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