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Hematology (S) > HEMA 1 (Hemostasis) > Flashcards

HEMA 1 (Hemostasis) Flashcards

1
Q

What is hemostasis?

A

Derived from the Greek meaning “the stoppage of bld flow”

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2
Q

What are the different hemostatic components?

A

1) Extravascular
2) Vascular
3) Intravascular

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3
Q

What is extravascular hemostatic cmpt?

A

Involves the tissues surrounding a vessel, w/c become involved in hemostasis when a local vessel is injured

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4
Q

What is vascular cmpt of hemostasis?

A

Involves the vessels through w/c bld flows

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5
Q

What is the intravascular cmpt of hemostasis?

A

1) The key cmpts are PLTs and biochemicals (procoagulants) in the plasma
2) Such cmpts are involved in coagulation (clot / thrombus formation) / fibrinolysis

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6
Q

What are the 2 types of hemostasis?

A

1) Primary hemostasis
2) Secondary hemostasis

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7
Q

What is the characteristic of primary hemostasis?

A

Composed of bld vessels and PLT

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8
Q

What is the purpose of primary hemostasis?

A

Formation of PLT plug

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9
Q

What is the characteristic of secondary hemostasis?

A

Composed of coagulation factors

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10
Q

What is the purpose of secondary hemostasis?

A

Formation of stable fibrin clot

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11
Q

What are the steps in primary and secondary hemostasis after vessel injury?

A

1) Vasoconstriction
2) PLT adhesion
3) PLT activation and secretion
4) PLT aggregation
5) Fibrin-PLT plug formation

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12
Q

What are the characteristics of vasoconstriction?

A

1) Controlled by vessel smooth muscle
2) Enhanced by chemicals secreted by PLTs

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13
Q

What are the events that happen in PLT adhesion?

A

1) When vascular injury occurs, PLTs come in contact w/ subendothelium (collagen, fibronectin) and adhere to portions of it
2) The von Willebrwnd factor (vWF) binds to gp Ib/IX/V on the PLT membrane

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14
Q

What is the other term for PLT adhesion?

A

PLT adhesiveness

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15
Q

Why does PLT adhesion occur?

A

Because of the presence of vWF being deposited on the injured tissues

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16
Q

What are the events that happen in PLT activation and secretion?

A

1) Following activation, the PLT undergoes a shape change caused by contraction of microtubules
2) The PLT changes from disk-shape to a spherical shape w/ the extrusion of numerous pseudopods
3) At the same time, the PLT granules are secreted
4) During activation, ADP and Ca ion activates phospholipase A2
5) Phospholipase A2 converts membrane phospholipid to arachidonic acid
6) Arachidonic acid is converted by cyclooxygenase into prostaglandin endoperoxide
7) In the PLTs, prostaglandin is converted by thromboxane synthetase into thromboxane A2
8) Thromboxane A2 causes the release of Ca ions and promotes PLT aggregation and vasoconstriction

Note:
Aspirin acetylation permanently inactivates cyclooxygenase, blocking thromboxane A2 production and impairs PLT aggregation

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17
Q

What is the event that happens in PLT aggregation?

A

Interaction and adhesion of PLTs to 1 another to form initial plug at injury site

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18
Q

What must happen in fibrin-PLT plug formation?

A

Fibrin clot must be stabilized by coagulation factor XIII

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19
Q

What are the different bld vessel products?

A

1) Prostacyclin (PGI2)
2) Adenosine
3) Thrombomodulin
4) Heparan sulfate
5) Tissue plasminogen activator
6) vWF

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20
Q

What is the metabolic product of ATP and ADP?

A

Adenosine

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21
Q

What are the actions of PGI2?

A

1) Inhibits PLT activation
2) Stimulates vasodilation

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22
Q

What are the hemostatic roles of PGI2?

A

1) Anticoagulant
2) Reduces bld flow rate

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23
Q

What is the action of adenosine?

A

Stimulates vasodilation

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24
Q

What is the hemostatic role of adenosine?

A

Reduces bld flow rate

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25
Q

What are the actions of thrombomodulin?

A

1) Endothelial receptor for thrombin
2) Binds and inactivates thrombin and enhances anticoagulant and fibrinolytic action pf PRO C found in the plasma

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26
Q

What are the hemostatic roles of thrombomodulin?

A

1) Anticoagulant
2) Fibrinolytic

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27
Q

What are the actions of heparan sulfate?

