Diabetes Management and Treatment Recommendation in Primary Care. Disclosure

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1 Diabetes Management and Treatment Recommendation in Primary Care Sally K. Miller, PhD, AGACNP, AGPCNP, FNP-BC, FAANP Senior Associate Lecturer Fitzgerald Health Education Associates, LLC North Andover, MA Nurse Practitioner, Nevada Health Centers, Clinical Professor Drexel University College of Nursing and Health Professions Developed by: Margaret A. Fitzgerald, DNP, FNP-BC, NP-C, FAANP, CSP, FAAN, DCC, FNAP President, Fitzgerald Health Education Associates, LLC, North Andover, MA Disclosure No real or potential conflict of interest to disclose. No off-label, experimental or investigational use of drugs or devices will be presented. Fitzgerald Health Education Associates, LLC 2 Objectives Having completed the learning activities, the participant will be able to: Identify the mechanism of action of biguanides, glitazones, sulfonylureas, other insulin secretagogues, insulin, SGLT2, and other agents in the care of the person with type 2 DM. Fitzgerald Health Education Associates, LLC 3

2 Objectives (continued) Having completed the learning activities, the participant will be able to: (cont.) Describe the appropriate clinical scenario for the use of each of the above-mentioned products. Recognize precautions and contraindications in the use of these medications. Fitzgerald Health Education Associates, LLC 4 The Diabetes Epidemic: Global Projections, IDF. Diabetes Atlas 5 th Ed Fitzgerald Health Education Associates, LLC 5 Should we continue to think of type 2 diabetes as just too little insulin or insulin that is not used well? A disease where beta cell failure is inevitable? Or should we start thinking of this as a complex disease with profound multisystem ill effects? Fitzgerald Health Education Associates, LLC 6

3 Relative Function (%) Glucose (mg/dl) Glucose (mg/dl) Insulin (µu/ml) Physiologic Insulin Secretion: Healthy Pancreas hr profile Basal insulin B L D Basal glucose AM PM Time of Day 9 Role of physiologic basal insulin To suppress glucose production between meals and overnight Nearly constant levels 50 60% of daily insulin needs Role of physiologic bolus insulin To cover rise in glucose post nutrient ingestion Rises and falls 40 50% of daily insulin needs Adapted with permission from Bergenstal RM et al. In: DeGroot LJ, Jameson JL, eds. Endocrinology. 4th ed. Philadelphia, Pa: WB Saunders Co.:821 Fitzgerald Health Education Associates, LLC 7 T2DM:Insulin Resistance Effects with Resulting Insulinopenia Obesity IFG* Diabetes Post meal Glucose Uncontrolled Hyperglycemia Fasting Glucose Insulin Resistance Cell Failure *IFG=Impaired fasting glucose. Years of Diabetes International Diabetes Center, Minneapolis, MN, USA. Fitzgerald Health Education Associates, LLC 8 Decreased beta cell = Insulinopenia With Insulin Resistance To maintain NL glucose Patient can produce 5 8 as much insulin per day when compared to non IR person Estimated endogenous dose as high as 500 units/d Source: AACE Diabetes Guidelines, Endocr Pract, 2002;8 (Supp 1) Fitzgerald Health Education Associates, LLC 9

4 Pathophysiology of T2DM per ADA Abnormal islet cell function is a key and requisite feature of type 2 diabetes. In early disease stages, insulin production is normal or increased in absolute terms, but disproportionately low for the degree of insulin sensitivity, which is typically reduced. Fitzgerald Health Education Associates, LLC 10 Pathophysiology of T2DM per ADA (continued) However, insulin kinetics, such as the ability of the pancreatic b-cell to release adequate hormone in phase with rising glycemia, are profoundly compromised. Source: dc /-/dc1 Fitzgerald Health Education Associates, LLC 11 -Cell Function (%) * -Cell Function Decline Over Time l -12 IGT l -10 Postprandial Hyperglycemia l -6 l -2 Type 2 Diabetes Patients Treated with Metformin and/or Sulfonylureas Years from Diagnosis *Dashed line shows extrapolation backward from year 0 and forward from year 6 from diagnosis based on Homeostasis Model Assessment (HOMA) data from UKPDS. IGT =Impaired glucose tolerance. The data points for the time of diagnosis (0) and the subsequent 6 years are taken from the obese subset of the UKPDS population and were determined by the HOMA model. Adapted with permission from Lebovitz HE. Diabetes Rev. 1999;7: American Diabetes Association. l 0 Approximately 50% of β-cell Function Lost l 2 l 6 Approximately 75% of β-cell Function Lost l 10 l 14

