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Secondary Hemostasis and Fibrinolysis Flashcards

1
Q

Factor I Alternate names, pathway, group, function/role, site of production, monitored by what test

A

Alternate names: Fibrinogen

Pathway: Common

Group: Fibrinogen

Function/role: Substrate (only acted on by the enzyme without furthering the cascade)

Site of production: liver

Monitored with what test: PT, PTT, TT, Fibrinogen Assay

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2
Q

Factor II Alternate names, pathway, group, function/role, site of production, monitored by what test

A

Alternate names: Prothrombin

Pathway: Common

Group: Prothrombin

Function/role: Serine protease (Converts inert factors (zymogens) into active forms)

Site of production: Liver

Monitored with what test: PT, PTT

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3
Q

Factor III Alternate names, pathway, function/role, site of production

A

Alternate names: Tissue Factor

Pathway: Extrinsic

Function/role: Cofactor (extrinsic Xase)

Site of production: Tissue (nonvascular)

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4
Q

Factor V Alternate names, pathway, group, function/role, site of production, monitored by what test

A

Alternate names: Proacelerin

Pathway: Common

Group: Fibrinogen

Function/role: Cofactor (prothrombinase complex)

Site of production: Liver

Monitored with what test: PT, PTT

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5
Q

Factor VII Alternate names, pathway, group, function/role, site of production, monitored by what test

A

Alternate names: proconvertin

Pathway: Extrinsic

Group: Prothrombin

Function/role: Serine Protease

Site of production: Liver

Monitored with what test: PT

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6
Q

Factor VIII Alternate names, pathway, group, function/role, site of production, monitored by what test

A

Alternate names: antihemophilic factor

Pathway: Intrinsic

Group: Fibrinogen

Function/role: Cofactor (intrinsic Xase)

Site of production: liver

Monitored with what test: PTT

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7
Q

Factor IX Alternate names, pathway, group, function/role, site of production, monitored by what test

A

Alternate names: Christmas factor

Pathway: Intrinsic

Group: Prothrombin

Function/role: Serine protease

Site of production: Liver

Monitored with what test: PTT

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8
Q

Factor X Alternate names, pathway, group, function/role, site of production, monitored by what test

A

Alternate names: Stuart factor

Pathway: Common

Group: Prothrombin

Function/role: Serine protease

Site of production: Liver

Monitored with what test: PT, PTT

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9
Q

Factor XI Alternate names, pathway, group, function/role, site of production, monitored by what test

A

Alternate names: plasma thromboplastin antecedent

Pathway: Intrinsic

Group:Contact

Function/role: Serine protease, contact factor

Site of production: Liver

Monitored with what test: PTT

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10
Q

Factor XII Alternate names, pathway, group, function/role, site of production, monitored by what test

A

Alternate names: Hageman factor

Pathway: Intrinsic

Group: Contact

Function/role: Serine protease (Converts inert factors (zymogens) into active forms), contact factor

Site of production: Liver

Monitored with what test: PTT

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11
Q

Factor XIII Alternate names, pathway, group, function/role, site of production, monitored by what test

A

Alternate names: stabilizing factor

Pathway: Common

Group: Fibrinogen

Function/role: Transglutaminase—forms stable X-linked covalent bonds on fibrin

Site of production: BM monos, macs, and megakaryocytes

Monitored with what test: Urease

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12
Q

PK Alternate names, pathway, group, function/role, monitored by what test

A

Alternate names: Prekallikrein. Fletcher factor

Pathway: intrinsic

Group: contact

Function/role: Cofactor; contact factor

Monitored with what test: PT

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13
Q

HMWK Alternate names, pathway, group, function/role, monitored by what test

A

Alternate names: High Molecular Weight Kiminogen, Fitzgerald factor

Pathway: Intrinsic

Group: contact

Function/role: Platelet adhesion; stabilize FVIII; contact factor; serine protease complexed with HK

Monitored with what test: PTT

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14
Q

Which factors are Vitamin K dependent. Describe why these factors are Vitamin K dependent.

