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Durham Metabolic Acidosis

The Genomic Analysis Of Lactic Acidosis And Acidosis Response In Human Cancers

The Genomic Analysis Of Lactic Acidosis And Acidosis Response In Human Cancers

The Genomic Analysis of Lactic Acidosis and Acidosis Response in Human Cancers Julia Ling-Yu Chen, Joseph E. Lucas, Thies Schroeder, Seiichi Mori, Jianli Wu, Joseph Nevins, [...view 2 more...], Mark Dewhirst, Mike West, Jen-Tsan Chi [ view less ] Affiliations: Institute for Genome Sciences and Policy, Duke University, Durham, North Carolina, United States of America, Department of Molecular Genetics and Microbiology, Duke University, Durham, North Carolina, United States of America Affiliation: Department of Statistical Science, Duke University, Durham, North Carolina, United States of America Affiliation: Department of Radiation Oncology, Duke University, Durham, North Carolina, United States of America Affiliations: Institute for Genome Sciences and Policy, Duke University, Durham, North Carolina, United States of America, Department of Molecular Genetics and Microbiology, Duke University, Durham, North Carolina, United States of America Affiliations: Institute for Genome Sciences and Policy, Duke University, Durham, North Carolina, United States of America, Department of Molecular Genetics and Microbiology, Duke University, Durham, North Carolina, United States of America Affiliations: Institute for Genome Sciences and Policy, Duke University, Durham, North Carolina, United States of America, Department of Molecular Genetics and Microbiology, Duke University, Durham, North Carolina, United States of America Affiliation: Department of Radiation Oncology, Duke University, Durham, North Carolina, United States of America Affiliation: Department of Statistical Science, Duke University, Durham, North Carolina, United States of America Affiliations: Institute for Genome Sciences and Policy, Duke University, Durham, North Carolina, United States of America, Department of M Continue reading >>

Acid Base Flashcards | Quizlet

Acid Base Flashcards | Quizlet

2[Na] + [glucose/18] + [BUN/2.8]. If ethanol present, add (ethanol/4.6) to above equation Can cause both anion gap metabolic acidosis and metabolic alkalosis if has vomiting and normal PH, serum bicarbonate, and pCO2 Add 0.05 to abg ph if from central VBG. Add 0.03 to abg ph if from peripheral VBG Subtract 5 from central venous pCO2 to estimate arterial pCO2. Subtract 3-8 from peripheral pCO2 to estimate arterial pCO2 Methanol, uremia, DKA/Drugs (metformin, stavudine, topiramate), Phosphate/Paraldehyde, Ischemia/Isoniazid/Iron, Lactate, Ethylene glycol/ETOH, Starvation/salicylates For albumin. Add 2.5 to anion gap for every 1g/dl that serum albumin is decreased from 4 g/dl Diarrhea, Ureteral diversion, RTA, Hyperalimentation, Addison disease/ Acetazolamide/Ammonium chloride, Miscellaneous (Chloridorrhea, Amphotereicin B, Toluene) Bromism (ingestion of Bromo seltzer), Albumin low, Multiple Myeloma For every 1 that anion gap increases, serum bicarb drops 0.6 (Urine Na + urine K) - urine chloride. >0 means RTA 1 or 4. Caused by ingestion of osmotically active substances. Measured serum osm would be greater than calculated serum osm. Gap should be within 10. Wood alcohol, antifreeze. Delirium, papilledema, retinal hemorrhages, blurry vision Antifreeze. Delirium, oxalate crystals in urine Rubbing alcohol. Does not cause acid base disorder, when metabolized will show up as acetone in bloodstream. First causes elevated anion gap metabolic acidosis and then later normal anion gap metabolic acidosis as it results in renal tubular acidosis. Acid loss: vomiting, NG suction, over-diuresis, hypermineralcorticoid states ( conn's, Cushing), penicillins. HCO3 gain: administration of sodium bicarb, baking soda, citrate, lactate, acetate (liver converts all of these to bicarb) < 10 mEq/ Continue reading >>

