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Diabetes Pathophysiology PowerPoint Presentation

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Description : Check out this medical titled "Diabetes Pathophysiology" by Beverly Dyck Thomassian, RN, MPH, BC-ADM, CDE.

This medical talks about Diabetes mellitus (DM) is a group of metabolic disorders characterized by high blood sugar levels (hyperglycemia) resulting from defects in insulin secretion, insulin action, or both. Insulin is a hormone produced by the pancreas that regulates blood glucose levels.

The two types of diabetes are Type 1 diabetes and Type 2 diabetes.

The pathophysiology of diabetes involves several complex mechanisms that contribute to hyperglycemia. These mechanisms include Insulin resistance, Impaired insulin secretion, Increased glucose production, Abnormal glucagon secretion, etc.

Tags : Diabetes Pathophysiology, Diabetes mellitus, metabolic disorders, Type 1 diabetes, Type 2 diabetes, Insulin resistance, Impaired insulin secretion, Increased glucose production, Abnormal glucagon secretion, endocrinology

Published on : Apr 21, 2023 | Views : 1705 | Downloads : 12

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Diabetes Pathophysiology www.DiabetesEd.net Beverly Dyck Thomassian, RN, MPH, BC-ADM, CDE President, Diabetes Education Services
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Lecture Objectives Discuss the current impact of diabetes. Describe the pathway of pathophysiological defects associated with the development of diabetes Describe and differentiate between the different types: prediabetes, Type 1, Type 2, LADA and GDM Describe the laboratory tests used for the diagnosis of Diabetes Mellitus including FBG, OGTT, A1C, antibodies List the characteristics of Insulin Resistance.
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Quick Question What best describes the prevalence of diabetes in the U.S.? 30% of people above the age of 20 have type 2 diabetes. The prevalence of type 1 and type 2 diabetes are almost equal. 1 out 3 persons has type 2 diabetes. About 10% of Americans have diabetes.
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CDC Announces 35% of Americans will have Diabetes by 2050 Boyle, Thompson, Barker, Williamson 2010, Oct 22:8(1)29 www.pophealthmetrics.com
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Diabetes in America 2017 29 million or > 9.3% 27% don’t know they have it 37% of US adults have pre diabetes (86 mil)
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Age-adjusted Diabetes Prevalence 20 yrs or older, by race/ethnicity— U.S. 20014
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68% overweight or obese 34% BMI 30 +, 34% BMI 25-29 1/3 of all overwt people don’t get diabetes We burn 100 cals less a day at work Overall, food costs ~ 10-15% of income Calorie Intake is on the rise Obesity and Economics in America
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Now, let’s get to the Nitty Gritty
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Hormones Effect on Glucose Hormone Glucagon (pancreas) Stress hormones (kidney) Epinephrine (kidney) Insulin (pancreas) Amylin (pancreas) Gut hormones - incretins (GLP-1) released by L cells of intestinal mucosa, beta cell has receptors) Effect      
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GLP-1 Effects in HumansUnderstanding the Natural Role of Incretins Adapted from Flint A, et al. J Clin Invest. 1998;101:515-520Adapted from Larsson H, et al. Acta Physiol Scand. 1997;160:413-422Adapted from Nauck MA, et al. Diabetologia. 1996;39:1546-1553Adapted from Drucker DJ. Diabetes. 1998;47:159-169 Stomach: Helps regulate gastric emptying Promotes satiety and reduces appetite Liver:  Glucagon reduces hepatic glucose output Beta cells:Enhances glucose-dependent insulin secretion Alpha cells:  Postprandialglucagon secretion GLP-1 secreted upon the ingestion of food  Beta-cell response GLP-1 degraded by DPP-4 w/in minutes
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Signs of Diabetes Polyuria Polydipsia Polyphasia Weight loss Fatigue Skin and other infections Blurry vision Glycosuria, H2O losses Dehydration Fuel Depletion Loss of body tissue, H2O Poor energy utilization Hyperglycemia increases incidence of infection Osmotic changes
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Natural History of Diabetes Development of type 2 diabetes happens over years or decades Yes! NO
