thrombosis and fibrinolysis Flashcards
thrombosis pathologic event (3)
- disruption of blood flow
- platelet fibrin mass
- occlusion of the blood vessel
virchow’s triad
- blood flow
- coagulation factors
- blood vessel
fibrinogen to fibrin and
feedback to activate and amplify
this process to form the
fibrin clot.
thrombin burst
inhibitor of coagulation
protein C
tissue factor pathwaay inhibitor (TFPI)
regulates TF/FVIIa pathway
anti-thrombin III (AT-III)
inhibits thrombin, FIXa, FXa, FXIa
protein C and co-factor Protein S
are vit. K dependent and inhibit FVa and FVIIIa
Very ill patient with skin necrosis –
disseminated intravascular coagulation (DIC)
New onset neurologic symptoms –
stroke or cerebral vein thrombosis
Frequent miscarriages/fetal loss –
placental thrombosis
thrombophilia:
congenital deficiency states (3)
- AT-III
- Protein C
- Protein S
thrombophilia:
genetic mutations 4
- activated protein C resistance or factor Vleiden
- hyperhomocysteinemia- MTHFR
- prothrombin gene mutation
- PAI- mutations- affects fibrinolysis
other causes of thrombophilia (2)
- elevated levels of FVIII, IX, XI
2. elevated levels of lipoproteins
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)
Antiphospholipid Antibody Syndrome
Antiphospholipid Antibody Syndrome
- what do we see
- what is it
- occurs in females/males
- age?
- clinical
- _________ due to binding to phospholipid and prothrombin in vitro in the assays
- assays detect antibodies against
- despite prolonged PTT, it does not cause
- treatment
- venous/arterial thrombosis (recurrent fetal loss)
- immune mediated
- females>males
- any age
- clinical-thrombosis, livido reticularis, thrombocytopenia, migraine headaches
- Prolongation of clotting assays
- cardiolipin and B2 glycoprotein 1
- bleeding
- treat underlying disease process and prevent further thrombosis
protection against thrombosis (6)
- inactivation of activated coagulation factors
- decrease platelet activity
- increase blood flow
- activation of thrombomodulin
- fibrinolytic system dissolves clot
- RES clears soluble fibrin complexes
involves the vascular endothelium, vW protein and plateltets
primary hemostasis
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
secondary hemostasis
dissolution of the fribrin clot as a part of the wound healing process
fibrinolysis
nitric oxide inhibits
platelet activation
Alpha2-antiplasmin binds with plasmin to form the alpha2-AP/plasmin complex, which prevents
plasmin from breaking down fibrin within the fibrin clot (fibrinolysis).
Missense mutation of Arginine 506 to Glutamine 506 (Arg-506-Gln)
Activated Protein C resistance (Factor V Leiden)
G to A substitution of nucleotide 20210 in 3’ untranslated portion of the gene
Prothrombin Gene Mutation
Mutation in the gene for methylene tetrahydrofolate reductase (MTHFR)
Hyperhomocysteinemia
