UNIT IV: ENDOCRINE CONDITIONS
CHAPTER 15
Diabetes Mellitus
Carol Green-Hernandez, PhD, ARNP, FNP-BC, FNS • Rochelle F. Rubin, PharmD, BCPS
Diabetes mellitus is a disorder of endocrine function that affects metabolic and circulatory mechanisms. As a chronic disease, diabetes mellitus is characterized by glucose intolerance and distortions in fat metabolism, caused by either relative or absolute insulin deficiency. These two kinds of insulin deficiency are used to categorize the two primary variants of diabetes: Type 1 (formerly called insulin-dependent diabetes mellitus [IDDM]) and Type 2 (formerly called non-insulin-dependent diabetes mellitus [NIDDM]). This chapter focuses on Type 2 disease, and briefly covers Type 1 disease as well. Discussions dealing with gestational diabetes; maturity onset diabetes of the young (MODY), which occurs because of genetic defects of the beta-cells); other genetic syndromes associated with diabetes (such as Down, Klinefelter, and Turner syndromes), immune-mediated diabetes; diseases of the exocrine pancreas secondary to pancreatic trauma, infection, or disease; and drug- or chemically induced diabetes are outside the scope of this chapter and so are not covered.
ANATOMY, PHYSIOLOGY, AND PATHOLOGY
Type 1 Diabetes
Type 1 diabetes mellitus (T1DM) results from the absence of insulin secretion from the pancreatic beta-cells after beta-cell destruction by glutamic acid decarboxylase antibodies. This is typically mediated through an autoimmune process, though it may be idiopathic, with unknown etiology. Idiopathic T1DM lacks an autoimmune cause of beta-cell destruction. Both forms of T1DM are characterized by the absence of insulin secretion. All patients with T1DM are prone to ketoacidosis.
Type 2 Diabetes
Type 2 diabetes mellitus (T2DM) is a polygenic disease characterized first by insulin resistance, leading to compensatory hyperinsulinemia. At this time in the development of T2DM, the blood glucose level is normal, but high levels of circulating insulin disrupt lipid metabolism. As the resistance increases, compensatory hyperinsulinemia cannot keep up, so the blood glucose level rises. At levels of 140 mg/dL or more, the glucose is toxic to the beta-cells and to the sites where insulin works. Eventually, absolute hyperinsulinemia becomes relative hypoinsulemia. Exogenous insulin administration cannot override the body’s insulin resistance at this stage.
Abnormalities in hepatic glucose output are a secondary outcome rather than a primary cause of T2DM. Small amounts of insulin prevent hepatic glucose output. Much larger amounts of insulin are required to dispose of postprandial glucose loads. Although increased glucose output can complicate the course of T2DM, abnormalities in hepatic glucose metabolism are reversible with adequate disease management.
This process can continue for some time, even several years, before the overt onset of T2DM. Persons at this stage of metabolic challenge may have normal glucose tolerance, or only impaired glucose tolerance (IGT). This is an insulin-resistant state, but one for which there is metabolic compensation. Eventually, about 7% of persons with IGT develop T2DM in the United States every year. Who will develop this disease depends on several often interrelated factors, including genetic predisposition, ethnic heritage, overall health, lifestyle, and (possibly) environmental factors.
The onset of diabetes does not end its progression. If not diagnosed and adequately treated, T2DM will inexorably worsen, leading to complications and requiring more complex antidiabetic medication regimens. In this new era of obesity combined with an increase in longevity, patients frequently see their disease progress through beta-cell destruction, thus bringing endogenous insulin secretion to a grinding, permanent halt.
Yet another problem derived from poor glycemic control is the emergence of nonalcoholic fatty liver disease (NAFLD). Alarmingly, this common form of hepatic disease is increasing at a rapid rate in both Western and non-Western countries. The foremost reason for this trend is, of course, the ever-increasing worldwide epidemic of obesity. Besides obesity, the prevalence of NAFLD is also seen in T2DM, dyslipidemia, and insulin resistance. Other associated risks include hypopituitarism, hypothyroidism, polycystic ovary syndrome (PCOS), and hypogonadism.
CLINICAL WARNING:
In nondiabetics, both micro- and macrovascular diseases are seen as outcomes of increased serum glucose and insulin levels. These elevations commonly accompany normal aging, so their monitoring is the key to diabetes prevention in patients older than 55 years.
