Diabetes
Diabetes
Russell D. White
Matthew John
Basics
Description
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Group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. This hyperglycemia produces both long-term microvascular and macrovascular complications.
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Synonym(s):
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Type 1: Autoimmune diabetes; Insulin-dependent diabetes mellitus (IDDM)
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Type 2: Non-insulin-dependent diabetes mellitus (NIDDM)
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Epidemiology
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Type 1:
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5–10% of patients with diabetes
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Diagnosis usually before age 30 yrs
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Type 2:
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90–95% of patients with diabetes
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Diagnosis usually after age 40 yrs
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Incidence
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Most common endocrine disorder
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Increasing in incidence
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Estimated 23.6 million patients in U.S. (8% of the population)
Risk Factors
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Type 1:
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With or without family history
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Frequently, the patient or a 1st-degree relative has an autoimmune disease process.
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Autoantibodies often present before clinical diagnosis.
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Diagnosis or exacerbation of disease during adolescence or periods of stress
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Type 2:
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Genetic factors:
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Family history
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Familial hyperlipidemia
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Environmental factors:
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Sedentary lifestyle
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Inappropriate, calorie-laden diet
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High association with insulin resistance
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Gestational diabetes mellitus (GDM)
General Prevention
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Primary prevention:
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Exercise:
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Persons with diabetes should perform at least 150 min per week of moderate-intensity physical activity (50–70% of maximum heart rate) (1)[A].
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In the absence of contraindications, persons with type 2 diabetes should be encouraged to perform resistance training 3× per week (1)[A].
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Weight loss and calorie restriction
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Medical therapy
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Secondary prevention:
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Same as primary prevention
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Treat HTN, lipids
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Smoking cessation
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Screen/treat retinopathy
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Cardiac evaluation if indicated: Performing >4 hr/wk of moderate to vigorous aerobic and/or resistance exercise physical activity is associated with greater cardiovascular disease reduction than with lower volumes of activity in persons with type 2 diabetes (2)[B].
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Aspirin for prevention of myocardial infarction/stroke
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Excellent foot care
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Select appropriate exercise: Persons with type 2 diabetes should include resistance exercise 3× weekly, targeting all major muscle groups and progressing to 3 sets of 8–10 repetitions at a weight that cannot be lifted more than 8–10× (8–10 RM) (2)[A].
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Etiology
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Type 1: Autoimmune disease characterized by antibodies against islet cells, insulin, and enzymes
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Type 2: Hepatic and peripheral insulin resistance with triad of:
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Impaired insulin secretion
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Increased hepatic glucose production
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Decreased muscle glucose uptake
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Commonly Associated Conditions
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Dyslipidemia
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HTN:
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In patients with type 1 diabetes, HTN and any degree of albuminuria, angiotensin-converting enzyme (ACE) inhibitors have been shown to delay the progression of nephropathy (1)[A].
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In patients with type 2 diabetes, HTN, and microalbuminuria, both ACE inhibitors and angiotensin-receptor blockers (ARBs) have been show to delay the progression of macroalbunimuria (1)[A].
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Nephropathy
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Nonproliferative/proliferative retinopathy
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Neuropathies
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Infections
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Coronary artery disease/peripheral arterial disease
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Diabetic ketoacidosis
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Nonketotic hyperosmolar coma
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Other autoimmune disorders associated with type 1 diabetes (eg, autoimmune thyroiditis, vitiligo, gluten-sensitive enteropathy, etc.)
Diagnosis
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Fasting plasma glucose >125 mg/dL or
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Casual plasma glucose >199 mg/dL together with classic symptoms of disease or
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2-hr oral glucose tolerance test glucose >199 mg/dL following 75-g glucose load
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Definitive diagnosis requires any 2 of the preceding abnormal values preferably on 2 separate days or
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A1C ≥6.5%
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Prediabetes is defined as a blood glucose ≥100–125 mg/dL.
