Diabetes Care: Part One


Published on

An intensive presentation regarding all related to pharmaceutical care in diabetes with real life case examples

Published in: Health & Medicine
No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Diabetes Care: Part One

  1. 1. Week Diabetes Mellitus 2 Part I Anas Bahnassi PhD CDM CDE
  2. 2. Lecture Outline Definition, Classification, and Epidemiology Carbohydrate Metabolism Type -1 Diabetes Type-2 Diabetes Gestational Diabetes Long-term complications type-2 Prevention of type-1 and type 2 diabetes Medical Nutrition Therapy Pharmacologic Therapy
  3. 3. Definition, Classification, and Epidemiology A relative or an absolute lack of insulin Clinical characteristics are symptomatic glucose intolerance resulting in hyperglycemia and alterations in lipid and protein metabolism. Over the long term, these metabolic abnormalities contribute to the development of complications such as retinopathy, nephropathy, and neuropathy. Most cases of diabetes mellitus can be assigned to type 1 or type 2 diabetes. Gestational diabetes describes glucose intolerance that has its onset during pregnancy. Subclinical glucose intolerance or “prediabetes” is identified as impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT).
  4. 4. Definition, Classification, and Epidemiology Type 1 and Type 2 Diabetes Type 1 Characteristics Other names Percentage of diabetic population Age at onset Pancreatic function Pathogenesis Previously, type I; insulin-dependent diabetes mellitus (IDDM); juvenile-onset diabetes mellitus 5–10% Usually <30 yr; peaks at 12–14 yr; rare before 6 mo; some adults develop type 1 during the fifth decade Usually none, although some residual Cpeptide can sometimes be detected at diagnosis, especially in adults Associated with certain HLA types; presence of islet cell antibodies suggests autoimmune process Type 2 Previously, type II; non–insulin-dependent diabetes mellitus (NIDDM); adult-onset diabetes mellitus 90% Usually >40 yr, but increasing prevalence among obese children Insulin present in low, “normal,” or high amounts Defect in insulin secretion; tissue resistance to insulin; ↑ hepatic glucose output
  5. 5. Definition, Classification, and Epidemiology Type 1 and Type 2 Diabetes Type 1 Characteristics Family history Obesity History of ketoacidosis Clinical presentation Treatment Type 2 Generally not strong Strong Uncommon unless “overinsulinized” with exogenous insulin Often present Common (60–90%) Moderate to severe symptoms that generally progress relatively rapidly (days to weeks): polyuria, polydipsia, fatigue, weight loss, ketoacidosis Insulin MNT Physical activity Amylin mimetic (pramlintide) Mild polyuria, fatigue; often diagnosed on routine physical or dental examination Rare, except in circumstances of unusual stress (e.g., infection) MNT, Physical activity Antidiabetic agents (biguanides, nonsulfonylurea insulin secretagogues, sulfonylureas, thiazolidinediones, α-glucosidase inhibitors, incretin mimetics/analogs, DPP-4 inhibitors) Insulin, Amylin mimetic (pramlintide)
  6. 6. Definition, Classification, and Epidemiology Type 1 Diabetes (a)5% to 10% of the diagnosed diabetic population has type 1 diabetes (b)It usually results from autoimmune destruction of the pancreatic β-cells. (c)Little or no pancreatic reserve, tendency to develop ketoacidosis, and require exogenous insulin to sustain life. (d)The incidence of autoimmune-mediated type 1 diabetes peaks during childhood and adolescence, but can occur at any age. Type 2 Diabetes (a) Type 2 diabetes is the most prevalent (b) Heterogeneous disorder that is characterized by (a) Obesity, (b) β-cell dysfunction, (c) Resistance to insulin action, (d) increased hepatic glucose production. (c) Incidence and prevalence of diabetes increase dramatically with age.
  7. 7. Carbohydrate Metabolism (post-prandial) Food Digested Inhibits hepatic glucose production by suppressing glucagon and its effects.  Glucose Conc. Insulin Released Glucose is converted to free fatty acids and stored as triglycerides. Stimulates the uptake of amino acids and their conversion to protein The liver does not require insulin for glucose transport, but insulin facilitates the conversion of glucose to glycogen and free fatty acids. The latter are esterified to triglycerides, which are transported by very-lowdensity lipoproteins (VLDLs) to adipose and muscle tissue.