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A1c Test Measures glycation of RBC’s over 2-3 months Weighted mean (50% preceding month) Each 1% ~ 29mg/dl Accuracy: affected by some anemias, hemoglobinopathies A measurement of glucose in fasting and postprandial states African Americans may have false lows
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A1c and Estimated Avg Glucose (eAG) A1c (%) eAG 5 97 6 126 7 154 8 183 9 212 10 240 11 269 12 298 eAG = 28.7 x A1c-46.7 ~ 29 pts per 1% Translating the A1c Assay Into Estimated Average Glucose Values – ADAG Study Diabetes Care: 31, #8, August 2008 Order teaching tool kit free at diabetes.org
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Quick Question What factors would make you suspect type 1 diabetes? a. Pt has a history of celiac disease b. Pt presents with low HDL cholesterol c. Friend tells you she has been eating "tons of sweets“ d. Pt is slightly overweight
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What Kind of Diabetes? AJ, a 12 year old female admitted to the ICU with a blood glucose of 476 mg/dl and a pH of 7.1. What further questions and or testing is needed to determine if patient has type 1 or type 2 diabetes?
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Type 1 Diabetes
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Dr. Banting and Best with Marjorie at University of Toronto
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Insulin Finally Available - 1922
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The Miracle of Insulin Patient J.L., December 15, 1922 February 15, 1923 Miracle of Insulin
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What Does Type 1 Look Like? Justice Sonia Sotomayor Bret Michaels Mary Tyler Moore Nick Jonas
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Type 1 Rates Increasing Globally 23% rise in type 1 diabetes incidence from 2001-2009 Why? Autoimmune disease rates increasing over all Changes in environmental exposure and gut bacteria? Hygiene hypothesis Obesity?
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Incidence of Type 1 in Youth General Pop 0.3% Sibling 4% Mother 2-3% Father 6-8% Rate doubling every 20 yrs Many trials underway to detect and prevent (Trial Net)
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Type 1 – 10% of all DiabetesGenetics and Risk Factors Auto-immune pancreatic beta cells destruction Most commonly expressed at age 10-14 Insulin sensitive (require 0.5 - 1.0 units/kg/day) Combo of genes and environment: Autoimmunity tends to run in families Higher rates in non breastfed infants Viral triggers: congenital rubella, coxsackie virus B, cytomegalovirus, adenovirus and mumps.
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How do we know someone has Type 1 vs Type 2? Type 1 Positive antibodies GAD ICA IAA and others Younger people develop quickly Older people take longer to develop Body wt and presentation
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Autoantibodies Assoc w/ Type 1 Panel of autoantibodies – GAD65 - Glutamic acid decarboxylase – ICA - Islet Cell Cytoplasmic Autoantibodies IAA - Insulin Autoantibodies
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Type 1 Summary Autoimmune pancreatic destruction Need insulin replacement therapy Often first present in DKA At risk for other autoimmune diseases Eval coping strategies
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Type 1 Diabetes Associated with other immune conditions Celiac disease (gluten intolerance) Thyroid disease Addison’s Disease Rheumatoid arthritis Other
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Type 1 back in hospital 14 yr old admitted for 3rd time this month for DKA Admission BG 648. She is 5’6 inches and weighs 100-110 lbs They ask you to provide diabetes education. What top 3 things are you going to assess for? If no action taken, what could this lead to?
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Disordered Eating “DiaBulimia” People with type 1 diabetes give themselves less insulin than needed to lose weight Tends to start in adolescence, more likely to occur in women than men. Signs: unexplainable spikes, A1c, weight loss, lack of marks from fingerpricks, lack of prescription refills for diabetes meds, records that don’t match A1c. Treatment – Mental health specialist and team
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Patti Labelle "divabetic” “I have diabetes, it doesn’t have me”
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Path to Type 2 Diabetes
