CIGABA DA LIPID METABOLISM DA CIKIN SAUKI: hanzarin matsalar da bayyanar cututtuka

Canje-canje na jijiyoyin jiki na Atherosclerotic halayen kusan dukkan mutane ne da suka wuce shekaru 40, bambance-bambance suna cikin yanayin canji kawai. Haɓaka atherosclerosis yana da alaƙa da ayyukan haɓakar jigilar cholesterol zuwa bango na ɓangaren ɓangaren ɓangare na ƙananan ƙarfi mai laushi sosai da kuma aiwatar da cire ƙwaƙwalwar ƙwayar cuta daga bango na jijiyoyi ta amfani da tsoka mai yawa na lipoproteins. Idan rabo daga "low and low density lipids / high lipids lipids" an kiyaye shi azaman 3: 1, atherosclerosis baya faruwa koda da babban abun ciki (sama da 6,21 mmol / L) na ƙwayar plasma. A cikin aikin asibiti, ana amfani da coeffrol na atherogenicity:

inda CO shine yawan adadin cholesterol, SLVP shine maida hankali akan yawan kuzarin lipid cholesterol.

Wannan jigon yana da kyau a cikin jarirai, a cikin mutane masu shekaru 20-30, ƙimar da take tsakanin 2 zuwa 2.8, tsufa fiye da shekaru 30 (ba tare da alamun asibiti na atherosclerosis) ba, yana cikin kewayon 3.0-3.5, kuma a cikin mutane tare da cututtukan zuciya na zuciya ya wuce 4, yawanci ya kai 5-6 ko sama.

A halin yanzu, an yi imanin cewa ainihin a cikin ci gaba na atherosclerosis sune canje-canje mai mahimmanci a cikin tsarin da aikin ƙwayoyin jijiya na jijiyoyin bugun jini. Duk wani lalacewar endothelium (aikin toxins, hadaddun rigakafi, matsakanci mai kara kumburi, cholesterol, lipoproteins da aka inganta, da dai sauransu) yana ƙaruwa da lalacewarsa, yana haifar da shigar azzakarin monocytes a ƙarƙashin endothelium da canjinsu zuwa macrophages.

A saman macrophages akwai masu karɓa don duka biyu marasa daidaituwa da ingantattun ƙwayoyi masu ƙarancin ƙarfi. Wadannan masu karɓa ba su rage aiki yayin tarawar cholesterol a cikin macrophages. Karshen, mai tattara lipids, ya zama cikin sel mai kumburi (dauke da dumbin cholesterol mai yawa). Endothelium, an cika shi da sel mai kumburi, zai fara aiki, kuma macrophages suna haɗuwa da jini. Suna ɓoye abubuwa masu alama da yawa a cikin mahallin, gami da waɗancan nau'ikan ƙwayoyin tsoka masu santsi waɗanda ke da masu karɓa don abubuwan haɓaka. Yaduwar sel mai santsi daga tsakiyar Layer da ƙaura zuwa cikin ɓoyayyen ciki yana farawa. Abubuwan da aka tara sunadaran ƙwayoyin tsoka mai santsi waɗanda aka cika su da ƙoshin kitse mafi yawanci suna zama jigilar mahaifa.

Gyara ƙwayoyin tsoka mai santsi waɗanda suke haɗuwa da ƙwaƙwalwar ƙwaƙwalwar ƙwayar cuta, elastin da sauran abubuwan haɗin haɗin matrix na ƙwayar mahaifa na ƙwaƙwalwar ƙwaƙwalwar mahaifa. A fibrous plaque siffofin. A nan gaba, lalata atheromatous na plaques, haɓakar lu'ulu'u mai narkewa da gwal mai narkewa, wanda ke damun nama da ke kewaye da shi, yana haifar da taƙaita lalacewar tasoshin da ƙwayar jini, wanda zai haifar da bugun zuciya da bugun jini, mai yiwuwa ne. A farkon matakan atherosclerosis, rikice-rikice na gida da na tsari na cholesterol da lipoproteins - dyslipo-proteininemia - suna faruwa. A mafi yawancin lokuta, abun da ke cikin barbashi na atherogenic a cikin jini, babban bangaren wanda shine sinadarin cholesterol, yana haɓaka a matsayin furotin - apoprotein B. Wannan yana haifar da ƙimar iskar shaƙa na ƙananan wadataccen lipoproteins, tarin wadataccen ƙarancin wadataccen lipoproteins da kuma samar da filayen atherosclerotic. Tare da ƙananan taro na lipoproteins mai yawa na jini a cikin jini (a cikin 30% na lokuta), atherosclerosis na hanzari na faruwa ko da ƙananan matakin jimlar cholesterol (ƙasa da 5.18 mmol / l).

