diabetes mellitus global and national prevalence of diabetes global and national prevalence of...
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Diabetes MellitusDiabetes Mellitus
Global and national prevalence of Global and national prevalence of diabetesdiabetes
Types of diabetesTypes of diabetes Pathogenesis of diabetesPathogenesis of diabetes Classification and criteria for lab Classification and criteria for lab
diagnosis of diabetesdiagnosis of diabetes Lab investigations for a patient of Lab investigations for a patient of
diabetesdiabetes MCQ’sMCQ’s
Patient J.L., December 15, 1922
February 15, 1923
The Miracle of The Miracle of InsulinInsulin
Diabetes MellitusDiabetes Mellitus
““Diabetes is a dreadful Diabetes is a dreadful
affliction,---------”. affliction,---------”.
Areteus of Cappadosia in 2Areteus of Cappadosia in 2ndnd Century. Century.
It continues to be a sinister disease, if It continues to be a sinister disease, if
not taken care of.not taken care of.
Sheikh M.Z, Diabetes Mellitus: The Continuing Challenge,
JCPSP 2004 Vol.14(2), 63-64
Diabetes a Diabetes a globalglobal epidemic epidemic
YearsYears Diabetics Diabetics (Million) (Million)
19981998 135135
20032003 170170
20252025 300300Sheikh M.Z, Diabetes Mellitus: The Continuing Challenge,
JCPSP 2004 Vol.14(2), 63-64
WHO ranks Pakistan 7th on diabetes
prevalance list- (The Nation ; English Daily- 15th
Nov 2008)
Pakistan ranked eighth in the world for Diabetes Mellitus (1995),
After India, China, USA, Russia, Japan, Brazil, and Indonesia.Asian and
other developing countries have higher prevalence of
diabetes mellitus as compared to Western population
Sheikh M.Z, Diabetes Mellitus: The Continuing Challenge,
JCPSP Vol.14(2) 63-64 ,
WHO Estimates
Diabetes Diabetes epidemiologyepidemiology in in PakistanPakistan
YearsYears Diabetics Diabetics (Million)(Million)
19951995 4.34.3
20252025 14.514.5
Sheikh M.Z, Diabetes Mellitus: The Continuing Challenge,
JCPSP 2004 Vol.14(2) 63-64
The provincial prevalence of diabetes The provincial prevalence of diabetes mellitus- Pakistanmellitus- Pakistan
Basit .A et al, Frequency of Chronic Complications of type II Diabetes
JCPSP 2004 Vol.14 (2): 79-83
*Shera AS et a; Pak national diabetes survey, J of Primary Care Diab, 2010 Vol 4 79-83
Province Province DiabetesDiabetes
BalochistanBalochistan 8.4%8.4%
Kyber Pakhtun Khwa Kyber Pakhtun Khwa (KPK)(KPK)
11.1%11.1%
SindhSindh 13.9%13.9%
Punjab*Punjab* 10.910.9
GenderGender prevalence of prevalence of DMDM
Sheikh M.Z, Diabetes Mellitus: The Continuing Challenge,
JCPSP 2004 Vol.14(2) 63-64
Diabetes MellitusDiabetes Mellitus
MalesMales 16.2%16.2%
FemalesFemales 11.7%11.7%
Impaired Glucose Tolerance
MalesMales 8.2%8.2%
Females 14.3%
SURGESURGE IN DIABETES MELLITUS IN DIABETES MELLITUS
Developing countriesDeveloping countries > 200%> 200%
Developed countries > 45%Developed countries > 45%
Type 2 diabetes, will be 90% of all cases..
