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Diabetes Update Pennsylvania Association of Developmental Disabilities Nurses
Gutman Diabetes Institute Einstein Medical Center, Philadelphia Patricia C. Adams, RN, CDE Abilify (aripiprazole) Clozaril (clozapine) Geodon (ziprasidone) Risperdal and Risperdal Consta (risperidone) Seroquel (quetiapine) Symbyax (Zyprexa [olanzapine] and Prozac [fluoxetine] combination) Zyprexa and Zyprexa Zydis (olanzapine) The Gutman Diabetes Institute
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Objectives Distinguish the different types of diabetes
Discuss appropriate administration of insulin Discuss prevention and treatment of hypoglycemia Review of ADA recommendations for anti- psychotic drugs and obesity Mean age of RN 46 UKPDS released 1998 Type 2 DCCT released 1993 type 1 DPP 2002 Gutman Diabetes Institute
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Diabetes Update Diabetes - Epidemic Proportions Glucose Toxicity
25.8 million Americans (8.3% of population) 18.8 million have been diagnosed 7.0 million are unaware they have the disease Lipid Toxicity 3/8/2011 1 in 4 hospitalized patients has diabetes and 1/3 only learn of their disease during hospitalization. Hyperglycemia is an independent predictor of infection in patients undergoing heart surgery. Almost 1/3 cardiac surgery patients have diabetes. DM major cause of heart disease & stroke Leading cause of kidney failure, non traumatic lower limb amputations, & new cases of blindness among adults in the US. Need to identify elevated blood glucose in all hospitalized patients 174 billion: Total costs of diagnosed diabetes in the United States in 2007 $116 billion for direct medical costs $58 billion for indirect costs (disability, work loss, premature mortality) After adjusting for population age and sex differences, average medical expenditures among people with diagnosed diabetes were 2.3 times higher than what expenditures would be in the absence of diabetes. The American Diabetes Association has created a Diabetes Cost Calculator that takes the national cost of diabetes data and provides estimates at the state and congressional district level. Factoring in the additional costs of undiagnosed diabetes, prediabetes, and gestational diabetes brings the total cost of diabetes in the United States in 2007 to $218 billion. $18 billion for people with undiagnosed diabetes $25 billion for American adults with prediabetes $623 million for gestational diabetes Gutman Diabetes Institute
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Diabetes Areas Requiring Control Glycemic Control
A1C < 7% (ADA Standards) < 6.5% (AACE Standards) Blood Pressure Control Goal is 130/80 ACE vs ARB; Diuretics Lipid Management Statins Blood pressure goal is 130/80. Strong linear relationship between blood pressure and mortality. The lower the pressure, the longer you live. May take several drugs to achieve goal blood pressure. All diabetes and hypertension patients should be treated with an ACE inhibitor or ARB. Add a thiazide if blood pressure control not achieved. Gutman Diabetes Institute
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Cardiovascular Risk Lipids Total Cholesterol < 200
HDL > 45 (Men) > 55 (Women) LDL < 100; <70 (Hx of cardiac disease) Triglycerides (Tg) < 150 Aspirin (81 – 325) mg daily >21 yrs) Now the thinking is that an HDL>60 is preferred. Gutman Diabetes Institute
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Recommendations: Dyslipidemia/Lipid Management
Treatment recommendations and goals Statin therapy should be added to lifestyle therapy, regardless of baseline lipid levels, for diabetic patients: with overt CVD (A) / LDL < 70 without CVD who are >40 years of age and have one or more other CVD risk factors (A) / LDL < 100 This set of seven slides summarize recommendations for screening, treatment, and goals for dyslipidemia/lipid management in patients with diabetes Slide 3 of 7 – Treatment Recommendations and Goals (Slide 2 of 6) Statin therapy should be added to lifestyle therapy, regardless of baseline lipid levels, for diabetic patients With overt CVD (A) Without CVD who are over the age of 40 years and have one or more other CVD risk factors (A) Discuss the impact of dm on density of cholesterol ADA. VI. Prevention, Management of Complications. Diabetes Care 2011;34(suppl 1):S29. Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S29.
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Diabetes Update Type 1 Type 2 Gestational Approximately 5%
7 – 14% of all pregnancies 5 – 10% have type 2 following delivery 20 – 50% chance of developing diabetes in the next 5 – 10 years Gutman Diabetes Institute
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What is a normal blood glucose level?