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BMI – Visual Image
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2. Classification and DM Diagnosis Pre Diabetes & Type 2- Screening Guidelines Start screening at age 45 or for anyone who is overweight (BMI  25, Asians BMI  23 ) with one or > additional risk factor: First-degree relative w/ diabetes Member of a high-risk ethnic population Habitual physical inactivity PreDiabetes History of heart disease
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Diabetes 2 - Who is at Risk? (ADA Clinical Practice Guidelines) Risk factors cont’d HTN - BP > 140/90 HDL < 35 or triglycerides > 250 baby >9 lb or history of Gestational Diabetes Mellitus (GDM Polycystic ovary syndrome (PCOS) Other conditions assoc w/ insulin resistance: Severe obesity, acanthosis nigricans (AN)
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Acanthosis Nigricans
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Acanthosis Nigricans (AN) Signals high insulin levels in bloodstream Patches of darkened skin over parts of body that bend or rub against each other Neck, underarm, waistline, groin, knuckles, elbows, toes Skin tags on neck and darkened areas around eyes, nose and cheeks. No cure, lesions regress with treatment of insulin resistance
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What is Type 2 Diabetes? Complex metabolic disorder …. (Insulin resistance and deficiency) with social, behavioral and environmental risk factors unmasking the effects of genetic susceptibility. New Diagnosis? Call 800 – DIABETES to request “Getting Started Kit” www.Diabetes.org
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Natural Progression of Type 2 Diabetes -20 -10 0 10 20 30 Years of Diabetes Relative -Cell Function Plasma Glucose Insulin resistance Insulin secretion 126 mg/dL Fasting glucose Postprandial glucose Prior to diagnosis After diagnosis Adapted from Bergenstal et al. 2000; International Diabetes Center.
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Life Study – Mrs. Jones Mrs. Jones is 62 years old, overweight and complaining of feeling tired and urinating several times a night. She is admitted with a urinary tract Infection. Her WBC is 12.3, glucose 237. She is hypertensive with a history of gestational diabetes. No ketones in urine. What are her risk factors, signs of diabetes What type of diabetes does she have? Does she have insulin resistance?
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What Do You Say?Mrs. Jones asks you What is type 2 diabetes? Will this go away? Will I get complications? Will I need to take diabetes medication for the rest of my life? How come I got diabetes? Do I have to check my blood sugars?
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Quick Question What is the preferred approach when providing diabetes education with patients? Provide patient centered self-management support Instruct all patients to meet national standards Highlight risk of complications when goals aren’t met Remind them that insulin treatment can be beneficial.
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Comparison of Type 1,Type 2, LADA Insulin Resistance xxx 0 x
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Diabetes is also associated with Fatty liver disease Obstructive sleep apnea Cancer; pancreas, liver, breast Alzheimer’s Depression
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Other Types of Diabetes Gestational Other specific types of diabetes
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Gestational DM ~ 7% of all Pregnancies GDM prevalence increased by ∼10–100% during the past 20 yrs Native Americans, Asians, Hispanics, African-American women at highest risk Immediately after pregnancy, 5% to 10% of GDM diagnosed with type 2 diabetes Within 5 years, 50% chance of developing DM in next 5 years.
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Increasing Prevalence –A public health perspective Body weight before and during pregnancy influences risk of GDM and future diabetes Children born to women with GDM at greater risk of diabetes Focus on prevention
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Postpartum after GDM 50% risk of getting diabetes in 5 years Screen at 6-12 wks post partum Repeat at 3 yr intervals or signs of DM Encourage Breast Feeding Encourage weight control Encourage exercise Make sure connected with health care Lipid profile/ follow BP Preconception counseling
