Response to Stimulatory and Inhibitory Tests of Antidiuretic Hormone Release in Diabetes Insipidus

1977 ◽  
Vol 52 (2) ◽  
pp. 11P-11P
Author(s):  
P. H. Baylis ◽  
D. A. Heath
Keyword(s):  
Diabetes Insipidus ◽  
Antidiuretic Hormone ◽  
Hormone Release

Disorders of Antidiuretic Hormone Secretion

1992 ◽  
Vol 3 (2) ◽  
pp. 370-378 ◽  
Author(s):  
Joyce Batcheller
Keyword(s):  
Diabetes Insipidus ◽  
Antidiuretic Hormone ◽  
Critically Ill ◽  
Blood Volume ◽  
Urine Output ◽  
Hormone Secretion ◽  
Team Approach ◽  
Antidiuretic Hormone Secretion ◽  
Intracellular Volume ◽  
Age And Sex

Depending upon the age and sex of a human, water constitutes 55% to 80% of the body’s weight and provides a milieu vital for survival. Water imbalance is common among the critically ill. Excessive increases or decreases in body water can be lethal. There are numerous pathologic and iatrogenic causes for water imbalance, the most troublesome being disorders of antidiuretic hormone (ADH) secretion. Antidiuretic hormone plays a pivotal role in conserving water by increasing reabsorption of water by the kidney. Without the influence of ADH (as is seen in diabetes insipidus), a person would be required to ingest between 5 and 15 L of water daily to match urinary losses. Conversely, excessive ADH secretion would reduce urine output in adults to as little as 500 mL per day, dangerously diluting blood volume and expanding intracellular volume. This is what causes the symptoms of the syndrome of inappropriate ADH (SIADH). The care of patients who are critically ill and have disorders of ADH secretion can be challenging. The challenge lies in the recognition and treatment of the disorder. A collaborative team approach helps patients achieve and maintain the delicate balance of body fluids

scholarly journals Pengelolaan Central Diabetes Insipidus Pasca Cedera Kepala Berat

2019 ◽  
Vol 8 (2) ◽  
pp. 99-104
Author(s):  
Bona Akhmad Fithrah ◽  
Marsudi Rasman ◽  
Siti Chasnak Saleh
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Diabetes Insipidus ◽  
Antidiuretic Hormone ◽  
Central Diabetes Insipidus ◽  
Young Generation ◽  
Posterior Pituitary ◽  
Challenging Problem ◽  
Mortality And Morbidity ◽  
Post Traumatic

Cedera otak traumatika adalah salah satu penyebab kematian dan kesakitan tersering pada kelompok masyarakat muda. Hasil akhir dari cedera kepala berat dapat menyebabkan gangguan kognitif, perilaku, psikologi dan sosial. Salah satu konsekuensi dari cedera kepala berat adalah terjadinya disfungsi hormonal baik dari hipofise anterior maupun posterior. Angka kejadian disfungsi hormonal ini sekitar 20-50%. Salah satu yang paling menantang dan sering terjadi adalah diabetes insipidus (DI) dan Syndrome inappropriate antidiuretic hormone (SIADH). Angka kejadian diabetes insipidus pasca cedera kepala diduga sebesar 1-2,9% dengan berbagai tingkatannya. Pada beberapa kasus bersifat sementara tapi beberapa kasus terjadi bersifat menetap. Pada laporan kasus ini akan dibawakan sebuah kasus diabetes insipidus pasca cedera kepala berat. Pasien mengalami cedera kepala berat, hingga dilakukan decompressive craniectomi dan trakeostomi. Untuk perawatan lanjutan pasien dirujuk ke Jakarta. Saat menjalani terapi lanjutan ini pasien terdiagnosis diabetes insipidus Pada kasus ini diabetes insipidus tidak timbul langsung setelah cedera kepala tetapi baru timbul lebih kurang satu bulan setelah cedera kepala. Diabetes insipidus dikelola dengan menggunakan desmopressin spray dan oral disamping mengganti cairan yang hilang. Pada kasus ini desmopressin sempat di stop sebelum akhirnya diberikan terus menerus dan pasien diterapi sebagai diabetes insipidus yang menetap. Managing Central Diabetes Insipidus in Post Severe Head Injury PatientAbstractTraumatic brain injury is the cause of mortality and morbidity in society mostly in male-young generation. The last outcome of traumatic brain injury might be deficit in cognitive, behavioral, psychological and social. the consequences of traumatic brain injury might be hormonal disfunction from anterior and posterior pituitary. The incidence around 20-50%. The most challenging problem is diabetes insipidus (DI) and syndrome of inappropriate antidiuretic hormone (SIADH). The incident of post traumatic diabetes insipidus around 1-2,9% with several degree. In certain case its only occurred transiently but some report it could be permanent. In this case report will find one case post traumatic diabetes insipidus. This pasien had severe traumatic brain injury and underwent decompressive craniectomy and tracheostomy. For further therapy patient was referred to Jakarta. In this further treatment patient diagnosed with diabetes insipidus. Diabetes insipidus doesn’t occurred since the first day of injury but occurred almost one month after. Diabetes insipidus managed with desmopressin spray and oral beside replace water loss. For a few days desmopressin stop but diabetes insipidus occurred again so desmopressin given daily both spray and oral and the patient had therapy as diabetes insipidus permanent. 

scholarly journals Coexistence of central diabetes insipidus and salt wasting: the difficulties in diagnosis, changes in natremia, and treatment.

