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Summative Assignment Diabetes

By bluewitty21 Apr 19, 2015 2518 Words
Summative Assignment – Diabetes
Part 1: -

Diabetes is a disease in which the body’s cells have an inability to absorb glucose due to either the pancreas not being able to generate insulin or the cells not reacting to the reduced amount of insulin being produced, these are diagnosed as type 1 and type 2 respectively. Carol is the case study being used, she was diagnosed with type 1 diabetes at the age of 7 and she is also 6 weeks pregnant.

As type one diabetes is an autoimmune disease the immune system is malfunctioning, so when the patient is exposed to a virus the bodies’ reaction can be more severe than that of an unaffected individual. There have been 18 regions of the genome found with HLA genes which code for immune response proteins, therefore linked to developing diabetes. Two of the regions of several genes have been labeled IDDM1 and IDDM18. (McCarthy, 2010) The beta cells in the Islets of Langerhans are attacked by the antibodies produced by the immune cells to destroy the virus, and it is here where the insulin producing  cells are located. (Bardsley, 2004) The virus’s presence causes auto-reactive CD4+ T cells to be generated; these secrete cytokines that in turn stimulate the production of CD8+ T cells. It is these CD8+ T lymphocytes that are cytotoxic and cause the destruction of the patients  cells located within the islets of Langerhans. This process of cell destruction is also believed to be part of the development of the disease causing the original lack of insulin, which is a negative feedback cycle. (Yoon et al, 2005) The localised apoptosis significantly affects glucose regulation within the blood as the  cells are gradually destroyed. As the  cells reduce in number the amount of glucose able to be absorbed into the cells also decreases which causes the blood glucose to rise, this can be fatal. When the bodies’ glucose demand increases which can be due to infection, (the most common being due UTI’s and pneumonia), the oxidation of substrates like proteins and lipids occurs. The bi- products of this process are ketones that cause a large decrease in pH. This occurs in a negative feedback loop that increases the severity of the symptoms and can cause death. (Palmer, 2004) This can be related back to Carol as being pregnant her growing foetus will put strains on her body, which are heightened due to having type 1 diabetes. It will be necessary for her to see her nurse and midwife more regularly to check her blood glucose levels and help reduce the risk of ketoacidodis and hyperglycaemia.

There are a number of symptoms that are related to diabetes one of which is polyuria (frequent urination), due to the lack of insulin, glucose levels in the blood increase. As the glucose works its way through the renal system not being able to be absorbed osmotic diuresis occurs. This is when the kidneys adjust to the high glucose levels by retaining water within the tubules lumen, which follows on to increase urine flow. Dehydration is likely to occur with polyuria through loss of water; this can also lead on to cause polydipsia (increased thirst). (Campbell et al, 2008)

Polydipsia can also occur on its own as a symptom of diabetes, but it is caused by similar reasons as polyuria. When the glucose levels in the blood increases osmotic pressure, taking water away from other areas as the body tries to regulate its concentration. This results in the feeling of thirst to try and help alleviate the dehydration caused. As urine is produced there is a loss of sodium in the fluid. Sodium is hugely important for the body as it is in the bones and extracellular fluids; it is also vital for muscle contractions and pH balance. Increased water absorption in the kidneys causes the hypothalamus to send a message to the posterior pituitary gland to release lower levels of an antidiuretic. This results in a rise in the osmic concentration, which stimulates osmoreceptors in the hypothalamus.

Another symptom is unexplained weight loss, the patient would generally be eating more frequently which can cause confusion for the reason it is happening. The weight loss is caused by an increase in glucose demand of the body, which means that, in the absence of glucose availability to cells, fats and proteins become oxidized. The chemical reaction occurring is the reason for loss of muscle mass and generalized weight loss. (Mader, 2010) This can cause serious complications for the healthy growth of Carols baby, if she is loosing weight then the baby may not gain the nutrients it needs to grow normally and healthily.

Polyphagia (increased appetite) can occur as one of the main symptoms of Diabetes, it is caused when the body is incapable of producing enough ATP due to high glucose levels, which affects the metabolism rates. A knock on effect of this can be over eating due to the hunger, which can lead to hyperglycaemia. (Marieb et al 2014) Nutrition and diet are especially important for Carol as she will also have increased hunger because of her pregnancy, so the amount she eats and what it is can considerably change the health of her foetus and how at risk she is of having complications.

