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
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
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
4
Q
necessary for platelet adhesion to collagen
carrier protein for coagulation factor viii:c
A
von willebrand factor
5
Q
a platelet aggregation inhibitor and vasodilator
A
prostacyclin
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
7
Q
hereditary vascular defects: thin vessel walls cause mucous membrane bleeding
A
hemorrhagic telangiectasia
8
Q
hereditary vascular defects: abnormally collagen production causes hyperelastic skin and joint abnormalities
A
ehlers-danlos syndrome
9
Q
vitamin c deficiency
impairs proper collagen synthesis and vessel integrity
A
scurvy
10
Q
committed myeloid progenitor cell in response this growth factor gives rise to megakaryocytes
A
thrombopoietin
11
Q
the process in which the nucleus divides without cytoplasmic division during the earliest thrombocyte stage
A
endomitosis
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
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
14
Q
invagination of the plasma membrane that becomes the future site of platelet fragmentation
A
demarcating membrane system
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
16
Q
2-4micrometers in size appearing as pale blue cells with azurophilic granules
no nucleus
A
mature platelets
17
Q
platelet zones: exterior coat int he peripheral zone and contains glycoprotein receptor sites
A
glycocalyx
18
Q
platelet zones: contains the phospholipid membranes, which serve as a surface for interaction of coagulation factors in secondary hemostasis
A
submembrane area
19
Q
platelet zones: contains microtubules, cytoskeleton, actin and myosin
A
sol gel (structural area)
20
Q
platelet zones: contains the granules, lysosomes, mitochondria, peroxisomes, and glycogen; controls platelet function in response to caogulation
A
organelle zone
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
22
Q
platelet zones: contain adp, atp, serotonin, and calcium in the organelle zone
A
dense bodies/delta granules
23
Q
platelet zones: contain hydrolase enzyme
A
lysosomes
24
Q
platelet zones: regulator of intracellular calcium concentration in the membrane systems
A
dense tubular system
25
platelet zones: releases granular contents through channels leading to the surface of the platelet in the membrane systems
open cannalicular system
26
reference range for platelets at healthy individuals
150-450 x 10^9/L
27
life span of platelets
8-12 days
28
platelet secreted proteins: stimulates vasoconstriction when vessel injury occur
serotonin
29
platelet secreted proteins: stimulate platelet aggregation and vasoconstriction
thromboxane a2
30
platelet secreted proteins: contacts the thrombus at the end of the coagulation process
actomyosin
31
platelet factors: neutralizes heparin
pf4
32
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
pf3
33
proper platelet function sequence
adhesion
release of granule contents
aggregation
clot retraction
34
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
adhesion
35
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
aggregation
36
proper platelet function: follows clot formation, dependent on the thrombasthenin and glycoprotein receptors iib/iiia, restores normal blood flow to the vessel
clot retraction
37
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
von willebrand disease
38
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
bernard soulier syndrome
39
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
glanzmann thrombasthenia
40
storage pool defects: characterized by large platelets, thrombocytopenia, and an absence of alpha granules
patients are prone to lifelong mild bleeding tendencies
gray-platelet syndrome
41
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
wiskott-aldrich syndrome
42
storage pool defects: characterized by a lack of dense body granules
patients exhibit occulocutaneous albinism and are prone to hemorrhage
hermansky-pudlak syndrome
43
interfere with cyclo-oxygenase enzymes preventing thromboxane a2 synthesis and subsequent aggregation
aspirin and nsaids
44
adenosine diphosphate (adp) receptor inhibitors
blockage of this receptor inhibits platelet aggregation
clopidogrel bisulfate
ticlopidine
45
block iib/iiia glycoprotein receptors, preventing aggregation
eptifibatide and similar anti-platelet medications
46
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
primary thrombocytosis
47
