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
1. Discuss Recent Statistics and Trends
2. Describe the Various Forms Of Diabetes and
3.
4.
5.
6.
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
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
NATIONAL & GLOBAL EPIDEMIC
1994
2003
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
DIABETES & ETHNICITY
 American Indians/
Alaska Native
 African Americans
 Hispanic/Latinos
 Non-Hispanic Whites
Source: ADA and the CDC – 2/08
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 EnergyDense Food
DIABETES MELLITUS
WHAT 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!
DIABETES MELLITUS DEFINED
 A GROUP 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
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
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
CLASSIFICATION OF DIABETES
TYPE 1
 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
TYPE 2
 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
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
PATHOPHYSIOLOGY OF TYPE 1 DIABETES
IN 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
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
NATURAL HISTORY OF TYPE 2
DIABETES
Up to 15 Years of Abnormalities Before the Diagnosis is Made
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
DIAGNOSING DIABETES
CRITERIA FOR DIAGNOSIS
 FASTING PLASMA GLUCOSE
≥ 126 mg/dL
 RANDOM PLASMA GLUCOSE
≥ 200 mg/dL
 2 HOUR GTT
≥200 mg/dL
 HbA₁c
≥6.5 % **
 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
**New Guideline
2010
Glycosylated Hemoglobin
HbA₁c
 Glucose Attached to Red
Blood Cells
 Reflects the Average Over 3
Months
Correlation With Blood Sugar
Levels:
HbA1c 6 ~Plasma Glucose 126
HbA1c 7~Plasma Glucose of 154
 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
The Higher the HbA1c, the
Greater Risk of Diabetic
Complications Including
Retinopathy
TESTING IN ASYMPTOMATIC PATIENTS
BMI≥ 25 kg/m² (overweight)
Plus Risk Factors
 Physical Inactivity
 1˚ Relative with Diabetes
 High Risk Ethnic Group
 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)
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
SHORT TERM COMPLICATIONS OF
DIABETES
HYPOGLYCEMIA
(Low Blood Sugar)
HYPERGLYCEMIA
(High Blood Sugar)
LONG TERM COMPLICATIONS OF
DIABETES(HYPERGLYCEMIA)
Whole Body May Be
Affected
 Retinopathy
 Nephropathy
 Neuropathy
 Cardiovascular
 Dermatologic
 Musculoskeletal
 Infectious Disease
 Vasculopathy
TREATMENT GOALS
NONPREGNANT ADULTS
 A₁c < 7.0%
 Fasting Plasma Glucose
70-130 mg/dL
 Peak Postprandial Plasma
Glucose
< 180 mg/dL
PREGNANT ADULTS
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%
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
DCCT
(Diabetes Control and Complication Trial 1993)
 First Clinical Evidence That Near Normalization Of
Blood Glucose In Type 1 Diabetics Reduced The Risk
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
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
TREATMENT STRATEGIES
 Ongoing
Assessment
 Lifestyle Changes
 Medications
 Prevent/Minimize
Complications
 Appropriate
Referral
ONGOING ASSESSMENT
 HISTORY
 PHYSICAL EXAM
 LABORATORY
 GLUCOSE
MONITORING
 SPECIALTY CARE
 LIFESTYLE
CHANGES
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
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
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
Ankle Brachial Index (ABI)
 Ratio of Systolic Blood Pressures at the Ankle &