Mood changes are another known side effect of diabetes. It is caused from lack of glucose reaching the brain; in a healthy individual the brain absorbs 20-25% of the bodies glucose supply. This means when diabetes is present and the glucose levels fluctuate abnormally it is likely the patient will fall to a low mood and possibly feel more aggressive. There have also been link made with hyperglycaemia and he sufferer experiencing memory loss and depression. (Campbell et al, 2008) For Carol the mood swings may be heightened due to her pregnancy and oscillating hormone levels.

Hyperglycaemia is a symptom of having raised glucose levels in the blood, ketoacidosis is the fatal complication of the increased glucose and reduced insulin levels. The metabolism of fats in the absence of glucose produces ketones that alter the blood pH, making it more acidic. This is a serious, acute condition (ketoacidosis) and if left untreated can cause death. Hyperglycaemia surfaces with increased gluconeogenesis, (the process in which glucose is produced preventing the body developing hypoglycaemia) and increased glycogenolysis. (the break down of glycogen which helps to regulate blood glucose levels) (Kitabchi et al 2009)

Pregnant women are at risk of developing gestational diabetes, as Carol already has type 1 she is placed at risk of its symptoms and complications becoming worsened. The risk of congenital anomalies increases by ten times the regular occurrence, (Casson et al, 1997) there is also increased incidence of newborns having impaired long term development, and motor functions. (Ornoy, 2005) At 6 weeks of pregnancy all the major organs have developed and the cardiovascular system has already started to work, so it is very important that she is monitored closely and has frequent ultrasounds. A few other problems that can occur with the baby are fetal distress, jaundice, hypoglycaemia and respiratory distress syndrome. (SIGN, 2005; Temple et al, 2002)

Part 2: -

Obesity can be defined as when excess fat accumulates in the subcutaneous tissues. Once an individuals body mass index (BMI) is 30 or over, they would be considered as clinically obese. (Mader, 2010) The illness has been closely connected with type 2 Diabetes, when there is an inability to absorb glucose due to the cells not reacting to the reduced amount of insulin being produced.

It is believed that the risk of developing type 2 diabetes increase when an individuals BMI raises over 25, it multiplies 10-40 fold once the BMI is 30 or more. The accumulation of abdominal fat which can be measured using the waist: hip ratio is most accountable as being a type 2 diabetes risk factor, over that of the extent of obesity. (Whitmore, 2010)

Lipotoxicity caused by the excessive deposition of lipid molecules in the liver, kidneys and muscle also enhances the risk of developing type 2 diabetes. More specifically, excess adipose tissue that can cause increased fatty acid production is linked with the onset and progression of impaired glucose tolerance. With this in mind, it has been found that around three-quarters of diabetes sufferers have a past history of obesity. (Day, 2011) Also, the World Health Organization has stated that 90% of type 2 diabetes sufferers are either overweight or obese. (Whitmore, 2010) There is much conflict over the connections between obesity and developing diabetes. This is due to other factors involved like age, gender, duration and distribution of the adiposity and ethnicity.

For an individual who is obese, plasma free fatty acid (FFA) concentrations are increased due to expansion of fat mass. It is also found that in type 2 diabetes sufferers, elevated plasma free fatty acid levels are frequent. This is also related to the progression from impaired glucose tolerance to developing type 2 diabetes. When plasma FFA concentrations are high, it has been associated with cardiovascular risk factors connected with insulin resistance for example, hypercuricaemia and dyslipidaemia. (Fagot-Campagna, 1998) When there is a high FFA concentration, dysfunction of the  cells is caused. This is connected to impaired glucose tolerance and an increased blood glucose level, which increases the risk of developing diabetes. The basic physiological purpose of free fatty acids is providing energy to body tissues like the liver, renal cortex and the cardiac muscle. It is during exercise and other activities that energy demand increases, this in turn causes the rate of lipolysis to rise, meaning a higher level of fatty acids from the break down of triglycerides. (Boden, 2002)

Results from in vitro studies have suggested that chronically high plasma free fatty acid levels are connected to -cell dysfunction in type 2 diabetes. It is thought that the adipose tissue is the site of insulin resistance. There is a decrease in insulin-mediated suppression of lipolysis. This in turn causes a rise in the levels of circulating free fatty acids; insulin resistance is the result of this negative feedback cycle. (Boden , 2002) The insulin resistant fat cells are unable to store excess fat; the adipocytokines in turn cannot store lipids, which consequently overflow into the muscle, liver and  cells. The resulting effect is skeletal muscle and hepatic insulin resistance. (Whitmore, 2010)

Genomewide association scans have been able to detect 40 genes that can be connected with type 2 diabetes, some also with  cell dysfunction. It is thought that these genes can predict up to 15% of type 2 diabetes risk. (Eckel et al, 2011) It has been found that the transcription factor TCF7L2 located on chromosome 10 can mutate pancreatic islet function. There are also other variants located on chromosomes’ 6 and 9 that are known cyclin-dependant kinase regulators. At each point these susceptibility alleles are positioned, there is a 15 to 20% increase in the risk of developing diabetes. (McCarthy, 2010) Genetic variants which influence body-mass index (BMI) and obesity have also shown clear results. When a population-based study into the ranges of BMI was carried out 30 different loci were identified. The strongest association is with the fat-mass and obesity related gene. There are also results, which support the idea of obesity being a hypothalamic function disorder.

