Presentation on theme: "Diabetes Mellitus: “Not So Sweet”"— Presentation transcript:
1Diabetes Mellitus: “Not So Sweet” Prutha Dave, RN, BSNMSN 621 Spring 2009Alverno College
2Let’s Learn About Type II Diabetes: Home Page Click Below For InstructionsOn Navigating the Tutorial:Tutorial ObjectivesNavigationQuick FactsPatho & GeneticsMini QuizClick Below To Take The Pre-Test:Signs & SymptomsMini QuizPre - TestTests & DiagnosisMini QuizClick Below To Start The Tutorial:Treatment & MedicationsMini QuizTutorialPatient EducationMini QuizImage retrieved with permission from:http://www.fredscorner.nl/animations.html
3Navigation 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 QuizNote: An incorrect answer page will ONLY allow you to return BACK to the QUESTION.
4Objectives 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.
5Quick FactsIn 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:
61. How is Diabetes diagnosed? a. Two separate fasting glucose measurements of 126 mg/dL or higherb. Using symptoms such as polydypsia, polyphagia, and polyuriac. A hemoglobin A1C level of 6.5%
7Image retrieved from: Prutha Dave`Family Photos Correct! Yay! Great Job!Two measurements are required to ensure reproducibility and thereforedecrease false positives and increase specificity.Image retrieved from: Prutha Dave`Family Photos
8Image retrieved from: Prutha Dave`Family Photos Oops! Try Again!Click On The Question To Return To It:Question 1Question 2Question 3Question 4Question 5Image retrieved from: Prutha Dave`Family Photos
92. A deficiency in which of the following results in hyperglycemia? a. Glucagonb. Insulinc. Ketonesd. Cortisol
10Correct! Yay! INSULIN helps to LOWER blood glucose concentration by MOVING GLUCOSE into BODY TISSUES for energyImage retrieved with permission from:http://www.fredscorner.nl/animations.html
113. What is the Metabolic Syndrome? Seen in patients with very slow metabolismb. Seen in patients who lack growth hormone, insulin, and cortisolc. Seen in patients with the following cluster of abnormalities: obesity, hyperlipidemia, hypertension, and glucose intolerance
12Image 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
134. 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)
14Image 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
155. What are the most common signs of Type II Diabetes? a. Palpitations, restlessness, and diarrheab. Dehydration, hypotension, and fatiguec. Excessive laughter, bad body odor, and hair lossd. Weight gain, blurred vision, and excessive thirst
17PathophysiologyCan be due to absolute insulin deficiency or insulin resistanceA metabolic disorder which is characterized by disturbances in carbohydrate, lipid, and protein metabolism caused by an imbalance between insulin availability and insulin needResults 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
18Video: What Happens in Type II Diabetes? Click OnVideo To ViewVideo retrieved from with permission from:
19InsulinA polypeptide which has a direct effect in lowering blood glucose levelThree actions:Promotes glucose uptake by target cells and provides for storage as glycogenPrevents fat and glycogen breakdownIncreases protein synthesis by inhibiting gluconeogenesis
20Insulin ProductionMade by the beta cells of the pancreas (islets of Langerhans)Composed of two polypeptide chains: A and BInitially made as a larger molecule: proinsulin and then cleaved to the active form of insulinOther cleavage product is the inactive C-peptide
21Insulin Release Glucose enters cell Glycolysis makes ATP ATP production causes K+ channel to close and depolarize the cellDepolarization opens voltage sensitive Ca2+ channels (Ca2+ enters cell)Ca2+ influx causes insulin release by exocytosisImage retrieved with permission from
22Insulin Action Travels through the portal circulation to the liver Binds to membrane receptorActivates intracellular enzymes to increase protein, glycogen, and fat synthesis, as well as increasing glucose transportersImage received with permission from:
23Glucagon: Another Polypeptide Antagonist of InsulinReleased during periods of fasting to maintain blood glucoseReleased by pancreatic alpha cellsCauses glycogen breakdown, gluconeogenesis, protein degradation, all resulting in elevation of blood glucoseIn diabetes, can have a negative effect as glucagon production goes unchecked as cells are starved of glucose resulting in exacerbation of hyperglycemiaImage retrieved with permission from:
24PathogenesisGenetic 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
25Beta 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:
26Genetics 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 FactorsEnvironmental Factors
27Genetic 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 aboutSpecific CandidateGenesAssociated withDMThese genetic polymorphisms can affect theutilization of blood glucose.(Radha et al, 2003)
28Polymorphic 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 GenesGenes Related to Insulin SecretionGenes Related to Insulin ResistanceGenes Related to Obesity
29Insulin 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
30Insulin Resistance Genes Glucose Transporter Gene (GLUT) –acts as a sensor to the B-celland as a major signaling molecule.Peroxisome Proliferator ActivatedReceptor Gene y (PPAR-y) –a transcription factor geneassociated in the regulation of adipocyte geneexpression and glucose metabolism.Insulin Receptor Substrate Gene (IRS) –this gene is shown to be associatedwith decreased insulin sensitivity.(Radha et al, 2003)Images retrieved from: Microsoft Word Clipart 2003
31Obesity Related GenesResearch has shown that variations in obesity genes have resulted in insulin resistance followed with the onset of Diabetes Mellitus. (Radha et al, 2003)Adiponectin GenesCLICK TO DISCOVER MORESingle nucleotidepolymorphisms within this gene have been associated with a risk for Type II Diabetes.Leptin Receptor GenesCLICK TO DISCOVER MOREMutations of this genehave been associated with hyperglycemia.Uncoupling Protein 2 GenesCLICK TO DISCOVER MOREStudies with these genes have shown to beassociated with obesity and DM.Mutations may also cause interferencewith glucose homeostasis.
