DOCSLIB.ORG

Chapter 68 Ends of the Capillaries

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Chapter 68 Ends of the Capillaries Fluid and Electrolyte PART Disorders VI These forces favor movement into the interstitial space at the arterial Chapter 68 ends of the capillaries. The decreased hydrostatic forces and increased oncotic forces, which result from the dilutional increase in albumin concentration, cause movement of fluid into the venous ends of the Electrolyte and Acid-Base capillaries. Overall, there is usually a net movement of fluid out of the intravascular space to the interstitial space, but this fluid is returned to Disorders the circulation via the lymphatics. An imbalance in these forces may cause expansion of the interstitial volume at the expense of the intravascular volume. In children with hypoalbuminemia, the decreased oncotic pressure of the intravascular 68.1 Composition of Body Fluids fluid contributes to the development ofedema . Loss of fluid from the Larry A. Greenbaum intravascular space may compromise the intravascular volume, placing the child at risk for inadequate blood flow to vital organs. This is especially TOTAL BODY WATER likely in diseases in which capillary leak occurs because the loss of Total body water (TBW) as a percentage of body weight varies with albumin from the intravascular space is associated with an increase in the age (Fig. 68.1). The fetus has very high TBW, which gradually decreases albumin concentration in the interstitial space, further compromising the to approximately 75% of birthweight for a term infant. Premature infants oncotic forces that normally maintain intravascular volume. In contrast, have higher TBW than term infants. During the 1st yr of life, TBW with heart failure, there is an increase in venous hydrostatic pressure decreases to approximately 60% of body weight and remains at this from expansion of the intravascular volume, which is caused by impaired level until puberty. At puberty, the fat content of females increases more pumping by the heart, and the increase in venous pressure causes fluid than that in males, who acquire more muscle mass than females. Because to move from the intravascular space to the interstitial space. Expansion fat has very low water content and muscle has high water content, by of the intravascular volume and increased intravascular pressure also the end of puberty, TBW in males remains at 60%, but TBW in females cause the edema that occurs with acute glomerulonephritis. decreases to approximately 50% of body weight. The high fat content in overweight children causes a decrease in TBW as a percentage of ELECTROLYTE COMPOSITION body weight. During dehydration, TBW decreases and thus is a smaller The composition of the solutes in the ICF and ECF are very different percentage of body weight. (Fig. 68.3). Sodium (Na+) and chloride (Cl−) are the dominant cation and anion, respectively, in the ECF. The sodium and chloride concentra- FLUID COMPARTMENTS tions ([Na+], [Cl−]) in the ICF are much lower. Potassium (K+) is the TBW is divided between 2 main compartments: intracellular fluid most abundant cation in the ICF, and its concentration ([K+]) within (ICF) and extracellular fluid (ECF). In the fetus and newborn, the the cells is approximately 30 times higher than in the ECF. Proteins, ECF volume is larger than the ICF volume (Fig. 68.1). The normal organic anions, and phosphate are the most plentiful anions in the ICF. postnatal diuresis causes an immediate decrease in the ECF volume. The dissimilarity between the anions in the ICF and the ECF is largely This is followed by continued expansion of the ICF volume, which determined by the presence of intracellular molecules that do not cross results from cellular growth. By 1 yr of age, the ratio of ICF volume to the cell membrane, the barrier separating the ECF and the ICF. In ECF volume approaches adult levels. The ECF volume is approximately contrast, the difference in the distribution of cations—Na+ and K+—relies 20–25% of body weight, and the ICF volume is approximately 30–40% on activity of the Na+,K+-adenosine triphosphatase (ATPase) pump and of body weight, close to twice the ECF volume (Fig. 68.2). With puberty, membrane ion channels. the increased muscle mass of males causes them to have a higher ICF The difference in the electrolyte compositions of the ECF and the volume than females. There is no significant difference in the ECF ICF has important ramifications in the evaluation and treatment of volume between postpubertal females and males. electrolyte disorders. Serum concentrations of electrolytes—[Na+], [K+], The ECF is further divided into the plasma water and the interstitial and [Cl−]—do not always reflect total body content. Intracellular [K+] fluid (see Fig. 68.2). The plasma water is 5% of body weight. The blood is much higher than the serum concentration. A shift of K+ from the volume, given a hematocrit of 40%, is usually 8% of body weight, although intracellular space (ICS) can maintain a normal or even an elevated