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hema 2 Flashcards

1
Q

Hemostasis

A

Process of cessation/stopping of bleeding (in the presence of vessel injury) thru clot formation & dissolution

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2
Q

Clot dissolution

A

prevents unwanted/excessive clot formation with the help of
circulating INHIBITORS

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3
Q

Prothrombotic substance

A

induces production of clot

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4
Q

Antithrombotic/fibrinolytic

A

induces blood clot dissolution

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5
Q

Antithrombotic/fibrinolytic

A

induces blood clot dissolution

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6
Q

Primary hemostasis

A

Vasoconstriction→ Platelet Adhesion→ Platelet Aggregation→ Platelet Secretion

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7
Q

Secondary Hemostasis

A

Coagulation → Fibrin Clot Formation → Fibrin Stabilization

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8
Q

Inhibitors

A

A substance that retards or stops a process or chemical reaction Inhibit either coagulation or fibrinolysis

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9
Q

Thrombus

A

A blood clot that obstructs a blood vessel

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10
Q

Embolus

A

A mass (clot) of blood or foreign matter
carried in the circulation Dislodged thrombus

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11
Q

Coagulation

A
  • Process of forming a FIBRIN CLOT
    Clinical significance:
  • Defected coagulation factors may cause excessive blood clotting
  • Disseminated Intravascular Coagulation (DIC)
    • Continuous blood clot formation
      Treatment: use of anticoagulant (heparin / warfarin) as therapy
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12
Q

Fibrinolysis

A
  • Enzymatic breakdown of blood clot
  • Fibrinolytic factors are activated
    when the injured vessel has
    developed a stable fibrin clot
  • Blood clot inside the vessel must be
    dissolved to avoid thrombus
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13
Q

Arteriosclerosis

A

Abnormal thickening and hardening of the arterial walls, causing loss of elasticity & impaired blood circulation

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14
Q

Atherosclerosis

A

A form of arteriosclerosis in which lipids, calcium, cholesterol, and other substances deposit on the inner walls of the arteries

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15
Q

Monophyletic

A
  • All blood cells are derived from single progenitor cells
  • The widely accepted theory
  • The Pluripotential hematopoietic stem cell
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16
Q

Polyphyletic

A

Suggests that all cell lineages have its own stem cell of where it came from

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17
Q

Myeloid progenitor

A

gives rise to the RBCs, platelets, and WBCs (except
lymphocytes) precursors.

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18
Q

cytoplasmic fragmentation of megakaryocytes

A

Platelets are formed through this. (platelet precursor) during thrombopoiesis / platelet shedding

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19
Q

Lymphoid progenitors

A

gives rise T cell, NK cell, and B cell precursors.

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20
Q

Vascular Intima

A

Innermost vascular lining (made out of Simple SECs)
Endothelial Cells (Endothelium) – comprising the epithelium is involved in clotting process by producing and storing clotting components, which will be secreted to activate platelets and coagulation factors.

Supporting the ECs – Internal elastic lamina composed of elastin & collagen (fibroblasts)

Sub-endothelial CT – Veins (Collagen & Fibroblast) / Artery (Collagen,

Fibroblast & Smooth Muscle Cells)
 Fibroblasts produce collagen

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21
Q

Vascular Intima

A

Innermost vascular lining (made out of Simple SECs)
Endothelial Cells (Endothelium) – comprising the epithelium is involved in clotting process by producing and storing clotting components, which will be secreted to activate platelets and coagulation factors.

Supporting the ECs – Internal elastic lamina composed of elastin & collagen (fibroblasts)

Sub-endothelial CT – Veins (Collagen & Fibroblast) / Artery (Collagen,

Fibroblast & Smooth Muscle Cells)
 Fibroblasts produce collagen

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22
Q

Vascular Media

A

Middle layer

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23
Q

Vascular Adventitia

A

Outermost layer

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24
Q

CONNECTIVE TISSUE MATRIX

A

Regulates the permeability of the inner vessel wall
Site where the important substances needed for activation is found (subendothelial collagen)

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25
Q

ENDOTHELIUM

A

Highly active metabolically due to its stored components needed for hemostasis, coagulation, and fibrinolysis.

Involved in clotting process by producing or storing clotting components

Releases prothrombotic components when injured

Releases antithrombotic /fibrinolytic components once healed.

