Diabetes Mellitus: “Not So Sweet” Prutha Dave, RN, BSN davep@alverno.edu MSN 621 Spring 2009 Alverno College

Let’s Learn About Type II Diabetes: Home Page Click Below For Instructions On Navigating the Tutorial: Tutorial Objectives Navigation Quick Facts Patho & Genetics Mini Quiz Click Below To Take The Pre-Test: Signs & Symptoms Mini Quiz Pre - Test Tests & Diagnosis Mini Quiz Click Below To Start The Tutorial: Treatment & Medications Mini Quiz Tutorial Patient Education Mini Quiz Image retrieved with permission from:http://www.fredscorner.nl/animations.html

Navigation Click on to go to next slide. Click on to go back to previous slide. Click on to go to the home page. Click on to return back to where you were. Click on to learn more about the topic. Role the mouse over or click underlined words to learn more about them. Click on to take a quick quiz after each section. Mini Quiz Note: An incorrect answer page will ONLY allow you to return BACK to the QUESTION.

Objectives of this Tutorial After completion of this tutorial the participant will gain a better understanding of Diabetes Mellitus, also known as Type II Diabetes. Also the participant will be able to care for a patient with the disease more effectively. Topics Covered include: Pathology & Causes. Symptoms & Treatment. Labs/Diagnosis & Patient Education.

Quick Facts In type 2 diabetes, either the body does not produce enough insulin or the cells ignore the insulin. There are 23.6 million children and adults in the United States, or 7.8% of the population, who have diabetes. Significant risk factor for coronary heart disease and stroke. Leading cause of blindness and end stage renal disease. Major contributor to lower extremity amputations. Can be successfully managed with the right patient education. Usually affects older adults but becoming common in obese adolescents. Image retrieved with permission from: http://www.india-shopping.net/india-ayurveda-products/image/diabetes.gif

1. How is Diabetes diagnosed? a. Two separate fasting glucose measurements of 126 mg/dL or higher b. Using symptoms such as polydypsia, polyphagia, and polyuria c. A hemoglobin A1C level of 6.5%

Image retrieved from: Prutha Dave`Family Photos Correct! Yay! Great Job! Two measurements are required to ensure reproducibility and therefore decrease false positives and increase specificity. Image retrieved from: Prutha Dave`Family Photos

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2. A deficiency in which of the following results in hyperglycemia? a. Glucagon b. Insulin c. Ketones d. Cortisol

Correct! Yay! INSULIN helps to LOWER blood glucose concentration by MOVING GLUCOSE into BODY TISSUES for energy Image retrieved with permission from:http://www.fredscorner.nl/animations.html

3. What is the Metabolic Syndrome? Seen in patients with very slow metabolism b. Seen in patients who lack growth hormone, insulin, and cortisol c. Seen in patients with the following cluster of abnormalities: obesity, hyperlipidemia, hypertension, and glucose intolerance

Image retrieved from: Prutha Dave`Family Photos Correct! Yay! Metabolic syndrome is a combination of abnormalities including high triglycerides, low HDL’s, HTN, and inflammation. Image retrieved from: Prutha Dave`Family Photos

4. Which of the following class of oral hypoglycemic medications can cause excessive hypoglycemia? a. Biguanides (Metformin) b. ACE inhibitors (Lisinopril, Captopril) c. Sulfonylureas (Glyburide, Glipizide) d. Statins (Lipitor, Crestor)

Image retrieved from: Prutha Dave`Family Photos Correct! Yay! Sulfonylureas increase insulin levels and the rate at which glucose is removed from the blood, it is important to know that they can cause hypoglycemic reactions. Image retrieved from: Prutha Dave`Family Photos

5. What are the most common signs of Type II Diabetes? a. Palpitations, restlessness, and diarrhea b. Dehydration, hypotension, and fatigue c. Excessive laughter, bad body odor, and hair loss d. Weight gain, blurred vision, and excessive thirst

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Pathophysiology Can be due to absolute insulin deficiency or insulin resistance A metabolic disorder which is characterized by disturbances in carbohydrate, lipid, and protein metabolism caused by an imbalance between insulin availability and insulin need Results in an inability to transport glucose into the cells of the body, thus causing a breakdown of fat and muscle protein (Porth, 2005) Image retrieved with permission from:http://professional.diabetes.org/Multimedia_Display.aspx?TYP=8&CID=53310

Video: What Happens in Type II Diabetes? Click On Video To View Video retrieved from with permission from: http://professional.diabetes.org/ResourcesForProfessionals.aspx?typ=17&cid=60425