  8. 8. Carbohydrate Metabolism (fasting) Fasting  Glucose Conc. Min. Glucose for CNS Other Hormones Released Glycogen to Glucose Insulin Release Inhibited Amino acids to glucose TG to Fatty Acids
  9. 9. Type-1 Diabetes Postprandial is first affected then fasting levels affected when 8090% of β-cells are destroyed Autoimmune destruction of β-cells triggered by environmental factors (Virus, Toxin). Pathogenesis  Immediate or first phase insulin response BUT glucose remains normal Antigens (human leukocyte antigen [HLA]-DR3 or HLA-DR4), and circulating insulin antibodies. Asypmtomatic period during βcells destruction
  10. 10. Type-1 Diabetes Treat with insulin Blurred vision due to osmotic changes in the lens Glucose provides an excellent medium for infections Insulin secretion compromised Progressive fasting hyperglycemia occurs Clinical Presentation Ketonemia, ketonuria, and, ultimately, ketoacidosis Weight loss, metabolism of glycogen and fatty acids to ketones Gluc. Conc.> 180 mg/dL, glucosuria osmotic diuresis Symptoms of polyuria with compensatory polydipsia appear
  11. 11. Type-1 Diabetes Honeymoon Period Decreased blood glucose concentrations and markedly decreased insulin requirements. Lasts weeks… up to a year Increasing exogenous insulin requirements are inevitable and should be anticipated. During this time, patients should be maintained on insulin even if the dose is very low, because interrupted treatment is associated with a greater incidence of resistance and allergy to insulin .
  12. 12. Type-2 Diabetes Impaired insulin secretion and resistance to insulin action. Factors such as obesity and a sedentary lifestyle also contribute to the development of insulin resistance Pathogenesis Stronger association with FH, no relation with HLA circulating ICA s are absent Impaired glucose utilization, increased hepatic glucose production, and excess glucose accumulates in the circulation The pancreas produces more insulin in an attempt to overcome insulin resistance
  13. 13. Type-2 Diabetes Basal insulin levels are typically normal or elevated at diagnosis. β-cells lose their ability to respond to  glucose conc. leading to  insulin secreted and insulin resistance is worsened Pathogenesis Early-phase insulin release in response to glucose often is reduced resulting in postprandial hyperglycemia Insulinotropic substances such as incretin hormones levels are altered. Evidence suggests that decreased peripheral glucose uptake and utilization in muscle is the primary site of insulin resistance and results in prolonged postprandial hyperglycemia
  14. 14. Metabolic Syndrome Genetic Predisposition Environmental factors: Obesity Age Sedentary lifestyle β-cells Defect IFG, IGT, Diabetes type-2 Lipid Disorder HTN, Stroke Insulin Resistance Increased Insulin Secretion CVD Other Conditions
  15. 15. Type-2 Diabetes Symptoms are mild and gradual Fatigue, polyurea, polydipsia, but no ketosis. Insulin maybe needed for many Treat with MNT, phys activity, oral antidiabetic Clinical Presentation Microvascular complications at diagnosis  7-10 yrs undiagnosed diabetes  endogenous insulin promote lipogenesis  weight loss not common. Enough insulin to prevent lipolysis Macrovascular disease is evident at diagnosis
  16. 16. Normal and diabetic glucose levels Normal Fasting <100 (5.6) ½, 1, 1½ hr <200 (11.1) 2 hr <140 (7.8) Impaired glucose tolerance <126 (7.0) ≥200 (11.1) 140–200 (7.8–11.1) ≥200 (11.1) ≥200 (11.1) Impaired fasting glucose Diabetes (nonpregnant adult) 100–125 (5.6–6.9) ≥126 (7.0)
  17. 17. Diagnosis criteria –Diabetes Mellitus (1) Classic signs and symptoms of diabetes (polyuria, polydipsia, ketonuria, and unexplained weight loss) combined with a random plasma glucose ≥200 mg/dL (11.1 mmol/L). (2) A FPG ≥126 mg/dL (7.0 mmol/L). Fasting means no caloric intake for at least 8 hours. (3) After a standard oral glucose challenge (75 g glucose for an adult or 1.75 g/kg for a child), the venous plasma glucose concentration is ≥200 mg/dL (11.0 mmol/L) at 2 hours and >200 mg/dL (11.0 mmol/L) at least one other time during the test (0.5, 1, 1.5 hours); this is the OGTT.