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26
Q

NORMAL HEMOSTASIS

A

PRIMARY (Coagulation)→ SECONDARY (Coagulation)→ FIBRINOLYSIS (Blood Clot Dissolution)

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27
Q

2 MAJOR PARTS OF PHYSIOLOGIC HEMOSTATIC SYSTEM

A

CELLULAR COMPONENT
PLASMA PROTEINS

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28
Q

CELLULAR COMPONENT

A

Platelets
Endothelial cells
Neutrophils
Monocytes

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29
Q

PLASMA PROTEINS

A

Group of plasma proteins which participates in:
* Clot Formation (Coagulation)
* Dissolution of Clots (Fibrinolysis)
* Naturally Occurring Serine Protease
Inhibitions (Anti-Coagulation)

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30
Q

VASCULAR DAMAGE

A

Upon injury, the body immediately constricts blood vessel to decrease blood flow Not only the endothelial cells are affected, but also the connective tissue matrix The damaged CT collagen (sub-endothelial) then activates platelets Platelet activation is then followed by adhesion, aggregation, and secretion

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31
Q

VASOCONSTRICTION

A

Narrowing of the diameter of blood vessels

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32
Q

von Willebrand Factor (vWF)

A

Promotes platelet adhesion
Binds to PLATELET via platelet glycoprotein membrane receptor (GP Ib/IX/V)

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33
Q

CLINICAL SIGNIFICANCE Bernard-Soulier Syndrome (BSS)

A

Absent: GP Ib/IX/V platelet membrane receptor Structure: Giant platelet s/ macrothrombocytes Risk: Bleeding tendencies

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34
Q

CLINICAL SIGNIFICANCE Bernard-Soulier Syndrome (BSS)

A

Absent: GP Ib/IX/V platelet membrane receptor Structure: Giant platelet s/ macrothrombocytes Risk: Bleeding tendencies

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35
Q

CLINICAL SIGNIFICANCE vWF Disease

A

vWF: Absent or Defective
No platelets can attach to subendothelium Risks: Bleeding tendencies

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36
Q

Platelet adhesion REVERSIBLE

A

Platelet binds to NON-PLATELET SURFACES (Sub-endothelial Collagen) Activation → change in structure → exposure of GP Ib/IX/V → vWF linkage to the receptor → which will then link the PLATELET to exposed sub-endothelial COLLAGEN

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37
Q

Platelet aggregation IRREVERSIBLE

A

PLATELET binds to one another (PLATELET ↔ PLATELET)
When platelets are activated → exposure of GP IIb/IIIa receptor → allows binding of FIBRINOGEN (in the presence of calcium) as well as vWF and FIBRONECTIN → which will then allow binding of one platelet to another

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38
Q

Fibrinogen (Factor I)

A

Binds to GP IIb/IIIa receptors on adjacent platelet and joins them together in the presence of IONIZED / ACTIVATED CALCIUM (Ca2+)

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39
Q

CLINICAL SIGNIFICANCE Glanzmann Thrombasthenia

A

Absent: GP IIb/IIIa platelet membrane receptor

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40
Q

CLINICAL SIGNIFICANCE Afibrogenemia

A

Lack of Fibrinogen (Total absence)

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41
Q

CLINICAL SIGNIFICANCE Hypofibrogenemia

A

↓ Levels of normal fibrinogen

42
Q

CLINICAL SIGNIFICANCE Dysfibrogenemia

A

Dysfunctional/Defective fibrinogen

43
Q

Risks

A

Bleeding and compromised platelet aggregation

44
Q

PLATELET SECRETION IRREVERSIBLE

A

Platelets discharged the contents of their granules RODAKS: Occurs during AGGREGATION
HENRY’S: Occurs during the late stage of platelet activation

45
Q

Platelet α-granules (Large Molecules)

A

β-Thromboglobulin Factor V
Factor XI
Protein S Fibrinogen
VWF
Platelet Factor 4 Platelet-Derived Growth Factor

46
Q

Platelet Dense Granules (Small Molecules)

A

Adenosine diphosphate (activates neighboring platelets) Adenosine triphosphate Calcium (helps platelets clump) Serotonin (Vasoconstrictor)

47
Q

During Activation

A

ADP and Ca2+ → Activates → Phospholipase A2
Phospholipase A2 → converts Membrane Phospholipids → into Arachidonic Acid Cyclooxygenase → converts Arachidonic Acid → into Prostaglandin Endoperoxidase

