Final Flashcards
(122 cards)
1
Q
This is defined as an alteration in the coagulation system that predisposes a person to form clots:
A
Hypercoagulability
2
Q
____ in US suffer from blood clots per year, with a __% mortality rate:
A
> 200k
30% (most due to PE)
3
Q
In order for thrombosis to present clinically, at least __ risk factor needs to be present to overcome the natural ____ to protect against clot formation:
A
1
inhibitory process
4
Q
List the 3 types of natural plasma inhibitors of coagulation factors:
A
- Serine-protease inhibitors
- Protein C
- TFPI (tissue factor pathway inhibitor)
5
Q
List the two types of Serine-protease inhibitors:
A
- AT (anti-thrombin)
* HC-II (heparin cofactor II)
6
Q
Combining __ with AT increases it’s effectiveness 200x:
A
heparin
7
Q
AT is synthesized in the ___ and has a half life of ___ days:
A
liver
2-3 days
8
Q
____ is a major inhibitor of 2a and 10a:
A
AT
7a, 11a, and 9a also somewhat inhibited
9
Q
AT deficiency is autosomal __, occurs mostly between ages ____, and results in ___:
A
dominant
15-35
clotting
10
Q
List some causes of acquired AT deficiency:
A
- liver disease
- consumption coagulopathy
- Renal disease protein loss
- continued heparin use
11
Q
HC-II is a minor inhibitor of ___:
A
Thrombin
12
Q
The major inhibitor of thrombin is ___, and the minor inhibitor is ___:
A
major: AT
minor: HC-II
13
Q
Does HC-II inhibit any other coag factors besides thrombin:
A
No
14
Q
With HC-II, you need a ____ concentration of heparin to inhibit thrombin:
A
higher
15
Q
Symptoms of HC-II deficiency range from ___ to ___:
A
asymptomatic
venous/arterial thrombosis
16
Q
Which has a higher affinity for heparin, AT or HC-II:
A
AT
which is why HC-II requires more heparin to affect tests
17
Q
Protein C is activated by ____, which is found in _____, and it is regulated by___:
A
- Activated by: Thrombomodulin, found in epithelial cells
* Regulated by: 5a
18
Q
___ degrades factors 8a and 5a:
A
Protein C
19
Q
Protein C inactivates _____:
A
PAI-1
20
Q
____ inactivates PAI-1:
A
Protein C
21
Q
Increased 5a ____ Protein C activation, while decreased 5a ___ Protein C activation:
A
- more 5a= enhances
* less 5a= inhibits
22
Q
Is Protein C Vit K dependant:
A
yes
23
Q
Protein C deficiency is among the most common causes of______ :
A
hypercoagulability
24
Q
Protein C deficiency is autosomal ___ and affects ___% among those with inherited venous thrombosis:
A
- dominant
* 6-10%
25
List some causes of acquired Protein C deficiency:
liver disease
DIC
warfarin therapy
Severe infection/shock
26
How is Functional Protein C activity tested for:
* mix pt plasma w/ PC def plasma
* Run APTT
* if it corrects: no deficiency
27
List the two lab tests used to check for Protein C activity/deficiency:
* Functional PC Activity
| * Antigen Assay
28
___ is used to determine the mechanism of deficiency (decreased production OR abnormal protein) in testing for Protein C:
Antigen Assay
29
Protein S exists in these two forms:
* Free form (40% of total PS, acts as cofactor to active PC)
| * Bound form (C4b-Bp)
30
_____ exists in a free form and a bound form, with the free form making up 40%:
Protein S
31
List some causes of Acquired Protein S Deficiency:
```
coumadin therapy & L-asparaginase
Pregancy
Oral contraceptives
Low Vit K levels
liver disease
DIC
```
32
T/F
| Deficiency of TFPI has yet to be associated with thromboembolitic disease:
True
33
____ may play a significant role in preventing clot formation, though a deficiency of it has not yet been associated with thromboembolitic disease:
TFPI
34
TFPI inhibits 9a and 10a by binding __ and __:
7 and 3
35
___ inhibits 9a and 10a by binding 7 and 3:
TFPI
36
TFPI inhibits __ and __ by binding __ and __:
* inhibits: 9a and 10a
| * by binding: 7 and 3
37
TFPI + 7 + 3 inhibits ___ and __:
9a and 10a
38
HIT/HIIT is due to an antibody to ___:
heparin-PF4 complex
39
Lipoprotein a (LPa) inhibits fibrinolysis by competing with ___ for binding with ___:
fibrinogen
| fibrin
40
LPa binds __ and ___:
* fibrinogen (blocking fibrin from binding)
| * TPA
41
Prothrombin Nucleotide ______ Mutation increases prothrombin level and DVT risk:
G20210
42
_____Mutation increases prothrombin levels and increases DVT risk:
Prothrombin Nucleotide G20210 Mutation
43
T/F
| Hyperhomocysteinemia is a risk factor for DVT:
True
44
__% of those with dysfibrinogenemia have recurring ___:
20%
| clots`
45
Unfractionated Heparin therapy is monitored via ____, and extended use can lead to ____:
APTT
| HIT/HITTS (heparin-PF4 Ab)
46
____does not require monitoring since it is cleared by the kidneys:
LMWH
47
LMWH does not require monitoring since it is cleared by the __:
kidneys
48
Asprin, Plavix, and Pradaxa are all ____ agents:
anti-platelet
49
Both alternative anticoagulants- Hirudin is from ____, Danaparoid is similar to LMWH except there is no ___ available:
leeches
| antidote
50
Aspirin is an ____ agent that works by inhibiting ___, which deactivates ___:
anti-platelet
cyclo-oxygenase
TXA2
51
Plavix is an ____ agent that works by inhibiting ____:
anti-platelet
| inhibits ADP binding
52
Pradaxa is an ___ agent that works be inhibiting _____:
Thrombin
53
T/F
| Unfractionated heparin therapy is monitored via PT:
False, it is monitored via APTT
54
___ is similar to LMWH, except there is no antidote available:
Danaparoid
55
___ is the inactive form of Plasmin:
Plasminogen
56
____ is the enzymatic dissolving of fibrin clot:
fibrinolysis
57
___ works by breaking down polymer bonds and release FDP's:
Plasmin
58
___ is the key enzyme in fibrinolysis:
Plasmin
59
List the two forms of Plasminogen:
* Glu- Plasminogen
| * Lys- Plasminogen
60
Plasminogen is synthesized in the __, has a half life of __, a plasma content of __mg/dL, and comes in _ forms:
* liver
* half life~ 2 days
* 20mg/dL
* 2 forms (Glu and Lys)
61
Which form of Plasminogen is more readily converted to active plasmin by activators:
Lys
62
____ is capable of being cleaved, results in lysine as new terminal amino acid:
Glu-Plasminogen
63
Glu-plasminogen becomes extended when bound to ___:
fibrin
64
List the 4 endogenous plasminogen activators:
* Urokinase
* t-PA
* Scu-PA
* Other
65
List the two exogenous plasminogen activators:
* Urokinase
| * Streptokinase
66
The primary source of plasminogen activators are in the _____:
blood vessel endothelium
67
____ is the primary plasminogen activator in the GI system:
Urokinase
68
Levels of ___ fluctuate rapidly in response to exercise, venous occlusions, alcohol and drugs, DDAVP, and steroids:
t-PA
69
If patient shows no increase in t-PA activity, they are at an increased risk for ___:
DVT
70
Scu-PA has a half-life of __mins and is rapidly inhibited by __:
5-10 mins
| PAI-1
71
T/F
| Other sources of plasminogen activation inlcude: initation of coag contact factors 11a and 12a, kallikrein, and HMWK:
True
72
Is urokinase an endogenous or exogenous plasminogen activator:
both
73
List the 3 drawbacks for use of Urokinase (u-PA):
* expensive
* lower affinity for fibrin than t-PA
* commonly develop hypofibrinogenemia
74
Which has a higher affinity for fibrin, u-PA or t-PA::
t-PA (which is one reason why it is used as a therapeutic fibrinolytic agent)
75
Streptokinase is not an ____, it is derived from ___:
not an enzyme
| derived form Streptococci
76
___ forms 1:1 complex with plasminogen which exposes an active serine site:
Streptokinase
77
The major drawback of _____ is that it can create immune response with Ab development:
Streptokinase
78
___ is the primary substrate of PAI-1:
t-PA
79
Regulation of fibrinolysis is dependent on the interaction of t-PA with ____:
PAI-1
80
Excess of PAI-1 is associated with ____, and risk is significantly higher in patients w/ MI <45 years old:
thrombotic disease
81
T/F
| PAI-1 is an acute phase reactant:
True
82
_____ is synthesized by blood vessel endothelium and released in inactive state, is an acute phase reactant, and it's primary substrte is t-PA:
PAI-1
83
Where is PAI-1 synthesized:
blood vessel endothelium
| is released in inactive state, must interact with t-PA
84
Plasmin has a half life of ___:
seconds
85
Plasmin degrades both ___ and ____:
* fibrin clots
| * native fibrinogen
86
Fragment X is composed of _ and _ fragments:
Y and D
| think D-E-D monomer
87
Fragment Y is composed of _ and _ fragments:
D and E
88
___ is cleaved cross linked fibrin:
D-dimer
89
Y and D fragments make up __:
Fragment X
90
D and E fragments make up __:
Fragment Y
91
___ degrades both fibrin clots and native fibrinogen:
Plasmin
92
Plasmin products have an ___ effect on coag system:
inhibitory
93
Alpha 2-antiplasmin inhibitor forms a 1:1 complex with ___:
plasmin
94
Plasmin forms a 1:1 complex with ___, which protects it from inhibitor by binding to same site as inhibitor, therefore inhibitor cannot bind and ____ proceeds:
alpha 2-antiplasmin inhibitor
| clot lysis
95
With alpha 2-antiplasmin inhibitor, plasmin activity is limited to area of ___ deposition:
fibrin
96
Alpha 2-macroglobulin, C1 inactivator, and alpha 1-antitrypsin are all ______:
plasmin inhibitors
97
Only 3 cases of congenital ___abnormalities have been reported:
Plasminogen
98
Low levels of t-PA = recurrent ___:
clotting events
99
Alpha 2-antiplasmin inhibitor = severe ____ tendency:
hemorrhagic
100
Alpha 2-antiplasmin inhibitor is bound to fibrin by ___:
8a
101
RVVT is used to differentiate __ from ___ deficiency:
8 from 10
102
In RVVT, you substitute venom for ____:
```
tissue thromboplastin
(venom does not require F7)
```
103
Increased Stypven time points to a deficiency in one of these three factors:
*10, 5, 2
104
Stypven time would be ___ in a F7 deficiency:
normal
105
___ cleaves A & B peptides:
Fibrin
106
Fibrin cleaves A/B peptides, leaving fragment___, then factor__ causes them to polymerize, giving crosslinking that forms ____:
* X (D-E-D monomer, or Y+D)
* F13a
* fragment Y (D-E)
107
The principle of the FDP test is latex particles coated with Ab's to human fibrinogen _____fragments:
D and E
108
T/F
| Serum is used for FDP, while Sodium citrate is used for RVVT:
True
109
Normal D-dimer level is
1
110
Does the D-dimer test detect breakdown products from both cross-linked fibrin AND fibrinogen:
No. Only cross-linked fibrin
111
Thrombin+TM+Protein C =
APC (Activated Protein C complex)
112
APC + Protein S =
powerful anticoagulant
| inactivates 5a, 8a, PAI-1
113
APC + Protein S = a powerful anticoagulant that inactivates these three things:
5a, 8a, PAI-1
114
In the functional Protein C activity assay, protein C in plasma is activated by __, the amount activated is determined by rate of hydrolysis by substrate; amount of product released is ___ to amount of Protein C:
venom
| proportional
115
What 3 thing make up the APC (activated protein C complex):
Thrombin
TM
Protein C
116
APC + ___= powerful anticoagulant that inactivates 5a/8a/PAI-1:
Protein S
117
Protein C needs _____ to inhibit 5a and 8a:
Protein S
118
In functional Protein S activity assay testing, there is a ___ relationship between Protein S and ____:
linear
| clot time
119
Protein S values may be falsely low in samples with elevated ___ levels due to improper venipuncture, cold activation on storage, or clinical conditions:
F7a
120
Reference range for PT:
11.5-14 seconds
121
ISI allows for calibration of various ___ to an international standard:
thromboplastins
122
Reference range for APTT:
20-45 seconds