32Environmental 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 ActivityUncontrolled Diet VirusesToxins (Smoking)
33What is one function of insulin? MINI QUIZ: TEST YOUR KNOWLEDGEWhat is one function of insulin?a. Promote weight lossb. Causes glycogen breakdownc. Increases protein synthesisd. Elevate blood glucose
34Correct! Great Job!INSULIN promotes glucose uptake, prevents fat and glycogen breakdown, and Increases Protein Synthesis! Good Reading!
36The 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
37Image retrieved from: Prutha Dave`Family Photos Correct! Great Job!Glucagon production can have a NEGATIVE effect if it goes unchecked as cells are starved ofglucose resulting in exacerbation of hyperglycemiaImage retrieved from: Prutha Dave`Family Photos
43Tests 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 MOREORAL GLUCOSE TOLERANCE TEST : CLICK TO LEARN MOREHbA1c : CLICK TO LEARN MORE
44How The Diagnosis is Made Normal ResponseFasting 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.
45Impaired 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.
46A 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.
47MINI QUIZ: TEST YOUR KNOWLEDGE Which of the following tests is not used for a routine diagnosis of Type 2 Diabetes?Fasting GlucoseOral GlucoseHbA1cFinger Stick
48Image retrieved from: Prutha Dave`Family Photos Correct! Great Job!Good Job. The HbA1C test is a measurement of glycosylated hemoglobin and is a usefultool for monitoring glycemic control but is not recommended for diagnostic purposes.Image retrieved from: Prutha Dave`Family Photos
53Images retrieved from: Microsoft Word Clipart 2003 TreatmentsAim to control blood glucose levelsOral medications which lower blood glucose by a variety of mechanismsInjectable Insulin which directly lowers blood glucosePrevention and reversal of diabetes can be achieved by a strict diet, exercise, and weight loss.Images retrieved from: Microsoft Word Clipart 2003
54Oral Medications Drugs that cause increased insulin release Sulfonylureas (Glyburide, Glipizide)Sitagliptin (Januvia) *newer drugExanatide (Byetta) *newer drugDrugs that sensitize cells to insulinBiguanides (Metformin)Thiazolidinediones (Rosiglitazone, Pioglitazone)Drugs that block carbohydrate absorptionAcarboseCLICK TO REVEAL MEDICATIONSCLICK TO REVEAL MEDICATIONSCLICK TO REVEAL MEDICATIONS
55CLICK TO LEARN THE MECHANISM SulfonylureasDrugs such as Glipizide and GlyburideMechanism: Stimulate insulin secretion by closing the Beta cell’s K+ channel causing depolarization and calcium influx. See prior slideSide Effects:HypoglycemiaRashesGI upsetHyponatremiaCLICK TO LEARN THE MECHANISM
56CLICK TO LEARN MECHANISM BiguanidesMajor drug in this class is MetforminMechanism: Makes liver more sensitive to insulinGreat at inducing weight lossSide Effects:Diarrhea, abdominal painLactic Acidosis- serious and potentially fatalThus avoid in patients with renal insufficiency, liver dysfunction or CHFCLICK TO LEARN MECHANISM
57CLICK TO LEARN MECHANISM ThiazolidinedionesMajor drugs in this class are Rosiglitazone (Avandia) and Pioglitazone (Actos)Mechanism: Makes peripheral tissues such as fat and muscle more sensitive to insulinSide Effects:Weight gainLiver toxicityFluid retention and edemaContradicted in CHFCLICK TO LEARN MECHANISM
58CLICK TO LEARN THE MECHANISM AcarboseMechanism: Inhibits enteric enzymes that break down complex carbohydrates, resulting in partial malabsorption of carbohydrates.Side Effects:BloatingAbdominal discomfortDiarrheaFlatulenceCLICK TO LEARN THE MECHANISM
59Insulin FormulationsRegular 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).