5 Old vs. Newer Models of T2DM Therapy Old model Pancreatic beta cells burn out over time Inevitable outcome of insulin resistance and beta cell exhaustion Newer model Certain therapies help preserve beta cell function Lifestyle and medications implicated Fitzgerald Health Education Associates, LLC 13 Should we focus on fasting glucose? Postprandial glucose? Early and intensive glycemic control, using regimens which re-create a physiological insulin profile, controlling postprandial as well as fasting glucose levels, offers the most promise for preserving beta-cell function, decreasing disease progression, and reducing the chronic complications of diabetes. Source: Fitzgerald Health Education Associates, LLC 14 Targets for Glycemic Control (Criteria for DM dx Assumed)

6 Targets for Glycemic Control ADA Biochemical index NL Goal Hemoglobin A1C (proportion of hemoglobin) Fasting (preprandial) plasma glucose Peak postprandial (1 2 h post meal) plasma glucose Bedtime <6% (0.06) <7%* (0.07) <100 mg/dl (5.6 mmol/l) <140 mg/dl (7.8 mmol/l) <120 mg/dl (6.7 mmol/l) mg/dl ( mmol/l) <180 mg/dl (10 mmol/l) mg/dl (5 8.3 mmol/l) Fitzgerald Health Education Associates, LLC 16 Goal A1C in Special Circumstances <6% (0.06 for certain individuals, particularly with low hypoglycemia risk, anticipated long life expectancy and no CVD For older adults who are frail or have anticipated life expectancy of 5 years, A1C goal should be 8% (0.08, as the risks of hypoglycemia outweigh the benefits of stringent glycemic control. Source: %20Sean/Documents/January%20Supplement%20Combined_Final.pdf AACE Medical Guidelines for Clinical Practice for Developing a Diabetes Mellitus Comprehensive Care Plan, available at Fitzgerald Health Education Associates, LLC 17 Online Calculator of Estimated Average Glucose (eag) Available at Calculator.aspx

7 Relative Function (%) Glucose (mg/dl) PPG vs. FBG A1C<7.3% (0.073 PPG 70% contributor % ( Roughly 50:50 contributors PPG and FBG A1C>10.3% (0.103 FBG 70% contributor Source: Fitzgerald Health Education Associates, LLC 19 T2DM: Insulin Resistance Effects with Resulting Insulinopenia Obesity IFG* Diabetes Post meal Glucose Uncontrolled Hyperglycemia Fasting Glucose Insulin Resistance Cell Failure Decreased beta cell = Insulinopenia *IFG=Impaired fasting glucose. Years of Diabetes International Diabetes Center, Minneapolis, MN, USA. Fitzgerald Health Education Associates, LLC 20 Lifestyle Modification and Beta Cell Function Associated with beta cell loss Physical inactivity Obesity Visceral fat Associated with beta cell preservation Physical activity Weight loss, especially reduction in visceral fat Fitzgerald Health Education Associates, LLC 21

8 Visceral vs. Subcutaneous Fat Fitzgerald Health Education Associates, LLC 22 American Diabetes Association Standards of Medical Care Available at /UserFiles/0%20- %20Sean/Documents/January%20Su pplement%20combined_final.pdf

9 When choosing medications for the treatment of T2DM, consider: Where is the major problem with glucose control? Postprandial? Fasting? Both? Which work against insulin resistance? Which work to increase insulin availability? Which work to off-load glucose? Fitzgerald Health Education Associates, LLC 26 Intervention in T2DM: Oral and Injectable s References %20Sean/Documents/January%20Supplement%20C ombined_final.pdf Prescribing Information for Each Product

