1
Q
Anticoagulant Ratio for Sodium Citrate tube
A
1 part anticoagulant, 9 parts whole blood
2
Q
What factors decrease if testing is delayed?
A
Factor V and VIII (“Labile” Factors)
3
Q
PT Reference Range
A
12-15 seconds
4
Q
PTT Reference Range
A
25-35 seconds
5
Q
INR Reference Ranges
A
Normal: 1-1.5
Therapeutic for Venous Thrombosis: 2-3
Therapeutic for Arterial Thrombosis: 3-4
6
Q
D-Dimer is created when
A
cross-linked fibrin is broken down by plasmin
7
Q
Two types of correction testing
A
50/50 with Normal Plasma (NP)
50/50 with Saline
8
Q
Correction with saline suggests
A
circulating inhibitors
9
Q
Correction with normal plasma suggests
A
factor deficiency
10
Q
Pre-Kallekrein Screening Test
A
PTT with longer incubation time. If correction seen, suggests PK deficiency.
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)
12
Q
Bethesda Titer
A
- Test to determine the strength of a FVIII:C inhibitor
- 1 Bethesda Unit leaves 50% FVIII:C in plasma
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
14
Q
Low Molecular Weight Heparin
A
Similar function to heparin, much less immunogenic, longer half-life
15
Q
TT Reference Range
A
15-19 Seconds
16
Q
Coumadin
A
- Vitamin K antagonist
- Testing looks like a factor deficiency
- Correction with NP
- No correction with saline
17
Q
Vitamin K Factors
A
II, VII, IX, and X
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
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
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
21
Q
Dilute Russell Viper Venom Time
A
- Uses exogenous Xase
- dRVV + Phospholipid + CaCl2
- if dRVV time > control, suggests LA
22
Q
Factor Assays
A
- Measure activity, NOT concentration
- Report as “% activity”
23
Q
Factor Activity Reference Range
A
50-150%
24
Q
Factor XIII is measured using
A
- Factor Assay
- 5M Urea (Clot Solubility Test)
25
Clot Solubility Test interpretation
If clot lyses within 24 hours, <5% FXIII activity OR FXIII inhibitor
26
Laurel Rocket Assay
- Rare
- Gel Immunoassay
- Measures amount, not activity
- Most used for Vwf:Ag, VIII Ag, IX Ag
27
PIVKA
- Common
- Gel Immunoassay after decarboxylating FII
- Most used for Vitamin K Deficiency
28
Reptilase Time
- 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
29
Stypven Time (ST)
- "Russell Viper Venom Time"
- exogenous Xase
- Prolonged PT and normal ST = FVII deficiency
30
Activated Clotting Time (ACT)
- Whole blood clotting time
- tube contains clot activator
- Normal: 80-125 seconds
31
TEG: R (ROTEM: CT)
- Time to initial fibrin formation
- Normal = 4 - 8 min
32
TEG: α
- Rapidity of fibrin buildup
- Normal = 47° - 74°
33
TEG: K (ROTEM: CFT)
- Clot strengthening
- Normal = 1 - 4 min
34
TEG: MA (ROTEM: MCF)
- Clot strength
- Normal = 55 - 73 mm
35
TEG: LY30 (ROTEM: LI30)
- Rate of clot breakdown measured at 30 minutes (LY60/LI60 is at 60 minutes)
- Normal = 0 - 8 %
36
Acceptable HCT range for unmodified coag testing
25-55%
37
Principle of fibrometer
Clot completes electrical circuit
38
Principle of Helena coagulation instrument
Clot alters the optical density
39
Principle of Sysmex CA-500
Clot detected by scattered light at 660 nm (red light)
40
Principle of Mini-Vidas
ELFA-2 immunoassay sandwich method, fluorescent detection
41
What diseases are associated with increased FSPs?
- Liver disease
- DIC
- Primary fibrinolysis
42
Prothrombin consumption test
- Tests PF3 availability
- PT on serum
- >25s is normal, <25s is abnormal
43
Glycocalyx function
Endothelial lining that serves various clotting and non-clotting processes
44
Glycocalyx is made of
proteins and mucopolysacharides
45
Substances that cause vasoconstriction
- Serotonin
- Thromboxane A2
- Endothelin
46
Substances which counteract vasoconstriction. Where do they come from?
- Prostacyclin
- Come from endothelial cells
47
Heparan sulfate and thrombomodulin--source and function
- Endothelial cells
- inhibit fibrin formation
48
Molecule that binds endothelial cells together
Fibronectin
49
Two major platelet receptors important for primary hemostasis
- GP Ib
- GP IIb/IIIa
50
Arachidonic acid on platelets...
stimulates aggregation and vasoconstriction
51
What is the most abundant protein in a platelet?
