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Joey Makes the Travel Soccer Team
Transcript of Joey Makes the Travel Soccer Team
Early symptoms that are noticeable in children are increased thirst, increased hunger, and weight loss. The prolonged elevated glucose level is what will lead to this particular combination of symptoms. As described by Ozougwu, J. C., Obimba, K. C. Belonwu, C. D., and Unakalamba, C. B., “When the capacity of the kidneys to absorb glucose is surpressed, glucosuria ensues. Glucose is an osmotic diuretic and an increase in renal loss of glucose is accompanied by loss of water and electrolyte. The result of the loss of water (and overall volume) leads to the activation of the thirst mechanism (polydipsia). The negative caloric balance, which results from the glucosuria and tissue catabolism leads to an increase in appetite and food intake that is polyphagia” (Ozougwu, Obimba, Belonwu, and Unakalamba, 2013). This explains the symptoms that are going to be present with this disease process.
The pathophysiology of type 1 diabetes is centered around the autoimmune destruction of the body’s own insulin producing beta cells. As mentioned by Kathleen Gillespie within the article Type 1 diabetes: pathogenesis and prevention “Type 1 diabetes is characterized by autoimmune destruction of insulin-producing β cells in the pancreas by CD4+ and CD8+ T cells and macrophages infiltrating the islets” (Gillespie, 2006). As mentioned within the article The pathogenesis and pathophysiology of type 1 and
type 2 diabetes mellitus, in addition to the loss of insulin production “the function of pancreatic α-cells is also abnormal and there is excessive secretion of glucagons in IDDM patients. Normally, hyperglycemia leads to reduced glucagons secretion, however, in patients with IDDM, glucagons secretion is not suppressed by hyperglycemia” (Ozougwu, Obimba, Belonwu, and Unakalamba, 2013). This process exacerbates the already impaired regulation of blood glucose levels and is a main factor contributing to how quickly DM1 patients develop diabetic ketoacidosis.
According to the website of a coconut water brand, O.N.E., (2016), coconut water has 930 mg of potassium, 95 mg of sodium, and 17 g of sugar in a 16.9 fluid ounce bottle. The electrolyte balance Joey could have experienced from rehydrating with coconut water is hyperkalemia. Also, the disease process of diabetes mellitus contributes to this electrolyte imbalance. "Hyperglycemia leads to a shift of water and potassium from the intracellular to the extracellular compartment" (Grossman & Porth, 2014, p.1324).
The complication that Joey has developed is diabetic ketoacidosis. Joey has excess glucose in his blood that he is unable to use because of the disease process of type 1 diabetes mellitus. He is playing soccer and he needs more energy to continue playing. The body will need to make the fuel Joey needs from adipose tissue or proteins. Insulin "normally inhibits lipolysis, thus preventing fat catabolism" (Huether & McCance, 2012, p.465). Since Joey's diabetes is not being controlled by insulin, the body can break down the fat into fatty acids. The liver converts fatty acids from adipose tissue to ketones for the body to use as energy (Grossman & Porth, 2014, p.1074). Ketoacidosis happens "when ketone production by the liver exceeds tissue use" (Grossman & Porth, 2014, p.1074). The excess ketones lower the pH of the blood causing a type of metabolic acidosis called diabetic ketoacidosis. The ketones are what makes the funny smell of Joey's breath mentioned.
The four goals for treating diabetic ketoacidosis are "to improve circulatory volume and tissue perfusion, decrease blood glucose, correct the acidosis, and correct the electrolyte imbalances" (Grossman & Porth, 2014, p. 1324). Insulin would be given to decrease the blood glucose levels. By administering insulin, Joey's cells will be able to use the glucose to make ATP, instead of using adipose tissue. With the inhibition of lipolysis, fatty acids cannot be converted to ketones and there will not be a drop in blood pH, which causes acidosis. Insulin would also bring in some potassium into the cells with the glucose.
Humulin Insulin (Regular Insulin):
Antidibetic, short-acting insulin
Emergency treatment of DKA or coma, and can be used in combination with intermediate or long-acting insulin to provide better control of blood glucose.
Hypersensitivity to insulin.
Renal impairment/failure, hepatic impairment/failure, thyroid disease, pregnancy, children and infants.
Ketoacidosis: Adult IV 2.4-7.2 units loading dose, followed by 2.4-7.2 units/h continuous infusion.
Profuse sweating, nausea, tremulousness, palpitation, and hypoglycemia.
Alochol, guanethidine, dextrothyroxine, epinephrine, furosemide, serum glucose, and propranolol.
up to 13h.