1996 ◽  
Vol 7 (12) ◽  
pp. 2527-2532
Author(s):  
S Laredo ◽  
K Yuen ◽  
B Sonnenberg ◽  
M L Halperin
Keyword(s):  
Diabetes Insipidus ◽  
Antidiuretic Hormone ◽  
Urine Volume ◽  
Extracellular Fluid ◽  
Central Diabetes Insipidus ◽  
High Rate ◽  
Salt Wasting ◽  
Positive Balance ◽  
Clinical Tools ◽  
Negative Balance

Both central diabetes insipidus (DI) and a high rate of excretion of sodium (Na) and chloride (Cl) contributed to the development of polyuria and dysnatremia in two patients during the acute postoperative period after neurosurgery. To minimize difficulties in diagnosis and projections for therapy, two available (but not often used) clinical tools were helpful. First, the osmole excretion rate early on revealed the co-existence of central DI and an osmotic diuresis. The osmoles excreted were largely Na salts; after antidiuretic hormone acted, this electrolyte diuresis caused the urine flow rate to be much higher than otherwise anticipated. Interestingly, part of this saline diuresis occurred when the extracellular fluid volume was contracted. The tool to explain the basis for the dysnatremias was a tonicity balance. Hypernatremia, which developed before treatment of central DI, was primarily a result of a positive balance for Na rather than a large negative balance for water. Moreover, hyponatremia that developed once antidiuretic hormone acted was primarily a result of a negative balance for Na; the urine volume was large and its Na concentration was hypertonic. To prevent a further decline in the plasma Na concentration, either the Na concentration in the urine should be decreased by provision of urea or a loop diuretic while replacing all unwanted water and electrolyte losses; alternatively, the fluid infused should have a similar Na concentration and volume as the urine (infuse hypertonic saline).

Vasopressin Effects on Plasma Renin Activity in Male and Female Rats

1978 ◽  
Vol 55 (3) ◽  
pp. 301-307 ◽  
Author(s):  
I. W. Henderson ◽  
R. J. Balment ◽  
J. Ann Oliver
Keyword(s):  
Plasma Renin Activity ◽  
Diabetes Insipidus ◽  
Antidiuretic Hormone ◽  
Plasma Renin ◽  
Renin Activity ◽  
Female Rats ◽  
Male Rats ◽  
Adrenergic Blockade ◽  
Male And Female ◽  
Male And Female Rats

1. The influence of gonadal and pituitary factors on the plasma renin response to exogenous vasopressin was examined in anaesthetized rats. 2. Plasma renin activity (PRA) was measured in Brattleboro rats (with and without hypothalamic diabetes insipidus) and Long-Evans male and female rats, before and after single intravenous injection of antidiuretic hormone (ADH) or saline. 3. Control saline injections did not change PRA. ADH reduced PRA in male, but increased PRA in female rats. Rats with diabetes insipidus displayed the greatest changes and were used in subsequent experiments. Extrarenal renin activity (nephrectomized rats) gave qualitatively similar responses to ADH. Plasma renin concentration, which was also measured with PRA in intact and nephrectomized male and female rats with diabetes insipidus, increased in the females and decreased in the males after ADH. 4. Castration, 24 h before study, abolished the ADH-induced fall in PRA, and testosterone implanted before castration did not restore the response. Cyproterone acetate reversed the ADH effect in males, so that PRA then rose after ADH. Hypophysectomized male rats, with depressed basal plasma renin activities, also showed a reduced PRA after ADH. 5. Ovariectomy had little effect on the ADH-induced renin release and the response was similar at oestrus, metoestrus and dioestrus. In hypophysectomized female rats ADH reduced PRA; a male pattern of response was seen in hypophysectomized female rats. 6. In both sexes PRA responses to ADH were blunted but not abolished by β-adrenergic blockade (propranolol). α-Adrenergic blockade (phenoxybenzamine) had little influence on the male response but in females the typical increase disappeared so that ADH reduced PRA. 7. It is concluded that pituitary hormones, including gonadotrophins and gonadal factors as well as adrenal sex steroids, appear to affect significantly the interplay between antidiuretic hormone and the renin—angiotensin system.

scholarly journals Studies of the Mechanism of Antidiuretic Hormone Release

2015 ◽  
pp. 95-100
Author(s):  
N. A. Thorn ◽  
J. T. Russell ◽  
G. Dahl ◽  
M. Gratzl
Keyword(s):  
Antidiuretic Hormone ◽  
Hormone Release
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