Diabetes > 126 mg/dl < 126 mg/dl > 100 mg/dl < 100 mg/dl Pre-Diabetes Normal 70 mg/dl A1C > 6.5% FPG> 126 mg/dl OGTT > 200 mg/dl (75g glucose load) RPG > 200 mg/dl with symptoms of hyperglycemia Ask participants, “What is a ‘normal’ blood glucose level?” Acceptable levels of glycemic control have progressively declined with improved understanding of the mechanism of diabetes complications. Currently, the “normal” range of blood glucose is 70 to 99 mg/dl. Patients with fasting blood glucose values 100 to 125 mg/dl are classified with impaired fasting glucose (IFG) or pre-diabetes. Fasting blood glucose values consistently above 126 mg/dl are associated with increased rates of diabetes complication and constitute the basis for clinical diagnosis. Diabetes Care 2005;28:S4-S36 Diabetes Care 2005;28:S37-S42 Criteria for the diagnosis of diabetes A1C 6.5%. The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay.* OR FPG 126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h.* 2-h plasma glucose 200 mg/dl (11.1 mmol/l) during an OGTT. The test should be performed as described by the World Health Organization, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.* In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose 200 mg/dl (11.1 mmol/l). *In the absence of unequivocal hyperglycemia, criteria 1–3 should be confirmed by repeat testing. Position Statement care.diabetesjournals. Diabetes Care, Clinical Practice Recommendations, 2011
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*At-risk BMI may be lower in some ethnic groups.
Criteria for Testing for Diabetes in Asymptomatic Adult Individuals Testing should be considered in all adults who are overweight (BMI ≥25 kg/m2*) and have additional risk factors: Physical inactivity First-degree relative with diabetes High-risk race/ethnicity (e.g., African American, Latino, Native American, Asian American, Pacific Islander) Women who delivered a baby weighing >9 lb or were diagnosed with GDM Hypertension (≥140/90 mmHg or on therapy for hypertension) HDL cholesterol level <35 mg/dl (0.90 mmol/l) and/or a triglyceride level >250 mg/dl (2.82 mmol/l) Women with polycystic ovarian syndrome (PCOS) A1C ≥5.7%, IGT, or IFG on previous testing Other clinical conditions associated with insulin resistance (e.g., severe obesity, acanthosis nigricans) History of CVD The three primary criteria for testing for diabetes in asymptomatic adult individuals (Table 4) are summarized on two slides; this slide (Slide 1 of 2) includes: Testing should be considered in all adults who are overweight (BMI ≥25 kg/m2) and have additional risk factors Testing should be considered in adults of any age with BMI ≥25 kg/m2 and one or more of the known risk factors listed on this slide It is important to know that the at-risk BMI may be lower in some ethnic groups, such as Asians *At-risk BMI may be lower in some ethnic groups. ADA. Testing in Asymptomatic Patients. Diabetes Care 2011;34(suppl 1):S14. Table 4. Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S14. Table 4.
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Diabetes in Severe Mental Illness
2 – 3 fold increased mortality rate associated with physical illness Most common cause of death – CVD More likely to be overweight, smoke, inactive More likely to have family hx diabetes, Limited access to primary care, cardiovascular risk screening European article also found Lack of disease ownership by psychiatrist vs primary care. Diabetes is already leading cause of CVD and independent risk factor Adults tx with SGA, 2 times greater risk for diabetes, dislipidemia, htn, cvd Gutman Diabetes Institute
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ADA Consensus Baseline monitoring at initiation of antipsychotic medications Personal/family hx diabetes, obesity, dislipidemia, hypertension, CVD Calculate BMI Waist circumference BP, Fasting blood glucose, Fasting Lipid profile Interval monitoring 4, 8, & 12 weeks after initiation of therapy Weight gain > 5% consider change in therapy Gutman Diabetes Institute
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ADA Consensus Consideration of metabolic risks when starting SGAs
Patient, family, and care giver education Baseline screening Regular monitoring Refer to specialized services, when needed Morrato, Newcomer, et looked into rate of testing after release of ADA consensus statement. Of interest is the following points Metabolic testing remained suboptimal for SGA users. Retrospective look at insurance claims Study 2001 – 2006, by end of % of SGA useres received no baseline glucose monitoring; 90% received no lipid assessment Causes of low adherence to evidence based treatment recommendations “Low awareness, lack of medical consensus, low self efficacy to enact change and failure to overcome the inertial of previous practice. Another explanation offered is that physicians treat guidelines more as options as opposed to true standards and professional organizations such as the ADA, APA cannot enforce adherence” Gutman Diabetes Institute