A

Facilitates y-carboxylation of the factors (II, VII, IX, X, PC, PS) which leads to an extra group being added to the y-carbon. Ca+2 binds to this site; induces conformational charge that allows the factor to bind to phospholipids Acarboxy proteins: Vitamin K dependent factors produced by the absence of vitamin K

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15
Q

Describe or diagram the coagulation cascade. Order the reactions from activation of the extrinsic and intrinsic pathways to fibrin formation and discuss each reaction/component.

A
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16
Q

Discuss the conversion of fibrinogen to a stabilized fibrin polymer.

A

Step 1
• Thrombin cleaves Fibrinopeptides A (α) and B(β) from the central E domain of the fibrinogen molecule
• Result: Fibrin Monomer (unstable)

Step 2
• Fibrin monomers spontaneously polymerize
• Result: unstable Fibrin Polymers (Note: Fibrin polymers are the endpoint for the PT and PTT test)

Step 3
• Factor XIIIa forms covalent bond between adjacent D-domains
• Result: Stable (stronger) fibrin

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17
Q

What is the proper specimen for most coagulation tests and the ratio of anticoagulant to blood in the container? What happens if the proper ratio is not obtained?

A 
Sodium Citrate (binds Calcium)
9:1 ratio blood to anticoagulant. An underfilled tube would result in too much anticoagulant and would falsely prolong hemostasis test results such as the PT and PTT. An overfilled tube would result in not enough anticoagulant and would falsely decrease hemostasis test result.
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18
Q

Fibrinogen Group

A

Acted on by thrombin
Unstable—lose activity when stored
Absent in serum—consumed during clotting
Members: Factor I (Fibrinogen), Factor V, Factor XIII, Factor VIII

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19
Q

Contact Group

A

Initial activation of intrinsic pathway
Stable and present in serum after clotting
Members: Factor XI, Factor XII, PK, HK

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20
Q

Prothrombin Group

A

Vitamin K Dependent (needs to bind Ca+2)
Have GLA-domain
Area where vitamin K dependent carboxylation occurs
Stable in stored plasma and serum
Members: Facter II, Factor VII, Factor IX, Factor X, Protein C and S

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21
Q

Prothrombin Time (PT)

Purpose

Principle

Reagents Involved

Normal Reference Interval

Significance of Abnormal Results

A

Purpose: 1) Screen for extrinsic or common pathway factor/inhibitor deficiencies
2) Monitor oral anticoagulant therapy

Principle: Measure the time from activation of the extrinsic pathway to fibrin formation

Reagents Involved: 1) Tissue thromboplastin (rabbit brain with Ca)

Normal Reference Interval: 10-13 seconds

Significance of Abnormal Results: Decreased: not clinically significant
Increased: Extrinsic of common pathway factor deficiency or inhibitor, or taking oral anticoagulants

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22
Q

Fibrinogen Assay

Purpose

Principle

Reagents Involved

Normal Reference Interval

Significance of Abnormal Results

A

Purpose: To quantitatively measure the amount of fibrinogen present

Principle: TT is inversely proportionally to the fibrinogen concentration. Establish a standard curve and use the patient’s thrombin time result to plug into the curve and determine the concentration of fibrinogen

Reagents Involved: Thrombin Reagent

Normal Reference Interval: 200-400 mg/dL

Significance of Abnormal Results: Increased: usually not clinically significant
Decreased: fibrinogen deficiency, fibrin inhibitors

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23
Q

Thrombin Time

Purpose

Principle

Reagents Involved

Normal Reference Interval

Significance of Abnormal Results

A

Purpose: 1) Evaluates the conversion of fibrinogen to fibrin 2) Screens for heparin

Principle: Add excess thrombin reagent to sample, measure the time it takes until clot forms

