Valley: Hemostasis Flashcards
(185 cards)
1
Q
What are the 4 steps involved in primary hemostasis?
A
- Adhesion of platelets to damages vascular wall
- Activation of platelets
- Aggregation of platelets
- Production of fibrin
2
Q
Adhesion of platelets to damages vascular walls (requires ———, also known as factor —)
A
Von willebrand’s factor; 8
3
Q
Activation of platelets (requires —, which is factor —)
A
Thrombin ; 2a
4
Q
Aggregation of platelets (requires — and ——)
A
ADP and thromboxane A2
5
Q
Production of fibrin (requires —, —, and ——— coagulation factors)
A
Extrinsic, intrinsic, and final common pathways
6
Q
Platelets have an average life span of — to —days
A
8-12
7
Q
Normal platelet count is — to — cells per ml
A
150,000 to 400,000
8
Q
Approximately — of the platelet pool is sequestered in the spleen
A
33%
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
10
Q
Von willebrand’s factor promotes — adhesion
A
Platelet
11
Q
Von willebrand’s factor is manufactured, and released from, ——.
A
Endothelial cells
12
Q
What is the most common inherited coagulation defect?
A
Von willebrand’s disease
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)
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
15
Q
What is a side effect that occurs in children with the use of DDAVP?
A
Hyponatremia
16
Q
DDAVP causes — in type 2B von willebrand’s disease.
A
Thrombocytopenia
17
Q
— is the standard treatment for von willebrand’s disease.
A
DDAVP (desmopressin)
18
Q
Von willebrand’s factor can be increase by giving what 3 things?
A
- Desmopressin (DDAVP)
- Cryoprecipitate
- Purified factor VIII
19
Q
What 3 factors do cryoprecipitate contain?
A
- Factor VIII
- Factor 1 (fibrinogen)
- Factor XIII
20
Q
Patients who do not respond to desmopressin with von willebrand’s disease should receive — or —.
A
Cryoprecipitate or factor VIII concentrate
21
Q
What is treated to inactivate HIV and hepatitis viruses?
A
Pooled factor VIII concentrate
22
Q
— combines with the thrombin receptor on the platelet surface to activate the platelet.
A
Thrombin (factor II)
23
Q
Among the numerous mediators released from the activated platelets, what are the 2 that promote platelet aggregation?
A
- ADP
- Thromboxane A2
24
Q
— activates the platelet.
A
Thrombin (factor II)
25
Thromboxane A2 and ADP uncover — receptors.
Fibrinogen
26
When fibrinogen attaches to its receptors, thereby linking platelets to each other the clot is still — and —.
Water-soluble and friable
27
— aggregates platelets.
Fibrinogen (factor I)
28
Cyclooxygenase (COX) is rendered non-functional because the — group of aspirin causes acetylation of cyclooxygenase.
Acetyl
29
— is the rate-limiting enzyme in the conversion of arachidonic acid to thromboxane A2.
Cyclooxygenase
30
When considering aspirin, without — then platelet aggregation is impaired.
Thromboxane A2
31
What are the 5 most common pharmacological causes of abnormal platelet aggregation?
1. Aspirin
2. NSAIDs
3. Plavix (clopidogrel)
4. Ticlopidine (Ticlid)
5. Dipyridamole (Persantine)
32
What is the main difference with aspirin and NSAIDs?
NSAIDs depression of thromboxane A2 production by platelets is temporary (~24-48hrs), not permanent
33
Which antiplatelet drug is an anti-ADP agent (life-time of the platelets)
Plavix (clopidogrel)
34
Which antiplatelet drug inhibits ADP-induced fibrinogen aggregation of platelets?
Ticlopidine (ticlid)
35
How early should you discontinue Ticlopidine (ticlid)?
14 days before surgery
36
Which antiplatelet drug increases cAMP in platelets?
Dipyridamole (persantine)
37
cAMP prevents — of platelets
Aggregation
38
How early do you discontinue dipyridamole (persantine)?
24 hours before surgery
39
How do anti-fibrinogen receptor (GPIIb/IIIa) drugs work?
“cap” and block the fibrinogen receptor (GPIIb/IIIa), preventing attachment of fibrinogen resulting in no linking of platelets and no aggregation
40
How early should eptifibatide (integrilin) be discontinued?
24 hours before surgery
41
How early should abciximab (ReoPro) be discontinued?
72 hours before surgery
42
How early should tirofiban (aggrastat) be discontinued?
24 hours before surgery
43
— activates the platelet.
