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Books on the topic 'Sodium Ion Cells'

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Published: 6 September 2023

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1

S, Aronson Peter, ed. Na⁺-H⁺ exchange, intracellular pH, and cell function. Orlando: Academic Press, 1986.

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2

1950-, Karmazyn M., Avkiran M, and Fliegel Larry 1956-, eds. The sodium-hydrogen exchanger: From molecule to its role in disease. Boston: Kluwer Academic Publishers, 2003.

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3

Ian, Glynn, Ellory J. C, and Company of Biologists, eds. The sodium pump: Proceedings of the Fourth International Conference on Na, K-ATPase, held at the Physiological Laboratory, Cambridge, in August 1984. Cambridge, U.K: Company of Biologists, 1985.

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4

E, Vance Dennis, and Vance Jean E, eds. Biochemistry of lipids, lipoproteins, and membranes. Amsterdam: Elsevier, 1991.

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5

Adragna, Norma, and Peter Lauf. Cell Volume and Signaling. Springer, 2014.

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6

Cell Volume and Signaling (Advances in Experimental Medicine and Biology). Springer, 2005.

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7

Egan, Brian N. Hyponatremia/Hypernatremia. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0037.

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lSodium is the most abundant cation in the extracellular fluid and is important for regulation of plasma water concentrations and cell volume. Sodium cannot readily cross the blood-brain barrier, and changes in plasma sodium levels by altering free water movement can expand or shrink brain cells. Changes in brain cell volume can cause brain cell dysfunction and apoptosis. Correction of both high and low sodium levels must be done gradually, as rapid correction of dysnatremias can also damage brain cells. In this chapter we review the physiology of sodium regulation, and discuss the clinical implications of these disorders as well as present a treatment plan for safe correction.
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8

Rich, Mark M. Critical Illness Neuropathy, Myopathy, and Sodium Channelopathy. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0033.

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Skeletal muscle weakness is a common problem that complicates recovery from critical illness. The primary causes of weakness include neuropathic disorders, myopathic disorders, and mixed disorders. Recent studies have demonstrated that reduced excitability of the nerve and muscle cell membranes might contribute to weakness during the acute stages of the polyneuropathy and myopathy encountered in critically ill patients. In both tissues, an acquired sodium channelopathy can lead to increased inactivation of channels, leading to inexcitability an paralysis. Experimental sepsis models have demonstrated a similar reduction in excitability in myocardial cells as well as in motor neurons within the spinal cord. The presence of a channelopathy in multiple tissues raises the possibility that reduced excitability of neurons within the CNS might contribute to septic encephalopathy. If this is the case, a single therapy to improve excitability might treat failure of a number of electrically active tissues.
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9

Na+-H+ exchange, intracellular pH, and cell function. Orlando: Academic Press, 1986.

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10

(Editor), Morris Karmazyn, Metin Avkiran (Editor), and Larry Fliegel (Editor), eds. The Sodium-Hydrogen Exchanger: From Molecule to its Role in Disease. Springer, 2003.

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11

Slimp, Jefferson C. Neurophysiology of Multiple Sclerosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.003.0003.

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Any discussion of the pathomechanisms and treatments of MS benefits from an understanding of the physiology of the neuronal membrane and the action potential. Neurons and glia, are important for signal propagation, synaptic function, and neural development. The neuronal cell membrane, maintains different ionic environments inside and outside the cell, separating charge across the membrane and facilitating electrical excitability. Ion channels allow flow of sodium, potassium, and calcium ions across the membrane at selected times. At rest, potassium ion efflux across the membrane establishes the nerve membrane resting potential. When activated by a voltage change to threshold, sodium influx generates an action potential, or a sudden alteration in membrane potentials, that can be conducted along an axon. The myelin sheaths around an axon, increase the speed of conduction and conserve energy. The pathology of MS disrupts the myelin structures, disturbs conduction, and leads to neurodegeneration. Ion channels have been the target of investigation for both restoration of conduction and neuroprotection.
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12

Hoorn, Ewout J., and Robert Zietse. Approach to the patient with hyponatraemia. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0028.