48
Q

In Platelet

A

Prostaglandins with the action of Thromboxane Synthetase → activates
Thromboxane A2

49
Q

Thromboxane A2

A

Caused ionized calcium to be release Promoted platelet aggregation Promotes Vasoconstriction

50
Q

Aspirin Acetylation / Aspirin Like Effect

A

Permanently inactivates CYCLOOXYGENASE Blocks THROMBOXANE A2 production Impairment of PLATELET FUNCTION (Aspirin Effect)

51
Q

Platelet Membrane

A

Key surface for coagulation enzyme-cofactor-substrate complex formation

52
Q

Zymogens (Procoagulants)

A

Inactive form of enzymes
* Pre-Kallikrein
* FXII
* FXI
* FIX
* FX
* FVII
* Prothrombin (FII) * FXIII

53
Q

Cofactors

A

Binds, stabilized,and enhance activity of their respective enzymes / zymogens
* HMWK
* Tissue Factor
* FVIII
* FV
* Protein Z
* Protein S
* Thrombomodulin

54
Q

Control protein

A

Serve the important function of regulating the coagulation process to avoid unnecessary blood clotting

55
Q

Fibrinogen substrate

A

Fibrinogen is the substrate for the enzymatic action of thrombin (the primary enzyme of the coagulation system).

56
Q

When a PROCOAGULANT becomes ACTIVATED

A

A lowercase “a” appears behind the numeral

57
Q

become activated in the coagulation process.

A

Both ZYMOGENS & COFACTORS

58
Q

Factor I

A

Fibrinogen

59
Q

Factor II

A

Prothrombin

60
Q

Factor III

A

Tissue Thromboplastin (crude mixture of TF and Phospholipid)

Tissue factor (in other references)

61
Q

Factor IV

A

Calcium is referred to by its name or chemical symbol NOT by its numeral

62
Q

Factor V

A

Proaccelerin

Labile Factor, Ac globulin

63
Q

Factor VI

A

VI was withdrawn from the naming system and never reassigned because it was known that it is just the activated form of Factor V

64
Q

Factor VII

A

Proceonvertin

Stable Factor, SPCA (1949) serum prothrombin conversion accelerator

65
Q

Factor VIII

A

Antihemophilic Factor

AHG, Antihemophilic Factor A

66
Q

Factor IX

A

Plasma Thromboplastin Component

Christmas Factor, Antihemophilic Factor B

67
Q

Factor X

A

Stuart Factor

Stuart-Prower Factor

68
Q

Factor XI

A

Plasma Thromboplastin Antecedent

PTA, Antihemophilic Factor C

69
Q

Factor XII

A

Hageman factor

Glass or contact factor

70
Q

Factor XIII

A

Fibrin-stabilizing factor

FSF

71
Q

Prekallekrein

A

Fletcher factor

72
Q

HMW Kininogen

A

Fitzgerald factor

73
Q

vWF

A

Factor VIII –related antigen

74
Q

FIBRINOGEN GROUP

A

I, V, VIII, XIII

Consumed during the process of coagulation Absent in serum

CALCIUM DEPENDENT

Vitamin K
INDEPENDENT

75
Q

PROTHROMBIN GROUP

A

II, VII, IX, X

Adsorbable & affected by Coumadin (PIVKAS)

CALCIUM AND Vitamin K
DEPENDENT

INHIBITED by Warfarin

76
Q

CONTACT GROUP

A

XI, XII, PK, HMWK

NOT consumed during the process of coagulation Present in serum

Calcium and vitamin K
INDEPENDENT

Involved in INTRINSIC Coagulation Pathway

77
Q

Intrinsic pathway

A
  • Reaction system that begins with FXII and culminates in fibrin polymerization
  • Coagulation experts identified the activation of FXII as the primary step in coagulation because this factor could be found in blood, whereas TF could not. * XII, pre-K, HMWK, XI, IX, VIII, X, V, prothrombin (II), and fibrinogen (I)
  • IXa:VIIIa complex in the intrinsic pathway is crucial to the activation of factor X.

