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MTLE > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

vascular structure: controls the vascular permeability and blood flow rate
lines the vessel wall
upon injury, increased vascular permeability occurs, allowing leakage of plasma proteins and blood cell migration to site of injury

A

endothelium

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2
Q

vascular structure: composed of smooth muscle cells and connective tissue with collagen fibers
exposure of collagen causes platelet activation; activates the intrinsic pathway of secondary hemostasis

A

subendothelium

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3
Q

vascular structure: produces or releases substances important in hemostasis
produces von willebrand factor, prostacyclin
tissue factor in vessels is exposed during vessel damage and activates the extrinsic pathway of secondary hemostasis

A

vascular endothelium

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4
Q

necessary for platelet adhesion to collagen
carrier protein for coagulation factor viii:c

A

von willebrand factor

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5
Q

a platelet aggregation inhibitor and vasodilator

A

prostacyclin

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6
Q

endothelial surface receptor
forms a complex with thrombin to inhibit factors v and viii in secondary hemostasis through the protein c system

A

thrombomodulin

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7
Q

hereditary vascular defects: thin vessel walls cause mucous membrane bleeding

A

hemorrhagic telangiectasia

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8
Q

hereditary vascular defects: abnormally collagen production causes hyperelastic skin and joint abnormalities

A

ehlers-danlos syndrome

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9
Q

vitamin c deficiency
impairs proper collagen synthesis and vessel integrity

A

scurvy

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10
Q

committed myeloid progenitor cell in response this growth factor gives rise to megakaryocytes

A

thrombopoietin

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11
Q

the process in which the nucleus divides without cytoplasmic division during the earliest thrombocyte stage

A

endomitosis

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12
Q

20-50micrometers
round nucleus contains 2-6 nucleoli and fine chromatin
scant basophilic cytoplasm contains no granules; irregularly shaped with cytoplasmic tags

A

megakaryoblast

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13
Q

increases size with a range of 20-80 micrometers
indented or lobulated nucleus contains variable number of nucleoli with coarsening chromatin
basophilic cytoplasm with granules beginning to appear; cytoplasmic tags present
demarcating membrane system begins to form

A

promegakaryocyte

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14
Q

invagination of the plasma membrane that becomes the future site of platelet fragmentation

A

demarcating membrane system

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15
Q

increases in size up to 100micrometers
largest cell in the body
contains a multilobulated nucleus with very coarser chromatin and variable number of nucleoli
cytoplasm has many small granules that stain purple with wright’s stain
represents 1% of nucleated bone marrow cells

A

megakaryocyte

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16
Q

2-4micrometers in size appearing as pale blue cells with azurophilic granules
no nucleus

A

mature platelets

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17
Q

platelet zones: exterior coat int he peripheral zone and contains glycoprotein receptor sites

A

glycocalyx

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18
Q

platelet zones: contains the phospholipid membranes, which serve as a surface for interaction of coagulation factors in secondary hemostasis

A

submembrane area

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19
Q

platelet zones: contains microtubules, cytoskeleton, actin and myosin

A

sol gel (structural area)

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20
Q

platelet zones: contains the granules, lysosomes, mitochondria, peroxisomes, and glycogen; controls platelet function in response to caogulation

A

organelle zone

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21
Q

platelet zones: this predominate in the organelle zone and contain a number of different proteins, with some most prominent being fibrinogen, vWF, beta thromboglobulin, platelet-derived growth factor, platelet factor 4

A

alpha granules

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22
Q

platelet zones: contain adp, atp, serotonin, and calcium in the organelle zone

A

dense bodies/delta granules

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23
Q

platelet zones: contain hydrolase enzyme

A

lysosomes

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24
Q

platelet zones: regulator of intracellular calcium concentration in the membrane systems

A

dense tubular system

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25
Q

platelet zones: releases granular contents through channels leading to the surface of the platelet in the membrane systems

A

open cannalicular system

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26
Q

reference range for platelets at healthy individuals

A

150-450 x 10^9/L

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27
Q

life span of platelets

A

8-12 days

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28
Q

platelet secreted proteins: stimulates vasoconstriction when vessel injury occur

A

serotonin

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29
Q

platelet secreted proteins: stimulate platelet aggregation and vasoconstriction

A

thromboxane a2

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30
Q

platelet secreted proteins: contacts the thrombus at the end of the coagulation process