A

1) Coats the endothelial cell surface
2) Weakly enhances activity of antithrombin-III (w/c is a plasma anticoagulant)

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28
Q

What is the hemostatic role of heparan sulfate?

A

Anticoagulant

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29
Q

What are the actions of tissue plasminogen activator?

A
  1. Converts plasminogen to plasmin, w/c plays an impt role in fibrinolysis
  2. Released only on appropriate stimulus, such as vessel injury, to prevent clot formation at the site of injury
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30
Q

What is the hemostatic role of tissue plasminogen activator?

A

Fibrinolytic

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31
Q

What are the actions of vWF?

A
  1. PRO secreted by endothelium into subendothelium
  2. Required for PLT adhesion to site of vessel injury
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32
Q

What is the hemostatic role of vWF?

A

Coagulation

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33
Q

What are the characteristics of vWF?

A
  1. Synthesized by:
    a. Endothelial cell
    b. Megakaryocyte
  2. Stored in:
    a. Endothelial cell (Weibel-Palade bodies)
    b. PLTs
  3. VIII/vWF
    a. Entire molecule as it circulates in the plasma
    b. Composed of VIII:C and VIII:vWF portions
  4. VIII:vWF
    a. Portion of molecule responsible for binding to endothelium and supporting normal PLT adhesion and fxn
  5. VIII:C
    a. Portion of molecule acting in intrinsic pathway
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34
Q

What is PLT?

A
  1. Are not true cells because they are small fragments of megakaryocyte cytoplasm
  2. Produced by megakaryocyte
  3. Fxn in both primary (adhesion, secretion, aggregation) and secondary hemostasis (coagulation)
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35
Q

What are the characteristics of PLT?

A
  1. Normal value: 150,000 - 400,000/uL
  2. Size: 2 - 4 um
  3. Volume (MPV): ~7 fL
  4. Shape:
    a. Discoid shape (inactive)
    b. Spherical w/ pseudopod (activated)
  5. Lifespan: 8 - 12 days
  6. Storage: 1/3 in the spleen
  7. Appearance in Wright-stain:
    a. Violet-purple granular appearance
    b. Look like specks of dust
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36
Q

What are the roles of PLT in hemostasis?

A
  1. Adhere to injured vessel
  2. Aggregate at the injury site
  3. Promote coagulation on their phospholipid surface
  4. Release biochemicals impt to hemostasis
  5. Induce clot retraction
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37
Q

What are the events / characteristics of clot retraction for PLT?

A
  1. Interaction of Gp IIb/IIIa w/ the PLT cytoskeleton
  2. The contractile abilities of activated PLTs also result in contraction (/ retraction) of formed clots
  3. Actinomysosin / thrombosthenin
  4. In the test tube, clot retraction may be quantitatively assessed
  5. Delayed / incomplete clot retraction:
    a. Thrombocytopenia
    b. Glanzamann’s thrombasthenia
  6. Gp IIb/IIIa is required for clot retraction
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38
Q

What is reticulated PLT?

A

Newly released circulated PLTs that have residual RNA

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39
Q

Morphologic differentiation of megakaryocytic cell series

Given stage: Megakaryoblast

  1. Stage
  2. Granules
  3. Cytoplasmic tags
  4. Nuclear features
  5. PLT visibility
  6. Other info
A
  1. Megakaryoblast
  2. Absent
  3. Present
  4. 1 nucleus
  5. Not visible
  6. Earliest recognizable PLT precursor
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40
Q

Morphologic differentiation of megakaryocytic cell series

Given stage: Promegakaryocyte

  1. Stage
  2. Granules
  3. Cytoplasmic tags
  4. Nuclear features
  5. PLT visibility
  6. Other info
A
  1. Promegakaryocyte
  2. Few
  3. Present
  4. 2 nuclei
  5. Not visible
  6. Formation of demarcating membrane system
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41
Q

Morphologic differentiation of megakaryocytic cell series

Given stage: Megakaryocyte

  1. Stage
  2. Granules
  3. Cytoplasmic tags
  4. Nuclear features
  5. PLT visibility
  6. Other info
A
  1. Megakaryocyte
  2. Numerous
  3. Usually absent
  4. 2 / more nuclei
  5. Not visible
  6. PLT shedding
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42
Q

Morphologic differentiation of megakaryocytic cell series

Given stage: Metamegakaryocyte

  1. Stage
  2. Granules
  3. Cytoplasmic tags
  4. Nuclear features
  5. PLT visibility
  6. Other info
A
  1. Metamegakaryocyte
  2. Aggregated
  3. Absent
  4. 4 / more nuclei
  5. Visible
  6. Last stage of thrombocyte formation
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43
Q

What is endomitosis?

