MASTERS (MSN) PRESENTATION FOR DIABETES MELLITUS

Diabetes mellitus education

1. Diabetes Mellitus: Type 1 and Type 2 This Photo by Unknown Author is licensed under CC BY-NC-ND By Jordan Hart RN BSN

2. AGENDA LEARNING OBJECTIVES By the end of this lesson to student will be able to describe and understand the following: understanding of pathophysiology regarding diabetes (type 1 and 2) understanding of risk factors in developing type 2 diabetes understanding of signs and symptoms of diabetes with diagnoses and treatments understanding of key terms and elements in understanding the disease process of diabetes understanding of lifestyle accommodations involved in diabetes understanding of ways to monitor blood glucose and monitor for emergencies such as HHS and DKA

3. Anatomy and Physiology of the Pancreas This Photo by Unknown Author is licensed under CC BY-SA-NC

4. Anatomy and Physiology of the Pancreas The pancreas is an accessory organ and exocrine gland of the digestive system, as well as a hormone producing endocrine gland Its endocrine function involves the release of insulin and glucagon into the bloodstream, two important hormones responsible for regulating glucose, lipid, and protein metabolism The pancreas aids in hormonal regulation by releasing insulin (beta cells) and glucagon (alpha cells) The pancreas is in the epigastric, left hypochondriac, and a portion of the umbilical abdominal regions Insulin and Glucagon play a delicate balanced role in regulating the blood glucose levels Moore, K. L., Dalley, A. F., & Agur, A. M. R. (2014). Clinically Oriented Anatomy (7th ed.). Philadelphia, PA: Lippincott Williams & Wilkins

5. Defining Diabetes Mellitus (DM) Diabetes is primarily a disorder of carbohydrate metabolism; however, insulin deficiency disrupts metabolism of proteins and lipids as well. Symptoms mainly result from a deficiency of insulin, from cellular resistance to insulin’s actions, or both (Lehne et al., 2021) leads to an increased concentration of glucose in the bloodstream (hyperglycemia) 3 different types of DM Type 1 DM Type 2 DM Gestational DM Pathophysiology of DM Type 1: characterized by autoimmune destruction of pancreatic beta cells, resulting in absolute insulin deficiency Type 2: primarily arises from insulin resistance in peripheral tissues, often coupled with progressive beta cell dysfunction Lehne, R. A., Burchum, J. R., Rosenthal, L. D., Jones, B. O., & Neumiller, J. J. (2021). Lehne’s Pharmacology for Nursing Care . http://repository.poltekkes-smg.ac.id/index.php?p=show_detail&id=17425&keywords =

6. Types of Diabetes Mellitus

7. Type 1 dm Known as insulin dependent DM Accounts for 5% of all DM cases T1DM can develop at any age, but it usually develops during childhood or adolescence. Very common to develop ketoacidosis primary defect in T1DM is destruction of pancreatic beta cells, the cells responsible for insulin synthesis Insulin levels are reduced early in the disease and usually fall to zero late Beta cell destruction is the result of an autoimmune process Autoimmune process in T1DM leads to patient’s immune system inappropriately wages war against its own beta cells Possible trigger genetics, environmental, infectious factors Lehne, R. A., Burchum, J. R., Rosenthal, L. D., Jones, B. O., & Neumiller, J. J. (2021). Lehne’s Pharmacology for Nursing Care. http://repository.poltekkes-smg.ac.id/index.php?p=show_detail&id=17425&keywords=

8. Type 2 DM Most prevalent form of DM, 90 to 95% of cases Can begin at any ag, but most common in middle age population Little risk for ketoacidosis In contrast to patients with T1DM, many people with T2DM are capable of insulin synthesis insulin is still produced; its secretion is no longer tightly coupled to plasma glucose content, release of insulin is delayed, and peak output is subnormal The liver, muscles, and adipose tissue (target tissue for insulin) exhibit insulin resistance Decreased insulin resistance in these tissues lead to cells that are less able to take up and metabolize the glucose available to them T2DM is tightly linked to weight gain and obesity. Lehne, R. A., Burchum, J. R., Rosenthal, L. D., Jones, B. O., & Neumiller, J. J. (2021). Lehne’s Pharmacology for Nursing Care. http://repository.poltekkes-smg.ac.id/index.php?p=show_detail&id=17425&keywords=

9. Gestational DM diabetes that appears in the pregnant patient during pregnancy and then subsides after delivery the placenta produces hormones that antagonize insulin’s actions production of cortisol, a hormone that promotes hyperglycemia, increases threefold during pregnancy Increased cortisol and placental actions can lead to possible increase in the body's need for insulin glucose can pass freely from the maternal circulation to the fetal circulation hyperglycemia in the mother will stimulate excessive secretion of insulin in the fetus The resultant hyperinsulinism can have multiple adverse effects on the fetus Lehne, R. A., Burchum, J. R., Rosenthal, L. D., Jones, B. O., & Neumiller, J. J. (2021). Lehne’s Pharmacology for Nursing Care. http://repository.poltekkes-smg.ac.id/index.php?p=show_detail&id=17425&keywords=

10. Characteristics Type 1 DM Type 2 DM Age of Onset Usually, childhood or adolescence Usually older than 40 years; however, this is occurring more and more frequently among younger people Etiology Autoimmune process Unknown, but there is a strong familial association, suggesting heredity is a risk factor Insulin levels Reduced early in the disease and completely absent later Levels may be low (indicating deficiency), normal, or high (indicating resistance) Blood glucose Levels fluctuate widely in response to infection, exercise, and changes in caloric intake and insulin dose Levels are generally more stable than in type 1 diabetes Speed of onset Abrupt Gradual Body composition Usually thin and undernourished at diagnosis Frequently Obese Ketosis Common, especially if insulin dosage is insufficient Uncommon https://youtu.be/bFnO8Uc9gjQ Lehne, R. A., Burchum, J. R., Rosenthal, L. D., Jones, B. O., & Neumiller, J. J. (2021). Lehne’s Pharmacology for Nursing Care. http://repository.poltekkes-smg.ac.id/index.php?p=show_detail&id=17425&keywords=

