It is a group of metabolic disorders characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart and blood vessels. The vast majority of cases of diabetes fall into two broad ehio-pathogenetic categories. In one category (type I diabetes), the cause is an absolute deficiency of insulin secretion. Individuals, at increased risk of developing this type of diabetes can often be identified by serological evidence of an autoimmune pathologic process occurring in the pancreatic islets and by genetic markers. In the other much more prevalent category (type II diabetes), the cause is a combination of resistance to insulin action and an inadequate compensatory insulin secretary response. In the latter category, a degree of hyperglycemia sufficient to cause pathologic and functional changes in various target tissues, but without clinical symptoms, may be present for a long period of time before diabetes is detected.
Diagnostic Criteria
- Poly-symptoms PLUS casual plasma glucose greater than or equal to 200 mg/dl.
- Fasting blood sugar glucose greater than or equal to 120 mg/dl.
- 2 hours plasma glucose greater than or equal to 200 mg/dl during an oral glucose tolerance test (OGTT).
N.B In the absence of unequivocal hyperglycemia with acute metabolic decomposition, these criteria should be confirmed by repeating on a different day
Treatment
Non drug treatment
- Regular physical exercise
- Diet control (avoid simple sugars, low saturated fat and cholesterol).
Drug treatment
Type 1 diabetes mellitus
Insulin (Remember that there is no single standard for insulin administration)
Adults of normal weight may be started with 20-25 units of intermediate acting insulin a day and increased to maintain a blood sugar level of 80-120 mg/dl. Fast acting insulin may also be considered in situations where control of post- pradial hyperglycemia is essential.
(For S/E, C/I and Dosage forms, see page 113)
Type 2 diabetes mellitus
Glibenciamide, p.o. 2.5 to 20 mg, daily or divided into two doses
S/E: hypoglycemia;
C/I: hepatic impairment, renal insufficiency;
D/I: with alcohol, flushing.
Dosage form: Tablet, 5 mg
AND/OR
Metformin (often used for obese patients), 500-2000 mg p.o. daily in divided doses.
S/E: anorexia, nausea, vomiting, abdominal discomfort and diarrhea;
C/I: renal diseases, hepatic disease, alcoholism.
Dosage forms: Tablet, 500 mg.
Diabetic foot ulcer:
Appears to be due to abnormal pressure distribution secondary to diabetic neuropathy. Callus formation is usually the initial abnormality. Vascular disease with diminished blood supply contributes to development of ulcers, and infection is common, often caused by multiple organisms. Patients should be advised to inspect their feet daily and to keep them clean and to wear properly fitting shoes. Moreover, those patients with neuropathy should be advised not to walk barefooted.
Diagnosis: |
Clinical Gram stain and culture from the discharge. X- ray of the affected foot |
Treatment:
Non Drug Treatment
Proper wound care, including debridement
Drug Treatment
First Line
Ampicillin, i.v, 1 g 6 hourly for 2-3 weeks.
(For S/E, C/I and Dosage forms, see page 7)
PLUS
Gentamicin 5-7 mg/kg i.v daily in divided doses for 10-14 days
(For S/E, C/I and Dosage forms, see page 25)
OR
A third generation cephalosporin, e.g.Ceftazidime, 1 gm i.v every 8 hourly or ceftriaxone 1-2 g i.v. or i.m 12 hourly for 7-10 days.
(For S/E and C/I see under ceftriaxone page 5).
Dosage form: Injection, 0.5 g, 1g, and 2g, in Vial.
PLUS
Gentamicin, 5mg/kg i.v daily in divided doses for 10-14 days.
(S/E, C/I and dosage forms, see page 25).
PLUS
Metronidazole, 750 mg, p.o. tid or 500mg IV every 6 hr, for 10-14 days.
(For S/E, C/I and dosage forms, see page 1)