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Hyponatraemia is the most common electrolyte disorder in hospitalized patients and is primarily a water balance disorder. Therefore, hyponatraemia is due to a relative excess of water in comparison with sodium in the extracellular fluid volume. Hyponatraemia is usually due to the release of vasopressin despite hypo-osmolality; this secretion is either ‘appropriate’ (i.e. due to a low intravascular volume) or ‘inappropriate’. The diagnostic approach to hyponatraemia relies on the assessment of the time of development, symptoms, and volume status, along with laboratory parameters such as urine sodium and urine osmolality. Complications are mainly neurological and usually depend on the rate of development and correction. If hyponatraemia develops acutely, treatment should be directed towards counteracting the water shift to or brain cells. Conversely, in more chronic cases of hyponatraemia, treatment should be directed at the underlying cause, while avoiding over-correction.
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13

Zietse, Robert, and Ewout Hoorn. Approach to the patient with hypernatraemia. Edited by Robert Unwin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0029_update_001.

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Hypernatraemia is much less common than hyponatraemia, and its prevalence is higher in certain populations, including children, the elderly, and critically ill patients. A common feature is that patients affected have been unable to drink water to correct the disorder. Hyponatraemia and hypernatraemia are both primarily disorders of water balance. Hypernatraemia is caused by a relative deficit of total body water in comparison to total body sodium. Both disorders are often associated with disturbances in the hormone governing water balance, arginine vasopressin (antidiuretic hormone). Hypernatraemia may be due to an inability to secrete vasopressin or a resistance to its actions in the kidney. The diagnostic approach relies on the assessment of the time of development, symptoms, and volume status, along with laboratory parameters such as urine sodium and urine osmolality. If hypernatraemia develop acutely, treatment should be directed towards counteracting the water shift to or from brain cells. In more chronic cases, treatment should be directed to the underlying cause while avoiding overcorrection.
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14

Suri, Ajay, and Jean R. McEwan. Anti-anginal agents in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0037.

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Angina is chest pain resulting from the lack of blood supply to heart muscle most commonly due to obstructive atherosclerotic. Intensive care unit patients are subject to various stresses that will increase the demand on the heart and are in a pro-thrombotic state. Patients in an intensive treatment unit may be sedated and so cardiac ischaemia may be detected by electrocardiogram, haemodynamic monitoring, and echocardiographic imaging of function. These signs may indicate critical coronary perfusion heralding a myocardial infarction and are alleviated by anti-anginal drugs. Beta-blockers and calcium channel blockers are the usual first-line treatments for angina, but may not be ideal in the critically-ill patient. Nitrates reduce blood pressure without typically affecting heart rate. Nicorandil is a similar mechanism of action and tends to be given orally, while ivabridine, an If channel blocker, is a newer anti-anginal, which acts by reducing heart rate, while not affecting blood pressure. Ranolazine is the one of the newest anti-anginal agents and is believed to alter the transcellular late sodium current thereby decreasing sodium entry into ischaemic myocardial cells.
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15

The Na, K-pump: Proceedings of the 5th International Conference on Na, K-ATPase held at Fuglso Conference Center, Denmark, June 14-19, 1987 (Progress in clinical and biological research). A.R. Liss, 1988.

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16

The Na, K-pump: Proceedings of the 5th International Conference on Na, K-ATPase held at Fuglso Conference Center, Denmark, June 14-19, 1987 (Progress in clinical and biological research). A.R. Liss, 1988.

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17

Kleinzeller, Arnost. Current Topics in Membranes and Transport: Na+ - H+ Exchange, Intracellular Ph, and Cell Function (Current Topics in Membranes). Academic Pr, 1986.

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18

Kleinzeller, Arnost. Current Topics in Membranes and Transport: Na+ - H+ Exchange, Intracellular Ph, and Cell Function (Current Topics in Membranes). Academic Pr, 1986.

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19

Ahuja, Christopher S., and Michael Fehlings. Neuroprotection for Spinal Cord Injury. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0015.