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Blood Glucose Regulation
Pancreas Muscle Insulin Secretion Release of GIP & GLP - 1 + + Intestine: Glucose Absorption BLOOD GLUCOSE Peripheral Glucose Uptake Incretins are intestinal hormones that are released in response to ingestion of food. They stimulate (text uses amplify) an insulin response in a glucose dependent state. Also, have role in satiety, gastric emptying. Inhibited by enzyme DDP-IV GIP Gastric inhibitory peptide GIP 1 Glucagon like peptide 1 Secretion liver - gluconeogenesis, peripheral glucose uptake muscle and fat Stimulated by glucose Amplified by GLP1, GIP Inhibited by glucose, Free Fatty Acids, Glucagon – increases hepatic gluconeogenesis Stimulated by glucose Inhibited by Somatostatin, insulin + Brain & Nervous System Fat Gutman Diabetes Institute
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Type 1 Diabetes Type 2 Diabetes Initially little insulin production
Evolves into no insulin production Exogenous insulin required daily Auto-immune response Genetic component 5 - 10% prevalence Slow, Insidious 6.5 years to manifest as elevated FBG Elevated postprandial blood glucose levels Damage vessel endothelium Insulin Resistance Beta Cell Deterioration Gutman Diabetes Institute
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Type 1 & 2 Comparison Type 1 Type 2 Age of Onset Usually <30
Rapid Slowly - years Insulin Availability Little to None Some Progressive Insulin Resistance Develops w/Time Usually present Treatment Exogenous insulin always needed Daily injections MNT, Activity, Oral Agents, Insulin Complications Develop w/Time Present at Dx Gutman Diabetes Institute
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Type 2 Diabetes: A Dual-Defect Disease
Genes Genes Impaired insulin secretion Insulin resistance ± Environment IGT IGT Type 2 diabetes Gutman Diabetes Institute
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Genes Vs. Jeans Dr. James Gavin! Gutman Diabetes Institute
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The Progressive Nature of Type 2 Diabetes
Normal Impaired glucose tolerance Type 2 diabetes Late type 2 diabetes complications Insulin sensitive Hyperglycaemia Normal insulin secretion Insulin resistance Normoglycaemia β-cell exhaustion Insulin resistance Fasting plasma glucose Insulin sensitivity Insulin secretion Adapted from Bailey CJ et al. Int J Clin Pract 2004;58:867–876. Groop LC. Diabetes Obes Metab 1999;1 (Suppl. 1):S1–S7.
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How Do Oral Diabetes Medicines Work?
Glucosidase Inhibitors TZD’S DPP IV Inhibitors Secretagogues Biguanides Increase insulin action Increase insulin secretion Decrease hepatic glucose Decrease breakdown of GLP-1- increase insulin secretion The classes of oral agents used for treating type 2 diabetes act on the major sites of defects associated with the disease. Their actions range from increasing insulin secretion (by the secretagogues) to suppressing hepatic glucose output (the biguanides) to delaying gastrointestinal glucose absorption (the -glucosidase inhibitors) to increasing insulin sensitivity (the thiazolidinediones). 5 new drug classes either under development or recently approved by FDA for diabetes management – long-acting GLP-1 analogues, (Byedtta) dipeptidyl peptidase (DPP) IV inhibitors (Januvia, Onglyza), islet hormone therapy (Symlin), and endocannabinoid receptor antagonists (rimonabant-Acomplia). In the pipeline – Pill allow urine loss in urine Trade Generic Diabeta Glyburide Micronase Glucatrol glipizide Amaryl Glimepiride Prandin Repaglinide Starlix Nateglinide Precose Acarbose Miglitol Glyset Pio Actos Sitagliptin Januvia Saxagliptin Onglyza Slow glucose absorption Glyburide Glipizide Glimepiride Repaglinide Nateglinide Pioglitazone Rosiglitazone Metformin Metformin XR Metformin/Glyburide Acarbose Miglitol Sitaglipton Saxaglipton Gutman Diabetes Institute
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Terminology: Physiologic Insulin Use AKA “Think like a Pancreas”
Basal Amount needed to prevent excess gluconeogenesis and ketogenesis Prandial Amount needed to cover discrete meals and/or nutritional supplements Tube Feedings, IV dextrose, TPN Gutman Diabetes Institute
