Nursing Care Of Patients With Diabetes Mellitus

NURSING CARE OF PATIENTS WITH DIABETES MELLITUS Definition • •

Diabetes is a chronic disorder of altered carbohydrate, fat and protein metabolism caused either by a relative or absolute lack of insulin Greek verb diabetes meaning "to run through" Latin Mellitus meaning "honey" Results of the disease

• • •

persistent hyperglycemia Impaired leukocyte activity long term vascular and neurologic degeneration Islets of Langerhans

• • •

Consist of three types of cells (little islands) in the pancreas which secrete hormones Alpha cells secrete Glucogon which is released in response to low levels of glucose, protein ingestion and exercise Delta cells secrete gastrin & somatostatin which inhibit release of insulin Insulin

• • •

Hormone secreted by the beta cells in the islets of Langerhans in the pancreas Primary function is to transport glucose into cells to be used for energy (brain, nerve, hepaticytes, intestinal mucosa cells & kidney tubule cells don’t need insulin) Insulin affects carbohydrate, fat, & protein metabolism & lowers blood glucose levels Carbohydrate Metabolism

• • •

Insulin attaches to the receptors on the cell wall causing glucose to be transported into the cell Insulin also causes the liver to convert glucose into glycogen for storage (glucogenesis) When glucose blood levels get low the liver reconverts the glycogen back into glucose (glucogenolysis) resulting in raising blood sugar levels Fat Metabolism

•

Glucose that is not needed by the body is converted into fat & triglyceride with the help of insulin ( lipogenesis) Protein Metabolism

• •

Insulin also promotes the entry of amino acids into cells and decreases the rate at which amino acids are released from cells Protein is not stored by the body - If you eat it and it’s not needed the nitrogen is stripped and thrown away by the kidneys and the rest is stored as fat Counter Regulatory Hormones

•

•

When the blood sugar gets too low the Alpha cells of the islets of Langerhans begin to secrete Glucagon which causes the liver to begin to convert the glycogen into glucose and dump it into the blood stream Epinephrine causes a similar but weaker effect Counter Regulatory Hormones

• •

Cortisol (from the adrenal cortex) causes the conversion of protein & fat into glycogen & then into glucose Somatotropin and Somatastatin also affect blood glucose levels Absence of Insulin

•

Without insulin the glucose cannot get into cells which results in hyperglycemia & cell starvation. Protein cannot be manufactured because the cells have no amino acids from which to manufacture it. The liver begins to convert glycogen into glucose and dump it into the blood stream which causes even higher glucose levels Absence of Insulin

•

Since the cells are starving the body begins to convert fat into usable glycerol and this conversion releases ketone bodies into the blood stream Ketones

•

•

Ketones are eliminated by the kidneys and can be measured in the urine. High ketone levels are an indication of high blood sugar levels. (Acitest) The ketones combine with sodium & the sodium is replaced with H+ which in turn causes acidosis The body tries to correct the acidosis by increasing the respiratory rate and depth (Kussmals respirations) Absence of Insulin

•

• •

The kidneys also try to throw away the extra glucose, but to do so they must throw away some water with it (& some electrolytes) - so the patient gets dehydrated because of the large urine output The kidneys usually will not spill glucose until the blood levels get to about 180 (normals 70 -110) the level at which a person spills sugar varies and is called the renal threshold Because of the dehydration the patient gets thirsty Diabetes Mellitus

• • • •

Leading cause of blindness in adults between ages 20 - 74 Accounts for 30% of new cases of end stage renal disease Accounts for 50 - 60% of adult deaths from coronary heart disease Accounts for 40 - 50% of nontraumatic amputations for foot or ankle ulcers Diabetes Mellitus

• •

725,000 new cases are diagnosed each year Health care expenditures of $105.2 billion in 1992 (14.6% of total health care expenditures)

Etiology and Pathophysiology • • •

Type 1 (also known as Juvenile & Insulin Dependent Diabetes) is an autoimmune disease More than 90% of these patients have antibodies directed against their own islet cells Studies show that Type I Patients have human leukocyte antigen molecules on chromosome 6 (HLA-DR3,-DR4) Etiology and Pathophysiology

