AHI – Diabetes Management

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DM Type I
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autoimmune disorder where the body does not produce insulin for glucose metabolism; acute and sudden onset, typically manifests at a young age
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DM Type 2
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a Metabolic Disorder that accounts for 90 to 95 percent of all diabetes cases wherein either the pancreas does not make sufficient insulin or body cells are resistant to its effects (insulin resistance) *usually occurs in older patients, but is seen increasingly in younger pts
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Three Main Types of Diabetes
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1) DM Type I 2) DM Type 2 3) Gestational Diabetes
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S/S DM Type 1
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Polyuria Polydipsia Polyphagia Fatigue Weakness Weight loss Irritability and mood changes
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Criteria for Diagnosing Diabetes
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1) *A1C = ≥6.5%* (Glycated Hemoglobin, Glycosylated Hemoglobin, Hemoglobin A1c, A1C, HbA1c) 2) Fasting plasma glucose (FPG) = *≥126 mg/dL (7.0 mmol/L)* 3) 2-h plasma glucose ≥200 mg/dL (11.1 mmol/L) during an OGTT 4)A random plasma glucose ≥200 mg/dL (11.1 mmol/L)
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Hemoglobin A1C
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% of hemoglobin that is coated with glucose, used for diagnosis of diabetes b/c it is not as susceptible for spikes as blood glucose levels are
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Prediabetic Criteria
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FPG = 100-126 AB1C = 5.7-6.4% OGTT = 140-199
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Normal Lab Values Relevant to Diabetes
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A1C = < 6.5% (5%) FPG = 70-110 (<99) pH = 7.35-7.45
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Tx for DM Type I
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*Insulin therapy* – Most should be treated with multiple dose injections (3-4 per day of basal and prandial insulin) or continuous subcutaneous insulin infusion Education: how to match prandial insulin dose to carbohydrate intake, premeal blood glucose, and anticipated activity
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Onset, Peak, Duration of Lispro
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O = 15 min P = 0 -1.5 hrs D = 3-4 hrs
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Onset, Peak, Duration of Asparte (Rapid Acting Insulin)
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O = immediate P = 45 min – 1.5 hrs D = 3-4 hrs
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Onset, Peak, Duration of Regular Insulin (Short Acting Insulin)
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O = 30 min – 1 hr P = 2-3 hrs D = 3-6 hrs
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Onset, Peak, Duration of NPH (Intermediate Acting)
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O = 2-4 hrs hrs P = 4-10 hrs D = 10-16 hrs
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Onset, Peak, Duration of Glargine (Long-Acting)
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O = 1-2 hrs P = none (plateaus throughout duration) D = 24+ hrs *commonly used as Basal Insulin
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Administration of Insulin
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Before meals Blood glucose testing and administration of insulin should occur within 30 minutes of each other Injection Proper injection sites Gently pinch skin and give at 90° angle (if very thin 45°) Document blood glucose, and insulin administration Be aware of NPO status, impending tests, and when meals are delivered A hypoglycemia management protocol should be adopted and implemented by each health care setting
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Blood glucose testing should be done within __ minutes of administration.
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30
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Monitoring Blood Glucose
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Important for detecting episodic hyperglycemia and hypoglycemia Patient training is crucial Supplies immediate information about blood glucose levels
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Continuous Glucose Monitor tests glucose in ____ .
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interstitial fluid
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Adrenalin can make blood sugar ___ .
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go up
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Exercise can also have the effect of ____ blood glucose by using the available sugar during activity.
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lowering.
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Order of NI for Diabetic Pt
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1) Vital Signs 2) Fingerstick 3) Administer Insulin 4) Complete Bedside Assessment 5) AM Care 6) Education
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Beta cell dysfxn begins ___ years before presentation of DM Type 2.
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10-12
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Etiology of DM Type 2
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The overabundance of free fatty acids contributes to insulin resistance. As the progression to type 2 diabetes continues, pancreatic insulin-producing cells become exhausted from overwork and damage occurs.
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Non-modifiable Risk Factors for DM Type 2
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Increased age Certain ethnicities (Native Americans, African Americans, Hispanic and/or Asian) Genetic factors
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Modifiable Risk Factors for DM Type 2
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Overweight Sedentary lifestyle Dietary components Perinatal factors, nutrition in utero
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As one’s ___ goes up, their risk for Diabetes Type 2 also increases.
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BMI
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Clinical Manifestations of DM Type 2
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Feeling tired and weak Passing large volumes of urine, especially during the night Having frequent infections (ex. yeast infections –> high blood sugar) Having blurred eyesight Weight loss Excessive hunger and thirst
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Factors Affecting BG Levels in Hospital Setting
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• Changing IV glucose rates • TPN and enteral feedings • Lack of physical activity • Unusual timing of insulin injections • Use of glucocorticoids • Unpredictable or inconsistent food intake • Fear of hypoglycemia • Cultural acceptance of hyperglycemia
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Some non-diabetic medications may _____ blood glucose levels in pts.
