Haemostasis Flashcards
What are the compounds secreted by thrombocytes when they are activated, and what does each of them cause?
- ADP – activate platelets further
- Serotonin – vasoconstriction
- Thromboxane A2 (TxA2) – Vasoconstriction and aggregation
- Calcium & presence of phospholipids – allows for coagulation reactions
Name compounds released by platelets that responsible for vasoconstriction during haemostasis.
- Serotonin
- Thromboxane A2
List the cells that the platelets are derived from developmentally
- Multipotent stem cells
- Myeloid precursor cells
- Megakaryocytes
What are the compounds that initiate the internal and external coagulation cascades.
- External (tissue factor) pathway – tissue factor
- Internal (contact activation) pathway – thrombin, factor XIIa, a nucleation site (eg glass in a laboratory)
What are the enzymes directly responsible for transforming fibrinogen to a clot?
•Thrombin (factor II) turns it into fibrin. Factor XIII cross-links it into a clot
What are the enzymes that are specifically part of the intrinsic (contact activation) coagulation pathway (i.e. not part of the common or extrinsic pathways)?
- Factor I – no. this is fibrinogen and part of the common pathway
- Factor II – no. this is thrombin and part of the common pathway
- Factor III – no. this is tissue factor (also known as thromboplastin) and part of the extrinsic pathway
- Factor IV – not specifically. This is calcium.
- Factor V – no. This is not an enzyme (it is a co-factor) and it is part of the common pathway
- Factor VI – no. does not exist
- Factor VII – no. Part of the extrinsic pathway.
- Factor VIII – not quite. This is a co-factor that is part of the intrinsic pathway
- Factor XI – yes
- Factor X – nearly. part of common pathway as well as intrinsic pathway
- Factor XI – yes.
- Factor XII – yes.
- Factor XIII – No. part of common pathway
What is the role of vitamin K in haemostasis?
•It is necessary for the production in the liver of Ca-dependent proteases: II, VII, IX, X
What conditions might lead a patient develop a vitamin K deficiency?
•Warfarin toxicity, poor absorption of vitK (eg lack of bile salts)
What is the aetiology (including environmental & genetic influences) of haemophilia A?
•Genetic. X-linked (recessive), factor VIII mutation
What is the aetiology (including environmental & genetic influences) of haemophilia B?
•Genetic. X-linked (recessive), factor IX mutation
Give an overview of how the body responds to an injury in a blood vessel.
- Formation of a haemostatic plug physically protects and coats the surface of injury initially; this involves platelet adhesion, activation and aggregation.
- Coagulation creates a large scale meshwork that can close off blood vessels and make a protective surface for repair.
- Vasoconstriction decreases the local flow of blood. It accelerates coagulation, as well as minimising blood loss
Explain the role platelets play in haemostasis.
- Platelets contribute to all three aspects of haemostasis.
- Platelets contribute to vasoconstriction by releasing vasoconstrictor compounds (serotonin, TxA2)
- The form the primary haemostatic plug
- And they secrete or provide compounds that encourage coagulation (including their phospholipids)
List 4 differentiated cell types that develop from the lymphoid precursor cells
- NK cells
- T cells
- B cells
- Plasma cells
List 4 differentiated cell types that develop from the myeloid precursor cells
- Megakaryocytes (thrombocytes are not cells because they do not have nuclei, so they are “formed elements”)
- Red blood cells
- Eosinophils, basophils, mast cells
- Monocytes, macrophages
- neutrophils
Explain platelet activation.
- It is when platelets change dramatically (usually in response to ADP or exposed collagen).
- A) Their shape becomes more spindly (less regular or rounded),
- B) their metabolism goes up,
- C) they exocytose many granules, and
- D) their membrane gains proteins (eg GP2b/3a).
- Many of the reactions of the clotting cascade can only take place on the membrane of an activated platelet, and Platelet aggregation requires binding proteins only present on the platelet membrane when activated.
PT becomes longer when the extrinsic pathway is compromised, while APTT becomes longer when the intrinsic pathway is compromised. Both PT and APTT become longer when the common coagulation pathway is compromised. Bleeding time becomes longer if the common pathway (or both the extrinsic pathway AND the intrinsic pathway) or total platelet activity is compromised/reduced. Given this information, fill In the following table concerning how each clinical condition will affect the timings (or platelet count) as shown below
