Nursing Care of the Diabetic Patient – Flashcards
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"Prediabetes" and Metabolic Syndrome
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impaired glucose tolerance (IGT) or impaired fasting glucose (IFG) develop diabetes within 10 years Long-term damage occurring in heart, blood vessels, etc. Usually no symptoms, but must watch for diabetes symptoms
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Impaired Glucose Tolerance IGT
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Fasting glucose levels higher than normal (>100 mg/dl, but <126 mg/dl)
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Impaired Fasting Glucose IFG
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2-hour plasma glucose higher than normal (between 140 and 199 mg/dl)
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Metabolic Syndrome
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Cluster of abnormalities that increase risk for cardiovascular disease and diabetes, including, Insulin resistance, ? triglycerides, ? LDLs & ? HDLs, Hypertension, Central obesity
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Highest rate of diabetes in the world
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native Americans and Alaskan natives
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Obesity Epidemic= Type II Diabetes Epidemic
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over 90% of patients with Diabetes has type 2 usually over 35 80-90% are overweight abdominal/visceral obesity most powerful risk factor
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Acute Complications:Hypoglycemia
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BG < 70 mg/dl Early S/S: confusion, irritability, diaphoresis, weakness, tremors, hunger Late S/S: double vision, confusion, seizures, coma
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Mild Hypoglycemia
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give 15 grams of oral carbohydrates. Can take 10-15 minutes for symptoms to disappear
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Moderate and Severe Hypoglycemia
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Rx for glucagon, not self-injected AE: nausea after injection Glucagon stimulates the liver to release sugar, if glycogen is available
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Acute Complications: DKA
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caused by a profound deficiency of insulin and is characterized by hyperglycemia, ketosis, acidosis, and dehydration. most likely in DM type 1
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Anion Gap
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difference between primary measured cations (sodium Na+ and potassium K+) and the primary measured anions (chloride Cl- and bicarbonate HCO3-) in serum. This test is most commonly performed in patients who present with altered mental status, unknown exposures, acute renal failure, and acute illnesses. Gap > 12 = metabolic acidosis
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DKA Triad
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Hyperglycemia (500-800 mg/dl) or (27.8-44.4 mmol/L) Metabolic Acidosis (anion gap > 12) Ketosis (of the urine)
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DKA Triggers
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Insulin Deficiency Iatrogenic (glucocorticoids, anti-psychotics, high dose thiazide diuretics) Infection: UTI, PNA Inflammation: pancreatitis, cholecystitis Ischemia / Infarction: MI, stroke, gut ischemia Intoxication: alcohol, cocaine, drugs
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DKA: Lab Findings
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Hyperglycemia: > 250 mg/dL in serum, + glucose on urinalysis Acidemia (pH 12: Anion gap = [Na] - [Cl] - [bicarbonate] Hyperosmolality >290 mOsm/L : 2 Na + 2 K + BUN/3 + glucose/18 Hyponatremia: fluid shift out of cells, dilutes sodium, causes cerebral edema and brain swelling Azotemia: 2/2 dehydration ^WBC and amylase Hyperkalemia: from fat breakdown = acidosis
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DKA Nursing Management
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monitor ABGs, mental status, volume status, BG q hr, electrolytes to close ion gap q 2-4 hr
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Acute Complications: HHS
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Hyperosmolar hyperglycemic syndrome high mortality rate Less common than DKA PTs over 60 y/o Ketoacidosis does NOT occur Few early S/S Neuro S/S due to ^ osmolality (slurred speech, SZ, coma) Hx dehydration, Na+ high BG > 400 mg/dl Tx: CORRECT DEHYDRATION: 8-9 L replacement over 48 hrs
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DKA and HHS: Nursing Interventions Similar
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Establish IV access quick Monitor cardiac, VS, K+, Blood gas Give: IV (HHS Pt greater fluid requirement) Insulin therapy: may not be for HHS -lytes PRN per order Assess: Renal status UOP, CP status, LOC
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Diabetes ManagementNursing Care Plan
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Focus on Monitoring, Management, Medication, Meal Planning, and Movement
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Normal insulin secretion
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Normal BG: 70-120 mg/dl High peak at breakfast, low peak at lunch, moderate peak at dinner, levels off during night
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Types of insulin
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rapid-acting, short-acting, intermediate-acting, long-acting
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Lispro (Humalog)
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Rapid, 5-15 min; give AC, Peak: 30-90 min, Duration; 5 hours
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Aspart (Novolog)
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Rapid: 10-20 min; Peak: 30-90 min Duration: 3-5 hours
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Rapid Insulins
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Humalog & Novolog
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Humulin R
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Regular: 30 min; Give AC Peak: 2-4 hours Duration: 12 hours
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Novolin R
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Regular: 30 min; Give AC Peak: 2-4 hours Duration: 12 hours
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Regular Insulins
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Humulin R & Novolin R
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Humulin N
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Intermediate NPH; 2 hours Peak: 4-10 hours Duration: 16 hours
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Novolin N
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Intermediate NPH: 90 min Peak: 4-12 hrs Duration: 24 hours
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Glarine (Lantus)
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Long Acting: 2-4 hours Peak: none, DO NOT MIX Duration: about 24 hours
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Problems with insulin therapy
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Hypoglycemia Allergic reactions Lipodystrophy Somogyi effect Dawn phenomenon Use of sliding scale in acute care settings: problem is that you are often 'chasing the sugar'
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New physiologic subcutaneous insulin protocols
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use basal, nutritional, and correctional insulin. These are weight based. Person weighing 65 kgs gets same amount of insulin as 120 kgs.
