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By Prof\ Sameh Shamaa Prof Of medical Oncology and Internal medicine Mansoura Faculty Of Medicine HEMOSTASIS
HEMOSTASIS
Def:- stoppage of bleeding from the blood vessels Mechanisms (I) v.c of blood vessels (II) platelet plug formation (III) Blood coagulation (fibrinogen fibrin) (IV) Clot retraction (V) fibrinolysis to dissolve the clot
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: plasma glycoproteins 2fibrinogen Willebrand factor ,which also presents inside the platelets
:Mechanisms
.v.c of the bl. vessel-1 Platelets adhesion to subendothelial layer, ( Willebrand- 2 )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 .Aggregation of platelets- 4 .Formation of capillary plug- 5
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Family history Duration (recent onset or since childhood) Duration of the bleeding episode. Circumstance of bleeding (spontaneous, after trauma, or surgery)
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2) Investigations :
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1) Capillary resistance test of Hess 2) Platelets count 3) Bleeding time time needed for the platelet plug formation If . N. ------ Normal 1ry homeostasis . ------ platelet or vascular defect.
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4) Other tests only done if there is a prolonged bleeding time with normal platelet count - Measurement of capillary resistance - Measurement of Willebrand factor - Platelets function tests (Adhesiveness, Aggregation) - other tests for platelets (clot retraction, prothrombin consumption).
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Coagulation of Blood
Def :- represent the conversion of fibrinogen (soluble protein) to fibrin (insoluble) meshwork which occludes the point or vessel rupture.
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systems of coagulation
I-urgent system. Extrinsic system. 12-20'' (seconds) In vivo only. Due to tissue damage. II-delayed system Intrinsic system. 4-8' (minutes) In vivo & in vitro due to contact with foreign surface
Tissue factor activation of contact system X < ------------------------------------IX a < ---------------- IX Xa 2- prothrombin thrombin 3-fibrinogen Fibrin
HEMOSTASIS
EXTRINSIC SYSTEM
FACTORS NICESSORY ARE: Factor X Tissue factor and Factor VII Tissue F. VIIa Xa X VII
INTRINSIC SYSTEM
Necessary factors: XII (Hageman factor) - Contact system XI Kallikrene kininogene - F. IX - F. VIII - F. X - Ca. ++ - phospholipids of the platelets membrane HEMOSTASIS
Contact System: Foreign surface |--------------------------------------------------| Kalierne XII kininogene Fragmentation XIIa XI XIa
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platelets V Xa
Ca++
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Insoluble Fibrin
Physiological anticoagulants
1- Serine protease inhibitors :inhibit the coagulation cascade. 2-Neutralizers of activated coagulation factors (components of protein C system)
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1-Protein C: synthesized in the liver, vit. K dependant, activated by thrombin. 2-Thrombomodulin. 3-Protein S and C4b-binding protein. HEMOSTASIS
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
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Measurement
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
(2) One stage prothrombin time: general exploration or the extrinsic pathway (Quick time) .N : 16-18 sec +addition of tissue thromboplastin ca++ to decalcified plasma ---> measure .the time till coagulation occur Affected by factors VII, X, V, II & )fiboinogen (only severe defect
HEMOSTASIS
(3) partial thromboplastin time (PTT) or CKT(cephaline koalin time) General exploration of the intrinsic pathway clotting time of recalcified plasma in the presence of phospholipid (cephaline), while koalin powder for activation of Hageman factor'. Affected by factors XII, XI, IX, VIII, X, II
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(4) 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 proteinswhich inhibits the polymerisation of monomers of fibrin. (e.g myeloma protein
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(5) Deficiency of F XIII (fibrin stabilizing factor ) detected by noting the solubility of fibrin
in 5M urea or 1% monochloroacetic acid (can't dissolve fibrin in the presence of factor XIII).In congenital defect of f. XIII ---> dissolution of the clot in <10.
(7) Detection of coagulation inhibitors: 1-Inhibitors for a specific factor (especially F. VIII) usually ---> severe hemorrhage 2-Inhibitors against platelets or tissue phospholipids ---> prolongation of tests of coagulation (Quick or CKT) e.g L.E but usually no hemorrhagic manifestations 3- if there is of Quick test or CKT or thrombine:50% of normal plasma + 50% of patient plasma (incubation at 370c for I hour) repeat the test If become normal ---> factor defect if no correction ---> presence of inhibitors. HEMOSTASIS
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4- Quick N., CKT: either: I- Hemophilia Aor B. 2- Rarely ---> defect of one factor of the contact system (XII, or XI or others)
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in 3, 4..5 dosage of the factors with suspected deficiency, also search for inhibitors. Ex: - Quick, normal dosage of factors---> hyperfibriongenemia which inhibit the test - Quick +CKT + no F. defect --->? Inhibitors, e.g. antiphospholipides.
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Thank You
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