  18. 18. Diagnosis criteria –Diabetes Mellitus Individuals with FPG values or OGTT values that are intermediate between normal and those considered diagnostic of diabetes are considered to have “prediabetes” or IFG or IGT. The categories of FPG values are as follows: a) A normal FPG is <100 mg/dL (5.6 mmol/L). b) An FPG of 100 to 125 mg/dL (5.6–6.9 mmol/L) is IFG. c) An FPG ≥126 mg/dL (7.0 mmol/L) indicates a provisional diagnosis of diabetes that must be confirmed, as described. The corresponding categories when the OGTT is used for diagnosis are as follows: a) A 2-hour postload glucose (2-hPG) <140 mg/dL (7.8 mmol/L) indicates normal glucose tolerance. b) A 2-hPG ≥140 mg/dL (7.8 mmol/L) and <200 mg/dL (11.1 mmol/L) indicates IGT. c) A 2-hPG ≥200 mg/dL (11.1 mmol/L) indicates a provisional diagnosis of diabetes, which must be confirmed by a second test.
  19. 19. Risk Factors for Type 2 Diabetes Mellitus Adults Children Overweight (≥25 kg/m2) Physical inactivity Overweight (BMI >85th percentile for age and sex; or weight >120% of ideal for height) Family history of diabetes (first- or second-degree relative) Ethnic predisposition Ethnic predisposition Family history of diabetes (first-degree relative) Previous IFG or IGT History of PCOS, GDM, or macrosomia Maternal history of diabetes (including GDM) Clinical conditions associated with insulin resistance Signs of insulin resistance (e.g., acanthosis nigricans) (e.g., severe obesity and acanthosis nigricans) Hypertension (≥140/90 mmHg or on antihypertensive therapy) Conditions associated with insulin resistance (e.g., Dyslipidemia hypertension, dyslipidemia, or PCOS) • HDL-C <35 mg/dL (0.90 mmol/L) • Triglyceride >250 mg/dL (2.82 mmol/L) • CVD
  20. 20. Goals of therapy (American Diabetes Association) Monitoring Parameter Fasting plasma glucose 2 hr postprandial plasma glucose 2–4 am plasma glucose HbA1c Urine ketones School Age (6–12 years) (mg/dL) 90–180 Adolescents and Young Adults (13–29 years) Pregnancy (mg/dL) (mg/dL) 90–130 60–90 Not routinely recommended 100–180 Not routinely recommended 90–150 ≤120 <7.0% <8.0% Absent to rare Absent to rare <7.5% Absent to rare 5–6% Rare Adults (mg/dL) 70–130 <180 >70 >60
  21. 21. ADA lipids goals for adults Low-density lipoproteins <100 mg/dL (<2.6 mmol/L) Triglycerides <150 mg/dL (<1.7 mmol/L) High-density lipoproteins • Men • Women >40 mg/dL (>1.0 mmol/L) >50 mg/dL (>1.3 mmol/L) More stringent goals (i.e., <70 mg/dL [1.8 mmol/L]) may be considered for individuals with overt cardiovascular disease
  22. 22. A case approach understanding R.P. is a 43-year-old woman visiting the drop-in clinic to obtain a routine physical examination for her new job. PMH Significant for GDM. was told (last child born 3 years ago) that she had “borderline diabetes,” which resolved each time after giving birth. FH Significant for type 2 diabetes hypertension, and CVD.
  23. 23. A case approach understanding Medications denies tobacco or alcohol use. SH She tries to walk 15 minutes twice a week. Had her last baby 3 yrs ago. PE Significant for moderate central obesity (5 feet 4 inches; 160 lbs; BMI, 30.2 kg/m2), BP 145/85 mmHg. R.P. denies any symptoms of polyphagia, polyuria, or lethargy. She has documented hypertension and an FPG value of 119 mg/dL, measured 2 months prior.