Insulin A polypeptide which has a direct effect in lowering blood glucose level Three actions: Promotes glucose uptake by target cells and provides for storage as glycogen Prevents fat and glycogen breakdown Increases protein synthesis by inhibiting gluconeogenesis

Insulin Production Made by the beta cells of the pancreas (islets of Langerhans) Composed of two polypeptide chains: A and B Initially made as a larger molecule: proinsulin and then cleaved to the active form of insulin Other cleavage product is the inactive C-peptide

Insulin Release Glucose enters cell Glycolysis makes ATP ATP production causes K+ channel to close and depolarize the cell Depolarization opens voltage sensitive Ca2+ channels (Ca2+ enters cell) Ca2+ influx causes insulin release by exocytosis Image retrieved with permission from http://professional.diabetes.org/Multimedia_Display.aspx?TYP=8&CID=53313

Insulin Action Travels through the portal circulation to the liver Binds to membrane receptor Activates intracellular enzymes to increase protein, glycogen, and fat synthesis, as well as increasing glucose transporters Image received with permission from: http://upload.wikimedia.org/wikipedia/commons/thumb/8/8c/Insulin_glucose_metabolism.jpg/400px-Insulin_glucose_metabolism.jpg

Glucagon: Another Polypeptide Antagonist of Insulin Released during periods of fasting to maintain blood glucose Released by pancreatic alpha cells Causes glycogen breakdown, gluconeogenesis, protein degradation, all resulting in elevation of blood glucose In diabetes, can have a negative effect as glucagon production goes unchecked as cells are starved of glucose resulting in exacerbation of hyperglycemia Image retrieved with permission from: http://www.endocrineweb.com/insulin.html

Pathogenesis Genetic and Environmental factors can lead to insulin resistance & decreased release. This causes decreased glucose uptake and increased glucose output resulting in hyperglycemia and Type II Diabetes. Image received with permission from:http://professional.diabetes.org/Multimedia_Display.aspx?TYP=8&CID=53319

Beta Cell Dysfuntion: Another Sign Initial decrease in beta cell mass. Increased apoptosis of cell and decreased regeneration. Long standing insulin resistance – causing the beta cells to get TIRED. Glucotoxicity, Lipotoxicity. Amyloid disposition causing dysfuction. (Porth, 2005) Image retrieved with permission from: http://www.bodyclinicindonesia.com/library/beta_cell.jpg

Genetics and Diabetes Mellitus There is a strong inheritance pattern for Type II Diabetes and it is a heterogeneous condition. Two major sets of factors play a role in the development of Diabetes Mellitus: Genetic Factors Environmental Factors

Genetic Factors Research shows that Diabetes Mellitus is polygenic  Meaning that it has different combinations of gene defects. Multiple “diabetogenic genes” or polymorphisms, each insufficient in themselves, must be present in order to cause diabetes. Click to Learn about Specific Candidate Genes Associated with DM These genetic polymorphisms can affect the utilization of blood glucose. (Radha et al, 2003)

Polymorphic Genes : Defects to Diabetes Mutations in the following “candidate” genes are seen in persons with Type II Diabetes and may directly contribute to the onset of the disease: *Click To Learn About Specific Genes Genes Related to Insulin Secretion Genes Related to Insulin Resistance Genes Related to Obesity

Insulin Secretion Genes Human Insulin Gene (INS) –transcription of the insulin gene is the restricting step for insulin synthesis and secretion. Beta Cell Genes (SUR/KIR 6.2) – these genes encode components of the B-Cell K ATP channel which mediate glucose metabolism and membrane depolaration to cause insulin realease. Pancreatic Duodenal Homedomain Gene (PDX 1) – a transcription factor gene which regulates pancreatic devleopment and islet cell function. (Radha et al, 2003) Images retrieved from: Microsoft Word Clipart 2003

Insulin Resistance Genes Glucose Transporter Gene (GLUT) – acts as a sensor to the B-cell and as a major signaling molecule. Peroxisome Proliferator Activated Receptor Gene y (PPAR-y) – a transcription factor gene associated in the regulation of adipocyte gene expression and glucose metabolism. Insulin Receptor Substrate Gene (IRS) – this gene is shown to be associated with decreased insulin sensitivity. (Radha et al, 2003) Images retrieved from: Microsoft Word Clipart 2003

Obesity Related Genes Research has shown that variations in obesity genes have resulted in insulin resistance followed with the onset of Diabetes Mellitus. (Radha et al, 2003) Adiponectin Genes CLICK TO DISCOVER MORE Single nucleotide polymorphisms within this gene have been associated with a risk for Type II Diabetes. Leptin Receptor Genes CLICK TO DISCOVER MORE Mutations of this gene have been associated with hyperglycemia. Uncoupling Protein 2 Genes CLICK TO DISCOVER MORE Studies with these genes have shown to be associated with obesity and DM. Mutations may also cause interference with glucose homeostasis.

