Izigaba zokukhula kwe-atherossteotic plaque

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I-Atherossteosis yisifo esingapheli esingesikhathi eside senhliziyo nemikhumbi emikhulu, ebonakala ngomonakalo odongeni olungejwayelekile kanye nokubekwa kwezixuku zabantu abaphakathi kwaso ngokuvalwa okwengeziwe kwe-lumen nokukhula kwezinkinga ezivela ebuchosheni, enhliziyweni, izinso, emikhawulweni ephansi.

Lesi sifo uqobo senzeka ikakhulukazi kwabaluphele, yize manje kufakwa i-cholesterol encane ezindongeni zemithambo yegazi ngisho nasezinganeni nasebasha.

Uma kungekho ukwelashwa okufanele, i-atherosulinosis yanoma yikuphi ukwenziwa kwasendlini kuholela ku-ischemia ne-hypoxia yezitho nezinhlelo, ushintsho lwe-trophic necrotic esikhunjeni nezicubu ezithambile.

Izimbangela zalezi zifo zingahlukaniswa ngamaqembu amabili - ziyaguquguquka futhi zingashintshi.

Esokuqala sifaka izizathu ezingathonywa ushintsho lwendlela yokuphila nemithi, nazi ezinye zazo:

  1. Indlela yokuphila yokuhlala phansi nomsebenzi wokuhlala phansi.
  2. Ukwephulwa kokudla okunengqondo - ukudla okungajwayelekile okunamafutha amaningi, ukudla okuthosiwe okune-cholesterol.
  3. Imikhuba emibi - ukuphuza ngokweqile, ukubhema.
  4. Ukucindezelwa ngokweqile nangokomqondo.
  5. I-Arterial hypertension nezinkomba zokucindezela okungaphezulu kuka-140 ngamamilimitha angama-90 we-mercury ekuphumuleni ngezilinganiso eziningana.
  6. Isifo sikashukela i-mellitus enokulawulwa okungekuhle kwe-glycemic kanye nezimo ezivame ketoacidotic.
  7. I-Hypercholesterolemia - ukukhuphuka kwenani eliphelele le-cholesterol (ngaphezu kwe-5.5 mmol / l), i-dyslipidemia - ukwephulwa kwesilinganiso esiphakathi kwama-lipotroteins amafrakhthi ahlukile (ukukhuphuka kwe-lipoproteins ephansi kwabantu, i-triglycerides, ukwehla kwezinga eliphakeme le-lipoprotein).
  8. Ukukhuluphala kwesisu okhalweni kwabesilisa kungaphezu kuka-102 cm, kuthi kwabesifazane kube ngaphezu kwama-88 cm.

Izici ezingeke zithonywe zibandakanya umlando womndeni onesisindo (i-hypercholesterolemia kanye ne-dyslipidemia, ukushona kwezihlobo zezifo zenhliziyo kuze kube seminyakeni engama-50), ubudala (emadodeni, isifo sokuqina kwezitho zofuzo sikhula ngemuva kweminyaka engama-45, kwabesifazane - emva kweminyaka engama-55), ubulili ( kuvame ukwanda emadodeni, njengoba ama-hormone ocansi abesifazane eba nomphumela wokuvikela emithanjeni yegazi).

Izindlela ze-pathogenetic zokwakheka kwe-plaque

Inhlanganisela ye-hyperlipidemia kanye nokulimazeka kwemithambo kuholela ekwakhekeni kwama-cholesterol ashintshiwe anamaphrotheni, nokudluliselwa kwawo ngaphansi komthamo wemithambo yegazi.

AmaLipid athunjwa ngama-macrophage, ajika abe ngamaseli ama-xanthomatous, akhula ngobukhulu ngosayizi.

Lawa maseli akhiqiza izinto zokukhula nokufuduka kwamangqamuzana amhlophe egazi namapuleti. Kukhona ukunamathela nokuhlanganiswa kwamaplathile, ukwabiwa kwezinto ezi-thrombotic.

I-plaque ikhula ngokushesha, ivimba i-lumen yomkhumbi ngenxa yokwakheka kohlaka lwezicubu ezithintekayo kanye nesondo.

Ngaphezu kwalokho, ngaphansi kwethonya lezinto zokukhula, kwakhiwa ama-capillaries ukuhanjiswa kwegazi ezinxekeni ezigcwele kakhulu. Isigaba sokugcina sentuthuko yi-necrosis enkabeni ye-plaque, i-sclerosis yayo nokubala.

Ushintsho lwe-morphological ngokuvela kwe-atherosclerosis lubonakala ngokuqubuka kwesifo, kusuka kokuncane kuya kokukhulu.

