Podcasts about acid base

In this episode we will be covering Facebook Live Questions 4/15-4/21/24  from Dana's free Facebook Group Registered Dietitian Exam Study Group with Dana RD! Don't forget to check out my recorded courses here.Looking for additional tutoring service? Visit my website! Interested in monthly group tutoring? Click here to learn more and apply.Free Downloads: danajfryernutritiontutoring.teachable.com/p/my-downloadable-462494

In this episode, we discuss the physiology and pathophysiology behind acid-base disorders. We then outline a 5 step approach to interpreting acid-base disorders. For reference, please refer to the infographic on our website at www.theinternatwork.com. Written by: Dr. Caroline Najjar, (Internal Medicine Resident)Reviewed by:  Dr. Bernard Unikowsky (Nephrologist) and Dr. Jesse Popov (General Internist)Sound editing by: Tony WalshSupport the show

rWotD Episode 2446: Acid–base reaction Welcome to random Wiki of the Day where we read the summary of a random Wikipedia page every day.The random article for Sunday, 14 January 2024 is Acid–base reaction.In chemistry, an acid–base reaction is a chemical reaction that occurs between an acid and a base. It can be used to determine pH via titration. Several theoretical frameworks provide alternative conceptions of the reaction mechanisms and their application in solving related problems; these are called the acid–base theories, for example, Brønsted–Lowry acid–base theory.Their importance becomes apparent in analyzing acid–base reactions for gaseous or liquid species, or when acid or base character may be somewhat less apparent. The first of these concepts was provided by the French chemist Antoine Lavoisier, around 1776. It is important to think of the acid–base reaction models as theories that complement each other. For example, the current Lewis model has the broadest definition of what an acid and base are, with the Brønsted–Lowry theory being a subset of what acids and bases are, and the Arrhenius theory being the most restrictive.This recording reflects the Wikipedia text as of 01:17 UTC on Sunday, 14 January 2024.For the full current version of the article, see Acid–base reaction on Wikipedia.This podcast uses content from Wikipedia under the Creative Commons Attribution-ShareAlike License.Visit our archives at wikioftheday.com and subscribe to stay updated on new episodes.Follow us on Mastodon at @wikioftheday@masto.ai.Also check out Curmudgeon's Corner, a current events podcast.Until next time, I'm Kimberly Neural.

ICUedu Acid-Base 2.0 Pocket Intensivist CardThis lecture has a lot of important visuals.  Here is is a link to the ICUedu.org subpage with the video lecture and a downloadable link to the key lecture visuals: https://www.icuedu.org/approachacidbase

Dan presented the talk “Metabolic Acidosis: The Eye Can Only See What the Mind Can Comprehend” at AMTC23. In this recording, he teaches you how to identify the prevalence of acid-base disorders including triple disturbances, how to calculate anion gap and determine the etiology of the gap, and how to identify adequacy of compensation for a primary metabolic acidosis. Get CE hours for our podcast episodes HERE! -------------------------------------------- Twitter @heavyhelmet Facebook @heavyliesthehelmet Instagram @heavyliesthehelmet Website heavyliesthehelmet.com Email contact@heavyliesthehelmet.com Disclaimer: The views, information, or opinions expressed on the Heavy Lies the Helmet podcast are solely those of the individuals involved and do not necessarily represent those of their employers and their employees. Heavy Lies the Helmet, LLC is not responsible for the accuracy of any information available for listening on this platform. The primary purpose of this series is to educate and inform, but it is not a substitute for your local laws, medical direction, or sound judgment. --------------------------------------------  Crystals VIP by From The Dust | https://soundcloud.com/ftdmusic Music promoted by https://www.free-stock-music.com

In this episode we will be covering Facebook Live Questions 9/19-9/24/23  free Facebook Group Registered Dietitian Exam Study Group with Dana RD! Don't forget to check out my recorded courses here.Looking for additional tutoring service? Visit my website! Interested in monthly group tutoring? Click here to learn more and apply.Learn more about  Group Tutoring at: https://www.danajfnutrition.com/monthlygrouptutoring 

