HEMOSTASIS

INTRODUCTION

 The term Hemostasis means prevention of blood loss.

 Hemostasis is the process of forming clots in the walls of damaged blood

vessels and preventing blood loss, while maintaining blood in a fluid state
within the vascular system.
EVENTS IN HEMOSTASIS

 4 Major Events
 Vascular Constriction
 Platelet Plug Formation
 Fibrin Formation
 Fibrinolysis
1. VASCULAR SPASAM

1- Sympathetic reflex
2- Release of vasoconstrictors (TXA2 and serotonin) from platelets
that adhere to the walls of damaged vessels.
2. PLATELET PLUG FORMATION

 Platelet adherence
 Platelet activation
 Platelet aggregation
 Formation of temporary haemostatic plug
3. FIBRIN FORMATION

 Formation of blood clot

 Clot begins to develop
 Severe trauma 15 to 20sec
 Minor trauma 1 to 2 min
General Mechanism

 Formation of prothrombin activator

 It catalyses conversion of prothrombin to thrombin
 Thrombin catalyses fibrinogen into fibrin.
 Fibrin stabilizing factor released from platelets entrapped in the clot.
 Thrombin that activate the FSF
 FSF create strong covalent bond
Blood clot

 The clot is a meshwork

 Fibrin fibres also adhere to damaged surfaces of blood vessels
CLOTTING FACTORS

 Factor I (fibrinogen)- Fibrinogen is a soluble plasma protein (MW

330000) which is acted upon by thrombin to form insoluble fibrin
clot.
 Factor II (prothrombin)- Inactive precursor of thrombin is formed
in liver.
 Factor III (tissue factor, tissue extract, thromboplastin)- This
converts prothrombin in the presence of factors V, VII, and Xa,
Calcium, and phospholipid.
 Factor IV (calcium)
 Factor V (labile factor, thrombogene or proaccelerin)- This
factor is reqd. for the conversion of prothrombin to thrombin by
tissue extract and plasma factors.
 Factor VII (stable factor, autoprothrombin I)- Factor VII is reqd.
for the formation of prothrombin activator by tissue extract.
 Factor VIII (antihemophilic globulin [AHG], antihemophilic
factor)- Factor VIII is reqd. for the formation of prothrombin
activator from blood constituents; it’ s consumed during clotting and
hence absent from serum. In vivo the half life of factor VIII is 10-
20h.
 Factor IX (Christmas factor, plasma thromboplastin component,
autoprothrombin II)- It’s needed for the formation of prothrombin
activator from blood constituents..
 Factor X (stuart-prower factor)- Converted to factor Xa either by
factors IXa & VIII or factor VII & tissue factor. Factor X can be activated
by other proteases such as trypsin or Russel’s viper venom.
 Factor XI (plasma thromboplastin acntecedent-PTA)- Also a beta2
globulin present both in serum & alumina treated plasma. It’s
thermolabile. Unlike factor XII, its activity increases when stored frozen
 Factor XII ( Hageman factor or contact factor)- It takes part in the
formation of prothrombin activator from blood constituents. It’s present in
both serum & plasma.
 Factor XIII (fibrin stabilizing factor)- This is plasma protein which causes
polymerization of soluble fibrin to produce insoluble fibrin.
 Fletcher factor Described by Hathway (1965). Deficiency resembles factor
XII deficiency. It’s a prekallikerin. Evidence indicating that prekallikerin is
activated by limited proteolysis.
 Fitzgerald factor Its heat stable. This appears to act after the activation of
Hageman factor & Fletcher factor but before the activation of factor XI. It’s
necessary for conversion of factor XI by Kaolin activated factor XII. It’s
reqd. for normal fibrinolysis & kinin formation.
 Von Willibrand factor (Vwf)
 4.FIBRINOLYSIS

 Plasminogen or profibrinolysin when activated forms plasmin

(fibrinolysin)
 Plasmin is a proteolytic enzyme that digests fibrin fibers and
protein coagulants such as fibrinogen, Factor V, Factor VIII,
prothrombin & Factor XII.
Methods of hemostasis

 Mechanical- Direct pressure, gauze pack, sutures

and ligation, staples.
 Chemical – pharmacological agents, topical
hemostatic agents
 Thermal
HEMOSTATIC
DISORDERS
TESTS FOR BLEEDING DISORDERS

 Clot retraction time

 Platelet count
 Coagulation time
 Bleeding time
 Prothrombin time
BLEEDING DISORDERS

 Afibrinogenaemia
 Purpura
 Hypoprothrombinemia
 Haemophilia (A,B,C)
 Von Willebrand disease
 AFIBRINOGENAEMIA

 A decrease or lack of fibrinogen may occur due to genetic defect.

 Dysfibrinogenaemia there may be normal concentration but fibrinogen

molecules are abnormal and there is bleeding disorder.

 Lack of fibrinogen leads to failure of haemostasis. which may be fatal.

 The condition is treated with fresh blood or fibrinogen injection.

PURPURA

 Its characterised by spontaneous petechial haemorrhage

under the skin and the mucous membrane.
 It may be due to:
 Thrombocytopenia
 Idiopathic thrombocytopenia Purpura
 Drugs induced(quinine, ergot, bismuth)
 Defects in the capillaries
 Treatment : transfusion of fresh blood, splenectomy
HYPOPROTHROMBINAEMIA

 Decreased prothrombin concentration in blood may result

due to:
 Liver damage
 Vitamin K deficiency
 There may be normal bleeding time in this condition but
coagulation time is prolonged.
 Treatment: injection of vitamin K, and antibiotics
 HAEMOPHILIA A
(CLASSIC HAEMOPHILIA)
 Is a hereditary bleeding disorder due to deficiency of
coagulation factor VIII (antihaemophilic factor)
 The bleeding tendency is related to factor VIII level. Patients
with mild haemophilia bleed only after major trauma or
surgery, those with moderately sever haemophilia bleed with
mild trauma or surgery, and those with severe disease bleed
spontaneously.
 Treatments: infusion of factor VIII.
gene therapy
avoid the use of aspirin.
HAEMOPHILIA B
(CHRISTMAS DISEASE)
 Is a hereditary bleeding disorder due to deficiency
coagulation factor IX.
 Clinical features same as haemophilia A, but less severe.
 Treatment: transfusion of factor IX.
Avoid aspirin.
HAEMOPHILIA C

 Rare genetic disorder caused by missing or defective blot

clotting protein called factor XI (plasma thromboplastin
antecedent)
 Clinical symptoms are oral bleeding, nasal bleeding, blood
in the urine etc.
von Willebrand disease
 Common congenital disorder and is transmitted in an
autosomal dominant pattern.
 Most cases are mild.
 Patients presents with mucosal bleeding.
 Bleeding decreases during pregnancy or estrogen use.
 Since the bleeding is mild, no treatment is necessary
except before surgery.
 Desmopressin acetate will be given.
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