- diabetes mellitus and its complications are now the third leading cause of mortality in the united...
TRANSCRIPT
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- DIABETES MELLITUS AND ITS COMPLICATIONS ARE NOW THE THIRD LEADING CAUSE OF MORTALITY IN THE UNITED STATES AND THE SECOND LEADING CAUSE OF BLINDNESS.
- DIABETES MELLITUS AND ITS COMPLICATIONS ARE NOW THE THIRD LEADING CAUSE OF MORTALITY IN THE UNITED STATES AND THE SECOND LEADING CAUSE OF BLINDNESS.
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-ESTIMATED PREVALENCE IN
U.S.A 3 - 6 % AND INCREASING
RAPIDLY
-ESTIMATED PRVALENCE IN
SAUDI ARABIA to 2003
18-24%
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-STROKE, M1 AND END – STAGE RENAL
DISEASE ARE FREQUENT CAUSES OF
MORTALITY.
-THE DISEASE IS FOUND THROUGHOUT THE WORLD AT VARYING PRVALENCE RATE.
- IN PIMA INDIANDS PREVALENEC RATE AT 50 %
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NIDDM IS MAJOR CAUSE OF MORBIDITY AND MORTALITY PREVAILING FROM,MACROVASCULAR DISEASE , BUT ALSO FROM SPECIFIC COMPLICATIONS OF DISABETES , RETINOPATHY , NEPHROPATHY AND NEUROPATHY.
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DIABETES MELLITUS IS ADISEASE
COMPLEX CHARACTERISED BY RELATIVE OR
ABSOLUTE INSUFFICIENCY OF INSULIN
SECRETION AND A CONCMMITANT
INTENSITIVITY OR RESISTANCE TO THE
METABOLIC ACTION INSULIN TARGET
TISSUE.
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NON INSULIN DEPENDENT DABETES ( NIDDM ) IS by FAR THE MOST PREVALENT FORM OF DIABETES WORLD – WIDE , FORMING MORE THAN 95 % OF ALL DIABETES IN MANY DEVELOPING COUNTRIES .
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Genetic Factors
HLA class 2 antigens in DR + DQ regions =
>90% Caucasian patients have either DR3 or DR4 , DR2 is protective.
Environmental Factors:
No Specific factors have been identified
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Viruses
The risk greater for children born between February-September
IgM antibodies against conxsackievirus found in
25-30% of new cases suggesting recent infection
( cont . )
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Coxsackievirus B RNA has been detected in 65% of children under the age of 7 years with newly diagnosed IDDM compared with 4% of controls which is consistent with recent Infection..
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(CONT)
Dietary Factors
Cow,s mild feeding fist 4 months indicated risk of subsequent IDDM, whilst breast feeting appeared protective.
Case controlled studies in Sweden have indicated a positive association between IDDM ,high protein intake and frequency of consumption of foods containing nitrosamine.
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(CONT)
Loss of first- phase insulin secretion in response to intravenous glucose is highly Predictive of early onset of diabetes .
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Islet cell antibodies in ICA are present in 80% of children at the time of diagnosis and have been detected up to 15 years before diagnosis of IDDM.
Long- term follow up has shown that family members with ICA are at greatly increased risk of progression to diabetes and this risk is directly related to persistence and strength of the ICA reaction.
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Other antibodies include:
insulin autoantibodies ( IAA)
antibodies to GAD ( Glutamate decarboxylase )
Protein tyrosine phosphatase IA-2
The presence of ICA together with 2 or more markers indicate a greater than 80% risk of progressing for insulin treatment in otherwise healthy family members .
( cont.)