Reagents Involved: Thrombin Reagent

Normal Reference Interval: 10-22 seconds

Significance of Abnormal Results: Decreased: not clinically significant
Increased: deficiency of fibrinogen; presence of heparin, FDPs or plasmin

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24
Q

Reptilase Time

Purpose

Principle

Reagents Involved

Normal Reference Interval

Significance of Abnormal Results

A

Purpose: 1) Evaluate the conversion of Fibrinogen to Fibrin 2) Screens for heparin (in conjunction with thrombin time)

Principle: Same as the thrombin time, except initiated with a different reagent (this reagent is not affected by the presence of heparin)

Reagents Involved: Reptilase (found in venom of Bothrops atrox snake)

Normal Reference Interval: 16-22 seconds
Significance of Results: increase = deficiency of fibrinogen

25
D-Dimer Assay Purpose Principle Reagents Involved Normal Reference Interval Significance of Abnormal Results
Purpose: To detect D-dimer fragments formed during fibrinolysis Principle: A latex with antibodies specific for the D-dimer fragment is used Reagents Involved: Latex coated with anti-d-dimer monoclonal antibodies Normal Reference Interval: \<250ng/mL Significance of Results: Increased conditions with increased fibrinolysis such as DVT or DIC
26
5M Urea Purpose Principle Reagents Involved Normal Reference Interval Significance of Abnormal Results
Purpose: To screen for deficiencies in Factor XIII Principle: Unstable fibrin is soluble in 5M urea after 24 hours Reagents Involved: 5M urea Normal Reference Interval: Clot present in 24 hours Significance of Results: Clot disappears between 0-24 hours = Factor XIII deficiency
27
Compare and Contrast Fibrin Degradation Products (FDPs) and D-dimers. Discuss their structure, the lab test(s) used to measure them, and the clinical application for the tests.
FSP are degradation products of fibrin and fibrinogen (Fragments X, Y, D, and E). Increases indicate increased fibrinolytic activity FDP is a latex screening test that doesn't distinguish between fibrin degradation products and fibrinogen degradation products D-Dimers are fibrin degradation products that contain "D" fragments that have been covalently bonded to one another by factor XIII
28
Discuss the different functionalities of thrombin
Procoagulant Functions: • Converts Fibrinogen and fibrin • Activates Factor XIII to XIIIa • Positive feedback for cofactors V, VIII, IX Anticoagulant Functions • Involved with activation of Protein C (inhibitor of fibrin formation) • Stimulates endothelial cells to release Tissue Plasminogen Activator Nitric Oxide and Prostacyclin
29
Antithrombin
Inactivates the serine proteases—thus inhibiting the coagulation cascade
30
Heparin Cofactor II
Inhibits thrombin only Most effective in extravascular locations Actions accelerated by heparin and dermatan sulfate
31
Protein C & S
They work together as major inhibitors of blood coag, vitamin K dependent made by liver Protein C—can only bind to free protein S—inhibits Va, VIIIa Protein S—cofactor for the protein C pathway, two different types (bound and free) • Bound to complement C4b binding protein, PC effects are low
32
Tissue Factor Pathway Inhibitor
An inhibitor of the extrinsic pathway. Binds to Factor Xa and neutralizes it, resulting in a conformation change that promotes binding of the Factor Xa/TFPI complex with the Factor VIIa/TF complex—resulting in its inhibition
33
Factor X deficiency Clinical manifestation, pathophysiology, lab results
Clinical manifestation: Mild to severe bleeding Pathophysiology: Inherited deficiency lab results PT, PTT: Increased Factor X assay: decreased Russell's Viper Venom — Abnormal