A

Multiple mitotic division w/out cell division, generating giant multinucleated / polypoid cells

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44
Q

What is thrombopoietin?

A

Hormone produced in the liver that stimulates thrombopoiesis

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45
Q

What is the # of PLTs produce by each megakaryocyte?

A

2,000 - 4,000 PLTs

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46
Q

What is PLT shedding?

A

Release of PLTs into the bone marrow sinus

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47
Q

What is demarcating membrane system (DMS)?

A
  1. Network formed by invagination of the plasma membrane
  2. Fxns as the future membrane system of PLT
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48
Q

What are the zones / areas in the PLT structure?

A
  1. Peripheral zone
  2. Submembrane area
  3. Sol-gel zone
  4. Organelle zone
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49
Q

What is peripheral zone (of the PLT structure)?

A

PLT’s outer membrane and related structures

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50
Q

What are the characteristics of peripheral zone (of the PLT structure)?

A
  1. Consists of:
    a. Surface coats (glycocalyx)
    b. Plasma membrane
    c. Submembrane area
  2. Glycoproteins are incorporated in the glycocalyx
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51
Q

What are the fxns of glyocalyx?

A

Provides surface to w/c some coagulation factors (I, V, VIII, X, XI, XII, XIII) may adhere

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52
Q

What are the fxns of sub-membrane area (of the PLT structure)?

A

Links the:
1. Membrane
2. Inner cell body

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53
Q

What is the sol-gel zone (of the PLT structure)?

A

Matrix / muscle and skeletal portion of the PLT

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54
Q

What are the characteristics of the sol-gel zone (of the PLT structure)?

A
  1. Influences communication of the organelles w/ the PLT’s external surroundings
  2. Maintains the shape of the PLT
  3. Consists of microtubule and microfilaments
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55
Q

What is the fxn of microtubules?

A

Give the PLT structural support

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56
Q

What does microfilaments do when PLT is stimulated?

A

They are projected outward forming pseudopodia

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57
Q

What is the importance of microfilaments?

A

They are necessary for contractile process of PLT

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58
Q

What is the characteristic of microfilaments?

A

Consists of 2 PROs such as:
1. Actin
2. Myosin

59
Q

What is the characteristic of organelle zone (of PLT structure)?

A

Consists of:
1. Granules
2. Dense bodies
3. Lysosomes
4. Mitochondria

60
Q

What is the fxn of organelle zone (of PLT structure)?

A

Serves as metabolic center to influence PLT fxn in response to exogenous stimuli such as:
1. Hypercoagulation
2. Viruses
3. Foreign bodies

61
Q

What are the glycoPROs (w/ their fxn) found in glycocalyx?

A
  1. Gp Ib/IX/V: for PLT adhesion
  2. Gp IIb/IIIa: for PLT aggregation
62
Q

What are the PLT granules?

A
  1. Alpha granules
  2. Dense granules
63
Q

What are the alpha granules?

A
  1. High molecular weight kininogen (HMWK)
  2. Fibrinogen (Factor I)
  3. Factor V
  4. vWF
  5. Platelet factor 4
  6. Thrombospondin
  7. Platelet-derived growth factor
  8. Beta thrombomodulin
  9. Plasminogen
  10. Alpha-2 antiplasmin
  11. C1 esterase inhibitor
64
Q

What are the dense granules?

A
  1. Ca
  2. ADP
  3. Serotonin
  4. ATP
  5. Mg
65
Q

What is PLT satellitism?

A

PLTs surrounds on:
1. Neutrophil
2. Monocyte (rare)

66
Q

What are the causes of PLT satellitism?

A
  1. Abnormal PROs
  2. EDTA
67
Q

Each coagulation factor (/ clotting factor) was assigned a Roman numeral in the order of its what?

A

Discovery

68
Q

True or False

All coagulation factors are glycoPROs synthesized in the liver

A

False, because nearly all are glycoPROs synthesized in the liver except factor VIII complex

69
Q

*What are the cmpts (w/ fxns and/or characteristics) of factor VIII complex?

