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Serum water concentration

Fig. 6. Seizures resulting from an inappropriately high rate of intravenous water delivery in a child undergoing appendectomy. Until the time when seizures developed, the patient received parenterally a multiple electrolyte fluid at the rate of approximately 3 liters per m per 24 hrs., those in charge failing to recognize the special influences of operation, ether anesthesia, morphine and demerol to depress the diuretic response. Hyponatremia and an increase in serum water concentration developed ultimately leading to water intoxication and seizures. (Kerrigan al. , 1955). Fig. 6. Seizures resulting from an inappropriately high rate of intravenous water delivery in a child undergoing appendectomy. Until the time when seizures developed, the patient received parenterally a multiple electrolyte fluid at the rate of approximately 3 liters per m per 24 hrs., those in charge failing to recognize the special influences of operation, ether anesthesia, morphine and demerol to depress the diuretic response. Hyponatremia and an increase in serum water concentration developed ultimately leading to water intoxication and seizures. (Kerrigan al. , 1955).
Describe the unique relationship between serum sodium concentration and total body water. [Pg.403]

The body s normal daily sodium requirement is 1.0 to 1.5 mEq/kg (80 to 130 mEq, which is 80 to 130 mmol) to maintain a normal serum sodium concentration of 136 to 145 mEq/L (136 to 145 mmol/L).15 Sodium is the predominant cation of the ECF and largely determines ECF volume. Sodium is also the primary factor in establishing the osmotic pressure relationship between the ICF and ECF. All body fluids are in osmotic equilibrium and changes in serum sodium concentration are associated with shifts of water into and out of body fluid compartments. When sodium is added to the intravascular fluid compartment, fluid is pulled intravascularly from the interstitial fluid and the ICF until osmotic balance is restored. As such, a patient s measured sodium level should not be viewed as an index of sodium need because this parameter reflects the balance between total body sodium content and TBW. Disturbances in the sodium level most often represent disturbances of TBW. Sodium imbalances cannot be properly assessed without first assessing the body fluid status. [Pg.409]

Although both water and sodium are required in this instance, sodium needs to be provided in excess of water to fully correct this abnormality. As such, hypertonic saline (3% NaCl) is often used. One can estimate the change in serum sodium concentration after 1 L of 3% NaCl infusion using the following equation 16... [Pg.409]

Hypernatremia is a serum sodium concentration greater than 145 mEq/L (145 mmol/L) and can occur in the absence of a sodium deficit (pure water loss) or in its presence (hypotonic fluid loss).19 The signs and symptoms of hypernatremia are the same as those found in TBW depletion. Symptoms of hypernatremia are evident with a serum concentration greater than 160 mEq/L (160 mmol/L) and usually consist of thirst, mental slowing, and dry mucous membranes. Signs and symptoms become more profound as hypernatremia worsens, with the patient demonstrating confusion, hallucinations, acute weight... [Pg.410]

Renal Effects. Ingestion of drinking water containing lead was found to be associated with evidence of renal insufficiency in humans (Campbell et al. 1977). Lead concentrations in drinking water were compared to PbB concentrations in 283 residents who ingested this water for a mean of 21.5 years. A highly significant correlation was found for these two parameters. In addition, elevated PbB concentrations were associated with renal insufficiency, reflected as raised serum urea concentrations and hyperuricemia. No renal biopsies were performed. [Pg.181]

The potent antidiuretic hormone AVP orchestrates the regulation of free water absorption, body fluid osmolality, cell contraction, blood volume, and blood pressure through stimulation of three G-protein-coupled receptor subtypes Vi-vascular types a and b, V2-renal, and V3-pituitary. Increased AVP secretion is the trademark of several pathophysiological disorders, including heart failure, impaired renal function, liver cirrhosis, and SIADH. As a consequence, these patients experience excess water retention or inadequate free-water excretion, which results in the dilution of sodium concentrations, frequently manifesting as clinical hyponatremia (serum sodium concentration <135mmol/L). This electrolyte imbalance increases mortality rates by 60-fold. Selective antagonism of the AVP V2 receptor promotes water... [Pg.528]

In rodents, copper administered by single intraperitoneal or subcutaneous injection is lethal at 3 to 7 mg Cu/kg BW (Table 3.7). Mice died when their drinking water contained 640 mg Cu/L (Table 3.7). In rats, copper accumulation in kidneys and lungs is similar regardless of route of administration (Romeu-Moreno et al. 1994). Concentrations of copper in serum of rats (Rattus sp.) reflect dietary copper concentrations in liver and kidney are directly related to serum Cu and ceruloplasmin (Petering et al. 1977). As serum Cu concentrations rise in rats, levels fall for serum cholesterol, triglycerides, and phospholipids (Petering et al. 1977). [Pg.203]

