Wound Closure Case Study

Type 1 diabetes is also called insulin-dependent because the pancreas produce little to no insulin due to the destruction of beta cell in pancreas(Bardsley et al, 2004). Therefore, the insulin have to be injected manually for body to function normally. (Seewaldt et.al, 2000) states that in type 1 diabetes, the beta cell located in the islets of Langerhans have antigen that cause the immune system to produce antibodies and kill the insulin producing cells. The autoimmune response is thought to be caused by the autoreactive CD4 and CD8 effector cells that recognise islet self-antigens, as an outcome there is greater than 90% destruction on insulin producing cell BACH (1994). Similarly, (Nakayama et al,2005) and (Kent et al, 2005) supports that insulin in itself is a

Diabetes Mellitus is a growing issue for health care providers internationally. The World Health organization estimated in 2013 there were 347 Million diabetics worldwide, predicting that Diabetes will be the 7th leading cause of death by 2030 (WHO, 2013). In both type 1 and type 2 diabetes Mellitus, factors such as poor compliance with diet and medication, infection, acute medical or surgical illness or trauma can lead to poor glycaemic control, precipitating a hyperglycaemic emergency such as Diabetic Ketoacidosis (DKA) (Scobie & Samaras, 2009). In Type 2 Diabetes, another equally dangerous

From observation, currently, the risk of delayed wound healing is managed, by nursing interventions and verbal health promotion, which may be due to the deficiency of packages designed for patients. This is supported by Collier (2003), who highlights the importance of nursing assessment, interventions and evaluation in improving wound healing. However, the importance of patients’ education, about balanced nutrition and dietary control of diabetes, may not be under estimated, as this may reduce the risk of infection and improve wounds healing (Casey, 1998, Dealey, 2005, Kemp, 2001, Timmons 2003, Ward, 2002). According to patients’ experience, their knowledge about nutrition helped them to achieve wound healing (Wound Care Information Network, 2008). For example, balanced proteins intake may encourage tissue repairs, as well as vitamin C intake may reduce the risk of infection, which may improve wound healing (Kemp, 2001, Ward,

Type 1 diabetes is an autoimmune disorder, in which the pancreas does not produce insulin. It usually begins in childhood or adolescence. In Type 1 diabetes, the body’s immune system destroys beta cells in the pancreas that produce insulin. Insulin is a hormone that converts sugar, starches, and food into energy. Without insulin, blood glucose levels become too high, which is known as hyperglycemia. To prevent hyperglycemia, people with Type 1 diabetes must take insulin daily to survive. Genetic and environmental factors affect the onset of Type 1 diabetes. [1] According to the American Diabetes Association, a predisposition to Type 1 diabetes is

About 10 to 20 percent of people with diabetes mellitus have Type 1, which occurs most often in children and young adults. The disease usually bags suddenly and symptoms can be severe (Goodheart 35). Type 1 diabetes in children is associated with the appearance of islet autoantibodies early in life, which is influenced by environmental factors. Once islet autoantibodies have developed, the progression to diabetes in antibody positive individuals is determined by the age of antibody appearance and by the magnitude of the autoimmunity in turn related to the age of the person. Characteristics that describe the magnitude of the autoimmunity can stage progression to Type 1 diabetes in islet autoantibody positive subjects regardless of genetic background or age (Achenbach et al.). There are very different incidences of Type 1 diabetes between countries that have similar prevalences of autoimmunity that suggests environment can influence the progression of Type 1 diabetes, but these studies suffer from relatively small numbers of people with islet autoantibodies (Achenbach et al.). Viruses and toxins can induce islet autoimmunity and it damages the body’s immune system. The body's immune system plays an essential role in Type 1 because it helps protect against

The researchers demonstrated that human liver cells would secrete insulin as well as control blood glucose levels in vivo by testing diabetic immunedeficient mice. They observed how well a mouse would improve the state of hyperglycemia. They observed the immunodeficient mice before and during the times of the study to attribute the change in the glucose blood levels were due to the liver

An acute cutaneous wound is one that is related to the skin and of a rapid onset, for example a burn, skin abrasions or a boil. As the wound is acute, it will have a short duration, lasting from several minutes to several days, and the cellular exudate is rich in neutrophil polymorphonuclear leucocytes with some macrophagates entering after the initial insult (S.Lakhani, S. Dilly, C. Finlayson, 2009). The process of wound healing is essential as otherwise we would likely bleed to death from the slightest little cut. There are several phases consisting of different sequences that allow or body to defend its selves when wounded, these include; firstly forming a blood clot around the wound to prevent excessive blood loss made possible by homeostasis, inflammation whereby the damaged and dead cells are removed from the body, proliferation during which replication of new tissue growth occurs and finally resolution occurs once the wound is closed and involves the realignment of collagen. With ages comes many changes in the body, changes to the skin are one of the primary causes for an alteration in the wound healing process as the dermis is thinner and subcutaneous tissue is diminished. Fewer capillaries are present and cell proliferation is decreased, which result in slower wound healing and atrophy of the glands as well as the skin and mucosa having a lower number of sensory receptors and these factors alone increase susceptibility to injury. (BE. Gould, RM.

