Group 2:

Anita Govind

April Windsor

Anton Vu
(SGL)
Tracie Hsiu-Hung Su
Topic 10: Case study B: Soldier with unexpected weight loss


A 28-year-old healthy soldier is preparing for deployment to northern Africa. He received his full vaccine series 3 months ago. Today, he was having his last “ hoorah” skiing with friends. Towards the end of the day, he noticed that he was far more fatigued than his friends and generally didn’t feel well. The following morning, he was seen in the medical clinic. The soldier shared that over the last few months began to experience weight loss despite ravenous appetite and increased dietary intake. He has to make frequent trips to the bathroom to urinate and has difficulty concentrating on her work because of fatigue. He drinks large volumes of coffee to help with a constant dry mouth and to combat his fatigue. At a clinic appointment, it was noted that his weight has dropped from 200 to 178 pounds. He is 6 feet 0 inches tall. Her urine is positive for sugar (2%) and ketones. A chemstick blood glucose level is 612 mg/dl. He had eaten breakfast 3 hours before the blood test.
1. Considering his presenting history and physical data, what form of diabetes mellitus is indicated? Explain why using the patho. Presenting symptoms: Fatigue, increased hunger, increased dietary intake, frequent urination, difficulty concentrating, dry mouth, and reports drinking lots of coffee.
Presenting signs: weight loss (200 lbs à 178 lbs), glycosuria, ketones in urine, RBS 612 mg/dL

With the presenting history and physical data, this patient is exhibiting diabetes mellitus type I (DM1). DM1 accounts for approximately 5% - 10% of all people with diabetes. Type 1 generally affects people under 40 years of age, and 40% develop it before 20 years of age (Michel, 2010). The classic symptoms of DM1 include polyuria, polydipsia, and polyphagia.
DM1 is characterized by destruction of β cells of the pancreas. There are two forms of DM1: immune mediated and idiopathic. In immune mediated type 1, the body’s own T cells attack and destroy pancreatic β cells, which are the source of insulin. In addition, auto antibodies to the islet cells cause a reduction of 80% to 90% of normal β-cell function before hyperglycemia and other manifestations occur. A genetic predisposition and exposure to a virus are factors that may contribute to the pathogenesis of immune-related type 1 diabetes (Michel, 2010). Idiopathic type 1 diabetes is a form of diabetes that is not related to autoimmunity but is inherited.
In DM1, there is a long preclinical period. The islet cell autoantibodies responsible for β-cell destruction are present for months to years before the onset of symptoms. Manifestations of DM1 develop when the pancreas can no longer produce sufficient amounts of insulin to maintain normal glucose. Once this occurs, the symptoms of diabetes will be rapid. Clinical manifestations will include rapid weight loss, and the classic signs of polyuria, polydipsia, and polyphagia.
DM1 is characterized by absolute insulin deficiency, and thus glucose cannot enter muscle and adipose tissue. Glucose produced by the liver is no longer opposed by insulin production. This leads to a rise in plasma glucose levels. “When the maximal tubular absorptive capacity of the kidneys is exceeded, glucose is lost in the urine, leading to glycosuria and osmotic fluid loss eventually leading to profound hypovolemia. Tissues dependent on insulin for glucose transport do not have glucose available as a substrate (Dawson, 2010).” The brain responds to this emergent situation by promoting eating behavior: increased thirst, which leads to increased urination and increased hunger. In addition, with continued insulin deficiency leads to fat metabolism, which leads to the production of fatty acids. The fatty acids undergo transformation to keto acids in the liver. Hepatic glyconeogenesis in response to tissue glucose deprivation also contributes to the increased