  24. 24. A case approach understanding What features of R.P.'s history and examination are consistent with an increased risk of developing type 2 diabetes? 1. Age 2. Ethnicity 3. Weight 4. Family history of diabetes 5. History of GDM 6. Documented IFG. Type 2 diabetes is also associated with other disorders such as hypertension. R.P. has not controlled hypertension and a family history of hypertension and CVD may indicate that she is predisposed to insulin resistance
  25. 25. A case approach understanding The physician orders another FPG for R.P., which comes back at 122 mg/dL. How should R.P. be managed at this time? 1. Education about risk for developing type 2 diabetes. 2. Institute lifestyle modifications (MNT, physical activity) aiming to lose weight, improve her CV health, and decrease her risk for developing diabetes. 3. A weight loss goal of 5% to 10% 4. Increase her level of moderate physical activity to at least 150 minutes/week. 5. Manage hypertension managed. 6. Metformin to prevent the development of type 2 diabetes is not recommended.
  26. 26. Treatment of Diabetes 1. Medical Nutrition Treatment (MNT) 2. Drugs (Insulin, oral hypoglycemic agents) 3. Exercise
  27. 27. Medical nutrition therapy Nutrition therapy is designed to help patients achieve appropriate metabolic and physiological goals. Unfortunately, patient acceptance and adherence to diet and meal planning is often poor. Type I diabetes Type 2 diabetes Adequate carbohydrates timed to match the peak of insulin Emphasize normalizing plasma glucose and lipid levels and maintain normal BP to prevent CVD Regularly scheduled meals and snacks are required to prevent hypoglycemic reactions A sustainable weight loss of 5% to 7% can be achieved through a structured programs that emphasize lifestyle changes, physical activity, and food intake that modestly reduces caloric and fat intake Patients who can “count carbohydrates” can inject rapid- or short-acting insulin matching their anticipated intake.
  28. 28. Exercise A key factor in the treatment of diabetes, particularly type 2. Obesity and inactivity contribute to the development of glucose intolerance in genetically predisposed individuals. Regular exercise reduces cholesterol, BP, weight, need for insulin or other agents, enhances insulin sensitivity, and improves psychological well-being by reducing stress. These effects are mediated through norepinephrine, epinephrine, growth hormone, cortisol, and glucagon, along with the suppression of insulin secretion
  29. 29. Overall goals of treatment Prevent acute and chronic complications. Periodic assessments of HbA1c coupled with regular measurement of fasting, preprandial, and postprandial glucose levels should be utilized to assess therapy. (1) Strive for glycemic control achieved. (2) Keep patients symptoms free. (3) Maintain normal growth and development in children. (4) Eliminate or minimize other cardiovascular risk factors. (5) Integrate the patient into the healthcare team.
  30. 30. Method of monitoring glycemic control (1) Urine ketone testing. (1) More recommended for type 1. (2) Should be checked when glucose level >300mg/dL (16.7mmol/L) (2) Plasma glucose (FPG, PPG) (1) Whole blood glucose (mg/dL) = Plasma glucose (mg/dL) ÷ 1.12 (2) Plasma glucose (mmol/L) = Plasma glucose (mg/dL) ÷ 18 (3) Self monitoring blood glucose. (1) (2) (3) (4) In type 1: correlate meals, exercise, and insulin dose. Pregnant women may have over control problems. Protect from hypoglycemia episodes. A must for intensive therapy patients.
  31. 31. Method of monitoring glycemic control (1) Continuous glucose monitoring. (2) Glycosylated hemoglobin. (1) It has become the gold standard for measuring chronic glycemia and is the clinical marker for predicting longterm complications, particularly microvascular complications. (2) It is the least affected by recent fluctuations in blood glucose. (3) measures the percentage of hemoglobin A that has been irreversibly glycosylated at the N-terminal amino group of the β-chain. (4) Alterations in RBC survival such as hemoglobinopathies, anemias, acute or chronic blood loss, and uremia may affect HbA1c values, resulting in inaccurate indications of glycemic control. Antioxidants such as vitamins C and E also may interfere with the glycosylation process
  32. 32. Factors affecting HbA1c Alterations in RBC Survival Hemoglobinopathies Anemias Hemolytic Iron deficiency Blood loss Decreased Decreased Decreased Decreased Assay Interference Uremia Hemodialysis Antioxidants Increased or no change No change Decreased
  33. 33. Physical and Chemical Properties of Human Insulin 21 amino acids α-chain β-chain 30 amino acids Monomers Dimers Zn++ Zn++ Self-aggregation in solution Hexamers (around Zn2+)
  34. 34. Rapid acting insulin Brand Onset min Peak min Duration hr Humalog or lispro 15-30 30-90 3-5 Novolog or aspart 10-20 40-50 3-5 Apidra or glulisine 20-30 30-90 1-2½ Role in glucose management Rapid-acting insulin covers insulin needs for meals eaten at the same time as the injection. This type of insulin is often used with longeracting insulin.