characterized by increased platelet production, usually in response, to thrombopoietin
platelet count is elevated by usually <1000 x 10^9/L
secondary/reactive thrombocytosis
48
regulates thrombopoiesis by inhibiting thrombopoietin
deficiency causes increased thrombopoietin and stimulates thrombopoiesis
iron
49
decrease in the number of platelets due to megakaryocyte hypoproliferation, ineffective thrombopoiesis, and increased loss/destruction
thrombocytopenia
50
this may result in up to 90% of platelets being sequestered
hypersplenism
51
increased destruction of damaged and normal platelets
splenic sequestration
52
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
platelet satellitosis
53
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
primary hemostasis
54
goal is generation of sufficient thrombin to convert fibrinogen to fibrin clot
involves activation of intrinsicic, extrinsic and common coagulation pathway factors
secondary hemostasis
55
includes the platelet plug formed in primary hemostasis and fibrin formed in secondary hemostasis
fibrin clot
56
activated when coagulation proteins are exposed to subendothelial collagen
intrinsic pathway
57
intrinsic pathway includes these:
XII
XI
prekallikrein
HMWK
IX
VIII
58
coagulation protein: hageman
XII
59
coagulation protein: plasma thromboplastin antecedent
XI
60
coagulation protein: fletcher
prekallikrein
61
coagulation protein: fitzgerald
hmwk
62
coagulation protein: plasma thromboplastin component / christmas factor
IX
63
coagulation protein: anti-hemophilic factor a
VIII
64
starts with the release of tissue factor from injured blood vessel endothelial cells and subendothelium
extrinsic pathway
65
coagulation protein: stable factor
VII
66
begins with factor X activation by either the extrinsic or intrinsic pathway
common pathway
67
common pathway includes these factors
X
V
II
I
68
coagulation protein: stuart-prower
X
69
coagulation protein: proaccelerin / labile factor
V
70
coagulation protein: prothrombin
II
71
coagulation protein: fibrinogen
I
72
coagulation protein: tissue factor
III
73
coagulation protein: calcium
IV
74
coagulation protein: fibrin stabilizing factor
XIII
75
coagulation protein: vWF
ristocetin cofactor
76
aka enzyme precursors or zymogens
found in plasma, along with non-enzymatic cofactors and calcium
coagulation factors
77
substrates having no biologic activity until converted by enzymes to active forms
zymogens
78
active forms of zymogens
serine proteases
79
assist in the activation of zymogens
cofactors
80
enumerate the cofactors
V
VII
tissue factor
high molecular weight kininogen
81
in its active form, factor XIII is a _____
transglutaminase
82
only substrate in the cascade that does not become an activated enzyme
fibrinogen
83
coagulation groups: contact group
prekallikrein
hmwk
XI
XII
84
produced in the liver
requires contact with a foreign surface for activation
all play a role in intrinsic coagulation activation
contact group
85
under the contact group, these reciprocally activate each other, while ____ is a cofactor in this process
XII and prekallikrein
hmwk
86
contact group: play a role in the inflammatory response, intrinsic fibrinolytic activation, kinin formation and activation of the complement system
XIIa
kallikrein
hmwk
87
coagulation groups: prothrombin group
II
VII
IX
X
88
required for the synthesis of functional factors with calcium binding sites necessary for binding to phospholipid surfaces
vitamin k
89
interfere with metabolism of vitamin K
vitamin K antagonists
oral anticoagulants (warfarin)
90
coagulation groups: fibrinogen group
I
V
VIII
XIII
91
produced in the liver
consumed in the clotting process
thrombin feedback on fibrinogen group factors depends on its concentration
fibrinogen group
92
activate factors V, VIII and XII and induce platelet aggregation
low thrombin levels
93
when thrombin levels are high, thrombin binds to ___ on the endothelial cell surface and activates the ____
thrombomodulin
protein c pathway
94
inhibit factors V and VIII (negative feedback on the cascade)
activated C and its cofactor protein S
95
fibrinogen group: serve as substrates for the fibrinolytic enzyme plasmin
I
V
VIII
96
fibrinogen group: found in platelets
I
V
97
fibrinogen alpha and beta fibrinopeptides are cleaved by ___ forming soluble ____
thrombin
fibrin
98
clot stabilization occurs, requiring thrombin activation of ____ and ____
XIII
calcium
99
VIII/vWF complex: synthesized in the liver is composed of two fractions, the anti-hemophiliac factor and antigenic property
