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Diabetes Mellitus

 Diabetes mellitus is a clinical syndrome characterized by hyperglycemia due to absolute or relative deficiency of insulin.

Aetiological classification 

A. Type 1 diabetes ( Insulin-dependent DM)

  • Immune-mediated
  • Idiopathic

B. Type 2 diabetes ( Not- insulin-dependent DM)

C. Other Specific types

  • Genetic defects of B-cell function
  • Genetic defects of insulin action 
  • Pancreatic disease
  1. Pancreatitis
  2. Pancreatectomy
  3. Neoplastic disease
  4.  Hemochromatosis
  5. Cystic fibrosis

D. Excess endogenous production of hormonal antagonists to insulin:

      Growth hormone                      - Acromegaly
      Glucocorticoids                       - Cushing's syndrome
      Thyroid hormones                   - Hyperthyroidism
      Catecholamine                          - Phaeochromocytoma
      Human placenta lactogen        - Pregnancy
     Glucagon                                  - Glucagonoma

E. Drug-induced

  • Corticosteroids
  • Thiazide diuretics
  • Phenytoin

F. Viral infections:

  • Congenital rubella
  •  Mumps
  • Coxsackie's virus B

G. Liver disease: Cirrhosis of the liver

  • DIDMOAD: DI ( Diabetes insipidus), Dm, Optic atrophy, Deafness.
  • Down syndrome
  • Turner's syndrome
  • Klinefelter's syndrome etc.

Pathophysiology

    Type 1 or IDDM, by the time IDDM appears, most of the beta cells in the pancreas have been destroyed. The destructive process is most likely autoimmune in nature. The pathogenic sequence involves genetic susceptibility followed by an environmental event that initiates the process in genetically susceptible individuals, which is probably viral. As a result, an inflammatory response in the pancreas called insulitis. There is an alternative or transformation of the surface beta cells that results in a lack of recognition as self by the immune system. Consequently, an immune response develops against the beta cells, and destruction occurs leading to DM.
 
In type 2 or NIDDM, there is little progress in the understanding, of the pathogenesis. There is a suggestion of a transmitted autosomal dominant trait being involved. No auto-immune mechanism is believed to preoperative. There are two clear physiologic defects in NIDDM: abnormal insulin secretion and resistance to insulin action in target tissues. 

      


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