it is higher in newborns and young infants; in premature newborns it serum [K+] despite massive losses of K+ from the ICS. This effect is seen is approximately 10% of body weight. The volume of plasma water can in diabetic ketoacidosis, in which significant K+ depletion is masked be altered by pathologic conditions, including dehydration, anemia, by transmembrane shift of K+ from the ICF to the ECF. Therefore, for polycythemia, heart failure, abnormal plasma osmolality, and hypoal- K+ and phosphorus, electrolytes with a high intracellular concentration, buminemia. The interstitial fluid, normally 15% of body weight, can serum level may not reflect total body content. Similarly, the serum increase dramatically in diseases associated with edema, such as heart calcium concentration ([Ca2+]) does not reflect total body content of failure, protein-losing enteropathy, liver failure, nephrotic syndrome, Ca2+, which is largely contained in bone and teeth (see Chapter 64). and sepsis. An increase in interstitial fluid also occurs in patients with ascites or pleural effusions. OSMOLALITY There is a delicate equilibrium between the intravascular fluid and The ICF and the ECF are in osmotic equilibrium because the cell the interstitial fluid. The balance between hydrostatic and oncotic forces membrane is permeable to water. If the osmolality in 1 compartment regulates the intravascular volume, which is critical for proper tissue changes, then water movement leads to a rapid equalization of osmolality, perfusion. The intravascular fluid has a higher concentration of albumin with a shift of water between the ICS and extracellular space (ECS). than the interstitial fluid, and the consequent oncotic force draws water Clinically, the primary process is usually a change in the osmolality of into the intravascular space. The maintenance of this gradient depends the ECF, with resultant shift of water into the ICF if ECF osmolality on the limited permeability of albumin across the capillaries. The decreases, or vice versa if ECF osmolality increases. The ECF osmolality hydrostatic pressure of the intravascular space, which is caused by the can be determined and usually equals ICF osmolality. Plasma osmolality, pumping action of the heart, drives fluid out of the intravascular space. normally 285-295 mOsm/kg, is measured by the degree of freezing-point 389 Downloaded for sumitr sutra ([email protected]) at Khon Kaen University Faculty of Medicine- library from ClinicalKey.com by Elsevier on March 11, 2020. For personal use only. No other uses without permission. Copyright ©2020. Elsevier Inc. All rights reserved. Chapter 68 ◆ Electrolyte and Acid-Base Disorders 389.e1 Keywords total body water fluid compartments edema intracellular fluid extracellular fluid osmolality hyperglycemia pseudohyponatremia point-of-care testing Downloaded for sumitr sutra ([email protected]) at Khon Kaen University Faculty of Medicine- library from ClinicalKey.com by Elsevier on March 11, 2020. For personal use only. No other uses without permission. Copyright ©2020. Elsevier Inc. All rights reserved. 390 Part VI ◆ Fluid and Electrolyte Disorders 100 PLASMA INTRACELLULAR 90 Cations Anions Cations Anions 80 Total body 70 water (TBW) eight 60 Naϩ (140) ClϪ (104) Kϩ (140) PhosϪ (107) 50 Intracellular fluid (ICF) 40 % Body W 30 20 Extracellular fluid (ECF) Ϫ 10 HCO3 (24) Ϫ 0 Prot (40) 2 468 6312 6912 15 Adult Birth ProtϪ (14) Months Years ϩ K (4) ϩ Na (13) Ϫ HCO3 (10) Age Caϩ (2.5) Other (6) Mgϩ (1.1) PhosϪ (2) Mgϩ (7) ClϪ (3) Fig. 68.1 Total body water, intracellular fluid, and extracellular fluid as a percentage of body weight as a function of age. (From Winters Fig. 68.3 Concentrations of the major cations and anions in the RW: Water and electrolyte regulation. In Winters RW, editor: The body intracellular space and the plasma, expressed in mEq/L. fluids in pediatrics, Boston, 1973, Little, Brown.) Urea is not only confined to the ECS because it readily crosses the cell membrane, and its intracellular concentration approximately equals its extracellular concentration. Whereas an elevated [Na+] causes a shift of water from the ICS, with uremia there is no osmolar gradient between the two compartments and consequently no movement of water. The only exception is during hemodialysis, when the decrease in extracellular urea is so rapid that intracellular urea does not have time to equilibrate. Intracellular This disequilibrium syndrome may result in shift of water into brain (30-40%) cells and leads to severe symptoms. Ethanol, because it freely crosses cell membranes, is another ineffective osmole. In the case of glucose, the effective osmolality can be calculated as follows: Effective osmolality =×21[]Na +[]glucose 8 Theeffective osmolality (also called the tonicity) determines the osmotic force that is mediating the shift of water between the ECF and the ICF. Hyperglycemia causes an increase in the plasma osmolality because it is not in equilibrium with the ICS. During hyperglycemia, there is shift of water from the ICS to the ECS.