A

actomyosin

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31
Q

platelet factors: neutralizes heparin

A

pf4

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32
Q

platelet factors: platelet phospholipid needed for proper platelet function and coagulation
needed in the production of thromboxane a2
provides a surface for fibrin formation, limiting the hemostatic response to the site of injury

A

pf3

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33
Q

proper platelet function sequence

A

adhesion
release of granule contents
aggregation
clot retraction

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34
Q

proper platelet function: platelets undergo a shape change and adhere to vascular surfaces, response to collagen exposure in subendothelium caused by vascular injury, dependent on binding of vWF at the gplb receptor site, can be activated by thrombin

A

adhesion

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35
Q

proper platelet function: fibrinogen attaches at the iib/iiia receptor of adjoining platelets, forming the initial platelet plug, platelets release non metabolic adp, serotonin and pf4
pf3 is released to provide the phospholipid surface needed for binding of clotting factors in secondary hemostasis

A

aggregation

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36
Q

proper platelet function: follows clot formation, dependent on the thrombasthenin and glycoprotein receptors iib/iiia, restores normal blood flow to the vessel

A

clot retraction

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37
Q

hereditary adhesion defects: decreased platelet adhesion causes mucous membrane bleeding that is variable in severity
lab: normal platelet count, prolonged bleeding time, decreased aggregation with ristocetin, variable aPTT, normal PT, decreased vWF:RCo, vWF:Ag

A

von willebrand disease

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38
Q

hereditary adhesion defects: giant platelets (increased mpv) that lack glyprotein Ib receptor; adhesion defect due to faulty binding of the platelets to von willbrand factor
lab: variable platelet count, platelet anisocytosis, prolonged bleeding time, decreased aggregation response to ristocetin, normal aPTT and PT, normal vWF:RCo, vWF:Ag and VIII:C

A

bernard soulier syndrome

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39
Q

hereditary aggregation and clot retraction defects: hemorrhagic disorders seen in populations where consanguinity is prevalent
lack of glycoprotein iib/iiia, the fibrinogen binding receptor
inability of fibrinogen to bind with platelets causes aggregation defects; lack of thrombasthenia/actomyosin causes clot retraction defect
lab: decreased aggregation response with ADP; epinephrine, and collagen, normal response with ristocetin

A

glanzmann thrombasthenia

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40
Q

storage pool defects: characterized by large platelets, thrombocytopenia, and an absence of alpha granules
patients are prone to lifelong mild bleeding tendencies

A

gray-platelet syndrome

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41
Q

storage pool defects: characterized by small platelets, thrombocytopenia, and a decreased amount of alpha granules and dense bodies
patients are prone to hemorrhage and recurrent infections

A

wiskott-aldrich syndrome

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42
Q

storage pool defects: characterized by a lack of dense body granules
patients exhibit occulocutaneous albinism and are prone to hemorrhage

A

hermansky-pudlak syndrome

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43
Q

interfere with cyclo-oxygenase enzymes preventing thromboxane a2 synthesis and subsequent aggregation

A

aspirin and nsaids

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44
Q

adenosine diphosphate (adp) receptor inhibitors
blockage of this receptor inhibits platelet aggregation

A

clopidogrel bisulfate
ticlopidine

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45
Q

block iib/iiia glycoprotein receptors, preventing aggregation

A

eptifibatide and similar anti-platelet medications

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46
Q

uncontrolled, malignant proliferation of plateletse, not in response to thrombopoietin, can be caused by essential thrombocythemia, polycythemia vera, and chronic myelogenous leukemia
associated with either hemorrhagic or thrombotic complications
platelet counts can be >1000 x 10^9/L

A

primary thrombocytosis

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47
Q

characterized by increased platelet production, usually in response, to thrombopoietin
platelet count is elevated by usually <1000 x 10^9/L

A

secondary/reactive thrombocytosis

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48
Q

regulates thrombopoiesis by inhibiting thrombopoietin
deficiency causes increased thrombopoietin and stimulates thrombopoiesis

A

iron

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49
Q

decrease in the number of platelets due to megakaryocyte hypoproliferation, ineffective thrombopoiesis, and increased loss/destruction

