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Hemostasis/Coagulation > Final > Flashcards

Final Flashcards

1
Q

This is defined as an alteration in the coagulation system that predisposes a person to form clots:

A

Hypercoagulability

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2
Q

____ in US suffer from blood clots per year, with a __% mortality rate:

A

> 200k

30% (most due to PE)

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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

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4
Q

List the 3 types of natural plasma inhibitors of coagulation factors:

A
  • Serine-protease inhibitors
  • Protein C
  • TFPI (tissue factor pathway inhibitor)
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5
Q

List the two types of Serine-protease inhibitors:

A
  • AT (anti-thrombin)

* HC-II (heparin cofactor II)

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6
Q

Combining __ with AT increases it’s effectiveness 200x:

A

heparin

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7
Q

AT is synthesized in the ___ and has a half life of ___ days:

A

liver

2-3 days

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8
Q

____ is a major inhibitor of 2a and 10a:

A

AT

7a, 11a, and 9a also somewhat inhibited

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9
Q

AT deficiency is autosomal __, occurs mostly between ages ____, and results in ___:

A

dominant
15-35
clotting

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10
Q

List some causes of acquired AT deficiency:

A
  • liver disease
  • consumption coagulopathy
  • Renal disease protein loss
  • continued heparin use
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11
Q

HC-II is a minor inhibitor of ___:

A

Thrombin

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12
Q

The major inhibitor of thrombin is ___, and the minor inhibitor is ___:

A

major: AT
minor: HC-II

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13
Q

Does HC-II inhibit any other coag factors besides thrombin:

A

No

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14
Q

With HC-II, you need a ____ concentration of heparin to inhibit thrombin:

A

higher

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15
Q

Symptoms of HC-II deficiency range from ___ to ___:

A

asymptomatic

venous/arterial thrombosis

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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

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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

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18
Q

___ degrades factors 8a and 5a:

A

Protein C

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19
Q

Protein C inactivates _____:

A

PAI-1

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20
Q

____ inactivates PAI-1:

A

Protein C

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21
Q

Increased 5a ____ Protein C activation, while decreased 5a ___ Protein C activation:

A
  • more 5a= enhances

* less 5a= inhibits

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22
Q

Is Protein C Vit K dependant:

A

yes

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23
Q

Protein C deficiency is among the most common causes of______ :

A

hypercoagulability

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24
Q

Protein C deficiency is autosomal ___ and affects ___% among those with inherited venous thrombosis:

A
  • dominant

* 6-10%

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25
Q

List some causes of acquired Protein C deficiency:

A

liver disease
DIC
warfarin therapy
Severe infection/shock

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26
Q

How is Functional Protein C activity tested for:

A
  • mix pt plasma w/ PC def plasma
  • Run APTT
  • if it corrects: no deficiency
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27
Q

List the two lab tests used to check for Protein C activity/deficiency:

A
  • Functional PC Activity

* Antigen Assay

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28
Q

___ is used to determine the mechanism of deficiency (decreased production OR abnormal protein) in testing for Protein C:

A

Antigen Assay

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29
Q

Protein S exists in these two forms:

A
  • Free form (40% of total PS, acts as cofactor to active PC)

* Bound form (C4b-Bp)

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30
Q

_____ exists in a free form and a bound form, with the free form making up 40%:

A

Protein S

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31
Q

List some causes of Acquired Protein S Deficiency:

A 
coumadin therapy & L-asparaginase
Pregancy
Oral contraceptives
Low Vit K levels
liver disease
DIC
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32
Q

T/F

Deficiency of TFPI has yet to be associated with thromboembolitic disease:

A

True

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33
Q

____ may play a significant role in preventing clot formation, though a deficiency of it has not yet been associated with thromboembolitic disease:

A

TFPI

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34
Q

TFPI inhibits 9a and 10a by binding __ and __:

A

7 and 3

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35
Q

___ inhibits 9a and 10a by binding 7 and 3:

A

TFPI

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36
Q

TFPI inhibits __ and __ by binding __ and __:

A
  • inhibits: 9a and 10a

* by binding: 7 and 3

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37
Q

TFPI + 7 + 3 inhibits ___ and __:

A

9a and 10a

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38
Q

HIT/HIIT is due to an antibody to ___:

A

heparin-PF4 complex

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39
Q

Lipoprotein a (LPa) inhibits fibrinolysis by competing with ___ for binding with ___:

A

fibrinogen

fibrin

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40
Q

LPa binds __ and ___:

A
  • fibrinogen (blocking fibrin from binding)

* TPA

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41
Q

Prothrombin Nucleotide ______ Mutation increases prothrombin level and DVT risk:

A

G20210

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42
Q

_____Mutation increases prothrombin levels and increases DVT risk:

A

Prothrombin Nucleotide G20210 Mutation

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43
Q

T/F

Hyperhomocysteinemia is a risk factor for DVT:

A

True

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44
Q

__% of those with dysfibrinogenemia have recurring ___:

A

20%

clots`

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45
Q

Unfractionated Heparin therapy is monitored via ____, and extended use can lead to ____:

A

APTT

HIT/HITTS (heparin-PF4 Ab)

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46
Q

____does not require monitoring since it is cleared by the kidneys:

A

LMWH

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47
Q

LMWH does not require monitoring since it is cleared by the __:

A

kidneys

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48
Q

Asprin, Plavix, and Pradaxa are all ____ agents:

A

anti-platelet

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49
Q

Both alternative anticoagulants- Hirudin is from ____, Danaparoid is similar to LMWH except there is no ___ available:

A

leeches

antidote

50
Q

Aspirin is an ____ agent that works by inhibiting ___, which deactivates ___:

A

anti-platelet
cyclo-oxygenase
TXA2

51
Q

Plavix is an ____ agent that works by inhibiting ____:

A

anti-platelet

inhibits ADP binding

52
Q

Pradaxa is an ___ agent that works be inhibiting _____:

A

Thrombin

53
Q

T/F

Unfractionated heparin therapy is monitored via PT:

A

False, it is monitored via APTT

54
Q

___ is similar to LMWH, except there is no antidote available:

A

Danaparoid

55
Q

___ is the inactive form of Plasmin:

A

Plasminogen

56
Q

____ is the enzymatic dissolving of fibrin clot:

A

fibrinolysis

57
Q

___ works by breaking down polymer bonds and release FDP’s:

A

Plasmin

58
Q

___ is the key enzyme in fibrinolysis:

A

Plasmin

59
Q

List the two forms of Plasminogen:

A
  • Glu- Plasminogen

* Lys- Plasminogen

60
Q

Plasminogen is synthesized in the __, has a half life of __, a plasma content of __mg/dL, and comes in _ forms:

A
  • liver
  • half life~ 2 days
  • 20mg/dL
  • 2 forms (Glu and Lys)
61
Q

Which form of Plasminogen is more readily converted to active plasmin by activators:

A

Lys

62
Q

____ is capable of being cleaved, results in lysine as new terminal amino acid:

A

Glu-Plasminogen

63
Q

Glu-plasminogen becomes extended when bound to ___:

A

fibrin

64
Q

List the 4 endogenous plasminogen activators:

A
  • Urokinase
  • t-PA
  • Scu-PA
  • Other
65
Q

List the two exogenous plasminogen activators:

A
  • Urokinase

* Streptokinase

66
Q

The primary source of plasminogen activators are in the _____:

A

blood vessel endothelium

67
Q

____ is the primary plasminogen activator in the GI system:

A

Urokinase

68
Q

Levels of ___ fluctuate rapidly in response to exercise, venous occlusions, alcohol and drugs, DDAVP, and steroids:

A

t-PA

69
Q

If patient shows no increase in t-PA activity, they are at an increased risk for ___:

A

DVT

70
Q

Scu-PA has a half-life of __mins and is rapidly inhibited by __:

A

5-10 mins

PAI-1

71
Q

T/F

Other sources of plasminogen activation inlcude: initation of coag contact factors 11a and 12a, kallikrein, and HMWK:

A

True

72
Q

Is urokinase an endogenous or exogenous plasminogen activator:

A

both

73
Q

List the 3 drawbacks for use of Urokinase (u-PA):

A
  • expensive
  • lower affinity for fibrin than t-PA
  • commonly develop hypofibrinogenemia
74
Q

Which has a higher affinity for fibrin, u-PA or t-PA::

A

t-PA (which is one reason why it is used as a therapeutic fibrinolytic agent)

75
Q

Streptokinase is not an ____, it is derived from ___:

A

not an enzyme

derived form Streptococci

76
Q

___ forms 1:1 complex with plasminogen which exposes an active serine site:

A

Streptokinase

77
Q

The major drawback of _____ is that it can create immune response with Ab development:

A

Streptokinase

78
Q

___ is the primary substrate of PAI-1:

A

t-PA

79
Q

Regulation of fibrinolysis is dependent on the interaction of t-PA with ____:

A

PAI-1

80
Q

Excess of PAI-1 is associated with ____, and risk is significantly higher in patients w/ MI <45 years old:

A

thrombotic disease

81
Q

T/F

PAI-1 is an acute phase reactant:

A

True

82
Q

_____ is synthesized by blood vessel endothelium and released in inactive state, is an acute phase reactant, and it’s primary substrte is t-PA:

A

PAI-1

83
Q

Where is PAI-1 synthesized:

A

blood vessel endothelium

is released in inactive state, must interact with t-PA

84
Q

Plasmin has a half life of ___:

A

seconds

85
Q

Plasmin degrades both ___ and ____:

A
  • fibrin clots

* native fibrinogen

86
Q

Fragment X is composed of _ and _ fragments:

A

Y and D

think D-E-D monomer

87
Q

Fragment Y is composed of _ and _ fragments:

A

D and E

88
Q

___ is cleaved cross linked fibrin:

A

D-dimer

89
Q

Y and D fragments make up __:

A

Fragment X

90
Q

D and E fragments make up __:

A

Fragment Y

91
Q

___ degrades both fibrin clots and native fibrinogen:

A

Plasmin

92
Q

Plasmin products have an ___ effect on coag system:

A

inhibitory

93
Q

Alpha 2-antiplasmin inhibitor forms a 1:1 complex with ___:

A

plasmin

94
Q

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:

A

alpha 2-antiplasmin inhibitor

clot lysis

95
Q

With alpha 2-antiplasmin inhibitor, plasmin activity is limited to area of ___ deposition:

A

fibrin

96
Q

Alpha 2-macroglobulin, C1 inactivator, and alpha 1-antitrypsin are all ______:

A

plasmin inhibitors

97
Q

Only 3 cases of congenital ___abnormalities have been reported:

A

Plasminogen

98
Q

Low levels of t-PA = recurrent ___:

A

clotting events

99
Q

Alpha 2-antiplasmin inhibitor = severe ____ tendency:

A

hemorrhagic

100
Q

Alpha 2-antiplasmin inhibitor is bound to fibrin by ___:

A

8a

101
Q

RVVT is used to differentiate __ from ___ deficiency:

A

8 from 10

102
Q

In RVVT, you substitute venom for ____:

A 
tissue thromboplastin
(venom does not require F7)
103
Q

Increased Stypven time points to a deficiency in one of these three factors:

A

*10, 5, 2

104
Q

Stypven time would be ___ in a F7 deficiency:

A

normal

105
Q

___ cleaves A & B peptides:

A

Fibrin

106
Q

Fibrin cleaves A/B peptides, leaving fragment___, then factor__ causes them to polymerize, giving crosslinking that forms ____:

A
  • X (D-E-D monomer, or Y+D)
  • F13a
  • fragment Y (D-E)
107
Q

The principle of the FDP test is latex particles coated with Ab’s to human fibrinogen _____fragments:

A

D and E

108
Q

T/F

Serum is used for FDP, while Sodium citrate is used for RVVT:

A

True

109
Q

Normal D-dimer level is

A

1

110
Q

Does the D-dimer test detect breakdown products from both cross-linked fibrin AND fibrinogen:

A

No. Only cross-linked fibrin

111
Q

Thrombin+TM+Protein C =

A

APC (Activated Protein C complex)

112
Q

APC + Protein S =

A

powerful anticoagulant

inactivates 5a, 8a, PAI-1

113
Q

APC + Protein S = a powerful anticoagulant that inactivates these three things:

A

5a, 8a, PAI-1

114
Q

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:

A

venom

proportional

115
Q

What 3 thing make up the APC (activated protein C complex):

A

Thrombin
TM
Protein C

116
Q

APC + ___= powerful anticoagulant that inactivates 5a/8a/PAI-1:

A

Protein S

117
Q

Protein C needs _____ to inhibit 5a and 8a:

A

Protein S

118
Q

In functional Protein S activity assay testing, there is a ___ relationship between Protein S and ____:

A

linear

clot time

119
Q

Protein S values may be falsely low in samples with elevated ___ levels due to improper venipuncture, cold activation on storage, or clinical conditions:

A

F7a

120
Q

Reference range for PT:

A

11.5-14 seconds

121
Q

ISI allows for calibration of various ___ to an international standard:

A

thromboplastins

122
Q

Reference range for APTT:

A

20-45 seconds

Hemostasis/Coagulation (3 decks)

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