Environmental Factors The complex interactions between genes and the environment make it difficult to identify a single factor that leads to Diabetes Mellitus. (Radha et all, 2003) Environmental Factors Include: Central Obesity Lack of Activity Uncontrolled Diet Viruses Toxins (Smoking)

What is one function of insulin? MINI QUIZ: TEST YOUR KNOWLEDGE What is one function of insulin? a. Promote weight loss b. Causes glycogen breakdown c. Increases protein synthesis d. Elevate blood glucose

Correct! Great Job! INSULIN promotes glucose uptake, prevents fat and glycogen breakdown, and Increases Protein Synthesis! Good Reading!

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The release of Glucagon has a positive effect on patients with Type II Diabetes: True or False? Image retrieved with permission from:http://www.fredscorner.nl/animations.html

Image retrieved from: Prutha Dave`Family Photos Correct! Great Job! Glucagon production can have a NEGATIVE effect if it goes unchecked as cells are starved of glucose resulting in exacerbation of hyperglycemia Image retrieved from: Prutha Dave`Family Photos

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Signs & Symptoms Sneaky onset Most common signs: The “Polys” Polyuria Polydipsia Blurred Vision Fatigue Skin Infections Paresthesias Weight loss at first Image retrieved with permission from: http://en.wikipedia.org/wiki/Diabetes

MINI QUIZ: TEST YOUR KNOWLEDGE Which symptom is the patient speaking of when she says she is having an abnormal touch sensation? Polyuria Gas Presyncope Paresthesias

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Tests and Diagnosis TESTS TO KNOW: Fasting Plasma Glucose: A blood test that measure the blood glucose level after a person has been fasting for at least eight hours. This is the fastest, most reproducible, and cheapest method to make the diagnosis. Oral Glucose Tolerance Test: A test in which a 75g dose of a sugary solution is given and then 2 hours later the blood glucose level is measured. This test is slightly more sensitive than the plasma glucose. Glycosylated Hemoglobin (HbA1c): Measures the percentage of red blood cells that have glucose bound to them and is useful in monitoring glycemic control. Not recommended for routine diagnosis. FASTING PLASMA GLUCOSE : CLICK TO LEARN MORE ORAL GLUCOSE TOLERANCE TEST : CLICK TO LEARN MORE HbA1c : CLICK TO LEARN MORE

How The Diagnosis is Made Normal Response Fasting Plasma Glucose (FPG) A fasting blood glucose level less than or equal to 110 mg/dl. This must be confirmed on a separate occasion. Oral Glucose Tolerance Test (OGTT) 2 hour postload glucose level of less than 140 mg/dl.

Impaired Fasting Glucose & Impaired Glucose Tolerance In essence, impaired fasting glucose and impaired glucose tolerance are the same thing, just measured differently. Impaired Fasting Glucose: A fasting glucose > 110 and < 126 mg/dl. This is considered a risk factor diabetes, but by itself, does not make the diagnosis of diabetes. The patient will require close monitoring. Impaired Glucose Tolerance: 2-hour glucose results from the OGTT that are > 140 and < 200 mg/dl.  This is also considered a risk factor for future diabetes.

A DIAGNOSIS OF DIABETES IS MADE WHEN: 1. Fasting Plasma Glucose level greater than 126 mg/dl on separate occasions. 2. Random blood glucose > 200 with classic symptoms. 3. Oral glucose tolerance tests show that the blood glucose level at 2 hours is > 200 mg/dl.  This must be confirmed by a second test on another day.

MINI QUIZ: TEST YOUR KNOWLEDGE Which of the following tests is not used for a routine diagnosis of Type 2 Diabetes? Fasting Glucose Oral Glucose HbA1c Finger Stick

Image retrieved from: Prutha Dave`Family Photos Correct! Great Job! Good Job. The HbA1C test is a measurement of glycosylated hemoglobin and is a useful tool for monitoring glycemic control but is not recommended for diagnostic purposes. Image retrieved from: Prutha Dave`Family Photos

Image retrieved from: Prutha Dave`Family Photos Almost! Try Again! Image retrieved from: Prutha Dave`Family Photos

True or False: For a diagnosis for Diabetes to be made a person must have a Fasting Plasma Glucose level greater than 126 mg/dl on only one occasion. True False

