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  • 1 SEMINAR ON DIABETES MELLITUS Submitted To: Submitted By Mr.Mohammed Nasim Jasmin T V Lecturer Msc Nursing 1st year Al- Shifa College of nursing Al- Shifa College of nursing Submitted On: 18-7-2013
  • 2 CENTRAL OBJECTIVE: At the end of session, the group will be able to acquire knowledge regarding diabetes mellitus and develop positive attitude towards care of patients with diabetes mellitus and will apply this knowledge in their daily practical situations. SPECIFIC OBJECTIVES: At the end of session, the group will be able to define diabetes mellitus understand types of diabetes mellitus describe classification of diabetes mellitus explain various signs and symptoms of diabetes mellitus explain various diagnostic studies used in diabetes mellitus discuss management of diabetes mellitus explain complications of diabetes mellitus
  • 3 INTRODUCTION Diabetes mellitus, a chronic disease characterized by elevated blood sugar levels, is a significant contributor to morbidity and mortality and throughout the world. Diabetes can cause debilitating and costly complications such as blindness, renal failure, lower extremity amputations, and cardiovascular disease. Much of the health and economic burden of diabetes can be averted through known prevention measures. Diabetes mellitus is known colloquially as "Sugar diabetes" as it results in excessively high levels of blood sugar and the presence of glucose in the urine. Symptoms of diabetes include a grossly exaggerated thirst, loss of weight, a sweet smell on the breath, a worsening appetite, and later on, cataracts can develop in the eyes. It certainly occurs in both dogs and cats, but is more common in the former. TERMINOLOGIES  Ketoacidosis: Ketoacidosis with an accumulation of ketone bodies, occurs primarily in diabetes mellitus  Gastroparesis: is a medical condition consisting of a paresis (partial paralysis) of the stomach also called delayed gastric emptying  Diabetes mellitus: It is a chronic multisystem disease related to abnormal insulin production, impaired insulin utilization, or both (American Diabetes Association) INCIDENCE According to recent estimates of epidemiology of Diabetes in India, approximately 285 million people worldwide (6.6%) in the 20–79 year age group will have diabetes in 2010 and by 2030, 438 million people (7.8%) of the adult population, is expected to have diabetes. Hospitalization rates for people with diabetes are 2.4 times greater for adults and 5.3 times greater for children than for the general population. The economic cost of diabetes continues to rise because of increasing health care costs and an aging population. Half of all people who have diabetes and who are older than 65 are
  • 4 hospitalized each year, and severe and life-threatening complications often contribute to the increased rates of hospitalization. ETIOLOGY AND PATHOPHYSIOLOGY Current theories link the causes of diabetes singly or in combination to genetic, autoimmune, viral and environmental factors. Regardless of its cause diabetes is a disorder of glucose metabolism related to absent or insufficient insulin supplies and or poor utilization of insulin that is available. NORMAL INSULIN METABOLISM Insulin is a hormone secreted by beta cells, which are one of four types of cells in the islets of Langerhans in the pancreas. Insulin is an anabolic, or storage, hormone. When a person eats a meal, insulin secretion increases and moves glucose from the blood into muscle, liver, and fat cells. In those cells, insulin: Transports and metabolizes glucose for energy Stimulates storage of glucose in the liver and muscle (in the Form of glycogen) Signals the liver to stop the release of glucose Enhances storage of dietary fat in adipose tissue Accelerates transport of amino acids (derived from dietary protein) into cells Insulin inhibits the breakdown of stored glucose, protein, and fat. During fasting periods (between meals and overnight) Pancreas continuously releases a small amount of insulin (basal insulin) another pancreatic hormone called glucagon (secreted by the alpha cells of the islets of Langerhans) is released when blood glucose levels decrease and stimulate the liver to release stored glucose. The insulin and the glucagon together maintain a constant level of glucose in the blood by stimulating the release of glucose from the liver. Initially, the liver produces glucose through the breakdown of glycogen (glycogenolysis). After 8 to 12 hours without food, the liver forms glucose from the breakdown of noncarbohydrate substances, including amino acids (gluconeogenesis).
  • 5 CLASSIFICATION TYPE 1 DIABETES MELLITUS Type 1 diabetes is characterized by destruction of the pancreatic beta cells which leads to alteration in the production of insulin. It is combined genetic, immunologic, and possibly environmental (eg, viral) factors contribute to beta cell destruction.  Genetic susceptibility is a common underlying factor in the development of type 1 diabetes. People do not inherit type 1 diabetes itself; rather, they inherit a genetic predisposition, or tendency, toward developing type 1 diabetes. genetic mutation causes killer (CD8) T-cell lymphocytes to attack and destroy the insulin-producing islet cells.  Autoantibodies against islet cells and against endogenous insulin have been detected in people at the time of diagnosis and even several years before the development of clinical signs of type 1 diabetes  Environmental factors, such as viruses or toxins, that may initiate destruction of the beta cells. Regardless of the specific etiology, the destruction of the beta cells results in decreased insulin production, unchecked glucose production by the liver, and fasting hyperglycemia. In addition, glucose derived from food cannot be stored in the liver but instead remains in the bloodstream and contributes to postprandial Hyperglycemia Onset of disease: it is associated with a long pre clinical period. The islet cell autoantibodies present for months to years before the onset of symptoms PRE-DIABETES MELLITUS People with pre-diabetes, which can lead to type 2 diabetes, heart disease, and stroke. People with pre-diabetes may have either impaired fasting glucose (IFG) or impaired glucose tolerance (IGT), or both. A person with IFG has a fasting blood glucose level of 100 to 125 mg/dL after an overnight fasting. In IGT, a person has a blood glucose level of 140 to 199 mg/dL after a glucose tolerance test lasting 2 hours. A significant number of those with pre-diabetes will develop the disease; however, many can delay or avoid type 2 diabetes with weight loss and increased physical activity.
