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Clinical Pathology > Hemostatsis COPY > Flashcards

Hemostatsis COPY Flashcards

1
Q

Normal Hemostasis occurs in 3 steps

A
  • Vasoconstriction
  • Platelet aggregation (1st)
  • Fibrin formation (2nd)
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2
Q

Primary Hemostasis

A

Platelet plug

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3
Q

Secondary Hemostasis

A

make platelet plug strong with fibrin

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4
Q

Big term to turn fibrinogen into fibrin

A

coagulation factors

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5
Q

what is the point of the coagulation cascade?

A

to create fibrin to strengthen platelet plug

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6
Q

Primary and Secondary hemostasis forms what?

A

Clot

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7
Q

What triggers primary hemostasis events?

A

Damage of the vascular wall exposes blood to

subendothelial tissue

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8
Q

What does endothelin do?

A

vasoconstrictor

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9
Q

What does nitric oxide and prostacyclin do?

A

vasodilator

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10
Q 
The platelet plug formation is the result of a series
of reactions (4)
A

adhesion

aggregation

release of granule content

morphological changes

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11
Q

What is adhesion dependent on?

A

interaction between:

platelets

and

the von Willebrand factor (VWF)

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12
Q

2 main glycoproteins on platelet

A

GP1b-V-IX

Integrin α2β1

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13
Q

where does VWF come from?

A

free floating

secreted by endothelial cells

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14
Q

VWF serves as a bridge between

A

collagen in the subendothelium

and

platelet membrane glycoprotein
Ib-V-IX (GP1b-V-IX)

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15
Q

Does adhesion occur better in large or small arterioles?

A

small

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16
Q

The adhesion process functions better under high

shear stress because

A

high shear unfolds the VWF

thus exposing the binding sites for GPIb-V-IX

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17
Q

Where does adhesion occur best?

large vein
small vein
large artery
small arteriole

A

small arteriole

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18
Q

What are the platelet receptors for collagen?

A

Integrin α2β1

GPVI

GPV

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19
Q

Aggregation happens with the conformational change of?

A

Integrin α2β1

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20
Q

What are the adhesive proteins of aggregation?

A

fibrinogen

VWF

fibronectin

thrombospondin

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21
Q

two most common

forms of severe inherited bleeding disease

A

Hemophilia A

Hemophilia B

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22
Q

Transmission of Hemophilia A and B

A

X-linked recessive traits

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23
Q

female carriers of hemophilia can also express a mild bleeding tendency, often manifest as

A

menorrhagia

heavy menstrual bleeding

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24
Q

Diagnosis of hemophilia (3)

A

1) combination of clinical and laboratory features.
2) (+) Family Hx in approximately 60% of cases
2) The clinical manifestations of hemophilia

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25
Q

Clinical features of severe hemophilia

A

episodes of spontaneous musculoskeletal bleeding
(~20-30/yr) with clinical events starting around 1-2
years of age

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26
Q

Clinical features of moderately severe hemophilia

A

usually do not manifest spontaneous bleeding

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27
Q

Clinical features of mild hemophilia

A

only bleed on provocation and can sometimes present late in adult life at the time of a surgical or dental intervention

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28
Q

Severe hemophilia factor level

A

<1%

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29
Q

Moderately severe hemophilia factor level

A

1-5%

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30
Q

Mild hemophilia factor level

A

5-40%

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31
Q

Laboratory diagnosis of hemophilia (2)

A

1) requires an accurate assessment of FVIII or FIX
levels with one-stage clotting assays

2) the initial phenotypic diagnosis of hemophilia is
complemented with molecular genetic testing to identify the causative FVIII or FIX mutation.

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32
Q

Current treatment of hemophilia - 3

A

1) involves various forms of protein replacement
therapy.

2) utilization of recombinant clotting factor
concentrates with prolonged circulating half-lives

3) gene therapy is now evident, that AAV-mediated
gene transfer is feasible and results in long-term
expression of therapeutic FIX levels in hemophilia B

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33
Q

most common inherited bleeding disorder in

humans

A

vWD

von Willebrand Disease

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34
Q

vWD

A

von Willebrand Disease

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35
Q

Who is more affected by vWD? males or females

A

females outnumber males by 2:1

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36
Q

How many subtypes of vWD?

