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تحلیل اصطلاحات پزشکی پاراگراف بیماریزایی دیابت قندی نوع 1 . امید طرازی زاده یزدی.

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Presentation Transcript
slide1

تحلیل اصطلاحات پزشکی پاراگرافبیماریزایی دیابت قندی نوع 1

امید طرازی زاده یزدی

slide3

Type 1 DM is the result of interactions of genetic, environmental, and immunologic factors that ultimately lead to the destruction of the pancreatic beta cells and insulin deficiency. Type 1 DM results from autoimmune beta cell destruction, and most, but not all, individuals have evidence of islet-directed autoimmunity. Some individuals who have the clinical phenotype of type 1 DM lack immunologic markers indicative of an autoimmune process involving the beta cells and the genetic markers of type 1 diabetes.

Diabetes Mellitus

دیابت قندی

gene + tic

Root = gene

Suffix = tic

تکوینی

immune + logy + ic

Root = immune

Suffix = logy

Suffix = ic

وابسته به علم ایمنی شناسی بدن

pancreat/o + ic

Root = pancreat

Suffix = ic

وابسته به غده لوزالمعده

auto + immune

Root = immune

Prefix = auto

خود ایمنی

Type 1 DM is the result of interactions of genetic, environmental, and immunologic factors that ultimately lead to the destruction of the pancreatic beta cells and insulin deficiency. Type 1 DM results from autoimmune beta cell destruction, and most, but not all, individuals have evidence of islet-directed autoimmunity. Some individuals who have the clinical phenotype of type 1 DM lack immunologic markers indicative of an autoimmune process involving the beta cells and the genetic markers of type 1 diabetes.

DM = Diabetis Mellitus

genetic = gene + tic

immunologic = immune + logy + ic

Pancreatic = pancreas + ic

autoimmune = auto + immune

slide4

These individuals are thought to develop insulin deficiency by unknown, nonimmune mechanisms and are ketosis prone; many are African American or Asian in heritage. The temporal development of type 1 DM is shown schematically as a function of beta cell mass in Fig. 344-6. Individuals with a genetic susceptibility have normal beta cell mass at birth but begin to lose beta cells secondary to autoimmune destruction that occurs over months to years. This autoimmune process is thought to be triggered by an infectious or environmental stimulus and to be sustained by a beta cell–specific molecule.

non + immune

Root = immune

Prefix = non

غیر ایمنی

Ket+ osis

Root = ketone

Suffix = sis

انباشتگی کتون در بدن

Infection + ous

Root = infection

Suffix = ous

عفونی

Stimulus

Root = stimulant

Suffix = us (noun endings)

محرک

These individuals are thought to develop insulin deficiency by unknown, nonimmune mechanisms and are ketosis prone; many are African American or Asian in heritage. The temporal development of type 1 DM is shown schematically as a function of beta cell mass in Fig. 344-6. Individuals with a genetic susceptibility have normal beta cell mass at birth but begin to lose beta cells secondary to autoimmune destruction that occurs over months to years. This autoimmune process is thought to be triggered by an infectious or environmental stimulus and to be sustained by a beta cell–specific molecule.

ketosis = ketone + osis

nonimmune = non + immune

infectious = infection + ous

stimulus = stimulant + us

slide5

In the majority, immunologic markers appear after the triggering event but before diabetes becomes clinically overt. Beta cell mass then begins to decrease, and insulin secretion progressively declines, although normal glucose tolerance is maintained. The rate of decline in beta cell mass varies widely among individuals, with some patients progressing rapidly to clinical diabetes and others evolving more slowly. Features of diabetes do not become evident until a majority of beta cells are destroyed (70–80%). At this point, residual functional beta cells exist but are insufficient in number to maintain glucose tolerance. The events that trigger the transition from glucose intolerance to frank diabetes are often associated with increased insulin requirements, as might occur during infections or puberty.

slide6

After the initial clinical presentation of type 1 DM, a "honeymoon" phase may ensue during which time glycemic control is achieved with modest doses of insulin or, rarely, insulin is not needed. However, this fleeting phase of endogenous insulin production from residual beta cells disappears as the autoimmune process destroys remaining beta cells, and the individual becomes insulin deficient. Some individuals with long-standing type 1 diabetes produce a small amount of insulin (as reflected by C-peptide production) and some individuals have insulin-positive cells in the pancreas at autopsy.

glyc + hemia + ic

Root = glyc

Suffix = hemia

Suffix = ic

قند خون

end + gen + ous

Root = gen

Prefix = end

Suffix = ous

درونی

auto + opsy

Auto = self

Opsy = view of

کالبد شکافی

After the initial clinical presentation of type 1 DM, a "honeymoon" phase may ensue during which time glycemic control is achieved with modest doses of insulin or, rarely, insulin is not needed. However, this fleeting phase of endogenous insulin production from residual beta cells disappears as the autoimmune process destroys remaining beta cells, and the individual becomes insulin deficient. Some individuals with long-standing type 1 diabetes produce a small amount of insulin (as reflected by C-peptide production) and some individuals have insulin-positive cells in the pancreas at autopsy.

glycemic = glyc + hemia + ic

endogenous = end + gen + ous

Autopsy = auto + opsy