Normal Anion Gap Acidosis

Normal Anion Gap Acidosis

In renal physiology , normal anion gap acidosis, and less precisely non-anion gap acidosis, is an acidosis that is not accompanied by an abnormally increased anion gap . The most common cause of normal anion gap acidosis is diarrhea with a renal tubular acidosis being a distant second. The differential diagnosis of normal anion gap acidosis is relatively short (when compared to the differential diagnosis of acidosis): Diarrhea : due to a loss of bicarbonate. This is compensated by an increase in chloride concentration, thus leading to a normal anion gap, or hyperchloremic, metabolic acidosis. The pathophysiology of increased chloride concentration is the following: fluid secreted into the gut lumen contains higher amounts of Na+ than Cl; large losses of these fluids, particularly if volume is replaced with fluids containing equal amounts of Na+ and Cl, results in a decrease in the plasma Na+ concentration relative to the Clconcentration. This scenario can be avoided if formulations such as lactated Ringers solution are used instead of normal saline to replace GI losses. [2] Continue reading >>

Common Laboratory (lab) Values Abgs

Common Laboratory (lab) Values Abgs

Difference between calculated serum anions and cations. Based on the principle of electrical neutrality, the serum concentration of cations (positive ions) should equal the serum concentration of anions (negative ions). However, serum Na+ ion concentration is higher than the sum of serum Cl- and HCO3- concentration. Na+ = CL- + HCO3- + unmeasured anions (gap). Normal anion gap: 12 mmol/L (10 14 mmol/L) 2] Based on the anion gap and patient history review potential causes: Normal anion gap (hyperchloremic) metabolic acidosis: Normal anion gap acidosis: The most common causes of normal anion gap acidosis are GI or renal bicarbonate loss and impaired renal acid excretion. Normal anion gap metabolic acidosis is also called hyperchloremic acidosis, because instead of reabsorbing HCO3- with Na, the kidney reabsorbs Cl-. Many GI secretions are rich in bicarbonate (eg, biliary, pancreatic, and intestinal fluids); loss from diarrhea, tube drainage, or fistulas can cause acidosis. In ureterosigmoidostomy (insertion of ureters into the sigmoid colon after obstruction or cystectomy), the colon secretes and loses bicarbonate in exchange for urinary Cl- and absorbs urinary ammonium, which dissociates into NH3+ and H+. Loss of HCO3 ions is accompanied by an increase in the serum Cl- concentration. The anion gap remains normal. Disease processes that can lead to normal anion gap (hyperchloremic) acidosis. Useful mnemonic (DURHAM): b) Ureteral diversion: Urine from the ureter may be diverted to the sigmoid colon due to disease (uretero-colonic fistula) or after bladder surgery. In such an event urinary Cl- is absorbed by the colonic mucosa in exchange for HCO3-, thus increases the gastrointestinal loss of HCO3-. c) Renal tubular acidosis: dysfunctional renal tubular cells causes an ina Continue reading >>

Dietary Acid Load, Subclinical Acidosis And Outcomes In Chronic Kidney Disease Scialla, Julia J. Duke University, Durham, Nc, United States

Dietary Acid Load, Subclinical Acidosis And Outcomes In Chronic Kidney Disease Scialla, Julia J. Duke University, Durham, Nc, United States