Thrombin
44
Aspirin — inhibits cyclooxygenase
Irreversibly
45
Aspirin inactivates the life time of the platelet, which is about — to — days.
8-12
46
NSAIDs — inhibit cyclooxygenase.
Reversibly
47
NSAIDs inhibit the platelet for — to — hours.
24-48 hours
48
The most common acquired blood clotting defect is due to inhibition of — production by aspirin or NSAIDs.
Cyclooxygenase
49
Which clotting factors are vitamin K dependent?
1972 ; 10,9,7,2
50
All procoagulant clotting factors are made in the liver except for which 3?
1. Von willebrand’s factor (VIII;vWF)
2. Tissue factor (factor 3)
3. Calcium (factor 4)
51
Factor VIII:vWF regulates the production or release of factor —.
VIII:C
52
Which clotting factor is the source of vascular wall and extravascular cell membranes; released from traumatized cells?
Tissue factor or thromboplastin (factor 3)
53
Which clotting factor is the source of diet?
Calcium (factor 4)
54
Which clotting factor is the source of vascular endothelial cells?
Von willebrand’s factor (factor VIII:vWF)
55
What 2 proteins are vitamin K dependent?
Protein C and protein S
56
After — aggregate, — is woven into platelets and cross-linked.
Platelets; fibrin
57
Cross-linked fibrin is — in water.
Insoluble
58
Cross-linking of fibrin strands requires coagulation factor —.
13
59
What 2 factors are included with the extrinsic pathway?
7 and 3
60
Damage outside of blood vessels triggers the release of — (factor —) from damaged cells.
Thromboplastin (factor 3, tissue factor)
61
Thromboplastin activates factor —.
7
62
Activated factor 7 activates factor —.
10
63
What 4 factors are involved with intrinsic pathway?
12, 11, 9, 8
64
What 4 factors are involved in the common pathway?
10, 5, 2, 1
65
What is needed for fibrin to start cross-linking?
Factor 13
66
Coumadin acts on the — and — pathways.
Extrinsic and final common
67
Coumadin is assessed by — and — blood tests.
PT and INR
68
Heparin acts on the — and — pathways.
Intrinsic and final common
69
Heparin is assessed by — and — blood tests.
PTT and ACT
70
The — pathway is initiated in response to damage occurring outside the blood vessel.
extrinsic
71
The coagulation factors of the extrinsic pathway are — and —.
III (also known as tissue factor or thromboplastin) and VII
72
The — pathway is initiated by damage inside the blood vessel.
intrinsic
73
The coagulation factors of the intrinsic pathway are —, —, —, and —.
XII, XI, IX, and VIII
74
The coagulation factors of the final common pathway are —, —, —, —, and —.
X, V, II, I and XIII
75
For 37 cents you can purchase the — pathway.
extrinsic
76
If you cannot buy the — pathway for $12, you can get it for $11.98.
intrinsic
77
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.
final common
78
Fibrin cross-linking occurs in the presence of factor —.
XIII
79
Warfarin (Coumadin) interferes with the — pathway.
Extrinsic
80
Prothrombin time (PT) and international normalized ratio (INR) assess the — pathway
Extrinsic
81
Heparin interferes with the — pathway.
Intrinsic
82
Partial thromboplastin time (PTT) and activated coagulation time (ACT) assess the — pathway.
Intrinsic
83
Most common inherited bleeding disorder?
Von willebrand’s disease
84
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)
Hemophilia A (factor VIII:C deficiency)
85
3 treatment options for hemophilia A?
Fresh frozen plasma (FFP), cryoprecipitate, and factor 8 concentrate
86
Christmas disease; factor 9 deficiency
Hemophilia B
87
The most important clue to clinically significant bleeding disorder in an otherwise healthy patient
remains the —.
history
88
The most common reason for coagulopathy in patients receiving massive blood transfusions is the lack of functioning —.
platelets
89
Platelets in stored blood are nonfunctional after —to— days.
1-2 days
90
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.
V and VIII
91
The only acceptable clinical indication for transfusion of packed red blood cells is to increase the ——— of the blood.
oxygen carrying capacity
92
All procoagulants except — are present in fresh frozen plasma (FFP).
platelets
93
Cryoprecipitate contains factor —, factor —, and factor —.
factor VIII, factor I, and factor XIII.
94
— is harvested from fresh frozen plasma as it is thawing.
cryoprecipitate
95
One unit of RBCs will increase hematocrit (Hct) —%, or —/dL.
3-4%, or 19/dL.