Load more

Recommended publications
  • Renal Physiology
    Renal Physiology Integrated Control of Na Transport along the Nephron Lawrence G. Palmer* and Ju¨rgen Schnermann† Abstract The kidney filters vast quantities of Na at the glomerulus but excretes a very small fraction of this Na in the final urine. Although almost every nephron segment participates in the reabsorption of Na in the normal kidney, the proximal segments (from the glomerulus to the macula densa) and the distal segments (past the macula densa) play different roles. The proximal tubule and the thick ascending limb of the loop of Henle interact with the filtration apparatus to deliver Na to the distal nephron at a rather constant rate. This involves regulation of both *Department of Physiology and filtration and reabsorption through the processes of glomerulotubular balance and tubuloglomerular feedback. Biophysics, Weill- The more distal segments, including the distal convoluted tubule (DCT), connecting tubule, and collecting Cornell Medical duct, regulate Na reabsorption to match the excretion with dietary intake. The relative amounts of Na reabsorbed College, New York, in the DCT, which mainly reabsorbs NaCl, and by more downstream segments that exchange Na for K are variable, New York; and †Kidney Disease allowing the simultaneous regulation of both Na and K excretion. Branch, National Clin J Am Soc Nephrol 10: 676–687, 2015. doi: 10.2215/CJN.12391213 Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Introduction The precise adaptation of urinary Na excretion to di- Health, Bethesda, Daily Na intake in the United States averages approx- etary Na intake results from regulated processing of an Maryland imately 180 mmol (4.2 g) for men and 150 mmol (3.5 g) ultrafiltrate of circulating plasma by the renal tubular for women (1).
    [Show full text]
  • Preventing Neurological Complications from Dysnatremias in Children
    Pediatr Nephrol (2005) 20:1687–1700 DOI 10.1007/s00467-005-1933-6 REVIEW Michael L. Moritz · J. Carlos Ayus Preventing neurological complications from dysnatremias in children Received: 30 November 2004 / Revised: 28 February 2005 / Accepted: 2 March 2005 / Published online: 4 August 2005 IPNA 2005 Abstract Dysnatremias are among the most common ongoing free-water losses or when mild hypernatremia electrolyte abnormalities encountered in hospitalized pa- (Na>145 mE/l) develops. A group at high-risk for neu- tients. In most cases, a dysnatremia results from improper rological damage from hypernatremia in the outpatient fluid management. Dysnatremias can occasionally result setting is that of the breastfed infant. Breastfed infants in death or permanent neurological damage, a tragic must be monitored closely for insufficient lactation and complication that is usually preventable. In this manu- receive lactation support. Judicious use of infant formula script, we discuss the epidemiology, pathogenesis and supplementation may be called for until problems with prevention and treatment of dysnatremias in children. We lactation can be corrected. report on over 50 patients who have suffered death or neurological injury from hospital-acquired hyponatremia. Keywords Hypernatremia · Hyponatremia · Cerebral The main factor contributing to hyponatremic encepha- edema · Myelinolysis · Fluid therapy lopathy in children is the routine use of hypotonic fluids in patients who have an impaired ability to excrete free- water, due to such causes as the postoperative state, Introduction volume depletion and pulmonary and central nervous system diseases. The appropriate use of 0.9% sodium Dysnatremias are a common electrolyte abnormality in chloride in parenteral fluids would likely prevent most children in both the inpatient and outpatient settings.
