NURS 5084 - Nursing - Essay On Diabetes

Running head: NURSING
Nursing
Name of the Student
Name of the University
Author Note

1NURSING
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