Diabetes mellitus (DM) is a disease in which altered carbohydrate metabolism leads to high blood glucose levels (Huether & Tomky, 1998). DM has several causes and can be categorized into several types (Table 10-1). DM also frequently occurs with other diseases and conditions, such as hypertension, metabolic syndrome, cardiac disease (Nathan et al., 2005) and vascular disease (Ganne et al., 2007).

Diabetes Type Cause
Type 1 Destruction of pancreatic beta cells, leading to reduced and finally no insulin secretion by the pancreas.
Type 2 Increased resistance of body tissues and cells to the action or actions of insulin.
Type 3 Possible new type of diabetes; described as a decrease in the secretion of brain insulin, which may be important for the survival of brain cells.
Type 4 Interference in insulin production, insulin secretion, blood glucose level regulation, or tissue sensitivity to the action or actions of insulin as a result of genetic, pancreatic, or hormonal problems. Several herbals and medications also can increase blood glucose levels.
Gestational Increased resistance of body tissues and cells to the action or actions of insulin as a result of the hormones of pregnancy.
Stress response Hormones released by the body in response to stressors (cortical hormones, epinephrine, norepinephrine) increase the release of glucose stores from the liver and muscle through glycolysis. These hormones also cause the manufacture of glucose from noncarbohydrate sources (e.g., proteins) through gluconeogenesis. Stressors that activate the stress response can be physical or emotional and may include invasive surgeries, traumatic injuries, taking an examination/test, or public speaking.

Type 1 Diabetes

Type 1 diabetes appears to arise from a complex genetic and environmental interaction that causes an individual’s immune system to attack and destroy pancreatic beta cells. Pancreatic beta cells are responsible for insulin secretion. As beta cells are destroyed, insulin production diminishes. However, more than 75% of the beta cells must be destroyed before hyperglycemia occurs. When all the beta cells have been destroyed, insulin production ceases, and insulin must be supplied from an alternative (outside) source.

Hyperglycemia causes an increased osmotic load in the blood vessels. Fluid transfers from the tissues or cells (area of lower osmotic pressure) to the blood vessels (area of higher osmotic pressure). This causes tissue cell dehydration and increased vascular volume. The kidneys respond to increased vascular volume by excreting additional fluid into the urine. This leads to increases in the volume and frequency of urination, a condition called polyuria.

With hyperglycemia, the renal tubules cannot reabsorb all the glucose, which is “spilled” into the urine. Glucose is a large molecule that takes fluid with it, leading to increased volume and frequency of urination. Electrolytes are excreted along with the large volume of fluid in the urine, and the result is severe electrolyte imbalances.

Even though the bloodstream has an overabundance of glucose, without insulin the glucose does not enter the cell. The cell is starving and in dire need of an energy source, therefore fatty acids are released and metabolized. During this process, ketones develop, leading to ketoacidosis, a severe metabolic condition (Table 10-2).

From Chernecky, C. C., & Berger, B. J. (2008). Laboratory tests and diagnostic procedures. (5th ed.). St. Louis: Elsevier.
Measurement Normal Serum Level Serum Level in Ketoacidosis
Glucose 70-100 mg/dL 350+ mg/dL
Ketone bodies 0.3-2.0 mg/dL 20+ mg/dL
Bicarbonate (HCO3) 22-26 mEq/L 5 mEq/L
Chloride (Cl) 97-107 mEq/L 90 mEq/L
PH 7.35-7.45 7.0 or lower
Anion gap 12-20 mEq/L Over 20 mEq/L

Type 2 Diabetes

Type 2 diabetes is caused by a not well understood interaction of genetic and environmental factors. Hyperglycemia in type 2 diabetes results from insulin resistance in the tissues. As tissues progressively decrease their response to a given concentration of insulin, less glucose enters the cell and therefore remains in the bloodstream. In response, pancreatic beta cells increase insulin secretion, raising the insulin level in the bloodstream. At a critical point, pancreatic beta cells are unable to increase insulin secretion any further in an attempt to counter the lack of tissue response to insulin, and hyperglycemia occurs. This process usually occurs slowly, over a prolonged period, and many people with type 2 diabetes are not even aware that they have developed the disease.