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0
50
100RELEASE
“HONEYMOON” PERIOD
OVERT DIABETES
PROGRESSIVE IMPAIRMENT IN INSULIN RELEASE
NORMAL INSUILN
TIME(YR)
BE
TA
-CE
LL
MA
SS
(%
OF
MA
X)
0
BIRTH
IMMUNOLOGIC ABNORMALITES
GENETIC PREDISPOSITION
NATURAL HISTORY OF BETA-CELL DEFECT
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DUE TO BETA-CELL RESERVE
INSULIN REQUIREMENT DECREASED
LASTS FOR UP TO 1 YR
PATIENT ALWAYS RELAPSES
TREATMENT PROPOSED TO EXTEND HONEYMOON PERIOD STILL EXPERIMENTAL
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RELATIONSHIPS OF TYPE I WITH OTHER AUTOIMMUNE DISEASES
ASSOCIATION BETWEEN HLA GENES AND DIABETES
PRESENCE OFANTI-ISULET AND/OR ANTI-INSULIN ANTIBIES
PRESENCE OF INFLAMMATORY CELLS AROUND ISLETS
EVIDENCE OF IMMUNE SYSTEM ACTIVATION
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0 50
Slow B cell failure Less insulitis GAD antibodies/ ICA HLA associations+
Years
Acute B cell failure
Insulitis
1AA/1A-2 antibodies/1CA/GAD antibodies HLA
associations +++
The spectrum of autoimmune diabetes
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0 50Years
? LADASlow type 1
Classic type 1
Type 1 in infancy
Clinical spectrum
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The clinical and immunogenetic characteristics of insulin
dependent diabetes mellitus change according to age at
presentation
1AA,insulin auto-antibodies:1A-2,protein1A-2:GAD,glutamate decarboxylase;ICA,islet cell
antibodies,LADA, latent autoimmune diabetes in the adult
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DR2
TYPE I DR3
DR4
A 2 ---------- BW51--------------- DR4
B8-------------B15 GENERALLY LOW IN POPULATION
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W.H.O. CLASSIFICATION
TYPE I ( INSULIN DEPENDET DIABETES MLLITUS IDDM)
HAVE LITTLE OR NO ENDOGENOUS INSULIN
ONSET OF DISEASE IS CLNICALLYABRUPT WITH : MARKED POLYURIA, POLYDIPSIA POLYPHAGIA WEIGHT LOSS, FATIGUE.
THESE PATIENTS ARE HIGHLY PRONE TO KETOSTS
THEY FREQUENT ARE PRESNT IN AND INITIAL ATTACK OF KETOACIDOSIS
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GENERALLY HAVE WEIGHT LOSS AND ARE FREQUENTLY AT OR BELOW IDEAL WEIGHT AND ARE THEREFORE PARTICULARY SENSITIVE TO INSULIN (ESPECIALLY REGULAR OR SOLUBLE INSULIN).
CAN OCCUR AT ANY AGE , BUT PEAKS IN THE
MIDDLE OF THE FIST DECADE AND AGAIN AT THE
TIME OF GROWTH ACCELERATION OF ADOLESCENCE.
OLD TERM – JUVENILE ONSET DIABETES MLLITUS .
TYPE I CONTD . .
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A PRODOMAL PHAE OF POLYUREA , POLYDYPSIA AND WEIGH LOSS MAY PRECEDE THE DEVELOPMENT OF KETOACIDOSIS BY A PERIOD OF MONTHS ( MOST COMMONLY 2 - 4 WEEKS ).
GENETIC PREDISPOSISTION ( FAMILY HISTORY LESS STRONGLY ASSOCIATED THAN WITH TYPE II ).
ASSOCIATED WITH SOME HLA HITOCMPATIBILTY ANTIGENS EG . B8, B15, DW3, DW4.
TYPE I CONTD…
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ASSOCIATED WITH ISLET CELL ANTIBODIES
VIRUS AETIOLOGY IS IMPLICATED ESPECIALLY COXACKIE B4 AND MUMPS.
SIGNIFICANT ASSOCIATION WITH CERTAIN AUTOIMMUNE DISORDERS - ADDISON ‘ S , HASHIMOTO’S TYROIDITS, HYPOPARATHYROIDISM, PERNICIOUS ANAEMIA
TYPE I CONTD .. .
