Diabetes Mellitus Part 1 Slides F2024 final student version PDF

Diabetes Mellitus Week 4 Prof. Elliott Diabetes Learning Objectives  Describe how the body obtains energy during a fasting state.  Describe the pathophysiology of diabetes and include the following hormones; insulin and counterregulatory hormones (specifically glucagon)....

Diabetes Mellitus Week 4 Prof. Elliott Diabetes Learning Objectives  Describe how the body obtains energy during a fasting state.  Describe the pathophysiology of diabetes and include the following hormones; insulin and counterregulatory hormones (specifically glucagon).  Describe the difference between endogenous and exogenous insulin.  Describe the differences between type 1 and type 2 DM.  What are the main signs and symptoms of type 1 and type 2 DM?  Describe the hemoglobin A1C test and its importance in diagnosing the monitoring DM.  Describe how to correctly teach your client to perform self- monitoring of blood glucose (accuchecks). How does this differ from a nurse performing accuchecks in an agency setting? 2 Diabetes Learning Objectives Describe the nutritional recommendations of a diabetic client. Discuss exercising with diabetes. Explain how illness changes the management of DM and how would you educate your client to care for themselves during a minor illness at home Discuss how stress/surgery changes the need for insulin? Discuss the reason for the 2 different routes of insulin. Can insulin be ingested? Why or why not? Compare and contrast the different types of insulin with regards to their onset, peak and duration of action. Include when the client should eat after administration of each type of insulin. Why is the intensive insulin therapy the preferred regimen to manage diabetes? 3  Definition  A chronic multisystem disease related to: Adults with  Abnormal insulindiabetes production have heart  Impaired insulin utilization disease death rates 2 to 4 times  or both higher than adults without diabetes.  Approximately 65 to 80% of people with The mellitus diabetes risk for(DM) stroke isasalso will die 2 to 4 a result of heart times disease or stroke higher among (CVA).people with  Canadians with DM are 2x as likely to die prematurely thandiabetes. people without DM 4 Etiology and Pathophysiology  Insulin  Promotes glucose transport from bloodstream into the cell  Decreases glucose in the bloodstream 5 Etiology and Pathophysiology 6 Deep Internal Anatomy Carbohydrates – glucose Cells need glucose Glucose needs insulin Insulin & Glucagon © Pat Thomas, 2006. Elsevier items and derived items © 2008, 2004, 2000, 1996, 1992 by Saunders, an imprint of Elsevier Inc. 7  Normal Insulin Secretion Bolus Insulin Basal Insulin Fig. 52-1. Normal endogenous insulin secretion. In the first hour or two after meals, insulin concentrations rise rapidly in blood and peak at about 1 hour. After meals, insulin concentrations promptly decline toward preprandial values as carbohydrate absorption from the gastrointestinal tract declines. After carbohydrate absorption from the gastrointestinal tract is complete and during the night, insulin concentrations are low and fairly constant, with a slight increase at dawn. Copyright © 2014 Elsevier Canada, a division of Reed Elsevier Canada, Ltd. 8  Etiology and Pathophysiology Insulin Stimulates storage of glucose as glycogen in liver and muscle Inhibits gluconeogenesis Enhances fat deposition ↑ protein synthesis The fall in insulin level during normal overnight fasting facilitates the release of stored glucose from the liver, protein from muscle, and fat from adipose tissue. 