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Coagulation Flashcards

1
Q

Anticoagulant Ratio for Sodium Citrate tube

A

1 part anticoagulant, 9 parts whole blood

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2
Q

What factors decrease if testing is delayed?

A

Factor V and VIII (“Labile” Factors)

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3
Q

PT Reference Range

A

12-15 seconds

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4
Q

PTT Reference Range

A

25-35 seconds

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5
Q

INR Reference Ranges

A

Normal: 1-1.5
Therapeutic for Venous Thrombosis: 2-3
Therapeutic for Arterial Thrombosis: 3-4

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6
Q

D-Dimer is created when

A

cross-linked fibrin is broken down by plasmin

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7
Q

Two types of correction testing

A

50/50 with Normal Plasma (NP)
50/50 with Saline

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8
Q

Correction with saline suggests

A

circulating inhibitors

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9
Q

Correction with normal plasma suggests

A

factor deficiency

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10
Q

Pre-Kallekrein Screening Test

A

PTT with longer incubation time. If correction seen, suggests PK deficiency.

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11
Q

Factor VIII:C Inhibitor

A
  • Antibody to FVIII
  • Most common specific inhibitor
  • Inc PTT, normal PT
  • Correction with NP at 0 hours, but not at 2 hours (gives antibody time to bind)
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12
Q

Bethesda Titer

A
  • Test to determine the strength of a FVIII:C inhibitor
  • 1 Bethesda Unit leaves 50% FVIII:C in plasma
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13
Q

Heparin

A
  • Acts as a co-factor with Antithrombin
  • Prolongs PTT, PT, and TT
  • No correction with NP
  • Correction with Saline
  • Correction with Protamine sulfate
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14
Q

Low Molecular Weight Heparin

A

Similar function to heparin, much less immunogenic, longer half-life

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15
Q

TT Reference Range

A

15-19 Seconds

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16
Q

Coumadin

A
  • Vitamin K antagonist
  • Testing looks like a factor deficiency
  • Correction with NP
  • No correction with saline
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17
Q

Vitamin K Factors

A

II, VII, IX, and X

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18
Q

Fibrin Split/Degradation Products (FSP/FDP)

A
  • Complex with fibrin monomers and prevent polymerization
  • Prolongs PTT, PT, and TT
  • No correction with NP
  • Correction with saline
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19
Q

Lupus Inhibitor/Anticoagulant

A
  • NOT specific to lupus
  • Inhibits the reagent in PTT testing (prolonged)
  • Usually doesn’t cause a bleeding problem
  • No correction with NP
  • Correction with saline
  • Correction with platelet neutralization
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20
Q

Tissue Thromboplastin Inhibition Test (TTIT)

A
  • Used to detect Lupus Anticoagulant
  • PT with dilute thromboplastin
  • Compare dilute to original PT
  • Ratio > 1:3 suggests LA
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21
Q

Dilute Russell Viper Venom Time

A
  • Uses exogenous Xase
  • dRVV + Phospholipid + CaCl2
  • if dRVV time > control, suggests LA
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22
Q

Factor Assays

A
  • Measure activity, NOT concentration
  • Report as “% activity”
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23
Q

Factor Activity Reference Range

A

50-150%

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24
Q

Factor XIII is measured using

A
  • Factor Assay
  • 5M Urea (Clot Solubility Test)
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25
Q

Clot Solubility Test interpretation

A

If clot lyses within 24 hours, <5% FXIII activity OR FXIII inhibitor

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26
Q

Laurel Rocket Assay

A
  • Rare
  • Gel Immunoassay
  • Measures amount, not activity
  • Most used for Vwf:Ag, VIII Ag, IX Ag
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27
Q

PIVKA

A
  • Common
  • Gel Immunoassay after decarboxylating FII
  • Most used for Vitamin K Deficiency
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28
Q

Reptilase Time

A
  • Snake venom (Bothrox atrox) that clots fibrinogen by a different pathway than thrombin
  • “Thrombin Time” that is unaffected by heparin
  • If increased, suggests FSPs, deficient or non-functioning fibrinogen
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29
Q

Stypven Time (ST)

A
  • “Russell Viper Venom Time”
  • exogenous Xase
  • Prolonged PT and normal ST = FVII deficiency
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30
Q

Activated Clotting Time (ACT)

A
  • Whole blood clotting time
  • tube contains clot activator
  • Normal: 80-125 seconds
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31
Q

TEG: R (ROTEM: CT)

A
  • Time to initial fibrin formation
  • Normal = 4 - 8 min
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32
Q

