US prescribing recommendations warn against the concurrent use of alcohol and/or other central nervous system depressants, but to date there have been no studies to assess the effects of azelastine nasal spray on the CNS in humans. More recent studies have shown similar degrees of somnolence (approx. 2%) compared with placebo treatment. The most common side effect is a bitter taste (about 20% of people). Due to this, the manufacturer has produced another formulation of azelastine with sucralose. The problem of bitter taste may also be reduced by correct application of the nasal spray (i.e. slightly tipping the head forward and not inhaling the medication too deeply), or alternatively using the azelastine/sucralose formulation.In addition, anosmia (loss in the ability to smell) can occur with nasal spray antihistamines (including both formulations of azelastine). Pharmacology
Pharmacodynamics
Azelastine has a triple mode of action:
Anti-histamine effect,
Mast-cell stabilizing effect and
Anti-inflammatory effect. Pharmacokinetics
The systemic bioavailability of azelastine is approximately 40% when administered intranasally. Maximum plasma concentrations (Cmax) are observed within 2–3 hours. The elimination half life, steady-state volume of distribution and plasma clearance are 22 h, 14.5 L/kg and 0.5 L/h/kg respectively (based on intravenous and oral administration data). Approximately 75% of an oral dose is excreted in feces. Pharmacokinetics of orally administered azelastine are not affected by age, gender or hepatic impairment. Metabolism
Azelastine is oxidatively metabolized by the cytochrome P450 family into its active metabolite, desmethylazelastine, and two inactive carboxylic acid metabolites. Chemical properties
The chemical nomenclature of azelastine is (±)-1-(2H)-phthalazinone, 4-[(4-chlorophenyl) methyl]-2-(hexahydro-1-methyl-1H-azepin-4-yl)-monohydrochloride. It is white, almost odorless with a bitter taste. References
External links
"Azelastine".
Calcium supplements are therefore often required to prevent symptoms of hypocalcemia and to restore lost bone mass.The patient is placed in a semi-Fowler position and the neck is extended. An abbreviated Kocher incision is made and the platysma muscle is dissected horizontally. The strap muscles are released off of the thyroid gland. Then the thyroid gland is mobilized and the parathyroid arterial blood supply is suture ligated. The entire parathyroid adenoma is identified and dissected out. Intraoperative PTH monitoring can begin at this time and will show falling PTH levels if the entire adenoma has been resected. Complications
While mild hypocalcemia is common after partial parathyroidectomy, some people experience persistently prolonged low calcium levels. This is called hungry bone syndrome. Despite the reactivation of unresected parathyroid glands producing normal to elevated levels of PTH, serum calcium continues to be low. The balance between calcium influx and efflux within the bone continues to be disrupted, favoring the former. The bone is said to be "hungry" as it consumes minerals without regard to PTH; calcium, magnesium, and phosphate continue to be deposited into the bones, resulting in hypocalcemia, hypomagnesemia, and hypophosphatemia. Prolonged calcium supplementation may be required. Hungry bone syndrome is particularly common in people who are on long-term regular dialysis. See also
List of surgeries by type

References
External links
"How is parathyroid surgery performed?". American Association of Endocrine Surgeons. Retrieved 11 May 2019. "Parathyroid gland removal". Medical Encyclopedia. Medline Plus. 3 December 2018. Retrieved 8 December 2018.