• • • • •

People at risk Strong Family history of diabetes African-American, Hispanic or Native American descent Obese History of delivering infants weighing > 9# (or gestational diabetes) Etiology and Pathophysiology

• •

Identical twins have 50% chance of both getting the disease (type 2) when one twin has it - but fraternal twins have 90% chance - strange! Studies are underway to test the Drug Imuran (an immunosuppressant) for diabetes prevention Classifications of Diabetes Mellitus

• • • •

Type 1 (also known as Juvenile & Insulin Dependent Diabetes) 10% of diabetics - abrupt onset Usually occurs before age 40 but can happen in older people B cells don’t produce insulin - must have insulin injections Classifications of Diabetes Mellitus

• • • •

Type 2 (AKA non-insulin dependent or Adult onset diabetes Usually occurs after age 40 B cells produce - maybe not enough - but most often the insulin will not bind to the receptor sites on the cells May be related to defective receptors, or not enough receptors, or the inside of the cell is defective More on Type 2 Diabetes

• • •

Insulin resistance stimulates a compensatory increased insulin production by beta cells in the pancreas These people can sometimes control their diabetes by staying on a strict diet and exercising If that doesn’t work they can be prescribed Oral hypoglycemic medications More on Type 2 Diabetes

• •

If the oral hypoglycemic meds don’t work they must get insulin Many type 2 diabetics require insulin during stress but return to oral hypoglycemics when the stress is relieved (they are not insulin dependent)

Gestational Diabetes • • •

Arises during pregnancy and usually disappears after delivery. associated with fetal mobidity requires tight control Women with gestational diabetes have increased risk of developing diabetes later in life Clinical Manifestations

• • • •

Type 1 Sudden onset of polyuria, polydipsia, and polyphagia. Weight loss despite increased food intake, extreme fatigus and pruitus and vaginal itching Thin under 40 YOA. Prone to developing ketosis Must take insulin Clinical Manifestations

• • •

Type 2 Rarely develop polyuria, polydipsia or polyphagia & if they do the symptoms are less severe than type 1 patients (women do have vaginitis leading to vaginal itching) Usually over 30 YOA and obese - can control disease with diet & exercise and can take oral hypoglycemics Diagnosis

• • • • • •

Symptoms of diabetes plus a casual blood sugar > 200 (casual = any time of day without regard to when they ate last) OR Fasting blood sugar of 126 mg/dl or higher (fasting = NPO >8hrs) OR 2 hour blood sugar level of >200 during a GTT (WHO guidlines) AND confirmed on the following day Diagnosis

• •

For gestational diabetes the figures are different but you will not be tested over pregnancy in this class (wait till next year!) Impaired glucose tolerance is more than normal limite (70 - 110) but not as high as the criteria for full blown diabetes. It is a warning sign that the patient could become diabetic, but with careful management can avoid it. GTT 2 hr FBS of >140 but<200 Management

• •

Diet - cornerstone of diabetic treatment - lack of adherence to the diet is the one area of self-management most responsible for poor control of diabetes most widespread & currently accepted diet is the exchange diet created by the American Diabetes Association Diabetic Diets

• • •

55-60% of total calories should be carbohydrates (complex preferred) 15 -20% protein Less than 30% fat cholesterol should be < 300 mg/day & sodium < 3 gm

Diabetic Diets •

•

some foods are free foods because they have fewer than 20 calories per serving (sugar free carbonated drinks, coffee, tea, lettuce, sugar free geletin and 1 tbsp catsup seasonings) All diabetic patients require diet education and many behavior modification Diet Education

• •

A specific # of calories is prescribed for each patient depending upon patient’s body weight, occupation, age, activities, and type of diabetes responses to the diet should be monitored & adjustments made as necessary Diet Education

• • • • •

Never skip meals Eat at regularly spaced intervals Recognize appropriate food portions Alcohol can cause hypoglycemia in patients on glucose lowering agents but is high in calories (eat CHO with drink) Alcohol may produce Antabuse effect porportional to the amount ingested with certain OHA’s Exercise

