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Normal Hemostasis Flashcards

1
Q

What is hemostasis?

A

The process involved when blood clots in response to an injury.

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2
Q

What is primary hemostasis?

A

Vessel constriction and platelet accumulation (plt plug).

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3
Q

What is secondary hemostasis?

A

Coagulation factors make fibrin.

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4
Q

What is fibrinolysis?

A

Break down of clot.

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5
Q

Deficiencies of coagulation stages results in?

A

Bleeding or hemorrhage.

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6
Q

Excess of coagulation stages results in?

A

Thrombosis or Clotting.

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7
Q

Damaged endothelial cells?

A
  1. produce and secrete vWF
  2. produce tissue factor
  3. expose collagen that secretes plt activating factor
  4. release plasminogen activator inhibitor, which inhibits fibrinolysis
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8
Q

Lifespan of platelets?

A

9 1/2 days

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9
Q

Platelet Peripheral Zone?

A

Outermost zone

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10
Q

Platelet Structural Zone?

A

Consists of microtubules and provides structure and support.

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11
Q

Platelet Organelle Zone?

A

Mitochondria, glycogen particles, and 4 types of granules.

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12
Q

Platelet Membrane systems?

A

Two systems of membranes.

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13
Q

Platelets in hemostasis must be adequate in both….?

A

Number and Function

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14
Q

Normal Platelet Range?

A

150,000-450,000x10*9/L

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15
Q

Formation of Platelet Plug Involves?

A 
Plt Adhesion                           A
Plt Activation                          A
Plt Shape Change                  S
Plt Secretion of Granules      S
Plt Aggregation                      A
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16
Q

Platelet Adhesion?

A

vWF (secreted by endothelial cells) to GPIb (plt receptor) to collagen (where plts adhere to collagen and promote spreading)
vWF becomes a bridge connecting plts to collagen fibers.
This promotes activation.

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17
Q

Platelet Activation?

A

Adhesion results in Activation which leads to shape change, secretion of granules, and aggregation.
*Only activated plts are able to proceed with the subsequent steps in formation of plt plug.

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18
Q

Platelet Agonists?

A

An agent that induces plt activation

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19
Q

Platelet derived agonists?

A

ADP, Serotonin, Platelet activating factor, thromboxane A2 (TXA2)

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20
Q

Non-platelet derived agonists?

A

Collagen, thrombin, epinephrine

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21
Q

Platelet Shape Change?

A

Disc shaped to spheres with spiny projections (pseudopods)
Allows greater chance of contact with each other
Become very sticky = aggregation

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22
Q

Platelet Secretion of Granules?

A

Release of alpha or dense granules

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23
Q

Thrombospondin?

A

Alpha granule: promotes plt to plt interaction

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24
Q

vWF?

A

Alpha granule: plt adhesion

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25
Q

Plt derived growth factor (PDGF)?

A

Alpha granule: promotes smooth muscle growth

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26
Q

ADP?

A

Dense granule: promotes plt aggregation

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27
Q

Calcium?

A

Dense granule: regulates plt activation/aggregation

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28
Q

Serotonin?

A

Dense granule: promotes vasoconstriction

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29
Q

Platelet Aggregation?

A

Attachment of plts to one another

Begins 10-20 sec after vessel injury

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30
Q

Platelet Plug or Primary Hemostatic Plug?

A

Clumping acts as plug and will stop bleeding
Plt plug is fragile and easily dislodged
Anchored by process of secondary hemostasis

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31
Q

Factor I

A

fibrinogen

32
Q

Factor II

A

prothrombin

33
Q

Factor III

A

tissue factor

34
Q

Factor IV

35
Q

Factor V

A

proaccelerin

36
Q

Factor VII

A

proconvertin (stable factor)

37
Q

Factor VIII

A

antihemophilic factor

38
Q

vWf

A

von Willebrand factor

39
Q

Factor IX

A

plasma thromboplastin component (PTC)

40
Q

Factor X

A

Stuart factor

41
Q

Factor XI

A

plasma thromboplastin antecedent (PTA)

42
Q

Factor XII

A

Hageman factor (contact factor)

43
Q

Factor XIII

A

fibrin-stabilizing factor

44
Q

HK (High molecular weight kininogen)

A

Fitzgerald factor

45
Q

PK (prekallikrein)

A

Fletcher factor

46
Q

Clotting factor characteristics?

A

Deficiency of the factor generally produces a bleeding tendency disorder (EXCEPT XII)
Factor can be assayed in lab
ALL are proteins

47
Q

Fibrinogen Group?

A 
I (fibrinogen)
V (proaccelerin) (is heat sensitive)
VIII (antihemophilic factor)
XIII (fibrin-stabilizing factor)
ALL factors are CONSUMED
PRESENT in PLASMA
ABSENT in SERUM
48
Q

Prothrombin Group?

A 
II (prothrombin)
VII (proconvertin)
IX (plasma thromboplastin component PTC)
X (Stuart factor)
Factors are NOT consumed EXCEPT II
PRESENT in PLASMA and SERUM EXCEPT II
Requires Vitamin K for synthesis( makes it possible for these factors to bind calcium)
49
Q

Contact Group?

A

XI (plasma thromboplastin antecedent PTA)
XII (Hageman factor or contact factor)
PK (prekallikrein/ Fletcher factor)
HK (high molecular weight kininogen/ Fitzgerald factor)
NOT consumed
PRESENT in PLASMA and SERUM
Requires contact with a surface for activation
Do not play an essential role in hemostasis except XI in vivo.

50
Q

In vitro (in test tubes)?

A

The initiation of the cascade occurs via two pathways: the extrinsic and intrinsic pathways.

51
Q

In vivo?

