Blood AHS 1 Flashcards
What is key in soft clot?
Platelets. Produced in bone marrow. Contain no usual cell contents. Vesicles containing blood clotting factors.
Three stages of clotting?
Primary / soft clot
Secondary / fibrin mesh
Degradation / fibrinolysis
Protease role in clotting?
Thrombin cleaves fibrinogen -> fibrin. Fibrin + factor XIIIa catalysis covalent secondary fibrin mesh clot.
What is zymogen activation?
Prothrombin (factor II) is inactive zymogen. Proteolytic cleavage by Factor Xa -> Thrombin (Factor IIa).
What is protease / function?
Enzyme cutting proteins by cleaving peptide bonds into polypeptides via hydrolysis (water breaking).
How do clots degrade?
Plasminogen activated by urokinase -> Plasmin (fibrin degrading product (FDP)).
What are common clotting disorers?
Vit K deficiency = decreased carboxylation (rodenticide inhibits gamma caboxylation).
Haemophilia
Von Willibrand’s disease = decreased platelet aggrigation seen on G.shephers & dobermans.
Blood components
55% Plasma. 45% Erythrocytes. <1 % leucocytes & platelets.
What are serum proteins? Function and electrophoresis
Transport (non-specific binding) and oncotic pressure maintenance (fluid distribution of intra and extra vascular compartments). 50% of liver output is Albumin (most abundant serum protein).
Electrophoresis separates proteins using agarose gel by charge using blue stain into class / components.
Decrease or increase of class/component = diagnostic tool.
How are serum enzymes used as diagnostic tool?
Change of gamma globulins: Decrease = immune suppression / deficiency (hypogammaglobulinaemia).
Broad increase: Chronic infection.
Specific gamma-globulin increase in y-band “multiple myeloma” (cancer), monoclonal expansion of single type of antibody producing cell. [Over producing is called paraproteinaemia].