  35. 35. Primary Structure of Lys(B28), Pro(B29)–Insulin Insulin Gly 23 Lispro Gly Glu 24 Glu Phe 25 Phe Tyr 26 Thr 27 Tyr 28 Thr Pro Lys 29 30 Lys Pro Thr Thr
  36. 36. Primary Structure of Asp(B28)-Insulin Insulin Gly 23 Aspart Gly Glu 24 Glu Phe 25 Phe Tyr 26 Thr 27 Tyr 28 Thr Pro Lys 29 30 Asp Lys Thr Thr
  37. 37. Primary Structure of Glu(B29), Lys(B3)–Insulin Insulin Phe 1 Glulisine Phe Val Asn Gln Pro Lys Thr 2 3 4 28 29 30 Val Lys Gln Pro Glu Thr
  38. 38. Asp Heinmann et al. Diabet. Med. 1996 Lys Pro Glu Lys 38
  39. 39. Short acting insulin Brand Regular (R) humulin or Actarapid Onset Duration Peak hr min hr 30-60 2-5 5-8 Velosulin (for use in the insulin 30-60 pump) 2-3 2-3 Role in glucose management Short-acting insulin covers insulin needs for meals eaten within 30-60 minutes
  40. 40. Intermediate acting insulin Brand NPH (N) Onset min 1-2 hours Peak hr 4-12 hours Duration hr Role in glucose management Intermediate-acting insulin covers insulin needs for about half the day or overnight. This type of insulin is 18-24 hours often combined with rapid- or short-acting insulin
  41. 41. Plasma insulin levels Action Profiles of Injected Human Insulin Regular 6–8 hours NPH 12–20 hours 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 Hours
  42. 42. Long acting insulin Brand Onset min Peak hr Duration hr No peak time; Lantus (insulin insulin is 1-1½ hour 20-24 hours glargine) delivered at a steady level Levemir (insulin detemir) 1-2 hours 6-8 hours Role in glucose management Long-acting insulin covers insulin needs for about one full day. This type of insulin is often combined, when needed, with rapid- or short-acting insulin Up to 24 hours 42
  43. 43. Primary Structure of Gly(A21), Arg(B31), Arg(B32)-Insulin Insulin A-chain Leu Glu Asn Tyr Cys Asn 16 17 18 19 20 21 Glargine Leu Glu Asn Tyr Cys Gly Insulin B-chain Phe Tyr Thr Pro Lys Thr 25 26 27 28 29 30 Glargine Phe Tyr Thr Pro Lys Thr Arg Arg
  44. 44. Primary Structure of Lys(B29)-N--Tetradecanoyl, Des(B30)-Insulin Detemir Gly Glu Phe Tyr Thr Pro Lys 23 Insulin 24 25 26 27 28 29 Gly Glu Phe Tyr Thr Pro • Fatty acid tail (myristic acid) added to human insulin • Complexes with albumin>20 hour action Lys Thr 30 Thr (CH2)4 NH CO R 44
  45. 45. Glucose infusion rates (mg/kg/min) Action Profiles of long acting insulin analogs – Glargine 6 NPH 5 4 Glargine 3 0.4 U/kg 2 Placebo 1 0 0 2 4 6 8 10 12 14 16 Time (h) 18 20 22 24 26 28 30
  46. 46. Glucose infusion rate (mg/kg/min) Action Profiles of long acting insulin analogs – Detemir 2.0 1.5 1.0 Detemir - high Detemir - low 0.5 0.0 -100 Placebo 100 300 500 700 900 Elapsed time (min) 1100 1300 1500
  47. 47. Premixed insulin Brand Onset min Duration Peak hr hr Humulin 70/30 30 2-4 14-24 Novolin 70/30 30 2-12 Up to 24 Novolog 70/30 10-20 1-4 Up to 24 Role in glucose management These products are generally taken two or three times a day before mealtime.