September 27, 2023: Titration: A Scientific Exploration into Acid-Base Reactions

We often draw blood gasses looking for an ACIDosis, but what about when you discover an ALKAlosis?In this episode, I share a story of a patient with a history of CHF, admitted for diuresis. She was initially improving but becames lethargic and difficult to arouse. We were surprised when her VBG showed alkalosis instead acidosis. Guest Sarah Lorenzini from the Rapid Response RN podcast, helped me make sense of our finding.Listen in to learn about this rare acid base imbalance that can occur as a result of a very common intervention.Check out Nicole Kupchik's exam reviews and practice questions at nicolekupchikconsulting.com. Use the promo code UPMYGAME20 to get 20% off all products.Do you need help with your resume, interviewing, or need career coaching? Check out Sarah at New Thing Nurse:Get 15% off of her resume and cover letter templates using the promo code UPMYGAMENursing students and new grad career services Experienced RN career servicesNP career servicesUp My Nursing Game is partnering with VCU Health Continuing Education to offer FREE continuing education credits for registered nurses. Click here to obtain nursing credit.See the show notes at upmynursinggame.com.The key moments in this episode are:00:02:32 - Patient background and presentation00:15:14 - Causes of metabolic alkalosis 00:20:18 - Treatment of diuretic induced metabolic alkalosis, 00:27:12 - Diagnostic reasoning, antibiotic stewardship 

Normal 261 – 280 mOsm/kg Indications Monitor: Electrolyte balance Acid-Base balance Hydration Evaluate function of antidiuretic hormone.   Description Osmolality is a measure of the particles in solution. The size, shape, and charge of the particles do not impact the osmolality   What would cause increased levels? Dehydration Azotemia Hypercalcemia Hyperglycemic Hyperosmolar Nonketotic State (HHNS) Hypernatremia Diabetes Insipidus Hyperglycemia Mannitol therapy Uremia Severe pyelonephritis Shock Ketosis   What would cause decreased levels? Hyponatremia Syndrome of Inappropriate Antidiuretic Hormone (SIADH) Overhydration

In this podcast episode, Dr. Edward G. Medeiros delves into the intricate world of acid-base balance through the lens of a nephrologist. He provides insights into the systematic approach required for handling different cases and emphasizes the significance of managing acidemia and alkalemia.For any suggestions or topics you'd like us to explore further, please don't hesitate to reach out to us at acpruleoutpod@gmail.com. We welcome your input and ideas!

Numerical acid base problems that require picking out the exact disorder and appropriate compensation show up on essentially every USMLE exam. In this podcast, I discuss a simple, but accurate approach to correctly answering these questions from an NBME/USMLE. This is one of those podcasts you should take notes on and listen through slowly. It … Continue reading Divine Intervention Episode 470: Numerical Acid-Base Problems on The USMLEs (a simplified, accurate approach)

Researcher Vicky van der Togt and virologist Dr Jeremy Rossman have spent the past 2.5 years trying to help Long Covid patients and research via their organisation Research-Aid Networks.   Their latest paper, published in Frontiers, hypothesises that it is an acid-base disruption that drives the symptomatology of Long Covid.  In this week's episode we discuss the impacts of dysregulated pH, how you can rebalance it and the results that they have observed.  Further research in this field has the potential to help with both Long Covid and a wide range of other diseases.Living with Long Covid? How was your week?Website - https://www.tlcsessions.net/Twitter - @SessionsTlc https://twitter.com/sessionstlcInsta - @tlcsessions https://www.instagram.com/tlcsessions

Stay with us! In the final episode of this series, Keith and Courtney introduce Acid-Base Balance and Disturbances. It has taken years for both of them to get to grips on some of the basics of this topic, and they spend the next hour breaking down what is going on and how to interpret the values in front of you. During the second half of this episode, they discuss some case-based scenarios.  Even if you are not utilising blood gas analysis in practice, it doesn't mean something acute is not happening to our patients under anaesthesia just because we can't see it, so it is still useful to understand. Keep up to date with the Burtons Academy: Facebook - Burtons Veterinary Equipment | Facebook Instagram - Burtons Veterinary Equipment (@burtonsveterinaryequipment) Twitter - Burtons Veterinary Equipment (@Burtonsvet) LinkedIn - https://www.linkedin.com/company/burtons-medical-equipment/

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In this episode we will be covering Facebook Live Questions 5/29-6/4  free Facebook Group Registered Dietitian Exam Study Group with Dana RD! Don't forget to check out my recorded courses here.Looking for additional tutoring service? Visit my website! Interested in monthly group tutoring? Click here to learn more and apply.

