This assignment will be looking at the pathophysiology of Type 1 diabetes, the effects this has upon Carol in terms of symptoms and how it may affect the developing embryo and foetus.
What is Type 1 Diabetes?
Diabetes type 1 is an organ specific autoimmune disease which develops in the pancreas and islet cell antibodies when the body’s immune system attacks and destroys insulin producing beta cells (Nelson-Piercy, 2005). This affects the metabolism of fats, proteins and carbohydrates as insulin facilitates the transformation of glucose to glycogen, changes glucose to fat and stimulates the oxidation of glucose for ATP production (Marieb and Hoehn, 2008). Insulin helps to maintain the homeostasis of blood sugar levels, increasing when levels are high and decreasing when low. This works by the insulin signaling pathway which includes an insulin receptor that is made up of two receptor subunits that are located on the outside of the cell membrane and two subunits that penetrate through the membrane. The extracellular subunits contain a binding site for insulin. When insulin binds to the extracellular subunits, it activates a chemical reaction that travels through the linked subunits into the cell. This sends chemical signals to proteins within the cell and causes them to alter their activity, which initiates the movement of glucose transporters to the cell membrane. Glucose transporters are the cells' method for transferring glucose through the cell membrane from the blood and into the cell. The glucose transporters are ever present inside organelles however, they are useless to transport glucose without activation from insulin. The binding of insulin to the cell leads to a rapid movement of the vesicles to the cell membrane, where they fuse with it and insert the glucose transporters. This gives the cell the ability to open itself to the transfer of glucose from the blood. When blood glucose levels decline, insulin ceases to bind to the cell receptors and the glucose transporters are moved back into the cell's cytoplasm.
Diabetes causes an imbalance to this natural process which has serious physiological and psychological effects on the individual with the condition. Causes
Evidence suggests that type 1 diabetes may be triggered in predisposed individuals by genetic and environmental factors. Research has identified the MHC (major histocompatibility complex) on chromosome 6 as being connected to autoimmune diseases and has traced type 1 to MHC class II genes within the leukocyte antigen region HLA-DQB1 and HLA-DRB1 (Nejentsev and Howson, 2007). However research is continuing as genetics doesn’t fully explain the development of type 1 diabetes as not everyone with diabetic parents will necessarily contract the disease. Other researchers have suggested that viral infections may trigger the disease such as Coxsackie B and rubella (Wylie and Bryce, 2008) as they can cause strong immune responses possibly infecting and damaging beta cells. This could lead on to and explain why beta cell antigens are produced, resulting in beta cells being attacked by the immune system. Pathophysiology
The pancreas contains the islets of Langerhans which produce many pancreatic hormones; through the beta cells it produces insulin. The immune system is designed to destroy foreign bodies however in type 1 diabetics the immune system attacks beta cells due to the antigens on the cell surface. Macrophages, dendritic and APC cells process beta cells and present the antigen to CD4+ T cells; this stimulates the secretion of cytokines activating beta cell-specific cytoxic CD8+ T cells which destroy the insulin producing cells (Joon and Yun, 2005). The secretion of insulin is controlled by the glucose concentrations in the blood stream. As the level of glucose rises in the blood, the insulin levels also increase. Insulin accelerates the transport of glucose from the blood into the cells, decreasing the blood glucose level,...
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