Lub hemostasis ntawm tib neeg lub cev yog tsim los ntawm peb qhov chaw:
1. Kev nruj ntawm cov hlab ntsha nws tus kheej 2. Platelets tsim ib qho embolus 3. Pib ntawm coagulation yam
Thaum peb raug mob, peb ua rau cov hlab ntsha hauv qab ntawm daim tawv nqaij puas, uas tuaj yeem ua rau cov ntshav nkag mus rau hauv peb cov ntaub so ntswg, ua kom tawv nqaij yog tawv nqaij, lossis los ntshav yog tias daim tawv nqaij puas lawm.Lub sijhawm no, lub cev yuav pib ua haujlwm hemostatic.
Ua ntej, cov hlab ntsha constrict, txo cov ntshav khiav
Qhov thib ob, platelets pib sib sau.Thaum cov hlab ntsha puas lawm, collagen raug pom.Collagen nyiam cov platelets mus rau qhov chaw raug mob, thiab cov platelets los ua ke los tsim ib lub ntsaws.Lawv sai sai ua ib qho thaiv uas tiv thaiv peb los ntawm los ntshav ntau dhau.
Fibrin txuas ntxiv mus, cia cov platelets txuas ntxiv kom nruj.Nws thiaj li muaj cov ntshav txhaws, tiv thaiv cov ntshav ntau tawm hauv lub cev thiab tseem tiv thaiv cov kab mob tsis zoo los ntawm peb lub cev los ntawm sab nraud.Nyob rau tib lub sijhawm, txoj kev coagulation hauv lub cev kuj tau qhib.
Muaj ob hom kev sib txuas sab nraud thiab sab hauv.
Extrinsic coagulation txoj kev: Pib los ntawm kev raug cov ntaub so ntswg puas rau ntshav sib cuag nrog yam III.Thaum cov ntaub so ntswg puas thiab cov hlab ntsha tawg, qhov cuam tshuam III ua ib qho nyuaj nrog Ca2+ thiab VII hauv cov ntshav los ua kom muaj txiaj ntsig X. Vim tias qhov xwm txheej III uas pib cov txheej txheem no los ntawm cov ntaub so ntswg sab nraud ntawm cov hlab ntsha, nws yog hu ua extrinsic coagulation pathway.
Intrinsic coagulation txoj kev: pib los ntawm kev ua kom muaj XII.Thaum cov hlab ntsha puas lawm thiab cov subintimal collagen fibers raug, nws muaj peev xwm qhib Ⅻ rau Ⅻa, thiab ces qhib Ⅺ rau Ⅺa.Ⅺa activates Ⅸa nyob rau hauv lub xub ntiag ntawm Ca2+, thiab ces Ⅸa ua ib tug complex nrog activated Ⅷa, PF3, thiab Ca2+ mus ntxiv activate X. Cov yam tseem ceeb ntawm cov ntshav coagulation nyob rau hauv lub saum toj no-hais txheej txheem yog tag nrho cov muaj nyob rau hauv cov ntshav plasma nyob rau hauv cov hlab ntsha. , yog li lawv tau lub npe hu ua intrinsic ntshav coagulation txoj kev.
Qhov xwm txheej no muaj lub luag haujlwm tseem ceeb hauv kev coagulation cascade vim yog kev sib koom ua ke ntawm ob txoj hauv kev ntawm qib X Factor X thiab yam V ua kom tsis muaj zog yam II (prothrombin) hauv cov ntshav rau active factor IIa, (thrombin).Qhov loj ntawm thrombin no ua rau ntxiv kev ua kom cov platelets thiab tsim cov fibers.Nyob rau hauv qhov kev txiav txim ntawm thrombin, fibrinogen yaj hauv plasma hloov mus rau hauv fibrin monomers;Nyob rau tib lub sijhawm, thrombin activates XIII mus rau XIIIa, ua fibrin monomers Lub cev fibrin txuas nrog ib leeg los tsim cov dej-insoluble fibrin polymers, thiab sib koom ua ke rau hauv ib lub network kom kaw cov qe ntshav, tsim cov ntshav txhaws, thiab ua kom tiav cov ntshav coagulation. txheej txheem.Qhov no thrombus nws thiaj li tsim cov pob khaus uas tiv thaiv qhov txhab thaum nws nce thiab tsim cov txheej txheem tshiab ntawm daim tawv nqaij hauv qab Platelets thiab fibrin tsuas yog qhib thaum cov hlab ntsha tawg thiab nthuav tawm, txhais tau hais tias hauv cov hlab ntsha noj qab haus huv lawv tsis tuaj yeem ua rau. clots.
Tab sis nws kuj qhia tau hais tias yog tias koj cov hlab ntsha tawg vim yog cov quav hniav, nws yuav ua rau cov platelets loj tuaj, thiab thaum kawg tsim cov thrombus ntau los thaiv cov hlab ntsha.Qhov no kuj yog cov txheej txheem pathophysiological ntawm kab mob plawv, myocardial infarction, thiab mob stroke.