A

3: type 1, type 2, and type 3

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37
Q

type 1 vWD

A

quantitative deficiency of
functionally normal VWF. In most populations this
accounts for ~65% of VWD cases

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38
Q

most common type of vWD

A

type 1 vWD

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39
Q

Type 2 vWD

A

represents a group of qualitative VWF variants (types 2A, 2B, 2M and 2N)
comprising approximately 30% of VWD

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40
Q

type 3 vWD

A

virtual absence of VWF (with
accompanying very low levels of FVIII) occurring in
approximately 1 in 1 million of the population

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41
Q

most rare type of vWD

A

type 3 vWD

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42
Q

consideration of diagnosis of vWD (non lab) - 3

A
  1. a personal history of excessive mucocutaneous bleeding
  2. laboratory test results consistent with VWD
  3. family history of the condition.
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43
Q

lab tests for diagnosis vWD

A
  1. the VWF:Ag

2. VWF activity assay (prior VWF:RCo test)

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44
Q

Clinical condition with bleeding AND thrombosis

A

liver cirrhosis

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45
Q

mucocutaneous bleeding suggests disorders of

A

platelets

von Willebrand factor (vWF)

vascular bleeding disorder

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46
Q

examples of mucocutaneous bleeding

A

petechiae, bruising, epistaxis, gastrointestinal bleeding and/or menorrhagia

47
Q

Bleeding into muscles and joints, soft tissues and

delayed surgical bleeding suggests disorders of

A

coagulation factors

48
Q

Initial tests to screen for bleeding disorders should

include:

A
  • a complete blood count (CBC)
  • blood film
  • whole blood platelet function testing
  • prothrombin time (PT)
  • activated partial thromboplastin time (APTT)
  • Factor XIII testing
49
Q

The main platelet functions required to maintain

vascular integrity and to ensure primary hemostasis are - 5

A
  1. adhesion
  2. activation
  3. secretion of various alpha and dense granule
  4. Aggregation
  5. procoagulant activity
50
Q

DIC - abbreviation

A

Disseminated Intravascular Coagulation

51
Q

Disseminated Intravascular Coagulation

A

pathological process characterized by the widespread activation of the clotting cascade that results in the formation of blood clots in the small blood vessels throughout the body

aka

systemic activation of hemostasis leads to
widespread intravascular fibrin deposition with
associated depletion of prohemostatic and
anticoagulant factors W/ secondary fibrinolysis

52
Q

What are the regulatory mechanisms that control the
extent of fibrin formation after coagulation is
triggered?

A

antithrombin mechanism,
the protein C–protein S system, the fibrinolytic
system, and the tissue factor pathway inhibitor
mechanism.

53
Q

main regulatory proteins of fibrin formation

A

antithrombin, protein C, and protein S

54
Q

What is Antiphospholipid syndrome?

A

autoimmune
disorder that increases the risk of venous and arterial
thrombosis as well as pregnancy complications
attributable to a reduction in placental perfusion

55
Q

Natural inhibitors of coagulation - 3

A
  1. Antithrombin (AT);
  2. Components of the protein C pathway (thrombomodulin,
    protein C, protein S)
  3. Tissue factor pathway inhibitor (TFPI)
56
Q

AT - abv

A

Antithrombin

57
Q

Components of the protein C

pathway - 3

A

thrombomodulin,

protein C, protein S

58
Q

TFPI - abv

A

Tissue factor pathway inhibitor

59
Q

Exclusionary test for low clinical probability for DVT

A

(-) D-dimer test

60
Q

Pretest Probability is defined as the probability of a patient having the target disorder before a diagnostic test result is known.

A

the probability of a patient having the target disorder before a diagnostic test result is known.

