What is Hemostasis? All you need to know

When a blood vessels is damaged, bleeding stop by a process is called hemostasis.

This process involves in :- 

1. Vas­cu­lar response ( which reduces blood flow).
2. Platelet plug formation. 
3. Clot for­ma­tion.

• Save

When a blood ves­sels is injured platelet comes in con­tact. The injured blood ves­sels clos­es ful­ly or par­tial­ly. In the mean time blood clot­ting out of blood ves­sel begins to coag­u­late. Coag­u­la­tion occurs in the blood comes out of ves­sels ( Extrin­sic Clot­ting). With­in the ves­sels by vasospasm (Intrin­sic clotting).

Mechanism of Coagulation 

Blood coag­u­la­tion takes place by the action of throm­bin (formed from pro­throm­bin) on sol­u­ble fib­rino­gen in the pres­ence of cal­ci­um ion and fib­rin threads are formed. About 12 pop­u­la­tion fac­tors are present in cir­cu­lat­ing plas­ma and the tis­sue sur­round­ing blood ves­sels. These fac­tors are inac­tive at nor­mal cir­cum­stances. When bleed­ing take place they are acti­vat­ed and coag­u­la­tion take place. Here below are the 12 fac­tors with their alter­na­tive name

Blood Coagulation

Four phas­es of Haemostasis :- 

1. Con­struc­tion of the injured blood ves­sel to dimin­ish blood flow.
2. For­ma­tion of platelet Aggregation. 
3. For­ma­tion of fib­rin mesh that bind to platelet aggre­gate, which give more sta­ble haemosta­sis plug.
4. Par­tial Com­plete dis­so­lu­tion of haemosta­sis plug.

Purpose of Coagulation 

Haemosta­sis facil­i­ties a series of enzy­mat­ic acti­va­tions that lead to the for­ma­tion of clot with platelet and fib­rin. This clot seals the injured are con­trols and pre­vents fur­ther bleed­ing while the tis­sue degen­er­a­tion process take place. Once the injury start heal the plug slow­ly dis­solves at the site of damage.

The process is asso­ci­at­ed with endothe­li­um platelets and hepa­to­cytes.

Endothe­li­um :- Clot­ting fac­tors III and VIII orig­i­nate from the endothe­lial cells while clot­ting fac­tors IV comes from plasma.

Platelets :- These are non- nucle­at­ed cells release pro­teins involved in clot­ting and platelet Aggregation.

Hepa­to­cytes :- The liv­er pro­duces the major­i­ty of the pro­teins that func­tion as clot­ting fac­tors and as anticoagulants.

Vaso­con­stric­tion:-With­in 30 min­utes of damage/ trau­ma to the blood ves­sels vas­cu­lar spasm ensures which leads to vasoconstriction.

Fibrin Clot Formation 

Two path­ways leads to fib­rin clot formation:

1. The intrin­sic pathway.
2. The Extrin­sic pathway.

The inac­ti­va­tion of throm­bin an area of restrict­ed blood flow response to an abnor­mal ves­sel wall with­out tis­sue injury is called out by intrin­sic pathway.

Involve­ment of fib­rin clot in response to tis­sue injury is car­ried out by Extrin­sic pathway. 

These path­ways con­verge in a final com­mon path­way which involves:-

1. Acti­va­tion of Pro­throm­bin to Thrombin.
2. Cleav­age of fib­rino­gen to fib­rin clot catal­ysed by Thrombin.

The extrin­sic path­way involves tis­sue fac­tor, fac­tor VII , fac­tor X and Ca++.

The Extrin­sic Pathway 

The tis­sue fac­tor binds to fac­tor VII and acti­vate it. The acti­vat­ed fac­tor ( VIIa) fur­ther acti­vates and fac­tor X and IX via pro­te­ol­y­sis. Acti­vat­ed IXa binds with its co fac­tor VIII ( VII­Ia) which leads the acti­va­tion of fac­tor X. Xa binds to acti­vat­ed fac­tor V ( Va) and Cal­ci­um and gen­er­ate pro­throm­bi­nase Com­plex that change pro­throm­bin to thrombin.

The Intrin­sic Pathway

With throm­bin pro­duc­tion occurs con­ver­sion of fac­tor XI to acti­vat­ed fac­tor XI ( XIa). Fac­tor XIa with acti­vat­ed VII and tis­sue fac­tor con­vert to IX to fac­tor IXa. Fac­tor VII­Ia and fac­tor Xa binds with fac­tor V ( Va) and con­verts pro­throm­bin to thrombin.

Fib­rin clot formation 

The final step to coag­u­la­tion cas­code involve the con­ver­sion of fib­rino­gen to fib­rin monomers which forms fib­rin mesh and results in fib­rin clot. This reac­tion is acti­vat­ed by fac­tor XIII to fac­tor XIIIa.

Clin­i­cal Significance 

• Car­dio­vas­cu­lar.
• Renal.
• Immuno­log­i­cal.

Vit­a­min k Deficiency 

• Inad­e­quate Vit­a­min k lev­els lead to an impair­ment in the syn­the­sis of coag­u­la­tion fac­tors VIII , IX , X and prothrombin. 
• In Vit­a­min K defi­cien­cy the PT and PTT may be pro­longed. Vit­a­min k is a fat sol­u­ble Vit­a­min obtained from both dietary intake and from the pro­duc­tion of intesti­nal bacteria.