A 23-year-old female presents with frequency absent of infection. The final diagnosis is Diabetes Insipidus. She is treated with dDAVP.
The Expected Level of Sodium
Excessive volume of hypotonic urine is excreted as a result of a disease process brought on by Diabetes insipidus (DI) (Christ-Crain et al., 2019). Since there are such symptoms as polyuria and polydipsia during DI, subsequent hypernatremia and increased osmolarity occur. An expected level of serum sodium concentration([Na1]) in the course of hypernatremia is approximately 145 mmol/L (Evenhuis et al., 2021).
Reason for Osmolarity Elevation
Hypotonic fluid loss due to diuresis occurred to this patient during DI. Hypernatremia rises ECF osmolality and tonicity, causing water loss and producing a cell shrinkage force Serum osmolality is usually higher than 295 mOsm/kg during DI (Evenhuis et al., 2021). Losing water increases blood concentration of sodium, calcium, glucose, substances that are contained in plasma including albumin, amylase, bilirubin, creatinine kinase (CK), and others.
Comparing Central and Neurogenic Diabetes
There are two types of DI such as central occurring due to the pituitary gland or the hypothalamus deficit of hormone arginine vasopressin (AVP) and nephrogenic which is caused by the resistance of kidneys to AVP (Christ-Crain et al., 2019). Central and nephrogenic Diabetes Insipidus are typically developed for various reasons, but hereditary origins should not be ruled out, particularly when symptoms occur in early childhood (Christ-Crain et al., 2019).
The Mechanism of dDAVP.
dDAVP and free water deficit replacement are still basic treatment methods for central DI (Garrahy & Thompson, 2020). This patient is affected by central DI and is treated by dDAVP that is the first generation artificial equivalent to ADH or vasopressin (AVP) characterized by hemostatic and anti-metastatic activity. (Garona et al., 2020). DAVP plays a role as a selective agonist of the arginine vasopressin type 2 receptor (AVPR2) existing in cancer cells and microvascular endothelium. Oral dDAVP has substituted nasal dDAVP becoming a more consistent way of dealing with chronic central diabetes insipidus (Garrahy & Thompson, 2020).
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.
Evenhuis, J., Epstein, S. E., Della-Maggiore, A., & Reagan, K. L. (2021). Congenital pituitary cyst resulting in a dipstick central diabetes insipidus and secondary hypernatremia in a cat. Journal of Feline Medicine and Surgery Open Reports, 7(1), 2055116921990294.
Garrahy, A., & Thompson, C. J. (2020). Management of central diabetes insipidus. Best Practice & Research Clinical Endocrinology & Metabolism, 34(5), 101385.
Garona, J., Pifano, M., Ripoll, G., & Alonso, D. F. (2020). Development and therapeutic potential of vasopressin synthetic analog [V4Q5] dDAVP as a novel anticancer agent. Vitamins and hormones, 113, 259-289.
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