Dietary Acid Load, Subclinical Acidosis and Outcomes in Chronic Kidney Disease Metabolic acidosis is a modifiable risk factor for chronic kidney disease (CKD) progression. It develops in advanced CKD due to impaired excretion of the daily load of nonvolatile acid that is generated from metabolism of dietary nutrients. Subclinical acidosis develops prior to overt acidosis and may also adversely affect clinical outcomes. Treatment of both overt and subclinical acidosis with alkali supplements slows renal disease progression in clinical trials, but use of alkali supplements may be associated with unacceptable risks in some CKD patients. Lowering nonvolatile acid load through dietary manipulation may be a complementary strategy to mitigate acidosis and improve outcomes earlier in CKD when subclinical, but not overt, acidosis is present. Using intensive patient-oriented research, we will perform detailed, direct measures of dietary intake, renal acid excretion, glomerular filtration rate and subclinical acidosis in participants with early stage 3 CKD with and without diabetes, and in healthy controls, to determine independent risk factors for subclinical acidosis. Using this rich source of data, we will also validate estimates of nonvolatile acid load against gold- standard measures for future research applications. Finally, we will directly measure nonvolatile acid load in 1000 participants from the Chronic Renal Insufficiency Cohort (CRIC) study, a diverse CKD cohort, and examine its association with hard clinical outcomes over long term follow-up. We anticipate that these research aims will establish nonvolatile acid load as a modifiable risk factor in CKD that may exert adverse effects by directly contributing to subclinical acidosis, which, by definition, escapes detec Continue reading >>

Short-term Effects Of The Dash Diet In Adults With Moderate Chronic Kidney Disease: A Pilot Feeding Study

Short-term Effects Of The Dash Diet In Adults With Moderate Chronic Kidney Disease: A Pilot Feeding Study

blood pressure , DASH diet , kidney disease , metabolic side effects There is a paucity of data on evidence-based dietary therapies that safely lower blood pressure (BP) in adults with chronic kidney disease (CKD). The same diets that lower BP in adults with normal kidney function have potential to adversely affect individuals with CKD. These diets typically emphasize liberal consumption of fruits and vegetables, whole grains, dairy, poultry, fish, legumes and nuts, and thereby have more potassium, phosphorus and protein than is currently recommended for patients with CKD [ 1 , 2 ]. If consumed in large quantities, these nutrients could cause acute or long-term electrolyte abnormalities, derangements in mineral metabolism and progressive kidney failure. The benefits and risks of evidence-based BP-lowering diets have not been rigorously tested among adults with moderate or severe CKD. The risks for patients with CKD to develop diet-related complications are influenced by several factors, such as the presence of comorbid conditions, medication use and severity of kidney dysfunction. For example, incidence of hyperkalemia and hyperphosphatemia substantially increases as kidney function worsens and is most prevalent among individuals with end-stage kidney disease [ 3 ]. Additionally, factors such as age >65 years, diabetes and use of renin angiotensin aldosterone system (RAAS) inhibitors are associated with earlier onset of metabolic complications [ 3 , 4 ]. This suggests that perhaps a subset of adults who are younger, non-diabetic, not taking RAAS inhibitors and/or have less severe CKD could safely benefit from diets that improve BP. The Dietary Approaches to Stop Hypertension (DASH) diet is an evidence-based treatment for hypertension [ 5 , 6 ]. It is rich in fruits and Continue reading >>

Mark W Dewhirst | Dvm, Phd | Duke University Medical Center, Durham | Dumc | Department Of Radiation Oncology

Mark W Dewhirst | Dvm, Phd | Duke University Medical Center, Durham | Dumc | Department Of Radiation Oncology

In the spring of 2002, The World Health Organization workshop 'Adverse Temperature Levels in the Human Body' brought together scientists with expertise in biological effects of hyperthermia to review the data and determine the evidence that could be used to evaluate potential adverse effects from human exposures to radiofrequency (RF) electromagnetic radiation in the range of 10-300 GHz. Standards for RF exposure in this frequency range are based currently on thermal effects. Information was reviewed on the ability of hyperthermia, either to the whole body or to part of the body to affect physiology, particularly the heart and circulatory system, to induce other thermoregulatory responses such as sweating, to affect the performance of simple and complex mental tasks, to induce various heat-related disorders such as heat stroke and to damage body tissue. Risks to a variety of organs were considered. In addition, thresholds for effects on developing embryos and foetuses and possible carcinogenic effects were also examined. These findings were discussed in the context of known cellular and biochemical responses of cells and tissues to hyperthermia. The experts judged the relevance of each study for informing decision-makers on the scientific basis for establishing safe exposure levels. The consensus was that standards should consider both temperature and time of exposure, whenever possible. These experiments investigate the biodistribution of radiolabelled MAb in a human glioma xenograft model after 4 h of local hyperthermia (HT) with a twofold purpose: to maximize the ratio of cumulative isotope activity in tumour relative to normal tissues, and to examine the temperature dependence of the effect. Restrained, unanaesthetized athymic nude mice bearing 150-200 mm3 s.c. hum Continue reading >>

