"Diabetes Insipidus" is a great example of a paper on the endocrine system. Diabetes insipidus (DI) is a disorder that manifests with polydipsia (increased thirst) and polyuria (excretion of urine in excessive amounts). Frequently, DI is provoked by insufficient production, storage, or release of an essential hormone, though, may also arise as a result of the kidney’ s incapability to interact with the hormone. The typical signs of DI include intense thirst and over-excretion of low-concentration urine. The daily urine output of patients with DI is within a 2-20 liters range, depending on the severity.
In contrast, the urine output of a healthy adult usually does not exceed 2.5 liters a day (Mayo Clinic, 2013). Some other symptoms may include fever, dry skin, diarrhea, vomiting, and weight loss. DI develops when the body fails to maintain fluid balance. Normally, the kidneys eliminate excess fluids from the bloodstream and accumulate this waste in the bladder before one urinates. If the system functions properly, the kidneys produce a smaller amount of urine when the body lacks water and vice versa. The control over fluid excretion is mostly conducted via the impact of vasopressin (anti-diuretic hormone – ADH).
The hormone is assembled in the hypothalamus and then deposited in the pituitary gland. When the body loses water, ADH is liberated into the blood. Vasopressin retains fluids by triggering water reabsorption in the kidney tubules. The malfunction in the fluid regulation system may occur on different levels, and that defines the form of DI. For instance, central DI means that the disruption occurred in the hypothalamus or pituitary gland. Major causes of this condition in adults include surgery, brain tumor, meningitis, or trauma.
If central DI presents in children, it is often due to genetic factors. On the contrary, nephrogenic DI develops because of a defect in the renal tubules. This irregularity prevents kidneys from responding to vasopressin. It may be either a result of chronic kidney disease or an inherited disorder or. Specific drugs, namely lithium and certain tetracylclines, are also able to evoke nephrogenic DI (Finch et al, 2003). As far as some other diseases may cause similar symptoms, the doctor performs a number of tests to differentiate between them.
Furthermore, the form of DI also must be determined. Typical tests for DI include water deprivation test, MRI, and urinalysis. When the water deprivation test is performed, the patient stops consuming fluids a few hours prior to the test. That allows the doctor to measure changes in urine output, urine density, and body weight. Performing urinalysis, the doctor estimates the chemical and physical characteristics of the urine. MRI of the brain gives the scope to detect abnormalities in the hypothalamus and the pituitary gland. The treatment approach depends on the form of DI.
Thus, the most efficient medication against central DI is desmopressin. Since there is a deficit of ADH, replacement therapy is needed to compensate for the shortage. Desmopressin can be taken orally, intravenously, or in a form of a nasal spray. Although the drug is safe, it is important to remember that its overdose may cause a reduced blood level of sodium and excessive water retention (Mayo Clinic, 2013). Nephrogenic DI cannot be cured with replacement medications. Instead, a low-salt diet is required to limit the volume of urine the kidneys produce (Loffing, 2004).
The patient will also have to drink enough fluids to avoid being dehydrated. Hydrochlorothiazide may be added in some cases.
Finch, C., Kelley, K., & Williams, R. (2003). Treatment of Lithium-Induced Diabetes Insipidus with Amiloride. Pharmacotherapy, 23(4), 546-550.
Loffing, J. (2004). Paradoxical Antidiuretic Effect of Thiazides in Diabetes Insipidus: Another Piece in the Puzzle. Journal of the American Society of Nephrology, 15 (11), 2948-2950.
Mayo Clinic. (2013). Diabetes Insipidus. Retrieved from http://www.mayoclinic.org/diseases conditions/diabetes-insipidus/basics/definition/con-20026841