CHAPTER 47 (Osborne) - Caring for the Patient with Diabetes

I. Introduction • diabetes mellitus (DM) - a group of metabolic disorders characterized by abnormal fuel

metabolism, all of which have hyperglycemia in common; results from defects in insulin secretion, insulin action, or both

• insulin• hormone secreted by beta cells in the Islet of Langerhans located in the pancreas• has a critical role in metabolism of carbs, fat and protein• essential in maintaining normal blood glucose levels

• diabetes-associated complications• retinopathy• nephropathy• neuropathy• stroke• CVD• PVD

• classifications of diabetes• age of onset (juvenile, adult-onset)• pharmacologic treatment (insulin, oral medications)• present criteria:

• Type 1• Type 2• gestational diabetes• other types

II. Types of Diabetes • 3 major types of diabetes:

1. Type 1 diabetes is a chronic autoimmune disorder in which there is a complete lack of insulin production

2. Type 2 diabetes is the most common form of diabetes, in which the body does not produce enough insulin or the cells ignore the insulin the body need so that it can use glucose, the bodies main fuel, for energy.

3. Gestational diabetes develops during pregnancy. It affects how cells use glucose.• prediabetes - a health condition without symptoms; the individual's blood glucose levels

are higher than normal but not high enough to be type 2 diabetes

A. Type I Diabetes Mellitus• type 1 diabetes mellitus (DM) - the complete lack of insulin production, which is

caused by autoimmune destruction of the insulin-producing pancreatic beta cells1. Epidemiology and Etiology

• frequently diagnosed before 30 y/o• latent autoimmune diabetes in adults (LADA) adult for of type 1 diabetes• 5-10% of all diagnosed diabetes in the US• usually thin or of normal weight at diagnosis• abrupt onset of symptoms

• results from genetics, environment and autoimmunitya) Genetics• familial predisposition exists, mode of inheritance still unknown• 6% if your sibling or father has type 1, 3% if your mother has it• 25-50% for monozygotic twins - evidence that there is an environmental trigger

b) Environmental• theory that there is a triggering event in at risk individuals, possibly:

• viral infections (congenital rubella syndrome, enteroviruses)• dietary factors (cow’s milk)• toxins (N-nitroso compounds, nitrates and nitrites)

c) Autoimmunity• circulating autoantibodies

• cytoplasmic islet cell antibodies (ICAs)• insulin autoantibodies (IAAs)• antibodies vs enzyme glutamic acid decarboxylase (GAD)• antibodies vs ilet tyrosie phosphatase

• presence of 1 or 2 of these antibodies plus alterations in insulin secretion is highly predictive of type 1

B. Type II Diabetes Mellitus• type 2 diabetes mellitus - results from decreased insulin production by the pancreas

and increased insulin resistance, which is characterized by an inability to use insulin effectively

1. Epidemiology and Etiology• frequently diagnosed after 30 y/o, but becoming more frequent in younger ages• 90-95% of all diabetes• dramatic increase in incidence in newly Westernized countries• those with type 2 are often overweight or obese at the time of diagnosis and a

strong family history of the disordera) Sedentary Lifestyle and Poor Dietary Patterns• studies show that high levels of activity protect against type 2• studies also show that lifestyle changes helps prevent type 2• poor dietary habits play a major role in the development of type 2 diabetes• there appears to be an association between the amount of caloric intake and de-

velopment of type 2 diabetes• high carbohydrate and low-fat diets appear to cause insulin sensitivity to deterio-

rate, but low-carb high-fat diets may decrease satiety and therefore leads to higher energy intake

• high-that diet combined with high alcohol intake may contribute to the develop-ment of diabetes

b) Ethnicity• there is wide variability in the risk of type two diabetes among different racial and

ethnic groups• highest to lowest incidence: American Indians, African Americans, Hispanics,

