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  • 20 Hiperglikemia

    Загружено:

    Listiyani Ismail
    21 просмотров9 страниц
    The document outlines the pathogenesis of type 2 diabetes through a series of diagrams showing the relationships between impaired insulin secretion from beta cells, increased hepatic glucose production, decreased glucose uptake, and other contributing factors. It shows how factors like increased free fatty acids, decreased incretin effect, increased glucagon secretion from alpha cells, and neurotransmitter dysfunction can impair insulin secretion and contribute to hyperglycemia. The final diagram outlines a sound treatment approach targeting these pathophysiological processes through medications like TZDs, GLP-1 analogues, DPP-4 inhibitors, sulfonylureas, metformin, and lifestyle changes to reduce lipolysis.

    Исходное описание:

    HIPERGLIKEMI

    Оригинальное название

    20.Hiperglikemia

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    © © All Rights Reserved

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    The document outlines the pathogenesis of type 2 diabetes through a series of diagrams showing the relationships between impaired insulin secretion from beta cells, increased hepatic glucose production, decreased glucose uptake, and other contributing factors. It shows how factors like increased free fatty acids, decreased incretin effect, increased glucagon secretion from alpha cells, and neurotransmitter dysfunction can impair insulin secretion and contribute to hyperglycemia. The final diagram outlines a sound treatment approach targeting these pathophysiological processes through medications like TZDs, GLP-1 analogues, DPP-4 inhibitors, sulfonylureas, metformin, and lifestyle changes to reduce lipolysis.

    Авторское право:

    © All Rights Reserved
    Скачайте в формате PPT, PDF, TXT или читайте онлайн в Scribd
    Отметить как неприемлемый контент
    21 просмотров9 страниц

    20 Hiperglikemia

    Загружено:

    Listiyani Ismail
    The document outlines the pathogenesis of type 2 diabetes through a series of diagrams showing the relationships between impaired insulin secretion from beta cells, increased hepatic glucose production, decreased glucose uptake, and other contributing factors. It shows how factors like increased free fatty acids, decreased incretin effect, increased glucagon secretion from alpha cells, and neurotransmitter dysfunction can impair insulin secretion and contribute to hyperglycemia. The final diagram outlines a sound treatment approach targeting these pathophysiological processes through medications like TZDs, GLP-1 analogues, DPP-4 inhibitors, sulfonylureas, metformin, and lifestyle changes to reduce lipolysis.

    Авторское право:

    © All Rights Reserved
    Скачайте в формате PPT, PDF, TXT или читайте онлайн в Scribd
    Отметить как неприемлемый контент
    из 9

    Pathogenesis of Type 2 Diabetes

    Islet b-cell

    Impaired
    Insulin Secretion

    Increased Decreased Glucose


    HGP Uptake

    HGP=hepatic glucose production.


    Pathogenesis of Type 2 Diabetes
    Islet b-cell

    Impaired
    Insulin Secretion

    Increased Decreased Glucose


    HGP Uptake
    Pathogenesis of Type 2 Diabetes
    Islet b-cell

    Impaired
    Insulin Secretion

    Increased Decreased Glucose


    HGP Uptake
    The Disharmonious Quartet

    Islet b-cell

    ↑ FFA Increased
    Lipolysis
    Impaired
    Insulin Secretion

    Increased
    HGP
    Decreased Glucose
    Uptake
    FFA=free fatty acids.
    The Quintessential Quintet

    Islet b-cell

    Decreased
    Incretin Effect

    Impaired
    Insulin Secretion
    Increased
    Lipolysis

    Increased
    HGP Decreased Glucose
    Uptake
    The Setaceous Sextet
    Islet b-cell

    Decreased
    Incretin Effect
    Impaired
    Insulin Secretion

    Islet a-cell

    Increased
    Lipolysis

    Increased
    Glucagon Secretion

    Increased
    HGP Decreased Glucose
    Uptake
    The Septicidal Septet

    Islet b-cell

    Decreased
    Impaired Incretin Effect
    Insulin Secretion Increased
    Lipolysis

    Islet a-cell

    Increased
    Increased Glucose
    Glucagon Secretion
    Reabsorption

    Increased
    HGP Decreased Glucose
    Uptake
    The Ominous Octet

    Islet b-cell

    Decreased
    Incretin Effect
    Increased
    Impaired Lipolysis
    Insulin Secretion

    Islet a-cell

    Increased Increased Glucose


    Glucagon Secretion Reabsorption

    Increased
    Decreased Glucose
    HGP
    Neurotransmitter Uptake
    Dysfunction
    Treatment of Type 2 Diabetes: A Sound
    Approach Based Upon Its Pathophysiology

    Islet b-cell
    TZDs
    GLP-1 analogues

    Impaired
     DPP-4 Inhibitors
    Sulfonylureas/
    Increased
    Lipolysis
    Insulin Secretion
    Meglitinides
    TZDs

    Metformin


    TZDs TZDs
    Metformin

    Increased
    HGP
    Decreased Glucose
    Uptake
    DPP-4=dipeptidyl peptidase-4.

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