Nursing Report: Pathophysiology of Type 1 Diabetes Mellitus

This nursing report provides a comprehensive overview of the pathophysiology of Type 1 Diabetes, detailing the mechanisms that lead to the disease. It begins by explaining how insufficient insulin action causes hyperglycemia, a key symptom. The report differentiates between autoimmune and non-immune Type 1 diabetes, highlighting the role of environmental and genetic factors in destroying pancreatic beta cells. It explores the T cell-mediated autoimmune disease process, including the infiltration of lymphocytes and macrophages, the production of autoantibodies, and the role of various antigens like glutamic acid decarboxylase (GAD) and zinc transporter 8. The report also discusses the relative inactivation of T regulatory cells, which further reduces insulin production. Furthermore, it examines the impact of abnormal cell functioning on glucagon levels, leading to hyperglycemia and hyperketonemia, and describes the related symptoms of polydipsia, polyuria, polyphagia, and weight loss. This report provides an in-depth understanding of the complex processes involved in the development and progression of Type 1 Diabetes.

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Insufficient functioning of insulin action causes inadequate glucose transfer from
blood circulation into liver and cells of skeletal muscles that causes hyperglycaemia, a
common symptom in all diabetes types. In hyperglycaemia, the glucose level increases in the
blood circulation. The type 1 diabetes is of two types: autoimmune and nonimmune.
Environment based genetic components plays a vital role in destroying beta cells in pancreas.
Type 1 autoimmune diabetes is known as type 1A diabetes. Nonimmune type 1 diabetes is a
less common term with respect to pancreatitis or idiopathic (type 1B) diabetes, a fulminant
disorder. Environmental factors are involved in developing diabetes mellitus type 1. Viral
infections such as enterovirus destroy the autoimmune beta cells. In diabetes mellitus type 1,
a T cell-mediated autoimmune disease; pancreatic beta cells are destroyed in genetically
susceptible individuals in these following stages.
1. Inflammation (insulinitis) and death of islets beta cell by infiltration of lymphocyte
and macrophage of islets. The surface of pancreatic islet cells expresses autoantigens that
circulates in blood stream and lymphatics, The antigens of these cells ingests the autoantigens
and activates CD4+ T helper 1 (Th1) lymphocytes that secretes interleukin 2 (IL-2) which in
turn activates beta-cell lymphocytes (autoanigen specific with cytotoxic in nature) that
undergoes proliferation and attack the cells of islets thereby secreting toxic perforins along
with granzymes. Interferon activating the macrophages and stimulating the inflammatory
cytokines release is secreted by lymphocytes of T helper. These IL-1 and TNF termed as
tumor necrosis factor causes the destruction of beta cells followed by apoptosis
2. Antibodies production against islet cells, insulin, glutamic acid decarboxylase
(GAD), and other cytoplasm proteins. IL-4 is produced by the activated lymphocytes
including the T helper 2 (Th2) that causes the further stimulation of B lymphocytes in order
to cause proliferation leading to production of antibodies. Autoantibodies of islet cells (ICAs)
are found to be present in the serum of the individuals far before the formation of deficient

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beta cells. A beta cell enzyme termed as Antiglutamic acid decarboxylase (antiGAD65) are
involves in the coordination of releasing insulin and this mechanism is helpful in forming
etiology variation in individual with diabetes. Apart from this enzyme, insulin autoantibodies
(IAAs) are the antibodies that act against insulin are found to occur in the destruction process
of beta-cell and active cells of islets. Zinc transporter 8 is another antigen of islet cells that
produces antigens against it and is found in the serum of individuals with diabetes type 1.
This protein product varies with the progression of the disease.
Another mechanism related to autoimmune function found in the diabetes type 1
pathogenesis is the relative inactivation off the cells involved in T regulation. The T
lymphocytes functions by inhibiting the response of immune system and self tolerance
regulation. These mechanism decreases with time leading to reduced beta-cell level and
reduced production of insulin.
Hyperglycemia, Glucagon, and Hyperketonemia- These conditions occur due to
abnormal cell functioning. Beta cells are responsible for producing insulin and amylin but
reduced level of insulin and glucagon with increased formation of glucagon from alpha cells
are prevalent in diabetes with type 1. The hepatic glucose and metabolism of fat is controlled
by insulin glucagon ratio in portal veins. Insulin and amylin paracrine functions in a normal
way. The abnormalities in beta cell level persist before the advent of diabetes with type 1.
Evidence based data have revealed that increased glucagon level with respect to insulin level
leads to hyperglycemia along with hyperketonemia. Therefore, hyperglycemia is caused by
abnormal functions of beta and alpha cells corresponding to reduced level insulin and amylin
with increased level of glucagon secretion in individuals with diabetes 1. Relative
hyperglucagonemia is a common form in diabetes mellitus and has been suggested by some
researchers that it is essential in the propagation of abnormality mechanism in diabetes.

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Polydipsia: Polydipsia is an abnormality caused by increased level of blood glucose.
In this abnormality, the water comes out of the body through osmosis and results in
dehydration of intracellular cells which increases the thirst
Polyuria: Polyuria occurs when hyperglycemia acts as osmotic diuretic when filtered
glucose exceeds normal limit with increased water loss in urine causing glycosuria.
Polyphagia: Polyphagia is an abnormality when the stores for cellular functioning of
carbohydrates, protein and fats are depleted that finally results in increased hunger in
individuals with this abnormality.
Weight loss: Osmotic diuresis leads to loss in body weight and causes tissue loss of
body due to energy production by utilising proteins and fats caused by insulin deficiency.