    [Show full text]
  • Clinical Aspect of Salt and Water Balance
    Misadventures in salt & water, as well as in acid-base balance Entertaining you is Friedrich C. Luft, Berlin Pflugers Arch 2015 Don’t just “do something” – stand there • 68 year-old woman presents disoriented at 18:00; had undergone tooth extraction that morning and, aside from a life-long mild bleeding tendency, had been quite normal • BP 130/85, pulse regular, respirations 18/min no localizing findings, no edema • Na 118, K 3.6, glucose 8, urea 4 (all mmol/L) • What now? An oil-immersion field showing a normal neutrophil flanked by two giant platelets (Bernard-Soulier syndrome). She had been given desmopressin. In addition, it had been hot so she was advised to “drink lots of water” Serum-Na depends on TBW, Na and K Water in H2 H2O O Na K Serum Na ≈ Naexch + Kexch Total-body H2O Edelman formula Volume Water out Na K Serum Na ≈ Naexch + Kexch total-body H2O Volume Clearance H2O (e) = V 1 - UNa+UK SNa Lots of spheres = little H2O ClH2O(e) neg When UNa+UK >SNa the ClH2O(e) neg and serum Na must fall Few spheres = much H O 2 When UNa+UK < SNa, the Cl (e) pos Cl (e) pos H2O H2O and serum Na must rise Actually, serum Na increased a little faster than we wanted so we infused some free water Had we given 3% saline, serum Na would have increased even faster Iatrogenic SIADH Clin Kidney J 2013;6:96-97 Paradoxal hyponatremia with isotonic electrolyte infusions • 65 year-old woman has meniscus surgery. At that time her Na was 141 mmol/L.
    [Show full text]
  • Body Fluids and Salt Metabolism
    Peruzzo et al. Italian Journal of Pediatrics 2010, 36:78 http://www.ijponline.net/content/36/1/78 ITALIAN JOURNAL OF PEDIATRICS REVIEW Open Access Body fluids and salt metabolism - Part II Mattia Peruzzo1, Gregorio P Milani2, Luca Garzoni1, Laura Longoni3, Giacomo D Simonetti4, Alberto Bettinelli3, Emilio F Fossali2, Mario G Bianchetti1* Abstract There is a high frequency of diarrhea and vomiting in childhood. As a consequence the focus of the present review is to recognize the different body fluid compartments, to clinically assess the degree of dehydration, to know how the equilibrium between extracellular fluid and intracellular fluid is maintained, to calculate the effective blood osmolality and discuss both parenteral fluid maintenance and replacement. Introduction Hyponatremia The first part of this review, published some months ago, Introduction outlined the physiology of the body fluid compartments, Hyoponatremia [4,6] is classified (Figure 1 left and mid- dehydration and extracellular fluid volume depletion [1]. dle panel) according to the extracellular fluid volume The second part will focus the causes underlying dysna- status, as either hypovolemic (= depletional) or normo- tremia and, more importantly, both the parenteral hydra- hypervolemic (= dilutional). Vasopressin is released both tion and the management of dysnatremia. in children with low effective arterial blood volume, by far the most common cause of hyponatremia in Dysnatremia everyday clinical practice, as well as in those with Under normal conditions, blood sodium concentrations normo-hypervolemic hyponatremia [8]. In hypovolemic are maintained within the narrow range of 135-145 hyponatremia vasopressin release is triggered by the low mmol/L despite great variations in water and salt intake.
    [Show full text]
  • And Ignore All Page & Fig #'S, They're No Longer Valid…
    EXAM 4 AP2 p 1 of 28 . Pat Jeffreys. Use this as a really big flash card….. ..and ignore all Page & Fig #’s, they’re no longer valid… Okay, let’s avoid being afraid of the new terminology & the alphabet soup that goes with it. Let’s just say it out loud ENOUGH times till it seems like we’ve ALWAYS had these words, got it? WE ARE IN THE RENAL CORPUSCLE, THE BOWMAN’S CAPSULE, @ THE GLOMERULAR CAPS : 1. Filtration Membrane = Is the walls of the G. capillaries that separate the Blood from the Filtrate Allows anything smaller than a protein to go through, ONLY. Proteins & bigger = too big. 2. Renal Fraction = % of BF through your ___ per minute = 20—25% 3. Filtration Fraction = % of the Renal Fraction that left the Blood to BECOME Filtrate (so...it’s a ___ of the Renal Fraction, yes?) 4. Okay, let’s talk about all the different pressures inside the Bowman’s Capsule. There’s 2 pressures involving the blood inside the G. Capillaries. 5. First there’s the BP of the blood in the capillaries, called the G. ___ ___. Relax. The symbols for it are : HPGC and it = ___ mm 6. The 2nd pressure of the blood in the caps is the G. ___ ___. Really ! Relax. The symbols for it are : OPGC and it = ___ mm 7. The 3rd pressure is NOT the blood, it’s the pressure outside the capillaries, where the filtrate is, IN the ____, and where the New filtrate is trying to go, kind of a pressure to make sure too much new stuff doesn’t come out, like a Pressure Policeman.