PATHOLOGY OF COMPLICATIONS SEEN IN DIABETES
Oxidative Stress and Antioxidants in T2DM
Hyperglycemia sets cell walls up for disequilibrium, with the result that they undergo lipid peroxidation and accumulation of its end product, malondialdehyde. This process of lipid peroxidation is, simply, one of rancidification, wherein reactive oxygen species (i.e., free radicals) are released at a rate that exceeds normal antioxidants’ abilities to combat them. These free radicals ensure that the cell’s metabolism will continue in chaos. Such chaos means that adenosine triphosphate (ATP) formation and enzymatic pathway synthesis of proteins are compromised. Lipid peroxidation and its associated malondialdehyde accumulation also can turn on the protein glycation process.
When euglycemia is restored in T2DM, reactive oxygen species production is reduced to normal. Research suggests that euglycemia not only protects against lipid peroxidation and its consequences, but can minimize or perhaps even mitigate the clinical complications of diabetes as well (Olokoba, Obateru, & Olokoba, 2012).
VASCULAR CHANGES
Data derived from the Action in Diabetes and Vascular Disease (ADVANCE) study have added to growing evidence that T2DM can lead to microvascular dysfunction. This dysfunction ranges from microalbuminuria and retinopathy to the development of macrovascular disease, including heart disease. This is a circuitious process, for a higher resting heart rate in patients with diabetes has been associated with the development of hypertension, leading to higher pressure gradients on the body’s microvasculature. Increased pressure gradients in turn underlie changes in the body’s macrovascular structure, underpinning the development of cardiac disease (Action in Diabetes and Vascular Disease, at http://ClinicalTrials.gov).
RETINOPATHY
Glycemic control affects the incidence of microvascular retinopathies in T1DM as well as maculopathies in T2DM. Microvascular changes can in fact be found relatively early in the course of T2DM, when glycemic control is poor. Research suggests that the frequency and incidence of retinopathy can be reduced in both T1DM and T2DM with adequate glycemic control from the time of diagnosis (Department of Health & Human Services, National Diabetes Fact Sheet, 2011). Of further benefit to vision health is dilated eye examination at time of diagnosis of T2DM. Dilated eye examination is also imperative within 5 years of initial diagnosis of T1DM. For both types, annual dilated screening examinations serve as the gold standard for eye health vigilance, with more frequent screenings in those patients with either diabetes type if proliferative changes are noted (American Diabetes Association, 2014).
EPIDEMIOLOGY
No race, no ethnic group, and neither gender can claim exemption from diabetes. Persons of all lifestyles, vegans or carnivores, smokers or not, are affected. Persons younger than 25 years who become diabetic are more likely to develop T1DM or, to a lesser extent, MODY. People older than 45 years are more likely to develop T2DM rather than T1DM. (Discussion of the increasing development of T2DM among the young, including children and adolescents, is outside the focus of this text.)
Overall, prevalence rates for T2DM have increased worldwide to an increasingly alarming extent. In 2011, there were approximately 366 billion people with the disease. By 2030, it is believed that more than 439 million people will be burdened with T2DM (Olokoba et al., 2012; Zimmet, Alberti, & Shaw, 2001).
DIAGNOSTIC CRITERIA
A suspected diagnosis of diabetes mandates further investigation by the primary care provider (PCP). The PCP should consider a diagnosis of diabetes when a patient presents with any of the findings outlined in Table 15.1.
A1c ≥6.5% (American Diabetes Association, 2014) FPG values:
FPG <100 mg/dL = normal
FPG ≥101 and 125 mg/dL = IFG
FPG ≥126 = conditional diagnosis of diabetes
OGTT with 50 g glucose, blood sugars ≥200 mg/dL at 2 hours should be investigated using an equivalent 75-g anhydrous glucose/water load; 140–200 mg/dL are classified as IGT. OGTT is not recommended for routine use.
Random plasma glucose ≥200 mg/dL with symptoms of hyperglycemia or hyperglycemic crisis.
A patient who presents with FPG between 100 and 125 mg/dL can be classified as having IFG.
These levels should be reconfirmed on a different day via repeat testing in any patient presenting without symptoms of hyperglycemia accompanied by acute metabolic decompensation.
FPG, finger prick glucose; IFG, impaired fasting glucose; IGT, impaired glucose tolerance; OGTT, oral glucose tolerance test.
Source: The International Expert Committee (2014).
HISTORY AND PHYSICAL EXAMINATION
The PCP’s history and physical examination should be thorough and careful if diabetes is to be diagnosed in a timely manner. History and physical data can alert the provider that a patient with other risk factors also risks glucose intolerance. Glucose intolerance can begin as impairment, but carries with it the risk of later overt diabetes. Table 15.2 presents questions specific to diabetes risk. Table 15.3 lists areas for physical examination that are indicated when screening for T2DM, as well as when providing ongoing care for the patient with diagnosed disease. It is important to note that 15% of patients already have evidence of complications at the time of diagnosis; these include retinopathy or neuropathy.
