Tasnudert n tnefsit n sskeṛ tettawi ɣer tezrawt n yisenfaren n tfizitologit ur nqeddec ara i yettawin ɣer unerni n sskeṛ.
Aṭṭan n sskeṛ d agraw n waṭṭanen imutayen yettwasken s yiswiren n sskeṛ (glukose) n yidammen yuεren i d-yettasen seg tuccḍiwin deg tuffɣa n insulin, deg tigawt n insulin neɣ deg sin.
Tasnudert n tnefsit n waṭṭan n sskeṛ tettawi-d assaɣ yemgaraden n yimgan, n twennaḍt d yimgan n tudert i yettekkan deg usnerni n waṭṭan.
Deg waṭṭan n sskeṛ n ṣṣenf 1, tafizitulujit n waṭṭan tettawi-d asenger amsellum n yiɣsan beta i d-yettgen tisent deg tεebbuḍt, d ayen i d-yettawin ɣer lexṣas deg usuffeɣ n tisent.
Ayagi yettawi ɣer urmir n usefrek n tneqqiḍin n sskeṛ deg idammen, yettawin ɣer hyperglycemia (askeṛ deg idammen yuli).
Deg sskeṛ n ṣṣenf wis 2, tafizitulujit n tnuḍin d tin yemgaraden ugar yerna tettawi-d deg-s ama d tuɣdaḍt n insulin ama d tuffɣa n insulin ur nqeddec ara.
Anmireg n insulin yettili-d mi ur d-ttarraḍent ara tsilunin n tfekka akken ilaq i insulin, ayen yettawin ɣer urmir n useqdec n glucose i lmend n trisiti.
Ayagi yettaǧǧa aburɣes ad d-yefk ugar n insulin akken ad yeεreḍ ad yeɣleb tuṭṭfa, maca s teɣzi n wakud, aburɣes yezmer ur yezmir ara ad yeddu d wayen i d-yettwaḥwaǧ, dɣa d ayen i d-yettawin ɣer usneqseq deg usuffeɣ n insulin.
Aṭṭan n sskeṛ n tadist, i d-yettilin deg tallit n tadist, yettmagga-d s ubeddel n wurman i yettawin ɣer tuṭṭfa n insulin.
Tasekkurt tessufuɣ-d ihurmunen izemren ad ḥebsen tigawt n tisent, ayen yettawin ɣer usnerni n tfesniwin n sskeṛ deg yidammen.
Tasnudert n tnefsit n waṭṭan n sskeṛ tettawi-d daɣen asiweḍ n twuɣa, am usexṣer n yizerfan n yidammen, n yiẓuran d izerfan, i izemren ad d-yawi uguren n tezmert imeqqranen am aṭṭanen n wul, n tnefsit, n tgeẓẓal d lexṣas n tmuɣli.
Asefhem n tfizitulujit n waṭṭan n ssker d ayen yesɛan azal meqqren i usnerni n yisufar n udawi d tsetratijit n uḥezzeb i waṭṭan-a azuran.
Biochemistry and pathophysiology of diabetes. Proceedings of conference on pathophysiology and treatment of diabetes mellitus. 1990. Mol Cell Biochem. 1992, 109 (2): 97-204.
Surampudi PN, John-Kalarickal J, Fonseca VA: Emerging concepts in the pathophysiology of type 2 diabetes mellitus. Mt Sinai J Med. 2009, 76 (3): 216-26.
Johnson D: Selected pathophysiology of diabetes. Semin Perioper Nurs. 1998, 7 (3): 164-78.
Hirsch IB: The changing faces of diabetes. Prim Care. 2003, 30 (3): 499-510.
Guthrie RA, Guthrie DW: Pathophysiology of diabetes mellitus. Crit Care Nurs Q. , 27 (2): 113-25.
Felig P: Pathophysiology of diabetes mellitus. Med Clin North Am. 1971, 55 (4): 821-34.
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['akked (6) azmul n tfekka neɣ n tuqqna tagensit n bab n yizerfan neɣ n umdan yettwafernen ad yexdem s yisem n bab n yizerfan. ']
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['Assaɣ']
['Ttxil-k azen-aɣ-d imayl ma tesεiḍ asteqsi / asumer.']
What is pathophysiology of diabetes?
Pathophysiology of diabetes refers to the study of the disordered physiological processes that lead to the development of diabetes mellitus.
Diabetes mellitus is a group of metabolic diseases characterized by high blood sugar (glucose) levels that result from defects in insulin secretion, insulin action, or both.
The pathophysiology of diabetes involves the complex interplay of genetic, environmental, and lifestyle factors that contribute to the development of the disease.
In type 1 diabetes, the pathophysiology involves an autoimmune destruction of the insulin-producing beta cells in the pancreas, leading to a deficiency in insulin production.
This results in an inability to regulate blood glucose levels, leading to hyperglycemia (high blood sugar).
In type 2 diabetes, the pathophysiology is more complex and involves both insulin resistance and impaired insulin secretion.
Insulin resistance occurs when the body's cells do not respond properly to insulin, leading to an inability to effectively use glucose for energy.
This causes the pancreas to produce more insulin to try to overcome the resistance, but over time, the pancreas may not be able to keep up with the demand, leading to a decrease in insulin production.
Gestational diabetes, which occurs during pregnancy, is caused by hormonal changes that lead to insulin resistance.
The placenta produces hormones that can block the action of insulin, leading to an increase in blood glucose levels.
The pathophysiology of diabetes also involves the development of complications, such as damage to blood vessels, nerves, and organs, which can lead to serious health problems like heart disease, stroke, kidney disease, and vision loss.
Understanding the pathophysiology of diabetes is crucial for developing effective treatments and prevention strategies for this chronic disease.
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