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Transcript of 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
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