10 Should we start or end with insulin therapy? Or perhaps both? Should we start with insulin? a 2- to 3-week course of intensive insulin therapy can successfully lay a foundation for prolonged good glycemic control. The ease with which normoglycemia is achieved on insulin may predict those patients who can later succeed in controlling glucose levels with attention to diet alone. Source: Fitzgerald Health Education Associates, LLC 29 Why start with insulin? Is the done deal for long-term insulin therapy? Consequences of hyperglycemia Induces insulin resistance Impairs β-cell function Correction of the hyperglycemia improves insulin sensitivity and insulin secretion Intensive insulin therapy most effective with presenting glucose 250 mg/dl (13.9 mmol/l). Fitzgerald Health Education Associates, LLC 30

11 Intensive Insulin Therapy at Time of T2DM Dx A two- to three-week course of intensive insulin therapy in a newly diagnosed type 2 diabetic which reverses the effects of glucose toxicity Possibly more effective than either oral agents or non intensive insulin therapy in obtaining long-term glycemic control Source: Fitzgerald Health Education Associates, LLC 31 Example of Individualized Dose Intensive Insulin Therapy Units of insulin per day=fasting blood glucose in mmol/l Example=Fasting blood glucose= 240 mg/dl=14 mmol/l 14 units per day=recommended insulin dose 50 60% basal, 40 50% bolus Glargine 8 units, 2 units aspart with each meal Source: Fitzgerald Health Education Associates, LLC 32 And what if the person will not check BG multiple times per day and/or inject multiple times per day? Consider single dose basal insulin Example Glargine Typically given at bedtime Evidence of less hypoglycemia if given in AM as a single dose See later in program for examples of doses Fitzgerald Health Education Associates, LLC 33

12 with intensified use=1 1.5% ( Sitagliptin (Januvia ), Saxagliptin (Onglyza ), Linagliptin Canagliflozin (Invokana ), dapagliflozin (Farxiga ), with intensified used=0.7-1% ( with intensified use=1 1.5% ( Sitagliptin (Januvia ), Saxagliptin (Onglyza ), Linagliptin Canagliflozin (Invokana ), dapagliflozin (Farxiga ), with intensified used=0.7-1% ( Increases synthesis and release of insulin b-cells and decreasing release of glucagon Delays intestinal carbohydrate by reducing postprandial digestion of starches and Increases synthesis and release of insulin b-cells and decreasing release of glucagon Delays intestinal carbohydrate by reducing postprandial digestion of starches and Metformin use increases risk of vitamin B12 deficiency due to B12 mal, risk appears dose- and length of use in excess of one year possibly associated with an increased risk of bladder cancer. Metformin use increases risk of vitamin B12 deficiency due to B12 mal, risk appears dose- and length of use in excess of one year possibly associated with an increased risk of bladder cancer. If starting insulin therapy, should you start other medication(s)? Example- Metformin (Glucophage ) with intensified use=1 2% ( Fitzgerald Health Education Associates, LLC 35 Insulin sensitizer, action of reducing hepatic glucose production and intestinal glucose Action on fasting and postprandial glucose, minimal to no inherent hypoglycemic risk Fitzgerald Health Education Associates, LLC 36

