How to write a nursing essay on Diabetes Insipidus

Diabetes insipidus is an apparent clinical pathologic condition characterized by polyuria and polydipsia. It is revealed when the serum sodium is significantly greater than 145 mEq/L while the serum osmolality also indicates greater than 300mOsm/Kg. The serum sodium would be elevated from the normal range for the 23-year-old patient presenting with diabetes insipidus. Sodium is extracellular cation that maintains intravascular volume. In the process of homeostasis, sodium and water are concentrated in urine by the action of the antidiuretic hormone (Christ-Crain et al., 2019). Deviation of antidiuretic hormone or sodium potassium channels results in hypernatremia characterized by excessive thirst and urination due to no further concentration of sodium and water to form urine.

The osmolality of the 23-year-old female with diabetes insipidus will be elevated due to inappropriate dilute urine due to either impairment of the central nervous about releasing antidiuretic hormone or impairment of the renal tubules, which impair homeostasis that fails to concentrate sodium and water to urine thus elevating the osmolality. The inability of the renal tubules to modify the concentration of the urinary solutes is also attributed to the elevated osmolality in diabetes insipidus.

Diabetes insipidus include central diabetes insipidus and nephrogenic diabetes insipidus. Central diabetes insipidus entails decreased secretion of the antidiuretic hormone in the pituitary gland (Christ-Crain et al., 2019). Occurs due to deviations occurring within the central nervous systems for instance the pituitary gland. Nephrogenic diabetes insipidus is categorized by decreased ability to concentrate urine due to resistance of arginine vasopressin action in the renal tubules. Both central and nephrogenic diabetes insipidus is caused due to the inability of the antidiuretic hormone to function within the renal tubules. Nephrogenic diabetes insipidus and central diabetes insipidus can either be congenital through hereditary genes or acquired, for instance, a tumor in the pituitary duct.

Deviating the homeostasis between the sodium extracellular cation and water causes excessive concentrated urination. The desmopressin acetate (dDAVP) acts by increasing the water permeability in the renal tubular cells, which decreases excessive urination and thus increases urine concentration (Christ-Crain et al., 2019). Administration of dDAVP counteracts the excessive passage of less concentrated urine, thus allowing urine concentrations before excreted.

References

Christ-Crain, M., Bichet, D. G., Fenske, W. K., Goldman, M. B., Rittig, S., Verbalis, J. G., & Verkman, A. S. (2019). Diabetes insipidus. Nature reviews Disease primers, 5(1), 1-20.

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