  • 6 TYPE 2 DIABETES MELLITUS Four main abnormalities related to type 2 diabetes are there  Insulin resistance Insulin resistance refers to decreased tissue sensitivity to insulin. Normally, insulin binds to special receptors on cell surfaces and initiates a series of reactions involved in glucose metabolism. In type 2 diabetes, these intracellular reactions are diminished, thus rendering insulin less effective at stimulating glucose uptake by the tissues and at regulating glucose release by the liver.  Marked decrease in the ability of pancreas to produce insulin Beta cell become fatigued from compensatory over production of insulin or when beta cell mass is lost  Inappropriate glucose production by the liver Instead of properly regulating the release of glucose in response to blood level glucose, liver does so in a haphazard manner that does not correspond to the body’s needs at the correct time  Alteration in the production of hormones and cytokines by adipose tissue Onset of disease: it is usually gradual. The person may go for many years with undetected hyperglycemia. If patient has marked hyperglycemia (eg: 500-1000mg/dL) a sufficient endogenous insulin supply may prevent DKA GESTATIONAL DIABETES Gestational diabetes is any degree of glucose intolerance with its onset during pregnancy. Hyperglycemia develops during pregnancy because of the secretion of placental hormones, which causes insulin resistance. For women who meet one or more of the following criteria,  selective screening for diabetes during pregnancy is now being recommended between the 24th and 28th weeks of gestation  age 25 years or older; age 25 years or younger and obese  family history of diabetes in first-degree relatives  member of an ethnic/racial group with a high prevalence of diabetes
  • 7 (eg, Hispanic American, Native American, Asian American, African American, or Pacific Islander) SECONDARY DIABETES Diabetes occurs because of another medical condition or due to treatment of a medical condition. These include cushing syndrome, hyperthyroidism, cystic fibrosis, recurrent pancreatitis etc. medications include corticosteroids, thiazides, phenytoin and atypical antipsychotics. This usually resolves when underlying condition resolved. CLINICAL MANIFESTATOINS Type 1 Diabetes mellitus  Classic symptoms are polyuria, polydipsia, polyphagia.  Osmotic effect of glucose produces manifestations of polydipisa and ployuria  Polyphagia is a consequence of cellular malnourishment when insulin deficiency prevents utilization of glucose for energy  Weight loss may occur as the body cannot get glucose and turns to other energy sources such as fat and protein  Weakness and fatigue may also be experienced, as body cells lack needed energy from glucose Type 2 Diabetes mellitus Clinical manifestations are non specific  Fatigue  Recurrent infections  Recurrent vaginal yeast infection  Prolonged wound healing  Visual changes DIAGNOSTIC STUDIES
  • 8  Random blood glucose Blood specimen is drawn without preplanning. Greater than or equal to 200 mg/dL in the presence of symptoms is suggestive of diabetes mellitus.  Fasting blood glucose Blood specimen is obtained after 8 hours of fasting. In the nondiabetic client the glucose level will be between 70 and 110 mg/dL. In the diabetic client glucose is _ 110 mg/dL but <126 mg/dL.  Postprandial glucose Blood sample is taken 2 hours after a highcarbohydrate meal. In the nondiabetic client, the glucose level will be between 70 and 110 mg/dL. In the client with diabetes mellitus, the result is greater than or equal to 140 mg/dL but <200 mg/dL.  Oral glucose tolerance test Diet high in carbohydrates is eaten for 3 days. Client then fasts for 8 hours. A baseline blood sample is drawn and a urine specimen is collected. An oral glucose solution is given and time of ingestion recorded. Blood is drawn at 30 minutes and 1, 2, and 3 hours after the ingestion of glucose solution. Urine is collected simultaneously. Drinking water is encouraged to promote urine excretion. In the
  • 9 nondiabetic client, the glucose returns to normal in 2 to 3 hours and urine is negative for glucose. In the diabetic client, blood glucose level returns to normal slowly; urine is positive for glucose.  Glycosylated hemoglobin or hemoglobin A1c Single sample of venous blood is withdrawn. The amount of glucose stored by the hemoglobin is elevated above 7.0% in the newly diagnosed client with diabetes mellitus, in one who is noncompliant, or in one who is inadequately treated. COMPLICATIONS OF DIABETES MELLITUS  Acute complications  Diabetic ketoacidosis (DKA) DKA is caused by an absence or markedly inadequate amount of insulin. This deficit in available insulin results in disorders in the metabolism of carbohydrate, protein, and fat. The three main clinical features of DKA are: • Hyperglycemia • Dehydration and electrolyte loss • Acidosis Pathophysiology DKA can develop despite the client’s compliance with the prescribed treatment regimen When the amount of glucose transported across cell membranes decreases, the liver increases its production of glucose. The blood glucose level becomes extremely elevated. The kidneys attempt to excrete the glucose, which is well beyond the renal threshold. In the process, excessive amounts of water, sodium, and potassium are excreted as well. The client becomes dehydrated; the skin is warm, dry, and flushed. Stored fat is broken down, causing ketones to accumulate in the blood and urine. As ketones mount, the pH of the blood becomes acidotic. The client begins breathing rapidly and deeply in an attempt to eliminate carbon dioxide and prevent it from forming carbonic acid, which would contribute even more to the acidotic state. If the condition is severe and prolonged, the client becomes comatose. Death results with untreated or ineffective treatment of DKA
  • 10 Assessment Findings Early symptoms are vague and become more definite and serious as increasing ketones accumulate in the bloodstream.  Weakness, thirst, anorexia, vomiting, drowsiness, and abdominal pain  The cheeks are flushed, and the skin and mouth are dry  The breath has an odor of acetone. Kussmaul respirations often are evident  The pulse is rapid and weak.  Hypotension  The client may become unresponsive but restless  Blood glucose levels are elevated to 300 to 1000 mg/dL or more. Urine contains glucose and ketones.  blood pH ranges from 6.8 to 7.3  serum bicarbonate level is decreased to levels from 0 to 15 mEq/L  lower partial pressure of carbon dioxide in arterial blood (PaCO2) to levels of 10 to 30 mm Hg.
