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102 Cards in this Set

  • Front
  • Back
Prothrombin Time
1. Test for
2.Reagent name
and its components
1.Tests for Extrinsic Pathway
2. Thromboplastin
a.TFIII- rabbit brain &Innovin
c.Ca++ to override NaCitrate
1. PT: which factors are being tested
2.Reference range
1. VII, X, V, II, I
2. 11-13 seconds
3.Proteins induced by Vit K absence or antagonists.
(anticoag drug produces incomplete form of factors)
1.INR Formula
2.Purpose of INR and
its values sensitivity to PIVKA
1. INR= (pt.PT/Normal PT) to power of ISI
2.The further the ISI is from 1 the less sensitive it is to PIVKA
1.Tests for
2.Name 2 reagents used
3.Which factors are tested
4.Reference Range
5. Heparin pt. value
1.Instrinsic Pathway
2.Activator reagent (Actin FSL) :contact activator and phospholipid
3. XII, XII, IX, VIII, X, V, II, I.
4. 27 - 35 sec
5. 2- 2.5 x more than normal
Specimen Requirements
1. What type tube
2. HCT adjustment: Low HCT vs. High HCT, how much anticoag?
3. Coag studies use ____
4. Platelet studies use___
1. Sodium Citrate
2. low:Need more ; high:need less
3. PPP (Platelet poor plasma)
4. PRP (Platelet rich plasma)
1. Prepared in ____tube
2.What temp and for how many hours?
3. Freeze at what temp?
1. plastic
2. refrigerator for 4 hours
3. -20 degrees
1. Factor I
2. High fibrinogen is associated with
3.Increased in what type people
1. Fibrinogen
2. MI and Stroke
3. Pregnant and smokers
1. Factor II
2.responsible for converting...
3.activates which factors
2.fibrinogen to fibrin
3.factors V, VII, XI, XIII
and protein C
1. Factor III
2.Found where?
3. Released from where
4. Cofactor for activation of ___
1. Tissue Factor III
2. in all tissues, especially brain, liver, lung, placenta
3. from injured tissues.
4. cofactor for actvtn of VII
1. Factor IV
2. required in
3. Low Ca++ a problem?
4. When do we add Ca and why
1. Calcium
2.several steps of cascade
3. no in vivo hemostasis
4. in coag tests to overcome anticoagulant
1. Factor V
2.When does activity decrease?
3.Works in complex with
4. Inactivated by?
1. Labile Factor
2.rapidly at room temp
3. Xa, Ca++ and PF3 to activate Prothrombin
4. Inactivated by Protein C
1. Factor VII
2. What activates this factor?
3. VIIa can also activate what factor? (in alternate pathway)
1.Proconvertin or stable factor
2. TFIII and Ca++
1. Factor VIII (1)
2. produced from?
3. heat stable or labile?
4. VIII deficiency
5.Inactivated by ?
1. Von willebrand
2. several tissues mostly liver
3. heat labile (fragile!)
4. Hemophilia A
5. Protein C
1.Factor VIII (2)
2.produced by ?
3. stored where
4. Platelet adhesion to_____
5. Deficiency in vWF
2.megakaryocytes and endothelial cells platelet alpha granules and endothelial cells.
5. Von willbrand Disease
1. Factor IX
2.Activated by which factors
3.Works in complex with?
4.Factor IX deficiency
1. Christmas factor
2. XIa and VIIa
3. with VIIIa, Ca++, PF3 to activate X
4. Hemophilia B
1.Factor X
2.Works in complex with___ activate _____
1.Stuart Prower
1.Va, Ca++, PF3 to activate (3) prothrombin
1.Factor XI
2.Contact factor?
3.Travels in blood complexed with?
4. deficiency:
1. (No other name)
2. It is a contact factor
3.High molecular weight kininogen
4. Only contact factor to cause bleeding- Hemophilia C
1.Factor XII
2.Contact Factor?
3.Activated by contact with?
