Vol. 5 No. 5 (2026), Articles
Vol. 5 No. 5 (2026)

ANEMIYA: RIVOJLANISH MEXANIZMLARI VA ORGANIZMDAGI FUNKSIONAL O‘ZGARISHLAR

Articles
Published 2026-09-22
Jo‘raqulova Jasmina Lazizjonovna
Samarqand davlat tibbiyot universiteti, Davolash ishi fakultetining 3-bosqich talabasi
Azimkulova Sabrina Karimovna
Samarqand davlat tibbiyot universiteti, Davolash ishi fakultetining 3-bosqich talabasi
Saidova Firuza Salomovna
Samarqand davlat tibbiyot universiteti, Patologik fiziologiya kafedrasi assistenti Samarqand, O‘zbekiston
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Keywords

anemiya, gemoglobin, eritrotsit, eritropoez, temir tanqisligi, gepcidin, ferroportin, eritropoetin, to‘qima gipoksiyasi, gemoliz, qon yo‘qotilishi, vitamin B12, folat, kompensator mexanizmlar, kislorod transporti.

Abstract

Anemiya — qonda gemoglobin miqdori va ayrim holatlarda eritrotsitlar soni yoki ularning funksional xususiyatlari organizmning fiziologik ehtiyojlarini ta’minlash darajasidan kamayishi bilan tavsiflanadigan ko‘p omilli gematologik sindromdir. Ushbu holatning klinik ahamiyati faqat gemoglobin konsentratsiyasining pasayishi bilan cheklanmay, to‘qimalarning kislorod bilan ta’minlanishi, hujayraviy energiya almashinuvi, yurak-qon tomir tizimi kompensator reaksiyalari, markaziy asab tizimi faoliyati va jismoniy ish qobiliyatining o‘zgarishi bilan bog‘liq. Anemiyaning rivojlanishida uchta asosiy mexanizm — eritrotsitlar ishlab chiqarilishining kamayishi yoki samarasiz eritropoez, qon yo‘qotilishi hamda eritrotsitlarning tezlashtirilgan parchalanishi — yetakchi o‘rin tutadi. Temir tanqisligi, folat va vitamin B12 yetishmovchiligi, surunkali yallig‘lanish, buyrak kasalliklari, irsiy gemoglobinopatiyalar va suyak ko‘migi patologiyalari anemiyaning turli patogenetik shakllarini yuzaga keltiradi. Ayniqsa, temir almashinuvida gepcidin–ferroportin tizimining buzilishi zamonaviy patofiziologik qarashlarda muhim o‘rin egallaydi. Yallig‘lanish sharoitida interleykin-6 ta’sirida gepcidin sintezining kuchayishi natijasida temirning ichakdan so‘rilishi va makrofaglardan chiqarilishi cheklanib, eritropoez uchun mavjud temir miqdori kamayadi. Gemoglobin pasayishiga javoban to‘qimalarda gipoksiya rivojlanadi, eritropoetin sekretsiyasi kuchayadi, yurak chiqishi ortadi va periferik qon tomir qarshiligi pasayadi. Uzoq davom etuvchi yoki og‘ir anemiyada kompensator mexanizmlar yetarli bo‘lmay qolib, yurak, miya, mushaklar va boshqa yuqori metabolik ehtiyojga ega organlarning funksional holati yomonlashadi. Maqolada anemiyaning asosiy rivojlanish mexanizmlari, temir va eritropoez metabolizmi, gipoksiyaning hujayraviy oqibatlari hamda yurak-qon tomir, asab, immun va mushak tizimlaridagi funksional o‘zgarishlar zamonaviy ilmiy ma’lumotlar asosida tahlil qilinadi.                                                        

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