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increase or decrease
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Nursing Care for Diabetic Pts
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• 24-hour coverage by nursing • Nursing often coordinates, and is aware of, the multiple services required by patient – Travel off unit, (eg, physical therapy, X-ray) – Amount of food eaten (carbohydrates) – Patient’s day-to-day concerns – Order changes (by various providers)
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Goals of Care for DM Pts
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Maintain steady control of blood glucose Decrease symptoms Promote well-being Prevent acute complications Delay onset and progression of chronic complications
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Nursing Assessment for DM
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Past health history (Table 49-13) Infections Medications Recent surgery Positive health history Obesity Current management strategies – How often they see their PCP – Education level – Nutritional habits
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Important Education for Pts with DM
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Symptoms Diagnosis Prevention Treatment Self-care Foot Care Exercise Nutrition Storage and dose preparation Syringes Blood glucose monitoring Interpretation of results Frequency of testing Blood glucose therapy goals
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Nursing Diagnosis for DM
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Knowledge Deficit: Pathophysiology Normal levels Effect of insulin & exercise Effects of stress, illness & infections Drugs, alcohol Self testing Signs/Symptoms of Hypoglycemia/ Hyperglycemia
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Oral Drug Therapy for DM
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Work to improve mechanisms by which insulin and glucose are produced and used by the body.
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Sulfonylureas
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increase insulin production from the pancreas 1) Glipizide (Glucotrol) 2) Glyburide (Micronase) 3) Glimepiride (Amaryl)
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Biguanides
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reduce glucose production by the liver, enhances insulin sensitivity and improves glucose transport 1) Metformin (Glucophage) – Temporarily discontinue metformin before IV contrast, resume after 48 hours and normal creatinine – Used for weight loss & lowering Cholesterol as well – CI for pts with liver disease or ETOH abuse
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Nutritional Therapy for DM
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+ Protein, – fats and carbohydrates, + fiber, – sweeteners, + replacers Less Alcohol Food labeling Exchange system, carbohydrate counting – ALL ABOUT BALANCE – Loss of 1-2 lbs a week does drastic improvement for HbAC1 %
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Exercise Therapy for DM
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Benefits of exercise (*decreases insulin resistance*) Risks related to exercise Screening before starting exercise program Guidelines for exercise – 30min/day moderate – 150 min/ week Exercise promotion
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Acute Complications of DM
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1) Diabetic ketoacidosis (DKA) 2) Hyperosmolar hyperglycemic syndrome (HHS) 3) Hypoglycemia – Too much insulin – Too little glucose
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Hypoglycemia
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*Blood glucose level < 70 mg/dL* Diet therapy: carbohydrate replacement Drug therapy: glucagon, 50% dextrose Prevention strategies for: – Insulin excess – Deficient food intake – Exercise – Alcohol consumption
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What can cause hypoglycemia?
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Insulin > demand Change in type of insulin Oral hypoglycemia Decreased caloric intake Increase in activity Decreased metabolism Excessive ETOH Adrenal insufficiency
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Glucagon IM has precautions for ___ .
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aspiration, as it can cause emesis (N/V)
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Hypoglycemia can lead to ….
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– LOC – seizures – coma – death
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Treat hypoglycemia with ___ carbs.
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simple -> absorbed faster!
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After giving glucose re hypoglycemic protocol, recheck after ___ .
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20 min
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S/S Hypoglycemia
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mood changes, tremor, pallor, diaphoresis, dizziness, blurred vision, HA, fatigue, hunger
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Clinical Manifestations of Diabetic Ketoacidosis (DKA)
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Dehydration (poor skin turgor, tachycardia, orthostatic hypotension) Lethargy and weakness Abdominal pain with anorexia and vomiting Kussmaul respirations (Body’s attempt to reverse metabolic acidosis) Acetone on breath (sweet, fruity odor) *Typically occurs in DM Type 1 that is poorly managed or undiagnosed*
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DKA Lab Findings
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BG > 250mg/dL (super high blood glucose) Arterial blood pH < 7.30 (low pH) Bicarb < 15mEq/L ( low HCO3) Urine +++ketones (keytones + in urine!)