The skin acts as a protective layer to the environment.Due to this key function, skin wounds are required to be productively repaired within a brief span outline .The wound healing process involves three systematic overlaid stages: inflammation, cell proliferation, and tissue regeneration. Wounded tissue experiences four stages to repair the injury hemostasis, inflammation, proliferation (granulation), and remodeling.After the injury Hemostasis immediately occurs.After the tissue disruption, the platelets start adhering to the presented collagen and to each other and Generally, inflammation starts 24 hours after injury . Neutrophils are the dominating cell marker in the inflammation stage. Alongside macrophages, neutrophils evacuate the cell

In type 1 diabetes the insulin producing beta cells are destroyed and therefore are unable to respond to an increase in blood glucose. The white blood cells of the immune system incorrectly identify the beta cells as foreign cells and begin an autoimmune response. Auto antibodies are produced in attempt to protect the body from foreign cell invasion, but instead destroy the beta cells.This causes little or no insulin to be secreted and BGL start to rise. As there is no insulin to bind to target cells such as the liver, muscle or fat cells to stimulate the uptake of glucose, the cells are unable to obtain sufficient amounts of energy to carry out their vital cellular functions. This triggers the release of glucagon, and gluconeogenesis and glycogenolysis begin to allow the cells to gain the required amount of glucose. Deprived of energy the body begins to breakdown fat and protein by gluconeogenesis. This explains symptoms such as fatigue or hunger even though BGL continue to increase as alternative sources are metabolised for energy. Although, this may suffice for the metabolic demands of cells, build up of ketones which are a byproduct of fat breakdown in the blood, causes ketosis. If ketones in the blood continue to escalate and prolong, then a potentially fatal condition called diabetic ketoacidosis may result: Glucagon secretion stimulates the beta-oxidation of

As mentioned above, diabetes can affect the body’s white blood cells, which lowers the efficiency of the immune system. If glucose levels are high the immune system will function very ineffectively, causing an increase in the risk of infection. These infections slow down the healing process of a wound, and can cause other health concerns. If an infection is left untreated or is not recognized, a diabetic patient risks the development of sepsis or gangrene, which often leads to the amputation of a limb in a diabetic

Type 1 diabetes mellitus has been shown to be the result of an autoimmune reaction to antigens of the beta cells of the pancreas. With an inability to secrete insulin, the body cannot utilise blood glucose and adaptions will occur in order to fuel the body’s energy needs. This poster will discuss the metabolic pathways that lead to hyperglycaemia and ketoacidosis in untreated diabetes mellitus.

A study by Cohen et al. (2008), supported previous reports of an association between psoriasis and diabetes mellitus. The age-adjusted proportion of diabetes was found to be significantly higher in psoriasis patients as compared to the control group. A possible explanation for the association between psoriasis and diabetes is the presence of chronic inflammation that occurs due to secretion of TNF-a and other proinflammatory cytokines such as IL-1 and IL-6, which precipitate both psoriasis and diabetes.

The levels of TNF-α are known to be higher in diabetes due to increased oxidative stress which endorses inflammation. Our results have validated the fact that NCs treatment has led to a noticeable but non-significant decrease in TNF-α levels as compared to different controls, resulting in rapid and efficient healing in diabetic wounds (Fig. 6.20). This might be because of the inhibitory effect of AgNPs on the release of IL-6 and TNF-α cytokines (Sarabahi 2012).

The immune system requires specific nutrients and consumption quantity in order to function efficiently. Diabetes is a rising healthcare problem emerging in developed countries today as society becomes increasingly dominated by a lifestyle of sedentary work and fast pace eating habits which are causing a rise in obesity and a decrease in nutritional awareness. According to the American Diabetes Association, approximately 29.1 million Americans are diabetic, which is 9.3% of the total population. With the disease on the rise, scientists are searching for answers, specifically to determine the exact cause of diabetes which is still unclear as of today. Although exactly how diabetes develops is unclear, recent research suggests that an elevated level of cytokines inflicting inflammation inside the body may play an important role in the development of type 2 diabetes. Therefore, new experiments are taking place as scientists are recognizing that there may be underlying immune responses that play key roles in the inflammation caused by improper regulation of glucose homeostasis.

Background: Diabetic nephropathy is the major micro-vascular complication of type 2 diabetes mellitus (T2DM) and is the main cause for end-stage kidney disease. In view of metabolic derangements of T2DM, we went further to investigate the role played by oxidized low density lipoprotein (ox-LDL), toll like receptor 4 (TLR4), lipocalin-2 (LCN2), and omentin-1 in DN. Patients and methods: 15 normo-albuminuria T2DM, 15 micro-albuminuria T2DM and 15 macro-albuminuria T2DM in addition to 15 healthy volunteer who served as control group were enrolled in this study. Demographic and clinical data were recorded. Plasma Ox-LDL, omentin- 1 and urinary LCN2 levels by immunoassy and TLR4 mRNA level with real time PCR were assessed. Results: TLR4 gene expression, Plasma ox-LDL, urinary LCN2 levels were increased in T2DM cases as compared to their allied control group with the higher values were for macro-albuminuria T2DM cases. Meanwhile Plasma omentin-1 level was decreased in T2DM cases when compared to their allied control group with least values were for macro-albuminuria T2DM cases. Also there were positive correlations between TLR4 mRNA, ox-LDL, urinary LCN2 levels and serum creatinine, fasting blood glucose, urinary albumin/creatinine ratio, meanwhile omentin 1 showed negative correlations with serum creatinine, fasting blood glucose, urinary albumin/creatinine ratio. Conclusions: Ox-LDL, TLR4, LCN2 and omentin 1 may confer a relevant role in diabetic nephropathy development and