4.Activates ____with_____
5.XIIa actiaves ____ to ____
1.Hageman Factor
2. Yes
3. with subendothelial tissue
4.Factor XI with cofactor HMWK
5. preakallikren to kallikrein
1.Kallikrrein can activate____
2.Kinins acts as :2 fx
3.Does deficiency in XII cause bleeding?
4.Lack of activation in fibrinoltic pathway causes____
1.kinin and fibrinolytic pathways
2. as vasodilator and smooth muscle relaxant to reestablish blood flow
4.abnormal clotting
1.Factor XIII
2.Activated by _____&_____
3.Between D domains and polymerized fibrin what does it form?
4.Deficiency detection thru
1. Fibrin stablilizing factor
2. Thrombin and Ca++
3. covalent bonds
4. Urea clot lysis
1.Prekallikrein (PK)
2.A contact factor?
3.Activated by ?
4.Attached to ____(a cofactor for PK activation)
5.Activates (2 answers)
and hydrolyzes ____from HMWK to initiate kinin system.
1. Fletcher Factor
2. Yes
3. XIIa
5. more XII and plasminogen to plasmin
6. bradykinins
1.High Molecular Weight Kininogen
2. Made from
3.Contact Factor?
4.Complexes with (2 answers)
5. Role in production of kinins
1. HMWK (Fitzgeral Factor)
2. Liver
4. XI and PK
5. Acts as a substrate for kallikrein
Fibrinogen assay
1.the assay is like TT with two exceptions:
2.Name of diluent
3.using a standard curve to convert clotting time to what units?
4.Reference range:
1.plasma diluted to 1:10 to minimize effect of heparin(an inhibitor)
2.Owrens Veronal Buffer
4. 170 - 410 mg/dl
Negative Feedback Control Mechanism
1.Activated by...
2.Functions of Protein C
1.Thrombin (IIa) activated thrombomodulin which activates protein C.
2.Inactivates Va and VIIIa,
liberates TPA from edothelial cells, a cofactor of protein S.
Protein S (Neg Feedback Cont.)
1.2 forms
2. Function
1. 60% bound to C4bBP and 40% free (the active molecule in coagulation)
2. serves as cofactor to Protein C.
Anti Thrombin III
1. Function
2.Heparins effect
3. Where is heparin found
1.Forms irreversible complex with factors XIIa, XIa, Xa, IXa and IIa to slowly neutralize these factors.
2.causes conformational change in the ATIII molecule which increases its effect.
3. In mast cells and tissue basophils.
Heparin Cofactor II
1. produced by
2. thrombin neutralization, regulates thrombin on the platelet surface
1.What are the Endogenous Plasminogen activators?
a.XIIa and Kallikrein
b.Activated Protein C -> Tissue plasminogen activator

2. Streptokinas, urokinase, TPA
Functions of Plasmin
1.Inactivates which factors
2. Degrades what factor
3.Explain Secondary Fibrinolysis
4.Primary Fibrinolysis
1.Va and VIIIa
3.Fibrin gets lysed within the clot.
4. Lysing of fibrinogen
Alpha 2 antiplasmin
2. Not very effective at what?
3.Plasminogen Activator Inhibitor 1(PAI-1) are released from
4. What is its function
1.inactivates free circulating plasmin and preventing it's function.
2. inactivating plasmin bound to fibrin
3. injured endothelial cells and activated platelets
4. to neutralize TPa
Thrombin Time
1. Tests for
2. Reagent:
3. Reference Range
1.tests for the adequacy of fibrinogen
2. dilute Thrombin
3. 20 - 30 seconds
50: 50 mix
1. Prolonged:
2. Corrected:
1. test should remain prolonged its due to inhibitor
2. test will correct if its factor deficiency.
Fibrin and Fibrinogen Degradation Products (FDP)
1.What type tubes?
2.TSI function
3.What are reagents
4.Normal pt values
1.TSI collection tubes with Thrombin
2. Neutralized plasmin
3. Lates particles coated with Anti-D & E and buffer.
4. 2 - 8 ug/ml
FDP Interpretation
1.Agglutination in undiluted specimen only.