9 52-10 Negative Feedback  Blood glucose level rises, pancreas secretes insulin  Blood glucose level falls, pancreas secretes glucagon Etiology and Pathophysiology  Counterregulatory hormones  Oppose the effects of insulin  Increase blood glucose levels  Helpmaintain normal blood glucose levels  Examples:  Glucagon,epinephrine, growth hormone, cortisol 12  A client with diabetes mellitus visits a primary care clinic. The client’s diabetes mellitus previously had been well controlled with glyburide daily, but recently the fasting blood glucose level has been 10.2 to 11.4 mmol/L. Which medication, if added to the client’s regimen, may have contributed to the hyperglycemia? A. Prednisone B. Atenolol C. Phenelzine D. Allopurinol 13 Etiology and Pathophysiology  Fasting State  Counter-regulatory hormones (especially glucagon) stimulate glycogen glucose  When glucose unavailable during fasting state  Lipolysis (fat breakdown)  Proteolysis (amino acid/protein breakdown) 14 40-15 15 Etiology and Pathophysiology Two most common types  Type 1  Type 2 Other common types  Prediabetes  Gestational Diabetes  Secondary Diabetes 16 Diabetes Mellitus (DM) Type 1 DM Type 2 DM  No  ↓ Insulin secretion insulin secretion and/or  ↓ sensitivity to insulin  Treatment:  Treatment:  Lifestyle modifications  Lifestyle and possibly: modifications  Oral antihyperglycemic  Insulin agents (OHAs) and/or  Insulin Type 1 Diabetes Mellitus  Most often occurs in children and people younger than 30 years of age Type 1 diabetes mellitus accounts for approximately 5% to 10% of all people with diabetes. 40% of those with type 1 diabetes mellitus have onset before the age of 20 years. The incidence of type 1 diabetes has increased by 3% to 5% over recent decades. 18 Type 1 Diabetes Mellitus Etiology and Pathophysiology  Result of longstanding process:  Progressive destruction of pancreatic  cells by body’s own T cells  Autoantibodies cause a reduction of 80% to 90% in normal -cell function before manifestations occur 19 Type 1 Diabetes Mellitus Etiology and Pathophysiology  Causes:  Genetic predisposition  Exposure to a virus  Idiopathic 20 Type 1 Diabetes Mellitus Onset of Disease  Long preclinical period  Antibodiespresent for months to years before symptoms occur Sudden develop  Manifestations weightwhen loss the pancreas can no longer produce Polydipsia insulin Polyuria  Rapid onset of symptoms Polyphagia 21 A patient is admitted with clinical manifestations of diabetes mellitus. Which findings is the nurse most likely to observe? Select all that apply  A. Excessive thirst  B. Weight gain  C. Constipation  D. Excessive hunger  E. Frequent urination 22 Type 1 Diabetes Mellitus Onset of Disease 23 Clinical Manifestations Type 1 Diabetes Mellitus  Classic symptoms  Polyuria (frequent urination)  Polydipsia (excessive thirst)  Polyphagia (excessive hunger)  Weight loss  Weakness  Fatigue 24 A patient with Type I diabetes typically has the following clinical presentation?  A.Thin, young with ketones in the urine  B. Overweight, young with no ketones present in the urine  C.Thin, older adult with glycosuria  D.Overweight, adult-aged with ketones present in the urine 25 Prediabetes  Individuals already at risk for diabetes  Blood glucose high but not high enough to be diagnosed as having diabetes  Characterized by impaired fasting glucose and impaired glucose tolerance  (6.1–6.9 mmol/L for impaired fasting glucose [IFG] and 7.1–11 mmol/L for impaired glucose tolerance [IGT]) 26 Prediabetes Test Result Dysglyce mia Category Fasting 6.1 to 6.9 Impaired plasma mmol fasting Glucose glucose A1C 6.0 to 6.4% Prediabetes OGTT 7.8 – 11.0 Prediabetes mmol/L 27 Prediabetes  Long-term damage already occurring  Heart, blood vessels  Usually present with no symptoms  Must watch for diabetes symptoms  Polyuria  Polyphagia  Polydipsia 28 A nurse working in an outpatient clinic plans a screening program for diabetes. Which of the following findings would indicate the patient has prediabetes. Select all that apply a. fasting glucose of 6.5 mmol/L b. hemoglobin A1C of 6.3% c. Glucose tolerance test 10 mmol/L d. fasting glucose of 5 mmol/L e. hemoglobin A1C 8 % 29 Type 2 Diabetes Mellitus  Most prevalent type of diabetes  Usually occurs in people over 35 years of age  “Dia-besity”  [risk ↑ with weight but be careful about body shaming/judgments]  Genetic basis  Greater in some high-risk populations  Increased rate in people of Indigenous, Latin American, South Asian, Asian, or African descent 30 Type 2 Diabetes Mellitus Etiology and Pathophysiology  Pancreascontinues to produce some endogenous insulin.  