2. Objectives Describe normal glucose metabolism Describe the pathophysiology of Type I and Type II DM Describe the two major types of diabetes with reference to genetics, the age incidence, and diagnosis Describe the following therapies for control of blood glucose. Diet Insulin Name and describe the major types of insulin available Describe situations in which the use of insulin in Type II Diabetes is clinically correct. Describe how to start a patient on insulin and how to counsel a patient
3. Objectives Distinguish the features of DM Type II from Type I List the classes of antidiabetic agents and discuss their mode of action Describe the pathophysiology, signs, symptoms, dignostic features and treatment of Diabetic Ketoacidosis and coma Hypoglycemia and insulin shock Lactic acidosis Hyperosmolar coma Discuss the dawn phenomenonandSymogyi effect, including their pathophysiology and management.
4. Objectives List and describe the following chronic complications of diabetes Retinal disease leading to blindness Renal disease Vascular disease Cardiac disease Dermatologic disorders Gastrointestinal disease Discuss the epidemiology of diabetes in the U.S. and explain its socio-economic impact.
5. Objectives Discuss the impact of diabetes on pregnancy and include the unique risks and management Explain short and ling term monitoring of diabetes. Describe patient education principles that may help diabetic patients adhere to their prescribed treatment plan
9. Pancreatic Physiology Endocrine and Exocrine activity Exocrine: Pancreatic Acini cells produce digestive juices Duct cells produce NaHCO3 Endocrinetissue contained inIslets of Langerhans Endocrine: ALPHA CELLS secrete Glucagon (25%) BETA CELLS produce Insulin (60%) DELTA CELLS produce Somatostatin (15%)
10. Primary Pancreatic Hormone Activity GLUCAGON Stimulates breakdown of glycogen in the liver Activates hepatic gluconeogenesis (makes sugar) INSULIN Anabolic hormone Facilitates entry of glucose into cells Stimulates the liver to store glucose in the form of glycogen Promotes the storage of carbohydrate and fat and protein synthesis
11. Insulin Biosynthesis, secretion and action Mature insulin molecule and C peptide are stored together and cosecreted from secretory granules in the beta cells Because the C peptide is cleared more slowly than insulin, it’s a useful marker of insulin secretion Glucose is the key regulator of insulin secretion Glucose levels >70 mg/dL stimulate insulin synthesis
12. Insulin Biosynthesis, secretion and action Insulin is secreted in a pulsatile pattern Small secretory bursts occur about every 10 minutes Superimposed upon greater amplitude oscillations of about 80-150 minutes Incretins also play a role in insulin secretion Released from GI tract neuroendocrine cells following food ingestion and amplify glucose-stimulated insulin secretion and suppress glucoagon secretion
13. Insulin Biosynthesis, secretion and action 50% is degraded in the liver after entering the portal venous system Unextracted insulin enters the systemic circulation where it binds to receptors in target sites
14. Somogyi Effect and Dawn Phenonemon Somogyi Effect: nocturnal hypoglycemia (from fasting) leads to a surge of counterregulatory hormones (glucagon and epinephrine) that produce hyperglycemia at around 7 AM Dawn Phenomenon: reduced tissue sensitivity to insulin between 5 and 8 AM
15. Diabetes Mellitus Syndrome with disordered metabolism and inappropriate hyperglycemia due to a deficiency of insulin secretion or to a combination of insulin resistance and inadequate insulin secretion to compensate. Several types exist and are caused by a complex interaction of genetics and environmental factors Factors that contribute to hyperglycemia include Reduced insulin secretion Decreased glucose utilization Increased glucose production
16. Diabetes Mellitus Metabolic dysregulation associated with DM causes secondary pathophysiologic changes in multiple organ systems that impose a tremendous burden on the individual and the health care system DM is the leading cause of ESRD, nontraumatic lower extremity amputations, and adult blindness
17. Diabetes Mellitus Classification Based on the pathogenic process that leads to hyperglycemia Two broad categories Type 1 – results from complete or near-total insulin deficiency Type 2 – heterogeneous group of disorders characterized by variable degrees of insulin resistance, impaired insulin secretion and increased glucose production
21. Diabetes Epidemiology 7th leading cause of death in 2007 Prevalence of 20.9% in individuals >60 years Prevalence is similar in men and women
22. Diagnosis of Diabetes 1Give 75 g of glucose dissolved in 300 mL of water after an overnight fast in persons who have been receiving at least 150–200 g of carbohydrate daily for 3 days before the test. 2A fasting plasma glucose 126 mg/dL is diagnostic of diabetes if confirmed on a subsequent day.