.
Brachial Arteries
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 Is Abnormal  Implies Vascular
Obstruction
Decreased ABI Often Associated With Uncontrolled
Diabetes (Hyperglycemia)
Asymptomatic in the Beginning
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
Neurologic Examination:
Peripheral Neuropathy
SEMMES-WEISS MONOFILAMENT
Reduced Sensation With Monofilament Testing
Decreased Vibratory Sensation
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
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
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
IS IT TIME FOR A BREAK YET?
SPECIALTY CARE
 PODIATRY
 OPHTHALMOLOGY
 AUDIOLOGY
 DENTAL
 ETC.
[Cardiology, Nephrology,
Gastroenterology, Psychiatry,
Psychology]
FOOT CARE
 DAILY FOOT
CHECKS/MIRROR
 PODIATRIST
 MONOFILAMENT
TESTING
 PROPER FOOTWEAR
 TEMPERATURE
AWARENESS
 STOP SMOKING
 NUTRITION/EXERCISE
 GLYCEMIC CONTROL
DIABETIC FEET GONE WRONG₁
DIABETIC FEET GONE WRONG₂
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
AUDIOLOGY
 Relationship Between
Diabetes & Hearing
Loss is
Controversial
 Diabetes is a WellKnown Risk Factor
& Poor Prognostic
Factor for SNHL
 Sudden Sensorineural
Hearing Loss
(SNHL)Otologic
Emergency
Sudden Sensorineural Hearing Loss in
Diabetes
 Comparison of Intratympanic, Oral and
Intravenous Dexamethasone Treatment on Sudden
Sensorineural Hearing Loss with Diabetes
 Conclusion: IT-DEX Treatment Is At Least As
Effective As IV-DEX Treatment For Sudden
Sensorineural Hearing Loss In Diabetes
 Local Treatment Less Likely to Elevate Blood
Sugar Compared to Systemic Therapy (PO or IV)
Source: Chi-Sung Han, Jong-Ryul Park, et al. Otolaryngology-Head & Neck Surgery (2009)141, 572-578.
VASCULATURE OF THE EAR
Blood Vessels of the Inner
Ear
Arteries of the Middle Ear
CHRONIC KIDNEY DISEASE & HEARING
LOSS
 Association of CKD &
Hearing Loss Known
for Decades
 Kidney & Stria Vascularis of
Cochlea Share
Physiologic,
Ultrastructural and
Antigenic Similarities
 Diabetes Often Results in
Chronic Renal Disease
 Therefore, the Link Between
Diabetes and Hearing
Loss May Be Indirect
But Exists
MALIGNANT OTITIS EXTERNA
 Osteomyelitis of the Ear Canal
 Often Involves the Adjacent