Today we have a special guest, Dr. Joel Topf, board-certified nephrologist and medical educator extraordinaire. Our listeners will likely recognize Dr. Topf from his prolific tweeting @Kidney_boy, as well as his numerous appearances on the Curbsiders podcast. He is a co-founder of the NephJC on Twitter, and host and founder of the NephJC podcast Freely Filtered. He is also host of the podcast Channel Your Enthusiasm, a deep dive monthly recap of the nephrology textbook Clinical Physiology of Acid Base and Electrolyte Disorders by Dr. Burton Rose (who, incidentally, is the creator of the original UpToDate). Dr. Topf wrote his own book on fluids, electrolytes and acid-base homeostasis.  He's the co-editor for the fourth edition of Nephrology Secrets and the first edition of The Handbook of Critical Care Nephrology. Dr. Topf joined us to talk about a new paper he co-authored on osmotic demyelination syndrome and hyponatremia. I'm also joined by Dr. Mita Hoppenfeld, hospitalist at the University of Utah, to talk about a new DOAC vs warfarin trial in On-X aortic valves, whether it's better to avoid hypertension or hypotension around time of surgery, and the diagnostic accuracy of CT abdomen scans without contrast. Check it out! Osmotic Demyelination and HyponatremiaApixaban vs Warfarin for On-X Aortic ValvePerioperative Blood Pressure Strategies Diagnostic Accuracy of CT Abdomen Without ContrastMusic from Uppbeat (free for Creators!):https://uppbeat.io/t/soundroll/dopeLicense code: NP8HLP5WKGKXFW2R

