Case Study

RENY M MATHEW
FCM-1

Whats the Plan

Meet The Patient
Background
Talk out the LOs
Treatment
Questions

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 blood
Major comorbidity factor
Type I and Type II

Whats The Difference

Type I 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)

Type II Diabetes
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

PLO: Look at the Histology of the Pancreas and how it is

Changed in the Manifestation of Type I vs. Type II Diabetes

Normal Pancreas: Islets of

Langerhans

What We See

Islet contains

cells- glucagon
cells- insulin
cells- somatostatin

What Do Those Cells Look Like

Islet TripleImmunostained
cells- glucagon (brown)
cells- insulin (pink)
cells- somatostatin (blue)

What Happens in Type I Diabetes

What Happens in Type II Diabetes

Amyloidosis
Brown = Insulin
Some studies do show

macrophage invasion
even in Type II
Eventually these patients
lose their -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

Questions?
THANKS!

References
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6.

Bonner-Weir, S., & OBrien, T. D. (2008). Islets in Type 2 Diabetes: In Honor of Dr.
Robert C. Turner. Diabetes, 57(11), 28992904. http://doi.org/10.2337/db07-1842
Braun, D. M. (n.d.). A560 Histology Slides. Retrieved March 30, 2016, from
http://medsci.indiana.edu/histo/docs/lab13_7.htm
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
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), S161S164.
http://doi.org/10.2337/dc08-s243
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), 2943.
http://doi.org/10.1007/s00281-010-0208-x
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), 895903. http://doi.org/10.1172/JCI14114