DIAGNOSTIC STUDIES
As noted in Table 15.1, the means for diagnosing T2DM is the hemoglobin A1c. Testing is not recommended for T1DM in patients who are healthy and who do not carry autoimmune risk. Patients aged 45 years and older should be screened for T2DM regardless of whether they are symptomatic. If the results of the screening laboratory test are normal, and in the absence of subsequent development of risk factors or diabetes symptoms, patients should continue to be screened at 3-year intervals, lifelong. More frequent testing should be considered in patients who are younger than 45 years and who:
Are obese (≥120% of desirable weight, or body mass index ≥25 kg/m2)
Report a first-degree relative who had diabetes
History Questions in Screening for Type 2 Diabetes (Age 18 Years and Above) |
Family history of diabetes? If yes, then T1DM or T2DM, and in whom?
Classic symptoms (polydipsia, polyphagia, unexplained weight loss)
Member of an ethnic group having a high incidence of T2DM (Native North American, African, Asian, Latino)
Birth weight and, if known, gestational age?
History of gestational diabetes? Of delivering an infant over 9 lb? Toxemia? Stillbirth?
Lifestyle stress?
Recent stressful event (positive or negative)?
Weight history (loss or gain)?
Previous history of diabetes treatment? If yes, then diet prescription, medications, self-management training? Glucose self-monitoring?
History of complications, including ketoacidosis/hypoglycemia?
Diet (including fluids) for food types, amounts, and how prepared for a typical day
Aerobic as well as anerobic exercise, noting type, amount of time, and frequency/week
Sleep history (Insomnia? Nightmares/terrors? Obstructive sleep apnea?)
Visual changes?
Numbness, tingling, or burning in hands or feet. This is bilateral rather than unilateral and, although primarily sensory, can involve motor nerve fibers. PN may progress from extreme pain to anesthesia and, in more extreme cases, can involve
Muscle weakness progressing to atrophy, with poor hand grasp or foot drop
Unexplained indigestion or abdominal pain? Diarrhea?
Infections, including vaginal or urinary tract? Candidiasis?
Interriginous infections/irritations (in skinfold areas)?
Impotence?
Coexistence of chronic disease, including hypertension, endocrine or autoimmune disease?
Atherosclerosis risks?
Medications?
Recreational drug use, including tobacco and alcohol (amount and frequency)?
PN, polyneuropathy; T1DM, Type 1 diabetes mellitus; T2DM, Type 2 diabetes mellitus.
Are members of an ethnic group at high risk of diabetes (e.g., Native North American, African, Asian, or Hispanic)
Were diagnosed with gestational diabetes mellitus or delivered a baby over 9 lb
Have high blood pressure (≥140/90 mmHg)
Have a HDL-C level of 35 mg/dL or less or a triglyceride level of 250 mg/dL or more
Were found previously to have either IGT or impaired fasting glucose (IFG)
Women with polycystic ovary disease
Most cases of diabetes can be diagnosed based on the A1c. Because no fasting is needed in order to assess a patient’s glycemic status, obtaining the A1c is more convenient to patient and clinician alike. The value for diagnosis of diabetes is an A1c of 6.5% or greater (American Diabetes Association, 2010; International Expert Committee, 2009). Because point-of-care testing methods are not yet consistent, their reliability cannot ensure an accurate diagnosis. A1c testing must therefore be done using a method certified by the National Glycohemoglobin Standardization Program, as derived from the standard set forth by the Diabetes Control and Complications Trial (DCCT; American Diabetes Association, 2010, 2012, 2014, 2013b).
Physical Examination for Type 2 Diabetes (Age 18 Years and Above) |
Height and weight
Blood pressure (may need to obtain orthostatic measurements as well)
Eyeground examination (preferably dilated, done by an ophthalmologist or licensed optometrist skilled in diabetes assessment) for signs of maculopathies and retinopathies. These can include:
retinal hemorrhages
scattered hard exudates
cotton-wool exudates (generally in concert with severe hypertension)
Oral examination (e.g., Candida)
Thyroid auscultation and palpation
Cardiac examination (e.g., S4)
Abdominal examination (e.g., hepatomegaly)
Examination of pulses via palpation and auscultation
Hand and finger examination (e.g., Dupuytren’s contracture? Trigger finger[s]?)
Thorough skin examination (including insulin injection sites if applicable; Acanthosis nigrans?)