  • 11  Serum sodium and potassium levels reflect the degree of dehydration (i.e., they may be elevated because they are concentrated in a low volume of body fluid Management Treatment depends on the severity of DKA. The main goals of treatment are to (1) reduce the elevated blood glucose, (2) correct fluid and electrolyte imbalances (3) Clear the urine and blood from ketones  Insulin is given intravenously - Insulin reduces the production of ketones by making glucose available for oxidation by the tissues and by restoring the liver’s supply of glycogen. Regular insulin is added to an IV solution and infused continuously. The amount of insulin and the rate of infusion depend on the blood glucose levels, but the rate may be in the range of 5 Units per hour. Isotonic fluid is instilled at a high volume, As insulin begins to lower the blood glucose level, the IV solution is changed to include one with glucose. This helps to avoid the potential for hypoglycemia.  Potassium replacements are given despite elevated serum levels to raise intracellular stores. Periodic monitoring of serum electrolytes and blood glucose levels is necessary. The urine is tested for glucose and ketones  Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS) HHNKS, an acute complication of diabetes, is characterized by hyperglycemia without ketosis. It is not unusual to find the blood glucose level well over 500 mg/dL, but the pH of the blood remains within the normal range of 7.35 to 7.45. Fluid and electrolyte imbalances accompany HHNKS. Pathophysiology Extreme hyperglycemia Severe osmotic dieresis
  • 12 Fluid volume deficit Decreased sodium Decreased potassium Decreased phosphorus Electrolyte imbalance Profound dehydration Hyperosmolality Hypovolemia Decreased renal perfusion hypotension hemoconcentation Oliguria tissue anoxia hyperviscosity Anuria increased lactic acid thrombosis Seizures Shock Coma Death Assessment Findings  Hypotension, mental changes, extreme thirst, dehydration,  tachycardia, and fever  Neurologic signs include paralysis, lethargy, coma, and seizures
  • 13  Symptoms of hypokalemia and hyponatremia usually are present.  Physical examination reveals dry mucous membranes and poor skin turgor  Blood glucose levels are exceedingly high and serum potassium and sodium levels are low.  The serum osmolarity is increased Medical Management  Treatment includes the administration of insulin  Correction of fluid and electrolyte imbalances.  A central catheter may be used to monitor the client’s hemodynamic response to fluid replacement.  Hypoglycemia Hypoglycemia, a low blood glucose level, is always a potential adverse reaction when administering medications for diabetes Pathophysiology and Etiology  When too much insulin (hyperinsulinism) is in the bloodstream relative to the amount of available glucose, hypoglycemia occurs.  The blood glucose level falls below 70 mg/dL. Because glucose is the primary source of cellular energy, especially for the brain  hypoglycemia tends to manifest in neurologic changes such as confusion, difficulty processing information, anxious feelings, emotional irritability, and headache.  The client feels hungry, a homeostatic mechanism to stimulate eating  If the condition is untreated, seizures, permanent brain damage, or death can occur.  Hypoglycemia occurs when a client with diabetes is (1) Not eating at all and continues to take insulin or oral antidiabetic medications (2) not eating sufficient calories to compensate for glucose- lowering medications
  • 14 (3) Exercising more than usual, this lowers available blood glucose.  Alcohol consumption also interferes with the liver’s ability to synthesize glucose from noncarbohydrates,  placing clients with diabetes who drink at higher risk for hypoglycemia. Assessment Findings  Initial symptoms include weakness, headache, nausea, drowsiness, nervousness, hunger, tremors, malaise, and excessive perspiration.  Some clients have characteristic personality or behavioral changes. Confusion and dizziness can occur.  If hypoglycemia is not corrected, symptoms can progress to difficulty with coordination.  The client may complain of double vision.  Although symptoms vary, each client tends to have a  uniquely repetitious pattern when hypoglycemia develops. Medical Management  The medical treatment for a hypoglycemic reaction is administration of 15 g of simple carbohydrate as soon as possible.  If the client is unconscious, glucose gel can be applied in the buccal cavity.  If the client does not respond after two administrations of rapidly absorbed carbohydrate the physician may order glucagon, a hormone that stimulates the liver to release glycogen, or 20 to 50 mL of 50% glucose is prescribed for IV administration.  Once the hypoglycemic symptoms are relieved, the client with diabetes is given complex carbohydrates such as graham crackers and milk to sustain and prolong an adequate level of blood glucose. CHRONIC COMPLICATIONS Although clients with diabetes can develop many complications, extremely common ones include peripheral neuropathy, nephropathy, retinopathy, and
