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DIABETES MELLITUS: A PRIMER FOR THE AUDIOLOGIST

DIABETES MELLITUS: A PRIMER FOR THE AUDIOLOGIST. Pamela D. Parker, M.D., F.A.C.O.G. Assistant Professor A.T. Still University School of Osteopathic Medicine Arizona November 2010 pparker@atsu.edu. EVERYTHING YOU ALWAYS WANTED TO KNOW ABOUT DIABETES BUT WERE AFRAID TO ASK. OBJECTIVES.

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DIABETES MELLITUS: A PRIMER FOR THE AUDIOLOGIST

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  1. DIABETES MELLITUS:A PRIMER FOR THE AUDIOLOGIST Pamela D. Parker, M.D., F.A.C.O.G. Assistant Professor A.T. Still University School of Osteopathic Medicine Arizona November 2010 pparker@atsu.edu

  2. EVERYTHING YOU ALWAYS WANTED TO KNOW ABOUT DIABETES BUT WERE AFRAID TO ASK

  3. OBJECTIVES • Discuss Recent Statistics and Trends • Describe the Various Forms Of Diabetes and Explain the Pathophysiology • Review Criteria For Diagnosis • Explain Acute and Chronic Complications • Outline Pharmacologic and Non-Pharmacologic Therapies • Recognize the Correlation Between Hearing Loss and Diabetes

  4. DIABETES STATISTICS • 7th Leading Cause Of Death In USA • 23.6 Million People (7.8%) Afflicted • 17.9 Million Diagnosed • 5.7 Million Undiagnosed • Men & Women Equally Affected • Native American/African American>Caucasian • Rising Prevalence: >1 Million New Cases Annually Since 2002

  5. NATIONAL & GLOBAL EPIDEMIC 1994 2003

  6. WHO IS AT RISK TO DEVELOP DIABETES? • + Family History • American Indian / Alaska Native • Hispanics/Latinos • African Americans • Pacific Islanders • Asians • History of Gestational Diabetes • Advancing Age • Obesity • Lack of Exercise • Co-Morbidities • Hypertension • Hyperlipidemia • Autoimmune Disorders

  7. DIABETES & ETHNICITY • American Indians/ Alaska Native • African Americans • Hispanic/Latinos • Non-Hispanic Whites Source: ADA and the CDC – 2/08

  8. GENETICS vs LIFESTYLE Pima Indians living in Mexico have a diabetes prevalence of 8%. Those who have emigrated to the USA have a diabetes prevalence of 50%. Why? More Sedentary Lifestyle; Increased Access To Energy-Dense Food

  9. DIABETES MELLITUSWHAT DOES IT MEAN? From the ancient Greek: DIABETES: siphon MELLITUS: honey; sweet Diabetic Individuals Urinate Excessively (“Siphon” Urine From the Body) Due to High Blood Sugar Practitioners would taste the urine of a patient to make the diagnosis!

  10. DIABETES MELLITUS DEFINED • AGROUP of Metabolic Disorders • Elevated Blood Sugar (Hyperglycemia) Due to Defects in: INSULIN SECRETION INSULIN ACTION BOTH • INSULIN is a HORMONE Converts Carbohydrate, Fats and Proteins Into Usable Energy Sources • CHO/Fat/Protein Metabolism Abnormalities Are Due to Deficient Insulin Action on Target Tissues

  11. What is a Hormone? • Όρµή – Greek for “set in motion” • Chemical Messengers • Endocrine Hormones --Secreted Directly Into the Blood Stream --Act On Distant Target Organs • Exocrine Hormones -- Released Through A Duct Into Tissues or Blood --Act On Nearby or Distant Targets

  12. GLUCAGON & INSULIN Two Main Pancreatic Hormones Control Blood Glucose  • GLUCAGON Produced By ALPHA (α)Cells ELEVATE Blood Sugar • INSULIN Produced by BETA(β)Cells LOWER Blood Sugar • These are Examples of Negative Feedback Mechanisms