Until the later stages of type 2 diabetes, varying amounts of insulin secretion allow some glucose to be transported into the cell for energy. Therefore fatty acids are not mobilized as an alternative energy source, nor is ketoacidosis a common complication. Instead, glucose continues to increase in the bloodstream, reaching levels of 600 mg/dL and higher, resulting in extremely high osmotic levels. This is called hyperglycemic hyperosmolar nonketotic (HHNK) coma. During HHNK, as a result of the very high serum glucose levels, fluid shifts from the tissues and is excreted in the urine (polyuria), further increasing osmotic levels. The degree of cognitive dysfunction (confusion, coma) is related to the dehydration and the osmotic level.


Several prescription and over-the-counter medications, as well as herbal preparations and supplements, affect blood glucose levels (Table 10-3 and Table 10-4). Medications that increase blood glucose levels may cause hyperglycemia and diabetes: they include corticosteroids (prednisone, dexamethasone), stress hormones (cortisol, epinephrine), sex hormones (androgens, estrogens), stimulants (ephedrine, amphetamines), some antipsychotics (clozapine, olanzapine), and the chemotherapeutic agent L-asparaginase.

Herb or Supplement Effect on Blood Glucose Level
Ackee Decrease
Agrimony Decrease
Aloe gel Decrease
Alpha lipoic acid Decrease
Annatto Increase
Astragalus Decrease
Banaba Decrease
Bean pod Decrease
Bilberry Decrease
Bitter melon Decrease
Black mulberry Decrease
Black psyllium Decrease
Black tea Increase or decrease
Blond psyllium Decrease
Blue cohosh Increase
Blueberry Decrease
Bugleweed Decrease
Burdock Decrease
Cassia cinnamon Decrease
Chanca piedra Decrease
Chinese cucumber root Decrease
Chromium Decrease
Cinnamon bark Decrease
Cocoa Increase
Coffee Increase or decrease
Cola nut Decrease
Corn silk Decrease
Country mallow Increase
Cowhage Decrease
Cumin Decrease
Damiana Decrease
Dandelion Decrease
Devil’s claw Increase
Devil’s club Decrease
Ephedra Increase
Eucalyptus dried leaf Decrease
Fenugreek Decrease
Flaxseed Decrease
Fo-ti Decrease
Ginger Decrease
Ginkgo leaf Increase or decrease
Ginseng (American, panax, Siberian) Decrease
Glycomannam Decrease
Glucosamine hydrochloride Increase
Glucosamine sulfate Increase
Goat’s rue Decrease
Green tea Increase or decrease
Guar gum Decrease
Guarana Increase or decrease
Gymnema Decrease
Horse chestnut Decrease
Hydrazine sulfate Decrease
Juniper Decrease
Kudzu Decrease
Lycium Decrease
Madagascar periwinkle Decrease
Marijuana Decrease
Maitake mushroom Decrease
Marshmallow Decrease
Melatonin Increase
Myrrh Decrease
N-acetyl glucosamine Increase
Niacin (niacinamine, vitamin B3) Increase
Olive leaf Decrease
Olive oil Decrease
Onion Decrease
Ribose Decrease
Sage Decrease
Solomon’s seal Decrease
Spinach Decrease
Stevia Decrease
Stinging nettle Decrease
Vanadium Decrease
Xanthan gum Decrease

Medication Effect on Blood Glucose Level
Allopurinol Decrease
Androgens Increase
Ascorbic acid (vitamin C) Increase
Aspirin Decrease
Betamethasone Increase
Clofibrate Decrease
Clozapine Increase
Cortisone Increase
Estrogens Increase
Dexamethasone Increase
Guanethidine sulfate Decrease
Haloperidol Increase
Heparin Increase
Hydrocortisone Increase
Isoniazid Decrease
L-asparaginase Increase
Levodopa Increase
Metaproterenol Increase
Methylprednisolone Increase
Olanzapine Increase
Phenylephrine Increase
Phenytoin Increase
Prednisolone Increase
Prednisone Increase
Pseudoephedrine Increase
Triamcinolone Increase