A

thrombocytopenia

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50
Q

this may result in up to 90% of platelets being sequestered

A

hypersplenism

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51
Q

increased destruction of damaged and normal platelets

A

splenic sequestration

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52
Q

platelets can adhere to neutrophils when exposed to edta
needs to redraw in sodium citrate to correct; multiply platelet count by 1.1 to correct for dilution factor in sodium citrate tube

A

platelet satellitosis

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53
Q

vascular system and platelets are involved
starts when platelets come in contact with exposed collagen, microfilaments, and the basement membrane of endothelial tissue
small blood vessels constrict, allowing platelets to adhere to exposed tissue, which causes adp/atp release

A

primary hemostasis

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54
Q

goal is generation of sufficient thrombin to convert fibrinogen to fibrin clot
involves activation of intrinsicic, extrinsic and common coagulation pathway factors

A

secondary hemostasis

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55
Q

includes the platelet plug formed in primary hemostasis and fibrin formed in secondary hemostasis

A

fibrin clot

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56
Q

activated when coagulation proteins are exposed to subendothelial collagen

A

intrinsic pathway

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57
Q

intrinsic pathway includes these:

A

XII
XI
prekallikrein
HMWK
IX
VIII

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58
Q

coagulation protein: hageman

A

XII

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59
Q

coagulation protein: plasma thromboplastin antecedent

A

XI

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60
Q

coagulation protein: fletcher

A

prekallikrein

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61
Q

coagulation protein: fitzgerald

A

hmwk

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62
Q

coagulation protein: plasma thromboplastin component / christmas factor

A

IX

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63
Q

coagulation protein: anti-hemophilic factor a

A

VIII

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64
Q

starts with the release of tissue factor from injured blood vessel endothelial cells and subendothelium

A

extrinsic pathway

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65
Q

coagulation protein: stable factor

A

VII

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66
Q

begins with factor X activation by either the extrinsic or intrinsic pathway

A

common pathway

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67
Q

common pathway includes these factors

A

X
V
II
I

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68
Q

coagulation protein: stuart-prower

A

X

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69
Q

coagulation protein: proaccelerin / labile factor

A

V

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70
Q

coagulation protein: prothrombin

A

II

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71
Q

coagulation protein: fibrinogen

A

I

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72
Q

coagulation protein: tissue factor

A

III

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73
Q

coagulation protein: calcium

A

IV

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74
Q

coagulation protein: fibrin stabilizing factor

A

XIII

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75
Q

coagulation protein: vWF

A

ristocetin cofactor

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76
Q

aka enzyme precursors or zymogens
found in plasma, along with non-enzymatic cofactors and calcium

A

coagulation factors

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77
Q

substrates having no biologic activity until converted by enzymes to active forms

A

zymogens

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78
Q

active forms of zymogens

A

serine proteases

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79
Q

assist in the activation of zymogens

A

cofactors

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80
Q

enumerate the cofactors

A

V
VII
tissue factor
high molecular weight kininogen

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81
Q

in its active form, factor XIII is a _____

A

transglutaminase

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82
Q

only substrate in the cascade that does not become an activated enzyme

A

fibrinogen

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83
Q

coagulation groups: contact group

A

prekallikrein
hmwk
XI
XII

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84
Q

produced in the liver
requires contact with a foreign surface for activation
all play a role in intrinsic coagulation activation

A

contact group

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85
Q

under the contact group, these reciprocally activate each other, while ____ is a cofactor in this process

A

XII and prekallikrein
hmwk

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86
Q

contact group: play a role in the inflammatory response, intrinsic fibrinolytic activation, kinin formation and activation of the complement system

A

XIIa
kallikrein
hmwk

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87
Q

coagulation groups: prothrombin group

A

II
VII
IX
X

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88
Q

required for the synthesis of functional factors with calcium binding sites necessary for binding to phospholipid surfaces

A

vitamin k

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89
Q

interfere with metabolism of vitamin K
vitamin K antagonists

A

oral anticoagulants (warfarin)

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90
Q

coagulation groups: fibrinogen group

A

I
V
VIII
XIII

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91
Q

produced in the liver
consumed in the clotting process
thrombin feedback on fibrinogen group factors depends on its concentration

A

fibrinogen group

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92
Q

activate factors V, VIII and XII and induce platelet aggregation

A

low thrombin levels

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93
Q

when thrombin levels are high, thrombin binds to ___ on the endothelial cell surface and activates the ____