  13. CLASSIFICATION OF DIABETES TYPE 1 TYPE 2 • Immune-Mediated • 5-10% of Diabetics • β Cell Destruction Lack of Insulin • Presence of Multiple Antibodies • Associated with Other Autoimmune Disorders • Previously Called: IDDM & Juvenile Onset Diabetes • Therapy: Insulin • Genetic Predisposition Plus Environmental • 90-95% of Diabetics • Insulin Resistance/Relative Deficiency • Not Autoimmune • Associated with Obesity • May Exist for Years Before Diagnosis is Made • Previously Called: NIDDM, Adult-Onset (AODM) • Therapy: Weight Loss; Lifestyle Changes; +/-Meds

  14. OTHER CATEGORIES OF DIABETES • GESTATIONAL DIABETES Develops During Pregnancy (7%) • Maturity Onset Diabetes of the Young (MODY) Autosomal Dominant Genetic Disorders • Endocrinopathies Diabetes Associated with Other Disorders (Acromegaly, Cushing Syndrome, Pheochromocytoma) • Inflammatory/Trauma • Drug-Induced • Viral-Induced Result of Uncontrolled Gestational Diabetes

  15. PATHOPHYSIOLOGY OF TYPE 1 DIABETESIN A NUTSHELL - HYPERGLYCEMIA • Absence of Insulin Affects 3 Target Tissues Liver/Fat/Muscle • Inability to Absorb Nutrients • Continuous Release of Glucose, Amino Acids, Fatty Acids into the Bloodstream • Micro & Macrovascular Damage • Cell Membranes Thicken STARVATION IN THE FACE OF PLENTY • All Tissues Susceptible to Damage From Hyperglycemia

  16. PATHOPHYSIOLOGY OF TYPE 2 DIABETES Interplay of Genetics and Environment(nurture/nature) Dual Defect: • Impaired β Cell Function  Decreased Insulin • Insulin Resistance  Decreased Peripheral Utilization of Glucose Increased Hepatic Glucose Production Excess Breakdown of Fat

  17. NATURAL HISTORY OF TYPE 2 DIABETES Up to 15 Years of Abnormalities Before the Diagnosis is Made

  18. SYMPTOMS OF DIABETES • Polyuria • Polyphagia • Polydipsia • Fatigue • Weight Change: Loss or Gain • Infections • Blurry Vision • Numb Feet OR • Irritability • Poor Work/School Performance • Diarrhea/Constipation • Muscle Cramps • Anxiety • Chest Pain • Fruity Breath • Impairment of Growth/Development

  19. DIAGNOSING DIABETES

  20. CRITERIA FOR DIAGNOSIS • FASTING PLASMA GLUCOSE ≥ 126 mg/dL • RANDOM PLASMA GLUCOSE ≥ 200 mg/dL • 2 HOUR GTT ≥200 mg/dL • HbA₁c ≥6.5 % ** **New Guideline 2010 • Gestational Diabetes – 2 Tier Testing 50 gm 1 Hour Testing 130 or 135 or 140 mg/dL 100 gm 3 Hour Testing 95/180/155/140 Or 105/190/165/145 mg/dL

  21. Glycosylated HemoglobinHbA₁c • Glucose Attached to Red Blood Cells • Reflects the Average Over 3 Months • More Accurate Than Fasting or Glucose Tolerance Testing -No Diurnal Variation -Not Altered By Stress -Patient’s Cannot “Cheat” • May Be Inaccurate if Hemoglobin is Abnormal (egThalassemia) or Rapid RBC Turnover • Costs More Than Traditional Blood Sugar Testing Correlation With Blood Sugar Levels: HbA1c 6 ~Plasma Glucose 126 HbA1c 7~Plasma Glucose of 154 The Higher the HbA1c, the Greater Risk of Diabetic Complications Including Retinopathy

