Pathophysiology of diabetes
Pathogenesis of Ulceration: Diabetic foot ulcers result from the synchronous activity of various causes. The real causes are noted to be fringe neuropathy and ischemia from fringe vascular malady.
Neuropathy : Over 60% of diabetic foot ulcers are the after effect of neuropathy. The advancement of neuropathy in influenced patients has been appeared in creature and in vitro models to be an aftereffect of hyperglycemia-actuated metabolic irregularities. One of the all the more usually portrayed instruments of activity is the polyol pathway. In the advancement of neuropathy, the hyperglycemic state prompts an expansion in real life of the chemicals aldose reductase and sorbitol dehydrogenase. This outcomes in the change of intracellular glucose to sorbitol and fructose.
Vascular Disease: Blood vessel infection (PAD) is a contributing component to the improvement of foot ulcers in up to half of cases. Advance, the hyperglycemia in diabetes is related with an expansion in thromboxane A2, a vasoconstrictor and platelet collection agonist, which prompts an expanded hazard for plasma hypercoagulability. In addition, smoking, hypertension, and hyperlipidemia are different variables that are normal in diabetic patients. Cumulatively, this prompts an expanded danger of ulceration in diabetic patients
- Insulin-Pancreatic hormone
- Gluconeogenesis
- Insulin Resistance
- Translocation of glucose
- Glucose and Glucagon
- Insulin Receptors
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