Describe the pathophysiology and clinical manifestations of diabetes mellitus.
Type 1 Diabetes Mellitus Formerly known as “Juvenile onset” or “insulin-dependent diabetes. Type 1 is the end result of a long-standing process in which the body’s own T cells attack and destroy pancreatic beta (B) cells, which are the source of the body’s insulin.
Autoantibodies (an antibody, produced by B cells in response to an altered “self” antigen on one type of the body’s own cells, that attacks and destroys these cells.) to the islet cells cause a reduction of 80% to 90% of normal B-cell functions before hyperglycemia and other manifestations occur.
Manifestation of type 1: diabetes develops when the person’s pancreas can no longer produce insulin. Once this occurs, the onset of symptoms is usually rapid, and the patient comes to the emergency department with impending or actual ketoacidosis. The patient usually has a history of recent and sudden weight loss, as well as the classic symptoms of polydipsia (excessive thirst), polyuria (frequent urination), and polyphagia (excessive hunger). Weight loss may occur as the body cannot get glucose and turns to other energy sources, such as fat and protein. Weakness and fatigue may also be experienced, as body cells lack needed energy from glucose. Ketoacidosis, a complication associated with untreated type1 diabetes, is associated with additional clinical manifestations.
Type 2 Diabetes Mellitus the pancreas usually continues to produce some endogenous (self made) insulin. However, the insulin that is produced is either insufficient for the needs of the body and /or is poorly utilized by the tissues. The presence of endogenous insulin is the major pathophysiologic distinction between type 1 and type 2 diabetes.
Manifestations of type 2 are often nonspecific, although it is possible that an individual with type 2 diabetes will experience some of the classic symptoms associated with type 1. Some of the more common manifestations associated with type 2 diabetes include fatigue, recurrent infections, recurrent vaginal yeast or monilia (Candida) infections,, prolonged wound healing , and visual changes. It appears so gradually that an individual may blame the symptoms on another cause, such as lack of sleep or increasing age, and before the person knows it, he or she may have complications.
Describe the collaborative care of the patient with diabetes mellitus:
Diagnostic – history and physical examination
Blood test – including fasting blood glucose, postprandial blood glucose, glycosylated hemoglobin (A1C), lipid profile, blood urea nitrogen and serum creatinine, electrolytes, TSH.
Urine – for complete urinalysis, microalbuminuria, and acetone (if indicated).
Funduscopic examination – dilated eye examination.
Neurologic examination – including monofilament test for sensation to lower extremities.
Monitoring of weight
Doppler scan (if indicated)
Foot (podiatric) examination.
Drug therapy – insulin, oral and other agents, enteric-coated aspiring (325mg), angiotensin-converting enzyme (CE) inhibitors, antihyperlipidemic drugs (if indicated)
Self-monitoring of blood glucose (SMBG)
Patient and family teaching and follow-up programs.
Describe the role of nutrition and exercise in the management of diabetes mellitus:
Factor Type 1
Total Calories increase in caloric intake possibly necessary to achieve desirable body weight and restore body tissues.
Effect of diet diet and insulin necessary for glucose control
Distribution of calories - equal distribution of carbohydrates through meals or adjustment of carbohydrates for insulin activity.
Consistency in daily intake – necessary for glucose control
Uniform timing of meals – crucial for NPH insulin programs; flexibility with multidose rapid-acting insulin.