Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt
Diabetes Cases.1 Ppt

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Editor's Notes

  • #7: Hyperglycemia in type 2 diabetics can be viewed as a continuum of progressive insulin resistance; this pathophysiology underscores the gradual development of increasing insulin resistance (first in muscle cells then in liver cells) with resultant hyperinsulinemia and culminating in beta cell failure and decreasing insulin levels. The stages in Diabetes can be characterized as follows: Stage 1: Normal glucose tolerance; some degree of hyperinsulinism but no evidence of impaired glucose tolerance (HgA1c under 5.5)Stage 2: Impaired glucose tolerance develops when muscles have significant insulin resistance and the raised insulin levels are not enough to bring the glucose to normal after a meal. Since the liver is more sensitive to insulin than muscle, fasting hyperglycemia has not developed (HgA1c= 5.5-6.1).Stage 3: Both muscle and liver demonstrate insulin resistance; the hyperinsulinemia does not prevent the liver from generating glucose in the fasting state and this is reflected in an elevated fasting glucose level (HgA1c = 6.2-7.5).Stage 4: The pancreas is now failing and the insulin levels start to falter. There is both moderately severe fasting hyperglycemia as the liver increases its glucose output as well as poorly controlled Diabetes (HgA1c = 7.6 - 10).Stage 5: The pancreas has overtly failed. The patient has severe fasting as well as severe insulin resistance; oral agents on their own will not correct this hyperglycemia (HgA1c is more than 10).Understanding these stages is important in managing diabetics more effectively. Thus, in a patient who is in stage 4, providing monotherapy is unlikely to work effectively. In such cases, both an insulin secretagogue (to stimulate insulin secretion) as well as an insulin sensitizer (to minimize insulin resistance) is needed to meet the moderately severe hyperglycemia that develops.Approved oral diabetic agents by mechanism of action include: Insulin secretagogues: Sulfonylureas and meglitinidesInsulin sensitizers: Metformin and thiazolidinediones
  • #37: Centralpontinemyelinolysis is a neurologic disease caused by severe damage of the myelin sheath of nerve cells in the brainstem, more precisely in the area termed the pons. It can also occur outside the pons. [1] The term \"osmotic demyelinization syndrome\" is similar to \"centralpontinemyelinolysis\", but also includes areas outside the pons. [2]