    [Show full text]
  • Disorders of Sodium and Water Balance
    Disorders of Sodium and Water Balance Theresa R. Harring, MD*, Nathan S. Deal, MD, Dick C. Kuo, MD* KEYWORDS Dysnatremia Water balance Hyponatremia Hypernatremia Fluids for resuscitation KEY POINTS Correct hypovolemia before correcting sodium imbalance by giving patients boluses of isotonic intravenous fluids; reassess serum sodium after volume status normalized. Serum and urine electrolytes and osmolalities in patients with dysnatremias in conjunction with clinical volume assessment are especially helpful to guide management. If an unstable patient is hyponatremic, give 2 mL/kg of 3% normal saline (NS) up to 100 mL over 10 minutes; this may be repeated once if the patient continues to be unstable. If unstable hypernatremic patient, give NS with goal to decrease serum sodium by 8 to 15 mEq/L over 8 hours. Correct stable dysnatremias no faster than 8 mEq/L to 12 mEq/L over the first 24 hours. INTRODUCTION Irregularities of sodium and water balance most often occur simultaneously and are some of the most common electrolyte abnormalities encountered by emergency med- icine physicians. Approximately 10% of all patients admitted from the emergency department suffer from hyponatremia and 2% suffer from hypernatremia.1 Because of the close nature of sodium and water balance, and the relatively rigid limits placed on the central nervous system by the skull, it is not surprising that most symptoms related to disorders of sodium and water imbalance are neurologic and can, therefore, be devastating. Several important concepts are crucial to the understanding of these disorders, the least of which include body fluid compartments, regulation of osmo- lality, and the need for rapid identification and appropriate management.
    [Show full text]
  • Physiology and Pathophysiology of Membrane Processes
    1 Physiology of membrane transports 1.1 General types of transports 1.2 Membrane processes in epithelial tissues Physiology and pathophysiology of 2 Pathophysiology of membrane transports 2.1 The cell membrane processes 2.2 Epithelia 2.3 Excitable tissues 1. Physiology of membrane transports 1.1 General types of transports Important: cellular pathology, kidney, gut, axcitable tissues 1. Bulk flow The basic purpose of transport processes at the cellular level (Fig. 1) Special instances: We look for: force, direction and factors („resistence“) Filtration across capillary wall: V´ = F * L * (∆P - ∆π) Osmosis (∆c, ∆π) → bulk flow across paracellular spaces and cytoplasmatic membranes Bulk flow → solvent drag : Flow of the solvent →↑rate of movement of a solute (over diffusion) Example: transfer of solutes across membranes by osmotically driven water (= bulk flow) 1 2. Diffusion = macroscopic flow of material from a region of high concentration to a region of lower concentration that results from the random Brownian motion of the 3. Volume resorption paracellularily across the wall of resorptive epithelia: molecules Ions: complicated by electric gradient – still „facilitated diffusion“ ∆c (small electrolytes), ∆π. No hydrostatic pressure drive Diffusion flow ≈ permeability * ∆c, i.e., linear relationship flow – Components: bulk flow (→ solvent drag) + diffusion concentration difference Plain diffusion across cellular membranes: Glycerol: no carrier, no charge, only ∆c 4. Facilitated diffusion Physiologically: water (mainly osmosis through carriers, however), Transcellular flows take place mainly through specialized transmembrane O2, CO2, NH3, ethanol, urea... proteins. Types of membrane transports – Fig. 2 Not ions Plain diffusion across paracellular shunts No substantial difference between bulk flow and diffusion Paracellular flows in leaky epithelial and endothelial layers take place through s.c.
