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ZEENAT AYAZ Diabetes mellitus
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Diabetes mellitus is a group of metabolic diseases characterized by elevated levels of glucose in the blood (hyperglycemia) resulting from defects in insulin secretion, insulin action, or both
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Insulin, a hormone produced by the pancreas, controls the level of glucose in the blood by regulating the production and storage of glucose. Transports and metabolizes glucose for energy Stimulates storage of glucose in the liver and muscle (in the form of glycogen)
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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 Also inhibits the breakdown of stored glucose, protein, and fat.
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Insulin Insulin and glucagon are hormones secreted by islet cells within the pancreas Insulin is normally secreted by the beta cells (a type of islet cells) of the pancreas Stimulus for insulin is high blood glucose levels
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Classification Type 1 diabetes (insulin-dependent diabetes mellitus) Type 2 diabetes (non-insulindependent diabetes mellitus) Gestational diabetes mellitus
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Type 1 Diabetes Mellitus Most often occurs in people under 30 years of age Peak onset between ages 11 and 13 Formerly known as “juvenile onset” or “insulin dependent” diabetes
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Type 1 Diabetes Mellitus Etiology and Pathophysiology Progressive destruction of pancreatic cells Autoantibodies cause a reduction of 80% to 90% of normal cell function before manifestations occur
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Type 1 Diabetes Mellitus Etiology and Pathophysiology Causes: Genetic predisposition Related to human leukocyte antigens (HLAs) Exposure to a virus
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Type 1 Diabetes Mellitus Onset of Disease Manifestations develop when the pancreas can no longer produce insulin Rapid onset of symptoms Present at ER with ketoacidosis
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Type 1 Diabetes Mellitus Onset of Disease Weight loss Polydipsia Polyuria Polyphagia
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Type 1 Diabetes Mellitus Onset of Disease Diabetic ketoacidosis (DKA) Occurs in the absence of exogenous insulin Life-threatening condition Results in metabolic acidosis
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Type 2 Diabetes Mellitus Accounts for 90% of patients with diabetes Usually occurs in people over 40 years of age 80-90% of patients are overweight
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Type 2 Diabetes Mellitus Etiology and Pathophysiology Pancreas continues to produce some insulin Insulin produced is either insufficient or poorly utilized by the tissues
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Type 2 Diabetes Mellitus Etiology and Pathophysiology Insulin resistance Body tissues do not respond to insulin Results in hyperglycemia
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Type 2 Diabetes Mellitus Etiology and Pathophysiology Inappropriate glucose production by the liver Not considered a primary factor in the development of type 2 diabetes
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Type 2 Diabetes Mellitus Etiology and Pathophysiology 17
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Type 2 Diabetes Mellitus Onset of Disease Gradual onset Person may go many years with undetected hyperglycemia 75% of type 2 diabetes is detected incidentally
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Gestational Diabetes Develops during pregnancy Detected at 24 to 28 weeks of gestation Risk for cesarean delivery, perinatal death, and neonatal complications
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Secondary Diabetes Results from another medical condition or due to the treatment of a medical condition that causes abnormal blood glucose levels Cushing syndrome Hyperthyroidism Parenteral nutrition
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Clinical Manifestations Diabetes Mellitus Polyuria Polydipsia (excessive thirst) Polyphagia In Type I Weight loss Ketoacidosis
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Clinical Manifestations Non-specific symptoms Fatigue and weakness Sudden vision changes Tingling or numbness in hands or feet Skin lesions or recurrent infections Prolonged wound healing Visual changes
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Clinical Manifestations 23
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Risk Factors for Diabetes Mellitus Family history of diabetes (i.e., parents or siblings with diabetes) Obesity (i.e., ≥20% over desired body weight or BMI ≥27 kg/m2) Race/ethnicity (e.g., African Americans, Hispanic Americans, Native Americans, Asian Americans, Pacific Islanders) Age ≥45 years Previously identified impaired fasting glucose or impaired glucose tolerance
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Risk factors (cont.) Hypertension (≥140/90 mm Hg) HDL cholesterol level ≤35 mg/dL (0.90 mmol/L) and/or tri- glyceride level ≥250 mg/dL (2.8 mmol/L) History of gestational diabetes or delivery of babies over 9 lbs
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ASSESSMENT AND DIAGNOSTIC FINDINGS high blood glucose level Fasting plasma glucose (FPG) levels of 126 mg/dL (7.0 mmol/L) or more random plasma glucose levels exceeding 200 mg/dL (11.1 mmol/L) on more than one occasion Plasma glucose values may be 10% to 15% higher than whole
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goal The main goal of diabetes treatment is to normalize insulin activity and blood glucose levels to reduce the development of vascular and neuropathic complications.