13 with intensified use=1 1.5% ( Sitagliptin (Januvia ), Saxagliptin (Onglyza ), Linagliptin Canagliflozin (Invokana ), dapagliflozin (Farxiga ), with intensified used=0.7-1% ( with intensified use=1 1.5% ( Sitagliptin (Januvia ), Saxagliptin (Onglyza ), Linagliptin Canagliflozin (Invokana ), dapagliflozin (Farxiga ), with intensified used=0.7-1% ( Increases synthesis and release of insulin b-cells and decreasing release of glucagon Delays intestinal carbohydrate by reducing postprandial digestion of starches and Increases synthesis and release of insulin b-cells and decreasing release of glucagon Delays intestinal carbohydrate by reducing postprandial digestion of starches and Metformin use increases risk of vitamin B12 deficiency due to B12 mal, risk appears dose- and length of use in excess of one year possibly associated with an increased risk of bladder cancer. Metformin use increases risk of vitamin B12 deficiency due to B12 mal, risk appears dose- and length of use in excess of one year possibly associated with an increased risk of bladder cancer. Rare risk for lactic acidosis with metformin use, nearly always with associated with identified risk factors, most commonly including presence of impaired renal or hepatic function, hypovolemia, low perfusion state including heart failure, and/or advanced age (>80 years). Considering metformin discontinuation in impaired renal function: Rational for discontinuation is to decrease lactic acidosis risk (90% renally eliminated). National Institute for Health - egfr below 45 ml/min per 1.73 m 2, absolute metformin discontinuation at egfr<30 ml/min per 1.73 m 2. Fitzgerald Health Education Associates, LLC 37 Metformin for DM prevention: Metformin therapy for prevention of type 2 diabetes can be considered in those at highest risk for developing diabetes, such as those with multiple risk factors, especially if demonstrated progression of hyperglycemia (i.e. A1C 6% {0.06 proportion}) despite lifestyle interventions mg per day as typical dose. Fitzgerald Health Education Associates, LLC 38 True or false? Metformin use is potentially associated with the following changes in lipid profile: LDL, HDL, TG. Metformin use increases risk of vitamin B 12 deficiency due to B 12 mal, risk appears dose- and length of

14 with intensified use=1 1.5% ( Sitagliptin (Januvia ), Saxagliptin (Onglyza ), Linagliptin Canagliflozin (Invokana ), dapagliflozin (Farxiga ), with intensified used=0.7-1% ( with intensified use=1 1.5% ( Sitagliptin (Januvia ), Saxagliptin (Onglyza ), Linagliptin Canagliflozin (Invokana ), dapagliflozin (Farxiga ), with intensified used=0.7-1% ( with intensified use=1 1.5% ( Sitagliptin (Januvia ), Saxagliptin (Onglyza ), Linagliptin Canagliflozin (Invokana ), dapagliflozin (Farxiga ), with intensified used=0.7-1% ( Increases synthesis and release of insulin b-cells and decreasing release of glucagon Delays intestinal carbohydrate by reducing postprandial digestion of starches and Increases synthesis and release of insulin b-cells and decreasing release of glucagon Delays intestinal carbohydrate by reducing postprandial digestion of starches and Increases synthesis and release of insulin b-cells and decreasing release of glucagon Delays intestinal carbohydrate by reducing postprandial digestion of starches and Metformin use increases risk of vitamin B12 deficiency due to B12 mal, risk appears dose- and length of use in excess of one year possibly associated with an increased risk of bladder cancer. Metformin use increases risk of vitamin B12 deficiency due to B12 mal, risk appears dose- and length of use in excess of one year possibly associated with an increased risk of bladder cancer. Metformin use increases risk of vitamin B12 deficiency due to B12 mal, risk appears dose- and length of use in excess of one year possibly associated with an increased risk of bladder cancer. with intensified use=1 2% ( Fitzgerald Health Education Associates, LLC 40 Increases insulin release beta cells Action on fasting and postprandial glucose, hypoglycemia risk, especially in elders, presence of impaired renal function, nocturnal, fasting, and 4 6 h after meals. Fitzgerald Health Education Associates, LLC 41 Due to failing beta cell function, typically less effective in older adults and/or after many years with T2DM, in the presence of Fitzgerald Health Education Associates, LLC 42