Carolyn Sangokoya's Research While Affiliated With Duke University Medical Center And Other Places

Carolyn Sangokoya's Research While Affiliated With Duke University Medical Center And Other Places

A variety of oncogenic and environmental factors alter tumor metabolism to serve the distinct cellular biosynthetic and bioenergetic needs present during oncogenesis. Extracellular acidosis is a common microenvironmental stress in solid tumors, but little is known about its metabolic influence, particularly when present in the absence of hypoxia. In order to characterize the extent of tumor cell metabolic adaptations to acidosis, we employed stable isotope tracers to examine how acidosis impacts glucose, glutamine, and palmitate metabolism in breast cancer cells exposed to extracellular acidosis.Acidosis increased both glutaminolysis and fatty acid beta-oxidation, which contribute metabolic intermediates to drive the tricarboxylic acid cycle (TCA cycle) and ATP generation. Acidosis also led to a decoupling of glutaminolysis and novel glutathione (GSH) synthesis by repressing GCLC/GCLM expression. We further found that acidosis redirects glucose away from lactate production and towards the oxidative branch of the pentose phosphate pathway (PPP). These changes all serve to increase nicotinamide adenine dinucleotide phosphate (NADPH) production and counter the increase in reactive oxygen species (ROS) present under acidosis. The reduced novel GSH synthesis under acidosis may explain the increased demand for NADPH to recycle existing pools of GSH. Interestingly, acidosis also disconnected novel ribose synthesis from the oxidative PPP, seemingly to reroute PPP metabolites to the TCA cycle. Finally, we found that acidosis activates p53, which contributes to both the enhanced PPP and increased glutaminolysis, at least in part, through the induction of G6PD and GLS2 genes.Acidosis alters the cellular metabolism of several major metabolites, which induces a significant degree o Continue reading >>

Metabolic Acidosis - Bi Cardiology Fellows

Metabolic Acidosis - Bi Cardiology Fellows

ELEVATED GAP ("MUDPILES") (or " PLUM SEEDS ") Diabetic ketoacidosis (ketoacids also in alcoholism and starvation) Lacticacidosis (circulatory or resp failure, sepsis, ischemic bowel/limb,seizure, malignancy, hepatic failure, DM, CO or cyanide poisoning,metformin, inborn errors of metabolism) OG = [serum osm] - [(Nax2) + (BUN/2.8) + (Glucose/18) + (Ethanol/4.3)] OG > 15 implies: Ethylene glycol, Methanol, Sorbitol, Mannitol, Isopropanol (delta Anion Gap)/ (delta Bicarb) Ratio Method If <1, there is an Elevated-AG and concurrent normal-AG acidoses If >2, there is an Elevated-AG acidosis and concurrent metabolic alkalosis "corrected bicarb" = delta gap + HCO3 [Remember: delta gap=AG - 12] If "corrected bicarb" is too high (>28), there is a coexistent metabolic alkalosis If "corrected bicarb" is too low (<22), there is a coexistent metabolic non-AG acidosis (hyperchloremic metabolic acidosis) Bicarb Gap = Na - Cl - 39 ( derivation of formula , Wrenn et al. ) If Bicarb Gap >6, there is an additional metabolic alkalosis If Bicarb Gap <-6, there is an additional non-AG acidosis Lactate (gray top tube on ice) and Ketones (gold top/SST tube); review the significance of lactate Miscellaneous (pancreatic fistula, ingestion of CaCl or cholestyramine, hyperparathyroidism, posthypocapnia) UAG = [Na + K]urine - [Cl]urine; normal=0 Also, UAG = 80 - [NH4+]; Keep in mind that UAG is an indirect assay for renal NH4+ excretion IfUAG is POSITIVE or only slightly NEGATIVE --> implies failure of kidneysto secrete NH4+ ; DDx=type I or IV RTA, or renal failure IfUAG is VERY NEGATIVE --> it implies relatively higher urine chloridewhich implies adequate NH4+ production ; DDx=GI causes, type II RTA,exogenous acid or dilutional decrease in pCO2 = 1.25 x (change in Bicarb) Anion Gap Correction: Red

