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Doria Flashcards

1
Q

PTT tests

A

Intrinsic pathway

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2
Q

PT tests

A

Extrinsic and common pathway

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3
Q

Normal PTT, abnormal PT

A

Problem in 7

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4
Q

Abnormal PTT, abnormal PT

A

Problem in common pathway

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5
Q

Blood collection

A

Venipuncture or syringe, trauma free, 2 tube technique if difficult collection, no clots, performed within 2 hours of collection

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6
Q

Anticoagulant

A

Sodium citrate for better preservation of V and VIII, 1:9 ratio of anticoagulant to whole blood, use plasma

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7
Q

Secondary hemostasis tests

A

Either screening or definitive testing, functional and measures time for clot formation after activator added, fibrin endpoint, factor concentration markedly decreased

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8
Q

Screening tests

A

Done after testing for bleeding time, APTT, PT, TT, and qualitative fibrinogen, nonspecific, lack sensitivity so normal screening doesn’t necessarily rule out factor deficiencies

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9
Q

Bleeding time

A

time required for bleeding to cease from a superficial cut to the skin influenced by depth, location and type of cut, skin thickness and skill of operator, drugs, platelet count, measures vessels, platelets and factors

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10
Q

Duke

A

Puncture in the ear

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11
Q

Ivy

A

forearm cut with a constant pressure of 40 mmHg

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12
Q

Template

A

Variation of Ivy, incision is consistent in length and depth utilizing a disposable device

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13
Q

PT

A

Best for abnormalities in extrinsic and common, measures time required to form a clot after tissue factor and calcium added, measure activation of VII/III and X, prolonged in factor deficiency or if inhibitor, prolonged in liver disease, oral anticoagulants, can be used to monitor Coumadin treatment

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14
Q

INR calculation

A

INR = (PT of patient/PT of control)

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15
Q

APPT

A

screening abnormalities in the intrinsic and common pathways and screen for lupus anticoagulant, requires activator the provides negative charge for activation of XII and adding a phospholipid membrane substitute for platelets and calcium, measures time required to form clot after addition of phospholipid and calcium, monitor heparin therapy, problems with reagent variability for IX

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16
Q

Activated clotting time

A

Variation of PTT, monitor high dose heparin treatment during and after heart bypass, coronary angioplasty or dialysis, artificial surfaces during surgery activates the clotting process requiring heparin, after surgery protamine sulfate added to inhibit heparin, PTT not reliable at high heparin dose

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17
Q

TT

A

measure time for a clot to form after addition of thrombin, prolonged TT indicates deficiency in fibrinogen, dysfibrinogenemia, the presence of circulating inhibitors or myeloma, can be used to monitor heparin therapy or detect heparin contamination

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18
Q

Reptilase time

A

Serine protease found in the Botox atrox snake and added to plasma will initiate clot formation, thrombin like enzyme that cleaves fibrinopeptide A, prolonged in hypofibrinogenemia, dysfibrinogenemia, presence of FDP and other circulating anticoagulants, not affected by heparin

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19
Q

Quantitative fibrinogen

A

Thrombin time measurements of varying dilutions of patient’s sample that is compared to a reference curve prepared from samples with known fibrinogen concentrations, fibrinogen concentration is inversely proportional to TT

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20
Q

Abnormal PT, normal APPT

A

Factor VII deficiency, verified by a factor VII assay

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21
Q

Abnormal PT, abnormal APPT

A

Rule out heparin contamination, need to differentiate between a factor deficiency in common pathway and circulating inhibitor

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22
Q

Normal PT, abnormal APPT

A

Factor deficiency in intrinsic or a lupus anticoagulant, need substitution studies or factor assay

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23
Q

Substitution studies

A

Mixing abnormal plasma from a patient and various blood components of known factor content followed by APPT and PT tests, correction of abnormal results indicates a factor deficiency, often bypassed by doing specific confirmatory tests for suspected deficient factors

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24
Q

Normal plasma

A

Contains all factors and is mixed with patient plasma to detect presence of circulating inhibitors

