Chapter 51- Assessment and Management of Patients with Diabetes PDF

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Assessment and Management of Patients with Diabetes...

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Chapter 51: Assessment and Management of Patients with Diabetes Disorder of Impaired Glucose Metabolism 798,000 new cases diagnosed each year In US, more than 25 million people (1/3 undiagnosed); in 2010 increased by 1.9 million Leading cause of:  Cardiovascular disease  Stroke  End-stage renal disease (ESRD)  Adult blindness  Non-traumatic lower limb amputations

Risk Factors: Epidemiology  Minorities disproportionately affected  Family history of diabetes  Obesity: BMI > 30  Age > 45  HTN: > 140/90  HDL 250 Normal Function of Insulin  Normal insulin metabolism = Insulin is a hormone s o Produced by the  cells in Islets of Langerhans o Anabolic hormone (storage): moves glucose from bloodstream to muscle & liver stored as glycogen, & adipose fat cells o Decreases glucose in the bloodstream by transporting glucose inside the cells o Released continuously into bloodstream in small increments with larger amounts released after food o Stabilizes glucose range to 70 to 120 mg/dL  Definition: Diabetes Mellitus o Abnormal insulin production o Impaired insulin utilization o Or both  Glucagon(counterregulatory hormone): oppose effects of insulin Pathophysiology  Disorder of glucose metabolism related to absent or insufficient insulin supply and/or poor utilization of available insulin.  Insulin metabolizes glucose for energy & tells liver to stop glucose release; with diabetes, this is unchecked  DM speeds up transport of protein from food into the cells in type 1 diabetic patients & increases breakdown of muscle mass  Insulin inhibits the breakdown of stored glucose, protein, & fat

Classification of Diabetes  Type 1 Diabetes: 5 % in adults with diabetes o Insulin-dependent o Complex genetic, immunologic, & environmental triggers genetic predisposition to β cell damage: o Autoimmune disease results in progressive destruction of the ß cells o Characterized by acute onset, usually before age 30 but may occur at any age  Destruction of β cell →↓insulin production  Glucose accumulates in blood stream, but glucose cannot enter cells without insulin  ↑glucose production by liver, breakdown of fat (increases ketone bodies)  Hyperglycemia → Kidney may not reabsorb glucose → appears in urine  When excessive glucose is excreted in urine → excessive loss of fluids and electrolyte (osmotic diuresis)  Type 2 Diabetes: 95% of adults with diabetes o Insulin-resistance  Body tissues do not respond to insulin  Insulin receptors are either unresponsive or insufficient in number o β cells fatigued from compensating, β-cell mass lost o Pancreas ↓ ability to produce insulin o Impaired insulin secretion  Enough insulin is present to prevent breakdown of fat (does not increase ketone)  A slow, progressive glucose intolerance  Gestational Diabetes o Any degree of glucose intolerance with its onset during pregnancy o Secretion of placental hormone causes insulin resistance o Risk: Severe obesity; prior hx gestational diabetes; family hx of diabetes, high risk ethnic/racial group o After delivery, blood glucose level return normal, or may develop type 2 DM  Latent Autoimmune Diabetes of Adults (LADA) o A subtype of diabetes: autoimmune beta cell destruction in pancreases o Clinical manifestations are the same with type 1 and type 2 diabetes Normal Insulin Secretion • Normal endogenous insulin secretion. In the first hour or two after meals, insulin concentrations rise rapidly in blood; they peak at about 1 hour. After meals, insulin concentrations promptly decline toward preprandial values as carbohydrate absorption from the gastrointestinal tract declines. After carbohydrate absorption from the gastrointestinal tract is complete and during the night, insulin concentrations are low and fairly constant, with a slight increase at dawn.

Diabetes Mellitus (DM): Assessment  Prevention o Type 2 diabetes can be prevent by lifestyle modifications (e.g., weight reduction)  Clinical manifestations o Three “P’s” (often in Type 1 DM with hyperglycemia)  Polyuria (due to osmotic diuresis)  Polydipsia (due to osmotic diuresis)  Polyphagia (due to catabolic state) o Fatigue, weakness o Sudden vision changes o Tingling pr numbness in hand, or feet o Slow healing of skin lesion or wounds o Recurrent of infections  Assessment and Diagnostic findings o Four methods of diagnosis  Glycosylated hemoglobin (A1C) ≥ 6.5%  Fasting plasma glucose level ≥126 mg/dL  Random or casual plasma glucose measurement ≥200 mg/dL plus symptoms (polyuria, polydipsia, and explained weight loss)  Two-hour OGTT (oral glucose tolerance test) level ≥200 mg/dL when a glucose load of 75 g is used (not recommended for routine clinical use)  History  Symptoms r/t hyper/hypoglycemia  Blood glucose monitoring results  Chronic complications of diabetes:  Eye, kidney, nerve, GU, cardiac, PVD, foot complication, etc.  Compliance with diet, exercise, medications  Use of tobacco, alcohol, OTC meds  Lifestyle, cultural, psychosocial factors  Physical o BP, BMI o Funduscopic examination: retinopathy (damage to small blood vessels) o Foot examination: ulcers, Skin examination: slowed healing, infections o Neurologic examination: peripheral neuropathy o GI problems: gastroparesis, constipation o Renal: nephropathy Goals of Diabetes Management

