thrombosis and fibrinolysis Flashcards

1
Q

thrombosis pathologic event (3)

A
  1. disruption of blood flow
  2. platelet fibrin mass
  3. occlusion of the blood vessel
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2
Q

virchow’s triad

A
  1. blood flow
  2. coagulation factors
  3. blood vessel
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3
Q

fibrinogen to fibrin and
feedback to activate and amplify
this process to form the
fibrin clot.

A

thrombin burst

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4
Q

inhibitor of coagulation

A

protein C

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5
Q

tissue factor pathwaay inhibitor (TFPI)

A

regulates TF/FVIIa pathway

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6
Q

anti-thrombin III (AT-III)

A

inhibits thrombin, FIXa, FXa, FXIa

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7
Q

protein C and co-factor Protein S

A

are vit. K dependent and inhibit FVa and FVIIIa

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8
Q

Very ill patient with skin necrosis –

A

disseminated intravascular coagulation (DIC)

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9
Q

New onset neurologic symptoms –

A

stroke or cerebral vein thrombosis

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10
Q

Frequent miscarriages/fetal loss –

A

placental thrombosis

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11
Q

thrombophilia:

congenital deficiency states (3)

A
  1. AT-III
  2. Protein C
  3. Protein S
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12
Q

thrombophilia:

genetic mutations 4

A
  1. activated protein C resistance or factor Vleiden
  2. hyperhomocysteinemia- MTHFR
  3. prothrombin gene mutation
  4. PAI- mutations- affects fibrinolysis
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13
Q

other causes of thrombophilia (2)

A
  1. elevated levels of FVIII, IX, XI

2. elevated levels of lipoproteins

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14
Q

Immune mediated disorder with production of antibodies (IgG, IgM, IgA) against proteins (β2-glycoprotein 1 and prothrombin) which interact with phospholipid within cell membranes (endothelial cells and platelets)

A

Antiphospholipid Antibody Syndrome

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15
Q

Antiphospholipid Antibody Syndrome

  1. what do we see
  2. what is it
  3. occurs in females/males
  4. age?
  5. clinical
  6. _________ due to binding to phospholipid and prothrombin in vitro in the assays
  7. assays detect antibodies against
  8. despite prolonged PTT, it does not cause
  9. treatment
A
  1. venous/arterial thrombosis (recurrent fetal loss)
  2. immune mediated
  3. females>males
  4. any age
  5. clinical-thrombosis, livido reticularis, thrombocytopenia, migraine headaches
  6. Prolongation of clotting assays
  7. cardiolipin and B2 glycoprotein 1
  8. bleeding
  9. treat underlying disease process and prevent further thrombosis
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16
Q

protection against thrombosis (6)

A
  1. inactivation of activated coagulation factors
  2. decrease platelet activity
  3. increase blood flow
  4. activation of thrombomodulin
  5. fibrinolytic system dissolves clot
  6. RES clears soluble fibrin complexes
17
Q

involves the vascular endothelium, vW protein and plateltets

A

primary hemostasis

18
Q

involves the progressive activation and amplification of the various clotting factors in the coag. cascade and results in the production of thrombin and a fibrin clot

A

secondary hemostasis

19
Q

dissolution of the fribrin clot as a part of the wound healing process

A

fibrinolysis

20
Q

nitric oxide inhibits

A

platelet activation

21
Q

Alpha2-antiplasmin binds with plasmin to form the alpha2-AP/plasmin complex, which prevents

A

plasmin from breaking down fibrin within the fibrin clot (fibrinolysis).

22
Q

Missense mutation of Arginine 506 to Glutamine 506 (Arg-506-Gln)

A

Activated Protein C resistance (Factor V Leiden)

23
Q

G to A substitution of nucleotide 20210 in 3’ untranslated portion of the gene

A

Prothrombin Gene Mutation

24
Q

Mutation in the gene for methylene tetrahydrofolate reductase (MTHFR)

A

Hyperhomocysteinemia