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Investigation of Pituitary Disease
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Thozhukat Sathyapalan, Stephen L. Atkin
The differential diagnosis of DI may also be facilitated by MRI of the pituitary and hypothalamus. In most healthy adults and children, the posterior pituitary emits a hyperintense signal in T1-weighted midsagittal images. This ‘bright spot’ is almost always present in patients with primary polydipsia but is invariably absent or abnormally small in patients with pituitary DI. It is usually also small or absent in nephrogenic DI, presumably because of high secretion and turnover of vasopressin. A normal bright spot virtually excludes pituitary DI, is unlikely in nephrogenic DI, and strongly suggests primary polydipsia.
Chronic Posttraumatic Stress
Published in Rolland S. Parker, Concussive Brain Trauma, 2016
Primary polydipsia may follow acute trauma to the head, and represents a disorder of thirst stimulation (Robinson, 1996). Ingested water produces a reduction of osmolality (concentration of brain fluids), which turns off the secretion of vasopressin. Urine is not concentrated and liquid excretion is higher. Primary polydipsia is characterized by drinking even greater amounts of fluid than in diabetes insipidus, perhaps more than 20 L/day.
Answers
Published in Neel Sharma, Tiago Villanueva, Data Interpretation Made Easy, 2013
The urine osmolality aft er ADH has not changed, implying nephrogenic diabetes insipidus. In cranial diabetes insipidus, the urine osmolality increases to more than 750 mosmol/kg aft er ADH. In primary polydipsia the urine osmolality aft er water deprivation is typically above 750 mosmol/kg.
Desmopressin and nocturnal voiding dysfunction: Clinical evidence and safety profile in the treatment of nocturia
Published in Expert Opinion on Pharmacotherapy, 2018
Global polyuria is defined as 24-h urinary output that exceeds 40 ml/kg body weight or above and can result in increased urinary frequency. Disease states such as diabetes mellitus, diabetes insipidus, hypercalcemia, and primary polydipsia can be associated with global polyuria [18]. Diabetes insipidus can be classified as central (neurogenic) due to insufficient antidiuretic hormone (ADH) synthesis by neurosecretory cells, or nephrogenic, in turn due to renal insensitivity to ADH. In contrast, NP is an abnormally large urine volume produced during the night-time, and the ICS defines NP as nocturnal polyuria index (NPI) >20% of daily urine output at night in young individuals and >33% in elderly [3,4,15]. Excessive urine production remains a commonly reported cause of nocturia with up to 93% of elderly patients having NP [19]. Given the difference used in the definition of 24-h polyuria and NP units (based on a 70 kg person of undefined gender voiding more than 40 ml/kg/24 h vs. patient age and urine production per time unit), it can be difficult to compare these two conditions. Patients with fluid overload states such as congestive heart failure, liver disease with hypoalbuminemia, nephrotic syndrome, or lower extremity venous stasis often exhibit NP [16].
Psychogenic polydipsia associated with sertraline treatment: a case report
Published in Psychiatry and Clinical Psychopharmacology, 2019
Esra Okyar, Leyla Bozatlı, Işık Görker, Serap Okyar
PP is a clinical condition in which the patient exhibits a compulsive consumption of fluids [5]. The development of hyponatremia is uncommon if there are no abnormalities in renal function. Sodium levels may decrease acutely or chronically. Acute hyponatremia is more severe and can threaten life by causing cerebral edema and brain death [6]. Hyponatremia can develop in 5–10% of patients with PP [10]. It has been reported in the literature that brain death occurred due to hypotonic hyponatremia by primary polydipsia in a 10-year-old male with mental retardation and attention deficit and hyperactivity disorder [13].