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Traumatic spinal cord injuries (SCI) often have a devastating impact on quality of life for patients and their families. Neuroprotection for spinal cord injury is aimed at improving functional outcomes by limiting secondary injury processes that occur within the first minutes, hours, and days following the primary injury. The primary mechanical trauma initiates a secondary injury cascade where ischemia, inflammatory cell infiltration, and cytotoxic changes in the microenvironment cause further cell death and loss of function. Time-sensitive neuroprotective measures targeting these secondary insults have emerged as key therapeutic strategies. This chapter summarizes current evidence-based neuroprotective treatments, such as blood pressure augmentation, early surgical decompression, and intravenous methylprednisolone, as well as important emerging interventions, including therapeutic hypothermia, sodium channel blockade using riluzole, and the anti-inflammatory actions of minocycline. The chapter concludes by summarizing the current guidelines that all practitioners should be well-versed in prior to providing care for patients with SCI.
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20

Frise, Matthew C., and Jonathan B. Salmon. Disorders of potassium in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0251.

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Plasma potassium levels are maintained in health between 3.5 and 5.0 mmol/L, and reflect total body potassium only in stable states at normal pH. Most true hyperkalaemia results from renal insufficiency. The goals of therapy are myocardial protection and return of plasma potassium to a safe level. Measures are commonly initiated above 5.5 mmol/L; above 6.5 mmol/L, aggressive measures should be adopted and calcium salts given if there are cardiac dysrhythmias or QRS-broadening. Glucose-insulin infusions and beta-2-agonists promote potassium shifts into cells. Diuretics and sodium bicarbonate may be helpful, but persistent hyperkalaemia is an indication for renal replacement therapy. Hypokalaemia may lead to dangerous arrhythmias, skeletal muscle weakness, ileus, and reduced vascular smooth muscle contractility. Rapid replacement should only be undertaken for severe hypokalaemia or in the context of arrhythmias. Once the extracellular deficit is corrected, there will usually be a continuing need for potassium supplementation to replenish intracellular stores.
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21

Esen, Figen. Disorders of magnesium in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0252.

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Plasma potassium levels are maintained in health between 3.5 and 5.0 mmol/L, and reflect total body potassium only in stable states at normal pH. Most true hyperkalaemia results from renal insufficiency. The goals of therapy are myocardial protection and return of plasma potassium to a safe level. Measures are commonly initiated above 5.5 mmol/L; above 6.5 mmol/L, aggressive measures should be adopted and calcium salts given if there are cardiac dysrhythmias or QRS-broadening. Glucose-insulin infusions and beta-2-agonists promote potassium shifts into cells. Diuretics and sodium bicarbonate may be helpful, but persistent hyperkalaemia is an indication for renal replacement therapy. Hypokalaemia may lead to dangerous arrhythmias, skeletal muscle weakness, ileus, and reduced vascular smooth muscle contractility. Rapid replacement should only be undertaken for severe hypokalaemia or in the context of arrhythmias. Once the extracellular deficit is corrected, there will usually be a continuing need for potassium supplementation to replenish intracellular stores.
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22

Mason, Peggy. The Neuron at Rest. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0009.

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Neuronal membrane potential depends on the distribution of ions across the plasma membrane and the permeability of the membrane to those ions afforded by transmembrane proteins. Ions cannot pass through a lipid bilayer but enter or exit neurons through ion channels. When activated by voltage or a ligand, ion channels open to form a pore through which selective ions can pass. The ion channels that support a resting membrane potential are critical to setting a cell’s excitability. From the distribution of an ionic species, the Nernst potential can be used to predict the steady-state potential for that one ion. Neurons are permeable to potassium, sodium, and chloride ions at rest. The Goldman-Hodgkin-Katz equation takes into consideration the influence of multiple ionic species and can be used to predict neuronal membrane potential. Finally, how synaptic inputs affect neurons through synaptic currents and changes in membrane resistance is described.
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23

Kleinzeller, Arnost. Current Topics in Membranes and Transport. Elsevier Science & Technology Books, 1988.

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24

Kleinzeller, Arnost. Current Topics in Membranes and Transport. Elsevier Science & Technology Books, 1990.

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25

Kleinzeller, Arnost. Current Topics in Membranes and Transport. Elsevier Science & Technology Books, 1987.