23. Diagnosis of Diabetes Person may have IFG and IGT They are at substantial risk of developing diabetes and have an increased risk of cardiovascular disease 25-40% risk of overt diabetes over next 5 years Fasting glucose – the most reliable and convenient test for identifying DM in asymptomatic individuals
25. Type 1 Diabetes General Considerations Caused by pancreatic islet B-cell destruction that leads to insulin deficiency Destruction is immune-mediated in > 90% of cases and idiopathic in the remainder Individuals with genetic susceptibility have normal beta cell mass at birth but begin to lose beta cells secondary to autoimmune destruction that occurs over months to years Autoimmune process is thought to be triggered by an infectious or environmental stimulus
26. Type 1 Diabetes Susceptibility involves multiple genes Major gene is located in the HLA region on chromosome 6 The rate of pancreatic B-cell destruction ranges from rapid to slow and varies among individuals Features of diabetes do not become evident until ~80% of beta cells are destroyed Prone to ketoacidosis Serum C-peptide negative 1–5 years after diagnosis; plasma glucagon is elevated
27. Type 1 Diabetes Immunologic markers Islet cell autoantibodies (ICAs) – present in >75% of those diagnosed with new-onset type 1 DM Testing for these can be useful in classifying type of DM and identifying nondiabetic individuals at risk of developing type 1 DM Environmental factors None have been conclusively linked to diabetes
28. Type 1 Diabetes Prevention No interventions have been proven successful in preventing type 1 DM in humans Demographics Typically onset of disease is prior to age 30 (10-14 most commonly) Suspect especially when hyperglycemia first appears in the nonobese or elderly
29. Type 1 Diabetes Incidence Highest in Scandinavia Lowest in China and parts of South America In the United States, average is 15 per 100,000 Incidences are higher in states densely populated with persons of Scandinavian descent such as Minnesota The global incidence is increasing, with an annual increase of ~3%
30. Type 1 Diabetes Symptoms and Signs Lean body habitus Increased thirst (polydipsia) Increased urination (polyuria) Increased appetite (polyphagia) with weight loss Ketoacidosis Paresthesias Recurrent blurred vision Vulvovaginitis or pruritus Nocturnal enuresis Postural hypotension from lowered plasma volume
31. Type I Diabetes Laboratory Tests Fasting plasma glucose ≥ 126 mg/dL or > 200 mg/dL 2 h after glucose load Ketonemia, ketonuria, or both Glucosuria Assess degree of glycemic control with glycosylated hemoglobin (hemoglobin A1c) reflects glycemic control over preceding 8–12 weeks Serum fructosamine Reflects glycemic control over preceding 2 weeks Helpful in presence of abnormal hemoglobins or in ascertaining glycemic control at time of conception among diabetic women
32. Type 1 Diabetes Laboratory tests Serum insulin or C-peptide Forms when proinsulin is broken down to form insulin and C-peptide C-peptide has a longer half life than insulin Islet cell antibodies Insulin autoantibody Screen for DM-associated conditions Microalbuminuria Dyslipidemia Thyroid function
33. Type 1 Diabetes Pharmaceutical treatment Insulin Goal is to design insulin regimens that mimic physiologic insulin secretion Insulin regimens usually include multiple-component insulin regimens, multiple daily injections or insulin infusion devices Most patients will require 0.5-1 U/kg/day of insulin divided into multiple doses, with ~50% of the insulin given as basal insulin
35. A multiple-component insulin regimen consisting of long-acting insulin,one shot of glargine to provide basal insulin coverage and three shots of lispro, or insulin aspart to provide glycemic coverage for each meal. The injection of two shots of long-acting insulin, NPH or detemir and short-acting insulin, lispro, insulin aspart (solid red line), or regular (green dashed line) B= breakfast L= lunch S= supper HS= bedtime = time of insulin injection Infusion pump which uses lispro or aspart
36. Diet/Nutrition Carbohydrate counting or exchange systems to estimate the nutrient content of a meal or snack Estimate of the carb content of a meal determines the bolus insulin dose for a meal or snack Want to coordinate and match caloric intake with the appropriate amount of insulin A common ratio is 1-1.5 units/10g of carb, but this must be individualized