Asian Americans, Whitesc) Obesity

• strongly associated with the development of type 2• central body obesity

• marker for glucose intolerance hyperinsulinemia and hypertriglyceridemia• type 2 and prediabetes are manifestations of an underlying disorder termed

metabolic syndromed) Metabolic Syndrome• A group of metabolic abnormalities that predispose individuals to CVD and type 2• Primary abnormalities

• insulin resistance• glucose intolerance• hyperinsulinemia• hypertriglyceridemia• decreased HDL cholesterol • central obesity• hypertension

• 3 or more abnormalities must be present:• high BP (> 130/85 mmHg)• hypertriglyceridemia (> 150 mg/dL)• low HDL (< 40 mg/dL in men, < 50 in women)• abdominal obesity (waist circumference > 102 cm in men, > 88 cm in women)• elevated fasting glucose (> 100 mg/dL)

• aka: insulin resistance syndrome - resistance and hyperinsulinemia leads to hy-perglycemia• causes an inflammatory process in the vascular endothelial lining ==> further

increases insulin resistance, increases hyperglycemia and damages the en-dothelium

C. Gestational Diabetes Mellitus• gestational diabetes mellitus (GDM) - a condition in which the onset of diabetes oc-

curs during pregnancy

D. Other Specific Types of Diabetes1. Monogenic Diabetes

a) Epidemiology, Etiology, and Risk Factors• neonatal diabetes mellitus (NDM) - monogenic diabetes (diabetes caused by a

single-gene mutation) that occurs in newborns and young infants• maturity-onset diabetes of the young (MODY) - monogenic diabetes that first

occurs during adolescence or early adulthoodb) Clinical Manifestations and Pathophysiologyc) Medical Management

2. Latent Autoimmune Diabetes in Adultsa) Epidemiology, Etiology, and Risk Factors• latent autoimmune diabetes in adults (LADA) - a genetically linked, hereditary

autoimmune disease that is sometimes referred to as type 1.5 diabetes; in this condition, the body mistakes the pancreas as foreign and responds by attaching and destroying the insulin-producing beta islet cells of the pancreas

b) Clinical Manifestations and Pathophysiologyc) Medical Management

3. Secondary Diabetes• secondary diabetes - the same as type 1 and type 2 diabetes in the regard that it

is caused by the pancreas’ inability to produce sufficient amounts of insulin, but oc-curs as a reaction to other internal diseases or conditions

a) Epidemiology, Etiology, and Pathophysiologyb) Clinical Manifestations, Laboratory Tests, and Medical Management

E. Prediabetes• prediabetes - a term used to identify people with glucose intolerance who are at in-

creased risk for developing diabetes

III. Physiology of Fuel Metabolism • pancreas

• exocrine - acini secrete digestive enzymes• endocrine - islets of Langerhans secrete hormones

• alpha cells - glucagon• beta cells - insulin• delta cells - somatostatin: inhibit release of insulin and glucagon• F cells - pancreatic polypeptide: role unknown

• fuel metabolism• effects of insulin

• synthesis of glycogen in liver and muscle• synthesis of protein in liver and muscle• synthesis of triglycerides in adipose tissue, and minimally in muscle• necessary for:

• glycolysis to make energy (ATP and NAD)• glucose transport (mostly to skeletal muscle)• suppression of gluconeogenesis, glycogenolysis, lipolysis• promotion of glucose uptake and utilization in tissues (especially in skeletal mus-

cle) - prevents hyperglycemia and maintaining proper glucose levels after meals• counterregulatory hormones - oppose the effects of insulin

• glucagon• hepatic gluconeogenesis• glycogenolysis• lipolysis• ketogenesis

• cortisol• protein catabolism• lipolysis

• provide precursors for gluconeogenesis and ketogenesis• growth hormone

• lipolysis• also provides precursors for gluconeogenesis and ketogenesis

• epinephrine• glycogenolysis• gluconeogenesis• lipolysis

• norepinephrine• primary metabolic goal after a meal: maintain normal blood glucose levels