96
1 cc/kg RBCs will increase Hct —%.
1
97
One unit of platelets will increase platelet count — - —/mm3.
5,OOO-lO,000
98
"Massive transfusion" is defined as 1 complete blood volume transfused within — hours.
24
99
Activated antithrombin binds factor — and factor — greatly and factors —, —, and — to a lesser degree.
thrombin (factor IIa) and factor Xa greater ; factors IX, Xl, and XII lesser
100
— works by increasing the effectiveness of antithrombin 1,000-fold or more
Heparin
101
Antithrombin is made in the — and neutralizes — pathway factors and — pathway factors by forming complexes with them
liver ; final common pathway factors and intrinsic pathway factors
102
— is a required cofactor for heparin
Antithrombin
103
Heparin binds to —
antithrombin III
104
Acquired antithrombin deficiency states are found in patients with what 2 issues?
Cirrhosis of the liver and Nephrotic syndrome
105
An antithrombin deficiency is the most common reason a patient is unresponsive to —.
heparin
106
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?
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
— forms a complex with antithrombin III.
Heparin
108
The — is prolonged by heparin. Heparin blocks the classical — and — pathways.
partial thromboplastin time (PTT) ; intrinsic and final common pathways
109
Protamine reverses the action of heparin by —.
neutralization
110
Warfarin (Coumadin) and other coumarin-like substances bind to the — receptor in the liver and competitively inhibit —.
vitamin K ; vitamin K
111
— is prolonged by warfarin. Warfarin and other coumarins block the classical — and — pathways.
Prothrombin time (PT) ; extrinsic (factor VII) and final common (factors II and X) pathways
112
Reombinant hirudin, ximelagatran, and argatroban are — inhibitors.
direct thrombin
113
Normal value for bleeding time?
3-10min
114
Normal value for platelet count?
150,000-400,000 cells/mL
115
Normal value for prothrombin time (PT)?
12-14 sec
116
Normal value for partial thromboplastin time (PTT)?
25-35 sec
117
Normal value for thrombin time (TT)?
<30 sec
118
Normal value for activate coagulation time (ACT)?
80-150 sec
119
Normal value for fibrinogen?
>150 mg/dl
120
— and — assess heparin
PTT and ACT
121
Heparinization is adequate if ACT — - — sec
> 400-450 sec
122
—, 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.
Plasminogen
123
— and — are the two agents that normally convert plasminogen to its active form, plasmin.
Tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA)
124
Plasmin breaks down —.
fibrin
125
— is synthesized in the liver and circulates in the blood
Plasminogen
126
-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
Tissue-type plasminogen activator (tPA)
127
-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
Urokinase-type plasminogen activator (uPA)
128
-produced by beta-hemolytic streptococci
-has little affinity for fibrin
-preformed antibodies to this may inactivate it
Streptokinase
129
What are the 3 plasminogen activators?
Tissue-type plasminogen activator (tPA), urokinase-type plasminogen activator (uPA), and streptokinase
130
Aprotinin (Trasylol) inhibits —.
plasmin
131
Epsilon aminocaproic acid (Arnicar, EACA) and tranexamic acid prevent the breakdown of — by preventing displacing the plasmin.
fibrin
132
Aprotinin and amicar work by inhibiting —.
plasmin
133
What is the one increased laboratory abnormality of clotting factors and enhanced fibrinolysis of DIC?
Fibrin degradation products
134
— is the "Most common cause of an isolated high PT"
Liver disease
135
Treatment for coagulation abnormalities with liver disease?
Replace clotting factors with fresh frozen plasma, cryoprecipitate, and vitamin K as needed
136
Treatment for coagulation abnormalities with renal failure?
Adequate dialysis and elevation of hematocrit, cryoprecipitate, and DDAVP
137
Transfused blood is deficient in — and coagulation factors — and —
platelets ; V and VIII
138
Diffuse bleeding during massive transfusion is generally caused by —.
thrombocytopenia
139
Treatment for coagulation abnormalities with massive blood transfusion?
Platelet transfusion (correct thrombocytopenia), fresh frozen plasma (supplies all coagulation factors), cryoprecipitate (source of factor I, VIII, and XIII)
140
When the endothelial lining of the blood vessel is damaged, platelets adhere to the subendothelial collagen. What substance anchors platelets to subendothelial collagen?
Von Willebrand's factor (VlII:vWF or VIII:R)
141
What clotting factor activates the platelet at the site of vascular injury?
thrombin (factor lIa)
142
What two substances, released from the activated platelet, stimulate platelet aggregation?