Neurological examination, including assessing for a positive Romberg sign (sometimes presents as swaying, destabilized pattern)
Sensory stimulation changes (peripheral neuropathy and, if indicated by history, abdominal)
Vibratory sense changes (peripheral neuropathy and, if indicated by history, abdominal)
Foot examination, looking for evidence of foot ulcers or infection not otherwise explained; peripheral neuropathy (PN)
Deep tendon reflex measurement (may be decreased, especially in presence of PN). Absence of ankle reflexes is an early sign
Gait analysis (may be unstable, especially in presence of PN)
If primary or differential diagnosis includes another endocrine disorder such as pheochromocytoma, Cushing syndrome, acromegaly, hemochromatosis, or pancreatic disease, be aware that secondary diabetes can occur in these patients (Olokoba et al., 2012)
Table 15.4 presents specific laboratory tests to order when diabetes is suspected.
CLINICAL WARNING:
The provider who finds a fasting plasma glucose (FPG) at 126 mg/dL or greater on two different occasions in a nonpregnant patient is advised to engage the patient in diabetes management.
Laboratory Evaluation at Suspicion or Diagnosis of Diabetes |
Fasting lipids (total cholesterol, high-density lipoprotein cholesterol, triglycerides, and low-density lipoprotein cholesterol)
Serum creatinine
Urinalysis for glucose, ketones, protein, and sediment
Microalbuminuria (timed specimen, or the microalbumin/creatinine ratio)
Urine culture if sediment or symptoms indicate need
Thyroid function tests if indicated
Electrocardiogram (establishing a baseline is important; obtain other measures if indicated)
TREATMENT OPTIONS, EXPECTED OUTCOMES, AND COMPREHENSIVE MANAGEMENT
Treating Diabetes
T2DM is characterized by consistent elevation of the blood glucose level and includes insulin resistance. Primary care management ideally leads to normalization of blood glucose and, if possible, improved glucose response to endogenous insulin in T2DM. The goal of treatment is to control the disease and ultimately to prevent or decrease complications arising from the damaging effects of chronic hyperglycemia. Sound management plans arise from appropriate treatment options, and so lead to individualized plans of care that can maximize positive outcomes for a patient. For this reason, the following discussion presents various treatment options appropriate in different clinical circumstances. This discussion is framed by appropriate management plans whose foci are optimal outcomes.
Matching Diagnosis to Treatment and Management
When symptoms of polydipsia, polyuria, and polyphagia present themselves in the absence of weight loss, current diagnostic guidelines support making a clinical diagnosis of T2DM based on the A1c. A threshold of ≥6.5% is the current criterion for the diagnosis of T2DM. If weight loss or other risk factors of autoimmune disease are present, consider evaluating insulin production by C-peptide level to determine diagnosis of T1DM (American Diabetes Association, 2014).
When discussing treatment options with the patient, the effective PCP recognizes the importance of ethnic and cultural influences. This recognition begins before planning interventions. Food customs and eating rituals differ from family to family. Specific ethnic or lifestyle habits greatly influence diet and meal planning. Similarly, cultural beliefs and values surrounding the body and perceived self-harm will influence the patient’s level of participation in self-monitoring and medical therapies. The PCP must inquire about and respect cultural influences, customs, beliefs, and values. This perspective is especially important when a patient’s cultural, religious, or ethnic background, or even lifestyle, differs from that of the provider.
Developments in self-care education and pharmaceutical advances have revolutionized the potential for healthy outcomes for people with diabetes. The Diabetes Complications and Control Trial (1993a, cited in American Diabetes Association, 2011, 2012, 2013, 2014) provided firm evidence that optimal control of blood glucose, defined as A1c of 6.5% or less, can delay or prevent long-term complications of diabetes. Furthermore, any level of improved control will decrease complication rates.
The purpose of this section is to present the most current standards of practice in a clear and practical way. This information can be used to frame a plan of care that helps the patient with diabetes to obtain optimal metabolic control. Hyperglycemia must be eliminated to control the progression of diabetes as well as to delay or prevent complications, including micro- and macrovascular problems. These two problems are discussed later in this chapter.
Goals of Diabetes Management
The immediate treatment goals in diabetes management include the achievement of optimal glycemic control based on an A1c of 6.5% or less and the absence of hypoglycemic episodes requiring assistance to treat. The overall goals of diabetic management are also dual: correction of metabolic irregularities and prevention of micro- and macrovascular complications.
Achievement of these goals depends on maintaining the target blood glucose level. If frequent high and low blood sugar levels are encountered in the face of desirable A1c, efforts must be made to smooth out glycemic control. Self-monitoring of blood glucose (SMBG) is critical to the success of this effort. SMBG and other components of diabetes management are discussed after the following section, as lifestyle assessment is an important first step in managing blood glucose.
Lifestyle Assessment and Intervention
The importance of understanding the patient’s activities of daily life cannot be overstated. Included in this assessment are meal planning, hours of sleep and activity, and variations in activities on a day-to-day, weekly, and seasonal basis. The provider also needs to assess the patient’s educational level, employment, household, and potential for community support. Cultural and ethnic practices and religious beliefs may play an important role in health decisions, food choices, times for ritual fasting, and celebrations. Family habits and customs also may affect the patient’s self-management of diabetes. Ascertaining insurance status is important, as this often determines whether the patient has access to both primary care and specialty providers, support services, medication, and supplies.
