pamela d. parker, m.d., f.a.c.o.g. assistant professor a.t. still university school of osteopathic...

Pamela D. Parker, M.D., F.A.C.O.G.Assistant Professor

A.T. Still University School of Osteopathic Medicine ArizonaNovember 2010

pparker@atsu.edu

OBJECTIVES

1.Discuss Recent Statistics and Trends2.Describe the Various Forms Of Diabetes

and Explain the Pathophysiology3.Review Criteria For Diagnosis4.Explain Acute and Chronic Complications 5.Outline Pharmacologic and Non-

Pharmacologic Therapies6.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 EPIDEMIC1994 2003

WHO IS AT RISK TO DEVELOP DIABETES?

+ Family HistoryAmerican Indian /

Alaska NativeHispanics/LatinosAfrican AmericansPacific IslandersAsiansHistory of

Gestational Diabetes

Advancing AgeObesityLack of ExerciseCo-MorbiditiesHypertensionHyperlipidemiaAutoimmune

Disorders

DIABETES & ETHNICITY

American Indians/Alaska Native

African AmericansHispanic/LatinosNon-Hispanic Whites

Source: ADA and the CDC – 2/08

GENETICS vs LIFESTYLEPima 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

DIABETES MELLITUSWHAT DOES IT MEAN?

From the ancient Greek:DIABETES: siphonMELLITUS: 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 DEFINEDA GROUP of Metabolic

DisordersElevated Blood

Sugar (Hyperglycemia) Due to Defects in: INSULIN SECRETION INSULIN ACTION BOTH

INSULIN is a HORMONEConverts 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 MessengersEndocrine 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 & INSULINTwo Main Pancreatic

Hormones Control Blood Glucose

GLUCAGONProduced By ALPHA (α) CellsELEVATE Blood Sugar

INSULIN Produced by BETA(β) CellsLOWER Blood Sugar

These are Examples of Negative Feedback Mechanisms

CLASSIFICATION OF DIABETESTYPE 1 TYPE 2

Immune-Mediated5-10% of Diabeticsβ Cell Destruction Lack

of InsulinPresence of Multiple

AntibodiesAssociated with Other

Autoimmune DisordersPreviously 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

OTHER CATEGORIES OF DIABETESGESTATIONAL

DIABETESDevelops 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/TraumaDrug-InducedViral-Induced

Result of Uncontrolled Gestational Diabetes

PATHOPHYSIOLOGY OF TYPE 1 DIABETESIN A NUTSHELL - HYPERGLYCEMIA

Absence of Insulin Affects 3 Target Tissues

Liver/Fat/MuscleInability to Absorb

NutrientsContinuous 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 InsulinInsulin Resistance

Decreased Peripheral Utilization of GlucoseIncreased Hepatic Glucose

ProductionExcess Breakdown of Fat

NATURAL HISTORY OF TYPE 2 DIABETES

Up to 15 Years of Abnormalities Before the Diagnosis is Made

SYMPTOMS OF DIABETESIrritabilityPoor Work/School

PerformanceDiarrhea/ConstipationMuscle CrampsAnxietyChest PainFruity BreathImpairment 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 % **

**New Guideline 2010

Gestational Diabetes – 2 Tier Testing50 gm 1 Hour Testing130 or 135 or 140 mg/dL

100 gm 3 Hour Testing95/180/155/140

Or

105/190/165/145 mg/dL

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 ifHemoglobin 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

TESTING IN ASYMPTOMATIC PATIENTSBMI≥ 25 kg/m²

(overweight) Plus Risk Factors

Physical Inactivity1˚ Relative with

DiabetesHigh Risk Ethnic

GroupPrior 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 AbnormalBlood 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 GOALSNONPREGNANT

ADULTSPREGNANT ADULTS

A₁c < 7.0%Fasting Plasma

Glucose70-130 mg/dL

Peak Postprandial Plasma Glucose

< 180 mg/dL

With Gestational Diabetes

Fasting Plasma Glucose ≤95

2 Hour Postprandial ≤120

With Preexisting DiabetesFasting 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 Kidney25% Reduction In Diabetes-Related Deaths18% Reduction In Myocardial Infarction

