Diabetes Mellitus type 1 is a chronic disorder of carbohydrate, fat and protein metabolism. A defective or deficient insulin secretary response, which translates into impaired carbohydrate (glucose) use, is a characteristic feature of diabetes mellitus (Goodman and Gillman’s, 2001).
Diabetes type 1 is also called insulin dependent diabetes mellitus (IDDM) and was previously referred to as juvenile onset diabetes. It occurs due to decreased insulin production and unchecked glucose production by the liver. Insulin enables the sugar to get out of the blood and into the cells where it is needed for the cells to function. Diabetes results from a severe, absolute lack of insulin resulting in reduction in Beta cell mass. Beta cells are a type of cell in the pancreas in areas called the islets of langerhans. These beta cells produce insulin. The function of insulin is to counter the action of a number of hyperglycemia-generating hormones and to maintain low blood glucose levels. Due to lack of insulin sugar will not be able to get into the cells so, there will be a high concentration in the blood. On the other hand, high amount of insulin shifts too much sugar into the cells and there will not be enough sugar left in the blood (Mohan, 2000). Lack of insulin affects them because insulin allows for the absorption of glucose by cells in the body and is secreted by the beta cells, in response to elevated glucose in the blood (Chatterjea, 2000).
To treat the high level of glucose insulin was given to the patient. Insulin works to lower blood glucose by promoting the transport of glucose into cells and by inhibiting the conversion of glycogen and amino acids to glucose (Smeltzer, 2004).
Ms. Rita Sharma was suffering from polyuria i.e. increased amount of urine (Smeltzer, 2004). When the blood glucose level is significantly elevated, (it is also mentioned in the above paragraph) the kidneys are unable to handle the workload and therefore allow the excess glucose to spill over into the urine. The glucose in urine acts osmotically i.e. higher concentration to lower concentration, to draw more water into the urine resulting in polyuria (Cotran, 2000).
Mrs. Rita Sharma’s urine was pale and turbid color. It occurs because concentration of glucose in the blood rises. The renal threshold for glucose is, usually 180 to 200mg/dl. When blood glucose increases, the kidneys may not reabsorb all the filtered glucose and the glucose than appears in the urine making it pale and turbid (Smeltzer et al, 2004).
She had a problem of Polydypsia, which means excessive thirst. As explained above, glucose in the urine increases, raising the osmotic pressure of the urine. This pulls the water along with the glucose in to the urine which leads to excessive urination called polyuria, causing a lack of overall body fluids making the blood hypertonic. This hypertonicity provokes the brain to initiate thirst as a compensatory mechanism of dehydration so that loss of water can be fulfilled (Chaudhuri, 2002).
She was suffering from a weight loss problem. Loss of tissue mass occurs in the insulin- dependent form of the disease (the consequence of glycosuria) that characterizes the illness. Role of insulin is to provide entry of glucose into the cells. Insulin deficiency results in non- utilization of glucose as it cannot enter into the cells leading to impaired synthesis of protein, fat and simultaneously causing accelerated breakdown of proteins and fats for production of energy leading to a catabolic state. It means there is an accelerated breakdown of fat and muscle secondary to insulin deficiency leading to weight loss.
Ms Rita Sharma’s blood pressure was 140/90mmhg. The reasons for the increased blood pressure are hyperinsulinemia, glucose intolerance and reduced level of HDL cholesterol. In a normal physiological state nitric oxide synthesis is stimulated by insulin besides decreased synthesis and responsiveness to non insulin resistant states have been associated with increased level of endothelin-1 and potent vasoconstrictor and proarthero sclerotic vascular hormone associated with hypertension (Kumar and Clark, 2005). The overall health management of Ms Rita was effective for recovery.
References
- Chatterjea, M. N. and Shinde, R. (2000) Text Book of Medical Biochemistry. 4th ed. New Delhi: Jaypee Brothers.
- Cotran, R. S., Kumar, V. and Collins, T. (2000) Pathologic Basis of Disease. 6th ed. India: Elsevier.
- Chaudhuri, S. K. (2002) Concise Medical Physiology. 4th ed. Calcutta: New Central book agency.
- Guyton, A. C. and Hall, J. E. (2006) Text Book of Medical Physiology. 11th ed. India: Elsevier.
- Goodman and Gillman’s. (2001) The Pharmacological Basis of Therapeutics. 10th ed. New York: McGraw-Hills.
- Kumar, P. Clark, M. (2005) Clinical Medicine. 6th ed. UK: Elsevier Saunders.
- Mohan, H. (2000) Text Book of Physiology. 4th ed. Delhi: Jaypee Brothers.
- Smeltzer, S. C. and Bare, B. G. (2004) Medical Surgical Nursing. 10th ed. London: Williams and Wilkins.