A certified diabetes educator (CDE) can assist the PCP in developing successful intervention strategies for patient teaching. The CDE is a nationally accredited role for professionals who have completed an extensive course of study through the American Diabetes Association. Most commonly, the CDE is a professional nurse (either BSN or MSN), a physician (MD or DO), a nutritionist (RD), a social worker (MSW), or a pharmacist (PharmD). The CDE has emerged as the recognized consultant for or provider of diabetes education. As a source of knowledge to the patient as well as the provider, CDEs are increasingly drawn into the patient–provider relationship. CDE services are often treated as reimbursable by third-party payers. Further information about CDEs as a resource is provided in the “Community Resources” section of this chapter.
Whether the sources of information and teaching are the provider, a CDE, or a combination of both professionals, it is important that information be given that will support the patient in managing his or her care in a systematic manner. This information includes but is not limited to:
Understanding the rationale for glycohemoglobin (GHB) testing
The relationship of meal planning, food, and exercise control to glycemic control
SMBG
Mode of action and side effects of medications
Sick-day management
Signs and symptoms of hypo- and hyperglycemia and their management
Possible acute and chronic complications
Taken as a whole, this information constitutes the survival skills for the person with diabetes. The following discussion focuses on each of these content areas that providers and patients need to understand for successful management of diabetes.
GHB Testing
GHB testing helps the provider to determine a patient’s blood glucose level for the 100 to 120 days before testing. A minor hemoglobin, GHB constitutes only 4% to 8% of the total hemoglobin. There are three components of GHB that are said to be glycosylated: A1a, A1b, and A1c. Hemoglobin A1c is the most commonly measured GHB. GHB analysis is useful because this component of the red blood cell’s hemoglobin combines with some of the bloodstream’s glucose load. This process is called glycosylation and is irreversible. In other words, how high a patient’s GHB level is depends on how much glucose was available in the bloodstream over the preceding 60 to 90 days. This determination is only an average of that glucose level, though, because red blood cells undergo a constant cycle of old cell destruction and new cell generation (Desai, 2009).
Refer to Table 15.5 for specific conditions that can affect GHB levels. GHB levels also can be increased or decreased by several conditions. Before making a final assessment of the GHB status of a patient, the provider should be aware of the coexistence of any of the states described in Table 15.6.
Meal Planning
Because “diet” is an emotionally charged and negative word, the concept of a meal plan is easier to accept and discuss. Many people plan their meals; people do not have to have a chronic disease to plan ahead for food. Meal planning is an important skill for patient learning. The provider must keep in mind that the primary goal of meal planning is control of blood sugar and lipid levels. Many patients can accomplish optimal glycemic control through planning meals, in combination with medications and activity. Planning includes meal composition, preparation methods, portion size, and condiments added. The provider should ask specific questions about favorite foods and about any food allergies or sensitivities, such as lactose intolerance.
Conditions That Interfere With Glycohemoglobin Determination |
Low values can occur with:
Sickle cell anemia
Chronic renal failure
Pregnancy
False elevations can occur whenever the lifespan of the red cell is lengthened, as in thalassemia
Conditions That Can Cause Increased or Decreased Glycohemoglobin Levels |
INCREASED LEVELS |
New diabetes Poor diabetic control Chronic renal failure Hemodialysis Iron-deficiency anemia Splenectomy Pregnancy |
DECREASED LEVELS |
Hemolytic anemia (due to increase in red cell turnover) Other hemoglobinopathies (due to decreased number of red blood cells) |
Clinical Pearls
Weight loss is a secondary target, and not easily sustained. In teaching meal planning, the provider should first aim at what can be done realistically to aid the patient in self-managing glycemic control. Very modest reductions in weight (3–10 lb) often yield dramatic improvements in glycemic control.
The provider should keep in mind that meal planning for the patient with diabetes includes 10% to 20% protein but not <0.8 g/kg/d, and no more than 10% saturated fats. Note that fat amounts may have to be adjusted downward if the lipid profile indicates a cardiovascular risk. The rest of the day’s calories should be derived from monounsaturated fats and complex carbohydrates. Both soluble and insoluble fibers should be consumed, and 20 to 35 g of soluble fibers should be eaten. Cholesterol intake should not exceed 300 mg/d (American Diabetes Association, 2011).