Insulin produced is insufficient or is poorly utilized by tissues. 31 Type 2 Diabetes Mellitus Etiology and Pathophysiology  Obesity (abdominal/visceral)  Most powerful risk factor  Genetic mutations  Lead to insulin resistance  Increased risk for obesity 32 Type 2 Diabetes Mellitus: Etiology and Pathophysiology  Four major metabolic abnormalities  1. Insulin resistance  Body tissues do not respond to insulin.  Insulin receptors are either unresponsive or insufficient in number.  Results in hyperglycemia 52-33 33 Type 2 Diabetes Mellitus: Etiology and Pathophysiology  2. Pancreas ↓ ability to produce insulin  β Cells fatigued from compensating  β-Cell mass lost  3. Inappropriate glucose production from liver  The liver’s response of regulating release of glucose is haphazard.  Not considered a primary factor in development of type 2 52-34 34 Type 2 Diabetes Mellitus: Etiology and Pathophysiology  4. Alteration in production of hormones and adipokines  Play a role in glucose and fat metabolism  Contribute to pathophysiology of type 2 diabetes  Two main adipokines  Adiponectin and leptin Individuals with metabolic syndrome at increased risk for type 2 diabetes mellitus  Cluster of abnormalities that increase risk for cardiovascular disease and diabetes  Characterized by insulin resistance 52-35 35 Gestational Diabetes  Develops during pregnancy  Detected at 24 to 28 weeks of gestation  Usually, normal glucose levels at 6 weeks post partum 36 Secondary Diabetes  Results from another medical condition:  Schizophrenia  Cushing’s syndrome  Hyperthyroidism  Immunosuppressive therapy  Parenteral nutrition  Cystic fibrosis  Usually resolves when underlying condition treated 37 Type 2 Diabetes Mellitus Onset  Gradualof Disease onset  Person may go many years with undetected hyperglycemia  Osmoticfluid/electrolyte loss from hyperglycemia may become severe  Hyperosmolar coma 38 Clinical Manifestations: Review Type 1 Diabetes Mellitus  Classic symptoms  Polyuria (frequent urination)  Polydipsia (excessive thirst)  Polyphagia (excessive hunger)  Weight loss  Weakness  Fatigue 52-39 39 Clinical Manifestations Type 2 Diabetes Mellitus  Nonspecific symptoms  May have classic symptoms of type 1  Fatigue  Weakness  Recurrent infections  Recurrent vaginal yeast infections  Prolonged wound healing  Visual changes 40 A patient with Type 2 diabetes may have all of the following except:  A. Blurry vision  B. Ketones in the urine  C. Glycosuria  D. Poor wound healing 41 Diagnostic Criteria:  Fasting plasma glucose over 7 mmol/L FPG ≥7.0 mmol/L Fasting = no caloric intake for at least 8 hours or A1C ≥6.5% (in adults) (Glycated hemoglobin) Using a standardized, validated assay, in the absence of factors that affect the accuracy of the A1C and not for suspected type 1 diabetes or 2hPG in a 75-g OGTT ≥11.1 mmol/L or Random PG ≥11.1 mmol/L CDA (2013) clinical guidelines, LHS 2011; Adams 2010 42 Random= any time of the day, without regard to the interval since 42 the last meal Diabetes Mellitus Diagnostic Studies  Hemoglobin A1C test  Recommended to be used as a diagnostic test  Useful in determining glycemic levels over the past 3 months  Shows the amount of glucose attached to hemoglobin molecules over RBC life span (~ 120 days)  Regular assessments required  Ideal goal: ≤7.0%  Normal range is 4 mmol/L Patient should eat regularly scheduled meal/snack to prevent rebound hypoglycemia One protein, one starch Check blood sugar again 45 minutes after treatment. 87 Hypoglycemia 88 Hyperglycemia Elevated (High) blood glucose Gradual onset of S&S Clinical manifestations include: Abdominal cramps Blurred vision Headache Glycosuria Increased urination Nausea, vomiting Weakness, fatigue Confusion, coma, death 89 Hypoglycemia results in which of the following? Select all that apply  A. Bradycardia  B. Diaphoresis  C. Palpitations  D. Clammy skin  E. Tremors