HEMOSTASIS

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HEMOSTASIS :

HEMOSTASIS Dr.ABHIJIT GOGOI, DEPARTMENT OF PHYSIOLOGY, UNIVERSITY OF FIJI HEMOSTASIS

HEMOSTASIS :

HEMOSTASIS Def:- stoppage of bleeding from the blood vessels Mechanisms v.c of blood vessels platelet plug formation Blood coagulation (fibrinogen fibrin) Clot retraction fibrinolysis to dissolve the clot HEMOSTASIS

PRIMARY HEMOSTASIS :

PRIMARY HEMOSTASIS includes the processes that result in the formation of the platelet plug. Necessary factors-: -The blood vessels : the vessel walls esp. the subendothelial layer. - The platelets - 2 plasma glycoproteins: - fibrinogen -Willebrand factor ,which also presents inside the platelets

Mechanisms: :

Mechanisms: 1-v.c of the bl. vessel. 2- Platelets adhesion to subendothelial layer, ( Willebrand factor is necessary for this stage) adhesion of platelets-  3- platelets secretion: their activation and secretion of ADP,adrenaline, noradrenaline –> aggregation & activation of other platelets. 4- Aggregation of platelets. 5- Formation of capillary plug.   HEMOSTASIS

Type and character of bleeding: - :

Type and character of bleeding: - Purpuric spots (capillary or platelets defect not characteristic of hemophilia) Hematoma, hemarthrosis or large ecchymoses at the site of trauma : suggests hemophilia (coagulation defect) Sudden severe bleeding from multiple sites after prolonged surgery or during obstetric procedures suggests acquired fibrinogen defect HEMOSTASIS

Capillary resistance test of Hess: :

Capillary resistance test of Hess: sphygmomanometer cuff above the cubital fossa and raise the pressure to 100 mm Hg (or midway between systolic & diastolic if systolic pressure <100) for 5 - 7' minutes-  deflation  '3 minutes later  count the number of petichea in area of 3 cm diameter, 1 cm below the cubital fossa  Normally up 10 if more than 20, means platelets or capillary wall defect HEMOSTASIS

Coagulation of Blood:

Coagulation of Blood Def :- represent the conversion of fibrinogen (soluble protein) to fibrin (insoluble) meshwork which occludes the point or vessel rupture. HEMOSTASIS

Blood clotting factors:

Blood clotting factors Factor I = Fibrinogen Factor II = Prothrombin Factor III = Tissue factor Factor IV = Calcium Factor V = Labile factor Factor VII = Stable factor Factor VIII = Antihemophilic factor A Factor IX = Antihemophilic factor B or Christmas factor

PowerPoint Presentation:

Factor X = Stuart Prower factor Factor XI = Antihemophilic factor C Factor XII = Hageman factor Factor XIII = Fibrin stabilising factor

First Step :Activation of factor X:

First Step :Activation of factor X BY One of 2 systems : 1 II Extrinsic system Intrinsic system HEMOSTASIS

systems of coagulation :

systems of coagulation Extrinsic system. Intrinsic system. In vivo only. In vivo & in vitro Due to tissue damage. due to contact with foreign surface ↓ ↓ Tissue factor activation of contact system ↓ ↓ X < ------------------------------------IX a < ---------------- IX ↓ Xa ↓ 2- prothrombin thrombin 3-fibrinogen Fibrin

EXTRINSIC SYSTEM :

EXTRINSIC SYSTEM FACTORS ARE: Factor X Tissue factor and Factor VII Tissue F. VIIa VII Xa X Blood vessel HEMOSTASIS

INTRINSIC SYSTEM :

INTRINSIC SYSTEM Necessary factors: - XII (Hageman factor) - Contact system XI Kallikrene kininogene - F. IX - F. VIII - F. X - Ca. ++ - phospholipids of the platelet’s membrane HEMOSTASIS

PowerPoint Presentation:

Contact System: Foreign surface |--------------------------------------------------| Kalierne XII kininogene Fragmentation XIIa XI XIa Rest of intrinsic pathway IX HEMOSTASIS

PowerPoint Presentation:

Rest of intrinsic pathway IX Platelets Ca ++ IXa X VIIIa VIII Xa II IIa HEMOSTASIS

Second Step: of Coagulation:

Second Step: of Coagulation Thrombin Formation: (IIa) Factors needed: - prothrombin (II) Ca++ platelets - Xa II V Ca++ - V (acceleririe) Xa - phospholipids - Ca + + IIa HEMOSTASIS

3rd Step :Fibrin Formation:

3 rd Step :Fibrin Formation Fibrin Formation:- ------------------------ IIa XIII XIIIa (Fibrinogen) -------------------- Ia (Soluble fibrin) Insoluble Fibrin HEMOSTASIS