Image retrieved from: Prutha Dave`Family Photos Correct! Yaayy! Must have a Fasting Plasma Glucose of 126 mg/dl or higher on TWO occasions. Great Job! Image retrieved from: Prutha Dave`Family Photos

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Images retrieved from: Microsoft Word Clipart 2003 Treatments Aim to control blood glucose levels Oral medications which lower blood glucose by a variety of mechanisms Injectable Insulin which directly lowers blood glucose Prevention and reversal of diabetes can be achieved by a strict diet, exercise, and weight loss. Images retrieved from: Microsoft Word Clipart 2003

Oral Medications Drugs that cause increased insulin release Sulfonylureas (Glyburide, Glipizide) Sitagliptin (Januvia) *newer drug Exanatide (Byetta) *newer drug Drugs that sensitize cells to insulin Biguanides (Metformin) Thiazolidinediones (Rosiglitazone, Pioglitazone) Drugs that block carbohydrate absorption Acarbose CLICK TO REVEAL MEDICATIONS CLICK TO REVEAL MEDICATIONS CLICK TO REVEAL MEDICATIONS

CLICK TO LEARN THE MECHANISM Sulfonylureas Drugs such as Glipizide and Glyburide Mechanism: Stimulate insulin secretion by closing the Beta cell’s K+ channel causing depolarization and calcium influx. See prior slide Side Effects: Hypoglycemia Rashes GI upset Hyponatremia CLICK TO LEARN THE MECHANISM

CLICK TO LEARN MECHANISM Biguanides Major drug in this class is Metformin Mechanism: Makes liver more sensitive to insulin Great at inducing weight loss Side Effects: Diarrhea, abdominal pain Lactic Acidosis- serious and potentially fatal Thus avoid in patients with renal insufficiency, liver dysfunction or CHF CLICK TO LEARN MECHANISM

CLICK TO LEARN MECHANISM Thiazolidinediones Major drugs in this class are Rosiglitazone (Avandia) and Pioglitazone (Actos) Mechanism: Makes peripheral tissues such as fat and muscle more sensitive to insulin Side Effects: Weight gain Liver toxicity Fluid retention and edema Contradicted in CHF CLICK TO LEARN MECHANISM

CLICK TO LEARN THE MECHANISM Acarbose Mechanism: Inhibits enteric enzymes that break down complex carbohydrates, resulting in partial malabsorption of carbohydrates. Side Effects: Bloating Abdominal discomfort Diarrhea Flatulence CLICK TO LEARN THE MECHANISM

Insulin Formulations Regular Insulin- (Clear solution) Short acting insulin and the only form given IV. Lente and Ultralente- (Cloudy solutions) Intermediate and Long acting versions of insulin. NPH- (Cloudy solution) Intermediate acting insulin. Usually given Subcutaneously (SubQ).

Synthetic Insulin Modified to have either very short or long half lives. Insulin Lispro (Humalog) and Insulin Aspart (Novolog) have a quicker onset and shorter duration than Regular Insulin. Insulin Glargine (Lantus) is a very long acting form of insulin. All are administered subcutaneously.

Characteristics of Insulin Type Onset (hr) Peak (hr) Duration (hr) Regular 0.5 2-5 6-8 Lispro/Aspart 0.2 0.7 2 NPH 2-4 6-10 14-18 Lente 1-3 6-15 18-26 Ultralente 4-6 8-30 24-36 Glargine None (Andreoli, 2004)

Profile of Action Image retrieved with permission from: http://www.endotext.org/Diabetes/diabetes20/figures/figure7.png

Dosing Regimens Intermediate and long acting insulin's are given to mimic the body’s natural 24 hour basal insulin secretion. Short acting insulin's are given pre-prandially to mimic nutrient stimulated insulin secretion.

Sample Regimens Image retrieved with permission from: http://www.deo.ucsf.edu/images/graphs/graph_intense_type2.gif

Side Effects of Insulin Hypoglycemia – too much Insulin can cause an abnormal decrease in blood glucose resulting in hypoglycemia. Lipohypertrophy at injection site Edema Weight Gain Promotes atherosclerosis at high doses Image retrieved with permission from: Microsoft Clipart 2003

MINI QUIZ: TEST YOUR KNOWLEDGE Which of the following patients would you want to avoid giving a Biguanide to? Patients with hypothyroidism Patients with pneumonia Patients with renal insufficiency and CHF Patients with overactive bladders

Correct! Great Job! Image retrieved with permission from:http://www.fredscorner.nl/animations.html 67

