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Evaluation and Investigation of Pituitary Disease
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
ADH deficiency leads to the production of large volumes of inappropriately dilute urine. This results in compensatory polydipsia, urinary frequency, nocturia, and enuresis. A 24-hr urine collection is performed to confirm excessive urine volume (>50 mL/kg/day) and low osmolality (<300 mOsmol/L). A water deprivation test, with close monitoring of plasma and urinary sodium and osmolalities, will confirm the inability to appropriately concentrate the urine in severe diabetes insipidus (DI).
Head and Neck
Published in Bobby Krishnachetty, Abdul Syed, Harriet Scott, Applied Anatomy for the FRCA, 2020
Bobby Krishnachetty, Abdul Syed, Harriet Scott
After pituitary surgery the most commonly affected electrolyte is sodium. This can be due to diabetes insipidus (DI) due to decreased secretion of ADH. Inappropriate water loss leads to hypernatraemia and increased serum osmolality in the context of large volumes of dilute urine. Treatment aims at replacement of water and ADH. Intranasal or intravenous desmopressin (Deamino D Arginine Vasopressin, DDAVP) has been the mainstay of treatment.
Critical Care and Anaesthesia
Published in Tjun Tang, Elizabeth O'Riordan, Stewart Walsh, Cracking the Intercollegiate General Surgery FRCS Viva, 2020
Rajkumar Rajendram, Alex Joseph, John Davidson, Avinash Gobindram, Prit Anand Singh, Animesh JK Patel
How is the serum sodium level regulated?Increase in serum osmolarity (>280–300 mOsm/kg) stimulates hypothalamic osmoreceptors, which cause thirst and release of ADH.ADH increases renal free water reabsorption resulting in the production of concentrated (i.e. low volume, high osmolarity) urine, returning serum osmolarity to normal.Aldosterone is released in response to hypovolaemia through the renin–angiotensin–aldosterone axis. This causes absorption of sodium at the distal renal tubule, which encourages water retention.Hypovolaemia increases sodium absorption in the proximal tubule.Hypervolaemia suppresses tubular sodium reabsorption, resulting in natriuresis.
Endothelial dysfunction: a therapeutic target in bacterial sepsis?
Published in Expert Opinion on Therapeutic Targets, 2021
Jean-Louis Vincent, Can Ince, Peter Pickkers
Arginine vasopressin (also called ADH) is a peptide produced in the supraoptic and paraventricular nuclei of the hypothalamus. After production in the hypothalamus, it is transported to the posterior part of the pituitary gland, where it is stored (Figure 5). Vasopressin is an important hormone in the regulation of osmolality and volume. Release from the neurohypophysis is regulated by the osmolarity of the blood, but in extreme circumstances, secretion also takes place in the context of volume regulation. Stretch receptors in the atria decrease their signal frequency as the atrial pressure decreases. Afferent nerves transmit this signal to the hypothalamus through the solitarius tract of the medulla, leading to increased vasopressin production. In addition, angiotensin II receptors are present in the hypothalamus which, when occupied with angiotensin II, also lead to increased production of vasopressin.
Heat-induced hypervolemia: Does the mode of acclimation matter and what are the implications for performance at Tokyo 2020?
Published in Temperature, 2020
Lorenz S. Kissling, Ashley P. Akerman, James D. Cotter
PVE occurs predominantly through stimulation of fluid conserving hormones and accruing albumin in the intravascular space. Principal fluid conserving hormones are the RAAS and ADH. The RAAS initiates with the release of renin, which then stimulates the adrenal cortex to release angiotensinogen, which is converted to angiotensin I, and angiotensin II. Angiotensin II is a potent vasoconstrictor, that limits the renal loss of sodium, increases water absorption, promotes thirst [79,80], and stimulates aldosterone production [81]. Aldosterone limits the excretion of sodium and preserves the sodium/water balance, total sodium content, and retains water through changes in osmotic pressures [82]. ADH is released from the posterior pituitary gland into the bloodstream, inducing water retention through the kidneys, vasoconstriction of arterioles, and stimulating thirst [83,84].
Approach to and management of abnormalities in plasma sodium
Published in Acta Clinica Belgica, 2019
We will not systematically discuss the various disease states associated with each category (see Table 1). Differentiating the hypervolemic (heart failure, liver cirrhosis, nephrotic syndrome) from the euvolemic or hypovolemic patient is usually simple because of the presencet of edema and/or ascites in the former. In the ‘hypervolemic’ patients, despite a large increase in the ECF volume, the ‘effective arterial blood volume’ (EABV) appears to be reduced and the kidneys respond in a manner virtually similar as in conditions associated with sodium depletion. There is an increase in ADH secretion due to the ‘hypovolemic stimulus’ (the major factor) and a decreased delivery of isotonic salt-containing fluid from the proximal to the distal nephron, both contributing to a decrease in electrolyte-free water excretion. Urinary sodium concentrations are low (UNa < 20 mmol/l), and serum urea or uric acid concentrations are normal or increased except in cirrhosis where both are sometimes low [7]. Vagal neuropathy could also play a role in producing high ADH levels in cirrhotic patients [8].