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Medical risks of exercise:
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Hypoglycemia
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Hyperglycemia/ketoacidosis in insulinopenic patients
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Asymptomatic coronary artery disease
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Peripheral arterial disease
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Exacerbation of retinopathy (weight lifting, high-altitude sports)
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Foot injuries
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Autonomic dysfunction (abnormal sweating mechanisms, asymptomatic heart disease or hypoglycemia, lack of normal heart rate response to exercise, orthostatic hypotension)
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Specific activities (rock climbing, SCUBA diving)
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Type 1:
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Metabolically unstable with classic symptoms
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3 P's: Polyuria, polyphagia, polydipsia
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Fatigue
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Weight loss
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Type 2:
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Weight gain/loss
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Complications often present at time of diagnosis of:
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Serious infection
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Pregnancy
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Acute coronary syndrome (14% of patients)
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Retinopathy (16%)
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P.119
History
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Classic symptoms: Polyuria, polydipsia, polyphagia
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Unexplained weight loss and ketoacidosis (type 1)
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Family history
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Coexisting problem, eg, serious infection, acute coronary syndrome, pregnancy, major trauma
Physical Exam
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May be normal in mild or controlled cases
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Acute signs:
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Ketoacidosis
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Weight loss
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Volume depletion
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Mental status changes
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Hypotension
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Abdominal pain
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Chest pain
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Chronic signs:
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Obesity (type 2)
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Diabetic retinopathy (microaneurysms, retinal hemorrhages)
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Cardiac arrhythmia
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Congestive heart failure
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Chronic infections, fever
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Neurologic sensation loss to monofilament testing
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Foot ulcers/infections
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HTN
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Microalbuminuria
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Renal failure
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“Stiff man” syndrome, ie, limited joint mobility
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Diagnostic Tests & Interpretation
Lab
Undiagnosed/uncontrolled cases:
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Elevated plasma glucose
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Elevated A1C
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Glycosuria, ketonuria
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Microalbuminuria/proteinuria (>30 µg albumin/mg creatinine in a random spot urine collection)
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Abnormal lipid profile
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Acidosis/decreased HCO3-
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Decreased K+ and Mg2+
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Elevated blood urea nitrogen (BUN) and Na+
Imaging
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Plain films, bone scan, or MRI to rule out stress fracture, Charcot foot, foreign body
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MRI is the diagnostic test of choice for osteomyelitis.
Diagnostic Procedures/Surgery
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Exercise testing should be considered in patients with diabetes who are considering activity/exercise greater than the activities of daily living.
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One may determine the 10-yr risk of cardiovascular disease using either of the statistical sites below to determine the relative risk of cardiac disease. Those with a 10-yr risk of 10% or greater should undergo exercise testing for further evaluation. Web site 1 is used for either type 1 or type 2 diabetes; Web site 2 is used for those with type 2 diabetes.
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American Diabetes Association's PHD (Personal Health Decisions): www.diabetes.lorg/phd/profile/default.jsp
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UKDPS Risk Engine: www.dtu.ox.ac.uk/index.html?maindoc%20=%20/riskengine/
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Differential Diagnosis
Secondary causes:
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Other pancreatic disease (eg, trauma, drug- or chemical-induced), genetic syndromes, Cushing syndrome, and acromegaly
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Steroid-induced
Treatment
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Long-term treatment
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Acute treatment
Pre-Hospital
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Check for hypoglycemia, hyperglycemia, and volume depletion.
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Measure glucose; administer oral glucose, SC/IM glucagon, IV glucose, and IV fluids as indicated.
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Precompetition anxiety may mimic hypoglycemia: Check glucose.
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Check blood sugar before exercise:
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Ideal range for type 1 athlete is 120–180 mg/dL.
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If <100 mg/dL, snack before exercise (20 g carbohydrate)
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If 100–250 mg/dL, exercise
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If >250 mg/dL, delay exercise, check ketones, and treat hyperglycemia and dehydration.
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If >250 mg/dL with no ketones, be cautious, and check blood sugar frequently during exercise.
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Consume 15 g carbohydrate/15 min during exercise <45 min; 15 g carbohydrate every 30 min if exercise >45 min.
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Consume 1.5 g/kg carbohydrate within 30 min of exercise completion; repeat 1–2 hr later. Fine-tune management based on training history.
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Delayed hypoglycemia occurs 6–28 hr after exercise. Check blood sugar 1–2× during the night after event.