Acidosis Induces Reprogramming Of Cellular Metabolism To Mitigate Oxidative Stress

Acidosis Induces Reprogramming Of Cellular Metabolism To Mitigate Oxidative Stress

Acidosis induces reprogramming of cellular metabolism to mitigate oxidative stress 1Institute for Genome Sciences & Policy, Durham, NC, USA 2Department of Molecular Genetics & Microbiology, Durham, NC, USA 1Institute for Genome Sciences & Policy, Durham, NC, USA 2Department of Molecular Genetics & Microbiology, Durham, NC, USA 1Institute for Genome Sciences & Policy, Durham, NC, USA 2Department of Molecular Genetics & Microbiology, Durham, NC, USA 1Institute for Genome Sciences & Policy, Durham, NC, USA 2Department of Molecular Genetics & Microbiology, Durham, NC, USA 1Institute for Genome Sciences & Policy, Durham, NC, USA 2Department of Molecular Genetics & Microbiology, Durham, NC, USA 3Department of Anatomy and Cell Biology, School of Medicine, National Taiwan University, Taipei, Taiwan Find articles by Chien-Kuang Cornelia Ding 1Institute for Genome Sciences & Policy, Durham, NC, USA 2Department of Molecular Genetics & Microbiology, Durham, NC, USA 1Institute for Genome Sciences & Policy, Durham, NC, USA 2Department of Molecular Genetics & Microbiology, Durham, NC, USA 1Institute for Genome Sciences & Policy, Durham, NC, USA 2Department of Molecular Genetics & Microbiology, Durham, NC, USA 3Department of Anatomy and Cell Biology, School of Medicine, National Taiwan University, Taipei, Taiwan 4Sarah W Stedman Nutrition and Metabolism Center, Durham, NC, USA 5Duke Institute of Physiology, Durham, NC, USA 6Department of Pediatrics, University of California Los Angeles School of Medicine, Los Angeles, CA, USA 7LABIOMED & SiDMAP, LLC, Torrance, CA, USA 4Sarah W Stedman Nutrition and Metabolism Center, Durham, NC, USA 5Duke Institute of Physiology, Durham, NC, USA 8Department of Pharmacology and Cancer Biology, Duke University, Durham, NC, USA 1Institute for Genome Scie Continue reading >>

Recognition Of Ckd After The Introduction Of Automated Reporting Of Estimated Gfr In The Veterans Health Administration

Recognition Of Ckd After The Introduction Of Automated Reporting Of Estimated Gfr In The Veterans Health Administration