Monitor blood glucose. Test urine for ketones. Monitor for hypoglycemia. Check BP, I&O every hour.
FSBS: 361 mg/dL
Joey Makes the Travel Soccer Team
By: Megan Peterson & Ashley Kirby
Height 5'3" (160cm)
Recent Weight loss despite increased caloric intake.
Recent development of blurry vision
Fainting episode following unsteady gait at soccer match, prompting EMS arrival, upon arrival FSBS was checked and found to be at 361mg/dL. A bystander also mentioned an altered breathing pattern.
Question #2 Cont.
The pathophysiology of type 1 versus type 2 DM differs in a few key ways. One major point is that type 2 DM is not considered an autoimmune disease process. There are key genetic factors involved in this process and it is mentioned within the article that there is a greater genetic correlation with type 2 then with type 1 that make the development of this disease much more likely, however environmental factors play a key role in the development of this disease. As mentioned by Ozougwu, J. C., Obimba, K. C. Belonwu, C. D., and Unakalamba, C. B., “the two main pathological defects in type 2 diabetes are impaired insulin secretion through a dysfunction of the pancreatic β-cell, and impaired insulin action through insulin resistance” (Ozougwu, Obimba, Belonwu, and Unakalamba, 2013). The difference seen here is that with type 1 there is a continued destruction of beta cells, where in type 2 there is a stress on the cells leading to overuse and burnout of the cells and a resistance to insulin systemically. Some of the genetic factors that can contribute are “obesity, over eating, lack of exercise, and stress as well as aging” (Ozougwu, Obimba, Belonwu, and Unakalamba, 2013).
The etiology of this disease is described by Ozougwu as “the result of an autoimmune reaction to proteins of the islets cells of the pancreas” (Ozougwu, Obimba, Belonwu, and Unakalamba, 2013). This simple definition describes a very complex and convoluted disease process. The autoimmune destruction of the islet cells is the primary distinction of this disease process.
As Gillespie points out “Like other organ-specific autoimmune diseases, type 1 diabetes has human leukocyte antigen (HLA) associations” (Gillespie, 2006). The author continues on to mention that there are two major combinations of this HLA gene (DR4-DQ8 and DR3-DQ2) that have been shown to be present in 90% of DM1 patients. This observation shows a definite link to genetics and the development of DM1.
Environmental factors continue to be studied at length with the correlation to DM1. There has been discussion of infection at an early age having shown increased risk for the development of DM1, Gillespie mentions that “The most popular candidates are viruses, with enteroviruses, rotavirus, and rubella being suspects. The strongest data to date have supported a role for rubella. Infants infected with congenital rubella syndrome are said to be at increased risk of type 1 diabetes” (Gillespie, 2006).
Cerebral edema "or brain swelling, occurs with an increase of water and sodium content causing an increase in brain volume" (Grossman & Porth, 2014, p.500). Joey is at risk for cerebral edema because "In the setting of hyperglycemia, extracellular osmolality rises, resulting in the movement of water into the extracellular space, thereby causing dilution of plasma sodium" (Watts & Edge, 2014, p.273). Sodium imbalances have effects on the brain, so sodium needs to be fixed slowly to prevent damage to the brain. It is thought that the treatment of giving insulin to lower glucose levels, sodium should also be given to reduce negative effects of water shifts in the brain (Watts & Edge, 2014, p.273).
Question #6 Cont.
Intravenous fluids, like normal saline, would be given to help with fluid volume and give some sodium intake. Electrolyte replacements should be given to replace the loss during treatment or due to polyuria in diabetics, Common "complications from ovetreatment of diabetic ketoacidosis are hypoglycemia and hypokalemia" (Grossman & Porth, 2014, p.1324).
Diabetes Mellitus 1 Pathophysiology
The pathophysiology of type 1 diabetes is centered around the autoimmune destruction of the body’s own insulin producing beta cells.
Diabetic Ketoacidosis Pathophysiology
"Diabetic ketoacidosis (DKA) is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. DKA usually occurs as a consequence of absolute or relative insulin deficiency that is accompanied by an increase in counter-regulatory hormones (ie, glucagon, cortisol, growth hormone, epinephrine). This type of hormonal imbalance enhances hepatic gluconeogenesis, glycogenolysis, and lipolysis.
Hepatic gluconeogenesis, glycogenolysis secondary to insulin deficiency, and counter-regulatory hormone excess result in severe hyperglycemia, while lipolysis increases serum free fatty acids. Hepatic metabolism of free fatty acids as an alternative energy source (ie, ketogenesis) results in accumulation of acidic intermediate and end metabolites (ie, ketones, ketoacids)." (Hamdy and Khardori, 2015).