VIII
100
coagulation portion that acts as a cofactor in the intrinsic coagulation pathway
VIII:C
101
antigenic property of factor VIII
VIII:Ag
102
VIII/vWF complex: synthesized by endothelial cells and megakaryocytes and its composed by two fractions,
von willebrand factor
103
needed for platelet adhesion to collagen in vivo
needed for a normal response to ristocetin on aggregation studies in vitro
vWF:RCo
104
antigenic property of vWF
vWF:Ag
105
coagulation factor: fibrinogen
I
106
coagulation factor: prothrombin
II
107
coagulation factor: tissue factor
III
108
coagulation factor: tissue thromboplastin
III
109
coagulation factor: calcium
IV
110
coagulation factor: proaccelerin
V
111
coagulation factor: labile factor
V
112
coagulation factor: accelerator globulin
V
113
coagulation factor: proconvertin
VII
114
coagulation factor: stable factor
VII
115
coagulation factor: serum prothrombin conversion accelerator
VII
116
coagulation factor: autoprothrombin I
VII
117
coagulation factor: anti-hemophilic factor
VIII:C
118
coagulation factor: antihemophilic globulin
VIII:C
119
coagulation factor: antihemophilic factor A
VIII:C
120
coagulation factor: platelet cofactor I
VIII:C
121
coagulation factor: plasma thromboplastin component
IX
122
coagulation factor: christmas factor
IX
123
coagulation factor: antihemophilic factor B
IX
124
coagulation factor: platelet cofactor 2
IX
125
coagulation factor: stuart prower factor
X
126
coagulation factor: autoprothrombin III
X
127
coagulation factor: plasma thromboplastin antecedent
XI
128
coagulation factor: antihemophilic factor C
XI
129
coagulation factor: hageman factor
XII
130
coagulation factor: glass factor
XII
131
coagulation factor: contact factor
XII
132
coagulation factor: fibrin stabilizing factor
XIII
133
coagulation factor: laki-lorand factor
XIII
134
coagulation factor: fibrinase
XIII
135
coagulation factor: plasma transglutaminase
XIII
136
coagulation factor: fibrinoligase
XIII
137
coagulation factor: fletcher factor
prekallikrein
138
coagulation factor: fitzgerald factor
hmwk
139
coagulation factor: flaujeac factor
hmwk
140
coagulation factor: williams factor
hmwk
141
coagulation factor: contact activation factor
hmwk
142
activated during coagulation and fibrinolysis
complement system
143
functions in lysing antibody-coated cells
complement
144
activates C1 and causes cleavage of C3 to C3a and C3b
plasmin
145
C': increases vascular permeability
C3a
146
C': causes immune adherence of erythrocytes to neutrophils, which enhances phagocytosis
C3b
147
kinin system contains these 4 plasma proteins
XII
XI
prekallikrein
hmwk
148
generates bradykinin and kallikrein
involved in chemotaxis and pain sensation
mediate inflammatory responses, promote vasodilation and activator of intrinsic coagulation and complement pathways
kinin system
149
keeps blood vessels clear
important in clot dissolution
fibrinolytic system
150
intrinsic activators of plasminogen
XIIa
kallikrein
hmwk
150
glycoprotein produced in the liver
zymogen found in the plasma
converted to plasmin by activators
plasminogen
151
extrinsic activators of plasminogen
tissue-type plasminogen activator (t-PA)
urokinase-type plasminogen activators (u-PA)
152
exogenous activators of plasminogen
t-PA
streptokinase
urokinase
153
not normally found in circulation
degrades fibrin clots, fibrinogen, factors V and VIII
activates the complement system
plasmin
154
produced in the liver
principal inhibitor of coagulation
inhibits the serine proteases
anti-thrombin
155
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
protein c and s
156
inhibits factor VIIa-tissue factor complex
tissue factor pathway inhibitor
157
inhibits thrombin, Xa, kallikrein, and plasma
alpha-2-macroglobulin
158
inhibits XIa and inactivates plasmin
alpha-1-antitrypsin
159
inhibits C1 from the complement cascade, and XIIa, XIa, kallikrein and plasmin
C1 inhibitor
160
principal inhibitor of fibrinolysis
neutralizes plasmin
alpha-2-antiplasmin
161
important inhibitor of fibrinolysis
prevents activation of plasminogen by t-PA
released from endothelial cell supon damage
plasminogen activator inhibitor-1
162
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
anti-thrombin deficiency
163
can cause superficial and deep vein thrombosis and/or pulmonary embolism
lab: immunologic and functional testing to diagnose
protein c or protein s deficiencies
164
all have autosomal recessive inheritance pattern