TEG: α

A
  • Rapidity of fibrin buildup
  • Normal = 47° - 74°
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33
Q

TEG: K (ROTEM: CFT)

A
  • Clot strengthening
  • Normal = 1 - 4 min
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34
Q

TEG: MA (ROTEM: MCF)

A
  • Clot strength
  • Normal = 55 - 73 mm
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35
Q

TEG: LY30 (ROTEM: LI30)

A
  • Rate of clot breakdown measured at 30 minutes (LY60/LI60 is at 60 minutes)
  • Normal = 0 - 8 %
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36
Q

Acceptable HCT range for unmodified coag testing

A

25-55%

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37
Q

Principle of fibrometer

A

Clot completes electrical circuit

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38
Q

Principle of Helena coagulation instrument

A

Clot alters the optical density

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39
Q

Principle of Sysmex CA-500

A

Clot detected by scattered light at 660 nm (red light)

40
Q

Principle of Mini-Vidas

A

ELFA-2 immunoassay sandwich method, fluorescent detection

41
Q

What diseases are associated with increased FSPs?

A
  • Liver disease
  • DIC
  • Primary fibrinolysis
42
Q

Prothrombin consumption test

A
  • Tests PF3 availability
  • PT on serum
  • > 25s is normal, <25s is abnormal
43
Q

Glycocalyx function

A

Endothelial lining that serves various clotting and non-clotting processes

44
Q

Glycocalyx is made of

A

proteins and mucopolysacharides

45
Q

Substances that cause vasoconstriction

A
  • Serotonin
  • Thromboxane A2
  • Endothelin
46
Q

Substances which counteract vasoconstriction. Where do they come from?

A
  • Prostacyclin
  • Come from endothelial cells
47
Q

Heparan sulfate and thrombomodulin–source and function

A
  • Endothelial cells
  • inhibit fibrin formation
48
Q

Molecule that binds endothelial cells together

A

Fibronectin

49
Q

Two major platelet receptors important for primary hemostasis

A
  • GP Ib
  • GP IIb/IIIa
50
Q

Arachidonic acid on platelets…

A

stimulates aggregation and vasoconstriction

51
Q

What is the most abundant protein in a platelet?

52
Q

Platelet alpha granules contain

A
  • vWF
  • Factor V
  • Fibrinogen
  • Plasminogen
53
Q

Platelet dense granules contain

A
  • Serotonin (vasoconstriction)
  • ADP/ATP (activates more platelets)
  • Calcium 2+ (promotes secondary hemostasis)
54
Q

Platelet alpha granules also contain these proteins that inactivate heparin:

A
  • Beta Thromboglobulin
  • Platelet factor IV
55
Q

Open Canalicular System

A

Deep, convoluted channels in the platelet cell surface that allows it to have a high SA:V ratio and assists in secretion and storage functions

56
Q

Intracellular calcium regulation system in platelets

A

Dense tubular

57
Q

The four major roles of platelets in hemostasis are:

A
  • Vessel surveillance
  • Formation of primary platelet plug
  • Surface for secondary hemostasis
  • Tissue healing
58
Q

The three steps of primary hemostasis are:

A
  • Adhesion
  • Activation
  • Aggregation
59
Q

Platelet Adhesion

A

Platelets bind to subendothelium using their GP Ib receptor via vWF

60
Q

Platelet Activation

A
  • Undergoes biochemical change
  • Changes shape
  • GP IIb/IIIa change conformation to bind fibrinogen
  • Membrane remodel to allow secondary hemostasis
61
Q

Define platelet agonist

A

induces platelet activation

62
Q

The 6 most important platelet agonists are

A
  • Collagen
  • ADP
  • epinephrine
  • thrombin
  • arachidonic acid
  • thromboxane A2
63
Q

Functions of Thromboxane A2

A
  • platelet activation
  • granule secretion
  • vasoconstriction
64
Q

Thromboxane A2 is made from/by

A

From: arachidonic acid
By: cyclooxygenase and thromboxane synthetase

65
Q

Platelet Aggregation

A
  • Platelets attach to each other, assisted by interactions between GP IIb/IIIa and fibrin
  • 2 phases: primary and secondary
  • Secondary is irreversible and requires ATP, triggered by ADP and Thromboxane A2
66
Q

Calcium’s role in primary hemostasis

A

Involved in aggregation (attachment between fibrinogen and GP IIb/IIIa)