2.undiluted and 1:5 dilutions
3. All 3 (with 1:20)
1. > or = 2 But <10 ug/mL
2. > or = 10 but <80 ug/ml
3. > or = 80 ug/ml
FDP will be positive in both primary and secondary fibrinolysis
1. Give examples
DIC (2), Deep Vein Thrombosis(2), Pulmonary Embolism (2), Following thrombolytic therapy, systemic fibrinolysis
D- Dimers
1. D-Dimers are present and positive only in ______fibrinolysis
2.Type of tube specimen
3. List Reagents
4. Test plasma is serially diluted with
2.Sodium Citrate Plasma
3. Lates particles coated with anti-D dimer monoclonal antibody and diluent buffer
4.glycine buffered saline
Reptilase Time
1.snake venom (Bothrops Athrox) is a____-like enzyme
2. Reptilase cleaves only _________
3.NOT inhibited by
4.sensitive to
5. Reference Range
6.Test is prolonged due to
2. fibrinopeptide A
3. Heparin or other thrombin inhibitors
4. dysfibrinogenimia
5. 16- 22 seconds
6. FDPs and paraproteins
Euglobulin Clot Lysis
1.Screening test of ____system
2.System removes inhibitors and measures reactions of:
1.fibrinolysis system
2. fibrinogen, plasminogen, and plasminogen activators.
(along with TPA)
Euglobulin Clot Lysis
1. Pt. plasma is diluted and acidified with _______.
2.Observe every___ for clot lysis, up to 10 hours.
3. Reference Range:
4.A pt. with increase fibrinolytic activity:_____hours
5.Pathway is deficient if clot remains at ___ hours
1. cold 1% acetic acid
2.10 minutes
3. >1 hour (usually < 4 hours)
4. < 1 hour
5. 10 hours
Hemophilia A
1.Deficient in what factor?
2.Lab findings:
a.Bleeding Time:
d.Confirm with Factor___assay
3. Acquired Factor VIII Deficiencies are:
1.Factor VIII
2.a.BT =normal
b.PT= normal
c.APTT= prolonged
d.Factor VIII
3.Auto antibodies to factor VIII and DIC
1.What are the treatments for Hemophilia A.
1.Purified factor VIII
and DDAVP :increase VIII in mild cases and appears to stimulate synthesis or release by liver.
Hemophilia B
2.Lab Findings:
2.Confirm with factor___assay
3.Acquired Factor IX Deficiencies are:
1.Factor IX
2.a.BT: normal
b.PT: normal
c.APTT: prolonged
3.DIC, Oral Anticoagulants, liver disease, Vit. K deficiency.
4. Factor IX concentrate, Prothrombin Complex Concentrate(PCC),FFP for minor bleeds
1.Def: Afibrinogenimia
1. Absence or very low
2.<100 mg/dl, hereditary
3.<100 mg/dl, functionally abnormal
Fibrinogen Deficiency -Factor I
1.Lab results
2.Fibrinogen activity
3.Acquired Fibrinogen Deficiencies:
1.a.BT=increase in ~50% people
b.PT = prolonged
c.APTT= prolonged
d.TT= prolonged
3. DIC
Liver Disease
Primary Fibrinolysis
Prothrombin- Factor II(autosomal recessive)
1.Clinical symptoms:
2.Acquired Prothrombin Deficiency
1.a.Heterozygotes: generally asymptomatic
b.Homozygotes: bleeding
2. DIC, Oral anticoagulants, Liver Disease, Vitamin K deficiency
Factor V Deficiency -Labile factor (autosomal recessive)
1.Clinical symptoms:
2.Acquired Deficiency:
1.Only homozygotes have symptomatic bleeding
Liver Disease
Factor VII Deficiency- Stable Factor (autosomal recessive)
1.Clinical symptoms:
2.Acquired Factor VII Deficiency:
1.Only homozygotes have symptomatic bleeding
2. DIC, Oral Anticoagulants, Liver disease, Vitamin K deficiency
Factor X Deficiency
1.Clinical Symptoms
2.Acquired Factor X deficiencies
3.Define Amyloidosis
1.a.heterozygotes: mild bleeding
b.Homozygotes:more severe bleeding
2.DIC, Oral anticoagulants, Liver Disease, Vitamin K deficiency, Amyloidosis.