1. Decrease symptoms 2. Promote well-being 3. Delay onset and progression of long-term complications. 4. Normalize insulin activity and blood glucose levels 5. Reduce incidence of complications o Retinopathy o Nephropathy o Neuropathy Diabetes Mellitus (DM): Management – Nutrition Therapy  Consistently following a meal plan: reduce caloric intake, pacing food intake and not skipping meals (decrease demands on pancreas)  Weight loss is the key to treatment  Meal planning and education o Caloric requirement (calorie-controlled diets) o Caloric distribution  Carbohydrates 50% to 60%  Fats 20% to 30%  Protein 10% to 20%  Fiber (improves blood glucose level) o Food classification systems  Exchange lists, Nutrition labels, Healthy food choice, My plate guide, Glycemic index DM: Nutritional Therapy  Diet teaching o Dietitian initially provides instruction. o Carbohydrate counting o USDA MyPyramid guide  An appropriate basic teaching tool o Plate method  Helps patient visualize the amounts of vegetable, starch, and meat that should fill a 9-inch plate o Alcohol  Moderate alcohol consumption can sometimes be safely incorporated into the meal plan if blood glucose levels are well controlled  High in calories, No nutritive value  Large amount converted to fats, increased risk of Diabetic ketoacidosis o Sweeteners  Artificial sweeteners is acceptable o Misleading food labels  “sugarless” or “sugar-free” may still provide calories equal to those of the equivalent sugar-containing products

DM: Glycemic Index (GI) Nutritional Therapy

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A low GI value (55 or less) are more slowly digested, absorbed and metabolized and cause a lower and slower rise in blood glucose Should be considered when a meal plan is formulated o For example, the GI of an apple is 52, regular milk 27, baked potato 93, cornflake cereal 119, and baked beans 69

DM: Exercise  ↑ insulin receptor sites and lowers blood glucose levels  Increases HDL  Contributes to weight loss  Improves circulation and muscle tone  Several small carbohydrate snacks can be taken every 30 minutes during exercise to prevent hypoglycemia; Best done after meals  Monitor blood glucose levels before, during, and after exercise  Exercise plans after medical clearance o Exercise plans after medical clearance, slowly with gradual progression o Blood glucose >250 m/dL with ketones in urine, should not begin exercise Monitoring Blood Glucose  Self-monitoring of blood glucose o Important for detecting episodic hyperglycemia and hypoglycemia o Patient education crucial o Requires at least three times before each meal o Keep a record of blood glucose results  Using a continuous glucose monitoring system  Testing for Hemoglobin A1c (HgbA1c) o Measure of glucose control for the past 3 months  Testing for Ketones o By-products of fat breakdown and accumulate in blood and urine; the signal of deficiency of insulin and Type 1 DM is deteriorating

Drug Therapy: Insulin  Required for type 1 diabetes  Prescribed for patient with type 2 diabetes who cannot control blood glucose by other means  Individuals with type 2 diabetes may need up to four injections per day to adequately control their blood glucose levels.  Prepared through genetic engineering  Storage of insulin o Do not heat/freeze. o In-use vials may be left at room temperature up to 4 weeks. o Extra insulin should be refrigerated. o Avoid exposure to direct sunlight.  Types of insulin o Rapid-acting (bolus): Lispro (Humalog), Aspart (Novolog), and glulisine (Apidra)  Injected 5 to 15 minutes before meal o Short-acting (bolus): Regular

 Injected 15 minutes before meal Intermediate-acting: NPH  2 injections to achieve 24-hour coverage o Premixed 70/30: NPH & Regular o Long-acting (basal): Glargine (Lantus), detemir (Levemir)  Injected once a day at bedtime or in the morning Insulin regimen o Usually, combination of a short-acting and a long acting insulin Complications of Insulin Therapy o Systemic allergic reaction (rare) o Insulin Lipodystrophy – localized reactions o Resistance to injected insulin – requires large dose to control symptoms o Hyperglycemia – elevated glucose level arising in the morning ü Dawn phenomenon: normal blood glucose level until 3 am, then begin to rise ü Insulin waning: progressive rise in blood glucose from bedtime to morning ü Somogyi effect: normal or elevated blood glucose at bedtime, a decreased at 2 – 3 am, then increases in the morning o

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tion. Different types of insulin may be used

Problems with insulin therapy: Somogyi effects  Somogyi effect: o Rebound effect in which an overdose of insulin causes hypoglycemia o Usually during mid-hours of sleep o Counterregulatory hormones released o Rebound hyperglycemia and ketosis may occur. Methods of Insulin Delivery  Insulin Pens  Jet Injections  Insulin Pump  Insulin syringes  Do not inject into site to be exercised, i.e. thigh.