  • 15 Vascular changes, stroke, dermopathy, atherosclerosis, CAD, gangrene, erectile dysfunction, infections  Macrovascular complications It is the disease of large and medium sized blood vessels that occur with greater frequency. These complications include cerebrovascular, cardiovascular and peripheral vascular diseases,  Microvascular complications It results from thickening of vessel membranes in capillaries and arterioles in response to conditions of chronic hyperglycemia  peripheral neuropathy Neuropathy is a general term that refers to pathologic changes in nerves. Neuropathies in clients with diabetes can affect motor, sensory, and autonomic nerves. Neuropathies develop 10 or more years after the onset of diabetes, but the incidence increases with the duration. Because their onset is gradual, the client usually is oblivious to the development in early stages. Pathophysiology and Etiology Neuropathy results from poor glucose control and decreased blood circulation to nerve tissue. Manifestations of peripheral neuropathies are more common among clients with diabetes who smoke and whose blood glucose level is poorly controlled. Because nitric acid dilates blood vessels, some believe that consistently elevated blood glucose levels lower nitric acid levels, impair circulation, and subsequently damage peripheral nerves.  Motor Neuropathy When motor nerves are affected, the muscles weaken and atrophy. Joint support is diminished. The feet widen. Eventually bone structure is affected, resulting in skeletal deformities, usually in the feet and ankles, with subsequent changes in gait. Areas of skin and soft tissue that are subjected to friction and pressure are
  • 16 prone to ulcerate If there is infection or impaired healing, portions of the affected extremity may require amputation.  Sensory Neuropathy Neuropathy involving sensory nerves leads to paresthesias, abnormal sensations such as prickling, tingling, burning, orneedle-like pain in the feet, legs, and sometimes hands. In severe cases, feeling is totally lost. This lack of sensitivity increases the potential for soft tissue injury without the client’s awareness.  Autonomic Neuropathy Neuropathy of autonomic nerves that affect organ functioning has several consequences. Gastroparesis, atony of the stomach, retards the movement of food from the stomach. If nerves that innervate the bladder are affected, the client does not sense the urge to void, and retained urine supports bacterial growth, causing frequent urinary tract infections. Incontinence also may occur when the bladder is overfilled. When autonomic nerves that affect cardiovascular function fail to function effectively, episodes of orthostatic hypotension occur. Signs and Symptoms  Pain is one of the leading symptoms  Skeletal muscles in the extremities become smaller.  The feet swell and become insensitive to temperature or other tactile stimuli  digestive, urinary, and sexual dysfunction  Dizziness when rising Management o Diet, exercise, and medication to control blood glucose levels. o Several medications can reduce pain, such as non-narcotic analgesics or a tricyclic antidepressant such as imipramine (Tofranil). o Nonpharmacologic pain relief can be facilitated with transcutaneous electrical nerve stimulation. o Elastic compression stockings
  • 17 o antihypotensive agent such as midodrine (ProAmatine), help reduce orthostatic hypotension. o Small, frequent meals and administration of metoclopramide (Reglan) are recommended for the relief of symptoms associated with gastroparesis. o Antibiotic therapy, increased oral fluid intake, and urinating every 3 hours helps eliminate urinary tract infections  Diabetic nephropathy Diabetic nephropathy refers to the progressive decrease in renal function that occurs with diabetes mellitus. Clients with type 1 diabetes are more likely to develop diabetic nephropathy, but clients with type 2 diabetes also are affected. Pathophysiology and Etiology Nephropathy is a consequence of glomerular deterioration resulting in impaired filtration of blood during urine formation. There are five stages of nephropathy, each characterized by a successive progression of renal dysfunction Essentially, the glomeruli excrete serum proteins, especially albumin, and lose their ability to excrete nitrogen waste products. Poor glucose control contributes to the onset of nephropathy. Although hypertension is an eventual consequence of diabetic nephropathy Assessment Findings In the early stages, the client does not manifest any obvious signs and symptoms.  Swelling of the feet and hands, most likely from the loss of albumin  BP increases gradually.  The client feels tired and weak.  Albumin in the urine.  Blood urea nitrogen and serum creatinine become elevated.  renal creatinine clearance is decreased Management
  • 18 Controlling both blood glucose levels and hypertension canprevent or delay the development of diabetic nephropathy clients with diabetes maintain their BP at or below 130/85mmHg. The target BP of clients with diabetes who already have developed proteinuria is at or lower than 125/75 mm Hg. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor antagonist slow the progressive nature of nephropathy A moderate reduction in dietary protein is beneficial. Smoking cessation is strongly recommended. Nursing Management  The nurse monitors the client’s blood glucose and hemoglobin A1c results.  check urine with a test strip to detect evidence of albuminuria.  The nurse provides additional teaching if the client’s blood glucose level is not controlled.  refers the client to programs that assist with smoking cessation or discusses the possibility of nicotine patches or gum to control further habituation.  The nurse explains the therapeutic regimen associated with prescribed antihypertensive drugs and dietary measures for lowering BP and complications from vascular disease  Diabetic retinopathy Diabetic retinopathy refers to pathologic changes in the retina that are experienced by persons with diabetes. On average, it develops 10 or more years after the onset of diabetes. The earlier retinopathy develops, the more likely it is that vision will rapidly deteriorate. Pathophysiology and Etiology Diabetic retinopathy is a consequence of inadequately controlled blood glucose levels, which cause vascular changes in the retina .