A

thrombomodulin
protein c pathway

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94
Q

inhibit factors V and VIII (negative feedback on the cascade)

A

activated C and its cofactor protein S

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95
Q

fibrinogen group: serve as substrates for the fibrinolytic enzyme plasmin

A

I
V
VIII

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96
Q

fibrinogen group: found in platelets

A

I
V

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97
Q

fibrinogen alpha and beta fibrinopeptides are cleaved by ___ forming soluble ____

A

thrombin
fibrin

98
Q

clot stabilization occurs, requiring thrombin activation of ____ and ____

A

XIII
calcium

99
Q

VIII/vWF complex: synthesized in the liver is composed of two fractions, the anti-hemophiliac factor and antigenic property

A

VIII

100
Q

coagulation portion that acts as a cofactor in the intrinsic coagulation pathway

A

VIII:C

101
Q

antigenic property of factor VIII

A

VIII:Ag

102
Q

VIII/vWF complex: synthesized by endothelial cells and megakaryocytes and its composed by two fractions,

A

von willebrand factor

103
Q

needed for platelet adhesion to collagen in vivo
needed for a normal response to ristocetin on aggregation studies in vitro

A

vWF:RCo

104
Q

antigenic property of vWF

A

vWF:Ag

105
Q

coagulation factor: fibrinogen

A

I

106
Q

coagulation factor: prothrombin

A

II

107
Q

coagulation factor: tissue factor

A

III

108
Q

coagulation factor: tissue thromboplastin

A

III

109
Q

coagulation factor: calcium

A

IV

110
Q

coagulation factor: proaccelerin

A

V

111
Q

coagulation factor: labile factor

A

V

112
Q

coagulation factor: accelerator globulin

A

V

113
Q

coagulation factor: proconvertin

A

VII

114
Q

coagulation factor: stable factor

A

VII

115
Q

coagulation factor: serum prothrombin conversion accelerator

A

VII

116
Q

coagulation factor: autoprothrombin I

A

VII

117
Q

coagulation factor: anti-hemophilic factor

A

VIII:C

118
Q

coagulation factor: antihemophilic globulin

A

VIII:C

119
Q

coagulation factor: antihemophilic factor A

A

VIII:C

120
Q

coagulation factor: platelet cofactor I

A

VIII:C

121
Q

coagulation factor: plasma thromboplastin component

A

IX

122
Q

coagulation factor: christmas factor

A

IX

123
Q

coagulation factor: antihemophilic factor B

A

IX

124
Q

coagulation factor: platelet cofactor 2

A

IX

125
Q

coagulation factor: stuart prower factor

A

X

126
Q

coagulation factor: autoprothrombin III

A

X

127
Q

coagulation factor: plasma thromboplastin antecedent

A

XI

128
Q

coagulation factor: antihemophilic factor C

A

XI

129
Q

coagulation factor: hageman factor

A

XII

130
Q

coagulation factor: glass factor

A

XII

131
Q

coagulation factor: contact factor

A

XII

132
Q

coagulation factor: fibrin stabilizing factor

A

XIII

133
Q

coagulation factor: laki-lorand factor

A

XIII

134
Q

coagulation factor: fibrinase

A

XIII

135
Q

coagulation factor: plasma transglutaminase

A

XIII

136
Q

coagulation factor: fibrinoligase

A

XIII

137
Q

coagulation factor: fletcher factor

A

prekallikrein

138
Q

coagulation factor: fitzgerald factor

A

hmwk

139
Q

coagulation factor: flaujeac factor

A

hmwk

140
Q

coagulation factor: williams factor

A

hmwk

141
Q

coagulation factor: contact activation factor

A

hmwk

142
Q

activated during coagulation and fibrinolysis

A

complement system

143
Q

functions in lysing antibody-coated cells

A

complement

144
Q

activates C1 and causes cleavage of C3 to C3a and C3b

A

plasmin

145
Q

C’: increases vascular permeability

A

C3a

146
Q

C’: causes immune adherence of erythrocytes to neutrophils, which enhances phagocytosis

A

C3b

147
Q

kinin system contains these 4 plasma proteins

A

XII
XI
prekallikrein
hmwk

148
Q

generates bradykinin and kallikrein
involved in chemotaxis and pain sensation
mediate inflammatory responses, promote vasodilation and activator of intrinsic coagulation and complement pathways