    [Show full text]
  • Effect of Phloretin on Water and Solute Movement in the Toad Bladder
    Effect of Phloretin on Water and Solute Movement in the Toad Bladder Sherman Levine, … , Nicholas Franki, Richard M. Hays J Clin Invest. 1973;52(6):1435-1442. https://doi.org/10.1172/JCI107317. Research Article It is generally believed that urea crosses the cell membrane through aqueous channels, and that its movement across the membrane is accelerated in the direction of net water flow (solvent drag effect). The present report presents evidence for a vasopressin-sensitive pathway for the movement of urea, other amides, and certain non-amides, which is independent of water flow. Phloretin, when present at 10-4 M concentration in the medium bathing the luminal surface of the toad bladder, strongly inhibits the movement of urea, acetamide, and propionamide across the toad bladder, both in the absence and presence of vasopressin. The vasopressin-stimulated movement of formaldehyde and thiourea is also reduced. Osmotic water flow, on the other hand, is not affected; nor is the movement of ethanol and ethylene glycol, or the net transport of sodium. On the basis of these studies we would conclude that the movement of many, if not all, solutes across the cell membrane is independent of water flow, and that a vasopressin-sensitive carrier may be involved in the transport of certain solutes across the cell membrane. Find the latest version: https://jci.me/107317/pdf Effect of Phloretin on Water and Solute Movement in the Toad Bladder SIERMM LEVINE, NIcHoLAs FRANKi, and RICHARD M. HAYS From the Department of Medicine, Division of Nephrology, Albert Einstein College of Medicine, Bronx, New York 10461 A B S T R A C T It is generally believed that urea crosses appeared to be accelerated in the direction of net water the cell membrane through aqueous channels, and that flow.
    [Show full text]
  • Sodium Toxicity in the Nutritional Epidemiology and Nutritional Immunology of COVID-19
    medicina Perspective Sodium Toxicity in the Nutritional Epidemiology and Nutritional Immunology of COVID-19 Ronald B. Brown School of Public Health Sciences, University of Waterloo, Waterloo, ON N2L 3G1, Canada; [email protected] Abstract: Dietary factors in the etiology of COVID-19 are understudied. High dietary sodium intake leading to sodium toxicity is associated with comorbid conditions of COVID-19 such as hypertension, kidney disease, stroke, pneumonia, obesity, diabetes, hepatic disease, cardiac arrhythmias, throm- bosis, migraine, tinnitus, Bell’s palsy, multiple sclerosis, systemic sclerosis, and polycystic ovary syndrome. This article synthesizes evidence from epidemiology, pathophysiology, immunology, and virology literature linking sodium toxicological mechanisms to COVID-19 and SARS-CoV-2 infection. Sodium toxicity is a modifiable disease determinant that impairs the mucociliary clearance of virion aggregates in nasal sinuses of the mucosal immune system, which may lead to SARS-CoV-2 infection and viral sepsis. In addition, sodium toxicity causes pulmonary edema associated with severe acute respiratory syndrome, as well as inflammatory immune responses and other symptoms of COVID- 19 such as fever and nasal sinus congestion. Consequently, sodium toxicity potentially mediates the association of COVID-19 pathophysiology with SARS-CoV-2 infection. Sodium dietary intake also increases in the winter, when sodium losses through sweating are reduced, correlating with influenza-like illness outbreaks. Increased SARS-CoV-2 infections in lower socioeconomic classes and Citation: Brown, R.B. Sodium among people in government institutions are linked to the consumption of foods highly processed Toxicity in the Nutritional with sodium. Interventions to reduce COVID-19 morbidity and mortality through reduced-sodium Epidemiology and Nutritional diets should be explored further.
