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CHAIR: Prof.Dr.B.Jayakumar . Diabetes Mellitus definition, classification & aetiopathogenesis. Introduction. The prevalence of Diabetes is increasing rapidly,particularly in children and young adults. One third of cases of Diabetes remain undiagnosed.
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Only few patients with Diabetes broadly achieve targets for blood pressure,lipid, or glucose management.
Second century understanding:
Greek Physician Aretaeus of Cappadocia
Diabetes mellitus may present with characteristic symptoms such as thirst, polyuria, blurring of vision, and weight loss.
The long-term effects of diabetes mellitus include progressive development of the specific complications of retinopathy with potential blindness, nephropathy that may lead to renal failure, and/or neuropathy with risk of foot ulcers, amputation, Charcot joints, and features of autonomic dysfunction, including sexual dysfunction.
Several pathogenetic processes are involved in the development of diabetes. These include processes which destroy the beta cells of the pancreas with consequent insulin deficiency, and others that result in resistance to insulin action.
II. Type 2 diabetes
D. Endocrinopathies— acromegaly, Cushing's syndrome, glucagonoma, pheochromocytoma, hyperthyroidism, somatostatinoma, aldosteronoma.
F. Infections— congenital rubella, cytomegalovirus, coxsackie.
H. Other genetic syndromes sometimes associated with diabetes— Down's syndrome, Klinefelter's syndrome, Turner's syndrome, Wolfram's syndrome, Friedreich's ataxia, Huntington's chorea, Laurence-Moon-Biedl syndrome, myotonic dystrophy, porphyria, Prader-Willi syndrome.
Genetic loci contributing susceptibility to Type 1 DM are polymorphisms in the promoter region of the insulin gene, the CTLA-4 gene, interleukin-2 receptor, and PTPN22.
Pancreatic islet molecules targeted by the autoimmune process include
These Genetic Environmental & Immunological factors interact leading to destruction of beta cells and insulin deficiency.
The reason(s) for the decline in insulin secretory capacity in type 2 DM is
Postreceptor defects in insulin-regulated phosphorylation/dephosphorylation plays the predominant role in insulin resistance.
Insulin receptor levels and tyrosine kinase activity in skeletal muscle are reduced, but these alterations are most likely secondary to hyperinsulinemia and are not a primary defect.
Failure to supressgluconeogenesis
Free Fatty Acid flux from adipocytes Increased lipid synthesis in hepatocytes.
4. Insulin promoter factor-1 (IPF-1; MODY 4) MODY 4 arises from mutations of the IPF1homeobox gene on chromosome 13.
Point mutations in mitochondrial DNA have been found to beassociated with diabetes mellitus and deafness.
Genetic abnormalities that result in the inability to convertproinsulin to insulin and the resultant carbohydrate intolerance have been identified
and 3. Rabson-Mendenhall syndrome
are two paediatric syndromes that
have mutations in the insulin receptor gene with subsequentalterations in insulin receptor function and extreme insulinresistance.
epinephrine) antagonize insulin action.
(e.g. Acromegaly, Cushing’s Syndrome, Glucagonoma and Phaeochromocytoma).
typically resolve when the hormone excess is removed.
diabetes in persons with insulin resistance.
binding to the insulin receptor.
recognition during pregnancy.
Insulin resistance related to the metabolic changes of late pregnancy, and
glucose load) or both are appropriate.
Immunolical markers: In contrast to type 2 DM, a long asymptomatic period of hyperglycemia is rare prior to the diagnosis of type 1 DM. A number of immunologic markers for type 1 DM are becoming available (discussed below), but their routine use is not recommended now.
Fasting > 7.0 (> 126)
Or2-h post glucose load > 11.1 (> 200)
Fasting (if measured) < 7.0 (< 126)
& 2-h post glucose load > 7.8 (> 140) & < 11.1(<200)
Fasting > 6.1 (> 110) & < 7.0 (< 126)and (if measured)
2-h post glucose load < 7.8 (< 140
Some investigators have advocated the hemoglobin A1C (A1C) as a diagnostic test for DM.
risk factor analysis and, if appropriate,use of an OGTT.
●Risk assessment for GDM should be undertakenat the first prenatal visit.
screening by measuring the plasma orserum glucose concentration 1 h after a50-g oral glucose load (glucose challengetest) and perform a diagnostic100-g OGTT on that subset of womenexceeding the glucose threshold valueon the glucose challenge test.
When the two-step approach is used, a glucosethreshold value _140 mg/dl identifies80% of women with GDM, and theyield is further increased to 90% by usinga cutoff of _130 mg/dl.