Recognition of CKD After the Introduction of Automated Reporting of Estimated GFR in the Veterans Health Administration Virginia Wang, Matthew L. Maciejewski, Bradley G. Hammill, Rasheeda K. Hall, Lynn Van Scoyoc, Amit X. Garg, Arsh K. Jain and Uptal D. Patel CJASN January 2014, 9 (1) 29-36; DOI: This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased. Background and objectives Early detection of CKD is important for slowing progression to renal failure and preventing cardiovascular events. Automated laboratory reporting of estimated GFR (eGFR) has been introduced in many health systems to improve CKD recognition, but its effect in large, United Statesbased health systems remains unclear. Design, setting, participants, & measurements Using Veterans Affairs (VA) laboratory and administrative data, two nonoverlapping national cohorts of patients receiving care in VA medical centers before (n=66,323) and after (n=16,670) implementation of automated eGFR reporting between 2004 and 2010 were identified. Recognition was assessed by the presence of new CKD diagnostic codes, use of additional diagnostic testing, outpatient nephrology visits, or overall CKD recognition (receipt of at least one of these outcomes) for each patient during the 12-month period after their first eligible creatinine or eGFR laboratory result. Generalized estimating equations were used to assess change before and after automated eGFR reporting. Results Overall CKD recognition increased from 22.1% of veterans before eGFR reporting to 27.5% in the post-eGFR reporting period (odds ratio [OR], 1.19; 95% CI, 1.12 to 1.27; P<0.001). Higher overall CKD recognition was driven largel Continue reading >>

Acid/base Disorders Hopmod Flashcards - Cram.com

Acid/base Disorders Hopmod Flashcards - Cram.com

What is the first and second step in determining an acid/base disorder? What is the differential for an elevated anion-gap metabolic acidosis? MUDPILES (Methanol, Uremia, DKA/Drugs, Phosphate, Ischemia/INH, Lactate, Ethylene glycol, starvation/salicylates) What is the differential for a normal anion gap metabolic acidosis? DURHAM (Diarrhea, Ureteral diversion, RTA, Hyperalimentaion, Addison's/Acetazolamide/Ampho, Misc How is the anion gaP affected by albumin? The anion gap decreases by 2.5 for every decrease in alb by 1 How can you evaluate for a concurrent normAl anion gap and elevated gap metabolic acidosis? By using the delta-delta. The change in bicarbonate should equal the change in The anion gap. what are the two likely causes of low anion gap met acidosis? What is the significance of an elevated urine anion gap (greater than zero)? A urine anion gap greater than zero signifies the kidney is not excreting acid appropriately, and there is either type 1 or type 4 renal tubular acidosis is present. how is respiratory compensation in metabolic acidosis calculated? Is this method appropriate for metabolic alkalosis? pCO2=1.5(HCO3)+8 +/- 2. It is only valid for met acidosis What four toxic substances (solvents) can cause an osmolar gap? Which cause delirium? Which cause ketosis? Which causes normal gap met acidosis? Methanol, Ethylene Glycol, Isopropyl alcohol and Toluene cause an osmolar gap. Methanol and Ethylene glycol cause delirium. Isopropyl alcohol causes ketosis (but not an acidosis). Toluene causes an elevated anion gap, but also causes an RTA, so a normal anion gap acidosis also develops. What toxic osmolarly active substances cause delirium and an elevated gap metabolic acidosis? How are they distinguished? Methanol and Ethylene glycol cause osmolar gap, met Continue reading >>

Mnemonic For Non-anion Gap Metabolic Acidosis

Mnemonic For Non-anion Gap Metabolic Acidosis

Mnemonic for NON-Anion Gap Metabolic Acidosis As Ive mentioned previously on this blog, the MUDPALES mnemonic for anion gap metabolic acidosis is one of the most successful medical mnemonics of all time. A less successful (and admittedly less useful) mnemonic exists for non-anion gap metabolic acidoses (NAGMA), which I learned as a resident. Its HARDUP, which stands for the following: H = hyperalimentation (e.g., starting TPN). R = renal tubular acidosis (Type I = distal; Type II = proximal; Type IV = hyporeninemic hypoaldosteronism. U = uretosigmoid fistula (because the colon will waste bicarbonate). P = pancreatic fistula (because of alkali lossthe pancreas secretes a bicarbonate-rich fluid). Practically speaking however, the two main causes you really have to remember for NAGMA are DIARRHEA or RENAL TUBULAR ACIDOSIS, which 90% of the time you can distinguish between based on the history alone. Another way to think about the differential diagnosis of NAGMA is to ask whether or not there is GI LOSS or RENAL LOSS of bicarbonate. If the history does not provide an obvious explanation, one can distinguish between GI versus renal bicarbonate losses by determining the urine anion gap (urine AG = urine Na + urine K urine Cl), where a positive value indicates renal bicarbonate loss whereas a largely negative value indicates extra-renal bicarbonate loss. Continue reading >>

Time To Ditch Dairy?

