Hemostasis Flashcards
(134 cards)
1
Q
The stages of hemostasis?
A
Primary
Secondary
Fibrinolysis
2
Q
What is primary hemostasis?
A
Formation of the platelet plug
3
Q
What is secondary hemostasis?
A
Coagulation
When the actual clot forms
4
Q
What is fibrinolysis?
A
Clot is dissolved
5
Q
What is the vessel itself’s initial response to injury?
A
Vasospasm
6
Q
What stimulates the vasospasm of the injured vessel to occur?
A
Disrupted endothelium
7
Q
What stage includes formation of the platelet plug?
A
Primary
8
Q
What initiates formation of the platelet plug?
A
Injury to vessel exposes endothelial collagen
9
Q
What coagulation factor is required for adhesion of platelets?
A
Von Wilebrand
vW
10
Q
What factor(s) activate platelets for the platelet plug?
A
Thrombin and tissue factor
11
Q
What is meant by platelet activation?
A
Platelets change shape
12
Q
What prostaglandin promotes platelet aggregation?
A
Thromboxane
13
Q
What substances are also included in the platelet plug?
A
Fibrinogen and thrombin
14
Q
Aggregation of platelets triggers further?
A
Attraction of more platelets
Platelet activation
15
Q
What kind of bleeding/injury do platelet plugs control?
A
Minute vessel breaks that occur constantly
-full clot not required
16
Q
Platelet counts under what allow spontaneous bleeding to occur?
A
< 20,000
17
Q
Intercerebral hemorrhage can occur from just a platelet count below?
A
< 20,000
18
Q
Thrombocytopenia means what? And what can you see with this as evidence of someone unable to form platelet plugs?
A
Low platelet count
Petechia
19
Q
Production of thromboxane requires what?
A
Cyclooxygenase (COX)
20
Q
What inhibits the production of the prostaglandin thromboxane?
A
Cox inhibitors interferes with the enzyme cyclooxygenase, which means it interferes with the production of thromboxane
21
Q
COX inhibitors interfere with what part of hemostasis?
A
Function of the platelets
- platelet aggregation
- formation of a platelet plug
22
Q
What COX inhibitor has temporary interference on hemostasis?
A
NSAIDs
23
Q
How long do NSAIDs interfere with platelet function?
A
1-2 days
24
Q
What cox inhibitor has permanent interference on platelet function?
A
Aspirin
25
Why is ASA interference considered permanent?
It lasts the life of a platelet
26
What is the life of a platelet?
8-12 days
| -1-2 weeks
27
How long does ASA interfere with platelet function?
1-2 weeks
28
What lab tests will tell platelet function, NOT count?
Bleeding time
29
What bleeding time may indicate bleeding risk?
Over 7-8 minutes
30
What platelet count constitutes thrombocytopenia?
< 100,000
31
What platelet count constitutes surgical bleeding risk?
< 50,000
32
What platelet count constitutes spontaneous bleeding?
< 20,000
33
What are the 4 A’s of platelet plug?
Activation
Adhesion
Aggregation
Attraction
34
What changes the platelet plug into a clot?
Fibrin
35
What is the inactive form of fibrin?
Fibrinogen
36
What factor converts fibrinogen into fibrin?
Thrombin
37
What is the inactive form of thrombin?
Prothrombin
38
What factor converts prothrombin into thrombin?
Factor X
39
What constitutes the chain of events that occur from factor X > fibrin formation?
The common pathway
40
The formation of fibrin requires what substances?
Fibrinogen
Calcium
Thrombin
41
The formation of thrombin requires what substances?
Prothrombin
Calcium
Factor X
42
What (old) 2 pathways were described to get to factor X?
Extrinsic and Intrinsic pathway
43
What factors are involved in the extrinsic pathway and what lab test would show abnormalities?
III
VII
PT
44
What factors are involved in the intrinsic pathway and what lab test would show abnormalities?
```
VIII
IX
XI
XII
PTT
```
45
What has replaced the intrinsic/extrinsic pathways?
The cell based theory
| -tissue factor theory
46
What factor does the cell based theory say triggers coagulation?
Factor III
47
What are the many names for factor III?
Tissue factor
Thromboplastin
Tissue thromboplastin
48
What are the phases of cell based theory?
Initiation
Amplification
Propagation
49
Describe initiation phase
Triggered by vessel injury to endothelial surface exposing tissue factor
Tissue factor and factor VII activate factor X
50
How much thrombin is created due to initiation phase
Only a small amount
51
Describe the amplification phase
XXX
52
How much thrombin is created from the activation stage?
Thrombin generation is gaining momentum
53
Describe the propagation phase
XXXX
54
This propagation phase is also the?
The common pathway
55
What is thromboelastogram?
Lab test: TEG
| -follows clot through initiation, complete formation, strength and lysis
56
What can TEG not detect?
vW disease or ASA effects
57
What is the R time on TEG?
Time to begin forming clot
58
What is the problem if R is prolonged in a TEG?
Coagulation factors
59
What is the K describe on a TEG?
Time of clot strengthening
60
What is the problem if K is prolonged on TEG?
Fibrinogen
61
What is MA on a TEG?
Measures the clot’s strength
62
What is the problem in the MA on a TEG?
Platelets
63
What is the determined by the time period after the MA?
Fibrinolysis
64
TEG waveforms
TEG waveforms
65
What is responsible for clot lysis?
Plasmin
66
How does plasmin dissolve the clot?
It removes the fibrin
67
What activates the plasminogen?
Tissue plasminogen activator
| -tPA
68
What inhibits plasmin?
Anti plasmin
| -supports clot
69
What class of drugs dissolve clots?