37. Type 1 Diabetes Other agents that improve glucose control Amylin (pramlintide) Usually cosecreted from pancreatic beta cells with insulin Pts who are insulin deficient are also amylin deficient SC injection before each meal - reduces postprandial glycemic excursion in type 1 and 2 diabetic pts Slows gastric emptying and suppresses glucagon Will decrease amount of short-acting insulin needed before the meal
38. Type 1 Diabetes Surgery Patients receiving simultaneous pancreas and kidney transplants have 85% chance of pancreatic graft survival and 92% chance of renal graft survival after 1 year Islet transplantation is minimally invasive Plagued by limitations and remains an area of investigation
40. Type 2 Diabetes General considerations Typically > 40 years of age Fasting plasma glucose ≥ 126 mg/dL more than once OGTT > 200 mg/dL 2 h after the oral glucose Often associated with hypertension, dyslipidemia, and atherosclerosis
41. Type 2 Diabetes Pathophysiology Characterized by impaired insulin secretion, insulin resistance, excessive hepatic glucose production and abnormal fat metabolism Obesity, especially central (hip-waist ratio) is very common (present in 80%) Early stages – glucose tolerance remains near normal, despite insulin resistance, because the beta cells increase their insulin output
42. Type 2 Diabetes Pathophysiology (cont’d) As the disease progresses, islets are unable to sustain the hyperinsulinemic state IGT develops, characterized by elevations in postprandial glucose Further decline in insulin secretion and increase in hepatic glucose production lead to overt diabetes with fasting hyperglycemia Ultimately, beta cell failure may ensue
43. Type 2 Diabetes Genetic considerations Strong genetic component Concordance in identical twins is between 70-90% If both parents have type 2, the risk approaches 40% for the offspring General considerations Prevalence of obesity in type 2 diabetes mellitus 30% in Chinese and Japanese 60–70% in North Americans, Europeans, and Africans Nearly 100% in Pima Indians and Pacific Islanders from Nauru or Samoa
44. Type 2 Diabetes General Considerations Enhancers of insulin resistance are aging, sedentary lifestyle, and abdominal-visceral obesity Both the tissue resistance to insulin and the impaired B-cell response to glucose are further aggravated by increased hyperglycemia, and both defects improve with decreased hyperglycemia
45. Type 2 Diabetes Demographics > 90% of all diabetics in the United States have type 2 diabetes (>18 million) Traditionally develops after age 40, but now more frequently at younger ages due to increased rates of obesity No gender predominance
46. Type 2 Diabetes Screening ADA recommends screening all individuals >45 years q3 years and earlier if they are overweight and have one additional risk factor for diabetes Many are asymptomatic and unaware they have the disease Type 2 DM may be present for up to a decade before diagnosis Treatment of type 2 DM may favorably alter the natural history of DM
47. Risk Factors for Type 2 Diabetes FH of diabetes (parent or sibling with type 2) Obesity (BMI >25) Habitual physical inactivity Race/ethnicity – AA, Latino, Native Amer, Asian or Pacific Islander Previously identified with IFG or IGT History of GDM or delivery of baby >9 lbs HTN (BP >140/90) PCOS or acanthosisnigricans
48. Type 2 Diabetes History Be sure to ask about DM relevant aspects such a weight, FH of DM, risk factors for CV disease, exercise, smoking and ethanol use If previously diagnosed with DM ask about type of therapy, prior HgbA1C levels, self-monitoring BG results, frequency of hypoglycemia, assessment of pt’s knowledge about diabetes, exercise and nutrition
49. Type 2 Diabetes Symptoms and Signs Often asymptomatic Obesity Polyuria Polydipsia Weakness or fatigue Recurrent blurred vision Vulvovaginitis or pruritus Slow wound healing Peripheral neuropathy Acanthosisnigricans
50. Acanthosisnigricans (AN) is a brown to black, poorly defined, velvety hyperpigmentation of the skin, usually present in the posterior and lateral folds of the neck, the axilla, groin, umbilicus, and other areas
51. Type 2 Diabetes PE Special attention should be given to DM-relevant aspects such as Weight or BMI Retinal examination Yearly evaluation by ophthalmologist BP >130/80 mmHg is considered HTN
52. Type 2 Diabetes PE Foot examination Peripheral neuropathy – vibratory sensation and light touch sensation with monofilament Calluses Foot deformities Peripheral pulses Insulin injection sites