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management There are five components of diabetes management Nutritional management Exercise Monitoring Pharmacologic therapy Education
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Treatment varies because of changes in lifestyle and physical and emotional status as well as advances in treatment methods. Therefore, diabetes management involves constant assessment and modification of the treatment plan by health professionals and daily adjustments in therapy by the patient.
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Diabetes Mellitus Acute Complications Hypoglycemia Diabetic ketoacidosis (DKK) Hyperosmolar hyperglycemic nonketotic syndrome (HHNS)
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hypoglycemia Type 1 or type 2 diabetes Blood glucose < 50-60 mg/dL Causes Too much insulin Overdose of oral antidiabetic agents Too little food Excess physical activity May experience S & S of hypoglycemia if there is sudden decrease in BS
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hypoglycemia Treatment Mild Immediate treatment 15 g rapid-acting sugar Severe Hospitalized Intravenous glucose Teach patients to carry simple sugar with them
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Life-threatening illness in type 1 Hyperglycemia Dehydration and electrolyte loss Acidosis Causes of DKA Decreased or missed dose of insulin, Illness or infection, Undiagnosed and untreated diabetes
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Without insulin, the amount of glucose entering the cells is reduced, and production and release of glucose by the liver is increased (lead to hyperglycemia). Excess glucose leads to polyuria (6.5 L/day) dehydration, sodium and potassium loss Burning of fat leads to ketosis Kidneys unable to excrete ketones, leads to ketoacidosis
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Diagnosis: Blood glucose (300 and 800 mg/dL) Treatment Rehydration (0.9-0.45% saline) Restoring Electrolytes (K + ) loss of potassium from body stores and an intracellular- to-extracellular shift of potassium Reversing Acidosis (reversed with insulin) Regular insulin infusion (5 units/hr) Hourly blood glucose monitoring
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Hyperosmolar hyperglycemic nonketotic syndrome (HHNS) 39 Is a serious condition most frequently seen in older persons. HHNS is usually brought on by something else, such as an illness or infection, dialysis, drugs that increase BS. Blood sugar levels rise resulting into glycosuria, polyuria, thirst. Severe dehydration will lead to seizures, coma and eventually death. HHNS may take days or even weeks to develop. Know the warning signs of HHNS.
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HHNS/ clinical manifestations 40 Hypotension, profound dehydration (dry mucous membranes, poor skin turgor), tachycardia, and variable neurologic signs (eg, alteration of sensorium, seizures, hemiparesis). Blood glucose level (600 to 1200 mg/dL) Treatment: fluid replacement, correction of electrolyte imbalances, and insulin.
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42 Diabetes Mellitus Chronic Complications Macrovascular (atherosclerotic plaque) Coronary arteries → (MI’s) Cerebral arteries → (strokes) Peripheral vessels → (ulcers, amputations, infection) Microvascular (capillary damage) Retinopathy Neuropathy Nephropathy
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Macrovascular Complications 43 Macrocirculation Blood vessel walls thicken, sclerose, and become occluded by plaque that adheres to the vessel walls. finally, blood flow is blocked. Complications Coronary artery disease Stroke Peripheral vascular disease
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Complication: CAD 44 CAD account for 50% to 60% of all deaths among patients with diabetes. High cholesterol and high triglycerides MI is twice as common in men and three times in women with diabetes, compared to people without diabetes. Silent MI Higher risk for a second infarction
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Complication: Stroke 45 People with diabetes have twice the risk of developing cerebrovascular disease. There is a greater likelihood of death from cerebrovascular disease. Recovery is slower with high BS. Hypertension plays a role
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Complication: Peripheral Vascular Disease 46 Diabetes-induced arteriosclerosis 2-3 times higher than in nondiabetic people S & S: diminished peripheral pulses and intermittent claudication (pain in the buttock, thigh, or calf during walking) Can lead to leg ulcers and gangrene and amputation.
