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Coag > Doria > Flashcards

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
Q

Serum

A

Lacks I, V, VIII, II, can correct VII, IX, X, XI, and XII deficiency

26
Q

Aged plasma

A

Lacks V and VIII, can correct I, II, VII, IX, X, XI, and XII deficiency

27
Q

Plasma adsorbed

A

Lacks II, VII, IX, and X, can correct I, V, VIII, XI, XII deficiency

28
Q

Factor assay

A

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
Q

Factor XIII

A

Not tested by PT or PTT

30
Q

Factor XIII assay

A

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
Q

Fibrinolysis tests

A

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
Q

Fibrin degradation products

A

Special tubes containing thrombin, reptilase to rapidly clot and trypsin inhibitor to prevent in vitro fibrinolysis

33
Q

D-Dimer

A

Beads coated with D-dimer antibodies and mixed with undiluted and 1:2 diluted plasma to check for agglutination, semiquantitative

34
Q

Euglobulin clot lysis

A

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
Q

Von Willebrand’s disease

A

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
Q

Von Willebrand Factor

A

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
Q

Clinical Von Willebrands

A

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
Q

Classifications of VW

A

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
Q

Testing for VW

A

abnormal bleeding time, confirmed with platelet aggregation studies, platelet count, PT, PTT, TT

40
Q

VW treatment

A

Replace with cryoprecipitate prepared by freezing plasma and precipitate contains vWF, VIII, fibrinogen and fibronectin, DDAVP, factor VIII concentrates

41
Q

Hemophilia

A

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
Q

Clinical Hemophilia

A

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
Q

Factor VIII hemophilia

A

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
Q

Factor IX hemophilia

A

Christmas disease, produced in lover, long arm of X chromosome, point mutations account for 95% of patients, no specific change

45
Q

Hemophilia labs

A

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
Q

Hemophilia therapy

A

replacement of factors, cryoprecipitate , DDACP, factor IX replacement, gene therapy

47
Q

Factor XI autosomal recessive disorders (ARD)

A

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
Q

Factor VII ARD

A

Quantitative and Qualitative defects, PT prolonged and normal PT, TT, platelet count, platelet function tests and fibrinolysis assays

49
Q

Factor V deficiency ARD

A

Parahemophilia, PT/PTT prolonged and normal TT, platelet count, platelet function tests and fibrinolysis assays

50
Q

Factor X deficiency ARD

A

Stuart Factor deficiency, PT/PTT prolonged and normal TT, platelet count, platelet function tests and fibrinolysis assays

51
Q

Prothrombin deficiency ARD

A

Rarest, PT/PTT prolonged and normal TT, platelet count, platelet function tests and fibrinolysis assays

52
Q

Factor XIII ARD

A

very rare, normal function even with low XIII levels, heterogeneous genetic disorder, urea solubility test abnormal and all screening assays normal

53
Q

Prekallikrein deficiency

A

Fletcher factor deficiency, detected by prolonged PTT and abnormal euglobin lysis, PTT corrected by serum, normal, aged, and adsorbed plasma

54
Q

HMwK deficiency

A

Fitzgerald factor deficiency, detected by prolonged PTT and abnormal euglobulin lysis test, PTT corrected by serum, normal, aged and adsorbed plasms

55
Q

factor XII deficiency

A

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
Q

Passavoy defect

A

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
Q

Afibrinogenemia

A

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
Q

Hypofibrinogenemia

A

mild disorder, autosomal recessive, abnormal if fibrinogen is less than 100 mg/dL

59
Q

Dysfibrinofenemia

A

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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