Dai rai yang, ana zinli a pathophysiology gaw hpa rai kun?
Pathophysiology of diabetes ngu ai gaw, ana zinli byin wa hkra galaw ai lam ni hpe hkaja ai lam re.
Diabetes mellitus ngu ai gaw, sai hta rawng ai chyaru (glucose) ni law wa ai majaw byin ai ana re.
Dai ana byin wa hkra galaw ya ai lam ni gaw, shinggyim masha a maumwi, shingra masa hte asak hkrung lam ni a majaw byin wa ai re.
Type 1 diabetes hta, ana byin ai lam gaw, insulin shapraw ai pancreas hta nga ai beta cells ni hpe autoimmune ana ni jahten kau ya ai majaw, insulin n pru wa ai.
Dai majaw, sai hta glucose n law wa ai majaw, sai hta sugar grai law wa ai.
Type 2 diabetes hta, ana byin ai lam gaw grau nna yak ai.
Insulin hpe n hkap la ai ngu ai gaw, hkum hkrang hta nga ai insulin hpe n lu jai lang ai majaw byin ai.
Dai majaw, pancreas gaw insulin n lu galaw hkra galaw wa ai. Raitim, aten na wa ai hte maren, insulin n lu galaw mat ai majaw, insulin n lu galaw mat ai.
Ma hkum hta na ma hkum kanu ni hta byin ai ma hkum hkalung ana (gestational diabetes) gaw, hormone galai shai ai lam a majaw byin wa ai rai nna, dai gaw insulin n lu galaw ai lam byin wa shangun ai.
Placenta gaw insulin hpe pat shingdang ya lu ai hormone ni hpe shapraw ya nna, sai hta glucose grau law wa shangun ai.
Dai hta n ga, sai lam, masin nra ni hte hkum hkrang daw shan ni hten za wa ai lam ni mung lawm ai. Dai gaw masin salum ana, stroke, nhkyun machyi ai hte myi hten ai zawn re ai manghkang ni byin wa chye ai.
Ndai ana hpe atsawm tsi lajang lu na matu hte, dai hpe koi lu na matu, ana kanu masa (pathophysiology) hpe chye na ra ai.
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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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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