Time To Ditch Dairy?

We didnt evolve drinking milk and most populations cant digest milk Milk and dairy products contain micronutrients and several bioactive constituents that may influence cancer risk and progression. However, little is known about the potential effect ofthese. Dairy products are a complex group of foods and composition varies by region, which makes evaluation of their association with disease risk difficult. For most cancers, associations between cancer risk and intake of milk and dairy products have been examined only in a small number of cohort studies, and data are inconsistent or lacking. Meta-analyses of cohort data available to date support an inverse association between milk intake and risk of colorectal and bladder cancer and a positive association between diets high in calcium and risk of prostate cancer. CONCLUSION: In general, dairy intake has not been linked to cancer, however high calcium intake has been in some studies. Be cautious against extra calcium supplementation if you already consume dairy. How could too much calcium promote prostate cancer? The theory: The active form of vitamin Dwhich we get mostly from sunlightmay protect the prostate.And calcium lowers levels of active vitamin D in the blood.Not all studies see a link between calcium and prostate cancer. And most men never reach the too-much-calcium range.Calcium may really be only a concern for men who get more than 2,000 mgs a day. One glass of milk delivers about 300 mg. This is based on the idea that the protein andphosphate in milk and dairy products make them acid-producing foods which cause our bodies to becomeacidified, promoting diseases of modern civilization. However, scientific evidence does not support this. Milk and dairy products neither produce acid upon metabolism nor cause meta Continue reading >>

Normal Anion Gap Metabolic Acidosis

Normal Anion Gap Metabolic Acidosis

Home | Critical Care Compendium | Normal Anion Gap Metabolic Acidosis Normal Anion Gap Metabolic Acidosis (NAGMA) HCO3 loss and replaced with Cl- -> anion gap normal if hyponatraemia is present the plasma [Cl-] may be normal despite the presence of a normal anion gap acidosis -> this could be considered a ‘relative hyperchloraemia’. Extras – RTA, ingestion of oral acidifying salts, recovery phase of DKA loss of bicarbonate with chloride replacement -> hyperchloraemic acidosis secretions into the large and small bowel are mostly alkaline with a bicarbonate level higher than that in plasma. some typical at risk clinical situations are: external drainage of pancreatic or biliary secretions (eg fistulas) this should be easily established by history normally 85% of filtered bicarbonate is reabsorbed in the proximal tubule and the remaining 15% is reabsorbed in the rest of the tubule in patients receiving acetazolamide (or other carbonic anhydrase inhibitors), proximal reabsorption of bicarbonate is decreased resulting in increased distal delivery and HCO3- appears in urine this results in a hyperchloraemic metabolic acidosis and is essentially a form of proximal renal tubular acidosis but is usually not classified as such. hyperchloraemic metabolic acidosis commonly develops during therapy of diabetic ketoacidosis with normal saline oral administration of CaCl2 or NH4Cl is equivalent to giving an acid load both of these salts are used in acid loading tests for the diagnosis of renal tubular acidosis CaCl2 reacts with bicarbonate in the small bowel resulting in the production of insoluble CaCO3 and H+ the hepatic metabolism of NH4+ to urea results in an equivalent production of H+ REASONS WHY ANION GAP MAY BE NORMAL DESPITE A ‘HIGH ANION GAP METABOLIC ACIDOSIS’ 1. Continue reading >>

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