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Usually available as U100, 1 mL contains 100 units of insulin Do not recap needle 45- to 90-degree angle, depending on fat thickness of the patient

Drug Therapy: Insulin  Insulin pump o Continuous subcutaneous infusion o Battery-operated device o Connected via plastic tubing to a catheter inserted into subcutaneous tissue in abdominal wall o Potential for tight glucose control

Drug Therapy: Oral Agents  Not insulin  Work to improve mechanisms by which insulin and glucose are produced and used by the body.  Work on 3 defects of type 2 diabetes: o Insulin resistance o Decreased insulin production o Increased hepatic glucose production  Interactions with other agents  -adrenergic blockers (cardiac patients) o Mask symptoms of hypoglycemia  Thiazide/loop diuretics o Can potentiate hyperglycemia by inducing potassium loss 1. Sulfonylureas include glipizide (Glucotrol, Glucotrol XL), glyburide (Micronase, DiaBeta, Glynase), and glimepiride (Amaryl). 2. Meglitinides include repaglinide (Prandin) and nateglinide (Starlix). 3. Metformin (Glucophage) is a biguanide glucose-lowering agent. 4. Acarbose (Precose) and miglitol (Glyset) are α-glucosidase inhibitors. 5. Thiazaolidinediones include pioglitazone (Actos) and rosiglitazone (Avandia).

Acute complication: Hypoglycemia  Hypoglycemia - < 70 mg/dL o Too much insulin or oral hypoglycemic agent, too little food, excessive physical activity  Clinical manifestations o Mild hypoglycemia  Sweating, tremor, tachycardia, palpitation, nervousness, hunger o Moderate hypoglycemia (CNS impairment)  Confusion, visual disturbances, slurred speech o Untreated can progress to loss of consciousness, seizures, coma, and death Acute complication: Hypoglycemia Management  If alert enough to swallow: o 15 of a simple carbohydrate – 2 or 3 glucose tablets, 0.5 cup juice

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o Avoid foods with fat: decrease absorption of sugar Emergency situations: patient is unconscious and cannot swallow o Glucagon injection (IM or subcutaneous) o Dextrose 50% in water 20 to 50 mL IV push – in the hospital settings Recheck blood sugar 15 minutes after treatment, and repeat until blood sugar >70 mg/dL. Providing patient education o Prevention o How to recognize symptoms of hypoglycemia o Carry simple sugar in case of hypoglycemia episodes o Glucose test for the patient who takes beta-blockers

Acute Complications: Diabetic Ketoacidosis (DKA)  Caused by profound deficiency of insulin: No insulin  Ketosis: body burns fat when glucose cannot enter cells  Associated with Type 1 DM  Life-threatening syndrome o Hyperglycemia o Metabolic Acidosis, Ketosis o Dehydration and electrolyte imbalance (e.g., potassium, sodium)  Precipitating factors o Illness o Infection o Inadequate insulin dosage o Undiagnosed and untreated type 1 DM  Prevention is important o Follow “sick day rules”  Never eliminate insulin doses when nausea and vomiting  Test blood glucose and urine ketones very 3 to 4 hours  Clinical manifestations o Abdominal pain, nausea, vomiting o Kussmaul respirations: Rapid deep breathing – Sweet fruity odor  Attempt to reverse metabolic acidosis o Polyuria, increased thirst  Diagnostic findings o Blood glucose level >250 mg/dL (13.9 mmol/L) o Metabolic acidosis: pH 350 after diuresis o Absent/minimal ketone bodies  Overall management is similar to DKA o Rehydration – IV infusion 0.9% or 0.45% NS then switch to D5W o Restoring electrolyte – potassium IV o IV Insulin infusion DKA       HHS      

Sudden onset (300 mg/dL pH 200 mg/dL, small dose of regular insulin SQ 6. Intraoperative: both Insulin infusion & Dextrose infusion with frequent titration based on glucose levels; give insulin SQ 30 minutes before D/C IV insulin infusion 7. Type 2 non-insulin dependent diabetics: may require doses

Hospitalized Patient with Diabetes 1. Goals: ü Help patient achieve control ü Monitor and manage potential complications 2. Assess patient’s usual routine for meals & meds →want to avoid mismatching 3. Adjust hospital routine to patient’s pattern to avoid hyperglycemia 4. Administer insulin when meal is served 5. Check IV solutions, meds (corticosteroids), altered diet (NPO, clear liquids, parenteral nutrition) 6. Hypoglycemia may occur if tube feeding stopped for an extended period of time 7. Older adult: hypoglycemia may be undetected, dehydration with elevated glucose levels...