ReferencesWe considered the complexity of the machinery to excrete ammonium in the context of research on dietary protein and how high protein intake may increase glomerular pressure and contribute to progressive renal disease (many refer to this as the “Brenner hypothesis”). Dietary protein intake and the progressive nature of kidney disease: the role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation, and intrinsic renal diseaseA trial that studied low protein and progression of CKD The Effects of Dietary Protein Restriction and Blood-Pressure Control on the Progression of Chronic Renal Disease(and famously provided data for the MDRD eGFR equation A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study GroupWe wondered about dietary recommendations in CKD. of note, this is best done in the DKD guidelines from KDIGO Executive summary of the 2020 KDIGO Diabetes Management in CKD Guideline: evidence-based advances in monitoring and treatment.Joel mentioned this study on red meat and risk of ESKD. Red Meat Intake and Risk of ESRDWe referenced the notion of a plant-based diet. This is an excellent review by Deborah Clegg and Kathleen Hill Gallant. Plant-Based Diets in CKD : Clinical Journal of the American Society of NephrologyHere's the review that Josh mentioned on how the kidney appears to sense pH Molecular mechanisms of acid-base sensing by the kidneyRemarkably, Dr. Dale Dubin put a prize in his ECG book Free Car Prize Hidden in Textbook Read the fine print: Student wins T-birdA review of the role of the kidney in DKA: Diabetic ketoacidosis: Role of the kidney in the acid-base homeostasis re-evaluatedJosh mentioned the effects of infusing large amounts of bicarbonate The effect of prolonged administration of large doses of sodium bicarbonate in man and this study on the respiratory response to a bicarbonate infusion: The Acute Effects In Man Of A Rapid Intravenous Infusion Of Hypertonic Sodium Bicarbonate Solution. Ii. Changes In Respiration And Output Of Carbon DioxideThis is the study of acute respiratory alkalosis in dogs: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC293311/?page=1And this is the study of medical students who went to the High Alpine Research Station on the Jungfraujoch in the Swiss Alps https://www.nejm.org/doi/full/10.1056/nejm199105163242003Self explanatory! A group favorite! It Is Chloride Depletion Alkalosis, Not Contraction AlkalosisEffects of chloride and extracellular fluid volume on bicarbonate reabsorption along the nephron in metabolic alkalosis in the rat. Reassessment of the classical hypothesis of the pathogenesis of metabolic alkalosisA review of pendrin's role in volume homeostasis: The role of pendrin in blood pressure regulation | American Journal of Physiology-Renal PhysiologyInfusion of bicarbonate may lead to a decrease in respiratory stimulation but the shift of bicarbonate to the CSF may lag. Check out this review Neural Control of Breathing and CO2 Homeostasis and this classic paper Spinal-Fluid pH and Neurologic Symptoms in Systemic Acidosis.OutlineOutline: Chapter 11- Regulation of Acid-Base Balance- Introduction - Bicarb plus a proton in equilibrium with CO2 and water - Can be rearranged to HH - Importance of regulating pCO2 and HCO3 outside of this equation - Metabolism of carbs and fats results in the production of 15,000 mmol of CO2 per day - Metabolism of protein and other “substances” generates non-carbonic acids and bases - Mostly from sulfur containing methionine and cysteine - And cationic arginine and lysine - Hydrolysis of dietary phosphate that exists and H2PO4– - Source of base/alkali - Metabolism of an ionic amino acids - Glutamate and asparatate - Organic anions going through gluconeogenesis - Glutamate, Citrate and lactate - Net effect on a normal western diet 50-100 mEq of H+ per day - Homeostatic response to these acid-base loads has three stages: - Chemical buffering - Changes in ventilation - Changes in H+ excretion - Example of H2SO4 from oxidation of sulfur containing AA - Drop in bicarb will stimulate renal acid secretion - Nice table of normal cid-base values, arterial and venous- Great 6 bullet points of acid-base on page 328 - Kidneys must excrete 50-100 of non-carbonic acid daily - This occurs by H secretion, but mechanisms change by area of nephron - Not excreted as free H+ due to minimal urine pH being equivalent to 0.05 mmol/L - No H+ can be excreted until virtually all of th filtered bicarb is reabsorbed - Secreted H+ must bind buffers (phosphate, NH3, cr) - PH is main stimulus for H secretion, though K, aldo and volume can affect this.- Renal Hydrogen excretion - Critical to understand that loss of bicarb is like addition of hydrogen to the body - So all bicarb must be reabsorbed before dietary H load can be secreted - GFR of 125 and bicarb of 24 results in 4300 mEq of bicarb to be reabsorbed daily - Reabsorption of bicarb and secretion of H involve H secretion from tubular cells into the lumen. - Thee initial points need to be emphasized - Secreted H+ ion are generated from dissociation of H2O - Also creates OH ion - Which combine with CO2 to form HCO3 with the help of zinc containing intracellular carbonic anhydrase. - This is how the secretion of H+ which creates an OH ultimately produces HCO3 - Different mechanisms for proximal and distal acidification - NET ACID EXCRETION - Free H+ is negligible - So net H+ is TA + NH4 – HCO3 loss - Unusually equal to net H+ load, 50-100 mEq/day - Can bump up to 300 mEq/day if acid production is increased - Net acid excretion can go negative following a bicarb or citrate load - Proximal Acidification - Na-H antiporter (or exchanger) in luminal membrane - Basolateral membrane has a 3 HCO3 Na cotransporter - This is electrogenic with 3 anions going out and only one cation - The Na-H antiporter also works in the thick ascending limb of LOH - How about this, there is also a H-ATPase just like found in the intercalated cells in the proximal tubule and is responsible for about a third of H secretion - And similarly there is also. HCO3 Cl exchanger (pendrin-like) in the proximal tubule - Footnote says the Na- 3HCO3 cotransporter (which moves