
a. I.
b. II.
c. VII.
d. XIII.

A

XIII

175
Q

What anticoagulant works on the extrinsic pathway, and what test assesses the effectiveness of this
anticoagulant? Anticoagulant&Test
a. Coumadin PT
b. Coumadin PTT
c. Heparin PT
d. Heparin PTT

A

Coumadin PT

176
Q

Cryoprecipitate contains coagulation factors
a. I, VIII, XIII.
b. II, VII, X.
c. I, VII, X.
d. II, X, XI.

A

I, VIII, XIII.

177
Q

When antithrombin III is activated by heparin, antithrombin III
a. releases factors I, III, VII, and XIII.
b. binds factors I, VII, and XIII.
c. releases factors II, IX, X, Xl, and XII.
d. binds factors II, IX, X, Xl, and XII.

A

binds factors II, IX, X, Xl, and XII.

178
Q

A patient who is scheduled for CABG surgery is heparinized, and the ACT is less than 300 seconds.
The result is the same after a second dose of heparin. Why is the patient unresponsive to heparin, and what is your next action?
Reason for unresponsiveness to heparin&Next Action
a. Deficiency of plasmin ; Give FFP
b. Deficiency of plasmin ; Cancel case
c. Deficiency of antithrombin III ; Give FFP
d. Deficiency of antithrombin III ; Cancel case

A

Deficiency of antithrombin III ; Give FFP

179
Q

Prothrombin time normally is
a. 3-5 seconds.
b. 12-14 seconds.
c. 25-35 seconds.
d. 80-150 seconds.

A

12-14 seconds.

180
Q

The reaction of protamine with heparin is a
a. neutralization reaction.
b. covalent reaction.
c. hydrogen bonding reaction.
d. counterbalanced reaction.

A

neutralization reaction.

181
Q

What substance converts fibrin to fibrin split products?
a. Tissue plasminogen activator
b. Amicar
c. Plasmin
d. Streptokinase

A

Plasmin

182
Q

Each of the following statements about aprotinin is true EXCEPT:
a. Aprotinin may cause an allergic reaction when administered to a patient for the first time.
b. Aprotinin may cause an anaphylactic reaction if administered to a patient for the second time.
c. Aprotinin is indicated for patients who are undergoing a sternotomy for the second time.
d. Aprotinin accelerates the breakdown of fibrin.

A

Aprotinin accelerates the breakdown of fibrin.

183
Q

Postoperative bleeding with continued oozing from wounds and catheter sites suggests what disorder?
a. Von Willebrand’s disease
b. Hemophilia A
c. Disseminated intravascular coagulopathy
d. Antithrombin III deficiency

A

Disseminated intravascular coagulopathy

184
Q

Each of the following is decreased in the patient with disseminated intravascular coagulopathy EXCEPT:
a. fibrin split products.
b. fibrinogen.
c. prothrombin.
d. factor VIII.

A

fibrin split products.

185
Q

What is the major cause of diffuse bleeding after a massive blood transfusion?
a. Antithrombin III deficiency
b. Thrombocytopenia
c. Factors V and VIII deficiency
d. Vitamin K deficiency

A

Thrombocytopenia

Cert Prep (20 decks)

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