  • 19 There are two types: nonproliferative retinopathy is the milder manifestation, and proliferative retinopathy, the more severe form, can lead to blindness.  In nonproliferative retinopathy, microaneurysms, outpouchings in retinal capillaries, develop from high vascular pressure and compromised circulation.  The stasis of blood flow interferes with transferring substances between the retina and blood vessels.  The deprived retinal cells swell  In the more advanced, proliferative form, damaged blood vessels are replaced with new ones that grow along the surface of the retina.  The newer blood vessels are more fragile  They tend to rupture and leak blood into the vitreous, the gel-like fluid that fills the posterior portion of the eye.  Inelastic scar tissue forms, which alters the shape of the retina, causes distorted vision, and pulls at the retina, increasing the potential for retinal detachment. Assessment Findings Clients with nonproliferative and proliferative retinopathy may not experience any visual changes for some time.  blurred vision  Visual acuity is diminished.  Ophthalmic examination reveals swelling near the macula of the eye, an area lateral to the optic nerve that provides acute central vision. Management  The client with diabetes is referred for an ophthalmic evaluation within 3 to 5 years after diagnosis  If there is evidence of retinal vessel changes, an ACE inhibitor such as lisinopril is prescribed to dilate the retinal blood vessels and improve blood flow  If vitreous hemorrhage already has occurred, some physicians prefer to let the condition resolve on its own, which may take up to 18 months.  Seal leaking or newly forming blood vessels with laser photocoagulation.
  • 20  A vitrectomy, removal of bloodied vitreous, also improves the clarity of vision.  In 2004, the FDA approved ovine hyaluronidase (Vitrase), a genetically engineered form of angiopoietin, a vascular growth factor that stimulates the repair of leaky retinal blood vessels.  Vascular disturbances Vascular disturbances affect many tissues and organs, in clients with diabetes, all the arteries and arterioles are more susceptible to accelerated atherosclerotic and arteriosclerotic changes than in clients without diabetes. Pathophysiology and Etiology A consistent finding in clients with diabetes is thickening of the arterial walls. The incidence of coronary artery disease also is increased. One possible explanation for obesity in clients with diabetes is that the brain may be insensitive to leptin, a chemical that signals satiation. A lack of response to leptin promotes overeating, which contributes to hyperlipidemia. Assessment Findings Peripheral vascular changes are one of the most common complications associated with diabetes  extremities are pale and cool due to decreased blood supply  Leg cramps  Gangrene develops if blood supply to the extremities is markedly diminished.  Uncontrolled infection leads to skin ulcers.  Myocardial infarctions occur at a much earlier age than among the nondiabetic population. . Medical and Surgical Management Atherosclerosis is managed with lipid-lowering measures such as a low- fat diet, exercise, and medications Vasodilators are prescribed to combat the effects of arteriosclerosis
  • 21 Drugs that reduce platelet aggregation (e.g., aspirin) are prescribed prophylactically Smoking cessation is advised Uncontrolled gangrene of the extremities can result in amputation  Infections Infection is very common due to defect in the mobilization of inflammatory cells and an impairment of phagocytosis by neutrophils and monocytes. Loss of sensation may delay the detection of an infection MANAGEMENT NUTRITIONAL THERAPY Diet is a major component of treatment for every person withdiabetes. Formulation of a diabetic diet depends on the client’s sex, age, height and weight, activity level, occupation, state of health, former dietary habits, and cultural background. Specific goals include the following  Maintain blood glucose level to as near normal as safely possible to prevent or reduce the risk for complications  Achieve lipid profiles and BP level that reduce the risk of cardiovascular complications  Modify lifestyle as appropriate for prevention and treatment of obesity , dyslipidemia, nephropathy  Address individual nutritional needs Food composition  Carbohydrates Carbohydrates and monodaturated fats should provide 45%-65% of total energy intake each day. It includes sugar, starches, fiber, low fat milk, fruits, and vegetables  Fats Fat should compose no more than 25-30% of meal plan  Protein It should less than 10% of total energy consumed
  • 22  Alcohol It is high in calories but no nutritive value and promotes hypertriglyceridemia. It has detrimental effects on the liver EXERCISE Exercise helps metabolize carbohydrates and control blood glucose levels because glucose-transporting receptors within skeletal muscles allow the muscles to take in glucose from the blood independent of insulin. This provides energy during exercise and lowers blood sugar. Exercise, therefore, reduces the need for insulin because blood sugar can be lowered without it, an advantage for those with diabetes. Exercise also improves circulation of blood, which is compromised in the client with diabetes. Exercise also lowers cholesterol and triglyceride levels and improves muscle tone. An exercise program for the client with diabetes specifies the type of exercise and the length of time to perform it. The program is tailored according to the client’s needs and life-style. Most importantly, the client needs to exercise consistently each day. Sporadic periods of exercise are discouraged because wide fluctuations in blood glucose levels can occur. It is necessary to regulate food and insulin requirements during times of increased activities PHARMACOLOGICAL MANAGEMENT Insulin Insulin is needed when a patient has inadequate insulin to meet specific metabolic needs. People with type 1 DM require exogenous insulin to survive and people with type 2 DM usually controlled by diet, exercise. May require exogenous insulin during periods of severe stress like illness and surgery Insulin has been available since 1925. It was initially extracted from beef and pork pancreases. In the early 1980’s, technology became available to produce human insulin synthetically. Synthetic human insulin has replaced beef and pork insulin. Now, insulin analogs are replacing human insulin. There are many forms of insulin to treat diabetes. They are classified by how fast they start to work and how long their effects last.