61
Q

Confirmatory test for high clinical probability for DVT

A

imaging diagnostic
techniques are required, typically compression
ultrasound for suspected DVT and computed
tomography of pulmonary arteries for suspected PE

62
Q

standard initial treatment for DVT

A

subcutaneous

low-molecular-weight heparin (LMWH) without monitoring.

63
Q

The antiphospholipid syndrome is

A

auto-immune disease characterized by thrombotic complications in both arteries and veins as well as fetal losses in combination with the presence of so-called
antiphospholipid antibodies in plasma of these patients

a disorder that manifests clinically as recurrent venous or arterial thrombosis and/or fetal loss

64
Q

Warfarin is used for

A

oral anticoagulant

65
Q

Warfarin MOA

A

vitamin K antagonist and blocks γ- carboxylation of a series of glutamic acid residues
during the synthesis of factors II, VII, IX, and X, and proteins C and S

66
Q

Which tests are used to monitor Warfarin?

A 
international normalized ratio (INR), and the partial
thromboplastin time (PTT)
67
Q

Heparin inhibits what?

A

thrombin - indirectly

68
Q

Heparin binds to…

A

antithrombin and increases its
ability to inhibit thrombin, factor Xa, and, to a lesser
extent, other serine protease coagulation factors.

69
Q

What is Heparin-induced thrombocytopenia (HIT)?

A

a complication of heparin therapy in which antibodies develop against complexes of heparin and
platelet factor 4 (PF4).

70
Q

What do target-specific oral anticoagulants do?

A

directly inhibit

either thrombin or factor Xa

71
Q

Antiplatelet therapy is used for

A

the prevention of recurrent stroke or myocardial infarction

72
Q

Coagulation Factor Name, Source, and Pathway

Factor I

A

Name: Fibrinogen

Source: Liver

Pathway: Common

73
Q

Coagulation Factor Name, Source, and Pathway

Factor II

A

Name: Prothrombin

Source: Liver

Pathway: Common

74
Q

Coagulation Factor Name, Source, and Pathway

Factor III

A

Name: Tissue Factor / thromboplastin

Source: Damaged tissues and activated platelets

Pathway: Extrinsic

75
Q

Coagulation Factor Name, Source, and Pathway

Factor IV

A

Name: Calcium Ions

Source: Diet, bones, platelets

Pathway: All

76
Q

Coagulation Factor Name, Source, and Pathway

Factor V

A

Name: Labile factor

Source: Liver and platelets

Pathway: Extrinsic and intrinsic

77
Q

Coagulation Factor Name, Source, and Pathway

Factor VII

A

Name: Proconvertin

Source: Liver

Pathway: Extrinsic

78
Q

Coagulation Factor Name, Source, and Pathway

Factor VIII

A

Name: Antihemophilic factor / Antihemophilic factor A

Source: Liver

Pathway: Intrinsic

79
Q

Coagulation Factor Name, Source, and Pathway

Factor IX

A

Name: Christmas factor / antihemophilic factor B

Source: Liver

Pathway: Intrinsic

80
Q

Coagulation Factor Name, Source, and Pathway

Factor X

A

Name: Stuart-Power factor / thrombokinase

Source: Liver

Pathway: Extrinsic and Intrinsic

81
Q

Coagulation Factor Name, Source, and Pathway

Factor XI

A

Name: Plasma thromboplastin antecedent / anthihemophilic factor C

Source: Liver

Pathway: Intrinsic

82
Q

Coagulation Factor Name, Source, and Pathway

Factor XII

A

Name: Hageman factor / contact factor / antihemophilic factor D

Source: Liver

Pathway: Intrinsic

83
Q

Coagulation Factor Name, Source, and Pathway

Factor XIII

A

Name: Fibrin-stabilizing factor

Source: Liver and platelets

Pathway: Common

84
Q

Vitamin K dependent factors

A

Factors: 2,7,9,10

II
VII
IX
X

Protein C

85
Q

Thrombin interacts with these factos

A

Factors: 1, 5, 8

I
V
VIII

86
Q

Abnormalities and common causes indicated by prolonged

Thrombin Time (TT)

