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Hematology > Unit 5 > Flashcards

Unit 5 Flashcards

1
Q

What does primary hemostasis include

A

Platelet production, destruction, function

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2
Q

What is Secondary Hemostasis

A

Coagulation cascade
Fibrinolysis

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3
Q

What is a clot

A

Soluble protein fibrinogen converts to insoluble fibrin

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4
Q

What does a clot do

A

Reinforces platelet plug

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5
Q

What is fibrinolysis

A

Dissolution of the fibrin clot

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6
Q

What does hemostasis depend on

A

1.Structure and integrity of blood vessels
2.Platelet concentration and function
3.Clotting factors

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7
Q

What are the 3 layers of tissue in blood vessels

A
  1. Tunica Intima
  2. Tunica Media
  3. Tunica Adventitia
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8
Q

What is the Tunica Intima

A

-A continuous, single layer of flattened epi cells
-Provides a protective environment for cellular elements of blood

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9
Q

What is Tunica Media

A

Composed of smooth muscle cells that can contract or expand to dilate or constrict lumen

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10
Q

What is Tunica Adventitia

A

Composed of collagen-anchors vessels to surrounding tissues

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11
Q

Why are normal epi cells negatively charged

A

Repel platelets and clotting proteins

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12
Q

What do injured Epi cells produce

A

-von Willebrand Factor
-Platelet activating factor

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13
Q

What does VWF do

A

-Aids in platelet adhesion to injured sites
-Carries a certain clotting protein (VIII)

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14
Q

What does exposure of tissue factor do

A

Exposes the receptor for clotting factor VII and will initiate the extrinsic coag pathway

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15
Q

Why are injured epi cells thrombogenic

A

with collagen exposure they become sticky which creates contact activation

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16
Q

what is contact activation

A

a protein complex forms on collagen which initiates the intrinsic coag pathway

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17
Q

What do blood vessels do after an injury

A

VASOCONSTRICTION
1. narrow the lumen to reduce blood loss
2. force platelets and plasma proteins into closer proximity to the vessel wall
3. stimulate and prolong platelet release of serotonin

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18
Q

What happens in Primary Hemostasis

A

Platelets:
-Adhere to injured vessel wall
-Aggregate to each other
- Form the primary hemostatic plug

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19
Q

How do mature MKs mature

A

Endomitosis

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20
Q

What is endomitosis

A

-Doubling of nuclear DNA content without dividing
-increase in cell size
-single nucleus goes from a round to highly lobulated nucleus

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21
Q

1 megakaryocyte = how many platelets

A

1,000-3,000

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22
Q

What is TPO

A

Thrombopoietin

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23
Q

What does TPO do

A

-Major factor regulating platelet development
-Influences MK and platelet production

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24
Q

Where is TPO produced

A

At a constant rate primarily in the liver

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25
Q

How does TPO work

A

Binds to MKs and MK precursors and stimulate
Binds to circulating platelets (prevent excessive production)

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26
Q

What is a result of an increased level of free active TPO

A

Thrombocytopenia

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27
Q

Normal reference range for PLT

A

150-450

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28
Q

How long do PLTs survive

A

9-12 days

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29
Q

What does GP-Ib do

A

Adheres PLT to damaged vessel
Major receptor for VWF

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30
Q

What does GP-IIb/IIIa do

A

Aggregates surrounding PLTs
Major receptor for fibrinogen

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31
Q

What do alpha granules of PLTs contain

A

Hemostatic proteins:
Clotting factors
VWF

Non-hemostatic proteins:
Growth factors for wound healing

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32
Q

What do dense bodies of PLTs contain

A

Serotonin
*induce/prolong vasoconstriction
Platelet aggregation agonists
*non-metabolic ADP *Epinephrine
Calcium
*important for secondary hemostasis

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33
Q

What are the strong agonists for PLTs

A

Collagen
Thrombin

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34
Q

What is collagen used for in PLTs

A

Exposed upon vascular injury
*VWF binds to collagen
*PLT GP-Ib binds to VWF (adhesion)

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35
Q

What does Thrombin used for in PLTs

A

Tissue Factor is exposed upon vascular injury
*Small amounts of thrombin are produced
*Thrombin attracts and activates PLTs
*Activated PLTs amplify thrombin production
*Leads to a stabilized fibrin clot

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36
Q

Platelet-derived Agonists can produce what other substances upon activation

A

Thromboxane A2 (TxA2)
Platelet activating factor (PAF)

37
Q

What do PLT-derived agonists release from their granules

A

ADP
Epinephrine
Serotonin

38
Q

What does aspirin do

A

COX inhibitor which prevents PLT aggregation

39
Q

How is Thromboxane A2 produced

A

-COX catalyzes the conversion of Arachidonic acid into Prostaglandin H2
-Prostaglandin H2 is then converted to TXA2