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Fill In The Blank: ________ insulin is the only form of insulin given intravenously. NPH Regular Lantus Aspart

Correct! Yay! Image retrieved with permission from:http://www.fredscorner.nl/animations.html 70

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Patient Education Patient education will be the single most important factor on helping a newly diagnosed patient manage their Diabetes. CLICK ON THE STAR to learn about outcomes and guidelines for Registered Nurses who are initiating Diabetes Self management education: IMPORTANT !! Patient Education

Patient Education Describing the diabetes disease process and treatment options Incorporating nutritional management into lifestyle Incorporating physical activity into lifestyle Using medication(s) safely and for maximum therapeutic effectiveness Click Here To Learn More!! Click Here To Learn More!! Click here to Learn More!! Click Here To Learn More!! (Funnell et al, 2009)

Patient Education Monitoring blood glucose and other parameters and interpreting and using the results for self-management decision making Preventing, detecting, and treating acute and chronic complications Developing personal strategies to address psychosocial issues and concerns Developing personal strategies to promote health and behavior change Click Here To Learn More!! Click Here To Learn More!! Click Here To Learn More!! Click Here To Learn More!! (Funnell et al, 2009)

How To Educate Self Management Describing the Disease Process: before beginning education about the disease process, perform a patient assessment to gain a better understanding of the Patient’s background such as cultural beliefs as well as readiness to learn. Teaching Nutritional Management: first learn about the patients current diet and any cultural influences that may affect diet. Not every patient will eat the same or like the same food that is recommended. Physical Activity: always, always promote any physical activity. Help the patients transition into incorporating an exercise regimen which is appropriate for them. Again, know that each patient is exercise. Safe Medication Use: make sure the patient understands the medication and why and how it will help manage the disease. Speak clearly and use simple terms. Also, recommending The use of a medication box may be of great help for the newly diagnosed Diabetic.

How To Educate Self Management Blood Glucose Monitoring: help the patient understand the need for blood glucose monitoring. Make sure they know how to use their specific device and have them do a repeat demonstration for you. Preventing Complications: teach patients to watch out for any changes in health status, and what specific symptoms to be aware of. Examples are eye sight changes or numbness and tingling. Psychosocial Issues: Promote discussing any thoughts or feelings associated with the new Diabetes diagnosis. Provide resources for patients to use when dealing with difficult psychosocial issues or concerns. Promoting Health: Always promote healthy lifestyle behaviors such as quitting smoking, eating healthy, exercising, and using a family or personal support system to incorporate these behaviors.

MINI QUIZ: TEST YOUR KNOWLEDGE What is one of the most important nursing practices before beginning patient education for new onset Diabetes? Making sure that the patient has all their medications in hand. Making sure that they exercise everyday for 2 hours Assessing the patients background and readiness to learn.

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Name a way that patients can remember to safely take their medications? Keep all their medication in one bottle.Slide 82 Just double up on medications the next day if they forget. Obtain a medication pill box with the days listed and with separate compartments for each day.

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The End : Credits *Thank you to my dear husband who put up with me through this crazy semester and for all his medical and technical expertise. *Thank you to my mom who motivated me to pursue my knowledge in Diabetes. Image retrieved with permission from:http://www.fredscorner.nl/animations.html

References American Diabetes Association, www.diabetes.org. Andreoli, T.E., & Carpenter, C.J., & Griggs, R.C., & Loscalzo, J. (2004) Cecil Essentials of Medicine. Philadelphia: Saunders. Funnell, M. et al. (2009) National Standards for Diabetes Self-Management Education, American Diabetes Association Diabetes Care, 32, S87-S94 DOI: 10.2337/dc09-S087 Hansen, L. (2003). Candidate genes and late-onset type 2 diabetes mellitus. Susceptibility genes or common polymorphisms? [Electronic Version]. Dan Med Bull, 50(4), 320-46. Jochen, A.L. (2005) Pharmacology of Insulin and Oral Sulfonylureas. Medical Pharmacology. Porth, C.M. (2005) Pathophysiology: Concepts of Altered Health States. Philadelphia: Lippincott Williams & Wilkins. Radha, V., & Vimaleswaran K.S., & Deepa R., & Mohan, V. (2003). The genetics of diabetes mellitus. Indian J Med Res, 117, 225-238. Rossini, A.A., & Mordes, J.P., & Handler, E.S. (1988). Perspectives in Diabetes: Speculations on Etiology of Diabetes Mellitus: Tumbler Hypothesis [Electronic Version]. Diabetes, 37, 257-61.