Sheikh M.Z, Diabetes Mellitus: The Continuing Challenge,
JCPSP 2004 Vol.14(2) 63-64
Normal Pancreatic Islets:Normal Pancreatic Islets:
ß cells ß cells Glucagon cellsGlucagon cells
Insulin Promotes Anabolism
Insulin lowers plasma glucose by:
1. Increasing glucose transport into most insulin sensitive cells
2. Enhancing cellular utilization and storage of glucose
3. Enhancing utilization of amino acids
4. Promoting fat synthesis
INSULIN
Glucagon Is Dominant In The Fasting State
Glucagon prevents hypoglycemia.Glucagon is secreted when plasma glucose
levels fall below 100 mg/dL.The liver is the primary target of glucagon.Glucagon stimulates glycogenolysis and
gluconeogenesis to increase glucose output by the liver.
Glucagon release is also stimulated by plasma amino acids.
GLUCAGON
Pathogenesis of Type Pathogenesis of Type 1DM1DM
Environment ?Environment ?
Viral infe..??Viral infe..??Genetic Genetic
HLA-DR3/DR4HLA-DR3/DR4
Severe Insulin deficiencySevere Insulin deficiency
ß cell Destructionß cell Destruction
Type 1 DMType 1 DM
Autoimmune Insulinitis Autoimmune Insulinitis
Putativetrigger
Circulating autoantibodies (ICA, GAD65)
Cellular autoimmunityCellular autoimmunity
Loss of first-phase insulin response (IVGTT)
Glucose intolerance (OGTT)
Clinicalonset—
only 10% of-cells remain
Time
-Cell mass 100%
“Pre”-diabetes
Geneticpredisposition
Insulitis-Cell injury
Eisenbarth GS. N Engl J Med. 1986;314:1360-1368
Diabetes
Natural History Of “Pre”–Type 1 Natural History Of “Pre”–Type 1 DiabetesDiabetes
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InsulinitisInsulinitis
Type 1 DM
Pathogenesis of Type 2 Pathogenesis of Type 2 DMDM
EnvironmentEnvironment
Obesity ???Obesity ???ß cell defectß cell defect
GeneticGenetic
ß cell ß cell
exhaustionexhaustion Type 2 DMType 2 DM
Insulin resistanceInsulin resistance
Relative Insulin Def.Relative Insulin Def.
IDDMIDDM
Abnormal SecretionAbnormal Secretion
J ack in the Box
Bacon Ultimate Cheeseburger
1020 Calories
71 grams of Fat
Average American
child or teen
watches 3-4 hours TV per day
I s I t Gluttony or Sloth??
H4046
Subcutaneous Fat Gluteal Fat Viceral Fat
Islets in Type 2 Diabetes:Islets in Type 2 Diabetes:
Loss of ß cellsLoss of ß cellsAmyloid depositsAmyloid depositsHyalinizationHyalinization
Adapted from Ramlo-Halsted BA, Edelman SV. Prim Care. 1999;26:771-789
Natural History of Type 2 Natural History of Type 2 DiabetesDiabetes
Macrovascular complicationsMicrovascular complications
Insulin resistanceInsulin resistance
ImpairedImpairedglucose toleranceglucose tolerance
UndiagnosedUndiagnoseddiabetesdiabetes Known diabetesKnown diabetes
Insulin secretionInsulin secretion Postprandial glucose
Fasting glucoseFasting glucose
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Type-1Type-1 Type-2Type-2 AgeAge: < 40 Years: < 40 Years DurationDuration: Weeks: Weeks KetonuriaKetonuria: Common: Common Insulin-Insulin- Dependent Dependent AutoantibodyAutoantibody: Yes: Yes Family HistoryFamily History: No: No Insulin levelsInsulin levels: very : very
lowlow IsletsIslets: Insulinitis: Insulinitis ComplicationsComplications: :
Acute & MetabolicAcute & Metabolic
> 40 Years> 40 Years Months to yearsMonths to years RareRare Independent *Independent * NoNo YesYes Normal or high *Normal or high * Normal / ExhaustionNormal / Exhaustion ComplicationsComplications
Late and vascular. Late and vascular.