Mastoid Bone
Pseudomonas is Common
Necrosis or Granulation of
Canal
Exquisitely Tender to Motion
Temp Often >39˚ C (102.2˚)
May Find Facial Paralysis,
Vertigo or Meningeal Signs
Intervention:
--Incision & Drainage/Culture
--Ototopical & Oral Antibiotics
--Possible IV Therapy In-Patient
Diabetics at Increased Risk 
Urgent Referral
Malignant External OtitisPus Draining
from Necrotic Ear Canal & Underlying
Osteomyelitic Bone; Swelling of Auricle
With Loss of Cartilaginous Architecture
DENTAL
 Lots Of
Microvasculature In The
Oral Cavity
 Also Home For Many
Bacteria
 Hyperglycemia Increases
Probability of Infection
 SOLUTION:
1) Good Oral Hygiene –
Flossing and Brushing
2) Dental Visit Twice Yearly
LIFESTYLE CHANGES
NUTRITION
PHYSICAL
ACTIVITY
TOBACCO
ALCOHOL
STRESS
REDUCTION
NUTRITION
 Meal Plans NOT DIETS
 LOW Glycemic Index
Choices
 Carbohydrate Counting
and Portion Control
are Important
 Consistent Meal Times and
Snacks
 THERE ARE NO GOOD
FOODS OR BAD FOODS
American Family Physician November 1, 2009;
80(9): 897-1026. EBMLow Glycemic Index
Diet lowered A1c levels & reduced
hypoglycemic episodes.
Select More Choices From The
Bottom Than the Top
CARBOHYDRATE COUNTING
GLYCEMIC INDEX
Flour Comparison
Glycemic Pyramid
INDIVIDUALIZE
PHYSICAL ACTIVITY
Physical Activity Can Positively
Impact Weight, Blood
Pressure, Bone Density, Mental
Health ,Glycemic Control
 There are Choices
--150 minutes/ week of
moderate-intensity aerobic
physical activity (yard work
counts)
--90 min/week of vigorous
aerobic exercise;
 No more than 2 consecutive days
of no activity;
 Resistance exercises 3X weekly
(if not contraindicated)
HARMFUL HABITS:
ENCOURAGE CESSATION
TOBACCO
ALCOHOL/DRUGS
STRESS REDUCTION
 Physical Activity
 Relaxation Techniques
– Yoga, Visualization
 Alternative Therapies
– Acupuncture,
Acupressure, Aroma
Therapy
 Formal Counseling if
Required
 DSME
MEDICATIONS – WHEN LIFESTYLE
CHANGE IS NOT ENOUGH
LACK OF INSULIN
INSULIN INSENSITIVITY ++
TYPE 1 DIABETES
INSULIN IS THE
ANSWER
• Rapid-Acting
• Intermediate-Acting
• Long-Acting
• Mixed
INSULIN – THE WONDER DRUG
TYPE 2 DIABETES:
MATCHING PHARMACOLOGY TO
PATHOPHYSIOLOGY
Insulin Secretagogues
Increase Pancreatic Insulin Output
α Glucosidase Inhibitors(Starch
Blockers)
Improve Glucose Metabolism In Small
Intestine(Starch Blockers)
Amylin Analogues
Potentiate Insulin Effects
Incretin Mimetics/Enhancers
Stimulate Insulin Secretion
Decrease Glucagon Secretion
Biguanides (Glucose Inhibitors)
Decrease Hepatic Glucose Output
+/- Improve Peripheral Insulin Sensitivity
Thiazolidenediones (Insulin
Sensitizers)
Increase Peripheral Insulin Sensitivity
+/- Decrease Hepatic Glucose Output
TARGETING THE TREATMENT
Insulin Secretagogues
Sulfonylureas
Glyburide, Glipizide, Glimepiride
Incretin
Mimetics/Enhancers
Exenatide, Lyraglutide
Non-Sulfonylureas
Nateglinide
Repaglinide
α Glucosidase Inhibitors
Acarbose
Miglitol
Biguanides
Metformin
Thiazolidenediones (TZDs)
Pioglitazone
Rosiglitazone
Amylin Analogues
Pramlintide
DRUGS COME FROM THE
STRANGEST PLACES
 Exenatide (Byetta)
 First Incretin Released




by FDA
GLP-1 Agonist
Slows Food Absorption
in Intestine 
Slower Insulin
Release
Decreases Glucagon
Release from Liver
Also Improves Insulin
Secretion by
Pancreas
 SOURCE: Gila Monster
Saliva!
WHAT ABOUT HYPOGLYCEMIA?
(Low Blood Sugar)
 Low Blood Sugar is Potentially
Dangerous
 Can Be a Side-Effect of Insulin &
Some Oral Agents
(Secretagogues)
 Glucose is the Sole Energy Source
for Brain & RBCs
 “Tight” Glycemic Control is Not a
Goal for All Individuals 
--Limited Life Expectancy;
--Recurrent Severe Hypoglycemia
--Advanced Disease
--Extensive Comorbidities
 DSME Includes Education For
Recognizing and Treating
Hypoglycemia
 GLUCAGON Injection I.M. or S.Q.
Signs & Symptoms of Hypoglycemia
MINIMIZING COMPLICATIONS
 Retinopathy
 CV disease
 Kidney disease
 Neuropathy
 Gastroparesis
 Impotence
 Autonomic
Neuropathy
 Etc. Etc.
HOW?
Diabetic SelfManagement
Education
• Paradigm Shift
• Patient-Centered
Goals
• Empowerment
• Shared Responsibility
DSME SURVIVAL SKILLS
 Self-Evaluation (Feet, Skin…)
 Blood Sugar Testing
 Management of Hypo and