associated with thrombosis, not hemorrhage
decreased activation of the fibrinolytic system
165
decreased activation of the fibrinolytic system: causes prolonged aPTT; factor XII assay confirms
factor XII deficiency
166
decreased activation of the fibrinolytic system: causes a prolonged aPTT that shortens in patient plasma incubated with kaolin
prekallikrein deficiency
167
decreased activation of the fibrinolytic system: causes a slightly prolonged aPTT
hmwk deficiency
168
decreased activation of the fibrinolytic system: characterized by thrombosis due to an inability to generate plasmin
plasminogen deficiency
169
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
factor V Leiden (activated protein C resistance
170
second most hereditary cause of thrombosis
caused by an amino acid substitution
may have slightly elevated prothrombin level
lab: pcr-based molecular assay
prothrombin gene mutation 20210
171
autosomal dominant trait
abnormal structure of fibrinogen
caused by gene mutations
associated with either bleeding or thrombosis
dependent on the specific gene mutation
dysfribrinogenemia
172
secondary thrombotic disorders: the body develops autoantibodies against platelet phospholipids; etiology is unknown
lupus anticoagulant and anti-cardiolipin antibodies
173
secondary thrombotic disorders: thrombotic event starts after tissue factor release during surgery, activating the extrinsic coagulation (dominant in vivo) pathway
post-operative status
174
secondary thrombotic disorders: risk of acquiring this increases because of the release of thromboplastic substances by neoplastic cells
malignancy
175
secondary thrombotic disorders: placenta is rich in tissue factor, which may enhance thrombosis
factor v and viii levels increase, contributing to clot formation
pregnancy
176
secondary thrombotic disorders: increase risk of venous thrombosis and renal artery thrombosis
estrogen oral contraceptives
177
secondary thrombotic disorders: results in decreased AT levels and increased PAI-1 causing thrombosis
morbid obesity
178
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
hyperhomocysteneinemia
179
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
von willebrand disease
180
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
factor viii:c hemophilia a, classic hemophilia deficiency
181
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
factor ix (hemophilia b, christmas disease) deficiency
182
mainly seen in the ashkenazi jewish population
characterized by clinical bleeding that is asymptomatic until surgery or trauma
factor xi (hemophilia c) deficiency
183
autosomal recessive trait
soft tissue bleeding
prolonged PT only
factor vii (stable factor) deficiency
184
autosomal recessive trait
soft tissue bleeding and chronic bruising
prolonged PT and aPTT
factor x (stuart-prower) deficiency
185
autosomal recessive trait
mild to moderate bleeding symptoms
prolonged PT and aPTT
factor V (owren disease, labile factor) deficiency
186
autosomal recessive trait
mild bleeding symptoms
prolonged PT and aPTT
factor ii (prothrombin) deficiency
187
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
factor i (fibrinogen)deficiency
188
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
factor xiii (fibrin-stabilizing factor) deficiency
189
major site of hemostatic protein synthesis
liver
190
hepatic disease can result in ____ synthesis of coagulation or regulatory proteins and causes impaired ____ of activated hemostatic components
decreased
clearance
191
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)
hepatic disease
192
needed for liver synthesis of functional factors II, VII< IX and X
produced by normal intestinal flora
vitamin K
193
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)
vitamin K deficiency
194
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
disseminated intravascular coagulation with secondary fibrinolysis
195
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
primary fibrinogenolysis
196
sample collection, handling and processing for coagulation: order of draw
coagulation > heparin, edta, sodium fluoride or clot-promoting additives
197
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
plastic- or silicone-coated
198
sample collection, handling and processing for coagulation: ratio of blood to anticoagulant
9:1 blood to 3.2% sodium citrate anticoagulant
199
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 ____
4 hours
24 hours
platelet-poor plasma
-20degC
200
