Hyperosmolarity

Deffebach, M. E., Salonen, R. O., Webber, S. E., and Widdiconibe, J. G. (1989), Cold and hyperosmolar fluids in canine trachea Vascular and smooth muscle tone and. ilbuniin flux. ]. Appi. Physiol. 66, 1309-1315. 

Stimulation of PKA and PKC inhibit NHE5 activity, as does hyperosmolarity, resembling the responsiveness of NHE3. NHE5 may also be regulated by the actin cytoskeleton, but further work is required to validate this notion and clarify the exact mechanism. 

Hyperosmolar drugs dehydrate local tissues, which causes irritation and increased peristalsis, with consequent evacuation of the fecal mass. Glycerin is a hyperosmolar drug. 

Hartman A, Dettmers C, Schott H, Beyenburg S. Cerebral blood flow and rheologic alterations by hyperosmolar therapy in patients with brain oedema. Acta Neurochir Suppl (Wein) 1990 51 168-169. 

Chronic or large ingestions of propylene glycol have been associated with the development of hyperosmolar anion-gap metabolic acidosis, renal dysfunction, hemolysis, cardiac arrhythmias, and seizures. 

Patients with hyperglycemic hyperosmolar nonketotic syndrome may require less insulin than DKA for acute glycemic control... 

Hyperosmolar Hyperglycemic State Hyperosmolar hyperglycemic state (HHS) is a life-threatening condition similar to DKA that also arises from inadequate insulin, but HHS occurs primarily in older patients with type 2 DM. DKA and HHS also differ in that HHS lacks the lipolysis,... 

Diarrhea Drug related Antibiotic-induced bacterial overgrowth Hyperosmolar medications administered via feeding tubes Antacids containing magnesium Malabsorption Hypoalbuminemia/gut mucosal atrophy Pancreatic insufficiency Inadequate GIT surface area Rapid GIT transit Radiation enteritis Tube feeding related Rapid formula administration Formula hyperosmolalty Low residue (fiber) content Lactose intolerance Bacterial contamination... 

Nausea and vomiting Gastric dysmotility (surgery, anticholinergic drugs, diabetic gastroparesis) Rapid infusion of hyperosmolar formula... 

LLE Left lower extremity NHDA Nonketotic hyperosmolar acidosis... 

Hyperglycemic hyperosmolar nonketotic syndrome Severe increase in serum glucose concentration without the production of ketones, leading to an increase in serum osmolality and symptoms... 

Hyperosmolar hyperglycemic state A potentially fatal short-term complication most commonly seen in older patients with type 2 diabetes caused by an insufficiency of insulin action that leads to alterations of osmolality and hyperglycemia, but without the ketosis and acidosis seen in diabetic ketoacidosis. 

Vasopressin is a peptide hormone produced by the hypothalamus and secreted by the posterior pituitary in response to stimulation. Normal stimuli for vasopressin release are hyperosmolarity and hypovolemia, with thresholds for secretion of greater than 280 mOsm/kg and greater than 20% plasma volume depletion. A number of other stimuli, such as pain, nausea, epinephrine, and numerous drugs, induce release of vasopressin. Vasopressin release is inhibited by volume expansion, ethanol, and norepinephrine. The physiological effect of vasopressin is to promote free water clearence by altering the permeability of the renal collecting duct to water. In addition, it has a direct vasoconstrictor effect. Consequently, vasopressin results in water retention and volume restoration. In patients with septic shock, vasopressin is appropriately secreted in response to hypovolemia and to elevated serum osmolarity (R14). 

Rapid intestinal transit may result in a false-positive breath test, in particular when hyperosmolar nonabsorbable substrates are used. A false-negative outcome in patients with culture-proven Gram-negative bacilli in the upper gut further query the sensitivity and usefulness of breath tests for clinical practice [10-13]. Positive microbial culture from small intestine is thus advantageous when major alterations of clinical management are considered. 

Hyperosmolar medium is known to be advantageous for the production of proteins such as antibodies in animal cell cultures [70, 71]. Likewise, raising the osmolarity of MS medium using mannitol was found to improve the accumulation of foreign pro-... 

Arima, H., Yamamoto, N., Sobue, K. etal. Hyperosmolar mannitol simulates expression of aquaporins 4 and 9 through a p38 mitogen-activated protein kinase-dependent pathway in rat astrocytes. /. Biol. Chem. 278 44525-44534,... 

Hepatic encephalopathy Hyperbilirubinemia Hypocalcemia Hypercalcemia Hyperparathyroidism Hypoparathyroidism Thiamine deficiency (Wernicke s) encephalopathy Diabetic ketoacidosis Nonketotic hyperosmolar coma Phosphate depletion Hypoglycemia Hypoxemia Hypercapnia... 

