Bleedingandcoagulationdisorders Hemostasis 141017100838 Conversion Gate01

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BLEEDING AND

COAGULATION DISORDERS

Dr. Shamshuddin Patel Sr.



HEMOSTASIS

• Def. : consequence of tightly regulatedprocesses that maintain blood in a fluid, clot-free state in normal vessels while

introducing the rapid formation of alocalized haemostatic plug at the site ofvascular injury.

- from Robbins Basic Pathology th edition

• Mechanism vasoconstriction formation of platelet plug coagulation cascade fibrinolysis



WHY BLOOD DOES NOT CLOTNORMALLY IN CIRCULATION?

• ENDOTHELIAL FACTORS: – smoothness of endothelial lining prevents platelet

adhesion

– negatively charged particles present over endothelial

lining repel the clotting factors• VELOCITY OF CIRCULATION, if decreases leads to

clotting

• PRESENCE OF NATURAL ANTICOAGULANTS IN

BLOOD, Ex: heparin, protein c,thrombomodulin

• SIMULTANEOUS ACTIVATION OF FIBRINOLYTICSYSTEM ALONG WITH CLOTTING MECHANISM.



Stages of

Heostas!s



5

Vascular Spasm

Vascular spasm results from the:

. !ocal myogenic contraction of the blood vesselsinitiated by direct damage to the vascular "all

#. $elease of !ocal autaco! factors from thetraumati%ed tissues and blood platelets, and

&. 'ervous re(exes initiated by pain nerve impulses orother sensory impulses that originate from thetraumati%ed vessel or nearby tissues.

). $elease of a vasoconstrictor substance,T"rom#o$a%& A' by the platelets "hich for the

smaller vessels are responsible for much of thevasoconstriction



M&c"a%sm o( t"& )lat&l&t)lu*

• *hen platelets come in contact "ith a damagedvascular surface, especially "ith collagen +bers in thevascular "all, the platelets themselves immediatelychange their o"n characteristics drastically

• hey begin to s"ell

• hey assume irregular forms "ith numerous irradiatingpseudopods protruding from their surfaces-

• heir contractile proteins contract forcefully and cause therelease of granules that contain multiple active factors

• hey become sticy so that they adhere to collagen in thetissues and to a protein called "o# W!$$e%&a#' fa(to&



)lat&l&t plu* (ormato%+ plat&l&ta!"&so%



M&c"a%sm o( t"& )lat&l&t )lu*,ormato%

• hey secrete large /uantities of ADP and theiren%ymes form T)&o%o*a#e A+

• The ADP and thromboxane in turn act on nearby

platelets to activate them as "ell, and• he sticiness of these additional platelets causes

them to adhere to the original activated platelets

• hus the damaged vascular "all activates

successively increasing numbers of platelets thatthemselves attract more and more additionalplatelets, thus forming a ,$ate$et ,$-g



)lat&l&t plu* (ormato%+ plat&l&tr&l&as& acto%



)lat&l&t plu* (ormato%+ plat&l&ta**r&*ato%



THE PLATELET ROLE IN

HEMOSTASIS



COAGULATION

• 0ormation of blood clotSta*&s o( clott%*

)"as& -+ Extrinsic and intrinsicpath"ays produceprothrombinase1prothrombin activator

)"as& '+ Prothrombinase converts

prothrombin to thrombin )"as& .+ hrombin converts soluble

+brinogen into insoluble +brin "hich

is the thread of the clot.



Clott%*

(actors %#loo!





E$tr%sc )at"/a0

1. Release of tissue factor: &raumatized tissue releases a

comle$ o! several !actors calledtissue factor or tissuethromboplastin

. !ctivation of Factor X: &issue!actor !urther comle$es with

Factor #II and( in the resence o!calcium ions( acts enzymaticallyon Factor X to !orm activated Factor X

•. Factor Xa forms prothrombin

activator" Factor Xa combines with tissue or latelet hosholiids as well as withFactor # to !orm the comle$called prothrombin activator

I E



1213 3

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HOW DOES BLOOD CLOT SUMMARY

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