COMMON MYTHS IN DIABETIC MEAL PLANNING
There are at least three myths about food and diabetes management that should be dispelled:
Myth 1: “Diabetes is a sugar disease. People with diabetes cannot eat sugar.” In fact, diabetes is an insulin disease. Sugars such as sucrose, fructose, maltose, and so on are only food stuffs that may affect the blood glucose level. As part of a balanced meal plan, different forms of sugar can be incorporated into a meal plan to add variety.
Myth 2: “All persons with diabetes must have a bedtime snack.” This myth is a holdover from the era when crude, long-acting insulins were used. These insulins exerted unpredictable peak actions; thus, it was deemed necessary to provide the patient with a hearty snack at bedtime. This myth pervades much of health care, contributing to fasting hyperglycemia both at home and in the hospital. Hepatic glucose output is maximal during the night, so additional caloric substrate is generally not required. Extra calories can lead to excessive weight gain.
Clinical Pearls
All patients on pharmacological therapy should keep some form of sugar at the bedside in case of overnight hypoglycemic symptoms. Easily stored sugars include glucose tablets and glucose gel.
Bedtime snacks are indicated in persons who need extra calories to maintain weight or if glycogen storage is limited, as in liver disease. These patients are prone to overnight hypoglycemia and may require a snack containing some mixed nutrients (e.g., 8 oz of 1% or skim milk and a slice of whole-grain bread/toast with 0.5 oz of low/no-fat cheese).
Juice and crackers are not recommended for bedtime consumption. Snacks containing only carbohydrate will provide only short-term fuel and, in fact, can potentiate higher blood glucose levels. Adding high-fat foods such as peanut butter may contribute to fasting hyperglycemia and general lipid excess in adults. Fats are not metabolized rapidly enough to prevent short-term hypoglycemia.
Myth 31: “‘Unsweetened’ and ‘no added sugar’ are the same as ‘sugar- free.’” All sugars, including fructose, can acutely elevate blood sugar levels. So-called “unsweetened” juice can deliver 20 to 30 g of carbohydrate in the form of fructose per 8-oz serving. This is nearly half the amount of a formal glucose tolerance test, which would raise the blood glucose of a person with diabetes to over 200 mg/dL. “Unsweetened” and “sugar-free” are not the same. Sugar-free foods provide few calories from carbohydrate (generally <4 calories per serving). Teach patients that any ingredient ending in “-ose” on a food label means that it contains a form of sugar.
Activity and Exercise
Exercise can have positive effects on glucose control across the lifespan. Exercise is the missing link in the diabetes plan of care. Exercise can overcome or reverse many common mistakes in meal planning and eating patterns. Moving from the theoretical recognition of its importance to the daily practice of exercise is one of the most challenging tasks in clinical practice. Prochaska and Norcross (1996) provide a model for understanding this barrier:
Stage 1: Precontemplation. The person is uninterested in changing a behavior.
Stage 2: Contemplation. The person is now interested in changing, but is not doing anything to act on this interest.
Stage 3: Preparation. The person is now interested in change and is acting on this interest occasionally.
Stage 4: Initial action. The person is now beginning a regular routine.
The PCP must be aware that the patient’s participation in exercise (or lack thereof) may fit within the confines of this model. This awareness can prevent frustration for provider and patient alike and may help providers work with patients toward initiating and sustaining stage 4.
Clinical Pearls
Encourage a nonexercising or rarely exercising patient to approach exercise as a stepwise progression.
Walking is an excellent form of exercise that is low in cost and easy to initiate in patients without neuropathic impingement. Walking 45 to 60 minutes each day is optimal and should be undertaken at least 6 but preferably 7 days a week (American Association of Clinical Endocrinologists, 2009).
Meal planning must be linked to daily activities. Some persons require an altered meal plan or different doses of medications if their activities vary widely, such as the weekend athlete who sits in front of a computer Monday through Friday and is active on Saturday and Sunday.
CLINICAL WARNING:
The provider needs to instruct the patient that exercise can alter the rate of insulin absorption. The patient should take care not to use any anatomic site for insulin injection that is used in exercising. For example, a runner or walker should avoid injecting the thigh before exercising. Because everyone responds differently to exercise, some patients may require insulin adjustments, whereas others may not.
A cardiac stress test or cardiology evaluation should be done in nonexercisers older than 40 years and in those with other cardiac risk factors. Refer to Chapter 8 for information about stress testing and exercise and cardiac disease.
Patients who have neuropathy or retinopathy should be taught to be very selective in their exercise routines and other activities in which they participate. Those with peripheral neuropathy will be safer using a treadmill than walking or running outside, where the terrain may be uneven or fraught with potential foot hazards. Patients with pre-proliferative and proliferative retinopathy should avoid all activities that increase intraocular pressure. These include weight-lifting and arm wrestling. Activities of daily living such as lifting or moving objects (e.g., grocery bags, furniture) also increase the risk of ophthalmic injury. Isometric exercise should be practiced only if the patient has had proper breath training.