34
Factor VII deficiency Clinical manifestation, pathophysiology, lab results
Clinical manifestation: Mild to severe bleeding Pathophysiology: inherited deficiency lab results PT: Increased Factor VII: Decreased
35
Factor XIII deficiency Clinical manifestation, pathophysiology, lab results
Clinical manifestation: Umbilical cord bleeding shortly after birth Excess bleeding after circumcision Spontaneous intracranial bleeding Pathophysiology: inherited deficiency lab results: PT, PTT, TT, Fibrinogen: Normal
36
Factor XII, HK, or PK deficiency Clinical manifestation, pathophysiology, lab results
Clinical manifestation: No bleeding symptoms Pathophysiology: Inherited deficiency lab results: PTT: Increased Factor XII, PK assay, HK assay: depend on deficiency
37
Hemophillia A Clinical manifestation, pathophysiology, lab results
Clinical manifestation: Severe bleeding common, Hemarthrosis. Deep and Delayed bleeding Pathophysiology: Deficiency in Factor VIII X linked Recessive lab results: Bleeding time, platelet count, platelet aggregation, PT, TT: Normal PTT: Increased Mixing Studies: correction Factor VIII: Decreased
38
Hemophillia B Clinical manifestation, pathophysiology, lab results
Clinical manifestation: Severe bleeding common, Hemarthrosis, Deep and Delayed bleeding Pathophysiology: Deficiency in Factor IX X linked Recessive Lab results: PT, TT, Fibrinogen: Normal PTT: increased Mixing studies: Corrected
39
Factor XI deficiency Clinical manifestation, pathophysiology, lab results
Clinical manifestation: Bleeding possible in 50% of cases Pathophysiology: Inherited deficiency Lab results: PTT: increased
40
Factor Assay Purpose, principle, reagents, result significance
Purpose: To quantitatively measure coagulation factors Principle: Modification of the PT or PTT. Specific factor deficient plasma is mixed with patient plasma. If the pt is deficient in the same factor it will be prolonged, if not deficient in the factor it will be normal Reagents Involved: Substrate plasms Reagents of PT and PTT Significance of Results: Prolonged — patient is deficient in that factor being analyzed
41
Mixing Studies Purpose, principle, reagents, result significance
Purpose: Differentiate between a true factor deficiency and a factor inhibitor Principles: Patient plasma is mixed in a 1:1 ratio with normal reagent plasma. A PT/PTT test is then performed on this mixture. If the patient is deficient in a coag factor, the normal plasma present will supply enough to the deficient factor to "correct" the PT/PTT result. If the patient has a circulating inhibitor, then the correction will not occur Reagents: Normal Reagent plasma Significance of Results: Correction = factor deficiency
42
Bethesda Titers Purpose, principle, reagents, result significance
Purpose: Determine amount of a specific coagulation inhibitor Principle: Equal volumes of normal pooled plasma and patient plasma are mixed,and a factor assary is ran, results are interpreted from a Bethesda chart Reagents: Normal pooled plasma and factor assay reagents Significance of results: Compare to Bethesda chart standard curve
43
Describe treatment options for the following conditions: Hemophilia A
cryoprecipitate or factor VIII concentrates; DDAVP possible
44
Describe treatment options for the following conditions: Hemophilia B
FFP; Factor IX concentrate
45
Afibrinogenemia Clinical manifestation, pathophysiology, lab results
Clinical Manifestation: Can be severe; may have spans without bleeding Pathophysiology: Inherited deficiency of Factor I Lab Results: PT, PTT, TT: Prolonged Fibrinogen: low, less than 5 mg/dL
46