sample collection, handling and processing for coagulation: temperatures testing must be performed at ___
37degC
201
evaluation tests: monitors unfractionated heparin therapy, screening tests for factors XII, XI, prekallikrein, HMWK, IX, VIII, X, V, II and I
aPTT
202
aPTT evaluation: reagents
platelet phospholipid substitute with an activator
calcium chloride
203
aPTT evaluation: prolonged aPTT can indicate
factors deficiencies in the intrinsic/common pathways
acquired circulating inhibitor: heparin, lupus inhibitor or antibody to a specific factor
204
aPTT evaluation: falsely long aPTT sources of error
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
aPTT evaluation: falsely short aPTT sources of error
hemolysis
small clot in tube
plasma containing platelets
206
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
prothrombin time
207
PT evaluation: reagents
thromboplastin source (tissue factor) with calcium chloride
208
PT evaluation: reference range
10.0-14.0 seconds
209
aPTT evaluation: reference range
23.0-35.0 seconds
210
means of standardizing PT reporting worldwide, not dependent on thromboplastin reagent or instrument used
used to monitor warfarin/coumadin therapy
no reference range
international normalized ratio (INR)
211
INR formula
INR = [patient PT in seconds/control PT in seconds]^ISI
212
thromboplastin reagent
number is provided by the manufacturer and is lot number and instrument specific
international sensitivity index (ISI)
213
PT evaluation: prolonged PT can indicate ____
factor deficiencies in the extrinsic/common pathways
factor reactivity less than 5-30%
warfarin therapy
214
PT evaluation: falsely long PT sources of error
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
PT evaluation: falsely short PT sources of error
small clot in tube
216
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
mixing study
217
mixing study: shortening of the time into the reference range indicates a ____
factor deficiency (hereditary or acquired such as warfarin therapy)
218
mixing study: partial or no correction indicates a ___
circulating inhibitor (heparin, lupus inhibitor, VIII inhibitor, IX inhibitor)
219
quantitative test for fibrinogen
thrombin reagent is added to diluted citrated patient plasma
fibrinogen level
220
fibrinogen level: this is obtained by using a standard curve and is inversely proportional to fibrinogen concentration
thrombin clotting time
221
qualitative/quantitative for fibrinogen
thrombin reagent is added to undiluted patient plasma and result is reported in seconds
thrombin time
222
causes of prolonged thrombin time
presence of heparin, degradation products or low fibrinogen
223
comparison of thrombin time and reptilase time in fibrin split products
TT: prolonged
RT: prolonged
224
comparison of thrombin time and reptilase time in hypofibrinogenemia
TT: prolonged
RT: prolonged
225
comparison of thrombin time and reptilase time in dysfibrinogenemia
TT: prolonged
RT: prolonged
226
comparison of thrombin time and reptilase time in immunologic antithrombin
TT: prolonged
RT: normal
227
comparison of thrombin time and reptilase time in heparin therapy
TT: prolonged
RT: normal
228
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
factor assays
229
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
5.0 urea clot solubility test
230
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
dilute russell viper venom test
231
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
activated clotting time
232
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
fibrin degradation products
233
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
d-dimer assay
234
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
unfractionated heparin therapy
235
inhibits serine proteases including XIIa, XIa, IXa, Xa, IIa, kallikrein
inhibition is immediate, immediately reversed by administration of protamine sulfate
antithrombin/heparin complex
236
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
warfarin/coumadin therapy
237
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
low-molecular weight heparin (enoxaparin sodium)
238
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
direct thrombin inhibitor (argatroban, lepirudin, bivalirudin)
239
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
fibrinolytic therapy
240
anticoagulant therapies: may be used in conjunction with other anticoagulant therapies to prevent recurrence of thrombotic events
anti-platelet medications (aspirin, plavix, ticlopidine, NSAIDS)