A

kinin system

149
Q

keeps blood vessels clear
important in clot dissolution

A

fibrinolytic system

150
Q

intrinsic activators of plasminogen

A

XIIa
kallikrein
hmwk

150
Q

glycoprotein produced in the liver
zymogen found in the plasma
converted to plasmin by activators

A

plasminogen

151
Q

extrinsic activators of plasminogen

A

tissue-type plasminogen activator (t-PA)
urokinase-type plasminogen activators (u-PA)

152
Q

exogenous activators of plasminogen

A

t-PA
streptokinase
urokinase

153
Q

not normally found in circulation
degrades fibrin clots, fibrinogen, factors V and VIII
activates the complement system

A

plasmin

154
Q

produced in the liver
principal inhibitor of coagulation
inhibits the serine proteases

A

anti-thrombin

155
Q

vitamin K-dependent regulatory proteins
activated when thrombin binds to thrombomodulin on the endothelial cell surface
inhibit factors V and VIII to provide negative feedback on the cascade

A

protein c and s

156
Q

inhibits factor VIIa-tissue factor complex

A

tissue factor pathway inhibitor

157
Q

inhibits thrombin, Xa, kallikrein, and plasma

A

alpha-2-macroglobulin

158
Q

inhibits XIa and inactivates plasmin

A

alpha-1-antitrypsin

159
Q

inhibits C1 from the complement cascade, and XIIa, XIa, kallikrein and plasmin

A

C1 inhibitor

160
Q

principal inhibitor of fibrinolysis
neutralizes plasmin

A

alpha-2-antiplasmin

161
Q

important inhibitor of fibrinolysis
prevents activation of plasminogen by t-PA
released from endothelial cell supon damage

A

plasminogen activator inhibitor-1

162
Q

genetic deficiency occurs in about 1:2000 in the general population
associated with deep vein thrombosis and pulmonary embolism
serine proteases not inhibited; negative feedback to cascade impaired
lab: antithrombin activity assay

A

anti-thrombin deficiency

163
Q

can cause superficial and deep vein thrombosis and/or pulmonary embolism
lab: immunologic and functional testing to diagnose

A

protein c or protein s deficiencies

164
Q

all have autosomal recessive inheritance pattern
associated with thrombosis, not hemorrhage

A

decreased activation of the fibrinolytic system

165
Q

decreased activation of the fibrinolytic system: causes prolonged aPTT; factor XII assay confirms

A

factor XII deficiency

166
Q

decreased activation of the fibrinolytic system: causes a prolonged aPTT that shortens in patient plasma incubated with kaolin

A

prekallikrein deficiency

167
Q

decreased activation of the fibrinolytic system: causes a slightly prolonged aPTT

A

hmwk deficiency

168
Q

decreased activation of the fibrinolytic system: characterized by thrombosis due to an inability to generate plasmin

A

plasminogen deficiency

169
Q

most common hereditary cause of thrombosis
caused by an amino acid substitution
protein c is incapable of inactivating factor V causing thrombin generation and subsequent fibrin clot formation
lab: pcr-based molecular assay to single-point mutation in the gene

A

factor V Leiden (activated protein C resistance

170
Q

second most hereditary cause of thrombosis
caused by an amino acid substitution
may have slightly elevated prothrombin level
lab: pcr-based molecular assay

A

prothrombin gene mutation 20210

171
Q

autosomal dominant trait
abnormal structure of fibrinogen
caused by gene mutations
associated with either bleeding or thrombosis
dependent on the specific gene mutation

A

dysfribrinogenemia

172
Q

secondary thrombotic disorders: the body develops autoantibodies against platelet phospholipids; etiology is unknown

A

lupus anticoagulant and anti-cardiolipin antibodies

173
Q

secondary thrombotic disorders: thrombotic event starts after tissue factor release during surgery, activating the extrinsic coagulation (dominant in vivo) pathway

A

post-operative status

174
Q

secondary thrombotic disorders: risk of acquiring this increases because of the release of thromboplastic substances by neoplastic cells

A

malignancy

175
Q

secondary thrombotic disorders: placenta is rich in tissue factor, which may enhance thrombosis
factor v and viii levels increase, contributing to clot formation

A

pregnancy

176
Q

secondary thrombotic disorders: increase risk of venous thrombosis and renal artery thrombosis

