NURS 6501 Week 9 Pathophysiology of Diabetes Insipidus

NURS 6501 Week 9 Pathophysiology of Diabetes Insipidus Essay Assignment Paper

Diabetes insipidus (DI) is related to an insufficiency of antidiuretic hormone (ADH) causing a partial or total inability to concentrate urine. Insufficient ADH activity leads to leads to high volumes of dilute urine causing increased plasma osmolality which results in frequent thirst (polydipsia) and frequent urination (polyuria, Huether, & McCance, 2017). In DI dehydration can develop quickly without fluid replacement and when a person cannot conserve more water than lost in the urine, serum hypernatremia and hyperosmolality occur. There are three forms of DI. The first is neurogenic and is caused by lesions on the hypothalamus, pituitary stalk, or posterior pituitary, disrupting ADH synthesis, transport or release (Huether & McCance, 2017). The other form nephrogenic DI is triggered by inadequate response of the renal tubules to ADH (Huether & McCance, 2017). In neurogenic drugs such as amphotericin B, carbonate, colchicines, demeclocycline, lithium, loop diuretics and general anesthesia, are factors known to cause kidney damage because it can inhibit the generation of cAMP in the tubules (Huether & McCance, 2017). The second is Central diabetes insipidus, and it is caused by inadequate antidiuretic hormone (ADH). Gestational DI is rare and caused by vasopressin as increase which usually causes mild symptoms that do not require treatment (Huether & McCance, 2017).

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Similarities and Differences

Both DM and DI are regulated by hormones in the endocrine system, and both alterations can potentially affect multiple body systems. The body system involved in DM are the liver and pancreas and, with DI the body systems are the hypothalamus and pituitary (Huether & McCance, 2017). DM relates to blood glucose levels and insulin resistance, and frequent monitoring of blood sugar is necessary, whereas with DI the hormone vasopressin influences the kidneys to concentrate urine, and therefore individuals must monitor for polyuria and polydipsia (Diabetes Insipidus, n.d.).

Patient Factors

DM has a strong genetic component, in both type I and II. Although in DM type II the factor is more of a combination genetic-environmental or behavioral factor involved (Huether, & McCance, 2017). In both DM type, I and II blood glucose must be monitored, therefore requiring education and re-education on the risks involved when an individual is noncompliant with controlling sugar levels. Treatment of DM includes regulating insulin levels with oral medications and insulin injections, along with lifestyle modifications including diet and exercise (Huether, & McCance, 2017).

DI can be genetic in that there are mutations in the genes affecting ADH synthesis, transport, and or release. DI is also the result of structural changes of the hypothalamus and pituitary glands hypothalamus and pituitary. Structural changes can result from trauma, infections or thrombosis, which are all likely due to an individual’s behavior (Huether, & McCance, 2017).

NURS 6501 Week 9 Pathophysiology of Diabetes Insipidus Essay Assignment Paper

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