54. Type 2 Diabetes Laboratory Tests Fasting plasma glucose ≥126 mg/dL or >200 mg/dL 2 h after glucose load Glucosuria Ketonuria on occasion without ketonemia Assess the degree of glycemic control with glycosylated hemoglobin (HbA1c) reflects glycemic control over preceding 8–12 weeks
55. Type 2 Diabetes Laboratory testing Screen for DM-associated conditions Microalbuminuria Dyslipidemia Lipoprotein abnormalities in obese persons with type 2 diabetes include High serum triglyceride (300–400 mg/dL) Low high-density lipoprotein (HDL) cholesterol (< 30 mg/dL) A qualitative change in low-density lipoprotein (LDL) particles Thyroid function
57. Long Term Treatment Goals Eliminate symptoms related to hyperglycemia Symptoms usually resolve when BG <200 mg/dL Reduce or eliminate the long-term microvascular and macrovascular complications Allow the pt to achieve as normal a lifestyle as possible
58. Long Term Treatment How to achieve these goals Pt education about DM, nutrition and exercise Provider education at every office visit + the use of a diabetes educator and dietician Nutritional recommendations Diet that includes fruits, vegetables, fiber-containing foods and low-fat milk Glycemic index – estimate of the postprandial rise in the BG when amount of that food is consumed
59. Glycemic Index Low glycemic index appears to reduce postprandial glucose excursions and improve glycemic control Short grain White Rice 72 White Bread 70 Graham Crackers 74 Broccoli 10 Corn 55 Potato (baked) 93 Sweet Potato 54 Apple 38 Watermelon 103 Honey 58 Fructose 23 Walnuts 15 Corn Chips 72 Milk (whole) 22 Yogurt (low-fat) 33
60. Diabetes Dietary Recommendations Cholesterol to 200 mg QD Protein intake to 10–35% of total calories Saturated fats to <7% of total calories Remainder of diet to consist of monounsaturated fats and carbohydrates with 20–35 g of dietary fiber
61. Long Term Treatment Exercise ADA recommends 150min/week (distributed over at least 3 days) of aerobic activity Reduces CV risk Reduces BP Maintains muscle mass Reduction in body fat and weight loss Lowers plasma glucose – during and following exercise Increases insulin sensitivity Formal exercise tolerance testing (stress test) is warranted in individuals prior to the start of an exercise program with any of the following: age>35 years, diabetes duration >10 years, microvascular complications, neuropathy, PAD
62. Long Term Treatment Monitoring of BG Patient’s measurements provide you with a picture of short-term glycemic control HbA1C reflects average glycemic control over the previous 3 months Self-monitoring of BG Frequency must be individualized Type 1 or type 2 on insulin - ≥3 times a day Type 2 on oral meds – 1-2 times a day with decreasing frequency as DM becomes controlled Monitor prior to a meal and supplemented with postprandial measurements
63. Type 2 Diabetes Pharmaceutical treatment Any therapy that improves glycemic control reduces “glucose toxicity” to the islet cells and improves endogenous insulin secretion However, type 2 DM is a progressive disorder and ultimately requires multiple therapeutic agents and often insulin
64. Classifications of glucose lowering agents Insulin secretagogues Drugs that stimulate insulin secretion Most effective in pt with relatively recent onset of DM (<5 years) Sulfonylureas (glyburide, glipizide, glimepiride) Meglitinide analogs (Prandin/repaglinide) D-phenylalanine derivative (Starlix/nateglinide) Side effects Can cause hypoglycemia, especially in the elderly Weight gain
65. Classifications of glucose lowering agents Biguanides Reduces hepatic glucose production and improves peripheral glucose utilization slightly Metformin (glucophage) Promotes modest weight loss Side Effects GI disturbances – nausea, bloating, diarrhea Lactic acidosis – can be prevented by avoiding use in renal insufficiency (creatinine >1.5 mg/dL) Must discontinue prior to radiographic contrast material
66. Classifications of glucose lowering agents αglucosidase inhibitors Reduce glucose absorption from the GI tract Reduce postprandial hyperglycemia acarbose, miglitol Not as potent as other oral agents at lowering the A1C Side effects Diarrhea, flatulence, abdominal distention (due to increased carbs/sugars in the large bowel)
67. Classifications of glucose lowering agents Thiazolidinediones (TZDs) Reduce insulin resistance Promote redistribution of fat from central to peripheral locations Circulating insulin levels decrease Pioglitazone (Avandia), rosiglitazone (Actos) Must measure LFTs prior to initiating therapy and q2 months for the 1st year of therapy Side effects Weight gain Peripheral edema and CHF – don’t use in CHF class III or IV