A

estrogen oral contraceptives

177
Q

secondary thrombotic disorders: results in decreased AT levels and increased PAI-1 causing thrombosis

A

morbid obesity

178
Q

secondary thrombotic disorders: linked to atherosclerosis, resulting in arterial and venous thromboembolism
mechanisms not fully understood by may be associated with a reduction in the localized activation of the protein C pathway

A

hyperhomocysteneinemia

179
Q

autosomal dominant trait
most common inherited bleeding disorder
abnormalities in both primary and secondary hemostasis
caused by a defect in a factor that is needed for platelet adhesion to collagen in primary hemostasis
mild to moderate bleeding, menorrhagia
abnormal platelet aggregation with ristocetin,variable aPTT and prolonged bleeding time

A

von willebrand disease

180
Q

sex-linked disorder transmitted on the x-chromosome by carrier women to their sons
accounts for 80% of the hemophiliacs
second most common hereditary bleeding disorder
bleeding symptoms are proportional to the degree of the factor deficiency, spontaneous bleeding occurs often and is especially bad in joint regions
prolonged aPTT only, factor viii:c assay to confirm

A

factor viii:c hemophilia a, classic hemophilia deficiency

181
Q

sex-linked recessive trait
accounts for 20% of the hemophiliacs, third most common hereditary bleeding disorder
bleeding symptoms are similar to those seen in hemophilia A
prolonged aPTT only; factor ix assay to confirm

A

factor ix (hemophilia b, christmas disease) deficiency

182
Q

mainly seen in the ashkenazi jewish population
characterized by clinical bleeding that is asymptomatic until surgery or trauma

A

factor xi (hemophilia c) deficiency

183
Q

autosomal recessive trait
soft tissue bleeding
prolonged PT only

A

factor vii (stable factor) deficiency

184
Q

autosomal recessive trait
soft tissue bleeding and chronic bruising
prolonged PT and aPTT

A

factor x (stuart-prower) deficiency

185
Q

autosomal recessive trait
mild to moderate bleeding symptoms
prolonged PT and aPTT

A

factor V (owren disease, labile factor) deficiency

186
Q

autosomal recessive trait
mild bleeding symptoms
prolonged PT and aPTT

A

factor ii (prothrombin) deficiency

187
Q

autosomal recessive trait; results from afibrinogenemia and hypofibrinogenemia
spontaneous bleeding of mucosa, intestines, and intracranial sites
prolonged bleeding time, decreased fibrinogen concentration, prolonged PT, aPTT and thrombin time

A

factor i (fibrinogen)deficiency

188
Q

autosomal recessive trait
spontaneous bleeding, delayed wound healing and unusual scar formation; increased incidence of spontaneous abortion
5.0 urea test abnormal; PT and aPTT normal; enzymatic and immunologic studies can be done

A

factor xiii (fibrin-stabilizing factor) deficiency

189
Q

major site of hemostatic protein synthesis

A

liver

190
Q

hepatic disease can result in ____ synthesis of coagulation or regulatory proteins and causes impaired ____ of activated hemostatic components

A

decreased
clearance

191
Q

acquired disorders of coagulation and fibrinolysis: prolonged PT, aPTT, bleeding time and possibly decreased platelet counts because of hypersplenism, alcohol toxicity, and disseminated intravascular coagulation (DIC)

A

hepatic disease

192
Q

needed for liver synthesis of functional factors II, VII< IX and X
produced by normal intestinal flora

A

vitamin K

193
Q

acquired disorders of coagulation and fibrinolysis: can result from oral antibiotics, warfarin or decreased absorption resulting from obstructive jaundice
breast-fed babies are more prone to this because it is sterile, which allows on bacterial intestinal colonization to occur
prolonged PT (VII, X, II) and prolonged aPTT (IX, X, II)

A

vitamin K deficiency

194
Q

acquired disorders of coagulation and fibrinolysis:
predisposing condition trigger systemic clotting
leads to systemic fibrinolysis and bleeding
triggered by G(-) septicemia, acute promyelocytic leukemia (FAB M3), obstetrical complications, massive tissue damage
prolonged PT, aPTT, thrombin time, decreased platelet court, antithrombin, fibrinogen concentrations, (+) fibrin and fibrinogen degradation products schistocytes
systemic thrombotic event causes multiple organ failure, systemic lysis leading to severe hemorrhage