  22. TESTING IN ASYMPTOMATIC PATIENTS BMI≥ 25 kg/m² (overweight) Plus Risk Factors • Physical Inactivity • 1˚ Relative with Diabetes • High Risk EthnicGroup • Prior Gestational Diabetes or Delivery of a 9+ lb Baby • Women with PCOS • Hypertension(Treated or Not) • HDL Cholesterol < 35 mg/dL • Triglycerides > 250 mg/dL • A₁C ≥ 5.7 or Previous Abnormal Blood Sugar Testing • History of Cardiovascular Disease • Clinical Conditions Associated with Insulin Resistance (Acanthosis Nigricans; Obesity)

  23. TESTING ASYMPTOMATIC INDIVIDUALS • If None Of These Criteria Exist, Begin Testing At Age 45 Years • If Testing Is Normal, Repeat Every 3 Years - More Often If Indicated Acanthosis Nigricans

  24. SHORT TERM COMPLICATIONS OF DIABETES HYPOGLYCEMIA (Low Blood Sugar) HYPERGLYCEMIA (High Blood Sugar)

  25. LONG TERM COMPLICATIONS OF DIABETES(HYPERGLYCEMIA) Whole Body May Be Affected • Retinopathy • Nephropathy • Neuropathy • Cardiovascular • Dermatologic • Musculoskeletal • Infectious Disease • Vasculopathy

  26. TREATMENT GOALS NONPREGNANT ADULTS PREGNANT ADULTS • A₁c < 7.0% • Fasting Plasma Glucose 70-130 mg/dL • Peak Postprandial Plasma Glucose < 180 mg/dL With Gestational Diabetes Fasting Plasma Glucose ≤95 2 Hour Postprandial ≤120 With Preexisting Diabetes Fasting 60-99 mg/dL 1 Hour Postprandial 100-129 mg/dL A₁c < 6.0%

  27. WHY TREAT TO “GOAL”? EBM Demonstrates That Reducing Glucose Close To “Normal” SIGNIFICANTLY REDUCES DIABETES COMPLICATIONS • DCCT - http://diabetes.niddk.nih.gov/dm/pubs/control/ • UKPDS - http://www.dtu.ox.ac.uk/index.php?maindoc=/ukpds/ • Others – see the ADA website

  28. DCCT (Diabetes Control and Complication Trial 1993) • First Clinical Evidence That Near NormalizationOfBlood Glucose In Type 1 Diabetics Reduced TheRisk Of Clinically Meaningful: --Retinopathy by 76% --Neuropathy by 60% --Nephropathy by 54% • However  Current Research Suggests “Too Tight” Control May Be Harmful In Some People – So Individualize

  29. UKPDS (United Kingdom Prospective Diabetes Study 1998) • Demonstrated The Same Patterns as the DCCT For Type 2 Diabetics • In Type 2 Diabetes - For Every 1% Reduction In the Hba1c Level There Was: • 35% Reduction In Microvascular Complications Of The Eye and Kidney • 25% Reduction In Diabetes-Related Deaths • 18% Reduction In Myocardial Infarction

  30. TREATMENT STRATEGIES • Ongoing Assessment • Lifestyle Changes • Medications • Prevent/Minimize Complications • Appropriate Referral

  31. ONGOING ASSESSMENT • HISTORY • PHYSICAL EXAM • LABORATORY • GLUCOSE MONITORING • SPECIALTY CARE • LIFESTYLE CHANGES

  32. PATIENT HISTORY • Age at Onset & Characteristics of Diabetes • Eating Patterns; Nutritional Status; Weight History • Growth & Development • Physical Activity • Review Previous Treatment Regimens • Psychosocial • Results of Glucose Monitoring Review Complications • Microvascular Retinopathy – Visual Changes Nephropathy - Proteinuria Neuropathy: Sensory – Feet Autonomic –GI; Sexual Dysfunction • Macrovascular Coronary Heart Disease (CHD) Cerebrovascular Disease (CVD) Peripheral Arterial Disease (PAD) • Dental • Otologic/Audiology

