Haematopoiesis and bleeding

Question 1

Detail the physiological process of haemostasis

Answer 1

1. Transient arteriolar vasoconstriction
   • Vascular spasm is the blood vessels’ first response to injury
   • The damaged vessels will constrict (vasoconstrict) which reduces the amount of blood flow through the area and limits the amount of blood loss
2. Primary haemostasis
   • When the platelets find an exposed area or an injury, they begin to form what is called a platelet plug, aggregating (sticking together) to seal the injury off
   • The platelet plug formation is activated by a glycoprotein called the Von Willebrand factor (vWF), which are found beneath the endothelium layer
   • They release chemical messengers such as adenosine diphosphate (ADP), serotonin and thromboxane A2 which cause more platelets to stick to the area and release their contents and enhance vascular spasms
3. Secondary hemostasis
   • Coagulation or blood clotting uses fibrin threads that act as a glue for the sticky platelets
   • As the fibrin mesh begins to form the blood is also transformed from a liquid to a gel like substance through involvement of clotting factors and pro-coagulants
   • Once this begins, red and white blood cells become caught up in the fibrin mesh which causes the clot to become even stronger
   • The release of Prothrombin also plays an essential part in the coagulation process because it allows for the formation of a thrombus, or clot, to form
   • This final step forces blood cells and platelets to stay trapped in the wounded area
4. Counter- regulatory mechanisms established
   • The endothelium releases tissue plasminogen activators, TPA, (fibrinolytic plasmin) and thrombomodulin (interferes with the coagulation cascade)
   • The purpose of this is to prevent inappropriate extension of the haemostatic plug

Question 2

Describe the coagulation cascade

Answer 2

• Happens during secondary haemostasis
• Has two initial pathways which lead tofibrinformation: the intrinsic pathway and the extrinsic pathway
• Fibrin doesn’t circulate in the blood freely, rather it circulates in its inactive form: as fibrinogen so that it doesn’t cause random clumps
• What helps change fibrinogen into its active form is thrombin
• Thrombin exists in its inactive form; prothrombin
• The extrinsic pathway starts the reaction, while the intrinsic pathway works to amplify the reaction
• Both pathways go through a cascade which eventuates into the thrombin, which eventuates into fibrin
• To regulate the coagulation cascade, the activation of thrombin leads to the generation of antithrombin, which acts as a negative feedback loop

Question 3

List the common bleeding disorders

Answer 3

Vascular disorders

Platelet disorders

Coagulation factor deficiencies

Question 4

Describe vascular disorders and related oral manifestations

Answer 4

Causes:
• Inherited: connective tissue disorders
• Acquired: scurvy coz of vitamin C deficiency

Oral manifestations:
• Petechiae (red dots on skin)

Question 5

Describe platelet disorders and related oral manifestations

Answer 5

Causes:
• Thrombocytopenia
• Leukaemia

Oral manifestations:
• Purpura (bruising)
• Petechiae (red dots on skin)
• Excessive bleeding

Question 6

Describe coagulation factor deficiencies and related oral manifestations

Answer 6

Causes:
• Haemophilia
• Von Willebrand disease
• Vitamin K deficiency
• Liver disease which affects Vit K absorption 
• Drug induced

Oral manifestations:
• Nosebleeds, Excessive bleeding