Phospholipids da polyunsaturated mai mai sun mallaki kaddarorin antiatherogenic. Sun iyakance yawan shan abinci na cholesterol a cikin karamin hanji, suna ta da sinadarin bile acid a hanta, da hana haduwa da sinadarai na karancin sinadarin ta hanyar hepatocytes, rage maida hankali kan rashin wadataccen lipoproteinon a cikin jini na jini, hana sinadarin roba na hadin gwiwa da kuma motsawar hadin gwiwar, hada karfi da jijiyoyin salula tare da hadin gwiwar hadahadar, da kuma hada karfi da hadin.

Cholesterol, triglycerides da cikakken mai mai sunadarai sun mallaki kaddarorin atherogenic. Haɗarin ƙwayoyin atherogenic lipoproteins a cikin jini na iya ƙaruwa saboda raguwa a cikin ƙimar kawar dasu daga jini zuwa hanta, haɓaka ƙima da aiki, da kuma keta metabolism na plasma lipoprotein, gami da haɓakar lipoproteins na rashin daidaituwa.

Rushewar ƙwayar cholesterol metabolism na faruwa a ƙarƙashin halaye masu zuwa: in babu ƙarancin mai karɓar ƙwayoyin lipoprotein mai yawa akan farfajiyar tantanin halitta. Musamman: endocytosis ba zai yiwu ba, a sakamakon: matakin wadannan lipoproteins a cikin plasma yana ƙaruwa (hereditary hypercholesterolemia shine nau'in II hyperlipoproteinemia) kuma rashin ingantaccen ƙwayar cuta wanda aka inganta shine: ƙwayoyin reticuloendothelial tsarin kama lipoproteins, wanda ke haifar da tarin ƙwayoyin cuta a cikin,

karuwa a cikin kusancin lipoproteins ga membrane saboda yawan cholesterol na matsanancin ƙwayar lipoproteins mai ƙarancin ƙarfi (nau'in III hyperlipoproteinemia): tasirin lalata kai tsaye da yawaitar ƙwayar cholesterol akan ƙwayar jijiya mai sanyin ƙarewa. A cikin lalacewa, adon farantin farashi da kuma sakin abubuwan ci gaba yana faruwa. Increasearuwar haɓakawa na haɓaka tsarin ƙwayoyin sel na lipoprotein, abubuwan da ke faruwa na microdamage, ƙaura daga leukocytes daga jijiyoyin jijiyoyin bugun gini a bango na jirgin ruwa, samuwar ƙwayar atherosclerotic a nan,

damuwa, wanda ke haɓaka ci gaban atherosclerosis. Anara yawan haɗuwa a cikin adrenaline da angiotensin a cikin jini yana haifar da raguwa a cikin ƙwayoyin endothelial, haɓaka gibba tsakanin su da tarin ƙwayoyin lipoproteins masu ƙarancin ƙarfi da ƙananan ƙarfi a cikin farantin medial,

yawan wadataccen lipoproteins mai yawa a cikin jini na jini (matakin su a cikin plasma yayi daidai da ajiyar cholesterol). Poarancin lipoproteins mai yawa na iya haifar da haifar da hadaddun ƙwayoyin rosette, tsarin rigakafi yana motsawa kuma bango na jijiyoyin jiki sun lalace,

low abun ciki na yawan yawa na lipoproteins, wanda, dangane da yanayin fibroblasts, endothelial da santsi ƙwayoyin tsoka, kama cholesterol. Kwalagin cholesterol yana farfadowa kuma yana hawa a matsayin wani ɓangare na yawan wadataccen lipoproteins zuwa hanta. Wadannan nau'ikan lipoproteins suna yin gasa ga masu karɓar ƙwaƙwalwar ƙwayoyi masu ƙarancin ƙarfi da ƙura mai yawa, suna hana cholesterol shiga sel. Suna samun damar kawar da cholesterol ta hanyar ruwa mai gwargwadon hankali game da gradient, kuma suna bayar da wuce haddi mai narkewar sinadarai da cholesterol ta hanyar masu karba zuwa ga mai kitse (depot),