A
  1. VIII: coagulant (VIII:C)
  2. vWF: produced by megakaryocytes and endothelial cells | activated at cold temp = VII and XI
70
Q

What are the different coagulation factors (w/ their preferred name and synonyms)?

A
  1. I (fibrinogen)
  2. II (prothrombin | prethrombin)
  3. III (tissue factor | tissue thromboplastin)
  4. IV (Ca ions)
  5. V (proaccelerin | labil factor, accelerator globulin [aCG])
  6. VII (proconvertin | stable factor, serum prothrombin conversion accelerator [SPCA])
  7. VIII (VIII:C) (antihemophilic factor [AHF] | antihemophilic globulin [AHG], antihemophilic factor A, PLT cofactor 1)
  8. IX (plasma thromboplastic component [PTC] | Christmas factor, antihemophilic factor B, PLT cofactor 2)
  9. X (Stuart-Prower factor | Stuart factor, Prower factor, autoprothrombin III)
  10. XI (plasma thromboplastin antecedent | antihemophilic factor C)
  11. XII (Hageman factor | glass factor, contact factor)
  12. XIII (fibrin stabilizing factor | Laki-Lorand factor, fibrinase, plasma transglutaminase, fibrinoligase)
  13. Prekallekrein (PK) (Fletcher factor)
  14. HMWK (Fitzgerald factor, Williams factor, Flaujeac factor, contact activation factor)
71
Q

What are the classifications of coagulation factors?

A
  1. Accdg to pathway
    a. Extrinsic pathway
    b. Intrinsic pathway
    c. Common pathway
  2. Accdg to properties
    a. Fibrinogen group
    b. Prothrombin group
    c. Contact group
72
Q

What are the factors present in extrinsic pathway?

A
  1. III
  2. VII
73
Q

What are the factors present in extrinsic pathway?

A
  1. III
  2. VII
74
Q

What are the factors present in intrinsic pathway?

A
  1. XII
  2. XI
  3. IX
  4. VIII
75
Q

What are the factors present in common pathway?

A
  1. I
  2. II
  3. V
  4. X
76
Q

What are the factors present in fibrinogen group?

A
  1. I
  2. V
  3. VIII
  4. XIII
  5. Ca dependent
77
Q

What are the factors present in prothrombin group?

A
  1. II
  2. VII
  3. IX
  4. X
  5. Vit K and Ca dependent
  6. Absorbable factors in Barium sulfate (BaSO4)
78
Q

Why are the factors present in contact group termed called as contact group?

A

Because they are activated by contact w/ (-)ly charged foreign particles

79
Q

What are the factors present in contact group?

A
  1. XII
  2. XI
  3. PK
  4. HMWK
80
Q

What is extrinsic pathway?

A

Activated by the release of tissue thromboplastin (factor III) into the plasma from the injured cells

81
Q

What is intrinsic pathway?

A

Activated when a vessel is injured, exposing the subendothelial basement membrane and collagen, both surfaces that promote coagulation

82
Q

What is common pathway?

A

Begins w/ the activation of factor X to factor Xa

83
Q

What is tissue factor / tissue thromboplastin?

A
  1. It is a transmembrane receptor for factor VIIa
  2. Tissue thromboplastin = mixture of tissue factor and phospholipid (Rodak)
84
Q

What are the characteristics of tissue factor?

A
  1. Found on extravascular cells such as:
    a. Fibroblast
    b. Smooth muscle cells
  2. Not found in endothelial cells under normal conditions
  3. High lvls are found in cells of the:
    a. Brain
    b. Lung
    c. Heart
    d. Kidney
    e. Testes
85
Q

What is vit K?

A

It is a quinone found in green leafy vegetables

86
Q

Vit K is produced by what?

A
  1. Bacteroides fragilis
  2. Escherichia coli
87
Q

What is the fxn of vit K?

A

Catalyzes an essential post-translational modification of the prothrombin group PROs = by γ-carboxylation of amino-terminal glutamic acid

Glutamic acid is modified to γ-carboxyglutamic acid when a 2nd carboxyl grp is added to the γ carbon

88
Q

What is vWF?

A

Large multimeric glycoPRO

89
Q

What are the fxns of vWF?

A
  1. Participates in PLT adhesion
  2. Transports factor VIII
90
Q

What are the characteristics of vWF?