60Synthetic InsulinModified 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.
61Characteristics of Insulin TypeOnset (hr)Peak (hr)Duration (hr)Regular0.52-56-8Lispro/Aspart0.20.72NPH2-46-1014-18Lente1-36-1518-26Ultralente4-68-3024-36GlargineNone(Andreoli, 2004)
62Profile of ActionImage retrieved with permission from:
63Dosing RegimensIntermediate 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.
64Sample RegimensImage retrieved with permission from:
65Side Effects of Insulin Hypoglycemia – too much Insulin can cause an abnormal decrease in blood glucose resulting in hypoglycemia.Lipohypertrophy at injection siteEdemaWeight GainPromotes atherosclerosis at high dosesImage retrieved with permission from: Microsoft Clipart 2003
66MINI QUIZ: TEST YOUR KNOWLEDGE Which of the following patients would you want to avoid giving a Biguanide to?Patients with hypothyroidismPatients with pneumoniaPatients with renal insufficiency andCHFPatients with overactive bladders
67Correct! Great Job!Image retrieved with permission from:http://www.fredscorner.nl/animations.html67
72Patient EducationPatient 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
73Patient EducationDescribing the diabetes disease process and treatment optionsIncorporating nutritional management into lifestyleIncorporating physical activity into lifestyleUsing medication(s) safely and for maximum therapeutic effectivenessClick Here To Learn More!!Click Here To Learn More!!Click here to Learn More!!Click Here To Learn More!!(Funnell et al, 2009)
74Patient EducationMonitoring blood glucose and other parameters and interpreting and using the results for self-management decision makingPreventing, detecting, and treating acute and chronic complicationsDeveloping personal strategies to address psychosocial issues and concernsDeveloping personal strategies to promote health and behavior changeClick Here To Learn More!!Click Here To Learn More!!Click Here To Learn More!!Click Here To Learn More!!(Funnell et al, 2009)
75How To Educate Self Management Describing theDiseaseProcess: beforebeginningeducation about thedisease process,perform apatientassessment to gaina betterunderstanding of thePatient’sbackground such ascultural beliefsas well asreadinessto learn.Teaching NutritionalManagement: firstlearnabout thepatientscurrent dietand anyculturalinfluences that mayaffect diet.Not everypatientwill eat thesame or likethe same foodthat is recommended.Physical Activity:always, alwayspromoteany physical activity.Help the patientstransitionintoincorporatinganexerciseregimen which isappropriatefor them. Again,knowthat each patient isexercise.Safe Medication Use:make sure thepatient understandsthe medication andwhy and how it willhelp manage thedisease. Speak clearlyand use simple terms.Also, recommendingThe use of amedication box maybe of great help forthe newly diagnosedDiabetic.
76How To Educate Self Management Blood GlucoseMonitoring:help thepatient understandthe need for bloodglucose monitoring.Make sure they knowhow to use theirspecific deviceand have them doa repeatdemonstrationfor you.PreventingComplications:teach patientsto watch out forany changes inhealth status, andwhat specificsymptoms to beaware of. Examplesare eye sightchanges ornumbness andtingling.Psychosocial Issues:Promote discussingany thoughts orfeelings associatedwith the newDiabetes diagnosis.Provide resourcesfor patients touse when dealingwith difficultpsychosocial issuesor concerns.Promoting Health:Always promotehealthy lifestylebehaviors suchas quitting smoking,eating healthy,exercising, andusing a family orpersonal supportsystem toincorporate thesebehaviors.
77MINI QUIZ: TEST YOUR KNOWLEDGE What is one of the most important nursing practices before beginning patient education for new onset Diabetes?Making sure thatthe patienthas all theirmedications in hand.Making sure that theyexercise everyday for2 hoursAssessing thepatients backgroundand readiness tolearn.
80Name a way that patients can remember to safely take their medications? Keep all their medication in one bottle.Slide 82Just 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.
83The 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
84References 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: /dc09-S087Hansen, L. (2003). Candidate genes and late-onset type 2 diabetes mellitus. Susceptibility genes or common polymorphisms? [Electronic Version]. Dan Med Bull, 50(4),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,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,