Underlying Pathophysiology of Type 1 Juvenile Diabetes

This clinical case discusses the pathophysiology of type 1 juvenile diabetes, including the destruction of beta cells in the pancreas. It also explores the associated co-morbidities, such as acute respiratory distress and increased pulse rate. The article provides insight into the risk factors that increase susceptibility to T1D and how it affects the immune system. Course code and college/university are not mentioned.

Running head: CLINICAL CASE 2
Underlying pathophysiology
Name of the Student
Name of the University
Author Note

1CLINICAL CASE 2
The pathophysiology of type 1 juvenile diabetes found in the 16 year old patient James
encompasses destruction of beta cells present in the pancreas. Beta cells are found in the islets of
Langerhans and their primary function is associated with the storage and release of insulin
hormone that brings about reduction in blood glucose concentration. Earliest abnormality in the
function of beta cells that are detectable before clinical onset of the disease includes loss of
insulin secretion, and loss of 1st phase insulin response to intravenous glucose (Atkinson,
Eisenbarth and Michels 2014, p.70). There are several individual risk factors, which can create
an influence on the auto-immune response towards these cells. Some of the risk factors that
might have increased susceptibility of James to suffer from T1D involve expansion of
autoreactive helper cells (CD4+ and CD8+), activation of innate immune system and presence of
autoantibody producing B cells (Ferreira et al. 2015, p.783). This results in a rapid decline in
insulin secretion followed by onset of T1D symptoms, thereby resulting in an increased glucose
output by liver and reduced uptake of glucose by the insulin sensitive tissues.
Figure 1- Schematic diagram for type 1 diabetes pathophysiology
(Source- Jansari et al. 2014)

2CLINICAL CASE 2
T1D have been found associated with acute respiratory distress in several individuals.
This can be attributed to the fact that diabetic ketoacidosis results in laboured breathing or rapid
breathing. Ketoacidosis encompasses short-term diabetes complications, caused due to elevated
blood glucose levels, in addition to increased levels of ketone in blood (Beyerlein et al. 2013,
p.802). Assessment of an increased pulse rate can be associated to the fact that T1D affects the
blood vessels and results in an acceleration of the process of atherosclerosis that lead to
hardening of the arteries (Cherney et al. 2014, p.28). This in turn altered the fluid dynamics of
the circulatory system and might have resulted in increased pulse rate. Presence of a high body
temperature might have occurred due to the effect of diabetes in slowing down the ability of the
body to fight against infections.
Elevated sugar levels in the blood and tissues facilitate the growth and infection of
bacteria, thereby weakening the immune system and resulting in the onset of fever (Herold et al.
2013, p.243). Increased blood glucose levels resulted in loss of fluids from the body at a faster
rate, thereby damaging the nerves involved in perspiration and resulting in dry skin (Piérard et al.
2013, p.107). Elevated blood glucose level lowers the ability of the immune system to fight with
lung infections, thereby contributing to accumulation of fluid and chest crackles in the patient.
Thus, it can be suggested that type 1 diabetes played significant role in development of the
associated co-morbidities.

3CLINICAL CASE 2
References
Atkinson, M.A., Eisenbarth, G.S. and Michels, A.W., 2014. Type 1 diabetes. The
Lancet, vol.383, no.9911, pp.69-82. Retrieved from:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4380133/pdf/nihms671875.pdf
Beyerlein, A., Wehweck, F., Ziegler, A.G. and Pflueger, M., 2013. Respiratory infections in
early life and the development of islet autoimmunity in children at increased type 1 diabetes risk:
evidence from the BABYDIET study. JAMA pediatrics, vol.167, no.9, pp.800-807. Retrieved
from: https://jamanetwork.com/journals/jamapediatrics/fullarticle/1704825
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von Eynatten, M. and Broedl, U.C., 2014. The effect of empagliflozin on arterial stiffness and
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M., Schuilenburg, H., Walker, N.M., Dunger, D.B. and Wallace, C., 2015. IL-21 production by
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https://link.springer.com/article/10.1007/s00125-015-3509-8
Herold, K.C., Vignali, D.A., Cooke, A. and Bluestone, J.A., 2013. Type 1 diabetes: translating
mechanistic observations into effective clinical outcomes. Nature Reviews Immunology, vol.13,
no.4, p.243. Retrieved from: https://www.nature.com/articles/nri3422

4CLINICAL CASE 2
Jansari, S., Devashri, N., Dhanani, A. and Chauhan, N., 2014. Differentiation of stem cells into
pancreatic β-cells: regenerative medicine for diabetes. International Journal of Biological and
Pharmaceutical Research, vol.5, pp.901-9. Retrieved from:
https://www.researchgate.net/profile/Neelam_Chauhan3/publication/267514394_DIFFERENTI
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Piérard, G.E., Seité, S., Hermanns-Lê, T., Delvenne, P., Scheen, A. and Piérard-Franchimont, C.,
2013. The skin landscape in diabetes mellitus. Focus on dermocosmetic management. Clinical,
cosmetic and investigational dermatology, vol.6, p.127. Retrieved from:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3658433/pdf/ccid-6-127.pdf