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SOURCE

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Source: Triplitt CL, Repas T, Alvarez C. Diabetes mellitus. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017. http://accesspharmacy.mhmedical.com/content.aspx?bookid=1861&sectionid=146065891. Accessed March 9, 2017.

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CONDITION/DISORDER SYNONYMS

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  • Juvenile-onset diabetes mellitus (DM)

  • Insulin-dependent DM

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DEFINITION

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  • Disorder of carbohydrate regulation caused by absolute deficiency of insulin production by pancreas.

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ETIOLOGY

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  • Autoimmune disorder usually developing in childhood or early adulthood probably initiated by exposure of genetically susceptible individual to unknown environmental agent.

  • Idiopathic type 1 DM is nonimmune form often seen in minorities, especially Africans and Asians, with intermittent insulin requirements.

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PATHOPHYSIOLOGY

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  • Immune-mediated destruction of pancreatic β-cells usually resulting in absolute deficiency of insulin.

  • A genetically susceptible individual must be exposed to a trigger that initiates the autoimmune process and destruction of pancreatic β-cells.

  • β-Cell destruction thought to occur during long preclinical period (9–13 years) associated with presence of immune markers.

  • Hyperglycemia occurs when 80–90% of β-cells are destroyed.

  • A transient remission (“honeymoon phase”) may precede established disease with associated risks for complications and death.

  • Factors initiating the autoimmune process unknown, but process mediated by macrophages and T lymphocytes with autoantibodies to β-cell antigens (eg, islet cell antibody, insulin antibodies)

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EPIDEMIOLOGY

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  • Accounts for 5–10% of all cases of DM

  • Prevalence of type 1 DM is increasing.

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PREVENTION AND SCREENING

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  • Presently no means of prevention.

  • Routine screening not recommended; screening for islet autoantibody status in high-risk family members may be appropriate in context of clinical trials.

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RISK FACTORS

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  • Parent or sibling with type 1 DM

  • Mother who had preeclampsia during pregnancy.

  • Respiratory infection shortly after birth.

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CLINICAL PRESENTATION

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SIGNS AND SYMPTOMS
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  • Onset: usually abrupt, <30 years old.

  • Patients often thin and prone to develop diabetic ketoacidosis (DKA) if insulin withheld or under conditions of stress.

  • 20–40% of patients present with DKA several days of.

    • Polyuria.

    • Polydipsia.

    • Polyphagia.

    • Weight loss.

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DIAGNOSIS

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LABORATORY TESTS
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  • Criteria for diagnosis of DM include any one of the following:

    • A1C ≥6.5%

    • Fasting plasma glucose ≥126 mg/dL (7.0 mmol/L)

    • 2-hour plasma glucose ≥200 mg/dL (111.1 mmol/L) during oral glucose tolerance test (OGTT) using 75 g anhydrous glucose in water.

    • Random plasma glucose concentration ≥200 mg/dL (111.1 mmol/L) with symptoms of hyperglycemia.

  • In absence of unequivocal hyperglycemia, confirm criteria 1 through 3 by repeat testing.

  • Normal fasting plasma glucose (FPG) <100 mg/dL (5.6 mmol/L)

  • Impaired fasting glucose defined as FPG of 100–125 mg/dL (5.6–6.9 mmol/L)

  • Impaired glucose tolerance diagnosed when 2-hour postload sample of OGTT is between 140 and 199 mg/dL (7.8 and 11.0 mmol/L).

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DIFFERENTIAL DIAGNOSIS
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