  33. PHYSICAL EXAMINATION • Height/Weight/BMI • Blood Pressure (Orthostatic)/ABI • Eyes – Looking for Retinopathy • Ears/Nose/Mouth/Throat • Skin (Injection Sites; Ulcers; Diabetic Skin Changes) • Feet -Comprehensive Exam • Musculoskeletal • Cardiovascular – Central And Peripheral • Neurologic

  34. OBESITY PARAMETERS Calculate The Body Mass Index BMI = Wt (Kg) ÷Ht(m2) < 18.5 Low 18.5 to 24.9 Healthy 25 to 29.9 Overweight > 30 Obese Central Obesity  if Waist Circumference Is Increased • Men >102 cm (40") • Women >88 cm (35") • Correlated With Cardiovascular Disease

  35. Ankle Brachial Index (ABI) • Ratio of Systolic Blood Pressures at the Ankle &BrachialArteries • Reflects Peripheral Arterial (Vascular) Disease (PAD) • Atherosclerotic Disease Usually Affects Lower Extremities Before Upper Extremities • Subjects With PAD Usually Also Have Coronary Artery Disease • ABI < 0.9 IsAbnormal Implies Vascular Obstruction • Decreased ABI Often Associated With Uncontrolled Diabetes (Hyperglycemia) • Asymptomatic in the Beginning .

  36. Neurologic Examination Central And Peripheral Nervous System - Routine Evaluation For Change In: • Proprioception • Vibration • Light Touch (Monofilament) • Reflexes • Evaluation For Autonomic Neuropathy If Indicated Proprioception

  37. Neurologic Examination:Peripheral Neuropathy SEMMES-WEISS MONOFILAMENT • Reduced Sensation With Monofilament Testing • Decreased Vibratory Sensation

  38. LABORATORY TESTING • BLOOD SUGAR FBS < 100; PPBS <140 • A1c - < 7 • RENAL FUNCTION Serum Creatinine Protein < 30 µg/mg(spot UA) • LIPIDS TC <200, TG < 150, LDLc<100 mg/dL • EKG

  39. CELIAC DISEASE TESTING • New Recommendation • All Children With Type 1 Diabetes & Anyone with Compelling Symptoms (Failure To Thrive; Poor Weight Gain; Malabsorption) • Strong Concordance Between Type 1 Diabetes & Celiac Disease  Autoimmune Link • If Negative, Consider Repeat Testing in Future

  40. GLUCOSE MONITORING • CHECK DON’T GUESS • Managing Diabetes Without BS Monitoring  Like Driving a Car with No Speedometer, Gas Gauge or Engine Lights --Lack Vital Information --Could Get Into Serious Trouble

  41. IS IT TIME FOR A BREAK YET?

  42. SPECIALTY CARE • PODIATRY • OPHTHALMOLOGY • AUDIOLOGY • DENTAL • ETC. [Cardiology, Nephrology, Gastroenterology, Psychiatry, Psychology]

  43. FOOT CARE • DAILY FOOT CHECKS/MIRROR • PODIATRIST • MONOFILAMENT TESTING • PROPER FOOTWEAR • TEMPERATURE AWARENESS • STOP SMOKING • NUTRITION/EXERCISE • GLYCEMIC CONTROL

  44. DIABETIC FEET GONE WRONG₁

  45. DIABETIC FEET GONE WRONG₂

  46. OPHTHALMOLOGY • Increased Incidence of Retinopathy, Cataracts, Macular Edema • Visual Blurring [From Hyperglycemia ]Will Improve When B.S. Decreases • Type 1 Diabetics Dilated Exam Within 5 Years of Diagnosis, Then Annual • Type 2 Diabetics Dilated Exam at Time of Diabetes Diagnosis (WHY?)Then Annual • Preconceptual: Before Pregnancy; Each Trimester; 6-8 Weeks Postpartum

  47. AUDIOLOGY • RelationshipBetweenDiabetes & Hearing Loss is Controversial • Diabetesis a Well- Known Risk Factor & Poor Prognostic Factor for SNHL • Sudden Sensorineural Hearing Loss (SNHL)Otologic Emergency

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