take hakkin matakai na cholesterol esterification a cikin yawa yawa na lipoproteins da sufuri tsakanin mutum azuzuwan na lipoproteins. Wannan yana rage karfin babban lipoproteins mai yawa don cire cholesterol daga kyallen takarda. A cikin marasa lafiya da cututtukan ƙwayar cuta na atherosclerosis, ƙwayoyin lipoproteins masu yawa suna wadatar cikin cholesterol, kuma ƙarancin lipoproteins yana wadatar cikin esters cholesterol,

lahani na ƙwayoyin cuta na apolipoproteins da masu karɓar su, lipoprotein da enzymes metabolism na jini (ƙirar gado na saurin atherosclerosis). A cikin hanta, ragin kira da catabolism na lipoproteins da ke kewaya cikin jini yana canzawa. A cikin iyalai daban-daban, an lura da lahanin kwayoyin da yawa waɗanda ke haifar da rashin daidaituwa na cholesterol ko dai a cikin sel ko kuma cikin lipoproteins da ke yawo cikin jini.

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Littattafai

1. Libov I. A., Cherkesova S. V., Roitman A. P. Harkokin zamani na dyslipoproteinemia da hanyoyin da suka dace da maganin su // Labaran Likita na Moscow. A'a 3. 1998. S. 34-37.
2. Thompson G. R. Jagora zuwa hyperlipidemia. MSD, 1990.
3. Spector A. V., Vasiliev E. E. Cardiology: makullin cutar. Vidar, 1996, p. 295-309.
4. Berk B. C., Weintraub W. S., Alexander R. W. Ingantaccen sinadarin C-mai kunnawa cikin “kunnawa” cutar sankarar jijiya // Am. J. Cardiol. 1990: 98: 2219-2222.
5. Haverkate F., Thompson S. G., Pyke S. D. M. et al, don Europeanungiyar Tattaunawa ta Turai akan romwararrakin Hankali da nakasa Angina Pectoris Nazarin. Prodaction na C-mai kunnawa mai gina jiki da haɗarin haɗari na jijiyoyi a cikin tsayayyiyar angina // Lancet. 1997, 349: 462-466.

Damuwa ta endothelial

Nazarin zamani sunyi imani da cewa matakin farko a cikin bunkasa atherosclerosis shine lalacewar farfajiya ta ciki. Akwai shaidu da yawa kan wannan ka'ida:

• Na farko, alluna na farko ana koyaushe a wuraren da ake yin jigilar kayayyaki. A lokacin rabuwa da babban jirgin ruwa, an kirkiro wani yanki mai rikitarwa, saboda haka, haɗarin lalacewar rufin ciki na jirgin a wannan wurin ya kasance koyaushe mafi girma.
• Abu na biyu, an daɗe da sanin cewa shan taba sigari yana da rawa wajen haɓaka cutar. Hayaƙin sigari kuma yana mummunan tasiri ga aiki na sel na endothelial, saboda saboda karuwa da adadin ƙwayoyin carbon monoxide wanda ke yaduwa cikin jini, an lura da hypoxia cell.
• Abu na uku, hauhawar jini yana kara nauyin jijiyar a tasoshin kuma shine mawuyacin hali wanda ke kara haɗarin haɓakar atherosclerosis.

Game da cholesterol

A yau akwai mutane kalilan waɗanda ba za su ji cewa rawar da ke cikin cholesterol a cikin ci gaban cututtukan ƙwayoyin cuta ba na da matukar muhimmanci. Amma ba kowa bane yasan menene wannan kayan. A halin yanzu, wannan shine ɗayan wakilan aji na sterols, wanda ke taka muhimmiyar rawa yayin gudanar da ayyukan ƙirar halitta na jiki. Babban ayyukan cholesterol:

• halittar bile acid
• kira na bitamin D3,
• samar da hormones na jima'i da kwayoyin adrenal.

Dangane da abincin, kimanin 300-500 MG na cholesterol yana shiga jikin mutum a kullun. A cikin samfuran, wannan lipid na iya kasancewa cikin yanayin kyauta ko ɗaure.