Isigaba sokuqala sokuthuthukiswa kwe-atherossteosis yi-dolipid, ayinazinguquko ezithile eziqondile. Kubonakala ngokukhula kokuqina kodonga lwe-vascular, ukwephula ubuqotho bayo - okugxilwe noma okuphelele, ukujuluka kwengxenye yegazi kwegazi esikhaleni se-subendothelial.

Ukuvuvukala kwe-Mucoid, ukunqwabelana kwe-fibrin ne-fibrinogen, amanye amaprotheni e-plasma, i-lipoproteins ephansi ne-cholesterol ayakhiwa.

Ukuthola lesi sigaba, kwanele ukusebenzisa ukuhlolwa komlando kokulungiswa kodonga lwamasipha futhi usebenzise udayi oluthile - i-thionine eluhlaza okwesibhakabhaka, lapho kubhekwe khona metachromasia futhi izindawo ezithintekile zigcwele ububende.

Isigaba sesibili - i-lipoidosis - ibonakala ngokufakwa kwe-cholesterol kanye ne-lipoprotein ngesimo semichilo yamafutha nezindawo eziphuzi ezingavuki ngaphezu kwezinga le-endothelium.

Izinguquko ezinjalo ekwakhekeni kwemithambo yegazi zingabonakala ngisho nasezinganeni nasentsheni, futhi azithuthuki ngokuzayo. Ama-lipid afakwa ngaphansi kwe-intima kuma-macrophage, noma amaseli we-foamy, namaseli wemisipha abushelelezi wemithambo yegazi. Kungenzeka futhi ukuthola lesi sigaba ngokomlando, ukubekwa kuqhutshwa yiSudan 4, 5, i-O ebomvu ebomvu.

Njengoba unikezwe ukuthi i-atherosclerosis yisifo esenzeka kancane kancane, lesi sigaba singakwazi ukuhlala isikhathi eside futhi singabangeli izimpawu ezibalulekile zomtholampilo.

Imikhumbi emikhulu, njenge-aorta, imithambo yegazi, imithambo yobuchopho, izinso nesibindi, ibhekana nezinguquko zokuqala ze-pathological.

Ukwenziwa kwendawo kwenqubo kuncike ezicini ze-hemodynamics ezindaweni zokufiphala kwemikhumbi, njengokufakelwa kwe-aortic emithanjeni ye-iliac.

Isigaba sesithathu sokuthuthuka kwe-atherosulinotic plaque yi-liposulinosis - ukwakheka kwemicu ye-elastic ne-collagen ku-endothelium, ukwanda kwama-fibroblasts, ukwahlukaniswa kwabo kwezici zokukhula kanye nokwakhiwa kwezicubu ezihlangene.

Ukuthuthukiswa okwengeziwe kwe-pathophysiological ye-atherosulinotic plaque

Ngokwe-morphologic, izigodi zikhushulwe ngaphezu kwezinga le-intima, ingaphezulu lomkhumbi liba namandla kakhulu, libe namandla kakhulu. Ama-plaque anjalo anganciphisa ukukhanya kwe-artery futhi aholele ku-ischemia yezitho nezinhlelo, ngokuya ngendawo, kuholele ezinkingeni ezifana nokushaywa, ukuhlaselwa kwe-ischemic kwesikhashana, ukufakwa kwe-myocardial, ukucekelwa phansi kwemikhumbi engxenyeni engezansi.

Isigaba esilandelayo sokuqhubekisela phambili kwezifo ngokweqile, sibonisa ukubola kwengxenye ephakathi ye-plaque, ukuhlukaniswa kwayo.

Amakristali e-cholesterol, amanoni acid, izingcezwana zemicu ye-collagen, amangqamuzana e-xanthoma kanye ne-T kanye ne-B lymphocyte atholakala kulesisindo esikhohlisayo. Lesi sigaqa sihlukaniswe emgodini womkhumbi yi-capsule ye-plaque, equkethe izicubu ezithintekayo.

Isigaba esilandelayo ulceration, sibonisa ngokudabukisa kolwelwesi lwesikhumba, kanye nokukhishwa kokuqukethwe kwalo kungena egazini, ukwakheka kwesilonda se-atheromatous. Ubungozi balesi sigaba ukungazethembi kwama-plaque anjalo, amathuba okuthuthukisa izilonda ze-ischemic kanye ne-thromboembolic ezinzima zezitho nezicubu.

Esakhiweni sokukhiqizwa kwesilonda, i-aneurysm ingahle ikhule - ukubonakala kodonga lwe-vascular, kanye nokuqhuma. Isigaba sokugcina senqubo ye-pathological ukufakwa kwethotho, okungukuthi, ukubekwa kukasawoti we-calcium kuyo.

Ngenxa yalokhu, indawo ethintekile yomkhumbi ihlanganiswe, i-patency ikhubazekile noma ayikho ngokuphelele.