  • 23 The types of insulin include: Rapid-acting Short-acting Intermediate-acting Long-acting Pre-mixed Fast-acting insulin These types of insulin are designed to take care of the sugar a person eats. They include:  Aspart — Starts to act in 5 to 15 minutes, peaks in 90 minutes, lasts 3 hours  Lispro — Starts to act in 5 to 15 minutes, peaks in 90 minutes, lasts 3 hours  Regular — Starts to act in 30 to 60 minutes, peaks in 2 hours, lasts 4 to 6 hours Intermediate and long-acting insulin These types of insulin, also called basal or background insulin, work continuously, similar to the way a normal pancreas produces insulin. They are absorbed slowly and last from 10 to 24 hours, . Basal insulin types include:  NPH — Starts to act about 2 hours after taking, peaks at 6 to 8 hours, lasts 10 to 16 hours  Glargine — Starts to act about 2 hours after taking, and can last 20 to 24 hours  Detemir – Starts to act about 2 hours after taking, and lasts between 14 and 24 hours Combination insulin Combination insulin mixtures have a later action with an earlier and stronger peak. The mixtures are tailored to a person’s individual needs. Combination insulin includes human and analog mixtures: Human mixtures combine NPH and regular insulin. classification Examples Rapid acting insulin Lispro clear
  • 24 Aspart clear Glulisine clear Short acting insulin Regular clear Intermediate acting insulin NPH cloudy Long acting insulin Glargine clear Detemir clear Combination therapy NPH cloudy Lispro cloudy Apart cloudy Insulin regimens The timing of insulin administration in relation to meal is very important Regimen Type of insulin Comments Once a day single dose Intermediate Or Long acting At bed time  One injection should cover noon meal  1 injection will last 24hrs with no peaks and less chance for hypoglycem ia  Does not cover postprandial blood sugars Twice a day Split mix dose NPH regular Or NPH rapid Before breakfast, 2 injections provide coverage for 24hrs
  • 25 and at dinner Three times a day Combination of mixed and single dose NPH regular Or NPH rapid Before breakfast and dinner as well as at bed time Three injections provide coverage or 24hrs Particularly during early hours Four times a day Multiple dose Regular or rapid injection Before breakfast, lunch and dinner AND NPH at bed time More flexibility is allowed at meal times and for amount of food intake Good postprandial control Basal bolus Before breakfast, lunch and dinner Long acting once a day, usually at bedtime Four injection srequired per day Storage of insulin As a protein insulin requires special storage considerations  Heat and freeze alters insulin molecules  Insulin vials that patient currently using may be left at room temperature for upto 4 weeks unless the room temperature is higher than 86o F or below freezing lessthan 37o F  Prolonged exposure to direct sunlight should be avoided  Prefilled syringes are stable upto 30 dayswhen stored in the refrigerator Administration of insulin Insulin is prescribed in units. 1 mL contains 100 units of insulin. The physician specifies both the dosage and the type of insulin to be used. When combining
  • 26 two types of insulin in the same syringe, the short-acting regular insulin is withdrawn into the syringe first and the intermediate- acting insulin is added next, a practice referred to as ‘‘clear to cloudy.’’ The mixture is administered within 15 minutes to ensure that the onset, peak, and duration of each separate insulin remains intact. Glargine (Lantus) insulin cannot be mixed with other types of insulin in the same syringe. Combination mixtures of insulin, such as Humulin 70/ 30, Novolin 70/30, and Humulin 50/50, eliminate the need for mixing insulins from two separate vials. Regular insulin can be administered intravenously and subcutaneously.  The intravenous route is used to treat severe hyperglycemia or prevent or control elevated blood sugar by adding it to a total parenteral nutrition solution that contains a high concentration of glucose.  The subcutaneous route is used most commonly for administering insulin insulin is absorbed more rapidly when injected in the abdomen than in the arms or thighs.  Clients with diabetes are taught to use the abdomen as the preferred site for self-administration. Subcutaneous injection sites require rotation to avoid lipoatrophy, breakdown of subcutaneous fat at the site of repeated injections, and lipohypertrophy, buildup of subcutaneous fat at the site of repeated injections, either of which eventually interferes with insulin absorption in the tissue.  Insulin is an anabolic hormone, it also causes weight gain.  Other techniques for injecting insulin subcutaneously include an insulin pen, jet injector, or insulin pump. Insulin Pen An insulin pen is a device in which a cartridge containing 150 to 300 units of insulin is loaded into an injecting pen with a disposable needle attached. Each time the insulin is injected, a new needle is attached. Once the device is loaded, the client  Selects the number of units for injection by dialing in the dose in 1- to 2- unit increments  cleans and pierces the skin,  injects the programmed amount
  • 27 Jet Injector A jet injector uses high pressure and rapid speed, rather than a needle, to instill insulin through the skin. The pressure transforms the liquid into a fine mist that is distributed over a wide area of tissue, resulting in faster absorption Although a jet injector offers several advantages, such as reducing pain at the site and eliminating the use of needles and their appropriate disposal, the cost tends to make this form of administration less practical. Insulin Pump An insulin pump provides a means for delivering insulin by continuous infusion. The device has three components: pump, tubing, and needle .The pump itself contains a reservoir for rapid-acting or short-acting insulin, a battery-operated infuser, and a computer chip that enables a person to regulate basal (continuous) and pre meal bolus doses in 0.05- to 0.1-unit increments. The pump, which is worn in a pouch or belt holder, is attached to tubing with a needle. The needle is inserted in the subcutaneous tissue of the abdomen and can remain in the same site for up to 3 days. Clients who are interested in controlling their diabetes with an insulin pump need to consider both its advantages and disadvantages Advantages • Resembles the normal pancreatic release of insulin • Decreases the necessity for multiple daily injections in different sites • Helps maintain consistent blood sugar levels; reduces the potential for episodes of hyperglycemia and ketoacidosis • Provides more flexibility for eating food at varying times during the day • Facilitates the instillation of smaller doses than those of insulin syringes