Amma ko da a ƙarshen maganar, tsarkewa da sakin cholesterol kyauta zai faru a cikin ƙananan hanji. A cikin hanji, ana amfani da cholesterol, ana amfani dashi don metabolic da sauran hanyoyin nazarin halittu.

Rarraba wannan lipid a cikin jiki ba shi da kyau. Yawancin dukkanin ƙwayar cholesterol ana ɗauka a cikin cortex na glandon adrenal, kwakwalwa, ƙwayar jijiya. Mafi sauƙin duka sune lipids a cikin nama na kashin haɗin kai da kasusuwa.

A ka’idar, ana iya aiwatar da sinadarin cholesterol a kusan kowace tantanin halitta na jiki. Koyaya, mafi yawanci ana samar da wannan kayan a cikin hanta kuma (a cikin adadi kaɗan) a cikin ƙananan hanji. A ƙarƙashin rinjayar wasu dalilai, haɓakar ƙwayar cholesterol yana ƙaruwa. Wadannan abubuwan sun hada da:

• bayyanar hasken rana
• rashin daidaituwa na hormonal tare da karuwa a cikin adadin kwayoyin hormones, insulin.

Shawara! Amma tare da haɓakar samar da glucocorticosteroids (kwayoyin homon da ke haifar da glandon adrenal) da kuma matsananciyar ƙarfi, ƙwaƙwalwar cholesterol, akasin haka, yana raguwa.

An gano cewa sterol a cikin jini na jini ba a cikin tsabta, amma a cikin nau'i na lipoproteins (hadaddun ƙwayoyin cholesterol tare da sunadarai). Lipoproteins sunzo cikin nau'ikan guda uku:

• ragu mai yawa (adadin su bai wuce 10% ba),
• low yawa (wannan shine mafi yawan nau'ikan irin wannan lipoproteins a cikin plasma kimanin 65-70%),
• babban yawa.

Ya danganta da rabo daga nau'in lipoprotein, an ƙaddara haɗarin haɓakar atherosclerosis. A saboda wannan, ana aiwatar da bincike na musamman tare da ƙudurin ɓarna, sannan a ƙididdige coefficient ta amfani da tsari na musamman.

Shawara! Amintaccen aminci dangane da haɓakar atherosclerosis shine rabo daga nau'in ƙwayar lipoprotein da aka lura da yara ƙanana, wanda suke dasu shine haɗin kai. A cikin matasa (kusan shekaru 20), madaidaicin rabo shine mai nuna alama daga 2 zuwa 3. A cikin mutane sama da 30, mahaifa bai kamata ya wuce 3.5 ba (don cututtukan zuciya, zai iya kai 6).

Tsarin aikin plaque

A cikin samar da plaque, matakai uku sun bambanta:

• lipoidosis: samuwar tabo mara nauyi ko tsiri a jikin bangon jirgin ruwa,
• liposclerosis: bayyanuwar fibrous nama,
• samuwar ƙwayoyin cuta mai rikitarwa, calcification.

Gefen lipid karamin abu ne (diamita ba ya wuce milimita 1.5) wanda aka kafa a saman jijiyarsa. Kwayoyin Foamy sune suka fi yawaita a cikin wannan halittar rawaya, sun haɗa da T-lymphocytes da fats. Bugu da kari, ƙwayoyin tsoka mai santsi da macrophages suna nan a cikin tsarin halittar.

Kamar yadda girman lips spots ke ƙaruwa, sai suka haɗasu, sakamakon haifar da tsiri tsararren yanki ɗaya. Dambatai da ratsi suna buɗewa a rukunin wuraren lalacewa ta ainihi.

Shawara! Wani takaddama game da lalacewar farjin ciki da samuwar ƙurar lipid an sanya su a cikin abubuwanda basu dace ba. Musamman ma, shan sigari, chlamydial ko kamuwa da kwayar cuta, hauhawar jini, da sauransu.

A cikin kanta, samuwar tabo baya haifar da lalacewar jirgin. Haka kuma, irin wadannan aibobi suna farawa tun suna yara. An yi imani cewa lokacin da shekara 25, halittun lipid na iya zama har zuwa rabin saman ciki na aorta. A cikin jijiyoyin halittar ƙwaƙwalwa waɗanda ke ciyar da kwakwalwa, irin waɗannan abubuwan suna bayyana ne kimanin shekaru 40.