Hypofibrinogenimia Clinical manifestation, pathophysiology, lab results
Clinical manifestation: Often asymptomatic; may have excess bleeding after trauma Pathophysiology: Inherited deficiency of Factor I Lab result: Platelet count, bleeding time, platelet aggregation test, PT, PTT: Normal TT: Increased Fibrinogen: 20-100mg/dL (low)
47
Describe treatment options for the following conditions: Factor I Deficiency
Cryoprecipitate; each blood type has different amounts of vWF: Type O have least, Type B has the most
48
Intrinsic Pathway Factors involved, triggers/activators, endpoint, tests to monitor
Increase Pathway: PK, HK, MF, XII, XI, IX, VIII Trigger: Autoactivation of contact factors Endpoint: activation of common pathway Test to monitor: PTT
49
Extrinsic Pathway Factors involved, triggers/activators, endpoint, tests to monitor
Factors involved: TF, VII Triggers: Tissue damage that releases TF Endpoint: Activation of common pathway Test to monitor: PT
50
Common pathway Factors involved, triggers/activators, endpoint, tests to monitor
Factors involved: X, V, II, I Triggers: Intrinsic and extrinsic Xase complexes Endpoint: fibrin formation Tests to monitor: PTT, PT
51
List and describe specific clinical symptoms associated with bleeding disorders related to: Platelet or Vascular Problems
Petechiae (small pinpoint bruises)
52
List and describe specific clinical symptoms associated with bleeding disorders related to: Coagulation Factor Problems
Hemarthrosis (joint bleeding); delayed bleeding; deep bleeding
53
Discuss inhibitors of single factors and therapy for low and high responders
Each coag factor has an inhibitor. The most common single inhibitors are VIII and IX. The inhibitors are autoantibodies specific for a factor. Low responders can be treated with large amounts of factor concentrates. High responders are difficult to treat. Recombinant F-VIIa show promise as a means of activating Factor X and bypassing the intrinsic pathway
54
Patient 1: Increased, Decreased or Normal? Bleeding Time - 5 minutes (1-10 min) Platelet Count - 220,000/uL (150,000 - 450,000) aPTT - 30 seconds (25 - 36 sec) PT - 17 seconds (10 - 13 sec) Mixing Studies - Corrected D-dimer - normal
BLEEDING TIME NORMAL PLATELET COUNT NORMAL PTT NORMAL PT ABNORMAL POSSIBLE DIAGNOSIS: EXTRINSIC PATHWAY FACTOR DEFICIENCY
55
Patient 2: Bleeding Time - 3 minutes (1 - 10min) Platelet Count - 310,000/uL (150,000 - 450,000) aPTT - 82 seconds (25 - 36 sec) PT - 27 seconds (10 - 13 sec) Fibrinogen Assay - 289 mg/dL (200 - 400 mg/dL) Mixing Studies - corrected D-dimer - normal
BLEEDING TIME NORMAL PLATELET COUNT NORMAL PTT ABNORMAL PT ABNORMAL FIBRINOGEN ASSAY NORMAL POSSIBLE DIAGNOSIS: COMMON PATHWAY FACTOR DEFICIENCY
56
Patient 3 Bleeding Time - \>15 minutes (1 - 10 min) Platelet Count - 220,000/uL (150,000 - 450,000) aPTT - 47 seconds (25 - 36 sec) PT - 11 seconds (10 - 13 sec) D-dimer - normal Platelet Aggregation Studies - abnormal with ristocetin
BLEEDING TIME: ABNORMAL PLATELET COUNT: NORMAL PTT: ABNORMAL PT: NORMAL DIAGNOSIS: VON WILLEBRAND FACTOR DEFICIENCY
57
Patient 4 Bleeding Time - 8 minutes (1 - 10 min) Platelet Count - 285,000/uL (150,000 - 450,000) aPTT - 30 seconds (25 - 36 sec) PT - 11 seconds (10 - 13 sec) D-dimer - abnormal (elevated)
BLEEDING TIME NORMAL PLATELET COUNT NORMAL PTT NORMAL PT NORMAL POSSIBLE DIAGNOSIS: INCREASED FIBROLYSIS
58
Patient 5: Platelet Count -302,000/uL (150,000 - 450,000) aPTT - 64 seconds (25 - 36 sec) PT - 12 seconds (10 - 13 sec) D-dimer - normal Mixing Studies - not corrected
PLATELET COUNT NORMAL PTT INCREASED PT NORMAL INTRINSIC PATHWAY INHIBITOR

Hemostasis (3 decks)

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