68. Classifications of glucose lowering agents GLP-1 receptor signaling “Incretins” Amplify glucose-stimulated insulin secretion Exenatide (Byetta) Suppresses glucagon and slows gastric emptying Most experience modest weight loss Suppresses appetite SC injection before morning and evening meal Only approved for adjunct or combo therapy with metformin, TZD or sulfonylurea Sitagliptin (Januvia) DPP-IV inhibitor, enhance incretin effect Promote insulin secretion and have a preferential effect on postprandial BG Oral medication and can be used in combination with metformin or a TZD
69. Classifications of glucose lowering agents Insulin therapy Can consider as initial therapy especially in lean individuals or those with severe weight loss, in those with underlying renal or hepatic disease, or those hospitalized or acutely ill Insulin is usually initiated as a single dose of long-acting insulin (determir (Levemir), glargine (Lantus)) and is most often started at bedtime Can use in combination with oral glucose-lowering agents (biguanides, αglucosidaseinhib, TZDs) As the disease progress the pt will often need prandial insulin coverage also
70. Classifications of glucose lowering agents Choice of initial glucose-lowering agent Level of hyperglycemia If FPG <200-250 mg/dL pts often respond to a single oral agent If FPG >250mg/dL pts often need >1 agent to reach goal Consider insulin if FPG >250-300mg/dL or in those who are symptomatic from hyperglycemia All oral agents except the αglucosidase inhibitors improve glycemic control to a similar degree (1-2% reduction in A1C)
72. Classifications of glucose lowering agents Combination therapy with oral agents Mechanisms of action are different so the effect on glycemic control is additive several drug combinations of TZD + metformin or sulfonylurea; metformin + sulfonylurea; DPP-IV with metformin are available
73. Diabetes Guidelines for ongoing medical care Self-monitoring of blood sugar HbA1c (2-4 times/year) Screen for microalbuminuria annually Serum lipids annually Feet examination by provider 1-2 times a year, daily by pt Diabetic eye examination annually
75. Diabetes Hemoglobin A1C There is an equation A 1% increase in A1C translates into a 35mg/dL increase in the mean glucose
76. Diabetes Complications May be present in up to 20-50% of newly diagnosed individuals with type 2 Retinopathy CV disease Nephropathy Neuropathy Diabetic ketoacidosis Hypoglycemia and altered awareness of hypoglycemia
77. Diabetes Prevention Goal of therapy is to prevent acute illness and reduce risk of long-term complications Type 2 DM is preceded by a period of IGT and a number of lifestyle modifications and pharmacologic agents prevent or delay the onset of DM Maintain a normal BMI Diet and exercise for 30 min/day five times/week ADA recommends consideration of Metformin (glucophage) in individuals with both IFG and IGT who are at high risk of progression to diabetes <60 years, BMI >35, +FH 1st degree relative, elevated TGs, reduced HDL, HTN or A1C >6%
79. Complications Acute Diabetic ketoacidosis Hyperglycemic Hyperosmolar State Chronic Duration and degree of glycemic control are the best predictors of complications Vascular Microvascular Retinopathy, neuropathy, nephropathy Macrovascular CAD, PAD, CV disease Nonvascular Gastroparesis, infections, skin changes, sexual dysfunction, cataracts, glaucoma, periodontal disease
80. Ocular Complications Diabetic retinopathy DM is the leading cause of blindness b/t the ages of 20-74 in the US Retinal vascular microaneurysms, blot hemorrhages, cotton wool spots eventually progress in most patients with continued hyperglycemia and lead to retinal ischemia Can be treated early with laser photocoagulation
82. Cardiovascular Complications DM major risk factor for cardiovascular disease in the US Annual incidence of cardiovascular death rate is increased by 3 times in diabetic men and by 4 times in diabetic women Risk factors for cardiovascular disease Insulin resistance Elevated urinary protein excretion Poor glycemic control Overweight or obesity Dyslipidemia HTN Sedentary lifestyle Smoking Monitoring of lipid levels and management of hyperlipidemia is essential in the prevention of macrovascular complications
83. Diabetic Nephropathy DM is the #1 cause of ESRD in the U.S. Leading cause of DM-related morbidity and mortality Begins with microalbuminuria defined as 30-300 mg/d After 10 years macroalbuminuria develops in 50% Overall risk of developing diabetic nephropathy is 20-40%