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100
90
80
70
60
50
40
30
20
10
COMA 5%
WEIGHT LOSS
35%
DKA 25%
%
POLYURIA 75%
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100
90
80
70
60
50
40
30
20
10
PH< 7.2
20%
HYPERGLYCEMIA AND/ OR
GLYCOSURIA 100%
KETONURIA 85%
HCO3<18 60%
%
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NIDDM IS ALMOSTCERTAINLY A HETEOGENOUS MIXTURE OF CONDITIONS CHARACTERISEDBY HYPERGLYCAEMIA , OF INSULIN RESISTANCE AND INSULIN HYOP-SECRETION AND LACK OF DEPENDENCE ON EXOGENOUS INSULIN TO MAINTAIN LIFE
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FOR MAJOR ABNORMLITIES APPEAR TO ACCOUNT
FOR THE INAPPROPRIATE HYPERGLYCMIA SEEM IN
TYPE II ( NIDDM) PATIENTS
1- DESCREASE IN QUANTITY INSULIN SECRETED
2- DELAY IN THE TIME OF RELEASE OF INSULIN
3- IMPAIRMET OF THE EFFCTS OF INSULIN ON THE PEREPHERAL TISSUES ( INSULIN RESISTANCE )
4- INCREASE IN HEPATIC GLUCOSE PRODUCTION
TYPE II ( NIDDM )
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DIABETES MELLITUS
TYPE I ( IDDM )
TYPE II ( NIDDM)
- OBESE
- NONBESE
GESTATIONAL DIABETES
OTHER TYPES
IMPAIRED GLUCOSE TOLERANCE ( IGT)
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Due primarily to a Beta cell defect resulting in inadequate insulin secretion for a given blood glucose level .
There is no significant increase in insulin resistance.
Various mutations in the giucokinase gene on
chromosomes 7p, probably account for 10-50% of cases of MODY .
Giucokinase – Mody is characterized by early onset ( often less than 18 months of age ) mild hyperglycaemia which is usually controIIed by diet alone until old age.
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Autosmal Dominant
Diagnostic Criteria
• Diagnosis before 25 years of age in atleast 2 family member .
•No requirement of insulin treatment 5 years after diagnosis and/or C- Peptide positivity.
•Convincing vertical transmission of type II Diabetes mellitus through at least three generations.
•Accounts upto 1% of Diabetes Mellitus population.
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1122334455Gene defectHNF4aGCKHNF1a1PF1HNF1B
Prevalence(%)51570<12
Glycaemia
Progressive deterioration in glycaemia
Mild stable hyperglycaemia
Progressive deterioration in glycaemia
Age of onset (years)
12-35Birth12-2814-4012-28
Other featuresLow glucose rise on OGTT
Sulphonylurea sensitivity
Cystic renal Chronic renal failure
ComplicationsYesVery rareCommon?Yes
Treatment
Progressive increase in requirements
Usually none except in pregnancy
Progressive increase in requirements Sulphonylurea first-line after diet failure
?
Progressive increase requirements
MODY
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GENETICS :
( STRONG FAMILY AGGREGATES ALMOST 100% CONCORDANCE RATE IN IDENTICAL TWINS ( PYKE ET AL )
RACE :
( DIABETES IN MIGRANT INDIANS)
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OBSITY :
(PIMA INDIANS NAURANS)
PHYSICAL INACTIVITY
LONGIVITY :
(DIABETES PREVALENCE INCREASES
WITH AGE E .G . PREVALENCE RATE > 30 % IN ELDERLY IN FINLAND)
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Two genes have been implicated so far : NIDDM 1 and NIDDM2
MODY (Autosomal Dominant )
-MODY 1, (HNF-4) extremely uncommon)
-MODY 2, (Glucokinase gene-impairs B-cell glucose
sensing)
-MODY 3, ( Hepatocyte Nuclear factor 1- ( HNF-1) are more common
Maternally inherited diabetes with deafness ( MIDD) Late onset IDDM
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SYNDROME CLINICAL FEATURES
Progressive cone dystrophy
Colour blindness Liver disease Deafiness Mental etardation
Turner,s 45,xo kayotype Short stature Gonadal dysgenesis
Thalassaemia Iron overland
Table 22.5
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SYNDROMESYNDROMECLINICAL FEATURESCLINICAL FEATURES
Alstrom
• Retinitis pigmentosa
• Deafness
• Obesity
Laurence-Moon-Biedl
• Retinits pigmentosa
• Obesity
• Polydactyly
• Hypogonnadism
Pseudo-Refsum• Retinitis pigmentosa
• Ataxia
• Muscle wasting
Genetic syndromes associated with an early onset NIDDM
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SYNDROMESYNDROMECLINICAL CLINICAL FEATURESFEATURES
Werner’s Premature senility Cataracts
Prader-Willi Obesity Short stature Mental retardation Micropenis
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TYPE II CONTD . . . THE CLINICALPRESENTATION VARIES GREATLY:
I . THEY MAY MANIFEST DM AFTER THE
DEVELOPMENT OF COMPLICTIONS ( E .G.RE
TIOPATHY ) .