40
Q

What does TXA2 do

A

activates GP IIb/IIIa which promotes PLT aggregation

41
Q

What does VWF carry

A

Clotting Factor VIII

42
Q

What step of PLT function requires Calcium

A

Aggregation

43
Q

What does fibrinogen do

A

Acts like a bridge and connects adjacent platelets

44
Q

What does In Vivo testing for

A

bleeding time

45
Q

What In Vitro testing for

A

platelet function analyzer

46
Q

platelet function analyzer (PFA) detects what

A

Closure time: the amount of time it took for the PLT plug to form

47
Q

The 3 pathways in 2nd Hemostasis

A

Intrinsic
Extrinsic
Common Pathway

48
Q

What is evaluated in In Vitro testing

A

PT
aPTT
TT

49
Q

What does PT evaluate

A

extrinsic and common pathway

50
Q

What does aPTT evaluate

A

intrinsic and common pathway

51
Q

What doe TT evaluate

A

Common pathway

52
Q

What is a zymogen

A

Inactive form of an enzyme

53
Q

What produces zymogens

A

mostly the liver

54
Q

What Coag Factors are in the intrinsic pathway

A

PK
HK
XII
XI
IX
VIII

55
Q

What are the names for PK

A

Prekallikrein
Fletcher Factor

56
Q

What are the names for HK

A

High Molecular Weight Kininogen
Fitzgerald Factor

57
Q

What is the common name for XII

A

Hageman Factor

58
Q

What is the common name for XI

A

Antihemophilic Factor C

59
Q

What is the common name for IX

A

Antihemophilic Factor B
Christmas Factor

60
Q

What is the common name for VIII

A

Antihemophilic Factor A
**carried in circulation by VWF

61
Q

What are the contact factors

A

PK
HK
XII
XI

62
Q

What activates Contact Factors

A

Collagen when exposed

63
Q

What is in the extrinsic pathway

A

Tissue Factor
VII

64
Q

What is tissue factor also known as

A

thromboplastin

65
Q

What makes up Extrinsic Tenase

A

VIIa:Ca2+

66
Q

What does extrinsic tenase do

A

Assembles TF expressing cells
Activate IX

67
Q

What is Factor X also known as

A

Stuart-Prower Factor

68
Q

What is Factor V also known as

A

Labile Factor

69
Q

What factor deteriorates at room temperature

A

Factor V: Labile Factor

70
Q

What is Factor II

A

Prothrombin

71
Q

What is the active form of Factor II

A

Thrombin

72
Q

What is Factor I

A

Fibrinogen

73
Q

What is the active form of Factor I

A

Fibrin

74
Q

What makes up Prothrombinase

A

Xa
Va
Ca2+
PL (phospholipid)

75
Q

What is Fibrinogen

A

Acute phase protein synthesized by the liver

76
Q

What is the role of fibrinogen

A

Acts a bridge between aggregated platelets
Precursor to fibrin mesh

77
Q

What are the 3 stages of conversion of fibrinogen to fibrin

A
  1. Proteolysis
  2. Polymerization
  3. Stabilization
78
Q

What happens in Proteolysis

A

Cleavage of Factor I into active Ia by thrombin
Results in fibrin monomer

79
Q

What happens in Polymerization

A

Spontaneous self-assembly into fibrin polymers

80
Q

What happens in stabilization

A

Intro of covalent bonds into fibrin polymers by XIIIa

81
Q

What will create the stable, crosslinked fibrin clot

A

Zymogen Factor XIII

82
Q

What activates XIII

A

thrombin

83
Q

What are the roles of thrombin

A

Activates: Fibrinogen, VIII, XIII
Stimulates endothelial cells to release VWF
A platelet agonist

84
Q

What is the sequence after vessel injury

A

Vasoconstriction
Platelet adhesion
Platelet aggregation
Coagulation cascade
Fibrin Stabilization

85
Q

What are the Vitamin K dependent factors

A

II
VII
IX
X

86
Q

What does Vit K do

A

y-carboxylation of glutamic acid
Adding carboxy group to negatively charged phosohlipid membrane via Ca2+

87
Q

What does Coumadin inhibit

A

Activity of epoxide reductase and prevents Vit K function

88
Q

How does Coumadin affect Vit K

A

Proteins are synthesized
y-carboxylation does not occur
Clotting factors can’t bind to phospholipid surface via Ca2+
Rendered nonfunctional

89
Q

What are naturally occurring inhibitors

A

Antithrombin
Tissue factor pathway inhibitor
Protein C & S

Hematology (4 decks)

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