25
Serum
Lacks I, V, VIII, II, can correct VII, IX, X, XI, and XII deficiency
26
Aged plasma
Lacks V and VIII, can correct I, II, VII, IX, X, XI, and XII deficiency
27
Plasma adsorbed
Lacks II, VII, IX, and X, can correct I, V, VIII, XI, XII deficiency
28
Factor assay
Definitive assay to confirm factor deficiency, ability of the patient's plasma to correct a prolonged APPT or PT of a known factor deficient plasma, factor activity curve constructed and plotted with Pt and APTT times
29
Factor XIII
Not tested by PT or PTT
30
Factor XIII assay
Urea solubility assay, stabilized fibrin clot obtained after adding CaCl to PPP and placed in another tube with 5M urea or 1% monochloretic acid, abnormal if clot dissolves after 24 hours at room temp
31
Fibrinolysis tests
Not detected by screening assays, when excessive fibrinolytic activity usually caused by disseminated intravascular clotting is suspected, testing for presence of fibrin degradation products in plasma
32
Fibrin degradation products
Special tubes containing thrombin, reptilase to rapidly clot and trypsin inhibitor to prevent in vitro fibrinolysis
33
D-Dimer
Beads coated with D-dimer antibodies and mixed with undiluted and 1:2 diluted plasma to check for agglutination, semiquantitative
34
Euglobulin clot lysis
Detection of increased fibrinolytic activity, euglobulin fraction prepared by precipitation with 1% acetic acid to remove fibrinolytic inhibitors, re-dissolved in saline and thrombin added to clot, plasmin activated to act on clot and incubated
35
Von Willebrand's disease
Deficiency or abnormal von Willebrand factor, most common inherited bleeding disorder in humans, plasma vWF binds to VIIIc to prevent degradation, the rest stored in megakaryocytes and endothelial cells
36
Von Willebrand Factor
glycoprotein of varying subunits, gene located on chromosome 12, necessary for activated platelets glycoprotein Ib to bind to collagen, for binding with factor VIII, produced in megakaryocytes and endothelial cells, first as monomers, then dimers, the ultimers
37
Clinical Von Willebrands
Manifestations depend on homozygosity and clinical variant, most patients have mild disease or asymptomatic and rare patients have severe life threatening manifestations, may look like a platelet problem if mild and coagulation like if severe
38
Classifications of VW
Type 1: 70%, classical form, mild manifestation, decreased VIIIvWF autosomal dominant Type 2: 15%, generally autosomal dominant, qualitative defect but with decreased production of larger multimeric forms of VIIIvWF Type 3: quantitative defect, absence of vWF in platelet and plasma, severe disease, varied patterns of inheritance
39
Testing for VW
abnormal bleeding time, confirmed with platelet aggregation studies, platelet count, PT, PTT, TT
40
VW treatment
Replace with cryoprecipitate prepared by freezing plasma and precipitate contains vWF, VIII, fibrinogen and fibronectin, DDAVP, factor VIII concentrates
41
Hemophilia
Sex-linked disorders involving VIII and IX, second most common hereditary bleeding disorder, 30% has no family history, women are carriers due to functioning gene on other X chromosome
42
Clinical Hemophilia
Dependent on factor levels, early bleeding, big joint bleeding, can be life threatening depending on site, mild deficiency may be symptomless unless surgery or trauma
43
Factor VIII hemophilia
Exists as 2 forms, VIIIc and VIIIvWF, VIIIc coagulant activity involved in fibrin formation, produced in liver, gene in long arm of X, large protein, VIIIc binds to VIIIvWF in blood, mutations in gene leads to disease
44
Factor IX hemophilia
Christmas disease, produced in lover, long arm of X chromosome, point mutations account for 95% of patients, no specific change
45
Hemophilia labs
Prolonged PPT, Hemophilia A PTT corrected by mixtures of normal plasma and serum, PT platelet count, platelet function tests, bleeding time, fibrinogen, fibrinolysis assays and TT are normal, confirm by factor assay
46
Hemophilia therapy
replacement of factors, cryoprecipitate , DDACP, factor IX replacement, gene therapy
47
Factor XI autosomal recessive disorders (ARD)
Hemophilia C, 4th most common, mild bleeding disorder if present, quantitative and qualitative, PTT prolonged, normal PT, TT, platelet count, platelet function tests and fibrinolysis assays
48
Factor VII ARD
Quantitative and Qualitative defects, PT prolonged and normal PT, TT, platelet count, platelet function tests and fibrinolysis assays
49
Factor V deficiency ARD
Parahemophilia, PT/PTT prolonged and normal TT, platelet count, platelet function tests and fibrinolysis assays
50
Factor X deficiency ARD
Stuart Factor deficiency, PT/PTT prolonged and normal TT, platelet count, platelet function tests and fibrinolysis assays
51
Prothrombin deficiency ARD
Rarest, PT/PTT prolonged and normal TT, platelet count, platelet function tests and fibrinolysis assays
52
Factor XIII ARD
very rare, normal function even with low XIII levels, heterogeneous genetic disorder, urea solubility test abnormal and all screening assays normal
53
Prekallikrein deficiency
Fletcher factor deficiency, detected by prolonged PTT and abnormal euglobin lysis, PTT corrected by serum, normal, aged, and adsorbed plasma
54
HMwK deficiency
Fitzgerald factor deficiency, detected by prolonged PTT and abnormal euglobulin lysis test, PTT corrected by serum, normal, aged and adsorbed plasms
55
factor XII deficiency
Hageman trait, no bleeding encountered but possible thromboembolic problems, detected by prolonged PTT and euglobulin lysis time, PTT corrected by serum, normal, aged, and adsorbed plasma
56
Passavoy defect
Prolonged PTT, corrected by long incubation and by normal plasma, original studies revealed autosomal dominant trait and associated with bleeding and similarities to prekallekrien deficiency
57
Afibrinogenemia
Autosomal recessive, no detectable factor I, severe disorder, bleeding starts early, PT, PTT, TT and bleeding time abnormal, low platelet count, treat with cryoprecipitate, fresh frozen plasma
58
Hypofibrinogenemia
mild disorder, autosomal recessive, abnormal if fibrinogen is less than 100 mg/dL
59
Dysfibrinofenemia
Structural alteration in factor I, most asymptomatic to mild bleeding, may present with thrombosis or both in same family, PT, PTT, TT and reptilase time are prolonged and antigen tests normal

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