TREATMENT STRATEGIESOngoing Assessment

Lifestyle ChangesMedicationsPrevent/Minimize

ComplicationsAppropriate Referral

ONGOING ASSESSMENTHISTORYPHYSICAL EXAM

LABORATORYGLUCOSE MONITORING

SPECIALTY CARE

LIFESTYLE CHANGES

PATIENT HISTORYAge at Onset &

Characteristics of Diabetes

Eating Patterns; Nutritional Status;

Weight HistoryGrowth &

DevelopmentPhysical ActivityReview Previous

Treatment RegimensPsychosocialResults of Glucose

Monitoring

Review Complications Microvascular

Retinopathy – Visual ChangesNephropathy - ProteinuriaNeuropathy: Sensory – Feet Autonomic –GI; Sexual

Dysfunction Macrovascular

Coronary Heart Disease (CHD)Cerebrovascular Disease (CVD)Peripheral Arterial Disease (PAD)

Dental Otologic/Audiology

PHYSICAL EXAMINATIONHeight/Weight/BMIBlood Pressure

(Orthostatic)/ABIEyes – Looking for

RetinopathyEars/Nose/Mouth/ThroatSkin (Injection Sites;

Ulcers; Diabetic Skin Changes)

Feet -Comprehensive Exam MusculoskeletalCardiovascular – Central

And PeripheralNeurologic

OBESITY PARAMETERSCalculate The Body Mass Index BMI = Wt

(Kg) ÷Ht(m2)

< 18.5 Low 18.5 to 24.9 Healthy 25 to 29.9 Overweight > 30 ObeseCentral 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 ArteriesReflects Peripheral Arterial (Vascular) Disease

(PAD)Atherosclerotic Disease Usually Affects Lower

Extremities Before Upper ExtremitiesSubjects With PAD Usually Also Have Coronary

Artery DiseaseABI < 0.9 Is Abnormal Implies Vascular

ObstructionDecreased ABI Often Associated With

Uncontrolled Diabetes (Hyperglycemia)

Asymptomatic in the Beginning

.

Neurologic ExaminationCentral 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 TESTINGBLOOD SUGAR FBS < 100; PPBS <140A1c - < 7RENAL FUNCTION

Serum Creatinine Protein < 30 µg/mg(spot UA)LIPIDS

TC <200, TG < 150, LDLc<100 mg/dLEKG

CELIAC DISEASE TESTINGNew RecommendationAll 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 MONITORINGCHECK DON’T GUESSManaging 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 CAREPODIATRY

OPHTHALMOLOGY

AUDIOLOGY

DENTAL

ETC.[Cardiology, Nephrology,

Gastroenterology, Psychiatry, Psychology]

FOOT CAREDAILY FOOT

CHECKS/MIRRORPODIATRIST

MONOFILAMENT TESTING

PROPER FOOTWEARTEMPERATURE

AWARENESSSTOP 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

AUDIOLOGYRelationship

Between Diabetes & Hearing Loss is Controversial

Diabetes is a Well-Known 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 EARBlood 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

DiseaseTherefore, 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 OtitisPus Draining from Necrotic Ear Canal & Underlying Osteomyelitic Bone; Swelling of Auricle With Loss of Cartilaginous Architecture

DENTALLots Of

Microvasculature In The Oral Cavity

Also Home For Many Bacteria

Hyperglycemia Increases Probability of Infection

SOLUTION:1) Good Oral Hygiene – Flossing and Brushing2) Dental Visit Twice Yearly

LIFESTYLE CHANGESNUTRITIONPHYSICAL ACTIVITY

TOBACCOALCOHOLSTRESS

REDUCTION

NUTRITIONMeal Plans NOT DIETSLOW Glycemic Index

ChoicesCarbohydrate 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. EBMLow Glycemic Index Diet lowered A1c levels & reduced hypoglycemic episodes.