All patients who undertake an exercise program or activities should be advised of the importance of careful foot evaluation before and after the activity. They should also be encouraged to use proper equipment and footwear, and to replace them when needed.
All patients who take insulin (especially in T1DM) should take special care when exercising. SMBG is mandatory for determining the need for extra calories before an activity. If the blood glucose level is <100 mg/dL, then a pre-exercise snack should be eaten that contains 20 to 25 g of carbohydrate. This snack proportion should be repeated after 30 minutes of exercise. If the blood glucose level is 100 to 250 mg/dL, then exercise without snacking is probably safe. The patient should be instructed to check the urine for ketones if the blood glucose level exceeds 250 mg/dL. If the urine is positive for ketones, the patient should delay exercise. The rationale for this delay is that inadequate levels of insulin in an exercising person with diabetes will result in an increased blood glucose level.
Home Glucose Monitoring
The American Diabetes Association (2014) recommends that all patients who take insulin also self-monitor their blood glucose levels. This activity is especially important in all pregnant women who have diabetes, regardless of the type. The provider should encourage SMBG in patients with unstable disease, those with a tendency toward hypoglycemia that occurs without forewarning, those with T2DM who are taking antidiabetic medication and whose glycemic control is tight, and in cases of ketoacidosis history. Whether T1DM or T2DM, all patients who manage their disease via intensive insulin regimens must use SMBG as part of their therapy. This latter group includes those who use an insulin pump or who self-inject their insulin multiple times daily.
Ideal SMBG monitoring regimens will vary in each individual patient. Recommended times to test SMBG readings include prior to meals and snacks, 2 hours after meals, at bedtime, prior to exercise, and whenever the patient may suspect low blood sugars. These readings give the most useful information about glucose control. Patients on insulin may use these values to adjust therapy. Patients without insulin can use these readings to determine where to target future therapy and identify meals that cause extreme glucose fluctuations.
There are many glucometers available. Package inserts provide excellent explanations on how to obtain a specimen and how to use the meter for its analysis and interpretation. Patients should be encouraged to bring their meters to the provider for one-on-one support and teaching about specimen collection and meter use. CDEs also are a good resource for up-to-date information related to meter choice and use.
Beginning Antidiabetic Medication
Food management and exercise may be enough for glycemic control in some patients with T2DM. Achievement of optimal blood sugar control usually requires antidiabetic medication. The previous discussion on meal planning, exercise, and SMBG serves as the foundation to beginning a medication regimen. However, medications alone cannot create optimal blood sugar levels in those with diabetes. For those who require medication, these modalities must be thought of as a threefold prescription. Together, they can assist the patient in maintaining the glucose profile close to normal, or at least within optimal ranges at any given point in time.
Sound clinical judgment is the hallmark of providing safe and effective health care. The PCP must assess each patient on an individual, case-by-case basis. In organizing the patient’s assessment and treatment plan, the provider should keep in mind the patient’s stage of insulin resistance, glucose toxicity, and ability to produce insulin.
All patients with T1DM will require insulin. Others who require insulin include patients with beta-cell damage (if not complete destruction) secondary to surgery or exposure to some toxins, including certain medications. Patients who have blood glucose levels exceeding 200 mg/dL, or A1c >9% may also require temporary or lifelong insulin therapy. Beta-cells can shut down when they are exposed to prolonged high glucose levels. This process is referred to as glucose toxicity. It is important to remember that some patients with T2DM can become extremely ill, with or without hyperglycemic hyperosmolar syndrome or diabetic ketoacidosis (DKA) states. These patients usually present over a period of weeks to months, and are often older than 30 years. They may have a history of obesity. Prolonged hyperglycemia can mean that this patient may present with marked weight loss. Persons with T2DM of many years’ duration can also experience deterioration of beta-cell function, eventually requiring complete insulin replacement (American Diabetes Association, 2014).
CLINICAL WARNING:
The patient with T1DM requires insulin at all times, and will have additional insulin requirements at times of illness and fasting. Withholding insulin in a person with T1DM who is vomiting can be a fatal mistake. Lack of insulin in T1DM allows the liver to produce ketones, precipitating illness and nausea and risking DKA.
The patient with T2DM will require insulin when ill or if the blood sugar level is very high. Insulin absence in T2DM (for whatever reason) will prevent the movement of nutrients to tissues. This will precipitate metabolic acidosis. Metabolic acidosis results from a lack of insulin in the hepatocyte, thus altering a metabolic pathway whose outcome is ketone production. Low doses of insulin are required to reverse this pathway. Increases in insulin dosage in persons taking insulin will be required at times of illness or fasting. Guidelines for these adjustments are discussed under sick-day management later in this chapter.