  48. 48. Mixed vs. Basal Insulin Regimens Outcome Analog mix vs. Human mix Analog mix vs. Long-acting analogs Analog mix vs. “Other regimens” Strength of Evidence FPG Similar Favors long-acting analog Unknown Moderate PPG Favors analog mix Favors analog mix Unknown High A1c Reduction Similar Favors analog mix Unknown High Hypoglycemia Similar Favors long-acting analog Unknown High Weight Similar Favors long-acting analog Unknown Moderate Mortality Unknown Unknown Unknown Unknown 48
  49. 49. A case approach understanding of type-1 diabetes A.H., a slender, 18-year-old woman who was recently discharged from the hospital for severe dehydration and mild ketoacidosis FPG = 190 mg/dL (normal, 70–100) RPG = 250 mg/dL (normal, 140 to <200). 4 weeks before she was hospitalized, Moved across country for Symptoms of polydipsia, nocturia (six times a night), fatigue, and a 12-lb weight loss over this period, which she attributed to the anxiety. PMH Remarkable for recurrent upper respiratory infections and three cases of vaginal moniliasis over the past 6 months.
  50. 50. A case approach understanding of type-1 diabetes FH Negative for diabetes, and she takes no medications. PE Within normal limits Weighs 50 kg and is 5 feet 4 inches tall. Laboratory results are as follows: FPG, 280 mg/dL (normal, <100); HbA1c, 14% (normal, 4%–6%); and trace urine ketones as measured by Keto-Diastix (normal, negative). LR FPG, 280 mg/dL (normal, <100); HbA1c, 14% (normal, 4%–6%); Trace urine ketones (normal, negative).
  51. 51. A case approach understanding of type-1 diabetes Which findings are consistent with type-1 diagnosis in A.H.? (1) classic symptoms of the disease (polyuria, polydipsia, weight loss, glucosuria, fatigue, recurrent infections). (2) A random plasma glucose above 200 mg/dL, and an FPG of 126 mg/dL or higher on at least two occasions. (3) Elevated HbA1c also is consistent with diabetes mellitus. (4) Features of A.H.'s history that are consistent with type 1 diabetes include: (1) Relatively acute onset of symptoms in association with a major life event (2) Ketones in the urine, (3) Negative family history (4) Relatively young age at onset.
  52. 52. A case approach understanding of type-1 diabetes A.H. will be started on insulin therapy. What are the goals of therapy? Will normal glucose levels prevent complications? (1) The goal is to prevent acute and chronic complications. (2) Physiological insulin therapy involves a complete program of diabetes management involves a balanced meal plan, exercise, frequent SMBG, and insulin adjustments based on these factors. (3) Lowering blood glucose concentrations through intensive insulin therapy in persons with type 1 diabetes slows or prevents the development of microvascular complications (DCCT Study)
  53. 53. A case approach understanding of type-1 diabetes What methods of insulin administration are available to achieve optimal glucose control? (1) A physiological insulin regimen is designed to mimic normal insulin secretion as closely as possible. (1) Insulin pump therapy (previously referred to as “continuous subcutaneous infusion of insulin” (2) Basal-bolus insulin regimens consisting of once to twice daily doses of basal insulin coupled with pre-meal doses of rapid or short-acting insulin
  54. 54. Factors Altering Onset and Duration of Insulin Action (1) Route of administration IV>IM>SC (2) Factors altering clearance: (1) Renal function. (2) Insulin antibodies (IgG). (3) Hyperthyroidism increases clearance and insulin action, making insulin control difficult. (3) Factors altering SC absorption: (1) Site of injection Site Abdomen Arm Hip Thigh Half-life absorption (min) 87 ± 12 141± 23 153± 28 164 ± 15 (2) Exercise increases absorption rate. (3) Heat increases absorption rate. (4) Massage increases absorption rate. (5) Smoking is controversial. (6) Jet injectors increases absorption rate. (7) Lipohypertrophy delays absorption. (8) More soluble insulin faster absorption. (9) Mixtures can mask the regular insulin. (10)More diluted insulin faster absorption. (11)Lower doses are absorbed faster.
  55. 55. A case approach understanding of type-1 diabetes How can insulin injections be administered to A.H. in a way that mimics physiological insulin release? Long acting insulin Short acting insulin
  56. 56. Estimating Total Daily Insulin Requirements Type 1 diabetes Initial dose 0.3–0.5 unit/kg Honeymoon phase With ketosis, during illness, during growth 0.2–0.5 unit/kg 1.0–1.5 units/kg Type 2 diabetes With insulin resistance 0.7–1.5 units/kg Estimating basal insulin Dose need to be adjusted according to SMBG results Basal requirements vary throughout the day, often increasing during the early morning hours. Basal requirements are approximately 50% of total daily insulin needs The basal requirement also is influenced by the presence of endogenous insulin, the degree of insulin resistance, and body weight.