• insulin levels increase - stimulates glucose uptake• excess glucose is stored as glycogen or lipids

• glucagon levels decrease• primary metabolic goal during fasting: provide glucose for the brain and nervous tis-

sue• glucagon levels increase

• stimulates hepatic glycogenolysis and gluconeogenesis = increased plasma glu-cose levels (mainly from gluconeogenesis)

• stimulates lipolysis = free fatty acids for energy, ketones for brain energy• insulin levels decrease

• fuel metabolism regulation:• hepatic glucose production• glucose uptake and utilization• insulin, glucagon and other counterregulatory hormones

• metabolic abnormalities in diabetes:• type 1 - complete loss of insulin

• increased free fatty acids from adipose tissue = increased ketone bodies = may re-sult in diabetic ketoacidosis

• type 2 - involves decrease in insulin production and resistance• resistance: inability of target tissues to achieve normal response• results from insulin deficiency and increase in glucagon and other counter regula-

tory hormones• hyperglycemia from:

• decreased insulin• hepatic gluconeogenesis• hepatic and muscle glycogenolysis

A. Pathophysiology of Type 1 Diabetes• environmental factors trigger an immune response• progressive loss of pancreatic beta cell mass - 80%-90% loss = overt type 1• honeymoon period - period after onset of overt type 1 characterized by endogenous

insulin production:• manifested by moderate reductions in insulin requirements up to normalization of

glucose tolerance• followed by loss of insulin production and dependence on exogenous insulin

B. Pathophysiology of Type 2 Diabetes• characterized by:

• decreased liver, muscle, and adipose tissue sensitivity to insulin• defect in insulin secretion from beta cells

• 3 stages:1. genetic factors and environment affect insulin sensitivity and secretion - initial pe-

riod of hyperinsulinemia, ability to maintain glucose tolerance2. insulin resistance increases - hyperinsulinemia becomes insufficient; associated

with enhanced lipolysis => free fatty acids increase => insulin resistance is exac-erbated => impaired glucose uptake => hyperinsulinemia ==> beta cell secretory defect d/t genetics/beta cell exhaustion ====> results in postprandial hyper-glycemia with normal fasting glucose

3. further increase in insulin resistance; impaired control of hepatic glucose produc-tion; hyperglycemia toxic to beta cells ==> insulin secretion declines slowly ====> results in fasting AND postprandial hyperglycemia

IV. Clinical Manifestations of Type 1 and Type 2 Diabetes • hyperglycemia - high blood glucose; characterized by glucosuria, osmotic diuresis,

polyuria, nocturia, hypotension, tachycardia, polydipsia, polyphagia, weight loss, fatigue• glucosuria - glucose in urine associated with an osmotic diuresis, an increase in urine

volume caused by an osmotic substance in the renal tubules (glucose)• polyphagia - increased appetite resulting from the significant loss of calories that occurs

through the loss of calories in the urine• Type 1 manifestations originate from hyperglycemia and ketosis• Type 2 manifestations originate from hyperglycemia• Manifestations

• glucosuria• osmotic diuresis• polyuria• nocturia• hypotension• tachycardia• polydipsia• polyphagia• weight loss• fatigue

A. Complications of Diabetes• Increased susceptibility to infection

• Inflammatory response is diminished• Slower than normal healing

• Cardiac disease• Neuropathies, retinopathies & nephropathies• PAD• Gastroparesis• Foot ulcers• Periodontal disease

• Skin infections, itching, dermopathy, blisters• Hearing loss• Hypertension• Stroke• Neurogenic bladder• Diabetic diarrhea• Ketoacidosis• Hyperosmolar hyperglycemic state• Sexual dysfunction

V. Laboratory Tests and Diagnostic Procedures • diabetes requires frequent blood glucose monitoring

• basis for diagnoses and therapeutic goals - adjustments in diet, physical activity, and pharmacologic therapy