A
  1. Composed of multiple subunits of 240,000 Daltons each
    => the subunits are produced by endothelial cells and megakaryocytes, where they combine to form multimers that range from 600,000 - 20,000,000 Daltons
  2. Stored in:
    a. PLTs (alpha-granules)
    b. Endothelial cells (Weibel-Palade bodies)
    => endothelial cells release ultra-large multimers of vWF into plasma, where they normally degraded into small multimers by a vWF-cleaving protease, ADAMTS-13 (a disintegrin-like metalloprotease w/ a thrombospondin type 1 motif, member 13), in bld vessels w/ high shear stress
    => in TTP, defective ADAMTS-13 enzyme activity is associated w/ ultralarge vWF multimers in the plasma, resulting in PLT aggregation and microvascular thrombosis

Vit K-dependents:
1. Procoagulants
a. II
b. VII
c. IX
d. X
2. Regulatory PROs
a. PRO C
b. PRO S
c. PRO Z

91
Q

What is the purpose of Ca?

A

Required for the assembly of coagulation complexes on PLT / cell membrane phospholipids

Serine proteases bind to (-)ly charged phospholipid surfaces, predominantly phosphatidylserine, through (+)ly charged Ca ions

92
Q

What are the characteristics of factor VI?

A
  1. Obsolete
  2. Activated factor (Va)
  3. Was withdrawn from the naming and never reassign
93
Q

What is serine protease?

A

Are proteolytic enzymes of the trypsin family

94
Q

What are the exs of serine proteases?

A
  1. Thrombin
  2. VIIa
  3. IXa
  4. Xa
  5. XIa
  6. XIIa
  7. pre-Kallekrein
95
Q

True or False

Each member has a reactive seryl AA residue in its active site and acts on its substrate by hydrolyzing peptide bonds, digesting the primary backbone, and producing smaller polypeptide fragments

A

True

96
Q

What is thrombomodulin?

A
  1. Transmembrane PRO constitutively expressed by vascular endothelial cells
  2. Cofactor of thrombin
97
Q

What is the fxn of thrombomodulin?

A

Thrombomodulin and thrombin activate PRO C, a coagulation inhibitory PRO, and thrombin activatable fibrinolysis inhibitor (TAFI), a fibrinolysis inhibitor
=> once thrombin is bound to thrombomodulin, it loses its procoagulant ability to activate factors V and VII, and through activation PRO C, leads to destruction of factors V and VIII, thus suppressing further generation of thrombin

98
Q

What is thrombin?

A

Considered as the key protease of coagulation pathway

99
Q

What is the primary fxn of thrombin?

A

To cleave fibrinopeptides A and B from the α and β chains of fibrinogen molecule, triggering spontaneous polymerization

100
Q

What are the fxns of thrombin?

A
  1. Activates cofactors V, VIII, and XI by (+) feedback mechanism
  2. Activates factor XIII, w/c forms covalent bonds between the D domains of the fibrin polymer to cross-link and stabilize the fibrin clot
  3. Initiates aggregation of PLTs
  4. When bounded to thrombomodulin, it activates PRO C pathway to suppress coagulation
  5. Activates TAFI to suppress fibrinolysis
101
Q

What is fibrinogen?

A
  1. Primary substrate of thrombin, w/c converts soluble fibrinogen to insoluble fibrin to produce a clot
  2. It is the most concentrated of all the plasma procoagulants
102
Q

What is the importance of fibrinogen?

A

Fibrinogen is essential to PLT aggregation because it links activated PLTs through their GP IIb/IIIa PLT fibrinogen receptor

103
Q

What is the cleaved fibrinogen called?

A

Fibrin monomer

104
Q

Why is intrinsic pathway called as its term?

A

Because XII is present in the bld

XII -> pre-Kallekrein -> HMWK -> XI -> IX -> VIII -> X -> V -> prothrombin -> fibrinogen

105
Q

Why is extrinsic pathway called as its term?

A

Because TF is not present in the bld

TF -> VII -> X -> V -> prothrombin -> fibrinogen

106
Q

What are the labile factors?

A
  1. V
  2. VIII
107
Q

What are the factors that are activated by cold temp?

A
  1. VII
  2. XI
108
Q

What is the normal value of fibrinogen?

A

200 - 400 mg/dL

109
Q

What is the most abundant clotting factor?