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Somogyi effect
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too much insulin Overdose of insulin causes hypoglycemia Usually during hours of sleep Counterregulatory hormones released Rebound hyperglycemia and possibly ketosis occur Also called Posthypoglycemic hyperglycemia
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Dawn phenomenon: "Liver Dump"
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hyperglycemia present on awakening in the morning Due to release of counter regulatory hormones in predawn hours (cortisol, glucagon, epinephrine...) Growth hormone/cortisol possible factors All people have this, whether or not they are diabetic. Surge of Cortisol around 5 AM. (Body's "let's get up signal?" Maybe reason shift workers have metabolic issues??? Avoid carbs at bedtime. Eat earlier.
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Drug TherapyOral Agents
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Work on three defects of type 2 diabetes: Insulin resistance Decreased insulin production Increased hepatic glucose production *Not insulin, improves body's ability to produce insulin and glucose
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Types of Oral Agents
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Sulfonylureas Meglitinides Metformin ?-Glucosidase inhibitors Thiazolidinediones
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Metformin
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First line drug for DM II; limits liver's output of glucose most prescribed medication for diabetes 2 in the world. S/S: diarrhea and stomach upset NOT for liver and kidney prob pts
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Thiazolidinediones
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Actos,reduce insulin resistance in muscle and fat tissue: (AVANDIA*BLACK BOX WARNING: HEART FAILURE)
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?-Glucosidase inhibitors
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Delay Carb absorption in small intestine.
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Beta blockers (Metoprolol, Atenolol)
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Drug interactions: Mask symptoms of hypoglycemia Prolong hypoglycemic effects of insulin
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Thiazide/loop diuretics
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Drug interactions: Can potentiate hyperglycemia By inducing potassium loss
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Cortisone
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Drug interactions: can elevated blood sugar
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Food therapy American Diabetes Association (ADA)
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within context of an overall healthy eating plan, person with diabetes can eat same foods as person who does not have diabetes
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Insulin Dosing: background, basal insulin repacement
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Approximately 40-50% of the total daily insulin dose is to replace insulin overnight, when you are fasting and between meals. This is called background or basal insulin replacement.
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Insulin Dosing: Bolus = Carbohydrate coverage
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The other 50-60% of the total daily insulin dose is for carbohydrate coverage (food) and high blood sugar correction. This is called the bolus insulin replacement. Bolus = Carbohydrate coverage
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One Unit regular insulin
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disposes about 12-15 grams of carbs ingested
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bolus dose for high blood sugar correction is defined as...
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how much one unit of rapid-acting insulin will drop the blood sugar.
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Generally, to correct a high blood sugar...
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one unit of insulin is needed to drop the blood glucose by 50 mg/dl. But drop in blood sugar can range from 15-100 mg/dl or more, depending on individual insulin sensitivities.
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The GENERAL CALCULATION for the body's daily insulin requirement is:
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Total Daily Insulin Requirement (in units of insulin) = Weight in Pounds ÷ 4 In kilograms: Total Daily Insulin Requirement (in units of insulin) = 0.55 X Total Weight in Kilograms Background dosing (basal) is about 50% of total.
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Type 1 DM: Emphasis
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Meal plan based on individual's usual food intake and is balanced with insulin and exercise patterns Insulin regimen managed day to day
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Type 2 DM: Emphasis
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Emphasis based on achieving glucose, lipid, and blood pressure goals Calorie reduction Low glycemic index foods: keep blood sugar even
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Exercise
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30 minutes brisk walking per day is goal. Combo of aerobic and strength training shown to be best.
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DiabetesChronic Complications: macro
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Angiopathy: Macrovascular (large and medium blood vessels) greater frequency and earlier onset in diabetes altered lipid metabolism common to DM
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Risk Factors for Macrovascular diabetic complications
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Obesity Smoking Hypertension High-fat intake Sedentary lifestyle
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DiabetesChronic Complications: micro
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Microvascular Result from thickening of vessel membranes in capillaries and arterioles In response to chronic hyperglycemia Is specific to diabetes unlike macrovascular
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Areas most noticeably affected by microvascular complications of diabetes
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Eyes (retinopathy) Kidneys (nephropathy) Skin (dermopathy) Problems usually appear after 10 to 20 years of diabetes
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Diabetic retinopathy
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Microvascular damage to retina Result of chronic hyperglycemia Most common cause of new cases of blindness in people 20 to 74 years *dilated eye exam annually
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Diabetic nephropathy
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damage to small blood vessels that supply the glomeruli of the kidney Leading cause of end-stage renal disease
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Critical factors for prevention/delay: diabetic nephropathy
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Tight glucose control Blood pressure management Yearly screening for: Microalbuminuria in urine, Serum creatinine
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Angiotensin-converting enzyme (ACE) inhibitors
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Used even when not hypertensive Angiotensin II receptor antagonists
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Diabetic neuropathy
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60% to 70% of patients with diabetes have some degree of neuropathy Nerve damage due diabetes Sensory versus autonomic neuropathy Sensory neuropathy
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Characteristics of Diabetic Neuropathy
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Loss of sensation, abnormal sensations, pain, and paresthesias
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Autonomic Complications
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Gastroparesis (Delayed gastric emptying) Cardiovascular abnormalities: Monitor lipidss; HG A1C Neurogenic bladder
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Silent" Heart Attacks
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Cardiovascular autonomic neuropathy (CAN) Patient often unaware she is having attack Symptoms: SOB, Weakness, fatigue, excessive perspiration. Abnormal heart rate control Beta blockers (atenolol, metoprolol) front line tx
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