Cells, Treatment, and Chromosome Analysis. About 4 X 105 CHO-K1 cells (Flow Laboratories, Scotland) were seeded into Ham s F10 medium (Flow) supplemented with 10 newborn calf serum (Flow). These cells were incubated at 37 °C and 5 C02 in 25-cm3 tissue culture flasks. Twenty-four hours later, the cells were exposed for 1 h at 37 °C to a maximum of 50 /zL of drinking water concentrate (neutral fraction) in a total volume of 3 mL of Ham s F10, without serum. As a positive control, 4-methoxyaniline, dissolved in DMSO, was used. [Pg.589]

Water Deficiency. This condition occurs when water output exceeds intake. Water is continually losl by way of the lungs, skin, and kidneys and dius a deficiency of body water will occur if a critical minimal supply is not maintained. Decreased intake when water is available is uncommon. Very rarely, a brain malfunction may interfere with one s sense of diirst. Increased output of water can result from many causes. For example, a person with diabetes insipidus who lacks ADH (antidiuretic hormone) or a person whose kidneys do not respond normally to ADH, as in instances of nephrogenic diabetes insipidus, will increase water output Other diseases which may cause excess excretion of water include osmotic diuresis, hypercalcemia, hypokalemia, chronic pyelonephritis, and sickle cell anemia, among others. Excessive water losses are also experienced in some cases with advanced age and in some burn cases. Two clinical features are good measures of dehydration—weight loss of the patient and an elevation of the serum sodium concentration. In situations of dehydration, the body initiates mechanisms which manipulate the transfer of water from one compartment to the next, retaining water in those cells and organs where it is most needed. [Pg.1721]

The secondary mineralocorticoid activity of glucocorticoids can lead to salt and water retention, which can cause hypertension. Although the detailed mechanisms are as yet uncertain, glucocorticoid-induced hypertension often occurs in elderly patients and is more common in patients with total serum calcium concentrations below the reference range and/or in those with a family history of essential hypertension (SEDA-20, 368 19). [Pg.7]

A potential risk of desmopressin is of water intoxication with resultant hyponatremia (48), and rapid falls in serum sodium concentration can result in seizures. The risk is increased in infants and patients receiving hypotonic intravenous fluids, and such patients need to be carefully monitored. [Pg.482]

Furosemide rarely causes the syndrome of inappropriate antidiuretic hormone secretion (SIADH) (although it has been found useful in treating some patients with SIADH who cannot tolerate water restriction (428)). In furosemide-induced cases (SEDA-7, 246), serum ADH concentrations were raised, total body sodium was normal, total body potassium greatly reduced, and intracellular water raised at the expense of extracellular fluid volume. However, such cases are rare, and no new cases have been published since this complication was reported in SEDA-7. [Pg.603]

A 54-year old man, who had taken lithium for 15 years without problems, suddenly developed food and water aversion, hypercalcemia (2.75 mmol/1), and lithium toxicity, with a serum lithium concentration of 4.3 mmol/1 (677). He was confused, delirious, and irritable. Hemodialysis produced a marked improvement in laboratory tests, which became normal after 9 days. [Pg.619]

Hyponatremia is caused by an excess of total body water relative to total body sodium and can result from a number of underlying conditions, including the syndrome of inappropriate antidiuretic hormone secretion (SIADH), cirrhosis, and congestive heart failure (CHF). In each of these conditions, inappropriate production of arginine vasopressin (AVP) [also known as vasopressin or antidiuretic hormone (ADH)], a neurohormone that regulates renal electrolyte-free water reabsorption, contributes to enhanced renal water retention, leading to decreased serum sodium concentrations.7 Hyponatremia can be characterized as hypervolemic, euvolemic, or hypovolemic... [Pg.175]

In mild cases of hyponatremia, treatment typically focuses on water restriction (< 800 mL/day) however this approach suffers from poor patient compliance due to thirst brought on by increasing serum osmolality.1,10 In cases of extreme hyponatremia, infusions of hypertonic saline are used to elevate serum sodium concentrations. Loop diuretics (e.g., furosemide) are often used as an adjunct to such treatment to offset potential volume overload.1 Hypertonic saline therapy is also suboptimal, as it carries a risk of overly rapid adjustment of plasma sodium levels, which can result in the rapid shift of water from brain tissue to the vascular space, triggering neural demyelination that can result in seizures, coma, quadriplegia, and even death.1... [Pg.176]