A

Fibrinogen

110
Q

What are the serine proteases in:
1. Extrinsic pathway
2. Intrinsic pathway
3. Common pathway

A
  1. VII
  2. PK, XII, XI, IX (present in serum and plasma)
  3. II, X
111
Q

What is prothrombinase?

A

Xa-Va

112
Q

What are the tenases in:
1. Intrinsic pathway
2. Extrinsic pathway

A
  1. VIIIa-IXa
  2. VIIa-IIIa-IV
113
Q

What is thrombin (/ factor IIa)?

A

Central regulatory component of coagulation

114
Q

What is the fxn of thrombin?

A

Can inhibit / accelerate coagulation

115
Q

What is tissue factor pathway inhibitor?

A

Principal regulator of tissue factor pathway

116
Q

What is the PRO C regulatory system?

A

Thrombin-thrombomodulin -> PRO C -> activated protein C (APC)-protein S -> inactivates factor Va and VIIIa

117
Q

What are the members of antithrombin and other serine protease inhibitors (Serpins)?

A
  1. Antithrombin
  2. Heparin cofactor II
  3. Protein Z-dependent protease inhibitor (ZPI)
  4. Protein C inhibitor
  5. α1-protease inhibitor (α1-antitrypsin)
  6. α2-macroglobulin
  7. α2-antiplasmin
  8. PAI-1
118
Q

What are the characteristics of antithrombin III?

A
  1. Synthesized in the liver
  2. 1st of the coagulation regulatory PRO to be identified
  3. 1st to be assayed routinely in clinical hemostasis lab
  4. SERPIN
119
Q

What is the fxn of antithrombin III?

A

Inhibits thrombin

120
Q

What is the characteristic of heparin cofactor II?

A

SERPIN

121
Q

What is the fxn of heparin cofactor II?

A

Primarily inactivates thrombin

122
Q

What is protein Z-dependent protease inhibitor (ZPI)?

A

Potent inhibitor of factor Xa

123
Q

What are the cmpts of the fibrinolytic system?

A
  1. Plasmin
  2. Plasminogen
  3. Tissue plasminogen activator (TPA)
  4. Urokinase plasminogen activator (UPA)
  5. Streptokinase (SK)
  6. Fibrin(ogen) degradation products / fibrin(ogen) split products
  7. D-dimer
  8. Fragment X, Y, E
124
Q

Fibrinolysis is dependent on what?

A

Enzyme plasmin

125
Q

What is the final stage of coagulation?

A

Fibrinolysis

126
Q

What are the fxns of plasmin?

A
  1. Digest / destroy fibrinogen, fibrin, factor V, and factor VIII
  2. Does not distinguish fibrinogen and fibrin
127
Q

What is the characteristic of plasmin?

A

Not normally present in the bld in an active form

128
Q

What is plasminogen?

A

Zymogen of plasmin

129
Q

What are the characteristics of plasminogen?

A
  1. Normally present in the plasma
  2. Homologous to Lp (a)
130
Q

What is the action done by plasminogen activators to plasminogen?

A

Plasminogen is converted to plasmin

131
Q

What is TPA?

A

It is released in vivo on endothelial cell damage

132
Q

What is the fxn of TPA?

A

Activates plasminogen

133
Q

What is the characteristic of UPA?

A

Purified from urine

134
Q

What may be administered to a pt to activate plasminogen?

A

UPA

135
Q

What is the fxn of UPA?

A

Activates plasmin

136
Q

What is the fxn of SK?

A

Activates plasminogen

137
Q

Where is SK derived from?

A

Streptococci

138
Q

What are the 2 fibrin(ogen) degradation products / fibrin(ogen) split products?

A
  1. Early degradation products
  2. Late degradation products
139
Q

What are the early degradation products?

A
  1. X
  2. Y
140
Q

What are the late degradation products?

A
  1. D (D-D dimer)
  2. E
141
Q

What are the fxns of D-dimer?

A
  1. Indicates fibrin (not fibrinogen) degradation products
  2. Verification of in vivo fibrinolysis
  3. Marker of thrombosis and fibrinolysis
142
Q

What is D-dimer?

A

Sp product of digestion of cross-linked fibrin

143
Q

How is fragment X, Y, and E produced?

A

Produced by digestion of either fibrin / fibrinogen by plasmin

144
Q

What regulates fibrinolysis?

A
  1. Plasminogen activator inhibitor 1 (PAI-1)
  2. α2-antiplasmin
  3. TAFI

Hematology (S) (5 decks)

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