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Hypoglycemia prevention 72 yr old, thin, lives alone, A1c 7.3%. History of MI, stroke. DM for 12 yrs, takes glyburide 10mg BID. Limited income. Creat 1.4. What strategies to Prevent hypo?
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Glycemic Threshold ValuesJohn White, PharmD, Diabetes Spectrum, 2007 Classification BG Physical Response Lower euglycemia 80-90’s Endogenous insulin Hypoglycemia 70’s Glucagon, adrenaline Symptoms 60s Growth hormone, cortisol 50’s Cognitive deterioration Neuroglycopenia 40’s 30’s Severe 20’s Coma, seizures neuroglycopenia 10 (shortage of glucose in the brain affects function of the neurons)
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Hypoglycemia Awareness autonomic symptoms adrenergically based after 2-5 yrs of type 1 dm, glucagon secretion impaired epinephrine secretion becomes primary mechanism to restore BG levels over time, epi response diminished or delayed decreases awareness of hypo and hormonal response
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Hypoglycemia Symptoms Autonomic Anxiety Palpitations Sweating Tingling Trembling Hypoglycemic Unawareness Neuroglycopenia Irritability Drowsiness Dizziness Blurred Vision Difficulty with speech Confusion Feeling faint
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Treatment of Hypoglycemia If blood glucose 70mg/dl or below: 10-15 gms of carb to raise BG 30 - 45mg/dl Retest in 15 minutes, if still low, treat again, even without symptoms Follow with usual meal or snack If BG less than 40, allow recovery time Severe hypo may require glucagon
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80 /20 Rule – Perfect Not Required
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Key points At the center of diabetes is someone living with it everyday. Focus on their successes Coach and support
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Thank You www.DiabetesEd.net
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Diabetes KetoAcidosis 135,000 Hospitalizations a year $2.4 billion U.S. dollars spent on treatment Often a cry for help ADA article on Hyperglycemic Crises
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DKA Precipitating Factors 25 -30% of time, illness and infection increases stress hormone release 50% inadequate insulin dosage initial manifestation of type 1 emotional stress - especially with teens, neglect or mismanagement
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Extreme Hyperglycemia – Diabetes KetoAcidosis (DKA) DKA - profound insulin deficiency Excess stress hormones such as glucagon, epinephrine, and cortisol render insulin less effective Excess glucose production by liver Lipolysis leads to FFA’s and ketones Osmotic diuresis, dehydration, lyte imbalances, acidosis
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DKA Signs and Symptoms hyperglycemia- leads to weakness, lethargy, malaise, headache GI symptoms - N/V, abd pain Kussmaul’s deep, rapid breathing hypothermia, acetone breath hyperpnea - to rid acidosis changes in mentation, hyporeflexia/tonia dehydration, ortho hypo
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Extreme Hyperglycemia – Hyperosmolar Hyperglycemic State (HHS) occurs in elderly pt’s w/ type 2 - esp if not closely monitored often precipitated by illness or stress symptoms may go unrecognized for wks massive fluid loss from osmotic diuresis burns, hyperglycemia, diarrhea, hemodialysis, diuretics, steroids MI, infections, hypertonic feedings
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DKA vs HHS Usually < 40 yrs old < 2 days symptoms Glucose >250 Serum Ketones: +++ pH low (<7.3) Anion Gap > 12 Usually Type 1 3 – 10% mortality Usually >60 yrs old > 5 days symptoms Glucose >600 Ketones: none to + pH normal (>7.3) Usually Type 2 10 - 20% mortality
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DKA - HHS Presentation and Action Labs NA - low to high K+ - moves into vascular space Hct and Hgb  dehydration BUN / Creatinine  WBC  (no infect) pH low to normal Action maintain insulin drip until ketone neg, glucose <200 maintain hydration check BG q1 hour assess lytes (esp K+) give sub-Q insulin before d/c IV insulin teach, teach, teach
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DKA and HHS 5 most important interventions Fluids (NS, 0.45 NS, D51/2 NS once glucose 300mg/dl) Insulin (.05 - 0.1unit/kg per hour) Potassium / lyte replacement (K+, Mg, Ca, Phos) Determine, treat precipitating cause Education to prevent future episodes