II . MAY HAVE SIGNIFICANT POLYRIA ,
POLYDIPSIA ,EASY FATIGUABILITY ETC .
III . MAY BE FOUND BY CHANCE ON ROUTINE
examination
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MILDTO AMRKED OBES IS PRESENT IN 80% TYPE II AT THE TIME OF DIAGNOSIS .
OBESITY IS A MAJOR RISK FACTOR RROBABLY DUE TO THE DECREASE INSULIN RECEPTOR DENSITY AND ABNORMAL COUPLING OF RECEPTOR TO METABOLIC PROCESS THAT OCCUR IN THE OBESE STATE
TYPE II CONTD. . .
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MOSTPATIENTS ARE DIAGNOSED AFTER
THE AGE OF 40 YEARS
OLD NAME - MANTURIY ONSET D.M .
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A GTT IS DOME FOR THOSE IN THE IMPAIRED TOLERANCE RANGE COMMON CAUSES OF TRANSIENT
CARBOHYDRTE INTOLERANCES :
PHYSICAL OR EMOTIONAL STRESS
INFECTION
UNDER NUTRITION
BED REST
TRAUMA
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NONOREGNANT ADULITS
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PLASMA OTHER CRITERIA
GLUCOSE ( mg/dI)
RANDOM > 200 CLASSIC SIGNS AND SYMPTOMS
OR
FASTING >126 ON AT
LEST 2 OCCASIONS
OR
FASTING < 126 SUSTAINED ELEVATED LASMA GLUCOSE DURING AT LEAST 2OGTTs
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OGTT SAMPLE PLASMA GLUCOSE VALUES ( mg/dI)
FASTING < 126
2 HOUR 126- 199
INTERVENING >200
*NONPREGANT
Dx OF IMPAIRED GLUCOSE
TOLERANCE IN ADULTS*
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WHO
DIABETICDIABETIC IMPAIRED GTIMPAIRED GTASTING ASTING >> 8 MMOL 8 MMOL/ / LL
HRS HRS >>11 MMOL11 MMOL / / LL
6- 8 MMOL / L6- 8 MMOL / L
8 – 11 MMOL / 8 – 11 MMOL / LL
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Diabetes mellitus in older adults is the commonest metabolic disorder in mainstream clinical practice
The disorder present an interplay between metabolic dysfunction, vasculopathy and the ageing process
Key Points
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cardinal features with enable clinicians to focus diabetes risk associated with functional decline, visual cognitive disorder depression, and vulnerability to hypoglycemia
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Interventions based on both vascular and rehabilitation models complement the metabolic approach to restructuring diabetes care for elderly
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Diabetes is suspected
Measure FPG or RPG
If FPG >7.8 or RPG > 11.1
If FPG 5.5-7.7 or RPG 7.8-11.0
If FPG < 5.5or RPG< 7.8
Perform OGTT ( 75g)
If FPG >7.8 and/or2hPG > 11.1
If FPG <7.8 and 2hPG 7.8-11.0
If FPG <7.8 and 2hPG< 7.8
Normal Impaired glucose tolerance
Diabetes
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20
18
16
14
12
10
8
6
4
2
0
Fasting 0.5 1.0 1.5 2.0
Diabetic
Impaired
glucose tolerance
Normal
Time after oral glucose ( hours)
Pla
sma
glu
c os e
(m
mo l
/lit
re)
Examples of the oral glucose tolerance test curve
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GLUCOSE INTOLERANCE DEVELOPS
DURING PREGNANCY
OCCURS IN 2% OF PRENGNANT WOMEN
ONSET USUALLY IN 2nd OR 3rd
TRIMESTER
INCREASED FEATAL SIZE AND MORBIDITY
GTT USUALLY RETURNS TO NORMAL AFTER PARTURITION
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Dx TEST INDICATED
CRIERION FOR POSITIVE SCREEN
1 HOUR PLASMA GLUCOSE > 140 mg / dI
If POSITIVE SCREEN
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1.DISEASES PRODUCING ANTI – INSULIN HOSRMONES.
