Several tests use glucagon to diagnose endocrine disorders. In patients with type 1 diabetes mellitus, a classic research test of pancreatic beta-cell secretory reserve uses 1 mg of glucagon administered as an intravenous bolus. Because insulin-treated patients develop circulating anti-insulin antibodies that interfere with radioimmunoassays of insulin, measurements of C-peptide are used to indicate beta-cell secretion.
C. Beta-Adrenoceptor Blocker Overdose
Glucagon is sometimes useful for reversing the cardiac effects of an overdose of β-blocking agents because of its ability to increase cAMP production in the heart independent of β-receptor function. However, it is not clinically useful in the treatment of heart failure.
D. Radiology of the Bowel
Glucagon has been used extensively in radiology as an aid to x-ray visualization of the bowel because of its ability to relax the intestine.
Transient nausea and occasional vomiting can result from glucagon administration. These are generally mild, and glucagon is relatively free of severe adverse reactions. It should not be used in a patient with pheochromocytoma.
Diabetes mellitus is defined as an elevated blood glucose associated with absent or inadequate pancreatic insulin secretion, with or without concurrent impairment of insulin action. The disease states underlying the diagnosis of diabetes mellitus are now classified into four categories: type 1, type 2, other, and gestational diabetes mellitus.
The hallmark of type 1 diabetes is selective beta cell (B cell) destruction and severe or absolute insulin deficiency. Type 1 dia betes is further subdivided into immune-mediated (type 1a) and idiopathic causes (type 1b). The immune form is the most com mon form of type 1 diabetes. Although most patients are younger than 30 years of age at the time of diagnosis, the onset can occur at any age. Type 1 diabetes is found in all ethnic groups, but the highest incidence is in people from northern Europe and from
Sardinia. Susceptibility appears to involve a multifactorial genetic linkage, but only 10–15% of patients have a positive family his tory. Most patients with type 1 diabetes have one or more circu lating antibodies to glutamic acid decarboxylase 65 (GAD 65), insulin autoantibody, tyrosine phosphatase IA2 (ICA 512), and zinc transporter 8 (ZnT8) at the time of diagnosis. These anti bodies facilitate the diagnosis of type 1a diabetes and can also be used to screen family members at risk for developing the disease.
Most type 1 patients with acute symptomatic presentation have significant beta cell loss and insulin therapy is essential to control glucose levels and to prevent ketosis.
and initially retain enough beta cell function to avoid ketosis.
They can be treated at first with oral hypoglycemic agents but then need insulin as their beta cell function declines. Antibody studies in northern Europeans indicate that up to 10–15% of “type 2” patients may actually have this milder form of type 1 diabetes (latent autoimmune diabetes of adulthood; LADA).
Type 2 diabetes is a heterogenous group of conditions characterized by tissue resistance to the action of insulin combined with a relative deficiency in insulin secretion. A given individual may have more resistance or more beta-cell deficiency, and the abnormalities may be mild or severe. Although the circulating endogenous insulin is sufficient to prevent ketoacidosis, it is inadequate to prevent hyperglycemia. Patients with type 2 diabetes can initially be controlled with diet, exercise and oral glucose lowering agents or non-insulin injectables. Some patients have progressive beta cell failure and eventually may also need insulin therapy.
Other Specific Types of Diabetes Mellitus