15 Incretin-based Therapies What is incretin? Group of GI hormones that influences blood glucose by causing increasing amount of insulin released from pancreatic beta cells post ingestion of carb-containing food or beverage This helps regulate blood glucose by largely preventing postprandial glucose elevation. Fitzgerald Health Education Associates, LLC 43 Incretin-based Therapies: Mechanism of Action GLP-1 agonists mimic incretin, activate GLP-1 receptor. Stimulates insulin release DPP-4 enzyme inactivation allows higher incretin levels. Incretin, GLP-1 receptor activation Inhibits glucagon release Lowering of blood glucose Fitzgerald Health Education Associates, LLC 44 Early vs. Later Use of Incretin-based Therapies Importantly, short-term studies have shown that incretins/incretin-based therapies protect β-cells (by enhancing cell proliferation and differentiation and inhibiting apoptosis) and stimulate their function (by recruiting β-cells to the secretory process and increasing insulin biosynthesis/ secretion). These therapies have the opportunity to interfere with the disease progression if used as an early intervention, when enough β-cell mass/function can still be preserved or restored. Source: Fitzgerald Health Education Associates, LLC 45

16 with intensified use=1 1.5% ( Sitagliptin (Januvia ), Saxagliptin (Onglyza ), Linagliptin Canagliflozin (Invokana ), dapagliflozin (Farxiga ), with intensified used=0.7-1% ( with intensified use=1 1.5% ( Sitagliptin (Januvia ), Saxagliptin (Onglyza ), Linagliptin Canagliflozin (Invokana ), dapagliflozin (Farxiga ), with intensified used=0.7-1% ( with intensified use=1 1.5% ( Sitagliptin (Januvia ), Saxagliptin (Onglyza ), Linagliptin Canagliflozin (Invokana ), dapagliflozin (Farxiga ), with intensified used=0.7-1% ( Increases synthesis and release of insulin b-cells and decreasing release of glucagon Delays intestinal carbohydrate by reducing postprandial digestion of starches and Increases synthesis and release of insulin b-cells and decreasing release of glucagon Delays intestinal carbohydrate by reducing postprandial digestion of starches and Increases synthesis and release of insulin b-cells and decreasing release of glucagon Delays intestinal carbohydrate by reducing postprandial digestion of starches and Metformin use increases risk of vitamin B12 deficiency due to B12 mal, risk appears dose- and length of use in excess of one year possibly associated with an increased risk of bladder cancer. Metformin use increases risk of vitamin B12 deficiency due to B12 mal, risk appears dose- and length of use in excess of one year possibly associated with an increased risk of bladder cancer. Metformin use increases risk of vitamin B12 deficiency due to B12 mal, risk appears dose- and length of use in excess of one year possibly associated with an increased risk of bladder cancer. Sitagliptin (Januvia ), Saxagliptin (Onglyza ), Linagliptin with intensified use= % ( Fitzgerald Health Education Associates, LLC 46 Increases insulin release, largely in response to increase blood glucose post meal. Action largely on postprandial blood glucose, minimal to no inherent hypoglycemia risk Fitzgerald Health Education Associates, LLC 47 Well tolerated, weight neutral. Indicated to improve glycemic control, in combination with insulin sensitizers or other Fitzgerald Health Education Associates, LLC 48

17 with intensified use=1 1.5% ( Sitagliptin (Januvia ), Saxagliptin (Onglyza ), Linagliptin Canagliflozin (Invokana ), dapagliflozin (Farxiga ), with intensified used=0.7-1% ( with intensified use=1 1.5% ( Sitagliptin (Januvia ), Saxagliptin (Onglyza ), Linagliptin Canagliflozin (Invokana ), dapagliflozin (Farxiga ), with intensified used=0.7-1% ( Increases synthesis and release of insulin b-cells and decreasing release of glucagon Delays intestinal carbohydrate by reducing postprandial digestion of starches and Increases synthesis and release of insulin b-cells and decreasing release of glucagon Delays intestinal carbohydrate by reducing postprandial digestion of starches and Metformin use increases risk of vitamin B12 deficiency due to B12 mal, risk appears dose- and length of use in excess of one year possibly associated with an increased risk of bladder cancer. Metformin use increases risk of vitamin B12 deficiency due to B12 mal, risk appears dose- and length of use in excess of one year possibly associated with an increased risk of bladder cancer. A1C, FPG, and 2-hour PPG Placebo-adjusted Results in a 24-week Study of Sitagliptin Phosphate A1C FPG 2-hr PPG n=229 n=234 n=201 (95% CI: 1.0, 0.6) (95% CI: 24, 10) (95% CI: 59, 34) A1C lowering appears to be related to degree of A1C baseline level. Source: Sitagliptin PI *Compared with placebo. Least squares means adjusted for prior antihyperglycemic therapy status and baseline value. Difference from placebo. Fitzgerald Health Education Associates, LLC 49 with intensified use=1 2% ( Fitzgerald Health Education Associates, LLC 50 Increases insulin release, largely in response to increase blood glucose post meal. Action largely on postprandial blood glucose, little inherent hypoglycemia risk Slows gastric emptying, often leading to appetite suppression and weight loss. Fitzgerald Health Education Associates, LLC 51