Medication
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Insulin secretagogues (ie, sulfonylureas, meglitinides): Decrease dose by 50% on exercise days.
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Biguanides (ie, metformin)
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Alpha-glucosidase inhibitors (ie, acarbose)
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DPP-IV inhibitors (ie, sitagliptin)
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Incretin mimetics (ie, exenatide, pramlintide)
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Insulin, SC:
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Decrease rapid-acting insulin dose by 30% for <1 hr of activity, 40% for 1–2 hr, 50% for >2 hr.
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Decrease intermediate-acting insulin dose by 50% prior to activity.
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When exercise lasts several hours, decrease basal insulin dose by 50% prior to activity.
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Very important to monitor frequently and determine individual insulin need according to type and duration of activity.
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Avoid regular or NPH insulin if possible owing to variability in absorption.
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Insulin pump therapy:
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Decrease basal rate by 50% 1 hr before intense activity and for 1–2 hr afterward.
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Reduce subsequent mealtime bolus by 30–50%.
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May temporarily suspend (discontinue) insulin pump therapy for 60 min for:
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Water sports (SCUBA, swimming, sailing)
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Contact sports (rugby, football, wrestling)
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P.120
Additional Treatment
Additional Therapies
Dozen diabetic tips:
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Have preexercise evaluation and exercise test, if indicated.
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Always exercise with a partner.
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Wear identification (Med-Alert) and have strategy for treating hypoglycemia.
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Use, do not simply possess, glucose-monitoring device with exercise.
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Athletes with well-controlled type 1 diabetes of <10 yrs' duration usually have few complications.
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Type 1 athletes of >10 yrs' duration often have dysregulation.
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Injection sites in type 1 athletes may affect absorption rate with exercise; certain medications in type 2 athletes may cause hypoglycemia.
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Meals should be ingested 3–4 hr before exercise.
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Avoid exercising during times of peak insulin activity (consider rapid-acting insulin).
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Check blood sugar before, during, and after exercise.
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Be aware of delayed hypoglycemia. Replenish glycogen stores in the “golden hour” after exercise based on duration/intensity of activity.
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Each diabetic athlete must be aware of personal pattern in blood glucose response to exercise based on training experience.
In-Patient Considerations
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Hypoglycemia:
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Admit for severe refractory hypoglycemia.
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Treat volume depletion.
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Administer parenteral or IV glucose, glucagon.
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Glucagon is ineffective if glycogen stores are depleted.
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Correct associated electrolyte abnormalities.
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Nonketotic hyperglycemia:
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Treat sometimes profound dehydration with isotonic crystalloid.
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IV or scheduled SC insulin
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Treat associated electrolyte abnormalities (ie, hypokalemia, hypomagnesemia).
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Diabetic ketoacidosis:
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Treat hypovolemia with isotonic crystalloid; transition to dextrose-containing fluid until acidosis resolves.
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IV or scheduled SC insulin until acidosis resolves
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Treat associated electrolyte abnormalities (ie, hypokalemia, hypomagnesemia).
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Ongoing Care
Treatment goals:
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Control blood glucose:
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Avoid blood glucose <70 mg/dL or >200 mg/dL.
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Maintain A1C within 1% of the upper limits of normal for reference laboratory.
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No severe hypoglycemia
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Treat associated problems:
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Strive to normalize weight.
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Avoid excessive alcohol use.
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Cease smoking.
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Treat associated diseases:
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HTN:
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Maintain BP <130/80 mm Hg.
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Select ACE inhibitors, ARBs, or some calcium-channel blockers (eg, amlodipine or diltiazem) for treatment.
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Avoid use of diuretics, β blockers, and verapamil in exercising persons.
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Hyperlipidemia: Maintain total cholesterol <200 mg/dL. Strive for low-density lipoprotein (LDL) cholesterol <100 mg/dL, <70 mg/dL in individuals with established cardiovascular disease. Strive for high-density lipoprotein (HDL) cholesterol >50 mg/dL in women and >40 mg/dL in men.
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Monitor/prevent macrovascular complications:
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Coronary artery disease:
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Common but often asymptomatic
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Screen with exercise testing according to ADA/ACSM recommendations.
