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RENY M MATHEWFCM-1
Case Study
What’s the Plan
Meet The PatientBackgroundTalk out the LOsTreatmentQuestions
Meet Patient A
Adolescent boy High BMI (>30) Patient had a high blood sugar that was not
coming down. There is no history of diabetes in immediate
family Some extended family members do have diabetes
Patient is somewhat responsive, but complains of fatigue
What is Diabetes
Body has an inability to produce enough (or any) insulin
Inability to uptake glucose from the bloodMajor comorbidity factorType I and Type II
Type I Diabetes Type II Diabetes
Also called child or juvenile diabetes (although it can occur at any age)
Onset is usually during childhood or adolescence
Occurs due to an autoimmune disease
Immune cells attack beta cells within the islets of Langerhans of the pancreas Patients are unable to produce
any Insulin Must take insulin (usually
through injection or pump)
Also called adult onset diabetes Patients are able to produce
insulin but are resistant to it Is now becoming more prevalent
in children as obesity epidemic grows
As time goes on, islet cells may stop producing insulin, may decrease, or levels may become low enough where taking insulin is required
Treatment usually starts with drugs that target insulin receptors As the disease progresses
Insulin is used
What’s The Difference
Normal Pancreas: Islets of Langerhans What We See
Islet contains α cells- glucagon β cells- insulin δ cells- somatostatin
PLO: Look at the Histology of the Pancreas and how it is Changed in the Manifestation of Type I vs. Type II
Diabetes
Islet Triple-Immunostained
What Do Those Cells Look Like
α cells- glucagon (brown)
β cells- insulin (pink)
δ cells- somatostatin (blue)
What Happens in Type I Diabetes
What Happens in Type II Diabetes
AmyloidosisBrown = InsulinSome studies do show
macrophage invasion even in Type II
Eventually these patients lose their β-cells as well Have to be on Insulin
Why Do We Care
Type I Diabetes Must treat with Insulin
Type II Diabetes Usually start with changes in diet and exercise Medicine to improve resistance Eventually onto insulin
What About our Patient
Adolescent Boy Could Be Type I
High BMI Could be Type II
Have to differentiate to determine long term treatment options GAD 65
Tests for antibodies
THANKS!
Questions?
References
1. Bonner-Weir, S., & O’Brien, T. D. (2008). Islets in Type 2 Diabetes: In Honor of Dr. Robert C. Turner. Diabetes, 57(11), 2899–2904. http://doi.org/10.2337/db07-1842
2. Braun, D. M. (n.d.). A560 Histology Slides. Retrieved March 30, 2016, from http://medsci.indiana.edu/histo/docs/lab13_7.htm
3. Differences Between Type 1 and Type 2 Diabetes. (n.d.). Retrieved March 24, 2016, from http://www.diabetes.co.uk/difference-between-type1-and-type2-diabetes.html
4. Donath, M. Y., Schumann, D. M., Faulenbach, M., Ellingsgaard, H., Perren, A., & Ehses, J. A. (2008). Islet Inflammation in Type 2 Diabetes From metabolic stress to therapy. Diabetes Care, 31(Supplement 2), S161–S164. http://doi.org/10.2337/dc08-s243
5. Rowe, P. A., Campbell-Thompson, M. L., Schatz, D. A., & Atkinson, M. A. (2011). The pancreas in human type 1 diabetes. Seminars in Immunopathology, 33(1), 29–43. http://doi.org/10.1007/s00281-010-0208-x
6. Viglietta, V., Kent, S. C., Orban, T., & Hafler, D. A. (2002). GAD65-reactive T cells are activated in patients with autoimmune type 1a diabetes. Journal of Clinical Investigation, 109(7), 895–903. http://doi.org/10.1172/JCI14114
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