Each year since 1997, the number of new diabetic cases has increased nationwide (CDC, 2007a). In 2004 alone, approximately 1.4 million adults were newly diagnosed with the disease (CDC-e, 2007a). The Centers for Disease Control and Prevention (CDC, 2005) estimate that 21 million Americans have diabetes, and an additional 41 million are prediabetic (CDC, 2005b). Prediabetes manifests as impaired glucose tolerance or impaired fasting glucose. The incidence of diabetes increases with advancing age, with most cases attributable to type 2 diabetes. However, although the incidence of diabetes increased for all age groups from 1997 to 2004 (CDC-c), the largest increase occurred among individuals age 18 to 44 (45%).


Type 2 diabetes occurs almost twice as often in African Americans and one and a half times as often in Hispanics as in Caucasians (CDC, 2007b). Native Americans by far are the ethnic group most highly at risk. More than one fourth of Native American adults living in the southeastern United States (27.8%) have diabetes (CDC, 2005a). Family history, advancing age (over 40), and gestational diabetes are uncontrollable risk factors for type 2 diabetes. However, hypertension, obesity, and lack of exercise are modifiable risk factors. Recent research has found genetic risk factors for diabetes: for type 2, these are human INS (insulin) gene promoter (Karaca et al., 2007), genes TCF7L2 (Owen & McCarthy, 2007) and CDKAL1 (Steinthorsdottir et al., 2007), and a mutant 128R allele of the E-selectin gene (Abu-Amero et al., 2007); for gestational diabetes, the genetic risk factor is a INS-VNTR class III gene (Litou et al., 2007).


Even though it is underreported, diabetes is the sixth leading cause of death in the United States. People with diabetes are twice as likely to die of heart disease and stroke and one and one half times more likely to have hypertension (CDC, 2005a). The incidence of retinopathy, nephropathy, and neuropathies is significantly higher in the diabetic population (CDC, 2005a), and these conditions are worsened by periods of poorly controlled serum glucose levels (–Diabetic control study, Genuth, 2006). Diabetes is the major contributing factor in new cases of blindness, end-stage renal disease, and nontraumatic lower limb amputations. The CDC’s National Center for Chronic Disease Prevention and Health Promotion estimates the death risk for individuals with diabetes to be twice that of the nondiabetic population (CDC, 2005c). Recent research has revealed racial and gender disparities among Medicare patients treated for diabetes mellitus; Caucasians appear to receive better treatment than African Americans, and women receive less intensive cholesterol treatment than men (Chou et al., 2007).


1. Fasting blood glucose test (FBG): 100 mg/dL to less than 126 mg/dL indicates prediabetes; 126 mg/dL or higher indicates diabetes (ADA, n. d. and WHO, 2007).

2. Oral glucose tolerance test (OGTT): 140 mg/dL to less than 200 mg/dL indicates prediabetes; 200 mg/dL or higher indicates diabetes (ADA, n. d. and WHO, 2007).

3. Nonfasting plasma glucose measurement: 200 mg/dL or higher indicates diabetes (ADA, n. d. and WHO, 2007).

4. Glycosylated hemoglobin (HgbA1c): 6% or higher is considered abnormal in most laboratories. This test is not usually used for diagnostic purposes, but rather to monitor blood glucose control over the past 90 days. An HgbA1c of less than 6.5% to 7% is considered good glycemic control (Genuth, 2006).

5. Polyuria

6. Polydipsia

7. Polyphagia

8. Unexplained weight loss

9. Increased incidence of recurrent infections (especially fungal or urinary tract infections)

10. Poor wound healing

11. Visual changes: Retinopathy develops in patients with type 1 diabetes who have vascular endothelial growth factor A (VEGFA) variants (Al-Kateb et al., 2007).

12. Unexplained foot wound or ulcer

13. Neuropathy

14. History of gestational diabetes or large for gestational age (LGA) fetus

Oct 19, 2016 | Posted by in NURSING | Comments Off on 10. DIABETES MELLITUS

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