Large fatty acid anions, particularly oleate and palmitate, are normally present in human serum at concentrations greatly exceeding their solubility in water (6,7,8). With HSA being normally at about 0.6mM, the total serum content of nonesterified fatty acids usually ranges from about the same level to a normal high of about 2mM or to 4mM... [Pg.320]

Elevated aluminum levels have been implicated as the cause of dialysis encephalopathy or dementia in renal failure patients undergoing long-term hemodialysis [85]. Some patients used aluminum-containing medications. Moreover, patients with renal failure cannot remove aluminum from the blood. Dialysis dementia can arise after three to seven years of hemodialysis treatment. Speech disorders precede dementia and convulsions. Since many hemodialysis units rely on systems to purify fluoridated tap water, it is likely that many patients are being exposed inadvertently to increased concentrations of fluoride and aluminum. Increased serum fluoride concentration and fluoride intoxication have been also observed in chronic hemodialysis patients. Arnow et al. [96] reported that 12 of 15 patients receiving dialysis treatment in one room became acutely ill, with multiple non-specific symptoms and fatal ventricular fibrillation. Death was associated with longer hemodialysis time and increased age compared with other patients who became ill. [Pg.176]

In the colon, semifluid material entering from the small bowel is thickened by absorption of water and salts (from about 1000 ml to 150 ml per day). If, owing to the action of an irritant purgative, the colon empties prematurely, an enteral loss of NaCl, KC1 and water will be incurred. In order to forestall depletion of NaCl and water, the body responds with an increased release of aldosterone (p.168), which stimulates their reabsorption in the kidney. However, the action of aldosterone is associated with increased renal excretion of KC1. The enteral and renal K losses add up to K+ depletion of the body, evidenced by a fall in serum K concentration (hypokalemia). This condition is accompanied by a reduction in intestinal peristalsis (bowel atonia). The affected individual infers constipation and again partakes of the purgative, and the vicious circle is closed. [Pg.176]

A standard solution of albumin (bovine serum) of concentration 4 mg/ml. Define the concentration accurately by diluting in water to give A279 of 0.140, corresponding to a concentration of 200 fig/ ml (determined from the molar absorption coefficient at 279 nm for albumin in aqueous solution of 45 000). Dilute this solution 1 4 to give a final concentration of 50 fig/m. ... [Pg.226]

Extensive early studies of in vitro and in vivo structure-activity relationships within the leucomycin family revealed correlations between the number and type of O-acyl substituents and the compounds antibacterial potency, efficacy in treating experimental infections, and serum antibiotic concentrations [26]. Consequently, esterification of all hydroxyl groups within several leucomycin-related macrolides was conducted to find derivatives with better antibiotic activity and pharmaceutical properties (such as greater water solubility and masking their extremely bitter taste). From such investigations with midecamycin, miokamycin was synthesized and characterized as a useful new macrolide antibiotic [24, 27]. It has now been commercially launched in several countries [5]. [Pg.269]

Bilirubin - an apolar, water-insoluble lipophile substance - is potentially toxic. It is bound to serum albumin and transported to the sinusoidal membrane of the liver cell as a bilirubin-albumin complex, (s. fig. 3.1) The binding capacity of albumin is exceeded only at a serum bilirubin concentration of >4—5 mg/dl. In the case of decreased albumin binding (e. g. in acidosis) or oversaturated binding capacity, there is a danger of toxic cell damage due to the diffusion of unbound bilirubin into the cells (in some cases accompanied by kernicterus). Neonates and premature babies are at particular risk because of their immature blood-cerebrospinal fluid barrier. Albumin-bound bilirubin can function as an antioxidant to intercept free radicals and/or O2 radicals. (93) (s. tab. 3.25)... [Pg.33]

Highly specific sodium electrodes have been developed in which the selectivity for sodium may be 10 times greater than that for potassium (C3, M19). With urine, the pH and potassium concentration should preferably be controlled, but this is unnecessary for blood. The potassium glass electrode is less selective and responds to NH/ and Na. Its selectivity may vary with age (M19). It can be used with blood only if corrections are made for sodium concentration according to Eq. (2) (M19, N2, N3), but when this is done, the electrode shows a linear response to potassium concentration. The precision of serum sodium and potassium measurements with electrodes was found to be better than those obtained by flame photometry (M19, N3). To compare the accuracy of the two methods, the results by flame photometry must be converted to concentrations in serum water. For most specimens, it was found that concentrations could be calculated satisfactorily from activity measurements and results by the two methods agreed (N3), but differences were noted with some samples. So far the cause of this has not been resolved, but it is possible that in future ionic activity will be recognized as a better diagnostic feature than ionic concentration (N3). [Pg.358]


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See also in sourсe #XX -- [ Pg.122 ]




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