Ukubonakaliswa kokuphazamiseka kwesakhiwo semithambo yegazi kungaba yi-polymorphic, okungukuthi, izingwegwe ezivuthiwe ezinezibalo namabala anamafutha zingabonakala ngasikhathi sinye.

Amapherishi e-atherossteotic ngokwawo angahlanganiswa yinkimbinkimbi ngokumpompela, ukushwabana kwegazi, nokuqhuma kwe-capsule.

Ngokomtholampilo, ama-plagi atherosselotic ahlukaniswe phakathi azinza futhi angaqina.

Kumaphetshana wohlobo lokuqala, isembozo sezicubu esisebenzayo sichazwa kahle, sinobukhulu, asithandi ukugqekeza nokukhipha okuqukethwe, futhi ngenxa yalokho asiholeli ezinkingeni ezinkulu ze-atherosclerosis. Lama-plaque abonakala ngenxa yezinkinga ezingamahlalakhona - i-ischemia engamahlalakhona yezitho noma izicubu, i-sclerosis yawo, i-dystrophy noma i-atrophy, i-angina pectoris ezinzile, ukungaguli kahle kwemithambo yegazi.

Ngohlobo lwesibili, ithayi livame ukukhala izinyembezi futhi kuphume i-nucleus yayo, izinkinga - ukuswelakala kwemithambo ye-acute kanye ne-ischemia yezitho zomzimba, i-angina engazinzile ne-acute coronary syndrome, ukungasebenzi kahle kobuchopho, i-gangrene yemikhawulo.

Okuyisisekelo ukwelashwa kwe-atherossteosis nokuvinjwa kwayo

Ukwelashwa kwama-plagi asezingeni le-atherosselotic avele atholakala emtholampilo futhi ngokunengqondo anendlela ehlanganisiwe, futhi kufaka phakathi ukulungiswa okuphoqelekile kwezinto ezingashintshiwe.

Le yinkimbinkimbi ifaka - ukulawulwa kokudla okunempilo, ukusetshenziswa kwemifino entsha nezithelo, okusanhlamvu, imikhiqizo yobisi kanye nokusungulwa kombuso wokuphuza.

Kubalulekile futhi ukuyeka ngokuphelele ukubhema, ukuphuza utshwala ngokulinganisela, ukwenza umsebenzi owanele womzimba (ukuhamba, ukugijima, i-aerobics).

Ukwelashwa okuyinhloko umuthi, lokhu kufaka phakathi izidakamizwa ezinesenzo sokwakheka kwemithi okuhloswe ngaso ukwehlisa i-cholesterol nezingxenyana zayo:

  • ama-statins (Atorvastatin, Lovastatin, Simvastatin);
  • imicu;
  • i-probucol;
  • i-nicotinic acid.

Kusetshenzisiwe futhi:

  1. ama-antiplatelet agents (Acetylsalicylic acid, Magnikor);
  2. ama-anticoagulants (heparin);
  3. izidakamizwa ze-vasoactive (Cilostazolum);
  4. ama-antispasmodics (Drotaverinum, Papaverineum);
  5. ukulungiswa kwamavithamini.

Ezimweni ezinzima zesifo, ngokushayisana okukhulu, izilonda eziyinqaba yezicubu ezithambile kanye nesigaxa se-gangrene, kusetshenziswa ukwelashwa okuhlinzwa - kusuka ekusebenzeni kokwehla kobuhlungu ukubuyisela ukujikeleza kwegazi (isiqubu, ukuhlinzwa okudlula, i-balloon angioplasty), ukususwa kwemithambo ethintekile (i-endarterectomy ne-prosthetics yomkhumbi eminye) ngaphambi kokungenelela ngenhloso ukususwa kwezicubu ezingasebenzi (i-necrectomy, ukunqunywa kwengalo).

Ukuvimbela ukwanda kwe-cholesterol nokukhula kwe-atherosclerosis kuyinto eyinhloko - kubantu abanempilo, futhi okwesibili - onesifo esivele satholakala.

Izinyathelo eziyinhloko zokuvimbela okuyinhloko ukudla okunempilo, ukusebenza ngokomzimba okulinganiselayo, ukuyeka imikhuba emibi, ukuqapha ingcindezi kanye namazinga e-cholesterol, ukuhlolwa okujwayelekile kwezokwelapha ngudokotela ojwayelekile.

Ukuze uvimbele okwesibili, kuyadingeka ukuthi uqale ngokuphathwa kwezifo ezihlangene, wehlise umfutho wegazi, uthathe ama-statin nama-antiplatelet agents, ukuxilongwa okufika ngesikhathi nokwelashwa kwezinkinga.

I-etiology ye-atherosulinosis ichazwa kuvidiyo kule ngxenye.

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