I. CLASSIFICATION AND I. CLASSIFICATION AND DIAGNOSIS OF DIABETESDIAGNOSIS OF DIABETES
Classification of DiabetesClassification of Diabetes
Type 1 diabetesType 1 diabetes ββ-cell destruction-cell destruction
Type 2 diabetesType 2 diabetes Progressive insulin secreting defectProgressive insulin secreting defect
Other specific types of diabetesOther specific types of diabetes Genetic defects in Genetic defects in ββ-cell function, insulin action-cell function, insulin action
Diseases of the exocrine pancreasDiseases of the exocrine pancreas
Drug- or chemical-inducedDrug- or chemical-induced
Gestational diabetes mellitusGestational diabetes mellitus
ADA. I. Classification and Diagnosis. Diabetes Care 2011;34(suppl 1):S12.
Criteria for the Diagnosis of DiabetesCriteria for the Diagnosis of Diabetes
HbA1CHbA1C ≥6.5% ≥6.5%OROR
Fasting plasma glucose (FPG)Fasting plasma glucose (FPG)≥126 mg/dl (7.0 mmol/l)≥126 mg/dl (7.0 mmol/l)
OROR
Two-hour plasma glucose ≥200 mg/dl (11.1 Two-hour plasma glucose ≥200 mg/dl (11.1 mmol/lmmol/l) during an OGTT) during an OGTT
OROR
A random plasma glucoseA random plasma glucose ≥200 mg/dl (11.1 ≥200 mg/dl (11.1 mmol/l)mmol/l)
ADA. I. Classification and Diagnosis. Diabetes Care 2011;34(suppl 1):S13. Table 2.
Prediabetes: IFG, IGT, Increased A1CPrediabetes: IFG, IGT, Increased A1C
Categories of increased risk for diabetes Categories of increased risk for diabetes (Prediabetes)*(Prediabetes)*
FPGFPG 100-125 mg/dl 100-125 mg/dl (5.6-6.9 mmol/l)(5.6-6.9 mmol/l): IFG: IFG
oror
2-h plasma glucose in the 75-g OGTT2-h plasma glucose in the 75-g OGTT140-199 mg/dl (7.8-11.0 mmol/l): IGT140-199 mg/dl (7.8-11.0 mmol/l): IGT
oror
A1C 5.7-6.4%A1C 5.7-6.4%
*For all three tests, risk is continuous, extending below the lower limit of a range and becoming disproportionately greater at higher ends of the range.
ADA. I. Classification and Diagnosis. Diabetes Care 2011;34(suppl 1):S13. Table 3.
Recommendations:Recommendations:Detection and Diagnosis of GDMDetection and Diagnosis of GDM
ScreeningScreening use use plasma glucose fasting plasma glucose fasting and 2 hours after breakfast,and 2 hours after breakfast, if abnormal go for 50 gram oral glucose if abnormal go for 50 gram oral glucose
challenge test.challenge test.
In pregnant women previously known to have diabetes, In pregnant women previously known to have diabetes, and and screening test abnormal go for screening test abnormal go for confirmatory test for diagnosis of GDM at 24-28 weeks gestation, using a 100 gram glucose- OGTT
Other investigations:
•Serum Urea.
•Serum Creatinine
•Serum Lipid profile: cholesterol; triglyceride; LDL-C; HDL-C.
•Serum sodium, potassium,
•24 hour urine for: protein; creatinine clearance; microalbumin;
•Spot urine for microalbumin
•Spot urine for albumin creatinine ratio- ACR
Other investigations and evaluations:
Blood complete picture
•Urine routine examination: glucose; protein/, albumin, WBC, sp gravity.
•Urine for ketone bodies
•Arterial blood gases-ABG’s
•Ultra sound liver- Fatty liver
•Fundoscopy- for diabetic retinopathy;
•Routine eye exam: diabetic cataract
•Blood pressure measurement
•Examination of feet- ulcer; poor sensations/neuropathy
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