  • 28 Disadvantages • Requires high motivation to control diabetes by frequently checking blood glucose levels and adjusting the infusion • Creates a potential for hyperglycemia if the pump fails, the tubing becomes kinked or obstructed, or the needle is displaced • Interferes or creates a nuisance factor when participating in active sports, sexual intercourse, or bathing; the pump can be temporarily disconnected without removing the needle, but doing so stops the delivery of insulin until it is reconnected Injection site selection for insulin The most common injection site is the abdomen (or stomach). The back of the upper arms, the upper buttocks or hips, and the outer side of the thighs are also used. These sites are the best to inject into for two reasons: They have a layer of fat just below the skin to absorb the insulin, but not many nerves - which means that injecting there will be more comfortable than injecting in other parts of your body. They make it easier to inject into the subcutaneous tissue, where insulin injection is recommended. Problems with insulin therapy  Allergic reactions: local inflammatory reactions may occur such as erythema, itching, burning around injection site. These may be self limiting within 1 – 3 months or may improve with a low dose if antihistamine drugs
  • 29  Lipodystrophy: atrophy of subcutaneous tissue may occur if same injection site used frequently  Somogyi effect: Somogyi effect is a rebound effect in which an overdose of insulin induces hypoglycemia. Usually ocuurs during night times. Counterregulatory mechanisms are released, stimulating lipolysis, gluconeogenesis, glycogenolysis which inproduces rebound hyperglycemia and ketosis  Dawn phenomenon: hyperglycemia that is present on awakening ikn the morning due to the release of counter regulatory hormones in the predawn hours Patient education on self administration of insulin  With one hand, stabilize the skin by spreading it or pinching up a large area  Pick up syringe with the other hand and hold it as a pencil  Insert needle straight into the skin  To inject the insulin, push the plunger all the way in  Pull needle straight out of skin  Press cotton ball over injection site for several seconds  Use disposable syringe only once and discard ORAL ANTIDIABETIC AGENTS Drug category & examples Mechanism Of action Side effects Second-Generation Sulfonylureas glimepiride (Amaryl), glipizide (Glucotrol), glyburide (DiaBeta, Glynase PresTab, Micronase) Stimulates insulin release; more potent than firstgeneration sulfonylureas Increased risk of cardiovascular mortality, anorexia, nausea, vomiting, heartburn, diarrhea, hypoglycemia, allergic skin reactions, insulin ‘‘burn out’’ Alpha-Glucosidase Delays digestion of
  • 30 Inhibitors acarbose (Precose), miglitol (Glyset) carbohydrates Abdominal pain, flatulence, diarrhea, hypoglycemia Give three times a day 15 min before each meal. Biguanide Compound metformin (Glucophage) Augments glucose uptake by tissues, especially muscles, decrease hepatic glucose production Anorexia, nausea, heartburn, diarrhea, lactic acidosis, hypoglycemia, allergic skin reactions, flatulence Thiazolidinediones (TZDs) rosiglitazone (Avandia), pioglitazone (Actos) Increases effects of circulating insulin, decrese endogenous glucose production Headache, pain, liver injury, hypoglycemia, hyperglycemia, infections, fatigue, risk for heart attack and heart failure Meglitinides repaglinide (Prandin) Stimulates insulin release Upper respiratory infections, hypoglycemia, hyperglycemia, headache Dipeptidyl peptidase IV (DPP-4) Inhibitor sitagliptin (Januvia Increases effects of incretin; prolongs the release of insulin and reduces production of glucose by the liver Upper respiratory tract infection; nasopharyngitis and headache. Adjuvant Drugs exenatide (Byetta Stimulate release of insulin Heartburn, headache, nausea,
  • 31 vomiting, diarrhea, weight loss, dizziness, pancreatitis Combination Drugs metformin and sitagliptin Combination product for use as adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes when mono-therapy is not controlling ; upper respiratory infection; headache. Amylin analog pramlintide Decrease gastric empying, glucagose secretion, endogenous glucose output from liver Hypoglycemia, nausea, vomiting, headache SURGICAL MANAGEMENT
  • 32 Pancreas Transplantation  Replacing the pancreas involves a whole or partial organ transplant.  The usual candidate is a client with type 1 diabetes who has renal failure and will benefit from a combined kidney and pancreas transplant.  Clients with type 2 diabetes are not offered the option of a pancreas transplant because usually their problem is insulin resistance, which does not improve with a transplant.  pancreas is both an exocrine and endocrine gland, transplanting it requires a means for exocrine enzymatic drainage and venous absorption of insulin.  Exocrine drainage is accomplished by establishing a duodenal or urinary bladder connection with the transplanted pancreas. Insulin is released into the portal vein, which carries blood to the liver.  As with any transplant, lifelong immunosuppressive drug therapy is required because without it, the new organ is destroyed. Islet Cell Transplantation  Some clients with type 1 diabetes are recipients of islet cell transplants, the insulin-producing components of the pancreas, rather than a transplant of the entire organ or part of the organ.  Two human pancreases are necessary to obtain sufficient numbers of islet cells for transplantation. The fragile islet cells must be transplanted within 12 hours of harvesting  After the pancreas is harvested, the islet cells are separated from the tissue and injected through the abdominal wall into the client’s portal vein, where they migrate to the liver and begin to release insulin NURSING MANAGEMENT  Imbalanced Nutrition: More than Body Requirements related to decreased activity, and habituation of pre illness eating habits  Provide three meals and snacks within prescribed caloric limits  Suggest free foods such as up to 1 cup of raw