A

disseminated intravascular coagulation with secondary fibrinolysis

195
Q

acquired disorders of coagulation and fibrinolysis: plasminogen is inappropriately activated to plasmin in the absence of clot formation, caused by certain malignancies
prolonged PT, aPTT and thrombin, low fibrinogen concentration, normal platelet count, rbc morphology and antithrombin concentration, present fibrinogen degradation products

A

primary fibrinogenolysis

196
Q

sample collection, handling and processing for coagulation: order of draw

A

coagulation > heparin, edta, sodium fluoride or clot-promoting additives

197
Q

sample collection, handling and processing for coagulation: glass tubes
to activate the intrinsic pathway, including the activation of the contact factors prekallikrein, XI and XII

A

plastic- or silicone-coated

198
Q

sample collection, handling and processing for coagulation: ratio of blood to anticoagulant

A

9:1 blood to 3.2% sodium citrate anticoagulant

199
Q

sample collection, handling and processing for coagulation: specimens must be processed ASAP following blood collection; recommendations include processing within ___ for aPTT and ___ for PT; centrifuge to obtain ___ and remove plasma from cells; can freeze plasma at ____

A

4 hours
24 hours
platelet-poor plasma
-20degC

200
Q

sample collection, handling and processing for coagulation: temperatures testing must be performed at ___

A

37degC

201
Q

evaluation tests: monitors unfractionated heparin therapy, screening tests for factors XII, XI, prekallikrein, HMWK, IX, VIII, X, V, II and I

A

aPTT

202
Q

aPTT evaluation: reagents

A

platelet phospholipid substitute with an activator
calcium chloride

203
Q

aPTT evaluation: prolonged aPTT can indicate

A

factors deficiencies in the intrinsic/common pathways
acquired circulating inhibitor: heparin, lupus inhibitor or antibody to a specific factor

204
Q

aPTT evaluation: falsely long aPTT sources of error

A

blood collection tube not full
large clot in tube
heparin contamination from line draw
hematocrit >55.0%
lipedimia/icterus only if optical method used

205
Q

aPTT evaluation: falsely short aPTT sources of error

A

hemolysis
small clot in tube
plasma containing platelets

206
Q

evaluation tests: monitor anticoagulaation therapy by vitamin K antagonists (warfarin/coumarin), screening tests for factor VII, X, V, II and I
principle: add thromboplastin reagent containing calcium chloride to citrated platelet-poor plasma, measure the time required for clot formation

A

prothrombin time

207
Q

PT evaluation: reagents

A

thromboplastin source (tissue factor) with calcium chloride

208
Q

PT evaluation: reference range

A

10.0-14.0 seconds

209
Q

aPTT evaluation: reference range

A

23.0-35.0 seconds

210
Q

means of standardizing PT reporting worldwide, not dependent on thromboplastin reagent or instrument used
used to monitor warfarin/coumadin therapy
no reference range

A

international normalized ratio (INR)

211
Q

INR formula

A

INR = [patient PT in seconds/control PT in seconds]^ISI

212
Q

thromboplastin reagent
number is provided by the manufacturer and is lot number and instrument specific

A

international sensitivity index (ISI)

213
Q

PT evaluation: prolonged PT can indicate ____

A

factor deficiencies in the extrinsic/common pathways
factor reactivity less than 5-30%
warfarin therapy

214
Q

PT evaluation: falsely long PT sources of error

A

blood collection tube not full
large clot in tube
heparin contamination from line draw
hematocrit >55.0%
lipedimia/icterus only if optical method used

215
Q

PT evaluation: falsely short PT sources of error

A

small clot in tube

216
Q

this is performed when the PT and aPTT is prolonged to differentiate a factor deficiency from a circulating inhibitor
patient plasma is mixed with normal pooled plasma and test(s) is (are) repeated

A

mixing study

217
Q

mixing study: shortening of the time into the reference range indicates a ____

A

factor deficiency (hereditary or acquired such as warfarin therapy)

218
Q

mixing study: partial or no correction indicates a ___

A

circulating inhibitor (heparin, lupus inhibitor, VIII inhibitor, IX inhibitor)

219
Q

quantitative test for fibrinogen
thrombin reagent is added to diluted citrated patient plasma

A

fibrinogen level

220
Q

fibrinogen level: this is obtained by using a standard curve and is inversely proportional to fibrinogen concentration