3.Amyloidosis: deposition of amyloid in various organs and tissues, binds factor X.
Hemophilia C (Autosomal recessive)
1.Clinical Symptoms
2.Acquired XI deficiency
1.Only homozygotes have symptomatic bleeding (mild to moderate)
2. DIC
Liver Disease
Factor XII Deficiency
1.Clinical symptoms:
2.Acquired XII deficiencies
1. NO bleeding problems but APTT is increased. Actually tend to have thrombosis problems.Deficiency in activation of Plasmin.
Liver Disease
PreKallekrein Deficiency
1.Clinical Symptoms
2.Lab result:
Rare and both autosomal recessive and autosomal dominant
1. May lead to thrombosis, no bleeding problems
2. APTT: increased
High Molecular Weight Kininogen Deficiency
(autosomal recessive)
1. Clinical symptoms
2.Lab result
1.clinically asymptomatic, some deep vein thrombosis and pulmonary embolus
2. APTT: prolonged
Factor XIII Deficiency
(Very rare) ~ 65 families
1.Clinical Symptoms
1.umbilical stump bleeding
poor wound healing
bruises resolve slowly
escessive scar formation
cranial hemmorhage
DIC (Disseminated Intravascular coagulation)
1.Causes include:
intravascular parasites
major tissue trauma
snake venoms
AProL- Acute Promyelocytic Leukemia
Complications of Pregnancy
DIC - Complications of pregnancy include:
dead fetus syndrome
amniotic fluid embolus
abruptio placentae
preeclampsia, eclampsia, HELLP
Increases in factors:VII, VIII, IX, XII and I
decrease protein S
1.Clinical symptoms
b.Bleeding from multiple sites due to overwhelming consumption of clotting factors (GI tract, UR tract, IV sites, nose, etc.)
c.often evidence of organ damage from fibrin deposition (due to microclot)
Lab Diagnosis
Secondary Fibrinolysis
PT= prolonged
APTT= prolonged
Fibrinogen= low
TT= prolonged
FDP= positive
D-dimer= positive
Plt count= low
PBS= red cell destruction
Laboratory Diagnosis
Primary Fibrinolysis
PT = prolonged
APTT= prolonged
Fibrinogen= low
TT= prolonged
FDP= positive
plt count= NORMAL
Chronic DIC
1. Also called ____
2. May be seen in____ and ___
3.less critical___and more diffuse_____
4.Proceeds ____
2. cirrhosis and metastatic cancer
3. bleeding , thrombosis
4. slowly
Liver Disease
1.Liver produces all factors except:
2.Results in:
4. Accumulate:
1.VIII (TF3?)
2.results in deficiency of factors and inhibitors
3.produce dysfunctional factors and inhibitors
4. Plasminogen activators
Renal Disease (Coag)
1.Tendency for
2.In DIC, _______ results in renal damage.
1.both thrombosis and bleeding. Nephrotic syndromes:lose some factors, ATIII, and Protein C in urine; uremic pt. have < platelet and platelet function.
Vitamin K Deficiency
1.Vitamin K Dependent factors
1.Factors, II, VII, IX, X
Protein C
Protein S
Factor VIII inhibitor
1.Acquired hemophilia: symptoms:
2. Examples of acquired hemophilia
1.severe, sudden onset, life threatening hemorrhage
2. Pregnancy, post partum, autoimmune disease, lmphoproliferative diseases, elderly with no apparent underlying disease (lupus, rheumatoid arthritis)
Factor VIII Inhibitor:
1.Lab diagnosis
c. 50:50 mix (APTT)
1.PT: normal
APTT: prolonged
50:50 mix APTT: prolonged
*Factor VIII inhibitors are time and temperature dependent
Lupus Anticoagulant
1.Specific?NotSpecific? for any coagulation factor.
2. Associated with bleeding?
3. Antiphospholipid Ab- where does it react?
4.Disease associated with:
1.NOT specific for any factor
2.NOT associated with bleeding
3.Doesnt react with endogenous platelet phospholipibd but in test systems.