Physiological anticoagulants:

Physiological anticoagulants 1- Serine protease inhibitors :inhibit the coagulation cascade. 2 -Neutralizers of activated coagulation factors (components of protein C system) HEMOSTASIS

1-Serine protease inhibitors::

1-Serine protease inhibitors: 1-Antithrombin (III). 2-Heparin and heparin like substance. 3-Alpha 1 antitypsin. 4-Alpha 2 macroglobulin HEMOSTASIS

2-Neutralizers of activated coagulation factors : (components of protein C system) :

2 -Neutralizers of activated coagulation factors : (components of protein C system) 1-Protein C: synthesized in the liver, vit. K dependant, activated by thrombin. 2-Thrombomodulin. 3-Protein S and C4b-binding protein . HEMOSTASIS

Fibrinolysis:

Fibrinolysis is the process wherein a fibrin clot , the product of coagulation , is broken down.Its main enzyme plasmin cuts the fibrin mesh at various places, leading to the production of circulating fragments that are cleared by other proteases or by the kidney and liver HEMOSTASIS

PowerPoint Presentation:

When plasmin breaks down fibrin, a number of soluble parts are produced. These are called fibrin degradation products (FDPs). FDPs compete with thrombin, and so slow down the conversion of fibrinogen to fibrin (and thus slows down clot formation).

Exploration of the coagulation:

Exploration of the coagulation whole blood clotting time Normally 4-10 minutes Generally ---> N. in platelets defects. ↑ = coagulation defect But not very sensitive: - only +ve when blood coagulation is very defective HEMOSTASIS

PowerPoint Presentation:

Thrombin time detect the defects in the conversion of fibrinogen ---> fibrin Measured by addition of thrombin to citrated patients plasma If polonged Abnormalities of fibornogen (hypo or hyper or dysfibrinogenemia) Heparin Presence of some abnormal proteins which inhibits the polymerisation of monomers of fibrin. (e.g myeloma protein

Normal Hemostasis:

Normal Hemostasis

PowerPoint Presentation:

Blood Coagulation & Tests Thrombin time

Who is likely to bleed:

Who is likely to bleed Obvious Cirrhosis Renal dysfunction Age Drugs Right heart failure

Vitamin K:

Vitamin K Warfarin affects factors II,VII,IX and X These are the vitamin K dependent factors Can reverse warfarin effect Takes time Available forms ?

Vitamin K deficiency:

Vitamin K deficiency Obstructive jaundice Malabsorption of Vit K dependent factors Older people at risk Post surgery at risk Treatment Oral or IV Vitamin K

Hepatic dysfunction - Cirrhosis:

Hepatic dysfunction - Cirrhosis Liver makes and degrades Coagulation is affected by decreased production and impaired degradation of activated factors Chronic DIC Splenomegaly Trearment only if bleeding Liver transplant

Hemophilia:

Hemophilia X linked bleeding disorders characterized by spontaneous development of large hematomes in deep tissues. May lead to joint bleeding, or into other closed structures Joint cavity bleeding leads to deformed joints bleeding may be spontaneous or asssociated with mild or moderate injury

Hemophilia types:

Hemophilia types Hemophilia A absent or decreased factor VIII Hemophilia B lack of factor IX similar in symptoms to Hemophilia A Hemophilia A is 10 times more common than hemophilia B

Hemophilia - Clinical Picture:

Hemophilia - Clinical Picture Mild- do not develop spontaneous bleeding, but do bleed after injury or surgery Many patients have sever disease Joint Bleeding results in severe disability hemarthroses chronic arthritis muscle bleeds Social, economic,psychological problems

Von Willebrand’s Disease:

Von Willebrand’s Disease Most frequent inherited bleeding disorder 1% - 1/100 of western population less severe than hemophilia Disease results from a decrease or absence of Von Willebrand factor for platelet adhesion Affects primary hemostasis

Von Willebrand’s Disease and Factor VIII:

Von Willebrand’s Disease and Factor VIII VW factor produced in megakaryocytes and endothelial cells Coded on chromosome 12 Autosomal dominant inheritance Large molecule, and multimeric Monomers undergoglycolisation and multimerization before secretion Different multimer size = disease

Von Willebrand’s Disease and Factor:

Von Willebrand’s Disease and Factor VW is carrier for factor VIII Factor VIII-VWf complex Factor VIII protein carried in circulation as complex with VWf Reacts with platelet via GP Ib Therefore can be problems with platelets and factor VIII

Clinical features of Von Willebrand’s Disease:

Clinical features of Von Willebrand’s Disease Generally mild bleeding - often unrecognized until surgery or injury epistaxis, menorrhagia, easy bruising, dental and post operative bleeding Can be severe in certain types Requires accurate diagnosis Requires specific treatment

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