Actin
52
Platelet alpha granules contain
- vWF
- Factor V
- Fibrinogen
- Plasminogen
53
Platelet dense granules contain
- Serotonin (vasoconstriction)
- ADP/ATP (activates more platelets)
- Calcium 2+ (promotes secondary hemostasis)
54
Platelet alpha granules also contain these proteins that inactivate heparin:
- Beta Thromboglobulin
- Platelet factor IV
55
Open Canalicular System
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
Intracellular calcium regulation system in platelets
Dense tubular
57
The four major roles of platelets in hemostasis are:
- Vessel surveillance
- Formation of primary platelet plug
- Surface for secondary hemostasis
- Tissue healing
58
The three steps of primary hemostasis are:
- Adhesion
- Activation
- Aggregation
59
Platelet Adhesion
Platelets bind to subendothelium using their GP Ib receptor via vWF
60
Platelet Activation
- Undergoes biochemical change
- Changes shape
- GP IIb/IIIa change conformation to bind fibrinogen
- Membrane remodel to allow secondary hemostasis
61
Define platelet agonist
induces platelet activation
62
The 6 most important platelet agonists are
- Collagen
- ADP
- epinephrine
- thrombin
- arachidonic acid
- thromboxane A2
63
Functions of Thromboxane A2
- platelet activation
- granule secretion
- vasoconstriction
64
Thromboxane A2 is made from/by
From: arachidonic acid
By: cyclooxygenase and thromboxane synthetase
65
Platelet Aggregation
- 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
Calcium's role in primary hemostasis
Involved in aggregation (attachment between fibrinogen and GP IIb/IIIa)
67
The capacity for platelets to stimulate formation of fibrin is called
Platelet Procoagulant Activity
68
Clot retraction
- occurs around 24 hours after formation
- reduces clot size up to 90%
- requires sufficient number of intact platelets
69
Fibrinogen reference range
200-400 mg/dL
70
Bleeding Time (BT) Reference Range
3-9 minutes
71
Petechiae
Small red dots--micro bruises from burst capillaries
72
Petechiometer
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
Platelet adhesion test Ref Range
31-83% retention of platelets
74
Clot Retraction Test Ref Range
0.76-0.9 ml of serum expressed
75
What conditions cause abnormal platelet function test?
- vWD
- Glanzman's Disease
76
Ecchymosis
larger red-purple spots
77
Purpura
Descriptive term "purple"
78
Who is affected by Senile Purpura? What is its etiology?
- Older adults
- Degeneration of supportive collagen
79
Epistaxis
Nosebleeds
80
Gingival bleeding
Bleeding from the gums
81
Menorrhagia
Menstrual bleeding lasting >7 days or that is unusually heavy
82
- Autosomal Dominant
- Lesions of dilated capillaries with abnormal connective tissue
- Bleeding from lesions
- Epistaxis
- Normal test results
Hereditary Hemorrhagic Telangectasia
83
- Autosomal Dominant
- Deceased AND abnormal synthesis of collagen
- Hyperextendable skin and joints
- Abnormal capillary fragility
- Possible abnormal BT
Ehlers-Danlos Syndrome (Rubber Man)
84
3 Types of Platelet Disorders
- Quantitative Decrease
- Quantitative Increase
- Qualitative Disorder
85
- Quantitative decrease
- Antibody to platelets
Idiopathic Thrombocytopenic Purpura (ITP)
86
- Quantitative decrease
- Microthrombi consisting of platelets circulate
- CNS damage and symptoms
- Non-immune
Thrombotic Thrombocytopenic Purpura (TTP)
87
- Quantitative decrease
- Can occur during/after massive transfusion
Dilutional Thrombocytopenia
88
- Plt count <1,000,000/ cumm
- Secondary to another condition
- transient
- BT and plt function normal
- Bleeding thromboses infrequent
Reactive Thrombocytosis
89
- Plt count >1,000,000/ cumm
- Malignant proliferation of megakaryocytes
- BT and plt function abnormal
- Bleeding/thromboses frequent
Thrombocythemia
90
- 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
Bernard Soulier Syndrome
91
- Qualitative Disorder
- Autosomal Recessive
- Deficient thrombasthenin
- Lack of Gp IIb/IIIa complex (no binding to fibrinogen)
- Platelet aggregation abnormal to all but ristocetin
Glanzman's Thrombasthenia
92
- 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)
Storage Pool Disease
93
- 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
Thromboxane A2 Deficiency
94
- Qualitative Disorder
- Deficient alpha granules
- Normal BT, Plt count, Clot retration, and aggregation studies
- Platelets appear agranular on smear
Grey Platelet Syndrome
95
- Qualitative Disorder
- Low aggregation with collagen
- Low secondary aggregation with ADP/epinephrine
Uremia
96
Types of Von Willebrand's Disease
Type 1: Produced by not released
Type 2: Produced, but not functional
Type 3: Not produced
MLS
flashcards
Decks in class (18)
# Cards
-
Hematology98
-
Big Bad Boards Box6
-
Urinalysis47
-
Micro Exam 120
-
Immunology Exam 148
-
Parasitology Exam 253
-
Immunology Exam 239
-
Immunology Exam 350
-
Blood Bank Exam 177
-
Abnormal WBCs and Leukemia92
-
Blood Bank Exam 269
-
Mycology Exam 1100
-
Coagulation96
-
Blood Bank Exam 353
-
Anaerobes Exam22
-
Chemistry Reference Ranges40
-
Chemistry Exam 172
-
Chemistry Exam 2107
