1.
Dipiro-Pharmacotherapy A Pathophysiologic Approach
2. Daneman D. Type 1 diabetes. Lancet 2006; 367:847–858.
3. Raffel LJ, Scheuner MT, Rotter JI. Genetics of diabetes. In: Porte D Jr, Sherwin RS, eds.
Ellenberg & Rifkin’s Diabetes Mellitus, 5th ed. Stamford, CT: Appleton & Lange,
1997:401–454.
4. Bennett P, Rewers M, Knowler W. Epidemiology of diabetes mellitus. In: Porte D Jr,
Sherwin RS, eds. Ellenberg & Rifkin’s Diabetes Mellitus, 5th ed. Stamford, CT:
Appleton & Lange, 1997:373–400.
5. American Diabetes Association. Diagnosis and classification of diabetes mellitus.
Diabetes Care 2007; 30(Suppl 1):S42–S47.
6. Gale EA. The rise of childhood type 1 diabetes in the 20th century. Diabetes
2002;51:3353–3361.
7. Froguel P, Zouali H, Vionnet N, et al. Familial hyperglycemia due to mutations in
glucokinase. Definition of a subtype of diabetes mellitus. N Engl J Med 1993; 328:697–
702.
8. American Diabetes Association. Standards for medical care in diabetes—2007. Diabetes
Care 2007;30(Suppl 1):S4–S41
9. Waris Qidwai, Tabinda Ashfaq Imminent Epidemic of Diabetes Mellitus in Pakistan:
Issues and Challenges for Health Care Providers JLUMHS SEPTEMBER-DECEMBER
2010; Vol: 09 No. 03
10. SARAH WILD, MB BCHIR, PHD1 GOJKA ROGLIC, MD2 ANDERS GREEN, MD,
PHD, DR MED SCI3 RICHARD SICREE, MBBS, MPH4 HILARY KING, MD, DSC
Global Prevalence of Diabetes Estimates for the year 2000 and projections for 2030,
Diabetes Care 27:1047–1053, 2004
11. Scott, G (March–April 2013). "The diabetic foot examination: A positive step in the
prevention of diabetic foot ulcers and amputation". Osteopathic Family Physician 5 (2):
73–78. doi:10.1016/j.osfp.2012.08.002.
12. R. Hakeem , A. Fawwad , Diabetes in Pakistan: Epidemiology, Determinants and
Prevention, Journal of Diabetology, October 2010; 3:4
13. Pharmacotherapy Handbook 7th edition
14. Michael J. Fowler, MD, Microvascular and Macrovascular Complications of Diabetes,
Clinical Diabetes Volume 26, number 2, 2008
15. Boulton in Diabetes, 30;36 2002
16. Selva Olid A, Solà I, Barajas-Nava LA, Gianneo OD, Bonfill Cosp X, Lipsky BA (4
September 2015). "Systemic antibiotics for treating diabetic foot infections". Cochrane
Database of Systematic Reviews.
17. Diabetes and kidney disease: MedlinePlus Medical Encyclopedia".www.nlm.nih.gov.
Retrieved 2015-06-27.
18. "Nonproliferative Diabetic Retinopathy (Includes Macular Edema)". Retrieved August
17, 2013.
19. Boulton AJ, Kirsner RS, Vileikyte L. Clinical practice. Neuropathic diabetic foot ulcers.
N Engl J Med 351(1):48-55, 2004.
20. A to Z drug facts
I. INTRODUCTION A. Defi nition. Th e American Diabetes Association (ADA) defi nes
diabetes mellitus as a group of metabolic diseases characterized by inappropriate
hyperglycemia resulting from defects in insulin secretion, insulin action, or both.
Symptoms of acute hyperglycemia include polyuria, polydipsia, polyphagia, weight loss,
blurred vision, fatigue, headache, and poor wound healing. Chronic hyperglycemia can
lead to damage and potentially failure of various organs, including the eyes, heart,
kidneys, blood vessels, and nerves. B. Classifi cation. Th ere are four clinical classes of
diabetes: type 1, type 2, gestational, and other s pecifi c types. 1. Type 1. Type 1 diabetes
mellitus (T1DM) is typically characterized by an absolute insulin defi ciency attributed to
an autoimmune destruction of the -cells of the islets of Langerhans. Aff ected individuals
will have autoantibodies to glutamic acid decarboxylase, pancreatic islet cells, and/ or
insulin. T1DM may be diagnosed at any age, but is most likely to be diagnosed prior to
the age of 30 years. 2. Type 2. Type 2 diabetes mellitus (T2DM) is the most common
form of DM and is typically identifi ed in individuals over the age of 30 years; however,
it has become a more prominent diagnosis in adolescents of certain ethnic origins (e.g.,
Hispanic, African American). Th ose diagnosed with T2DM are typically overweight or
obese, have a positive family history of diabetes, and/or exhibit signs of insulin resistance
(e.g., truncal obesity, high triglycerides, low high-density lipoprotein cholesterol [HDL-
C], acanthosis nigricans); autoantibodies found in T1DM are absent in T2DM. 3.
Gestational diabetes mellitus. Gestational diabetes mellitus (GDM) is a condition in
which women fi rst exhibit levels of elevated plasma glucose during pregnancy. Women
previously diagnosed with diabetes prior to pregnancy are excluded from this classifi
cation. Aft er pregnancy, the diagnostic classifi cation of GDM may be changed based on
postpartum testing (see III.B.2.b). 4. Other specifi c types. Secondary diabetes occurs
when the diagnosis of diabetes is a result of other disorders (e.g., Cushing syndrome,
acromegaly, cystic fi brosis, Down syndrome, pancreatic disorders) or treatments (e.g.,
glucocorticoids, antipsychotics). Monogenic DM (formerly maturity-onset diabetes of the
young) should be considered in children with an atypical presentation or response to
therapy. Adults may present with Latent Autoimmune Diabetes of the Adult (LADA),
which is a slow destruction of the pancreatic -cells similar to T2DM, but autoantibodies
are present as in T1DM. 5. Categories of increased risk for diabetes (prediabetes):
Individuals who have elevated blood glucose levels that do not meet diagnostic criteria
for diabetes, but that are too high to be considered normal, are classifi ed as having
prediabetes. Prediabetes is a high-risk category for the future development of T2DM.