A. Blood Glucose Levels• fasting (no food/drink except H2O for 10-12 hours)

• can be used in diagnosing prediabetes and diabetes• useful for daily monitoring of glycemic control• normal: 70-110 mg/dL; prediabetes 100-125; older adult 70-120

B. Oral Glucose Tolerance Tests• useful in confirming diagnosis of diabetes• fasting 10 hours prior• carbohydrate intake of 150 g/day for 3 days prior• no smoking during test

C. Self-Monitoring of Blood Glucose• used to make immediate decisions e.g., insulin dose prior to meals• used to make therapeutic decisions based on trends over time• preprandial, postprandial, or during presence of clinical symptoms• capillary blood glucose levels using glucometers

D. Continuous Blood Glucose Monitoring• continuous intermittent measurement of glucose level in interstitial fluid• sensor with a small cannula inserted into SQ tissue

E. Hemoglobin A1C Test• primary laboratory test used for monitoring longer term glucose control (2-3 months)• hemoglobin A1c (Hgb A1c) - a stable glycated hemoglobin complex formed when

glucose in the blood binds irreversibly to hemoglobin• normal: 2-5%; diabetic control: 2.5-6%; high average: 6.1-7.5%

F. Urinary Glucose• glucose is present in urine when blood levels are elevated

• presence warrants further testing

G. Urinary and Blood Ketones• ketones normally not present except following fasting and first morning urine of preg-

nant women• detectable urinary ketones = large amounts of serum ketones = DKA• serum acetone is > 50 mg/dL in DKA

H. Diabetes Diagnosis• National Guidelines for Establishing a Diagnosis of Diabetes

• fasting blood sugar over 126 mg/dL on more than one occasion w/ or w/o symp-toms

• casual serum blood glucose over 200 mg/dL with symptoms• 2 hour oral glucose tolerance test of over 200 mg/dL at 2 hours following 75 g glu-

cose intake• Additional criteria

• HgbA1c 6.5% or higher• C-peptide negative (no insulin produced)• Urine positive for glucose and/or ketones

I. Prediabetes Diagnosis• impaired glucose tolerance often occurs with metabolic syndrome• OGTT will show impaired glucose tolerance• some will not have metabolic syndrome• FPG = 110-125 mg/dL x2• OGTT = >140 and <200 @2hrs

VI. Medical Management • combination of pharmacologic and nonmusical therapy toward normalization of:

• blood glucose• BP• blood lipid levels

• Type 1 - insulin replacement therapy• Type 2 - insulin, oral medications, or a combination of both• other meds: antihypertensives, lipid-lowering drugs• important part of treatment: exercise, good nutrition, lifestyle changes

A. Goals of Diabetes Management• overall goal:

• prevention of chronic long-term complications• short-term goals - prevention of:

• severe hypoglycemia• hyperglycemia• acute complications such as DKA and HHS

• long-term goals:

• normalizing blood glucose levels• preventing systemic complications

• improvements in glycemic control = reduction of microvascular complications (i.e., neuropathy, nephroppathy, and retinopathy)• hypertension - associated with microvascular complications; lower BP reduced

them• CVD reductions - not statistically significant

• glycemic goals: • A1c < 7.0% (individualized)• preprandial 90-130• postprandial <180

• BP goal: <130/80• Lipid goals:

• LDL <100• triglycerides <150• HDL > 40

B. Management of Type 1 Diabetes• insulin replacement therapy via injection or pump1. Insulin Preparations

• synthetic human insulin produced by recombinant DNA technology - mimics the ab-sorption and biologic activity of endogenous insulin