84. Diabetic Nephropathy Treatment Glycemic control slows progression Strict BP control Start ACE or ARB Restrict protein intake to 0.8g/kg/day Nephrology consultation when GFR is <60 mL/min More likely to develop in: Males Relatives have had kidney disease or HTN Poor glycemic control Patient has HTN
85. Diabetic Neuropathy Most common complication of DM Type 2 Develops in ~50% of individuals with DM Peripheral neuropathy Most common is distal symmetric polyneuropathy Most frequently presents with distal sensory loss but may also have hyperesthesia, paresthesia and dysesthesia Begins in feet and spreads proximally, usually present at rest and worsens at night
86. Diabetic Neuropathy Autonomic neuropathy Involves the cholinergic, noradrenergic, and peptidergic Can involve multiple systems CV, GI, GU Postural hypotension and decreased CV response Gastroparesis Urine retention ED Treatment Check feet daily and take precautions (footwear) TCAs, anticonvulsants, duloxetine (Cymbalta) and pregabalin (Lyrica), gabapentin (Neurontin)
87. PV Disease of the Feet Screening and referral to footcare clinic for people with diabetes who are at high risk of developing foot ulcers reduces the risk of foot ulcers and major amputation
88. Foot structure Foot appearance Vascular status Neurosensory 128 Hz tuning fork base at great toe nail Monofilaments Deep tendon reflexes
89. Skin & Mucous Membrane Complications Protracted wound healing and skin ulcerations Shin spots – pigmented pretibial papules Granulomaannulare – erythematous plaques on the extremities or trunk Repetitive candidainfection
90. Infections Many common infections are more frequent and severe in the diabetic population “malignant” or invasive otitisexterna Pneumonia UTI Skin and soft tissue infections
91. Hypoglycemia Glucose level <55 mg/dL with symptoms that are relieved promptly after the glucose level is raised Most convincingly documented by Whipple’s triad Symptoms consistent with hypoglycemia Low plasma glucose concentration measured with a precise method (not a glucose monitor) Relief of symptoms after the plasma glucose is raised
93. Hypoglycemia Etiology and pathophysiology Most commonly a result of the treatment of diabetes Hypoglycemia in diabetes Impact and frequency More common in type 1 DM Pts suffer an average of twice a week with symptomatic hypoglycemia and once a year with a severe episode 2-4% die as a result of hypoglycemia Occurs in type 2 DM with sulfonylureas or insulin
94. Hypoglycemia Hypoglycemia in diabetes Conventional risk factors Relative or absolute insulin excess Insulin dose is excessive, ill-timed or the wrong type Influx of exogenous glucose is reduced (missed meal) Glucose utilization is increased (during exercise) Sensitivity to insulin is increased (improved glycemic control, increased fitness or weight loss) Endogenous glucose production is reduced (alcohol ingestion) Insulin clearance is reduced (renal failure)
96. Hypoglycemia Postprandial (reactive) hypoglycemia Occurs exclusively after meals Diagnosis requires documentation of Whipple’s triad after a mixed meal Early - rapid discharge of ingested carbohydrate into the small bowel followed by rapid glucose absorption and hyperinsulinism Particularly associated with dumping syndrome after gastrectomy
99. Hypoglycemia Laboratory Tests If history suggests prior hypoglycemia and a potential mechanism isn’t apparent Obtain plasma glucose, insulin, C-peptide under conditions when hypoglycemia would be expected, typically during fasting Treatment 3 glucose tablets (20g), 4 oz of juice, 6 oz of soda, or 7 lifesavers – if pt is able and willing 25g IV glucose or 1mg SC or IM glucagon - if pt is unable or unwilling to take orally
100. Hypoglycemia Treatment Fasting (postabsorptive) hypoglycemia Change dose of medication, no alcohol Endocrine tumor – surgical removal Reactive (postprandial) Hypoglycemia Dietary manipulation is an adjunct: reduce proportion of carbohydrates in the diet, increase the frequency and reduce the size of the meals
Why would a patient secrete less insulin?? Type 1 autoimmune disease where the islet cells in the pancreas have been destroyed by antibodies and no longer produce insulin. Type II the body has been exposed to high levels of blood glucose for so long that it is desensitized to elevated sugar and produces less insulin. Also, for the same reason, the pancreas wears out from producing increased insulin for an extended period of time and therefore no longer can produce insulin in sufficient levels.