Hyperglycemia
Nutrition Planning
Medications
Recognize S/S Infection
Regular Follow-up With Health
Care Providers
Sick Days/Travel Strategies
Medic Alert Bracelets
Appropriate Sharing of
Diagnosis
AADE CONCEPTUAL FRAMEWORK FOR
DSME
Healthy Eating
Being Active
Monitoring
Taking Medications
Problem Solving
Healthy Coping
Decreasing Risks
American Association of
Diabetes Educators
BLOOD PRESSURE MONITORING
GOALS
Systolic < 130 (SBP)
Diastolic <80 (DBP)
INTERVENTIONS
White Coat Hypertension
Lifestyle Changes if 130-139/8089
Medication(s) if ≥140 SBP or 90
DBP
DASH Diet
Ongoing Evaluation for
Nephropathy
DIETARY APPROACHES TO STOP
HYPERTENSION (DASH)
Dash Study: In Nondiabetic
Individuals, DASH Diet
Interventions 
Antihypertensive Effects
Similar To Those Of
Pharmacologic Monotherapy
--Cut Heart Disease 24%
--Cut Stroke 18%
IMMUNIZATIONS
VACCINES
INFLUENZA
PNEUMOCOCCAL
HEPATITIS B
VACCINES
BACKGROUND
RECOMMENDATIONS
 >36,000 Deaths Annually From
Annual Influenza Vaccine: All
Diabetics ≥6 Months Old
Pneumococcal Vaccine: All
“flu”
 Diabetics 6X More Likely to be
Hospitalized/3X More Likely to
Die From Complications of
Influenza & Pneumonia
 Anyone on Dialysis is at
Increased Risk for Hepatitis B
and C
Diabetics >2 Years Old;
-- Repeat One Time in
Individuals >64 Years of Age,
Who Were Previously
Immunized if the Vaccine Was
Given More Than 5 Years
Previously
Hepatitis B Vaccine: Series of 3
Shots
KEEPING TRACK
PRECONCEPTUAL COUNSELING
 Women With Pre-existing




Diabetes Have 2-5 X
Increased Risk of
Miscarriage & Stillbirth
Increased Incidence of Anatomic
Malformations of Heart
and Spine
Increased Preeclampsia, Fetal
Macrosomia, Cesarean
Delivery
Excellent Glycemic Control
BEFORE Conception as
Well as During Pregnancy
Specialized Testing (U/S, EKG,
Ophthalmology, NST, etc)
THE TEAM
Clinical Diabetic Educator
Registered Dietician
Clinician (Physician, PA, NP)
Podiatrist
Ophthalmologist
Dentist
Social Worker
Psychologist
Audiologist
Cardiologist
Nephrologist
Gastroenterologist
FAMILY INVOLVEMENT
 All Family Members Should
be “On the Same Page”
 No Reason Everyone Cannot
Eat the Same Food
 Encourage Family Exercise
 Express Caring but Do Not
Become Heavy Handed – WE
Are NOT The Food Police
BUT I’M AN AUDIOLOGIST…
 Know Your Patient’s




History & Meds
Watch For Otologic
Complications
Refer to Primary or
Specialty Care
Reinforce the Team
Goals
Swift Intervention for
Malignant Otitis
Resources

National Diabetes Education Program
1 Diabetes Way
Bethesda, MD 20892–3600
Phone: 1–800–438–5383
Fax: 703–738–4929
Internet: www.ndep.nih.gov

American Diabetes Association
National Service Center
1701 North Beauregard Street
Alexandria, VA 22311
Phone: 1–800–DIABETES (342–2383)
Fax: 703–549–6995
Internet: www.diabetes.org

American Association of Diabetes
Educators
100 West Monroe, Suite 400
Chicago, IL 60603
Phone: 1–800–338–3633 or 312–424–2426
Diabetes Educator Access Line: 1–800–
TEAMUP4 (832–6874)
Fax: 312–424–2427
Internet: www.diabeteseducator.org

Juvenile Diabetes Research Foundation
International
120 Wall Street
New York, NY 10005–4001
Phone: 1–800–533–2873 or 212–785–9500
Fax: 212–785–9595
Internet: www.jdrf.org
Anything from the Joslin Clinic
REFERENCES
 Diabetes Care, Volume 33, Supplement 1, January 2010
 Brazilian Journal of Otolaryngology 75(4):573-578, July/August 2009
 American Family Physician 79(1):29-36, January 1,2009
 American Family Physician 74(9):1510 – 1516, 2006
FOR NOW…..
ANY QUESTIONS