Diabetes Mellitus is a chronic progressive disease caused by relative or absolute insulin deficiency and decreased sensitivity to insulin. It can be diagnosed with a random blood glucose over 200 mg/dL, fasting glucose over 126 mg/dL on two occasions, or an abnormal oral glucose tolerance test. It is classified as primary/secondary and type 1/type 2 depending on etiology and pathogenesis. Type 1 is insulin-dependent and associated with autoimmunity while type 2 is non-insulin dependent and associated with insulin resistance. Complications include damage from advanced glycation end products, protein kinase C activation, and disturbances in the polyol pathway which can lead to macrovascular disease, nephropathy, and ocular complications. Diabet

1. DIABETES MELLITUS
YUZBASHEVA NIHAL 221B

2. Diabetes Mellitus is chronic
progressive disease caused by
relative or absolute insulin
deficiency, and is associated by
decreased or loss of the sensitivity
of tissues to insulin

4. DIAGNOSIS
 A random blood glucose concentration of 200 mg/dL
or higher, with classical signs and symptoms
(discussed next)
 A fasting glucose concentration of 126 mg/dL or
higher on more than one occasion
 An abnormal oral glucose tolerance test (OGTT), in
which the glucose concentration is 200 mg/dL or
higher 2 hours after a standard carbohydrate load (75
g of glucose).

5. CLASSIFICATION ACCORDING
ETIOPATHOGENECITY OF DISEASE
Primary(nosological)
Secondary(symptomatic)

6. CLASSIFICATION ACCORDING TO
PATHOGENESIS
• I Type – Insulin-dependent
Diabetes (I DM)
• II type – Non Insulin-depedent
Diabetes (II DM)

7. DM1 DM2
Genetic locus Ch.6 Unknown
Genetics HLA-D linked No HLA association
Pathogenesis Autoimmunity or immuno-
pathologic mechanisms
Insulin Resistance
Relative Insulin deficiency
Islet Cells Insulitis early; Marked
atrophy and fibrosis; Beta
cell depletion
No insulitis; Focal atrophy
amyloid; Mild beta cell
depletion
Age of Onset Young ages >40
Body Habitus Normal to wasted Obese
Plasma Insulin Low to absent Normal to high
Plasma Glucagon High, suppresible High, resistant
Acute Complication Ketoacidosis Hyperosmolar coma
Insulin Therapy Obligatory Non obligatory

10. COMPLICATIONS
Formation of advanced glycation end
products (AGEs)
Activation of protein kinase C.
Disturbances in polyol pathways.

11. PANCREAS

12. PANCREAS

13. DIABETIC MACROVASCULAR
DISEASE

14. HYALINE ARTERIOLOSCLEROSIS

15. DIABETIC MICROANGIOPATHY

16. DIABETIC NEPHROPATHY

17. DIFFUSE MESANGIAL SCLEROSIS

18. NODULAR
GLOMERULOSCLEROSIS

20. NEPHROSCLEROSIS IN A PATIENT
WITH LONG-STANDING DIABETES

21. OCULAR COMPLICATIONS OF
DIABETES

24. DIABETIC COMA
Keto-acidic Coma
Hyperosmolar non-ketotic Coma
Lactic Acidic Coma
Hypoglycemic coma

25. THANKS
FOR
YOUR
ATTENTIO
N!