• preparations are characterized by onset, peaks, and duration of action• goal: mimic normal pattern of basal and meal-stimulated insulin secretiona) Rapid-Acting Insulin• onset: 15 min; peak 1-2 hrs• most effective in reducing postprandial hyperglycemia• routinely administered right before meal/snack, but better if after to avoid hypo-

glycemiab) Short-Acting Insulin (regular insulin)• injected before meals approximately 30-45 minutes prior• rapid acting resemble endogenous insulin secretion more closely than this

c) Intermediate-Acting Insulin (NPH)• slow onset, prolonged peak effect (too high for basal), lengthened duration• to provide basal insulin coverage (2x/day)

d) Long-Acting Insulin• to provide basal insulin with relatively small peak action

e) Premixed Insulins• most common is 70/30 NPH/regular• helpful for patients who have difficulty mixing insulins but impossible to adjust

dose of one without affecting the otherf) Incretin Mimetics• incretin mimetic - a class of medications that enhances glucose-dependent in-

sulin secretion from the pancreatic beta cells• effect: reduction in postprandial glucose levels

g) Amylin Analog (Pramlintide)• synthetic analog of hormone secreted by beta cells• reduces postprandial blood glucose by slowing gastric emptying, suppressing

glucagon, and promoting satiety• injected SQ immediately before meals for

• improving glycemic control in type 2• adjuvant mealtime TX in type 1

2. Insulin Delivery Devices• pens, insulin cartridges• continuous subcutaneous insulin infusion (CSII) - a method of intensive insulin

therapy via pump that is used in the management of diabetes3. Insulin Regimens

• goal in type 1: normalize blood glucose levels by mimicking closely the basal and meal-stimulated insulin release

a) Twice-Daily Insulin Injection Regimen• NPH + regular/rapid-acting (prior to breakfast and dinner)• no flexibility in changing mealtimes• peak effect of NPH predisposes to hypoglycemia if meals are skipped

b) Three-Times-Daily Insulin Injection Regimen• NPH + regular/rapid-acting (B); regular/rapid-acting (D); NPH (HS)• last NPH peak coincides with secretion of growth hormone• useful for people with high fasting glucose levels on awakening• fasting hyperglycemia caused by:

• dawn phenomenon - fasting hyperglycemia without prior nocturnal hypo-glycemia; d/t secretion of growth hormone or pregnancy

• Somogyi effect - fasting hyperglycemia with prior hypoglycemiac) Four-Times-Daily Insulin Injection Regimen• NPH + regular/rapid-acting (B); regular/rapid-acting (L+D); NPH (HS)

d) Other Insulin Regimens• peakless (glargine) + rapid acting• insulin pump with short/rapid at a basal rate and manual bolus prior to meals

Nursing Management of insulin tx• instructing patients in insulin delivery technique• reviewing insulin delivery technique for those who have been on them before ini-

tial visit• instructing on their specific insulin regimens and assessing understanding• instructing pt on rel btw glucose monitoring and insulin regimen• instructing pt on how adjustments in insulin tx may affect glycemic control• understanding S&S of hypoglycemia and hyperglycemia

C. Management of Type 2 Diabetes• previous standard: diet and exercise, then drugs• present standard: oral medications as early intervention1. Oral Diabetes Medications

a) Sulfonylureas - enhance insulin secretion

• c/i: sulfa allergyb) Meglitinides - causes rapid secretion of insulinc) Alpha-Glucosidase Inhibitors - delay digestion and absorption of intestinal carbo-

hydrated) Biguanides - reduce hepatic glucose production; improve insulin sensitivity• cautious use in alcohol abusers; with contrast dyes and after any surgery

e) Thiazolidinediones - improve insulin sensitivityf) Dipeptidyl Peptidase-4 Inhibitors - increase postprandial insulin secretiong) Combinations of Oral Medications• different meds with varying mechanisms may be used in combination• general principles

• fails on one, combine rather than stop one and substitute another• near max dose for one, combine rather than increase dose• secondary failure of 2-drug combo is expected; add 3rd drug or better yet in-

sulin, or switch entirely to insulin2. Insulin Therapy for Type 2 Diabetes

• purpose: provide adequate insulin to supplement the reduction in insulin secretion and overcome insulin resistance