  57. 57. Estimating Total Daily Insulin Requirements Estimating premeal insulin The 500 rule (modified to 450 rule) : 500/total daily dose of insulin (TDD) = number of carobhydrate grams covered Using 50 U/day, 500/50 = 10. Therefore, 10 g carbohydrate would be covered by 1 unit of insulin lispro, glulisine, or aspart. This role is not quite applicable in type 2 because insulin resistance. It may underestimate insulin needs Correction factor The correction factor determines how far the blood glucose drops per unit of insulin given and is known as the “1700 rule.” For regular insulin, the rule is modified to the “1500 rule.” 1700/TDD = point drop in blood glucose per unit of insulin If a patient uses 28 U/day of insulin, their correction factor (or insulin sensitivity) would be 1700/28 = 60 mg/dL. Therefore, the patient can expect a 60 mg/dL drop for every unit of rapid acting insulin administered.
  58. 58. Patient’s selection criteria for intensive insulin therapy Type 1, otherwise healthy patients (>7 years of age) Women with diabetes who plan to conceive Pregnant patients with diabetes (pre-existing) Patients poorly controlled on conventional therapy (includes type 2 patients) Technical ability to test blood glucose concentrations Intellectual ability to interpret blood glucose concentrations and adjust insulin doses appropriately Access to trained and skilled medical staff to direct treatment program and provide close supervision
  59. 59. Avoid or use intensive insulin therapy cautiously in: Patients with counter-regulatory insufficiency β-Adrenergic blocker therapy Autonomic insufficiency Adrenal or pituitary insufficiency Patients with coronary or cerebral vascular disease Unreliable, noncompliant individuals, including those who abuse alcohol or drugs and those with psychiatric disorders
  60. 60. Hypoglycemia Blood glucose concentration <60 mg/dL: Patient may or may not be symptomatic. Blood glucose <40 mg/dL: Patient is generally symptomatic. Blood glucose <20 mg/dL can be associated with seizures and coma Blurred vision, sweaty palms, generalized sweating, tremulousness, hunger, confusion, anxiety, circumoral tingling, and numbness. Nocturnal hypoglycemia: nightmares, restless sleep, profuse sweating, morning headache, morning “hangover.” In one study, 80% of patients with nocturnal hypoglycemia had no symptoms. Signs and symptoms Ingest 10–20 g rapidly absorbed carbohydrate. Repeat in 15–20 min if glucose concentration remains <60 mg/dL or if patient is symptomatic. Follow with complex carbohydrate/protein snack if meal time is not imminent. Treatment
  61. 61. A case approach understanding of type-1 diabetes A.H. was instructed to inject herself with 12 units of Lantus each morning and give 4 units of Novolog with each meal. The initial goal of therapy is to achieve preprandial blood glucose concentrations of <180 mg/dL and to eliminate symptoms of hyperglycemia. Time 7 AM Glucose Concentration (mg/dL) 160–200 Noon 220–260 5 PM 130–180 11 PM 140–180 Occasional 3 AM tests averaged 160 mg/dL Urine is negative for ketones. She eats approximately four carbohydrate servings for breakfast (60 g) and two to four carbohydrate servings for lunch and dinner (30–45 g). She feels a bit better, and her weight has stabilized, but she still urinates two to three times nightly.
  62. 62. A case approach understanding of type-1 diabetes How would you interpret these results, and how should A.H.'s insulin doses be altered? (a) (b) (c) (d) (e) (f) Set glycemic goals Develop recommendations for pharmacologic therapy Evaluate the effectiveness of pharmacologic therapy, Instruct patients to interpret and respond to blood glucose patterns Evaluate the impact of dietary factors on glycemic control Modify therapy during acute/intercurrent illness or whenever patients receive medications known to affect glycemic control (g) Modify the management plan in response to a change in activity levels (h) Identify hypoglycemic unawareness
  63. 63. Pharmacottherapy Anas Bahnassi PhD CDM CDE abahnassi@gmail.com http://www.twitter.com/abpharm http://www.facebook.com/pharmaprof http://www.linkedin.com/in/abahnassi