A

Basically a single pathway known as the tissue factor pathway.
Tissue factor and factor VII (extrinsic pathway) will also activate the intrinsic pathway in vivo.
Intrinsic pathway is necessary for large amounts of fibrin.

52
Q

Intrinsic Pathway

A

PK (prekallikrein/ Fletcher factor)
HK (high molecular weight kininogen/ Fitzgerald factor)
XII (Hageman factor or contact factor)
XI (plasma thromboplastin antecedent PTA)
IX (plasma thromboplastin component PTC)
VIII (antihemophilic factor)

53
Q

Extrinsic Pathway

A

VII (proconvertin)

III (Tissue factor)

54
Q

Common Pathway

A 
X (Stuart factor)
V (proaccelerin) (is heat sensitive)
II (prothrombin)
I (fibrinogen)
XIII (fibrin-stabilizing factor)
55
Q

Extrinsic and Common Pathway

A

Requires tissue factor (not normally present in blood) to become activated.
Tissue factor is exposed when there is an injury to the blood vessel and it forms a complex with factor VII.

56
Q

Intrinsic and Common Pathway

A

Involves substances present in plasma.
Exposure to collagen activates factor XII and XI (contact group)
Uses accessory factors such as calcium.

57
Q

Common Pathway

A

Factor X is start of common pathway which when activated becomes Xa which activate II (prothrombin) to IIa (thrombin) which cleaves I (fibrinogen) resulting in fibrin strands and cleaves XIII which results in linking of the fibrin strands.

58
Q

Fibrinolysis

A

Process of removing fibrin

59
Q

Fibrinolysis cascade

A

Plasminogen>Plasmin>Fibrin>Fibrin Degradation Products (FDP)

60
Q

Plasminogen

A

Inactive plasminogen circulates in plasma.

As clotting begins, plasminogen binds to fibrin throughout the clot.

61
Q

Plasminogen Activators

A

Tissue Plasminogen Activator (tPA)
Urokinase type plasminogen activator (uPA)
Both activates plasminogen so that it can convert to plasmin

62
Q

Plasmin

A 
Initiates fibrinolysis (slow process)
Digests fibrin by hydrolysis to produce smaller fragments (cleaves fibrin)
63
Q

Fibrin Degradation or Split Products (FDP or FSP)

A

Dissolves clot as tissue repair is taking place.

Protein fragments that are cleared by liver.

64
Q

Detection of fragments in plasma?

A

Is a diagnostic value for some hemostatic disorders.
Plasmin splits fibrin into X and Y, then Y is split to D and E.
These fragments inhibit hemostasis from reoccuring and can be detected in the lab.

65
Q

The regulatory mechanisms of the coagulation cascade serve two main functions.

A

Limit the amount of fibrin clot formed.

Localize clot formation.

66
Q

Secondary Hemostasis Inhibitor (1)

A

Tissue factor pathway inhibitor (TFPI):
Glycoprotein found on endothelial cells
Serves as an anticoagulant by inhibiting factors Xa and VIIa.

67
Q

Secondary Hemostasis Inhibitor (2)

A

Activated Protein C and Protein S:
Both Vitamin K dependent inhibitors made in the liver.
They inactivate Factors Va and VIIIa.

68
Q

Secondary Hemostasis Inhibitor (following 3-6)

A

Serine Protease Inhibitors:
Known as serpins.
Inhibit target by trapping the enzyme with the serpin and resulting in loss of activity.

69
Q

Secondary Hemostasis Inhibitor (3)

A

Antithrombin III (AT):
Protein made in liver and endothelial cells which binds and directly inactivates thrombin and the other factors.
Inhibits thrombin, Factors IXa, Xa, and XIIa, kallikrein, plasmin.
*Most important inhibitor
*Key player with heparin
*If you dont have antithrombin, heparin won’t work.

70
Q

Secondary Hemostasis Inhibitor (4)

A

Alpha2-macroglobulin:

Inhibits kallikrein, plasmin, thrombin, Xa

71
Q

Secondary Hemostasis Inhibitor (5)

A

Alpha1-antitrypsin:

Inhibits factor XIa, thrombin, kallikrein, plasmin

72
Q

Secondary Hemostasis Inhibitor (6)

A

Heparin Cofactor II (HCII):

Inhibits thrombin

73
Q

Secondary Hemostasis Inhibitor (8)

A

C1-Inhibitor:
Inhibitor of the esterase activity of C1 from the complement cascade.
Also inhibits the contact system proteases F-XIIa, F-IXa, kallikrein, and PLN.
Major plasma protease inhibitor of F-XIIa, accounting for >90% of the plasma inhibitory activity.

74
Q

Secondary Hemostasis Inhibitor (7)

A

Protein Z (PZ):
Vitamin K dependent protein
Markedly enhances the inhibitory function of protein ZPI againt F-Xa.
ZPI:
Plasma serpin that inhibits F-Xa in a PZ-dependent manner.
Also inhibits F-XIa in the absence of PZ.

75
Q

Fibrinolytic Activator

A

Tissue Plasminogen Activator (TPA):
Produced in endothelial cells.
Aids in the regulation of fibrinolysis.
A thrombolytic agent (clot busting drug).
Approved in certain pt’s having a heart attach or stroke.

76
Q

Fibrinolytic Inhibitors (Inhibitors of plasminogen activation)

A 
Plasminogen activator inhibitor-1 and 2:
Inhibits tPA and uPA
Thrombin activated fibrinolysis (TAFI):
Suppresses plasminogen binding to fibrin
(These are both inhibitors of plasminogen activation)
77
Q

Fibrinolytic Inhibitors (Inhibitors of Plasmin)

A

Alpha 2- antiplasmin inhibitor:
Inhibits plasmin.
Alpha 2- macroglobulin:
Inhibits Plasmin.

Coagulation (14 decks)

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