•

Benefits of exercise: improved insulin sensitivity, potential improvement in glucose tolerance in some patients, promotion of weight loss and attainment of goal body weight, improved cardiovascular status, reduced cholesterol and triglyceride levels, potential reduction of insulin or oral hypoglycemic dosages, improved sense of well being Exercise

• • •

should be avoided if blood sugar is > 250 (increases secretion of glucagon and growth hormone, causing the liver to release more glucose) If blood glucose is low, the patient may need to eat a fruit exchange Diabetics on medication should always carry a simple carbohydrate when exercising (lemon drops)

Oral Hypoglycemic Agents • •

Sulfonylureas are used for type II diabetics who have some functioning beta cells It stimulates the beta cells to produce more insulin, reduces the accelerated rate of hepatic glucose production in type 2 diabetics, partially reduces the number of cellular insulin receptors Oral Hypoglycemic Agents

• •

First generation OHA’s Orinase, Dymelor, Tolinase, Diabenese Second generation (called that because they came on the scene later) Glucotrol, Micronase, DiaBeta, Glynase

•

2nd generation drugs have fewer adverse effects, are about 100 times more potent by weight & have more predictable time actions and half-lives - but they are expensive Metformin (Glucophage)

• • •

Not a sulfonylurea Not bound to plasma proteins, is not metabolized in the liver and is eliminated rapidly by the kidneys It lowers blood sugar but does not cause hypoglycemia Insulin

• •

Beta Cells stop producing insulin in Type 1 diabetics so they must have insulin to survive. Type 2 diabetics also must have insulin if their blood sugar is not controlled by diet and exercise or diet & exercise & OHA or in stress producing situations as a temporary measure Types of Insulin

• •

Beef (made from cow pancreas) was most commonly used kind until about 10 years ago) Pork was used by some people who did not respond well to the beef insulin -patients could have insulin allergies or reactions to proteins left in the insulin during the extracting process Humulin Insulin

• •

Humulin insulin is a biosynthetic insulin made by altering common bacteria (E-Coli) using recombinant deoxyriboneucleic acid (DNA) technology. It is identical to human insulin By adding chemicals, the length of time the insulin is active can be altered Catagories of Insulin

• • • •

Onset Peak Duration Rapid acting 1/2-1hr 2-4 hrs 5-7 hrs Intermediate 2-4 hrs 8-12 hrs 18-24 hr Long Acting 4-6 hrs 18-24 hrs >36hrs Examples of Insulins

•

Rapid acting - Regular (Humulin R,

Iletin I R, Semi Lente) •

Intermediate - NPH ( Humulin N,

Iletin NPH, Iletin I Lente) • • Regular

Long Acting - Ultra Lente, Humulin U Mixtures - 70/30 (70% NPH & 30%

Injections • • •

Some patients inject themselves several times a day Others inject themselves only once Goal of insulin treatment is to mimic the pattern of nurmal insulin secretion Preparation and Injecting Insulin

•

Will be discussed and practiced during clinical time Teaching about Insulin

• • • •

Store unopened insulin in the refrigerator. Do not freeze Store opened bottles that will be used within a month at room temperature Bring refrigerated insulin to room temperature before injecting Do not expose to sunlight Teaching about Insulin

•

• • • • •

Rotate injection sites to avoid lipodystrophy. Do not inject within 1 inch of the previous injection site. Best to use the abdomen for consistent absorption. Do not inject into a part which will be exercised that day Insulin pumps are available but they are expensive $4100 to $10,000 Blood Glucose Monitoring Many machines are available Patient should be matched to a machine (cognitive functioning and physical coordination) Many patients test their own blood sugar 4 times/day - but most only do it once while at home. Urine Testing

• • •

Testing urine for glucose is not considered accurate Testing urine for ketones is done frequently during pregnancy Ketones in the urine indicate that the body cannot utilize carbohydrates & is having to use fats for energy Glycosylated Hemoglobin