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Management of Macrovascualr changes 47 Prevention and treatment of risk factors for atherosclerosis. obesity, hypertension, and hyperlipidemia (exercise, stop smoking). Control of blood glucose levels may reduce triglyceride concentrations and can significantly reduce the incidence of complications.
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Microvascular Complications 48 Microcirculation Eyes Kidneys Nerves
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Complication: Diabetic Retinopathy 49 Leading cause of blindness in people ages 20 to 74 in US Almost all patients with type 1 diabetes and more than 60% of patients with type 2 diabetes have some degree of retinopathy after 20 years
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Diabetic Retinopathy 50 Changes in the retinal capillaries; lead to retinal ischemia. Changes include microaneurysms, intraretinal hemorrhage, hard exudates, and focal capillary closure. Yearly eye exams are recommended
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Complication: Diabetic Nephropathy 51 Disease of the kidneys (50% of RF due to DM) Characterized by albumin in the urine, hypertension, edema, renal insufficiency DM is the most common cause of renal failure First indication: microalbuminuria Treatment: ACE inhibitors, control BP and BS, prevent & treat UTI, low Na & protein diet.
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Complication: Diabetic Neuropathy 52 Disorder of the peripheral nerves, spinal cord, and autonomic nervous system Results: sensory and motor impairments, postural hypotension, delayed gastric emptying, diarrhea, impaired GU function Result from the thickening of the capillary membrane and destruction of myelin sheath which disrupt nerve conductions.
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Complication: Diabetic Neuropathy 53 Bilateral sensory disorders Appear first in toes, feet, and progress upward to fingers and hands Tingling, decrease in proprioception, and a decreased sensation of light touch Treatment Controlling BS delay the onset. Analgesics to control pain
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Complication: Autonomic Neuropathy 54 Involves numerous body systems such as: Cardiovascular (slight tachycardia, orthostatic hypotension & silent MI). Gastrointestinal (Delayed gastric emptying, N&V, early satiety, variation of BS absorption) Genitourinary (urinary symptoms of neurogenic bladder, UTI, erectile dysfunction) Hypoglycemic unawareness (DM diminish function of adrenal medulla)
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Foot and Leg Problems 55 50% -75% of lower extremity amputations are performed on people with diabetes. More than 50% of these amputations are thought to be preventable.
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Foot and Leg Problems Contributing factors 56 Neuropathy Peripheral vascular disease Immunocompromis e Injuries could be: Chemical Thermal Traumatic
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Foot Care 57 1. Take care of your diabetes. 2. Inspect your feet every day. 3. Wash your feet every day (dry between toes well). 4. Keep the skin soft and smooth. 5. Smooth corns and calluses gently. 6. Trim your toenails each week or when needed. 7. Wear shoes and socks at all times. 8. Protect your feet from hot and cold. 9. Keep the blood flowing to your feet. 10. Check with your health care provider.
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Special Issues in Diabetes Care 58 Patients with diabetes who are undergoing surgery Hyperglycemia (due to stress hormones) Hypoglycemia (being NPO) Hold morning insulin unless it is > 200 mg/dL. Diuresis leads to fluid and electrolytes imbalance
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Nursing Diagnoses 59 Risk for fluid volume deficit related to polyuria and dehydration Imbalanced nutrition related to imbalance of insulin, food, and physical activity Deficient knowledge about diabetes self-care skills/information
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Nursing Diagnoses 60 Deficient knowledge about diabetes self-care skills/information Potential self-care deficit related to physical impairments or social factors Anxiety related to loss of control, fear of inability to manage diabetes, misinformation related to diabetes, fear of diabetes complications
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Collaborative Problems/ Potential Complications 61 Fluid overload, pulmonary edema, and heart failure Hypokalemia Hyperglycemia and ketoacidosis Hypoglycemia Cerebral edema
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