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Human Insulins Regular NPH 70/30 Gutman Diabetes Institute
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Insulin Analogs Humalog (Lispro) Humalog Mix 75/25 NovoLog (Aspart)
NovoLog Mix 70/30 Apidra (Glulisine) Lantus (Glargine) Levemir (Detemir) *** review question. Know the different brands! Gutman Diabetes Institute
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Administer insulin as one would physiologically secrete insulin (Mimick the pancreas’ function)
Gutman Diabetes Institute
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Basal / Bolus Insulin Therapy
Novolog u100: _____ units with 1st ______units with 2nd ______units with 3rd meal @_____ Lantus u100 : _____ units in the morning @_____ Call your physician or diabetes educator: Blood glucose test times: 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 __________________________________________________________________________________________________________________________________________________________________________________________________________________________________________ Before breakfast 1 hour after breakfast 2 hours after breakfast Before lunch 1 hour after lunch 2 hours after lunch Before dinner (supper) 1 hour after dinner (supper) 2 hours after dinner (supper) Bedtime Early Sleeping Meal times: Hours of sleep: _____ _____ _____ ______________ Supplemental insulin: _____________________ BG test outcomes No. of Units Time Insulin sensitivity factor:______ Insulin to carb ratio:__________ Urine ketone tests:____________ ____________________________
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Premix (cloudy) Short acting insulin Intermediate acting insulin
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 Insulin type: Human u100 Premix R & NPH Onset (Begins to work) ½ - 1 hour following injection Peak action (Works the strongest) Dual following injection Effective duration following injection Actual maximum duration hrs Meal and Snack times AM / PM Onset Peak Duration 1st meal______ AM/PM _____ ____to____ 1st snack______ 2nd meal______ 2nd snack_____ 3rd meal______ 3rd snack _____ Bedtime______
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Insulin Action Times Type Starts Peaks Ends Lispro (Humalog) 5 min.
3 – 4 hr. Aspart (Novolog) 3 – 5 hr. Glulisine (Apidra) Regular 30 – 60 min. 2 – 4 hr. 6 – 8 hr. NPH 1.5 hours 4 – 12 hr. 10 – 16 hr. Gutman Diabetes Institute
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Dual (Lispro/Lispro Protamine) Dual (Aspart/Aspart Protamine)
Insulin Action Times Type Starts Peaks Ends Glargine (Lantus) 4 – 6 hr. None 24 hr. Levemir (Detemir) < 2 hr. 3 – 14 hr 16 – 24 hr. 70/30 0.5 – 1.0 hr. Dual (NPH/R) 12 – 20 hr. Mix 75/25 10 min. Dual (Lispro/Lispro Protamine) Mix 70/30 Dual (Aspart/Aspart Protamine) 75/25 peaks ½ - 4 hr. Mix 70/30 peaks 1-3/4 – 2-1/4 hr. Must administer aspart and lispro immediately if mixed with NPH. Can’t mix Glargine with any other insulin Gutman Diabetes Institute
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Insulin and Timing of Meals
70/30 – 30 minutes prior to meal Regular – 20 to 30 minutes prior to meal NPH – 20 to 30 minutes prior to meal Aspart- 5 – 10 minutes prior to meal Lispro- 5 – 10 minutes prior to meal Apidra - 5 – 10 minutes prior to meal Gutman Diabetes Institute
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Proper Matching Glucose Level 1 2 3 4 Time in Hours
Insulin Peak action For patients taking rapid-acting insulin (such as lispro or aspart), an effect is seen in blood glucose levels within about 15 minutes. The peak occurs in 30 to 90 minutes, depending on the patient, and the insulin should be out of the patient’s system in about 2 to 4 hours. 1 2 3 4 Time in Hours Gutman Diabetes Institute
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Improper Matching Hypoglycemia Hyperglycemia Glucose Level 1 2 3 4
Insulin Peak Action For patients taking rapid-acting insulin (such as lispro or aspart), an effect is seen in blood glucose levels within about 15 minutes. The peak occurs in 30 to 90 minutes, depending on the patient, and the insulin should be out of the patient’s system in about 2 to 4 hours. 1 2 3 4 Time in Hours Gutman Diabetes Institute
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You wouldn’t hold the pancreas, so don’t hold the lantus
Clinical Pearl Basal insulin You wouldn’t hold the pancreas, so don’t hold the lantus Gutman Diabetes Institute