  • 33  unlimited sugar free drinks if the client becomes hungry between meals or snacks.  Encourage client to drink 8 ounces of water before eating a meal  Advise client to eat slowly and wait 15 seconds between chewing thoroughly, swallowing, and taking the next bite  Risk for Imbalanced Fluid Volume related to hyperglycemia and polyuria  Monitor intake and output a deficit in fluid intake or excess urine output suggests a deficit in fluid volume.  Provide at least 1500 to 3000 mL of fluid per day  Risk for Injury related to orthostatic hypotension and impaired vision secondary to neuropathy and retinopathy  Assist client when rising from a sitting or lying position. Autonomic neuropathy causes orthostatic hypotension and the potential for fainting and falling  Have client dangle on the side of the bed before ambulating. Dangling allows a period during which blood flow is restored to the brain.  Keep the floor dry and the environment free of clutter  Risk for Impaired Skin Integrity related to loss of sensation in feet and impaired blood circulation  Examine skin and feet daily. Client may be insensitive to injuries and slow to heal because of peripheral neuropathy and vascular disturbances.  Assess skin for signs of breakdown, poor healing, change in color or temperature, or infection  Impaired blood supply compromises the integrity of the integument  Dry client’s skin well after bathing, especially in areas of the body that are dark and moist  Fungal infections are common increases and folds of skin  Inspect inside the client’s shoes for foreign objects or disrepair.  Risk for Ineffective Management of Therapeutic Regimen related to insufficient knowledge regarding diabetes self-management  Assess client’s ability and willingness to learn about diabetes and self- management  Teaching is more effective when the learner is capable and motivated to acquire information.  Teach client about insulin and how to self-administer using proper technique  Clients learn in various ways: verbal explanations, reading information, seeing a demonstration, or using a hands-on application
  • 34 HEALTH EDUCATION Blood glucose  Monitor blood glucose and record it in a diary  Take medication on time  Obtain a HbA1c blood test every 3 – 6 months  Carry some forms of glucose at all times Exercise  Begin a medically supervised exercise program  Learn how exercise affect blood glucose level Diet  Follow diet created by a dietitian  Eat slowly and chew food thoroughly  Choose food low in saturated fats  Limit amount of alcohol Other guidelines  Perform an annual eye examination and urine testing for protein  Examine feet at home  Know symptoms of hyper and hypoglycemia  Quit smoking REVIEW OF LITERATURE Alginate dressings for healing diabetic foot ulcers. Source Department of Nursing, Midwifery and Social Work, University of Manchester, Manchester, UK, M13 9PL. Abstract BACKGROUND: Foot ulcers in people with diabetes mellitus are a common and serious global health issue. Dressings form a key part of ulcer treatment, with clinicians and patients having many different types to choose from including alginate dressings. A clear and current overview of current evidence is required to facilitate decision-making regarding dressing use.
  • 35 OBJECTIVES: To compare the effects of alginate wound dressings with no wound dressing or alternative dressings on the healing of foot ulcers in people with diabetes mellitus. SELECTION CRITERIA: Published or unpublished randomized controlled trials (RCTs) that have compared the effects on ulcer healing of alginate dressings with alternative wound dressings or no dressing in the treatment of foot ulcers in people with diabetes. DATA COLLECTION AND ANALYSIS: Two review authors independently performed study selection, risk of bias assessment and data extraction. MAIN RESULTS: Included six studies (375 participants) in this review; these compared alginate dressings with basic wound contact dressings, foam dressings and a silver- containing, fibrous-hydrocolloid dressing. Meta analysis of two studies found statistically significant difference between alginate dressings and basic wound contact dressings. Pooled data from two studies comparing alginate dressings with foam dressings found statistically significant difference in ulcer healing . There was statistically significant difference in the number of diabetic foot ulcers healed when an anti-microbial (silver) hydrocolloid dressing was compared with a standard alginate dressing SUMMARY Lifestyle modification is the most cost-effective intervention for prevention of diabetes in high-risk groups in India. However, control of diabetes with diet, weight control and physical activity has been difficult and will not be sufficient for most of the patients. Moreover, the steady increase in the incidence of type 2 diabetes has significant socioeconomic Implications BIBLIOGRAPHY 1. Brunner and Suddarth’s, Text Book of Medical Surgical Nursing, 9th edition, 2005, Lippincott 2. John Luckmann, Medical Surgical Nursing, 3rd edition, 1987, Saunders Company, Philadelphia London
  • 36 3. Joyce M. Black, Jane Hokanson Hawks, Medical Surgical Nursing- Clinical Mangement for positive outcomes, 7th edition, 2005, Elsevier, India. 4. Lewis, Heitkemper & Dirksen Medical Surgical Nursing Assessment and Management of Clinical Problem (6th ed) (2000) Mosby 5. Haslett C., Chilvers E. R., Hunder J.A.A. & Boon, N. A. Davidson’s Principles and Practice of Medicine, 18th ed, (1999) Churchill living stone. 6. Nettina, Sandra, Lippincott Williams & Wilkins, The Lippincott Manuel of Nursing practice, 7th ed, 2001, Philadelphia 7. library.med.utah.edu/WebPath/TUTORIAL/DIABETES/DIABETES.htm 8. en.wikipedia.org/wiki/Diabetes_mellitus 9. diabetes.webmd.com/types-of-diabetes-mellitus 10.www.nlm.nih.gov/medlineplus/diabetesmellitus.htm