Thrombolytics
70
Name 3 plasminogen activators
TPA and analogues
Streptokinase
Urokinase
71
Name 3 plasmin inhibitors
Aprotinin
Amicar amiocarproic acid
Transexamic acid
72
What is the most common inherited bleeding disorder?
VonWillebrands disease
73
What is vonWillebrand’s needed for?
Adhesion of platelets
74
What medication can exacerbate vW symptoms?
ASA
| -should be avoided
75
What lab results are seen with vW?
Prolonged bleeding time
PT/PTT may be normal
PLT count may also be normal
76
What is the first line treatment for vW? Why?
DDAVP
| It treats the most common form of vW
77
What is DDAVP?
Analogue of vasopressin
78
What is given if vW patient does not respond to DDAVP?
FFP
| Non-recombinant factor VIII
79
Why must non-recombinant factor VIII be used?
Recombinant factor VIII is artificially created and does not contain vW
80
Where is factor VIII made?
In the liver
81
Where is vW synthesized?
By vessel endothelial cells
82
What is the relationship between vW and factor VIII?
vW with factor VIII combine to take part in coagulation
| -VIIIc is without vW
83
Hemophilia is an abnormality on which chromosome?
X
84
What lab value would show hemophilia?
Prolonged PTT
85
What is hemophilia A?
Deficiency of factor VIIIc
| -treatment is factor VIII
86
What is hemophilia B?
Deficiency of factor IX
87
What can treat both types of hemophilia?
FFP
88
What type of hemophilia can cryoprecipitate treat?
Hemophilia A
| -though controversial
89
Which type of hemophilia is more common?
Hemophilia A
90
What is the most common inherited defect in secondary hemostasis?
Hemophilia A
91
What is the most common inherited cause of abnormal bleeding?
VW disease
92
What is the most common inherited cause of abnormal secondary coagulation?
Hemophilia A
93
What is the most common cause of abnormal bleeding?
ASA
94
What is more common acquired bleeding problem or inherited?
Acquired
95
What are examples of acquired bleeding problems?
```
Liver disease
Decreased function VIII, IX, XI
RA
Colitis
Aging
Systemic lupus erythematous
```
96
What factors are NOT made by the liver?
VW: endothelium
Calcium: factor IV from diet
III: from damaged tissue
97
Liver disease causes what lab abnormalities?
Elevated PT and PTT
98
Vitamin K is required for the liver to synthesize what factors?
II
VII
IX
X
99
What contains all coagulation factors except platelets?
FFP
100
What does FFP also contain?
Anticoagulation factors like antithrombin III
101
What is in cryoprecipitate?
Factor VIII
Fibrinogen
XIII
102
What is stored banked blood deficient in?
Platelets
Factor V
Factor VIII
103
What factor has the shortest half life?
Factor VII
104
Why does stored banked blood has deficiencies?
Because of the process of removing the plasma
105
What is dilutional coagulopathy?
So much banked blood has been giving which doesn’t have factors V, VIII and platelets
106
What is usually the biggest problem with dilutional coagulopathy?
Low platelets
107
Platelets may be need if how much banked blood has been given?
10-15 units
108
With dilutional coagulopathy a patient’s factors have to fall below what % for coagulation to no longer be normal?
< 30%
109
What can be given with dilutional coagulopathy after platelet transfusion and bleeding still a problem?
FFP
110
Name some anti-coag factors
Antithrombin (antithrombin III)
Protein S
Protein C
Thrombomodulin
111
What drug class inhibits further clot formation?
Anticoagulants
112
What does Heparin augment?
Antithrombin III
113
Heparin interferes with which pathway?
Intrinsic
114
So what factors are affected by Heparin?
```
I
II
V
VIII
IX
X
XI
XII
By interfering with intrinsic pathway, it also interferes with the common pathway
```
115
How is the activity of Heparin monitored?
PTT
116
What explains heparin resistance?
Low antithrombin III
117
How is low antithrombin III treated?
FFP
| -so heparin resistance is treated with FFP
118
What is the most common cause of drug induced thrombocytopenia?
Heparin Induced Thrombocytopenia (HIT)
119
What is a risk of using direct thrombin inhibitors?
Increased risk of bleeding
| -it can not be reversed
120
Name direct thrombin inhibitors
Bivalirudin
Argatroban
Hirudin
Dabigatran
121
What direct thrombin inhibitor has the shortest half life?
Bivalirudin
122
Name direct factor X inhibitors
Fondaparinux
Rivaroxaban
Apixaban
123
What are the advantages of low molecular weight heparin?
```
Longer half life
More predictable
Less monitoring needed
Less platelet inhibition
Less HIT
```
124
What are the disadvantages of LMWHeparin?
Not reversible
125
How does Coumadin work?
Competes with vitamin K at the liver
126
What factors are affected by this vitamin K competition with Coumadin?
II
VII
IX
X
127
What pathway does Coumadin interfere with?
Extrinsic pathway
128
What test does Coumadin affect?
PT
129
What test is Coumadin monitored for therapeutic levels?
INR
| -ratio that tells you how much longer clotting takes
130
What is disseminated intravascular coagulation?
Uncontrolled coagulation activation
Widespread thrombosis of small vessels
Consumes clotting factors and platelets
131
What type of things can DIC be a secondary complication of?
```
Sepsis
Shock
Post op
Transfusion reaction
OB complications
Others
```
132
What are the symptoms of DIC?
```
Spontaneous diffuse hemorrhage
Decreased platelets
Decreased fibrinogen
Elevated PT
Elevated PTT
Elevated fibrin degradation products
```
133
What is the distinctive characteristic of DIC? (2 names)
Elevated fibrin degradation products
| AKA fibrin split products
134
What is the treatment of DIC?
Platelets and FFP
Treat underlying cause
Heparin is a controversial treatment
