Clinical Case Report: Exploring the Pathophysiology of Type 1 Diabetes

This clinical case report delves into the pathophysiology of Type 1 Diabetes (T1D) in a 16-year-old patient, focusing on the destruction of pancreatic beta cells responsible for insulin production. It highlights the earliest detectable abnormalities, including the loss of insulin secretion and impaired first-phase insulin response. The report identifies risk factors that contribute to the autoimmune response, such as autoreactive helper cells and autoantibody-producing B cells, leading to reduced insulin secretion, increased liver glucose output, and decreased glucose uptake by insulin-sensitive tissues. Furthermore, it discusses the association of T1D with acute respiratory distress, attributed to diabetic ketoacidosis and its effects on breathing, pulse rate, body temperature, and skin condition. The analysis concludes that T1D significantly contributes to the development of related co-morbidities, including lung infections and fluid accumulation.

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
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4CLINICAL CASE 2
Jansari, S., Devashri, N., Dhanani, A. and Chauhan, N., 2014. Differentiation of stem cells into
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