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Interventions for DKA
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Monitoring for clinical manifestations *Assessment of airway, level of consciousness, hydration status, blood glucose level* Management of fluid and electrolytes Drug therapy goal: to lower serum glucose by 75 to 150 mg/dL/hr Management of acidosis Client education and prevention – Severity of s/s will dictate treatment – Pt can end up on NG tube or respirator
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Hyperosmolar Hyperglycemic Syndrome (HHS)
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Severe hyperglycemia w/ serum glucose *>600mg/dL* Plasma osmolarity > 315 mOsm/kg Bicarb > 15 Arterial pH > 7.3 Serum ketones – negative or mildly elevated *HHNS occurs less often than DKA, but has a much higher mortality* – Patients >60, Type 2 DM, infections End result – hyperglycemia and volume depletion through osmotic diuresis. – Total body water losses can reach 8-12 liters
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BG levels can rise as high as ___ before s/s of HHS begin, because there is enough insulin in the body to combat the glucose levels before ketosis begins.
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600-800
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Typically, with pts who get HHS, an acute illness has impaired their ____.
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thirst mechanism
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Nursing Interventions for HHS
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Monitoring for clinical manifestations Fluid therapy: to rehydrate the client and restore normal blood glucose levels within 36 to 72 hr Continuing therapy with IV regular insulin at 10 units/hr often needed to reduce blood glucose levels Client education and prevention
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DKA vs HHS
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– usually < 40 y/o – S/S last under 2 days – Glucose levels 600-800 mg/dL – Sodium = normal or low – Potassium = irrelevant – BiCarb = low – Ketones = present – Serum Osmolality = < 350 mOsm/kg – Prognosis = 3-10% mortality
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HHS vs DKA
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– usually >60 y/o – S/S usually last > 5 days – Glucose levels = > 800 mg/dL – Sodium = normal or high – Potassium = irrelevant – BiCarb = normal – Ketones = not present – Serum Osmolality = > 350 mOsm/kg – Prognosis = 10-20% mortality
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Chronic Complications of Diabetes
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Cardiovascular disease (Primary cause of death in patients with DM) *silent ischemia* Cerebrovascular disease (Diabetic patients have at least twice the risk of CVA) Retinopathy (vision) problems – damage to blood vessels in retina – Leading cause blindness – *Need annual eye exams* Diabetic neuropathy Diabetic nephropathy Male erectile dysfunction due to nerve impairment *Complications for feet and lower extremities* – due to sensory neuropathy – and peripheral arterial disease
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Primary cause of death for pts with DM
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Cardiovascular Disease
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Diabetic Retinopathy
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– starts with “dirty lens” spots, “floaters” – damage to blood vessels in retina – can lead to blindness – annual eye exams necessary
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Interventions for DM Risk for Delayed Surgical Recovery
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Preoperative care – Careful assessment of cardiac risk factors –> EKG – May be relatively asymptomatic Intraoperative care – Glycemic control Postoperative care and monitoring includes care of: – Cardiovascular – Renal – Nutritional
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Contributing Factors to Risk for Complications of Feet and Lower Extremities in DM
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Risk factors Sensory neuropathy Peripheral arterial disease- 2x more common in diabetics Other contributors: *Smoking* Clotting abnormalities. Impaired immune function Autonomic neuropathy
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1 in __ diabetics will develop a foot ulcer in their lifetime.
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4
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Foot ulcers can become a big problem in DM pts because of …
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delayed healing that can lead to necrosis or amputation
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It is recommended that DM pts go to ____ annually.
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a podiatrist
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Interventions for Foot Care
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•Testing for sensation (monofilament, vibration) •Annual visit with comprehensive foot examination •Every visit if high risk •Appropriate foot wear •Teach patient daily skin assessment, may need mirror •Wash/dry daily •Avoid hot water; dry thoroughly between toes •Lubricate daily (not between toes) •Trim toes properly after bathing •No self-cutting of nails if: •Neuropathy, PAD, poor vision •Report nonhealing breaks in skin or any other concerns
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Interventions for Nursing Dx for DM: Risk of Injury Related to Disturbed Sensory Perception: Visual
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Blood glucose control Environmental management Incandescent lamp Clock method for meals Syringes with magnifiers Large-print reading materials Hand-held magnifiers
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DM and Infection
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Diabetic individuals more susceptible to infection Defect in mobilization of inflammatory cells Impairment of phagocytosis by neutrophils and monocytes Loss of sensation may delay detection. Treatment must be prompt and vigorous. (frequent yeast infections, neuropathy can delay awareness of s/s of infection, impaired wound healing)
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DM Gero Considerations
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Prevalence increases with age Hypoglycemic unawareness more common Presence of delayed psychomotor function could interfere with treating hypoglycemia Strict glycemic control may be difficult to achieve – cognitive dysfxn can interfere with Tx as well
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Some medications may _____ blood glucose levels.
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increase or decrease

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