    [Show full text]
  • Renal Physiology
    RenalCJASN Physiology ePress. Published on May 1, 2014 as doi: 10.2215/CJN.08580813 Regulation of Potassium Homeostasis Biff F. Palmer Abstract Potassium is the most abundant cation in the intracellular fluid, and maintaining the proper distribution of potassium across the cell membrane is critical for normal cell function. Long-term maintenance of potassium homeostasis is achieved by alterations in renal excretion of potassium in response to variations in intake. Understanding the mechanism and regulatory influences governing the internal distribution and renal clearance of potassium under normal circumstances can provide a framework for approaching disorders of potassium Department of Internal Medicine, commonly encountered in clinical practice. This paper reviews key aspects of the normal regulation of potassium University of Texas metabolism and is designed to serve as a readily accessible review for the well informed clinician as well as a Southwestern Medical resource for teaching trainees and medical students. Center, Dallas, Texas Clin J Am Soc Nephrol ▪: ccc–ccc, 2015. doi: 10.2215/CJN.08580813 Correspondence: Dr. Biff F. Palmer, Department of 1 Introduction Catecholamines regulate internal K distribution, with Internal Medicine, Potassium plays a key role in maintaining cell function. a-adrenergic receptors impairing and b-adrenergic recep- University of Texas 1 1 1 b – Southwestern Medical Almost all cells possess an Na -K -ATPase, which tors promoting cellular entry of K . 2-Receptor induced pumps Na1 out of the cell and K1 into the cell and 1 Center, 5323 Harry stimulation of K uptake is mediated by activation of the Hines Boulevard, 1 1 . 1 1 leads to a K gradient across the cell membrane (K in Na -K -ATPase pump.
    [Show full text]
  • Antidiuretic Hormone and Water Transfer
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Kidney International, Vol. 9 (1976) p. 223—230 Antidiuretic hormone and water transfer RICHARD M. HAYS Department of Medicine, Division of Nephrology, Albert Einstein College of Medicine, Bronx, New York There has been remarkable progress in recent years the rat collecting duct has also been shown to in- in our understanding of the physiology of antidiuretic crease following vasopressin administration [11]; re- hormone (vasopressin), from its synthesis and release cent studies with the isolated papillary collecting duct in the central nervous system to its action on the renal of the rabbit, however, have been stated to show tubular cell. Several recent reviews [1—5] have consid- no effect of vasopressin on urea permeability [14]. ered the physiology of antidiuretic hormone in detail, and only a brief summary will be given of the steps Activation and control of cyclic AMP leading to the permeability response of the collecting duct. The question to be emphasized in this article is Attachment of vasopressin to its receptor activates the following: how does vasopressin increase the rate adenylate cyclase, a membrane-bound enzyme that of osmotic water flow across the cell membrane? converts ATP to adenosine 3',5'-monophosphate (cyclic AMP) [IS]. The rise in the intracellular cyclic Synthesis, release and binding AMP level ranges from ten-fold in the rat inner me- dulla [16] to three-fold in rat outer medulla and toad Vasopressin is synthesized in the supraoptic and bladder [16, 17]. Many factors control the paraventricular nuclei of the hypothalamus, probably intracellular level of cyclic AMP, including phospho- along with the neurophysin that acts as its binding diesterase, prostaglandin E1, calcium, magnesium, protein within the central nervous system [6, 7].
    [Show full text]
  • Hypernatremia in Critically Ill Patients
    Journal of Critical Care (2013) 28, 216.e11–216.e20 Hypernatremia in critically ill patients☆,☆☆,★ Gregor Lindner MD a,⁎, Georg-Christian Funk MD b aDepartment of Emergency Medicine, Inselspital, University of Bern, 3010 Bern, Switzerland bDepartment of Respiratory and Critical Care Medicine, Otto Wagner Hospital, Wien, Austria Keywords: Abstract Hypernatremia is common in intensive care units. It has detrimental effects on various Hypernatremia; physiologic functions and was shown to be an independent risk factor for increased mortality in Intensive care; critically ill patients. Mechanisms of hypernatremia include sodium gain and/or loss of free water and Treatment; can be discriminated by clinical assessment and urine electrolyte analysis. Because many critically ill Sodium patients have impaired levels of consciousness, their water balance can no longer be regulated by thirst and water uptake but is managed by the physician. Therefore, the intensivists should be very careful to provide the adequate sodium and water balance for them. Hypernatremia is treated by the administration of free water and/or diuretics, which promote renal excretion of sodium. The rate of correction is critical and must be adjusted to the rapidity of the development of hypernatremia. © 2013 Elsevier Inc. All rights reserved. 1. Introduction Hypernatremia is defined as a serum sodium concentration exceeding 145 mmol/L [1]. The Edelman equation shows the serum sodium concentration (Na+) as a function of the total exchangeable sodium and potassium in the body and the total body water [2]. Equation 1 (while Na+ total body stands for total exchangeable sodium and K+ total body stands for total exchangeable potassium). ☆ Conflict of interest: No conflicts to declare.
    [Show full text]