4.SLE, various malignancies, autoimmune diseases, infections, AIDS, some healthy people, antibiotic and other drug exposure.
Lab Diagnosis for Lupus Anticoagulants
2.50:50 mix APTT
3.Dilute Russell Viper Venom Time (DVVT)
4.Platelet Neutralization Procedure (PNP)
5.Kaolin Clotting time (KCT)
1.APTT = prolonged
2.50:50 mix APTT = prolonged
3.DVVT = sensitive to LA, will be prolonged
4.Wash donor plt, freeze and thaw;if shortened by>10%, confirms LA
5. Kaolin initiate factor, LI inhibits process; KCT =Prolonged! if corrects = confirms LA
Massive Transfusions
1.Storage of labile factors. Lose which factors?
2.Citrate Toxicity:
how to fix?
____lose viability of stored blood.
1. Lose V and VIII affect screening tests but seldom cause bleeding problems.
2.Give Ca++
3.Platelets lose viability
1._______= clot occuring in a major vessel
2. _________= thrombus broken free from original site and lodges in capillaries of an organ.
2. Emboli
Non-Disease factors causing Thrombosis
1.Age, Immobilization, diet, lipid metabolism imbalance, elevated estrogens, trauma/surgery, smoking, inflammation, central venous catheter.
Disease Factors causing Thrombosis
Anti-phospholipid syndrome, myeloproliferative disorders, hepatic and renal disorders, malignancies, leukemia, Paroxysmal Nocturnal Hematuria, chronic inflammation
Congenital Thrombosis risk Factors
Deficiencies in:
b.Protein C
c.Free Protein S
Activated protein C resistance
Prothrombin 20210A
Plasminogen mutations
TPA deficiency and PAI-1 increase
Laboratory Evaluation of Thrombosis
PT, APTT, LA, Protein C and its pathway, Protein S and its pathway, Anti thrombin
Decreased Platelet Production:
A.Congenital Hypoplasia
1.Give 3 diseases
B.Neonatal Hypoplasia
1.give examples
A.1. Fanconi syndrome, Wiskott-Aldrich, May Hegglin (ineffective thrombopoiesis w/ large platelets bizarre, most assymptomatic)
B.1.newborns infected with Rubella-lack megakaryocytes, drugs ingested by mother.
Decreased Platelet Production
1.Acquired Hypoplasia
1.Irradiation, Drugs, Ethanol, early aplastic anemia, pernicious anemia and folate deficiency, viruses, Bacterial inf, Malignancies, Myelodysplastic syndrome.
INcreased Platelet Destruction Immune Mechanisms
1.Immune Thrombocytopenia Purpura
2.Drug Induced Immune Effects
3.Neonatal Autoimmune Thrombocytopenia
4. Neonatal Alloimmune Thrombocytopenia
5.Post Transfusion Isoimmune Thrombocytopenia.
6.Secondary Autoimmune Thrombocytopenia. (CLL, SLE)
Immune Thrombocytopenia (ITP)
1.Platelet count
2.Size of platelet
3.In bone marrow, what condition
4.Bleeting time?
5.Deficient __________
1.Platelt often <20,000
2.Large platelets
3.megakaryocyte hyperplasia
5.clot retraction
Drug Associated Thrombocytopenia
1.Give example
2.Side effects of heparin
1.Patient with Thrombosis
Heparin therapy.
2.Thrombocytopenia and thrombotic complications
Neonatal Alloimmune Thrombocytopenia
1. Ags cross placenta to____
then Ab cross placenta to__
Neonatal Autoimmune Tbctpna
1.due to:
2.neonate platelet count:
1.AGs to mother, ABs to fetus
1.passive transplacental transfer of Abs from mother with ITP.
2.normal to decreased
Non-immune Mechanisms of INcrased platelet destructions:
1.Give 3
*HELLP syndrome
2.Thrombotic Thrombocytopenic Purpura
3.Hemolytic Uremic Syndrome (HUS)
2.HELLP syndrome:
1.Hypertension, proteinuria, and seizures.