Select More Choices From The Bottom Than the Top

GLYCEMIC INDEXFlour Comparison Glycemic Pyramid

INDIVIDUALIZE

PHYSICAL ACTIVITYPhysical 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 REDUCTIONPhysical ActivityRelaxation

Techniques – Yoga, Visualization

Alternative Therapies – Acupuncture, Acupressure, Aroma

TherapyFormal Counseling if

RequiredDSME

MEDICATIONS – WHEN LIFESTYLE CHANGE IS NOT ENOUGH

LACK OF INSULIN INSULIN INSENSITIVITY ++

TYPE 1 DIABETESINSULIN IS

THE ANSWER• Rapid-Acting• Intermediate-Acting• Long-Acting• Mixed

INSULIN – THE WONDER DRUG

TYPE 2 DIABETES:MATCHING PHARMACOLOGY TO

PATHOPHYSIOLOGYInsulin Secretagogues

Increase Pancreatic Insulin Outputα Glucosidase Inhibitors(Starch

Blockers)Improve Glucose Metabolism In Small

Intestine(Starch Blockers)Amylin Analogues

Potentiate Insulin EffectsIncretin Mimetics/Enhancers

Stimulate Insulin SecretionDecrease 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 TREATMENTInsulin Secretagogues

SulfonylureasGlyburide, Glipizide,

Glimepiride

Non-SulfonylureasNateglinideRepaglinide

α Glucosidase InhibitorsAcarboseMiglitol

Incretin Mimetics/EnhancersExenatide, Lyraglutide

BiguanidesMetformin

Thiazolidenediones (TZDs)

PioglitazoneRosiglitazone

Amylin AnaloguesPramlintide

DRUGS COME FROM THE STRANGEST PLACES

Exenatide (Byetta)First Incretin Released

by FDAGLP-1 AgonistSlows 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 COMPLICATIONSRetinopathyCV diseaseKidney diseaseNeuropathyGastroparesisImpotenceAutonomic

NeuropathyEtc. Etc.

HOW?Diabetic Self-

Management 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 EatingBeing ActiveMonitoring

Taking MedicationsProblem SolvingHealthy Coping

Decreasing Risks

American Association of Diabetes Educators

BLOOD PRESSURE MONITORINGGOALS

Systolic < 130 (SBP)Diastolic <80 (DBP)

INTERVENTIONSWhite Coat HypertensionLifestyle Changes if 130-

139/80-89Medication(s) if ≥140 SBP

or 90 DBPDASH 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

VACCINESBACKGROUND

>36,000 Deaths Annually From “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

RECOMMENDATIONS

Annual Influenza Vaccine: All Diabetics ≥6 Months

OldPneumococcal Vaccine: All

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 TEAMClinical Diabetic Educator

Registered DieticianClinician (Physician, PA,

NP)Podiatrist

OphthalmologistDentist

Social WorkerPsychologistAudiologistCardiologistNephrologist

Gastroenterologist

FAMILY INVOLVEMENTAll 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 & MedsWatch For Otologic

ComplicationsRefer to Primary or

Specialty Care Reinforce the Team

GoalsSwift Intervention

for Malignant Otitis

Resources National Diabetes Education

Program1 Diabetes WayBethesda, MD 20892–3600Phone: 1–800–438–5383Fax: 703–738–4929Internet: www.ndep.nih.gov

American Diabetes AssociationNational Service Center1701 North Beauregard StreetAlexandria, VA 22311Phone: 1–800–DIABETES (342–2383)Fax: 703–549–6995Internet: www.diabetes.org

American Association of Diabetes Educators 100 West Monroe, Suite 400Chicago, IL 60603Phone: 1–800–338–3633 or 312–424–2426Diabetes Educator Access Line: 1–800–TEAMUP4 (832–6874)Fax: 312–424–2427Internet: www.diabeteseducator.org

Juvenile Diabetes Research Foundation International120 Wall StreetNew York, NY 10005–4001Phone: 1–800–533–2873 or 212–785–9500Fax: 212–785–9595Internet: 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