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26

Kleinzeller, Arnost. Current Topics in Membranes and Transport. Elsevier Science & Technology Books, 1986.

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27

Bronner, Felix, and Arnost Kleinzeller. Current Topics in Membranes and Transport. Elsevier Science & Technology Books, 1986.

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28

El Kenz, Hanane, and Philippe Van der Linden. The physiology of blood in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0011.

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Following the discovery of the ABO blood groups by Landsteiner in 1901, Albert Hustin described the first transfusion of a whole blood unit in 1914. The modern transfusion era really begins in 1916 with the discovery of sodium citrate as an anticoagulant by the same physician, allowing blood conservation in dedicated packs. Since that time, many advances have been made especially over the past two decades in the storage, the conservation, and the laboratory testing of blood components and in transfusion medicine practice. Transfusion of whole blood has been replaced by blood component therapy, which consists of the administration of packed red blood cells, fresh frozen plasma, or platelets. Although blood transfusion is safer than ever, the risk of complications will never reach zero. The risk of infectious transfusion-transmitted diseases has been markedly reduced by the implementation of extensive infectious disease testing, donor selection, and pathogen-inactivation procedures. In countries with a high human development index, the leading causes of allogeneic blood transfusion-related deaths actually resulted from immunological and septic complications. The first section of this chapter describes the structure, function, and immunological aspects of the different blood components that are routinely transfused today. The second section details the composition of the different blood components, their indications, the pre-transfusion compatibility tests, and the main adverse effects associated with their transfusion.
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29

Daudon, Michel, and Paul Jungers. Cystine stones. Edited by Mark E. De Broe. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0203_update_001.

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Cystinuria, an autosomal recessive disease (estimated at 1:7000 births worldwide), results from the defective reabsorption of cystine and dibasic amino acids (also ornithine, arginine, lysine, COAL) by epithelial cells of renal proximal tubules, leading to an abnormally high urinary excretion of these amino acids. Due to the poor solubility of cystine at the usual urine pH, formation of cystine crystals and stones ensues. Incidence of homozygotes is estimated at 1 in 7000 births worldwide, but is lower in European countries and much higher in populations with frequent consanguinity. Cystine stones represent 1–2% of all stones in adults and 5–8% in paediatric patients, with an equal distribution between males and females.Cystinuria is caused by inactivating mutations in the gene SLC3A1 or SLC7A9, both encoding proteins contributing to the function of the heterodimeric transport system of cystine.Cystine nephrolithiasis may present in infants, most frequently in adolescents or young adults, sometimes later. Cystine calculi are weakly radio-opaque. Stone analysis using infrared spectroscopy (or X-ray diffraction) allows immediate and accurate diagnosis. Urinary amino acid chromatography quantifies urinary cystine excretion, needed to define the therapeutic strategy.Urological treatment of cystine stones currently uses extracorporeal stone wave lithotripsy or flexible ureterorenoscopy with Holmium laser, that is, minimally invasive techniques. However, as cystine stones are highly recurrent, preventive therapy is essential.Medical treatment combines reduced methionine and sodium intake, to lower cystine excretion; hyperdiuresis (> 3 L/day) to reduce cystine concentration; and active alkalinization preferably using potassium citrate (40–80 mEq/day) to increase cystine solubility by rising urine pH up to 7.5–8. If these measures are insufficient to prevent recurrent stone formation, a thiol derivative (D-penicillamine or tiopronin), which converts cystine into a more soluble disulphide, should be added. Close monitoring and adherence of the patient to the therapeutic programme are needed to ensure life-long compliance, the key for successful prevention in the long term.
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30

Covic, Adrian, Mugurel Apetrii, Luminita Voroneanu, and David J. Goldsmith. Vascular calcification. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0120_update_001.