2. microangiopathic Hemolysis, Elevated Liver enzymes, Low Platelet count.
1.Thrombotic Thrombocytopenic Purpura
2.clinical and lab findings
1.Thrombi = arterioles and capillaries
Composed of platelets and vWF but very little fibrin or fibriogen
2. example: neurologic abnormalities
Hemolytic Uremic Syndrome
2.________(endotoxins) attach to renal glomerular capillary endothelial cells.Thrombi in Kidney
2.Clinical Lab findings
1.E coli.
Hemolytic Anemia
Renal Failure
1.Reactive Thrombocytosis:
secondary to______
2.Myeloproliferative Disorders are:
1.inflammation, trauma or other unrelated conditions
2.Polycethemia Vera
Chronic Myelogenous Leukemia
Primary myelofibrosis
Essential Thrombocytosis
Disorders of Platelet Adhesion
1.Give 2 diseases
2.Other Platelet Function problems
1.Bernard Soulier Syndrome and Von Willebrand disease
2.Autoimmune disorders,Myeloproliferative disorders, multiple myeloma and Waldenstrom's, Chronic liver disease(alcohol) and drugs
Bernard Soulier Syndrome
2.Lab findings
3.normal with all agents but________
1.glycoprotein Ib/IX on platelet
2.BT: increased
Platelets: decreased
vonWillebrand Disease
1.Type 1. which factors are reduced.
2.Type 2A decrease in ?
3.Type 3 _______ are absent
1.vWF and Factor VIII
2. high and intermediate weight multimers
3. all multimers
Von Willebrand Disease Lab Findings
1.Platelet count:
4.Bleeding time
5.Platelet aggregation
6.Ristocetin Cofactor Activity Assay
1.Platlete ct= nomral
2.PT = normal
3.APTT = normal
4.Bleeding time = increased
5. plt. agg = normal with all agents except ristocetin
6. measures ability of plasma vWf to agglutinate donor platelets in the presence of ristocetin
Disorders of Aggregation
1.3 disorders
1.Hereditary afibrinogenemia, Uremia, Glanzman thrombasthenia
Disorders of Aggregation:
Glanzmann Thrombasthenia
1.Bleeding time:
4.Platelet count:
5:Platelet Aggregation
6.Platelets lack ____and____
1.BT = increase
2.PT = normal
3.APTT= normal
4.plt Ct. = normal
5. normal only with ristocetin
6.GPIIb and IIIa
Disorders of Release Reaction
and definitions
1.lack dense granules
2.dilation of surface connecting tubular system (swiss cheese)
3.marked decrease in alpha granules plt, dec. alpha and dense granule
5.lack normal dense granule
6.inhibits cyclooxygenase
1.Storage pool disease
2.Hermansky-Pudlak syndrome
3.Gray platelet syndrome
4.Wiskott aldrich syndrome
5.Chediak Higashi
6.Aspirin Therapy
Vascular Disorders
Name 2 hereditary Vascular disorders and definitions
1.Hereditary Hemorrhagic Telangiectasia
=thin walled blood vessel, hemorrhages more easily
2.Ehlers - Danlos Syndrome= defect collagen production, inadequate connective tissue
Acquired Vascular Disorders
Name 2
1. Allergic Purpura = autoimmunity to components of vessel walls
2. Scurvy
Vitamin C deficiency, results in weakened capillary walls.
Aggregating Agents
for Studies
1.Add aggregatin agen to ____ while ____is a blank
2.Name the Agents
1.PRP , PPP is a blank
Arachidonic Acid
Single wave with lag phase
(often only see 1 phase)
Arachidonic Acid
Needs VWF (cofactor) and need GPIb
Factos Affecting Platelet Aggregation: 5 answers
2.Temp (37 degrees)
4.Time(at least 30 minutes)
5.Cuvette and stir bar size/shape
Bleeding time would be prolonged with what conditions:
VonWillbrand Disease
Aspirin Therapy
Coagulation Factors:
1.Adsorbed Plasma

2.Serum Fresh and Aged
1. I, V, VIII, XI, XII