Diabetes Therapies: Insulin
The purpose of all diabetes therapies is to achieve glycemic control as close to normal as possible without hypoglycemia. Insulin may be required for the maintenance of life or for the patient’s level of wellness. Thus, insulin must be prescribed in a proactive manner that directly involves the patient in decision making and management. By anticipating peaks and troughs of blood glucose levels based on lifestyle assessments and, ideally, home glucose monitoring results, the provider can work with the patient to achieve smoother glycemic control. Insulin adjustments should be made after a pattern of insulin response is clear. Adjustments are generally made over a period of 3 or more days, within the context of a patient’s diet, glucose levels, and exercise management. Once a dose is established, teaching, guidance, and support for self-administration of insulin must be provided. These activities can be done by a member of the health care team who is skilled in teaching this content. Individual insulin dose requirement will change over time as seasons of the year, activity level, dietary intake, personal metabolic rate, and physical and mental stress fluctuate.
Traditionally, insulin came from either beef or pork sources, which had the potential to elicit an antibody response in humans. Due to the safety concerns and improvements in technology, manufacturers in the United States discontinued production of all beef and pork insulin sources and now use only recombinant DNA production technology. Insulin is available in either U-100 or U-500, 100 or 500 units/mL, respectively, in the United States. U-500 regular insulin is available for insulin-resistant individuals who require significantly large doses of insulin to control their blood sugars. All other insulins are only available in the U-100 strength in the United States. Short-acting insulin was available in an inhalation formulation for a short time, but was removed from the market after poor uptake and acceptance by patients and providers.
Insulin is often categorized by the onset, peak, and duration of action of each preparation. These characteristics are determined by the ability of insulin to be absorbed into the bloodstream after subcutaneous injection, travel to the site of action, and interaction with insulin receptors (Tibaldi, 2012).
Table 15.7 lists prescribing information for the insulin preparations that are most widely available. Table 15.8 outlines methods for teaching insulin self-administration with an insulin vial and syringe. Table 15.9 describes methods for teaching insulin self-administration with an insulin pen.
Insulin Dosing
Patients with T1DM require full insulin replacement with exogenous insulin, as there is no more insulin production from the pancreas. Full insulin replacement needs vary per patient, with most patients started on initial insulin doses of 0.5 to 1 units/kg total daily dose (TDD). Patient with more insulin resistance will need higher doses, such as patients with a mixed T1DM with insulin resistance. The TDD is divided into 50% basal (background) insulin, and 50% bolus (mealtime) insulin, further divided into injections prior to three meals daily. Preferred regimens use either insulin glargine or insulin detemir as the background insulin, plus rapid-acting insulin (insulin aspart, glulisine, or lispro) for the bolus insulin doses three times daily before meals. Patient SMBG readings are then used to determine the need for insulin adjustments. To address elevated (or low) FPG readings, adjust the basal insulin. To address elevated (or low) postprandial blood glucose measurements or premeal blood glucose (BG) measurements at later meals in the day, adjust the insulin injection at the immediately preceding meal.
Patients with T2DM are often maintained on oral antihyperglycemic agents and use insulin in addition to the oral agents. Typical starting doses for T2DM patients are 0.2 units/kg in once daily basal (background) insulin in addition to oral agents, and titrated to optimal SMBG control. Bolus insulin with meals is added if needed for better BG control later in the day or after meals.
Clinical Pearls
Try to adjust insulin by 10% to 20% of TDD at a time using the patient’s SMBGs to determine which injection to add or subtract units of insulin.
Because it is difficult to control and can affect the rest of the day’s glycemic levels, target the fasting glucose first.
If the patient has not taken insulin before, begin with a TDD dose of 0.2 to 1.0 units/kg divided into multiple daily injections in the proportions outlined in Table 15.10.
CLINICAL WARNING:
The use of any short-acting insulin (such as regular) before bed is dangerous and generally should not be prescribed. Rapid-acting insulin is only used at bedtime for correctional doses, based on a patient’s elevated bedtime blood glucose, and only if instructed by the health care provider. If overnight hypoglycemia is a concern, a mid-sleep awakening for SMBG (3 a.m.) may be useful for safeguarding against hypoglycemia.
Hyperglycemia can cause transient or permanent visual blurring. Patients must be certain that they are administering the correct dose. If the provider and patient determine that visual, special learning, or self-management needs exist, then a CDE or a provider from a diabetes specialty practice group should be consulted. Either of these professionals can provide information and teaching about possible alternative insulin delivery systems or assistive devices. These include information about syringe magnifiers for enlarging the calibration, and insulin pens with memory functions to remind patients what doses were injected.
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