PHAEOCHROMOCYTOMA
CUSHING ‘S
ACHROMEGALY
GLUCAGONOMA
THROTOXICOSIS
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2. DRUGS
THIAZIDE DIURETICS
FRUSOMIDE ( LASIX )
STEROIDS
THYROID HORMONES
ORAL CONTRACETIVES
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COMPLICATIONS OF MANAGEMENT
-HYPOGLYCAEMIA
-KETOACIDOSIS
-LACTICACIDOSIS OTHER COMPLICATIONS
-INFECTIONS
-SOCIAL ETC
TREATEMENT
-DIET
-ORAL HYPOGLYCAEMICS
-INSULIN
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3.ASSOCIATED WITH MANY OTHER DISEASES
EG . MUSLAR DYSTROPHIES
DOWN ‘S
KLEINFELTER’S
TURNER ‘S
FREDERICK’ S ATAXIA
GLYCOGEN STORAGE DISEASE
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CLINICALFEATURES
TYPE IJUVENILE ONST
TYPE IIMATURITY ONSET
KETOSISOBESITYONSET
USUALUNCOMMON
ACUTE OR SUB ACUTE
RAREFREOUENT OFTEN INSIDOUS
EPIDEMIOLOGYINCIDENCE
AGE AT ONSET
PATHOLOGYISLETMASSBETACELLMASS INSULITIS ATONSET
PEAK AGE 12 - 14
MOSTLY < 40 YRS
< 10 % < 10 %
FREQUENT
RISES UNTIL 8TH
DECADE MOSTLY > 40 YRS
MODERATE RED.MODERATE RED.
PROBABLY ABSENT
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IMMUNOLOGYANTIPANCRETICCELL MEDIATEDIMMUNITYANTIPANCREATICCELL HUMORALIMMUNITY
35– 50 % AT ONSET
60 – 85 %
< 5 %
APPROX . 5 %
GENETICSCONCRODANCE WITH IDENTICAL TWITNSASSOCIATED EITHHLA
< 50 %
PRESENT
MOSTLY INVAR
PRESENT
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THE PRESENCE OF COMMONLY
ASSOCIATAED CONDITIONS SHOULD
BE EVALUATED EG:
-
•OBESITY
• HYPERTENSION
• HYPERLIPIDAEMIA
• MACROVASCULARDISEASE
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AT DIAGNOSIS , A COMPLETE HISTORY AND PHYSICAL EXAMINATION ARE ANDATORY AS MACROVASCLUAR ISEASE , AND SOMETIONS MICROVASCULAR COMPLICATIONS ARE RESENT AT DIAGNSIS OF NIDDM
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HETEROGENEOUS DISORDER
CHARACTERIZED BY :
DEFICIENT INSULIN SECRETION
INSULIN RESISTANCE
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•* Mature onset diabetes of the young is inherited in an autsomal dominant manner and associated with 8 cell dysfunction.
* Environmental factors important for NIDDM include physical inactivity, excessive consumption of food leading to obesity stress and some drugs
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•* Non-insulin dependent diabetes mellitus ( NIDDM ) is a heterogeneous disease in which a number of genetic and environmental factors interact to cause diabetes
•* Maternally inhented diabetes and deafness is a distinct subtype of NIDDM
Practice points
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Fasting plasma glucose(mM)
4
6 8 10 12
0
60
80
100
40
20
Mea
n p
iasm
a in
suli
n r
esp
onse
gu
rin
g O
GT
T (
U/m
l)Relationship between fasting glucose and insulin secretion
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HETEROGENEOUS DISORDER
CHARACTERIZED BY :
DEFICIENT INSULIN SECRETION
INSULIN RESISTANCE
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100
90
80
70
60
50
40
30
20
10
00 1 2 3 4 5 6 7 8 9 10
1 marker2 markers>3 markers
Follow – up(years)
IDD
M-f
ree
surv
ival
(%)
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