18 with intensified use=1 1.5% ( Sitagliptin (Januvia ), Saxagliptin (Onglyza ), Linagliptin Canagliflozin (Invokana ), dapagliflozin (Farxiga ), with intensified used=0.7-1% ( Increases synthesis and release of insulin b-cells and decreasing release of glucagon Delays intestinal carbohydrate by reducing postprandial digestion of starches and Metformin use increases risk of vitamin B12 deficiency due to B12 mal, risk appears dose- and length of use in excess of one year possibly associated with an increased risk of bladder cancer. Major adverse effect=n/v, usually better with dose adjustment, continued use, contraindicated in gastroparesis. Adjunct to improve glycemic control in T2DM when not adequately controlled with biguanide, sulfonylurea, others Exenatide is FDA approved as add-on therapy with insulin glargine, with or without metformin in T2DM with inadequate glycemic control on insulin glargine alone. Fitzgerald Health Education Associates, LLC 52 Incretin-based Therapies with Basal Insulin Basal insulin Primarily improves fasting plasma glucose (FPG) control Incretin-based therapies Glucose-dependent effect Largely benefit postprandial plasma glucose (PPG) control Requires functioning beta cells for clinical effect Source: b2e-b6f3-e885508feb4a Fitzgerald Health Education Associates, LLC 53 PK Implications with GLP-1 Agonists, Slower Gastric Emptying Pharmacokinetics (PK) Use does not affect of most medications Where peak concentrations necessary for clinical efficacy, medication should be taken at least 1 h prior to PKaltering medication injection Examples=Oral contraceptives, most antimicrobials Fitzgerald Health Education Associates, LLC 54

19 with intensified use=1 1.5% ( Sitagliptin (Januvia ), Saxagliptin (Onglyza ), Linagliptin Canagliflozin (Invokana ), dapagliflozin (Farxiga ), with intensified used=0.7-1% ( with intensified use=1 1.5% ( Sitagliptin (Januvia ), Saxagliptin (Onglyza ), Linagliptin Canagliflozin (Invokana ), dapagliflozin (Farxiga ), with intensified used=0.7-1% ( with intensified use=1 1.5% ( Sitagliptin (Januvia ), Saxagliptin (Onglyza ), Linagliptin Canagliflozin (Invokana ), dapagliflozin (Farxiga ), with intensified used=0.7-1% ( Increases synthesis and release of insulin b-cells and decreasing release of glucagon Delays intestinal carbohydrate by reducing postprandial digestion of starches and Increases synthesis and release of insulin b-cells and decreasing release of glucagon Delays intestinal carbohydrate by reducing postprandial digestion of starches and Increases synthesis and release of insulin b-cells and decreasing release of glucagon Delays intestinal carbohydrate by reducing postprandial digestion of starches and Metformin use increases risk of vitamin B12 deficiency due to B12 mal, risk appears dose- and length of use in excess of one year possibly associated with an increased risk of bladder cancer. Metformin use increases risk of vitamin B12 deficiency due to B12 mal, risk appears dose- and length of use in excess of one year possibly associated with an increased risk of bladder cancer. Metformin use increases risk of vitamin B12 deficiency due to B12 mal, risk appears dose- and length of use in excess of one year possibly associated with an increased risk of bladder cancer. Canagliflozin (Invokana ), dapagliflozin (Farxiga ), with intensified used=0.7 1% ( Fitzgerald Health Education Associates, LLC 55 Action largely by lowering plasma glucose levels by increasing the amount of glucose excreted in Primarily postprandial glucose effect. Hypoglycemic risk related to glucose offload, increased when used with insulin and insulin secretagogues. Fitzgerald Health Education Associates, LLC 56 Adverse effects=genital mycotic infection (~10% female, ~5% male), UTI, increased urination Modest weight loss (4 7 lbs { kg}), greater with higher dose Anticipate need for lower dose of insulin or insulin secretagogue to minimize hypoglycemia risk when use in Dose adjustment or medication discontinuation required in presence of renal impairment due to increased risk of adverse effects including electrolyte disturbances, less therapeutic effect. Can be used as add-on with metformin, sulfonylurea, others. FDA advisory about diabetic ketoacidosis and urosepsis risk with SGLT2 use. Fitzgerald Health Education Associates, LLC 57