11. Risk factors for DM Obesity Race Hypertension Physical activity Familial history Gestational diabetes Vera, M. V. (2024, April 29). 20 diabetes mellitus nursing care plans. Nurseslabs. https://nurseslabs.com/diabetes-mellitus-nursing-care-plans/

12. Clinical Manifestations Polyuria, Polydipsia, Polyphagia Fatigue, weakness, sudden vision changes, tingling or numbness in hands or feet, dry skin, sores that heal slowly and recurrent infection Onset of type 1 diabetes may be associated with nausea, vomiting, or stomach pains Increased blood glucose level (hyperglycemia) Weight loss (T1DM) or gain (T2DM) Vera, M. V. (2024, April 29). 20 diabetes mellitus nursing care plans. Nurseslabs. https://nurseslabs.com/diabetes-mellitus-nursing-care-plans/

13. Key Terms and Diagnostics of DM

14. Key terms and diagnostics Polyuria. Increased urination due to excess loss of fluid caused by osmotic diuresis. Polydipsia. Increased thirst because of fluid loss and dehydration. Polyphagia. Increased appetite resulting from the catabolic state caused by insulin deficiency and breakdown of proteins and fats. Fasting plasma glucose tolerance test (FPG)= 126 mg/dL or greater Glycosylated Hemoglobin(HbA1c) = 6.5% or greater Random Plasma Glucose test = 200 mg/dL or greater https://youtu.be/iUlYRyvQAIE Vera, M. V. (2024, April 29). 20 diabetes mellitus nursing care plans. Nurseslabs. https://nurseslabs.com/diabetes-mellitus-nursing-care-plans/ Oral Glucose Tolerance test (OGTT) = 200 mg/dL or greater (done usually if FPG could not lead to definite diagnoses

15. Management of diabetes

16. Treatment via medications: Type 1 versus type 2 Type 1 Diabetes Mellitus Type 2 Diabetes Mellitus integrated program of diet, self-monitoring of blood glucose, physical activity, and insulin replacement survival requires daily dosing with insulin essential to coordinate insulin dosage with carbohydrate intake Unsuccessful control can lead to hyper- or hypo- glycemia preventing long-term complications requires a comprehensive treatment plan Lifestyle measures (diet and physical activity) and drug therapy T2DM can be treated with a variety of oral and injectable drugs Most common oral drug is metformin (Glucophage), most common injectable is Insulin IV radiocontrast media that contain iodine pose a risk for acute renal failure, which could exacerbate metformin-induced lactic acidosis. To reduce risk, patients should discontinue metformin a day or two before elective radiography Rapid insulin- meals eaten at same time as injection Short-acting insulin-meals eaten within 30-60 mins of injection Intermediate-acting insulin- covers insulin needs overnight Lehne, R. A., Burchum, J. R., Rosenthal, L. D., Jones, B. O., & Neumiller, J. J. (2021). Lehne’s Pharmacology for Nursing Care. http://repository.poltekkes-smg.ac.id/index.php?p=show_detail&id=17425&keywords=

17. Lifestyle accommodations Make sure to check blood sugar before and after exercising Mayo Clinic. (2024, March 27). Diabetes - diagnosis and treatment - Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/diabetes/diagnosis-treatment/drc-20371451

18. Monitoring Blood Glucose General Glycemic Treatment Targets for Nonpregnant Adults with DM A1C < 7.0% Premeal plasma glucose 80-130 mg/dL Peak post meal plasma glucose <180 mg/dL These ranges depend on : Duration of diabetes Age/life expectancy Comorbid conditions Known cardiovascular disease or advanced microvascular complications Hypoglycemia unawareness Other individualized considerations Self-Monitoring of Blood Glucose (SMBG) Recommended for all patients who use insulin Glucometers are mainly used via finger prick that uses a small drop of capillary blood on a chemically treated strip Rapid test results Continuous Glucose Monitoring (CGM) CGM measures interstitial glucose (which correlates well with plasma glucose) Worn for a period of time (6 to 7 days) Reads interstitial glucose every 5 min or so (depending on device chosen) programmed to include sophisticated alarms for hypoglycemic and hyperglycemic excursions and can interface with insulin pumps and even smartphones Monitoring of Hemoglobin A1C provides an index of average glucose levels over the prior 2 to 3 months Provides a picture of long-term glycemic control no substitute for SMBG because A1C tells us nothing about acute, hour-to-hour swings in blood glucose Lehne, R. A., Burchum, J. R., Rosenthal, L. D., Jones, B. O., & Neumiller, J. J. (2021). Lehne’s Pharmacology for Nursing Care. http://repository.poltekkes-smg.ac.id/index.php?p=show_detail&id=17425&keywords=

19. PREVENTING HYPERGLYCEMIC EMERGENCIES FROM DM

20. Diabetic ketoacidosis (DKA) https://youtu.be/99KimaS6tTU VS HYPEROSMOLAR HYPERGLYCEMIC STATE (HHS) >250

21. Hyperglycemia vs hypoglycemia Charleson, K. (2024, January 17). Hypoglycemia vs. hyperglycemia. Verywell Health. https://www.verywellhealth.com/hypoglycemia-vs-hyperglycemia-5179943

22. THANK YOU Jordan Hart RN, BSN This Photo by Unknown Author is licensed under CC BY-ND