Lipotoxicity is a metabolic syndrome that occurs with non-adipose tissue only. The adipocytes in the body, although have adequate capacity for lipid storage are over faced with the fatty bi-product of lipolysis. This overflows to the liver, kidneys and skeletal muscles, which can then go on to cause cellular dysfunction and cell death. Due to the process of lipolysis concentrations of fatty acids significantly rise in the liver and muscle. The high levels of breakdown of triglycerides are caused by an increase in energy demand, for example during exercise. In type 2 diabetes there are a number of faulty insulin receptors, this is due to the  subunit not functioning properly and therefore the chemical messages not being able to be sent around the body. The excess fat present in an obese individual causes a layer of visceral fat around the organs, which can inhibit their regular necessary functions. When a patient develops type 2 diabetes the  cells in the pancreas are still able to produce a minimal amount of insulin, but there is an inability of the cells to react to the insulin and therefore a reduced amount of glucose is absorbed. Type 2 diabetes is usually easily managed through oral medications and regular medical check ups. (Mader, 2010) Obesity can affect the insulin sensitivity due to the capacity of the adipocytes being reached and excess lipids surrounding the organs. This lowers insulin sensitivity because the chronically raised lipid concentration will impair islet  cell function. (Day, 2011)

1. Bailey CJ, Day C (2011) Obesity in the pathogenesis of type 2 diabetes. British Journal of Diabetes and Vascular Disease 11(2), 55-61

2. Bardsley J, Want L (2004) Overview of Diabetes. Crit Care Nurs Q Vol 27, No. 2, pp. 106-112

3. Boden G, Shulman GI (2002) Free fatty acids and type 2 diabetes: defining their role in the development of insulin resistance and beta cell dysfunction, European Jounal of Clinical Investigation, 32, 14-23

4. Campbell R et al (2008) Biology (8th edition). San Francisco: Pearson Education Limited.

5. Casson et al (1997) Outcomes of pregnancy in insulin dependant diabetic women: results of a five year population cohort study. BMJ 315(7103): 275-8

6. Eckel RH, Kahn SE, Ferrannini E, Goldfine AB, Nathan DM, Schwartz MW, Smith RJ and Smith SR (2011) Obesity and type 2 diabetes: what can be unified and what needs to be individualized? Diabetes Care. 34(6) 1424-1430

7. Kitabchi A et al(2009) Hyperglycemic Crises in Adult Patients With Diabetes. Diabetes Care Vol 32, No. 7

8. Mader S (2010) Human Biology (11th edition). New York: McGraw. Hill.

9. Marieb E et al (2014) Human Anatomy and Physiology (9th edition). Essex: Pearson Education Limited

10. McCarthy, M.I. (2010) Genomics, Type 2 Diabetes and Obesity The New England Jounal of Medicine 363, 2339-2350

11. Ornoy A (2005) Growth and neurodevelopment outcome of children born to mothers with pregestational and gestational diabetes. Pediatr Endocrinol Rev 3(2): 104-113

12. Palmer R (2004) An overview of diabetic ketoacidodis. Nursing Standard Nov 17/ Vol. 19/ No. 10

13. Richard IG Holt and Neil A Hanley (2007) Essential Endocrinology and Diabetes (5th edition). Massachusetts: Blackwell Publishing.

14. SIGN (Scottish Intercollegiate Guidelines Network) (2005) Complications of pregnancy and fatal outcomes in pregnant diabetic patients managed in a tertiary hospital in Saudi Arabia.

15. Temple R et al (2002) Association between outcome of pregnancy and glycaemic control in early pregnancy in type one diabetes: population based study. BMJ 325(7375): 1275-6

16. Whitmore, C. (2010) Type 2 Diabetes and Obesity in Adults. British Journal of Nursing. 19(14) 880-886

17. Yoon J, Jun H (2005) Autoimmune Destruction of Pancreatic  cells. American Journal of Therapeutics 12, 580-591

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