20 American Diabetes Association Dia Care 2015;38:S41-S48 SU Insulin release TZD Insulin sensitizer DPP-4 inhibitor Insulin release post meal SGLT2 glucose excretion post meal GLP-1 RA Insulin release post meal 2015 by American Diabetes Association What about sliding scales? Per Standards of Medical Care in Diabetes One of the problems with slidingscale insulin regimens is that the sliding-scale regimen prescribed on admission is likely to be used throughout the hospital stay without modification, even when control remains poor. Fitzgerald Health Education Associates, LLC 60

21 Per Standards of Medical Care in Diabetes (continued) Additionally, sliding-scale insulin therapy treats hyperglycemia after it has already occurred, instead of preventing the occurrence of hyperglycemia. This reactive approach can lead to rapid changes in blood glucose levels, exacerbating both hyper- and hypoglycemia. Fitzgerald Health Education Associates, LLC 61 Resource of Insulin Sliding Scale Example InslnSldngScl.htm ~1 Unit Rapid-acting Insulin to Lower BS by 50 mg/dl (2.78 mmol/l): Low Dose If goal BS<150 mg/dl (8.3 mmol/l) BS= ( mmol/l): 1 unit BS= ( mmol/l): 2 units BS= ( mmol/l): 3 units BS= ( mmol/l): 4 units BS 350 (19.4 mmol/l): 5 units Less in renal impairment 50% renally excreted Fitzgerald Health Education Associates, LLC 63

22 Conclusion Where is the major problem with glucose control? Postprandial? Fasting? Both? What meds help where? Role of beta cell preservation? End of Presentation Thank you for your time and attention. Sally K. Miller, PhD, AGACNP, AGPCNP, FNP-BC, FAANP fhea.com Images/Illustrations: Unless otherwise noted, all images/illustrations are from open sources, such as the CDC or Wikipedia or property of FHEA or author. All websites listed active at the time of publication. Fitzgerald Health Education Associates, LLC 66

23 Copyright Notice Copyright by Fitzgerald Health Education Associates, LLC All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording or any information storage and retrieval system, without permission from Fitzgerald Health Education Associates, LLC Requests for permission to make copies of any part of the work should be mailed to: Fitzgerald Health Education Associates, LLC 85 Flagship Drive North Andover, MA Fitzgerald Health Education Associates, LLC 67 Statement of Liability The information in this program has been thoroughly researched and checked for accuracy. However, clinical practice and techniques are a dynamic process and new information becomes available daily. Prudent practice dictates that the clinician consult further sources prior to applying information obtained from this program, whether in printed, visual or verbal form. Fitzgerald Health Education Associates, LLC disclaims any liability, loss, injury or damage incurred as a consequence, directly or indirectly, of the use and application of any of the contents of this presentation. Fitzgerald Health Education Associates, LLC 68 Fitzgerald Health Education Associates, LLC 85 Flagship Drive North Andover, MA Fax Website: fhea.com Learning & Testing Center: fhea.com/npexpert Fitzgerald Health Education Associates, LLC 69