• type 2 may respond to oral meds but possibly require insulin over time• risk of heart failure in thiazolidinediones with type 2

Nursing Management re: oral hypoglycemic tx• instructing pt in prescribed oral meds• reviewing oral tx who have been on them prior to initial visit• instructing pt on rel btw glucose monitoring and oral hypoglycemic meds• helping them understand how adjustments may affect control• understanding S&S of hypo- and hyperglycemia

VII. Nutrition and DiabetesA. Micronutrients and Macronutrients in the DietB. Medical Nutrition TherapyC. Nutritional Needs of Hospitalized Patients

VIII. Exercise and Physical ActivityA. Exercise and Diabetes ComplicationsB. Exercise Prescriptions

IX. Management of Hospitalized Patients with DiabetesA. Hyperglycemia in Acute IllnessB. Target Glucose Levels for Hospitalized PatientsC. Insulin Protocols Designed to Meet Treatment Goals in Hospitalized PatientsD. Diabetic Ketoacidosis

• diabetic ketoacidosis (DKA) - a life-threatening complication precipitated by an acute or relative deficiency in insulin secretion that changes in relationship to develop-ment of insulin resistance and level of blood glucose and characterized by profound disturbances in metabolism of CHO, fat, and protein

E. Hyperosmolar Hyperglycemic Syndrome

• hyperosmolar hyperglycemic syndrome - (aka hyperosmolar hyperglycemic nonke-totic syndrome) a life-threatening complication characterized by serumm hyperosmo-larity, dehydration, and hyperglycemia; restricted to patients who cannot recognize their thirst or express their need for water

F. Hypoglycemia1. Hypoglycemia Unawareness• hypoglycemia - results from an imbalance between glucose production and glucose

utilization that occurs when glucose use exceeds glucose production• autonomic symptoms

• adrenergic - tremors, palpitations, nervousness, anxiety• cholinergic - sweating and hunger

• neuroglycopenic symptoms• irritability, confusion, drowsiness, weakness, difficulty speaking, unresponsive-

ness, unconsciousness, seizures, coma• hypoglycemia unawareness - the loss of autonomic nervous system responses to

low blood glucoseG. Etiology and Precipitating Factors of DKA, HHS, and Hypoglycemia

1. Pathophysiology of Diabetic Ketoacidosisa) Insulin Deficiency and Carbohydrate Metabolismb) Insulin Deficiency and Fat Metabolism• Kussmaul respirations - deep and rapid respirations accompanied by an ace-

tone odor to the breathc) Insulin Deficiency and Protein Metabolismd) Couterregulatory Hormones

2. Pathophysiology of Hyperosmolar Hyperglycemic Syndrome3. Pathophysiology of Hypoglycemia

H. Clinical Manifestations of DKA, HHS, and HypoglycemiaI. Primary Laboratory and Diagnostic ProceduresJ. Medical and Nursing Management of DKA, HHS, and Hypoglycemia

X. Chronic Complications of Diabetes and Associated Medical TreatmentA. Diseases of the Heart and Blood VesselsB. Kidney DiseaseC. Blindness and Other Visual DisordersD. Neuropathy

• diabetic peripheral neuropathy (DPN) - polyneuropathy most commonly seen in the legs, feet, and hands; a significant factor in the pathway leading to lower extremity ul-ceration, a potentially very serious complication of diabetes

E. Vascular and Neuropathic Complications Leading to Lower Extremity AmputationsF. Charcot DeformityG. Gastrointestinal DisturbancesH. Diabetic DiarrheaI. Oral/Dental ProblemsJ. Complications of PregnancyK. Foot ProblemsL. Health Promotion, Diabetes Education, and Cultural Implications

XI. Gerontological ConsiderationsXII. ResearchXIII. Summary