• • • •

Also called Hemoglobin A1c Provides an overview of the glucose levels for the previous 3 months Normals are 7% - 11% Greater than 15% indicates that the disease is out of control Acute Complications of DM

• •

Diabetic Ketoacidosis - occurs most often in type 1 diabetes seldom in type 2 Severe disturbances in protein, fat & carbohydrate metabolism resulting from profound insulin deficiency Diabetic Ketoacidosis

•

Patient develops severe hyperglycemia, osmotic diuresis, dehydration, hyperlipidemia, & metabolic acidosis. Ketones are lost in the urine & electrolytes are depleated Diabetic Ketoacidosis

•

•

Symptoms - hyperglycemia, polyuria, polydipsia, weakness, lethargy, anorexia, nausea, vomiting, blurred vision, headache, muscle aches, abdominal pain, sodium & potassium depletion Thirst, dry mucous membranes, loss of skin turgor, sunken eyeballs, renal failure, hypovolemic shock, Kussmals respirations, fruity smelling breath Diabetic Ketoacidosis

•

Treatment - Insulin is given IV in .45% NaCl to treat the hyperglycemia, 1 -2 liters of fluid in the first 2 -3 hours to treat the hypovolemia, and potassium to correct the electrolyte depletion Hyperglycemic Hyperosmolar Nonketotic Syndrome

•

•

Similar to Ketoacidosis but this occurs in Type II diabetics and Ketones are not found in the blood or urine (since the patient’s beta cells produce some insulin the body does not need to use fats etc and ketones do not develop Occurs slowly and almost always in elderly patients who are not getting enough fluids Hyperglycemic Hyperosmolar Nonketotic Syndrome

• • •

Watch for HHNK in patients who are receiving tube feedings (concentrated fluid without enough water Also in patients with diarrhea, vomiting, severe burns, dialysis Treatment is rehydrate, replace electrolytes Hypoglycemia

• •

Blood glucose levels fall below 50 Caused from taking too much insulin, not eating enough, excessive physical activity, ingestion of alcohol especially when not eating Hypoglycemia

•

Symptoms of mild hypoglycemia (50 -60 blood sugar) - sudden tremors, palpitations, diaphoresis & hunger - treat with 4 -6 ounces juice or 6 -10 life savers Hypoglycemia

•

•

Symptoms of moderate hypoglycemia - All of the above + headache, mood changes, irritability, inability to concentrate, confusion, slurred speech, irrational behavior, blurred vision, impaired judgement, drowsiness - treat with second dose of simple carbohydrate Severe hypoglycemia - unconscious, convulsing - treat with IV glucose or IM glucogon Somoyi Phenomenon

• •

Usually occurs at night episode of hypoglycemia & oversecretion of counterregulatory hormones which produces hyperglycemia Somogyi Phenomenon

•

•

Phenomenon suspected when blood sugar keeps going up despite increasing dosages of insulin or when patients wake with headache, nightmares or enuresis or unexplained N&V Treatment is decrease evening insulin dose & give bedtime snack Cost of Being a Diabetic

• • • •

Humulin N is $17.13 a bottle at Wal Mart Syringes are $16.96 for a box of 100 Glucose monitoring machines & test strips are expensive and have short expiration dates Glucophage 500mg is $30.98 for 50 tablets Management during illness

• • •

fever, influenza, vomiting & diarrhea can lead rapidly to hyperglycemia in diabetics Stress increases secretion of counter regulatory hormones glucogon, epinephrine and cortisol thereby raising blood glucose levels hyperglycemia leads to osmotic diuresis (fluid, glucose and electrolytes are lost) Call the Doctor

• • •

Blood glucose >250 & ketonuria lasts > 6 hrs Signs of dehydration occur (dry mucous membranes, lightheadedness, lethargy, decreased urine output) Symptoms of ketoacidosis occur (fruity odor to breath, abdominal pain, air hunger) Call the Doctor

• •

Patient cannot retain fluids or food or 4 hours Don’t stop taking insulin when sick Long Term Degenerative Changes of Diabetes Mellitus