Polymodal sensory neurons in C. elegans are also mechanoreceptors. Polymodal sensory neurons in C. elegans seem to fall into the TRP class of mechanoreceptors as they apparently rely on several TRP channels for mechanosensation [4]. These sensory neurons respond to nose touch, hyperosmolarity and volatile repellents by triggering a backward response in the worm the OSM-9 and OCR-2 channels apparently mediate these responses, and the pathways differ for each sensory modality. However, little is known about the transduction mechanism in these cells. 

The practice of diluting hyperosmolar EN formulations should be avoided unless necessary to increase fluid intake. 

Most studies were performed with hyperosmolar solutions. Hypertonic disruption is under clinical evaluation for enhanced delivery of small molecular weight cytostatic agents to brain tumours. Technically, the procedure is performed as a high-flow short-term infusion of 25% mannitol or arabinose under general anaesthesia. The underlying mechanism is a sequelae of endothehal cell shrinkage, disruption of tight junctions and vasodilatation by osmotic shift [72]. 

Compared to small molecules, barrier opening for high molecular weight compounds is of shorter duration [72]. Furthermore, a characteristic difference exists in the degree of barrier opening in tumour versus normal brain tissue. Barrier disruption was consistently found to be more pronounced for the normal BBB, which may limit the clinical applicability of hyperosmolar barrier opening, at least for cytotoxic drugs [76]. 

The smallest functional unit of the kidney is the nephron. In the glomerular capillary loops, ultrafiltration of plasma fluid into Bowman s capsule (BC) yields primary urine. In the proximal tubules (pT), approx. 70% of the ultrafiltrate is retrieved by isoosmotic reabsorption of NaCl and water. In the thick portion of the ascending limb of Henle s loop (HL), NaCl is absorbed unaccompanied by water. This is the prerequisite for the hairpin countercurrent mechanism that allows build-up of a very high NaQ concentration in the renal medulla In the distal tubules (dT), NaCl and water are again jointly reabsorbed. At the end of the nephron, this process involves an aldosterone-controlled exchange of Na+ against 1C or H. In the collecting tubule (C), vasopressin (antidiuretic hormone, ADH) increases the epithelial permeability for water, which is drawn into the hyperosmolar milieu of the renal medulla and thus retained in the body. As a result, a concentrated urine enters the renal pelvis. 

ADH, a nonapeptide, released from the posterior pituitary gland promotes re-absorption of water in the kidney. This response is mediated by vasopressin receptors of the V2 subtype. ADH enhances the permeability of collecting duct epithelium for water (but not for electrolytes). As a result, water is drawn from urine into the hyperosmolar inter-stitium of the medulla. Nicotine augments (p. 110) and ethanol decreases ADH release. At concentrations above those required for antidiuresis, ADH stimulates smooth musculature, including that of blood vessels ( vasopressin ). The latter response is mediated by receptors of the Vi subtype. Blood pressure rises coronary vasoconstriction can precipitate angina pectoris. Lypres-sin (8-L-lysine vasopressin) acts like ADH. Other derivatives may display only one of the two actions. 

Sodium chloride (hypotonic) - 0.45% Sodium chloride (hypotonic) is primarily a hydrating solution and may be used to assess the status of the kidneys, because more water is provided than is required for salt excretion. It also may be used in the treatment of hyperosmolar diabetes where the use of dextrose is inadvisable and there is a need for large amounts of fluid without an excess of sodium ions. 

Hyperglycemia and diabetes mellitus Hyperglycemia, in some cases extreme and associated with ketoacidosis or hyperosmolar coma or death, has been reported in patients treated with atypical antipsychotics. 

Glycerin Suppository [Laxative] Uses Constipation Action Hyperosmolar laxative Dose Adults. 1 adult supp PR PRN Feds. 1 infant supp PR daily-bid PRN Caution [C, ] Disp Supp SE D Interactions T Effects W/ diuretics EMS Monitor ECG and BP for signs of hypovolemia and electrolyte disturbances d/t D OD Unlikely but may cause severe D and dehydration symptomatic and supportive... 

Acute complications of diabetes include diabetic ketoacidosis, hyperglycaemic non-ketotic hyperosmolar coma, lactic acidosis and hypoglycaemia. 

Laxatives are used to increase stool frequency and reduce stool viscosity. Even with long-term use, bulk laxatives and pure osmolar laxatives do not predispose patients to formation of a cathartic-type colon and should be the initial agents used for chronic constipation after a structural obstructing lesion has been excluded. Laxatives are also used before radiological, endoscopic, and abdominal surgical procedures such preparations quickly empty the colon of fecal material. Nonabsorbable hyperosmolar solutions or saline laxatives are used for this purpose. Classification and comparison of representative laxatives are provided in Table 40.1. 

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