A

Abnormality: Fibrinogen or inhibition of thrombin by heparin

Cause:
DIC
Heparin Therapy

87
Q

Abnormalities and common causes indicated by prolonged

Prothrombin Time (PT)

A

Abnormality: Deficiency in on or more of Factors: VII, X, V, II, I (fibrinogen)

Cause:
liver disease
warfarin therapy
DIC

88
Q

Abnormalities and common causes indicated by prolonged

Activated partial thromplastin time (APTT)

A

Abnormality: Deficiency in one of more of factors: XII, XI, IX, VIII, X, V, II, fibrinogen

Cause:
Hemophilia
Christmas Disease

89
Q

Abnormalities and common causes indicated by prolonged

Fibrinogen quantitation

A

Abnormality: Fibronogen deficiency

Cause:
DIC
Liver disease

90
Q

Disorders of Primary Hemostasis

A
  • bleeding due to vessel wall abnormalities
  • bleeding due to reduced platelet number
  • bleeding due to decreased platelet function
91
Q

Thrombocytopenia

A

abnormally low level of platelets

92
Q

Test Findings For

DIC

A

Platelet: Decrease

APTT: Increase

PT: Increase

TT: Increase

93
Q

Test Findings For

Thrombocytopenia

A

Platelet: Decrease

APTT: Normal

PT: Normal

TT: Normal

94
Q

Test Findings For

vWD

A

Platelet: Normal

APTT: Normal

PT: Normal

TT: Normal

95
Q

Test Findings For

Vitamin K deficiency

A

Platelet: Normal

APTT: Increase

PT: Incrase

TT: Normal

96
Q

Which factor does the liver NOT produce?

A

Factor VIII

97
Q

DIC scores

A

if ≥ 5, compatible with over DIC: repeat daily

if

98
Q

Deficiency in which proteins incrase risk for venous thrombosis

A

Antithrombin

Protein C

Protein S

99
Q

Antithrombotic Therapies - 4

A
  • VITAMIN K ANTAGONISTS
  • ANTITHROMBIN-DEPENDENT PARENTERAL  ANTICOAGULANTS
  • TARGET-SPECIFIC ANTICOAGULANTS
  • ANTIPLATELET THERAPY
100
Q

Drugs that increase clearance of warfarin (decreased INR)

A

Barbituates

Rifampin

Hyperforin

101
Q

Drugs that decrease clearance of warfarin (increased INR)

A

Amiodarone

Fluconazole

Miconazole

Phenylbutazone

Sulfamethoxazole

102
Q

Adhesion mediated by

A

GPIb (receptor for vWF)

GPIa-IIa (receptor for collagen).

103
Q

Degranulation (release reaction) includes the release of

A

α and dense granules and the synthesis/release of thromboxane A2(TXA2)

104
Q

Platelet α granules contains large molecules - 5

A

fibrinogen

platelet derived growth factor (PDGF)

von Willebrand factor (vWF),

P-selectin,

platelet factor 4(PF4)

105
Q

Platelet dense granules contain small molecules - 4

A

adenosine diphosphate (ADP),

adenosine triphosphate (ATP),

serotonin (5-HT),

calcium

106
Q

Degranulation is stimulated by platelet agonists including: 6

A

epinephrine

ADP

thrombin

platelet activating factor (PAF)

collagen

TXA2

107
Q

Aggregation (attachment to other platelets) is mediated by

A

GPIIb/IIIa

108
Q

Intrinsic Pathway Factors

A

Factors include

XII
XI
IX
VIII
prekallikrein / high molecular weight kininogen (HMWK)
109
Q

Tenase complex on intrinsic pathway

A

Calcium
VIIIa
IXa

110
Q

Extrinsic Pathway Factor

A

VII

111
Q

Common Pathway Factors

A

X
II (prothrombin)
Fibrinogen (I)

112
Q

Common name of Factor Ia

A

fibrin

113
Q

Fibrinogen is a hexamer composed of pairs of… 3

A

Polypeptides:

α,β, and η

114
Q

Polymerized fibrin molecules are called

A

Protofibrils

Clinical Pathology (11 decks)

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