• •

•

Tight control reduces incidence and onset of complications Microvascular disease (thickening of the capillary basement membrane that surrounds the endothelial cells of the capillary, increased capillary permeability and capillary occlusion) Affects the areterioles, venules, & capillaries Diabetic Retinopathy

• • •

Leading cause of blindness in the United States Characterized by deterioration of the small blood vessels in the retina After 10 years of having diabetes 50% of all diabetics have it and 90% of those who have poor control of blood glucose levels

Diabetic Retinopathy • • •

All diabetic patients should undergo eye examination by an ophyalmologist annually Should have intraocular pressure measurement and dilated pupil fundus examination fluorescein angiography is performed to assess reinal vessels & macular edema Diabetic Neuropathy

• • •

Occurs in 70% of diabetic patients Prevalence increases with age and severity of hyperglycemia Results in loss of large and small myelin nerve fibers, connective tissue proliferation and thickening of the capillary basement membrane Diabetic Neuropathy

• •

Can have mononeuropathy such as carpal tunnel syndrome, extraocular motor paralysis & footdrop Most patients have numbness, tingling, burning, dull ache & cramping that begins in the digits & progresses to the foot and hand (worse at night) Diabetic Neuropathy

• •

This progresses to muscle weakness & sensory loss, an unbalanced gait, foot ulcers and lossof fine motor skills. Sensory neuropathy leads to loss of pain & pressure sensation & increases the risk of undetected injury, tissue ischemia or infection Diabetic Neuropathy

• • •

Additional systems can be affected: Autonomic nervous - causes orthostatic hypotension and mild persistent tachycardia or profuse sweating while eating, drying and cracking of the skin of the feet Gastrointestinal - gastroparesis (delayed emptying of the stomach, nausea & vomiting) Watery diarrhea (often at night without warning) followed by constipation Diabetic Neuropathy

• •

Urinary - frequent urinary tract infections and incontinence Sexual - Impotence in men and inability to have an orgasm Diabetic Nephropathy

• • •

Characterized by proteinuria, hypertension,edema and renal insufficiency Occurs in patients with Type 1 diabetes after 15 -20 years (30% to 40% progress to endstage renal disease) Occurs after 5 to 10 years with Type 2 diabetics Diabetic Nephropathy

•

deterioration of kidney function takes place over many years - first sign is protein in the urine

•

Nephrotic syndrome is diagnosed when protein excreted exceeds 3.5 g/d. When protein is lost in the urine the serum protein also decreases. Low serum protein causes decreased oncotic pressure and retention of fluid, weight gain edema, protein tissue wasting Diabetic Nephropathy

•

Nephrotic syndrome progresses to renal insufficiency when the GFR falls to >25 to 30 mL/min (normal is 125 mL/min) and the patient has elevated serum creatinine and blood urea nitrogen levels Diabetic Nephropathy

•

•

Uremia is the next progression (digression) & is diagnosed when the GFR is below 15 mL/min and serum creatinine is greater than 4 to 5 mg/dl (pt will have nausea, vomiting lethargy, anemia, hypertension & acidosis) Patients with nephropathy are at increased risk of renal failure following radiocontrase procedures such as IVP or CAT scans Assessment of Diabetic Patients

• • • •

Be sure to assess what the patient knows and whether the information they give is correct How willing are they to learn How well have they integrated the many lifestyle changes into their regimen Can they see to draw up their insulin? What is their educational level? Monitoring and Self Care

•

foot care : inspect feet daily for sores, blisters, swelling, redness, & tenderness. Wash feet daily using mild soap.Pat dry and apply Lanolin type lotion (not between toes). Test water bfore putting feet in it. Do not soak feet. War shoes with soft linings. Do not walk barefooted in the house or outside. More Foot Care

•

Do not use hot water bottle . Cut toenails straight and even with the toe. If fungus infected have the podiatrist care for them. Have a podiatrist treat any foot problems like corns or calluses. Do not cross legs at the knees or ankles Possible Nursing Diagnoses

• • • • • •

Anticipatory grieving Ineffective individual coping Fluid volume deficit Altered peripheral tissue perfusion Risk for injury Risk for altered health maintenance