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Vascular calcification (VC) is a common feature of patients with advanced CKD and it could be, at least in part, the cause of increased cardiovascular mortality in these patients. From a morphologic point of view, there are at least two types of pathologic calcium phosphate deposition in the arterial wall—namely, intima calcification (mostly associated with atherosclerotic plaques) and media calcification (associated with stiffening of the vasculature, resulting in significantly adverse cardiovascular outcomes). Although VC was viewed initially as a passive phenomenon, it appears to be a cell-mediated, dynamic, and actively regulated process that closely resembles the formation of normal bone tissue, as discovered recently. VC seems to be the result of the dysregulation of the equilibrium between promoters and inhibitors. The determinants are mostly represented by altered calcium and phosphorus metabolism, secondary hyperparathyroidism, vitamin D excess, high fibroblast growth factor 23, and high levels of indoxyl sulphate or leptin; meanwhile, the inhibitors are vitamin K, fetuin A, matrix G1a protein, osteoprotegerin, and pyrophosphate. A number of non-invasive imaging techniques are available to investigate cardiac and vascular calcification: plain X-rays, to identify macroscopic calcifications of the aorta and peripheral arteries; two-dimensional ultrasound for investigating the calcification of carotid arteries, femoral arteries, and aorta; echocardiography, for assessment of valvular calcification; and, of course, computed tomography technologies, which constitute the gold standard for quantification of coronary artery and aorta calcification. All these methods have a series of advantages and limitations. The treatment/ prevention of VC is currently mostly around calcium-mineral bone disease interventions, and unproven. There are interesting hypotheses around vitamin K, Magnesium, sodium thiosulphate and other potential agents.
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31

Lameire, Norbert, Raymond Vanholder, and Wim Van Biesen. Clinical approach to the patient with acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0222_update_001.

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The prognosis of acute kidney injury (AKI) depends on early diagnosis and therapy. A multitude of causes are classified according to their origin as prerenal, intrinsic (intrarenal), and post-renal.Prerenal AKI means a loss of renal function despite intact nephrons, for example, because of volume depletion and/or hypotension.There is a broad spectrum of intrinsic causes of AKI including acute tubular necrosis (ATN), interstitial nephritis, glomerulonephritis, and vasculitis. Evaluation includes careful review of the patient’s history, physical examination, urinalysis, selected urine chemistries, imaging of the urinary tree, and eventual kidney biopsy. The history should focus on the tempo of loss of function (if known), associated systemic diseases, and symptoms related to the urinary tract (especially those that suggest obstruction). In addition, a review of the medications looking for potentially nephrotoxic drugs is essential. The physical examination is directed towards the identification of findings of a systemic disease and a detailed assessment of the patient’s haemodynamic status. This latter goal may require invasive monitoring, especially in the oliguric patient with conflicting clinical findings, where the physical examination has limited accuracy.Excluding urinary tract obstruction is necessary in all cases and may be established easily by renal ultrasound.Distinction between the two most common causes of AKI (prerenal AKI and ATN) is sometimes difficult, especially because the clinical examination is often misleading in the setting of mild volume depletion or overload. Urinary chemistries, like calculation of the fractional excretion of sodium (FENa), may be used to help in this distinction. In contrast to FENa, the fractional excretion of urea has the advantage of being rather independent of diuretic therapy. Response to fluid repletion is still regarded as the gold standard in the differentiation between prerenal and intrinsic AKI. Return of renal function to baseline or resuming of diuresis within 24 to 72 hours is considered to indicate ‘transient, mostly prerenal AKI’, whereas persistent renal failure usually indicates intrinsic disease. Transient AKI may, however, also occur in short-lived ATN. Furthermore, rapid fluid application is contraindicated in a substantial number of patients, such as those with congestive heart failure.‘Muddy brown’ casts and/or tubular epithelial cell casts in the urine sediment are typically seen in patients with ATN. Their presence is an important tool in the distinction between ATN and prerenal AKI, which is characterized by a normal sediment, or by occasional hyaline casts. There is a possible role for new serum and/or urinary biomarkers in the diagnosis and prognosis of the patient with AKI, including the differential diagnosis between pre-renal AKI and ATN. Further studies are needed before their routine determination can be recommended.When a diagnosis cannot be made with reasonable certainty through this evaluation, renal biopsy should be considered; when intrarenal causes such as crescentic glomerulonephritis or vasculitis are suspected, immediate biopsy to avoid delay in the initiation of therapy is mandatory.
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