67
Q

The capacity for platelets to stimulate formation of fibrin is called

A

Platelet Procoagulant Activity

68
Q

Clot retraction

A
  • occurs around 24 hours after formation
  • reduces clot size up to 90%
  • requires sufficient number of intact platelets
69
Q

Fibrinogen reference range

A

200-400 mg/dL

70
Q

Bleeding Time (BT) Reference Range

A

3-9 minutes

71
Q

Petechiae

A

Small red dots–micro bruises from burst capillaries

72
Q

Petechiometer

A

Squeezes area of the forearm, watches for petechiae. >5 in 5 cm area means one or more of:
- High vessel permeability
- Low platelet count
- Abnormal platelet function

73
Q

Platelet adhesion test Ref Range

A

31-83% retention of platelets

74
Q

Clot Retraction Test Ref Range

A

0.76-0.9 ml of serum expressed

75
Q

What conditions cause abnormal platelet function test?

A
  • vWD
  • Glanzman’s Disease
76
Q

Ecchymosis

A

larger red-purple spots

77
Q

Purpura

A

Descriptive term “purple”

78
Q

Who is affected by Senile Purpura? What is its etiology?

A
  • Older adults
  • Degeneration of supportive collagen
79
Q

Epistaxis

A

Nosebleeds

80
Q

Gingival bleeding

A

Bleeding from the gums

81
Q

Menorrhagia

A

Menstrual bleeding lasting >7 days or that is unusually heavy

82
Q
  • Autosomal Dominant
  • Lesions of dilated capillaries with abnormal connective tissue
  • Bleeding from lesions
  • Epistaxis
  • Normal test results
A

Hereditary Hemorrhagic Telangectasia

83
Q
  • Autosomal Dominant
  • Deceased AND abnormal synthesis of collagen
  • Hyperextendable skin and joints
  • Abnormal capillary fragility
  • Possible abnormal BT
A

Ehlers-Danlos Syndrome (Rubber Man)

84
Q

3 Types of Platelet Disorders

A
  • Quantitative Decrease
  • Quantitative Increase
  • Qualitative Disorder
85
Q
  • Quantitative decrease
  • Antibody to platelets
A

Idiopathic Thrombocytopenic Purpura (ITP)

86
Q
  • Quantitative decrease
  • Microthrombi consisting of platelets circulate
  • CNS damage and symptoms
  • Non-immune
A

Thrombotic Thrombocytopenic Purpura (TTP)

87
Q
  • Quantitative decrease
  • Can occur during/after massive transfusion
A

Dilutional Thrombocytopenia

88
Q
  • Plt count <1,000,000/ cumm
  • Secondary to another condition
  • transient
  • BT and plt function normal
  • Bleeding thromboses infrequent
A

Reactive Thrombocytosis

89
Q
  • Plt count >1,000,000/ cumm
  • Malignant proliferation of megakaryocytes
  • BT and plt function abnormal
  • Bleeding/thromboses frequent
A

Thrombocythemia

90
Q
  • Qualitative Disorder
  • Autosomal Recessive
  • Lack of GP 1b on platelets
  • Loss of interaction between platelets and vWF (no adhesion to collagen or subendothelium)
  • Platelet aggregation normal to all but ristocetin
A

Bernard Soulier Syndrome

91
Q
  • Qualitative Disorder
  • Autosomal Recessive
  • Deficient thrombasthenin
  • Lack of Gp IIb/IIIa complex (no binding to fibrinogen)
  • Platelet aggregation abnormal to all but ristocetin
A

Glanzman’s Thrombasthenia

92
Q
  • Qualitative Disorder
  • Autosomal Dominant
  • Deficiency of dense granules
  • low release of ADP
  • No aggregation with collagen
  • No secondary aggregation with ADP or epinephrine (aggregation reverses)
A

Storage Pool Disease

93
Q
  • Qualitative Disorder
  • Deficient cyclo-oxygenase prevents conversion of arachadonic acid to Thromboxane A2
  • Can be caused by aspirin intake
  • No aggregation with collagen
  • No secondary aggregation with ADP/epinephrine (aggregation reverses
A

Thromboxane A2 Deficiency

94
Q
  • Qualitative Disorder
  • Deficient alpha granules
  • Normal BT, Plt count, Clot retration, and aggregation studies
  • Platelets appear agranular on smear
A

Grey Platelet Syndrome

95
Q
  • Qualitative Disorder
  • Low aggregation with collagen
  • Low secondary aggregation with ADP/epinephrine
96
Q

Types of Von Willebrand’s Disease

A

Type 1: Produced by not released
Type 2: Produced, but not functional
Type 3: Not produced

MLS (18 decks)

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