A

thrombin clotting time

221
Q

qualitative/quantitative for fibrinogen
thrombin reagent is added to undiluted patient plasma and result is reported in seconds

A

thrombin time

222
Q

causes of prolonged thrombin time

A

presence of heparin, degradation products or low fibrinogen

223
Q

comparison of thrombin time and reptilase time in fibrin split products

A

TT: prolonged
RT: prolonged

224
Q

comparison of thrombin time and reptilase time in hypofibrinogenemia

A

TT: prolonged
RT: prolonged

225
Q

comparison of thrombin time and reptilase time in dysfibrinogenemia

A

TT: prolonged
RT: prolonged

226
Q

comparison of thrombin time and reptilase time in immunologic antithrombin

A

TT: prolonged
RT: normal

227
Q

comparison of thrombin time and reptilase time in heparin therapy

A

TT: prolonged
RT: normal

228
Q

used to confirm a suspected factor deficiency, as suggested by a mixing study that shows correction
measures the ability of the patient plasma to correct the PT or aPTT result obtained with plasma known to be factor deficient

A

factor assays

229
Q

unstable clot that forms in factor XIII deficiency dissolves in urea solution in which a factor XIIIa stabilized clot remains intact for at least 24 hours

A

5.0 urea clot solubility test

230
Q

sensitive test tat uses snake venom as the reagent to activate factor X in the cascade
if the lupus inhibitor is present, the venom is neutralized, and the test is prolonged

A

dilute russell viper venom test

231
Q

whole blood is placed in a glass tube containing activity
determine time it takes the clot to form
blood is kept at 37degC during testing

A

activated clotting time

232
Q

latex particles are coated with antibody against fibrinogen and are mixed with patient serum
macroscopic agglutination indicates degradation products
non specific test that will be abnormal when either fibrin degradation products or fibrinogen degradation products are present

A

fibrin degradation products

233
Q

latex particles are coated with antibody against d-dimer
highly specific measurement for fibrin degradation products
does not detect fibrinogen degradation products
abnormal results indicate a clot has formed, been stabilized by factor XIIIa, and is being lysed by plasmin

A

d-dimer assay

234
Q

TOC to prevent extension of existing clots due to acute thrombotic events
therapy involves a bolus of heparin followed by continuous infusion
antithrombin must be present with levels of 40-60% of normal for heparin to work
monitor with aPTT, therapeutic range is approximately 1.5-2 times patient baseline aPTT value prior to treatment

A

unfractionated heparin therapy

235
Q

inhibits serine proteases including XIIa, XIa, IXa, Xa, IIa, kallikrein
inhibition is immediate, immediately reversed by administration of protamine sulfate

A

antithrombin/heparin complex

236
Q

oral anticoagulant
prescribed on an outpatient basis to prevent extension of existing clot and recurrences of thrombotic events and prophylactically it is often prescribed post surgery to prevent thrombosis
vitamin K antagonists
inhibits liver synthesis of functional prothrombin group factors II, VII, IX and X, factor VII is affected first
monitor with PT and INR

A

warfarin/coumadin therapy

237
Q

anticoagulant therapies: subcutaneous injection, requires antithrombin to work, fixed dose response reduces the need for laboratory monitoring, lower risk of heparin-induced thrombocytopenia, mainly an anti-Xa inhibitor, anti-IIa response is reduced

A

low-molecular weight heparin (enoxaparin sodium)

238
Q

anticoagulant therapies: inactivates thrombin only, does not require presence of antithrombin to work, used in place of unfractionated or low-molecular weight heparin when HIT suspected, these medications will prolong the PT, aPTT and thrombin time

A

direct thrombin inhibitor (argatroban, lepirudin, bivalirudin)

239
Q

anticoagulant therapies: tissue plasminogen activator, streptokinase or urokinase, can be used to lyse existing clots and reestablish vascular perfusion, these medications convert plasminogen to plasmin, plasmin destroys fibrin clots, factors I, V, and VIII, affects tests include PT, aPTT, thrombin time, fibrinogen, FDP, and D-dimer

A

fibrinolytic therapy

240
Q

anticoagulant therapies: may be used in conjunction with other anticoagulant therapies to prevent recurrence of thrombotic events

A

anti-platelet medications (aspirin, plavix, ticlopidine, NSAIDS)

MTLE (6 decks)

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