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Clinical Pearl Without insulin, in an insulin deficient individual, blood glucose will increase passively by as much as 45 mg/dl per hour even in the absence of food. Gutman Diabetes Institute
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Location, Location, Location
Lipohypertrophy can occur from repeated injections in one site. Gutman Diabetes Institute
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Glycemic Recommendations for Non-Pregnant Adults with Diabetes (1)
A1C <7.0%* Preprandial capillary plasma glucose 70–130 mg/dl* (3.9–7.2 mol/l) Peak postprandial capillary plasma glucose† <180 mg/dl* (<10.0 mmol/l) Recommended glycemic goals for nonpregnant adults (Table 10) are shown on three slides Slide 1 of 3 These recommendations are based on those for A1C values, with listed blood glucose levels that appear to correlate with achievement of an A1C of <7% The issue of preprandial versus postprandial self-monitoring of blood glucose (SMBG) is complex; in some epidemiological studies, elevated postchallenge two-hour oral glucose tolerance test (2-h OGTT) glucose values have been associated with increased cardiovascular risk independent of fasting plasma glucose (FPG) In diabetic subjects, some surrogate measures of vascular pathology, such as endothelial dysfunction, are negatively affected by postprandial hyperglycemia Postprandial hyperglycemia, like preprandial hyperglycemia, contributes to elevated A1C levels, with its relative contribution being higher at A1C levels that are closer to 7% However, outcome studies have clearly shown A1C to be the primary predictor of complications, and landmark trials such as the Diabetes Control and Complications Trial (DCCT) and the UK Prospective Diabetes Study (UKPDS) relied overwhelmingly on preprandial SMBG For individuals who have premeal glucose values within target but A1C values above target, a reasonable recommendation for postprandial testing and targets is monitoring postprandial plasma glucose 1-2 hours after the start of the meal and treatment aimed at reducing PPG values to <180 mg/dl to help lower A1C *Postprandial glucose measurements should be made 1–2 h after the beginning of the meal, generally peak levels in patients with diabetes. ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S21. Table 10. Reference American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care 2011;34(suppl 1):S Table 10.
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Control Hyperglycemia
Hyperglycemia needs to be controlled. Any glucose excursion causes endothelial damage Don’t relax with one good glucose reading Need to look at trends over 24 – 48 hours Need basal and prandial insulin coverage Rare to withhold basal insulin Insulin sliding scales do not work alone! Reactive vs proactive Variations in glucose have been shown to lead to oxidative stress, which may be the mechanism for most diabetes complications – Irl Hirsch. The variability is deleterious to the tubulointerstiitum than a constant high concentration of glucose. The best predictor of oxidative stress is overall glucose variability, not just postprandial hyperglycemia. Gutman Diabetes Institute
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Treating Hypoglycemia
DM medication given too early DM medication dosage too high Meals delayed or not eaten Give DM medication at right time Advocate for adjustment of medication Offer food when appropriate In some cases, hypoglycemia in the hospital is related to giving the patient his or her diabetes medications too early. Other times, the medication dosage may be too high for the amount of calories being consumed. Nurses should take care to ensure that these diabetes drugs are given at the most appropriate times. Glucose levels should be monitored, looking for trends, and adjustments should made when needed. Problems Nursing solutions Gutman Diabetes Institute
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Hypoglycemia Wait 15 minutes, - retest “Test don’t Guess”
Anything under 70 mg/dl is hypoglycemia Treat 16 grams of carbohydrate – “fast acting” Glucose gel – 15 grams Glucose Tabs –4 ½ cup juice or regular soda Wait 15 minutes, - retest Hypoglycemia is a BG less than 70 mg/dl and requires treatment to prevent further decreasing of blood glucose. Treatment is by protocol in hospitalized patients. Gutman Diabetes Institute
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Hypoglycemia This represents a patients BG pattern with over treatment of hypoglycemia. These wide variations in BG increase the risk for vascular and nerve complications. Excursions often considered higher risk of CVD. Gutman Diabetes Institute