Liposclerosis

Mataki na biyu a cikin samuwar kwayoyin halitta (plaque) shine haɓakar ƙwayar fibrous. A cikin yankin da aka ƙirƙiri (tsiri), ƙwayoyin matasa suna farawa a hankali, wanda ke haifar da haɓakar nama mai haɗuwa.

Lokacin da ya balaga, toshiyawar katanga tana faruwa kuma siffofin jaka - wani juzu'i wanda yake fitowa zuwa gindin jirgin. Wannan yana haifar da cikas ga kwararar jini. A farkon matakin farko na samuwar atherosclerotic, ƙwaƙwalwar ƙwayar cuta tana da ƙwaƙƙwaran ƙwayar lipid.

A wannan yanayin, tsarin haɗin nama yana da bakin ciki. Ana kiran wannan samu "rawaya", dan kadan yana shafar kwararar jini. Tunda kwatankwacin ƙwayar haɗin haɗi yana da bakin ciki, ya lalace cikin sauƙi.

A ƙarshen matakai na ci gaba, samuwar da aka kafa tana da tsarin mai aiki na tsoka mai haɗuwa. Ana kiranta da "farin plaque" kuma yana da mummunar tasiri a cikin hemodynamics (saurin jini).

Kirkirar kafa

Wannan matakin ci gaban cutar ana nuna shi ta hanyar haɓaka ƙimar ƙwayar tsoka a cikin ƙwaƙwalwar da aka riga aka kafa. Wannan yana haifar da halakar kasusuwan fibrous da faruwar cutar basur.

Lokacin da aka lalata tsarin ƙwaƙwalwar ƙwayar cuta, ulceration na faruwa, wanda shine babban dalilin ƙirƙirar suturar jini. A matakin karshe, ana ganin tara sinadarin alli a cikin kasusuwa na plaque, wanda ya kai ga harhadawa da kuma girman girman plaque.

Babban abin da ya haifar da samuwar atherosclerotic mai rikitarwa shine fitowar jini a bangon jirgin ruwa. Tare da rabuwa da suturar jini, zai iya rufe jirgin, yana hana jigilar jini sosai.

Shawara! A wannan mataki na haɓakar atherosclerosis ne marasa lafiya ke fuskantar rikice-rikice - haɓakar bugun zuciya na ischemic (tare da lalacewar tasoshin kwakwalwa), bugun zuciya (tare da haɓakar atherosclerosis na jijiya).

Tashin hankali

Tsarin da ke sama don ƙirƙirar plaque yana ba mu damar fahimtar sakamakon ci gaban atherosclerosis. Wannan shi ne:

• canje-canje hemodynamic sakamakon raguwar ƙwayar jijiyoyin bugun gini,
• ulceration na fibrous kwantena lokacin da ta lalata, da samuwar jini clots,
• ajiya na lemun tsami a cikin sallar nama, wanda hakan ke kara girmanta.

Iri Plaques

Tare da atherosclerosis, filaye na iya zama a tsaye kuma ba. Wannan kayan yana dogara da siffar, girma da kuma tsari. Fibrous nama ya fi rinjaye a cikin plaic sitirique, kuma lipid shine yake rinjaya a cikin mummunan yanayin. Tsarin tsayayye na tsaye yana ƙaruwa a hankali, saboda haka yanayin mai haƙuri ba ya canzawa shekaru. Karatun da ba su da tsayayyun suna da babban tsakiya da ƙumshi mai buɗe ido.

Irin wadannan lamuran cikin sauki sun katse kuma ulcerate, wanda hakan ke haifar da zubar jini. Kasancewar ire-iren filayen da ba su da tabbas shine ke taka rawa wajen haɓaka mummunar rikicewar cutar atherosclerosis.

Don haka, pathogenesis na atherosclerosis tsari ne mai matukar wahala. Wani rawar a ci gaban cutar ana wasa ba kawai ta abubuwan ciki ba, har ma da halaye marasa kyau na masu haƙuri da kansa. Yana ba da isasshen ciwan cututtukan ƙwayar cuta ga abinci mai ɗima, shan sigari, rashin motsa jiki, haka kuma cututtukan kamuwa da cuta da rushewar jijiyoyin jiki. Don hana haɓakar cutar, yana da daraja a lokaci-lokaci a lura da matakin ƙwayar cholesterol a cikin jini.