ADP and thromboxane A2
143
What substance links platelets together (aggregates them)?
fibrinogen (factor I)
144
What agents inhibit platelet aggregation by impairing cyclo-oxygenase?
aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs)
145
What clotting factors are found in the extrinsic pathway?
III (also known as tissue factor or thromboplastin) and VII
146
What clotting factors are found in the intrinsic pathway?
XII, XI, IX, and VIII
147
What clotting factors are found in the final common pathway?
I, II, V, X, XIlI
148
What clotting factor is considered the physiologic initiator of the coagulation cascade?
III (also known as tissue factor or thromboplastin)
149
What clotting factor promotes fibrin cross-linking?
XIII
150
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?
II, IX, X, XI, and XII (IX, XI and XII are in the intrinsic pathway; II and X are most profoundly inhibited)
151
What four clotting factors are vitamin K dependent? Which of these is in the extrinsic pathway?
II, VII, IX, and X (VII is in the extrinsic pathway)
152
How does heparin work?
heparin increases the activity of ("turns on") antithrombin III
153
How does coumadin work?
coumadin competitively inhibits the vitamin K- dependent clotting factors
154
What anticoagulant affects the extrinsic and final common pathways?
warfarin (coumadin)
155
What anticoagulant affects the intrinsic and final common pathways?
heparin
156
What two coagulation tests assess the extrinsic pathway?
prothrombin time (PT) and the international normalized ratio (INR)
157
What two coagulation tests assess the intrinsic pathway?
partial thromboplastin time (PTT) and activated coagulation time (ACT)
158
How does protamine work to reverse heparin? What kind of reaction is this?
protamine combines electrostatically with heparin (this is a neutralization reaction)
159
What enzyme is responsible for breaking down fibrin?
plasmin
160
What two pharmacological agents inhibit plasmin?
epsilon-aminocaproic acid (Amicar) and aprotinin (Trasylol)
161
Name three substances that convert plasminogen to plasmin?
urokinase plasminogen activator (uPA), tissue plasminogen activator (tPA), and streptokinase
162
When is aprotinin generally used in anesthesia? How does it work?
aprotinin is used for repeat sternotomies and works by inhibiting plasmin
163
What is the normal activated coagulation time?
80-150 seconds
164
What is the best test of primary hemostasis, or platelet function?
standardized skin bleeding time
165
What is the most common reason for coagulopathy after a massive blood transfusion?
lack of functioning platelets (thrombocytopenia)
166
What clotting factors are found in fresh frozen plasma?
all procoagulants
167
Cryoprecipitate contains what clotting factors?
factor I (fibrinogen), factor VIII, and factor XIIl
168
What are the typical manifestations of disseminated intravascular coagulopathy?
bleeding, with oozing from tubes, wounds, and vascular access sites
169
Transfused blood is deficient in what two coagulation factors?
factors V and VIII
170
What is the most common inherited coagulation defect?
Von Willebrand's disease
171
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
Cryoprecipitate
172
What antiplatelet agent prevents ADP-induced platelet aggregation?
a. Aspirin
b. Ibuprofen
c. Ketorolac
d. Ticlopidine
Ticlopidine
173
Each of the following clotting factors is made in the liver EXCEPT:
a. VIII:C.
b. IV.
c. X.
d. XII.
IV
174
The clotting factor that is responsible for cross-linking fibrin is
a. I.
b. II.
c. VII.
d. XIII.
XIII
175
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
Coumadin PT
176
Cryoprecipitate contains coagulation factors
a. I, VIII, XIII.
b. II, VII, X.
c. I, VII, X.
d. II, X, XI.
I, VIII, XIII.
177
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.
binds factors II, IX, X, Xl, and XII.
178
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
Deficiency of antithrombin III ; Give FFP
179
Prothrombin time normally is
a. 3-5 seconds.
b. 12-14 seconds.
c. 25-35 seconds.
d. 80-150 seconds.
12-14 seconds.
180
The reaction of protamine with heparin is a
a. neutralization reaction.
b. covalent reaction.
c. hydrogen bonding reaction.
d. counterbalanced reaction.
neutralization reaction.
181
What substance converts fibrin to fibrin split products?
a. Tissue plasminogen activator
b. Amicar
c. Plasmin
d. Streptokinase
Plasmin
182
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.
Aprotinin accelerates the breakdown of fibrin.
183
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
Disseminated intravascular coagulopathy
184
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.
fibrin split products.
185
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
Thrombocytopenia
