S18C227 - Tests of Hemostasis Flashcards

1
Q

Site of bleeding gives indication of bleeding diathesis

A
  • mucocutaneous, petechiae, ecchymoses, epsitaxis, GI/GU bleed or heavy perids is characteristic of a platelet d/o
  • purpura with thrombocytopenia indicates systemic illness
  • bleeding into joint and potential spaces and delayed bleeding is common with coagulation factor deficiencies
  • pts with both mucocutaneous and bleeding in deep apces may have DIC (platelet and coag factor abnormality)
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2
Q

Thrombus

A
  • DVT/PE
  • possibly underlying hypercoagulable state
  • acquired hypercoagulable d/o and inherited
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3
Q

acquired hypercoagulable d/o

A
thrombocythemia
polycythemia vera
paroxysmal nocturnal hemoglobinuria
antiphospholipid syndrome
cancer

-can have both arterial and venous thrombi

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4
Q

inherited hypercoagulable d/o

A
  • Factor V leiden
  • prothrombin mutations
  • hyperhomocysteinemia
  • protein C and S deficiencies
  • antithrombin

-tend to be just venous thrombi

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5
Q

normal coagulation formation

A
  • platelet plug forms (primary hemostasis)
  • then a cross-link of fibrin is produced over top to strengthen the plug (secondary hemostasis)
  • these rxns are counterregulated by the fibrinolytic system to limit the fibrin clot and prevent excessive clot formation
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6
Q

Primary Hemostasis

A
  • formation of platelet plug requires:
  • normal collagen
  • normal platelets
  • normal von WF (connects platelets to endothelium via glycoprotein Ib)
  • normal fibrinogen (connects platelets to each other via glycoprotein IIb and IIIa)
  • occurs in 20sec
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7
Q

Tests of primary hemostasis:

A

-platelet count: 150-300 is normal

in thrombocytopenia bleeding not a problem until platelets

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8
Q

Secondary hemostasis tests: PT and INR

A

PT and INR

  • PT 11-13s
  • INR 1
  • extrinsic clotting pathway factors VII, X, V, prothrombin and fibrinogen
  • prolonged PT: warfarin (inhibition of 1972 vit K dependent factors), liver dz (decr factors), Abx that inhibit vit K factors (cefotaxime)
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9
Q

Secondary hemostasis tests: aPTT

A

aPTT: 22-34s

  • activated partial thromboplastin time
  • intrinsic system
  • factors XII, XI, IX, VIII, X, V, prothrombin, and fibrinogen
  • prolonged if: heparin, factor deficiencies (factors have to be
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10
Q

Secondary hemostasis tests: fibrinogen level

A
  1. 1 – 11.8 μmol/L
    - low in DIC
    - elevated as an acute phase reactant
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11
Q

Secondary hemostasis test: mix testing

A
  • performed when an there is an abnormal result on screening test
  • pts plasma is mixed with normal plasma and screening is repeated
  • if mixing corrects the screening test then one or more factors are deficient
  • if mixing does not correct the test then there is an inhibitor present
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12
Q

Hemostatic tests: FDP

A

Fibrinogen degradation products

-

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13
Q

Hemostatic test: D-dimer

A
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14
Q

Hemostatic test: factor V leiden

A
  • looks for activated protein C resistance and confirmatory test analyzes DNA sequence of Factor V gene
  • screening assay uses aPTT with and w/o added activated protein C
  • mutation associated with thromboembolism in people
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15
Q

Hemostatic test: antithrombin

A
  • 30-45mg/dL
  • measures level of antithrombin
  • not vit K dependent
  • pts with deficiency require higher doses of heparin for anticoagulation therapy
  • deficiency causes thromboembolism in
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16
Q

Hemostatic tests: antiphospholipid antibodies

A

-IgG

17
Q

Hemostatic test: other

A
  • anti-factor Xa - used to monitor LMWH tx, may be elevated in renal dz
  • blood smear
18
Q

Secondary hemostasis: coagulation cascade

A
  • final product is cross-linked fibrin

- strengthens platelet plug

19
Q

Fibrinolytic system

A
  • limits size of fibrin clots that are formed
  • tPA is released from endothelial cells and is trigger for fibrinolytic process
  • tPA = tissue plasminogen activator
  • tPA converts plasminogen to plasmin which degrades fibrinogen and fibrin inot FDP and degrades cross-linked fibrin into d-dimers
  • antithrombin also inhibits hemostasis by binds factors XIIa, XIa, IXa and thrombin thereby inhibiting them (heparin potentiates this rxn
  • protein C and S bind together then inactive Facotrs Va and VIIIa, if there is a mutation in factor V (FVL) this prevents protein C from binding and inhibiting factor V leading to prolonged thrombogenic activity
  • therfore defects in antithrombin, protein C/S and FVL lead to hypercoagulable state and increased VTE