Pathophysiology ya vuvabyi bya chukele yi vula dyondzo ya ku cinca ka fambiselo ra miri leri vangaka vuvabyi bya chukele.
Vuvabyi bya chukele i ntlawa wa mavabyi ya ku cinca ka miri lama vangiwaka hi ku tlakuka ka mpimo wa chukele engatini (glucose) hikwalaho ka ku nga humesi kahle insulin, ku nga tirhi kahle ka insulin kumbe haswimbirhi.
Vuvabyi bya chukele byi vangiwa hi swilo swo hambana-hambana leswi katsaka xitekela, mbango ni ndlela leyi munhu a hanyaka ha yona.
Eka vuvabyi bya chukele bya type 1, pathophysiology yi katsa ku onhiwa ka tisele ta beta leti humesaka insulin eka pancreas, leswi vangaka ku kayivela ka insulin.
Leswi swi endla leswaku munhu a nga swi koti ku lawula mpimo wa chukele engatini, leswi vangaka hyperglycemia (ku tlakuka ka chukele engatini).
Eka vuvabyi bya chukele bya type 2, pathophysiology ya kona ya rharhangana swinene naswona yi katsa ku ala ku pomperiwa ka insulin ni ku nga humesi kahle insulin.
Ku ala ku dya insulin swi humelela loko tisele ta miri ti nga swi koti ku endla ntirho wa insulin, leswi endlaka leswaku tisele ti nga swi koti ku tirhisa glucose hi ndlela leyinene leswaku ti kuma matimba.
Leswi swi endla leswaku nxorhonxorho wa kholokholo wu humesa insulin yo tala leswaku wu kota ku lwisana ni vuvabyi lebyi, kambe hi ku famba ka nkarhi, nxorhonxorho wa kholokholo wu nga ha tsandzeka ku endla leswi lavekaka, leswi endlaka leswaku insulin yi nga humesiwi hi xitalo.
Vuvabyi bya chukele lebyi vaka kona loko wansati a tikile byi vangiwa hi ku cinca ka tihomoni leti endlaka leswaku miri wu ala ku pomperiwa insulin.
Placenta yi humesa tihomoni leti sivelaka insulin leswaku yi nga tirhi, leswi endlaka leswaku mpimo wa chukele engatini wu tlakuka.
Pathophysiology ya vuvabyi bya chukele yi katsa ku va ni swiphiqo, swo tanihi ku onhaka ka misiha ya ngati, misiha ya misiha ni swirho, leswi nga vangaka swiphiqo leswikulu swa rihanyo swo fana ni vuvabyi bya mbilu, ku oma ka misiha, vuvabyi bya tinso ni ku lahlekeriwa hi mahlo.
Ku twisisa ndlela leyi vuvabyi bya chukele byi nga ni khombo ha yona i swa nkoka leswaku ku ta endliwa matshungulelo lama tirhaka ni tindlela to byi sivela.
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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["na (6) ku sayina ka xiviri kumbe ka elektroniki ka n'wini wa mfanelo ya vuqambi kumbe munhu la pfumeleriweke ku endla hi vito ra n'wini wa mfanelo ya vuqambi. "]
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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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