Schizophrenia

Only available on StudyMode
  • Download(s) : 191
  • Published : April 17, 2012
Open Document
Text Preview
Nursing Management of Patient with Type 1 DM

A.R., a 61-year-old female from Project 4 Quezon City with a medical history chronic renal failure, The patient was scheduled to have her wound stitches removed. When suddenly she felt dizziness with cold clammy skin and uncontrolled urination. Usually patient with diabetes mellitus complains of dizziness and body weakness.

Pathophysiology

The symptoms of Type 1 diabetes mellitus are vague and the causes may be related to several factors. Type 1 diabetes affects approximately 5% to 10% of people with the disease; it is characterized by an acute onset, usually before 30 years of age (CDC, 2008). Type 1 diabetes is characterized by destruction of the pancreatic beta cells. Combined genetic, immunologic, and possibly environmental (eg. Viral) factors are thought to contribute to beta cell destruction. Although the events that lead to beta-cell destruction are not fully understood, it is generally accepted that a genetic susceptibility is a common underlying factor in the development of type 1 diabetes. People do not inherit type 1 diabetes itself but rather a genetic predisposition, or tendency has been found in people with certain human leukocyte antigen (HLA) types. There is also evidence of an autoimmune response in type 1 diabetes. This is an abnormal response in which antibodies are detected against normal tissues of the body, responding to these tissues as if they were foreign. Autoantibodies against islet cells and against endogenous (internal) insulin have been detected in people at the time of diagnosis and even several years before the development of clinical signs of type 1 diabetes. In addition to genetic and immunologic components, environmental factors, such as viruses or toxins that may initiate destruction of the beta cell are being investigated. Regardless of the specific cause, the destruction of the beta cells results in decreased insulin production by the liver, and fasting hyperglycemia. In addition, glucose derived from food cannot be stored in the liver but instead remains in the bloodstream and contributes to postprandial hyperglycemia. If the concentration of glucose in the blood exceeds the renal threshold for glucose, usually 180 to 200 mg/dL (9.9 to 11.1 mmol/L), the kidneys may appears in the urine (glycusuria). When excess glucose is excreted in the urine, it is accompanied by excessive loss of fluid and electrolyte. This is called osmotic dieresis. Because insulin normally inhibits glycogenolysis and gluconeogenesis, these process occur in an unrestrained fashion in people with insulin deficiency and contribute further to hyperglycemia. In addition, fat breakdown occurs, resulting in an increased production of ketone bodies, which are the byproducts of fat breakdown. Increased thirst and frequent urination, Extreme hunger, Weight loss Fatigue, Blurred vision, Dizziness and Body weakness are the common signs and symptoms of type 1 diabetes mellitus. Diabetic ketoacidosis occurs when a person with diabetes becomes dehydrated. As the body produces a stress response, hormones (unopposed by insulin due to the insulin deficiency) begin to break down muscle, fat, and liver cells into glucose (sugar) and fatty acids for use as fuel. These hormones include glucagon, growth hormone, and adrenaline. These fatty acids are converted to ketones by a process called oxidation. The body consumes its own muscle, fat, and liver cells for fuel.

In diabetic ketoacidosis, the body shifts from its normal fed metabolism (using carbohydrates for fuel) to a fasting state (using fat for fuel). The resulting increase in blood sugar occurs, because insulin is unavailable to transport sugar into cells for future use. As blood sugar levels rise, the kidneys cannot retain the extra sugar, which is dumped into the urine, thereby increasing urination and causing dehydration. Commonly, about 10% of total body fluids are lost as the patient...
tracking img