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Medical Nutrition Therapy
No longer a diabetic diet (ADA) Currently Carb Controlled Requires Individualization Need for Consistent Carbohydrates Some sweets OK Meals – 4.5to 5 Hours Apart Divide Protein and Fats Gutman Diabetes Institute
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Medical Nutrition Therapy
Consume Fewer Animal Fats Emphasize Low Fat Dairy Products Emphasize Monounsaturated Fats Emphasis upon Fiber Decrease Use of Sweets Decrease Use of Alcohol Emphasize need for everyone to eat this way. Remind about the impact of isolating someone and the emotions associated with diabetes. Be careful of the “Food police” Gutman Diabetes Institute
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The Plate Method Fill a quarter of your plate with starch or bread
The Plate Method is an easy to remember technique for meal planning. This method recommends a healthy distribution of carbohydrates, a lower fat intake, and a greater amount of fruits and vegetables. It can be used to eat healthfully, lose weight, and/or manage your diabetes. Fill a quarter of your plate with starch or bread Fill half your plate up with non starchy vegetables Fill a quarter of your plate with protein (choose lean cuts) “Carb counting is a complicated process. Requires thorough knowledge of labels, measuring all food. Above system has been proven to be in the “Ball Park” Females gms CHO a meal Males 60 – 75 gms CHO a meals Source: National Diabetes Education Program To learn more about how meal planning can help prevent or manage your diabetes, contact the Gutman Diabetes Institute, or
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Juice is a Carbohydrate Too!
Even Light Juice Cocktail Contains ˜ 8 gm CHO No Sugar Free Juices
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Sorbitol, xylitol, mannitol
Sugar Free Foods Non-nutritive sweeteners are OK Sugar contains 4 kcal/gm Sugar alcohols contain 2-3 kcal/gm End in “ol” May contain more carbohydrate than regular item Need to read the label Can cause diarrhea Sorbitol, xylitol, mannitol
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Physical Activity Role of Physical Activity
150 mins / week; most days of the week Cells More Receptive to Insulin Decreases Insulin Resistance Lowers Blood Glucose Integral Part of Diabetes Management Gutman Diabetes Institute
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Diabetic Ketoacidosis
Precipitating Factors Infection Insulin Omission Inadequate Amount of Insulin Newly Diagnosed Diabetes Gutman Diabetes Institute
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Diabetic Ketoacidosis
3 Clinical Features Hyperglycemia - >250 mg/dL Ketonuria or ketonemia Acidosis pH <7.3 and/or serum bicarb <15 mEq/L Gutman Diabetes Institute
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Diabetic Ketoacidosis
Absence or reduced effect of insulin Excess of counter regulatory hormones Glucagon Cortisol Growth hormone Catecholemines Gutman Diabetes Institute
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Diabetic Ketoacidosis
Clinical Presentation Presence of Acidosis Abdominal Pain Nausea Vomiting Anorexia Treatment Emergency measures / hospitalization IV fluids Insulin!!! Replacement of electrolytes Gutman Diabetes Institute
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Diabetic Ketoacidosis
Clinical Presentation Hyperglycemia 3 – 4 Days Metabolic Alterations < 24 Hours Respiratory Symptoms Kussmaul Respirations Kussmaul breathing is respiratory compensation for a metabolic acidosis, most commonly occurring in people with diabetes, diabetic ketoacidosis. Blood gases on a patient with Kussmaul breathing will show a low partial pressure of CO2 in conjunction with low bicarbonate because of a forced increased respiration (blowing off the CO2). Gutman Diabetes Institute
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Hyperosmolar Hyperglycemic State
Lab Values Glucose > 600 mg/dl No Ketones or Only Small Amounts Plasma Osmolality > 320 mOsm/kg Treatment focus on fluids, Insulin still needed for hyperglycemia (glucose toxic) Correct electrolyte imbalance ID / Tx underlying comorbidities Gutman Diabetes Institute
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Diagnostic Criteria; DKA vs HHS
Mild Moderate Severe Glucose 250 >250 .250 >600 pH <7.00 >7.30 BiCarb 15-18 10-15 <10 >15 Urine Ketones + small Serum Ketones Anion Gap >10 >12 <12 Mentation Alert Alert/Drowsy Stupor/Coma Gutman Diabetes Institute
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