Building Competency in Diabetes Education THE ESSENTIALS

PATHOPHYSIOLOGY| 3-21

Comparing type 1 and type 2 diabetes Table 4. Comparison of type 1 and type 2 diabetes

Type 1

Type 2

Pathogenesis

Polygenic

Polygenic

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Genetic predisposition and environmental influences that trigger an autoimmune destruction of pancreatic beta cells

Genetic predisposition and insulin resistance combined with insulin deficiency; one or the other may predominate

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May be idiopathic

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Insulin production

Minimal or absent insulin; variable rate of destruction

Progressive beta cell malfunction

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Production ranges from initial hyperinsulinemia to insulin deficiency Rate of malfunction may be affected by glucose control

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May be transient; “honeymoon” period

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Age at onset

Usually younger than 25 years, but variable, up to eighth decade of life (33) Usually classic: polyuria, polydipsia, polyphagia, weight loss, fatique. Often acute/severe, especially in children, but may be minimal/gradual in adults

Usually >25, but increasing in younger persons

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Clinical presentation

Onset variable, from slow to severe

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Impaired glycemia may be present five to eight years before diagnosis

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Body type

Usually lean, with notable pre-diagnosis weight loss

80–90% overweight or obese (central obesity)

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20–30% lean

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Family history (parents with diabetes)

Infrequent (5–10%)

Frequent (75–90%)

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