Laboratory Test: PT, APTT (measures XII, XI, IX, VIII)

78
Q

Extrinsic Pathway

A

Extrinsic Pathway
Formation of TF:VIIa has since proven to be the primary in vivo initiation mechanism for coagulation.
TF is NOT PRESENT in blood (released only if there is injury) VII, X, V, prothrombin (II), and fibrinogen (I)

Laboratory Test: PT

79
Q

Common pathway

A

Two pathways have in common: FX, FV, FII (Prothrombin), FI (Fibrinogen)

80
Q

INITIATION

A

occurs on tissue factor-expressing cells and produces 3% to 5% of the total thrombin generated

81
Q

PROPAGATION

A

occurring on platelets, which produces 95% or more of the total thrombin.

82
Q

Initiation phase

A

Refers to extrinsic tenase complex formation and generation of small amounts of FXa, FIXa, and thrombin.

83
Q

FVIIa

A

1%-2% - normally present in blood in activated form Mostly needed to be activated by TF

84
Q

Fibroblast & other sub-endothelial cells

A

Provide TISSUE FACTOR

85
Q

Tissue Factor

A

Cofactor to FVIIa

86
Q

Propagation phase

A

Reactions occur on the surface of the activated platelet, which now has all the components needed for coagulation

Platelets are activated at the site of injury by both the low-level thrombin generated in the initiation phase and by adhering to exposed collagen.

87
Q

Cofactors of FVa and FVIIIa

A

Activated by thrombin in the initiation phase bind to platelet membranes and become receptors for FXa and FIXa

88
Q

FIXa

A

Generated in the initiation phase binds to FVIIIa on the platelet membrane to form the intrinsic tenase complex IXa:VIIIa

89
Q

FXa binds to FVa to form the prothrombinase complex

A

Activates prothrombin and generates a burst of thrombin (produces 95% or more)

90
Q

Thrombin (FIIa)

A

Cleaves fibrinogen into a fibrin clot
Activates factor XIII to stabilize the clot
Binds to thrombomodulin to activate the protein C control pathway
Activates TAFI to inhibit fibrinolysis.

91
Q

FIBRINOLYSIS

A

FINAL STAGE of hemostatic activation
Fibrin degradation; restoring normal blood flow during vascular repair Systematic, accelerating hydrolysis of fibrin and plasmin

92
Q

2 ACTIVATORS OF FIBRINOLYSIS

A

Tissue Plasminogen Activator (TPA)
Urokinase Plasminogen Activator (UPA)

93
Q

PLASMINOGEN

A

Inactive form of PLASMIN present in circulating blood.
The 2 activators of fibrinolysis activates and converts plasminogen to plasmin Plasmin will then hydrolyze the fibrin clot

94
Q

TISSUE PLASMINOGEN ACTIVATOR (TPA)

A

TPA released from endothelial cells converts Plasminogen to Plasmin. Plasmin breaks down Fibrinogen & Stable Fibrin Clot creating fragments: Fibrin Monomer Degradation Product & Cross-linked Degradation Products (contains D- Dimers)

95
Q

UROKINASE PLASMINOGEN ACTIVATOR (UPA)

A

An intrinsic plasminogen activator secreted by urinary tract epithelial cells, monocytes, and macrophages
Converts Plasminogen to Plasmin

96
Q

Fragment X

A

The central E domain with the two D domains (D-E-D), minus some peptides cleaved by plasmin

97
Q

Fragment Y

A

The E domain after cleavage of one D domain (D-E).
D-E fragments are further digested to individual D & E Domains.

98
Q

Fragment XYDE

A

Produced by digestion of either fibrin or fibrinogen by plasmin

99
Q

Fragment D-D (D-Dimer)

A

Composed of two D domains from separate fibrin molecules (NOT FIBRINOGEN) cross-linked by the action of factor XIIIa
Specific product of digestion of cross-linked fibrin only Marker of thrombosis (stabilized clot) and fibrinolysis (dissolution of stabilized clot)

100
Q

Plasminogen Activator Inhibitor-1 (PAI-1)

A

Principal inhibitor of plasminogen activation, inactivating both TPA and UPA, thus preventing them from converting plasminogen to the active fibrinolytic enzyme plasmin.

101
Q

a2-antipaslmin

A

Synthesized in the liver and is the primary inhibitor of free plasmin Only a small amount of plasmin is technically present in blood, circulating

102
Q

Thrombin Activatable Fibrinolysis Inhibitor

A

Synthesized in the liver
Activated by the thrombin-thrombomodulin complex Activated TAFI: Functions as an anti-fibrinolytic enzyme

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