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Use aspirin therapy in primary prevention for type 1 or type 2 patients with family history of coronary artery disease, cigarette smoking, HTN, obesity, micro- or macroalbuminuria, hyperlipidemia, or age >30 yrs or in secondary prevention for diabetics with macrovascular disease.
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Peripheral arterial disease
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Cerebrovascular disease
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Monitor/prevent microvascular complications:
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Retinopathy:
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Type 1 patients >10 yrs of age should have a comprehensive dilated eye exam within 3–5 yrs of diagnosis and then yearly thereafter.
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Type 2 patients should have a comprehensive dilated eye exam soon after diagnosis and then yearly thereafter.
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Avoid activities in patients with moderate nonproliferative retinopathy (power lifting, heavy Valsalva), severe nonproliferative retinopathy (boxing, heavy competitive sports), and proliferate retinopathy (weight lifting, jogging, high-impact aerobics, racquet sports).
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Nephropathy:
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Screen diabetic patients for microalbuminuria: type 1 at puberty, after 5 yrs' duration, and then yearly thereafter; type 2 at diagnosis and yearly thereafter.
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Screening can be done as either a 24-hr urine collection, timed urine collection, or spot urine collection in the morning.
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Treat nephropathy with BP control, good glycemic control, use of ACE inhibitors, and mild protein restriction.
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Neuropathy:
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Annual 10-g monofilament testing
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Routine foot care education
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P.121 -
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Treat special foot problems.
References
1. American Diabetes Association: Standards of Medical Care in Diabetes-2009. Diabetes Care. 2009;32(Suppl 1):S13–S61.
2. Sigal RJ, Kenny GP, Wasserman DH, et al. Physical Activity/Exercise and Type 2 Diabetes: A consensus statement of the American Diabetes Association. Diabetes Care. 2006;29:1433–1438.
Additional Reading
American College of Sports Medicine and American Diabetes Association. Joint position statement: diabetes mellitus and exercise. Med Sci Sports Exerc. 1997;29:i–vi.
American Diabetes Association. Diabetes mellitus and exercise. Diabetes Care. 2000;23 (Suppl 1):S50–S54.
Sigal RJ, Kenny GP, Boule N, et al. Effects of aerobic training, resistance training, or both on glycemic control in type 2 diabetes; a randomized trial. Ann Int Med. 2007;147:357–369.
Codes
ICD9
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250.00 Diabetes mellitus without mention of complication, type II or unspecified type, not stated as uncontrolled
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250.01 Diabetes mellitus without mention of complication, type I (juvenile type), not stated as uncontrolled
Clinical Pearls
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Some diabetic athletes in good metabolic control can carbohydrate-load without ill effects.
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The ideal time to exercise is early morning or when in basal state (>3 hr since last meal).
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Physiologic factors that predispose to hypoglycemia include reduced fitness level, longer exercise time, greater exercise intensity, higher insulin dosage, insulin injection into or over exercising muscle, and massage or heat application to area of insulin injection.
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For exercise, avoid short- and intermediate-acting insulin owing to variability of absorption from day to day in the same person. Rapid-acting insulin is decreased by 25–75%; long-acting basal insulin is reduced in athletes with type 1 diabetes by as much as 50% with long periods of exercise (cycling, triathlons, tournament play). Further insulin adjustments are tailored to the individual athlete's response and are based on glucose patterns with exercise.
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As type 2 patients begin training, improve physical fitness, reduce body fat, and improve insulin resistance, the dosage of medications may be decreased.
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Anaerobic exercise may cause hyperglycemia secondary to catecholamine release. Type 1 patients who are insulinopenic may become hyperglycemic with exercise.
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The best way to determine metabolic needs is through careful testing during training to determine the individual's metabolic response to exercise.
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Insulin and insulin secretagogues (sulfonylureas and meglitinides) can cause hypoglycemia.
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Regulate an insulin pump during exercise by decreasing basal infusion rate by 50% and for 1–2 hr afterward; reduce subsequent meal-time bolus by 30–50%.
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The most common error among diabetic athletes is not measuring glucose before, during, and after exercise.