Haemostasis Flashcards
Haemostasis
Process by which bleeding stops
Why is Haemostasis important
Blood is important connective tissue
Keeps all organs nourished
Important blood loss is stopped quickly as a protective mechanism.
Minor blood loss consequences
Body’s homeostatic mechanisms maintain blood volume and cells
Moderate blood loss consequences
Headache
Fatigue
Nausea
Sweating
Dizziness
Rapid blood loss consequences
Clammy, cold, pale skin
Rapid, shallow breathing
Rapid heart rate
Confusion
Weakness
Blue lips and fingers
Loss of consciousness
What occurs when more than 20% of blood has been lost
Hypovolemic shock
Usually treated in hospital
Children and elderly most vulnerable
Primary stages of Haemostasis
Vasoconstriction
Platelet plug formation
Secondary stages of Haemostasis
Coagulation
Stages of Haemostasis
Vasoconstriction
Platelet plug formation
Coagulation
What occurs during first stage of Haemostasis
Construction of blood vessels.
Platelets adhere to damaged wall.
Platelets release serotonin and thromboxane.
Smooth muscle in vessel wall contracts.
What occurs during second stage of Haemostasis
Platelets clump around exposed collagen fibres.
Protein; Von Willebrand factor stabilised platelet plug.
Platelets release ADP chemicals to attract other platelets.
Platelet plug forms.
Bleeding time
Time taken for primary haemostasis to occur
2-7 minutes normally
Why would bleeding time be prolonged
Anti platelet drugs
Anaemia
Collagen disorders; von Willebrand disease
What does a blood clot consist of
Red/white blood cells
Platelets
Fibrin
What occurs during coagulation
Complex process; results in platelet plug stabilisation by fibrin strands.
Fibrin formed by fibrinogen.
How is extrinsic clotting pathway activated
Triggered by tissue factor (III), released by damaged epithelial cells.
How is extrinsic pathway measured
Prothrombin time
Normal value 11-16 seconds
How is intrinsic clotting pathway activated
Triggered by blood contacting with collagen fibres in the broken wall of blood vessel.
Initiated inside blood vessel.
Activation of factor XII.
How is intrinsic pathway measured
Activated partial thromboplastin time (aPTT)
What occurs during common pathway
Both extrinsic and intrinsic pathways fall into common pathway.
Prothrombin is converted into thrombin.
Thrombin converts fibrinogen into fibrin.
Factor XIII acts on fibrin to form fibrin mesh.
Stabilisation of fibrin clot.
Situations/factors which may inhibit blood clotting
Inherited diseases such as haemophilia A, B, C
Liver disease
Vit K deficiency
Von Willebrand disease
Anticoagulant medication
Indications of anticoagulant medication user
Atrial fibrillation
Deep vein thrombosis
Stroke
(Drugs that prevent blood clotting)
Anticoagulant medication
Warfarin
Rivaroxaban
Apixaban
Heparin
Dabigatran
Summary of coagulation cascade
- Initial injury, allow blood to escape into surrounding tissue.
- Vasoconstriction; tissue factor (III) released and smooth muscle wall contracts.
- Platelet plug formation; platelets adhere to each other and form temporary seal.
- Coagulation; fibrinogen converts into fibrin by thrombin, stabilises and strengthens clot.
What occurs during clot retractions
Contracts 90% of initial clot volume in 24hrs.
Actin and myosin pull clot tight.
Fibrin threads draw more closely.
Clot shrinkage pulls edges of damage blood vessel together.
Fibrinolysis
Clot breakdown.
Plasminogen trapped within clot converts into plasmin.
Plasmin breaks down fibrin.
Fibrinolysis is enhanced by
Sepsis
Severe trauma
Severe cancers
Increased consumption of fibrin with blood vessels.
Fibrinolysis is depressed by
Pregnancy
Alcoholic liver disease
Chronic renal disease
Hypothyroidism
Thrombosis
Formation of blood clot inside blood vessel, can block blood flow.
What causes thrombosis
Over activity of coagulation
Under activity of Fibrinolysis
Where does thrombosis often occur
Start at an area of vascular endothelial damage
Haemorrhage
Bleeding
How is haemorrhage controlled in dentistry
COMMON:
Pressure
Sutures
Packing with Haemostatic agents
UNCOMMON:
Electrosurgery
Lasters