sodium against chemical gradient NS uses negative charge inside cell to power it) is important for sensing acid-base changes in the cell. - Distal acidification - Occurs in intercalated cells of of cortical and medullary collecting tubule - Three main characteristics - H secretion via active secretory pumps in the luminal membrane - Both H-ATPase and H-K ATPase - H- K ATPase is an exchange pump, k reabsorption - H-K exchange may be more important in hypokalemia rather than in acid-base balance - Whole paragraph on how a Na-H exchanger couldn't work because the gradient that H has to be pumped up is too big. - H-ATPase work like vasopressin with premise H-ATPase sitting on endocarditis vesicles a=which are then inserted into the membrane. Alkalosis causes them to be recycled out of the membrane. - H secretory cells do not transport Na since they have few luminal Na channels, but are assisted by the lumen negative tubule from eNaC. - Minimizes back diffusion of H+ and promotes bicarb resorption - Bicarbonate leaves the cell through HCO3-Cl exchanger which uses the low intracellular Cl concentration to power this process. - Same molecule is found on RBC where it is called band 3 protein - Figure 11-5 is interesting - Bicarbonate resorption - 90% in the first 1-22 mm of the proximal tubule (how long is the proximal tubule?) - Lots of Na-H exchangers and I handed permeability to HCO3 (permeability where?) - Last 10% happens distally mostly TAL LOH via Na-H exchange - And the last little bit int he outer medullary collecting duct. - Carbonic anhydrase and disequilibrium pH - CA plays central role in HCO3 reabsorption - After H is secreted in the proximal tubule it combines with HCO# to form carbonic acid. CA then dehydrates it to CO2 and H2O. (Step 2) - Constantly moving carbonic acid to CO2 and H2O keeps hydrogen combining with HCO3 since the product is rapidly consumed. - This can be demonstrated by the minimal fall in luminal pH - That is important so there is not a luminal gradient for H to overcome in the Na-H exchanger (this is why we need a H-ATPase later) - CA inhibitors that are limited tot he extracellular compartment can impair HCO3 reabsorption by 80%. - CA is found in S1, S2 but not S3 segment. See consequence in figure 11-6. - The disequilibrium comes from areas where there is no CA, the HH formula falls down because one of the assumptions of that formula is that H2CO3 (carbonic acid) is a transient actor, but without CA it is not and can accumulate, so the pKa is not 6.1. - Bicarbonate secretion - Type B intercalated cells - H-ATPase polarity reversed - HCO3 Cl exchanger faces the apical rather than basolateral membrane- Titratable acidity - Weak acids are filtered at the glom and act as buffers in the urine. - HPO4 has PKA of 6.8 making it ideal - Creatinine (pKa 4.97) and uric acid (pKa 5.75) also contribute - Under normal cinditions TA buffers 10-40 mEa of H per day - Does an example of HPO4(2-):H2PO4 (1-) which exists 4:1 at pH of 7.4 (glomerular filtrate) - So for 50 mEq of Phos 40 is HPO4 and 10 is H2PO4 - When pH drops to 6.8 then the ratio is 1:1 so for 50 - So the 50 mEq is 25 and 25, so this buffered an additional 15 mEq of H while the free H+ concentration increased from 40 to 160 nanomol/L so over 99.99% of secreted H was buffered - When pH drops to 4.8 ratio is 1:100 so almost all 50 mEq of phos is H2PO4 and 39.5 mEq of H are buffered. - Acid loading decreases phosphate reabsorption so more is there to act as TA. - Decreases activity of Na-phosphate cotransporter - DKA provides a novel weak acid/buffer beta-hydroxybutyrate (pKa 4.8) which buffers significant amount of acid (50 mEq/d).- Ammonium Excretion - Ability to excrete H+ as ammonium ions adds an important amount of flexibility to renal acid-base regulation - NH3 and NH4 production and excretion can be varied according to physiologic need. - Starts with NH3 production in tubular cells - NH3, since it is neutral then diffuses into the tubule where it is acidified by the low pH to NH4+ - NH4+ is ionized and cannot cross back into the tubule cells(it is trapped in the tubular fluid) - This is important for it acting as an important buffer eve though the pKa is 9.0 - At pH of 6.0 the ratio of NH3 to NH4 is 1:1000 - As the neutral NH3 is converted to NH4 more NH3 from theintracellular compartment flows into the tubular fluid replacing the lost NH3. Rinse wash repeat. - This is an over simplification and that there are threemajor steps - NH4 is produced in early proximal tubular cells - Luminal NH4 is partially reabsorbed in the TAL and theNH3 is then recycled within the renal medulla - The medullary interstitial NH3 reaches highconcentrations that allow NH3 to diffuse into the tubular lumen in the medullary collecting tubule where it is trapped as NH4 by secreted H+ - NH4 production from Glutamine which converts to NH4 and glutamate - Glutamate is converted to alpha-ketoglutarate - Alpha ketoglutarate is converted to 2 HCO3 ions - HCO3 sent to systemic circulation by Na-3 HCO3 transporter - NH4 then secreted via Na-H exchanger into the lumen - NH4 is then reabsorbed by NaK2Cl transporter in TAL - NH4 substitutes for K - Once reabsorbed the higher intracellular pH causes NH4 to convert to NH3 and the H that is removed is secreted through Na-H exchanger to scavenge the last of the filtered bicarb. - NH3 diffuses out of the tubular cells into the interstitium - NH4 reabsorption in the TAL is suppressed by hyperkalemia and stimulated by chronic metabolic acidosis - NH4 recycling promotes acid clearance - The collecting tubule has a very low NH3 concentration - This promotes diffusion of NH3 into the collecting duct - NH3 that goes there is rapidly converted to NH4 allowing more NH3 to diffuse in. - Response to changes in pH - Increased ammonium excretion with two processes - Increased proximal NH4 production - This is delayed 24 hours to 2-3 days depending on which enzyme you look at - Decreased urine pH increases diffusion of ammonia into the MCD - Occurs with in hours of an acid load - Peak ammonium excretion takes 5-6 days! (Fig 11-10) - Glutamine is picked up from tubular fluid but with acidosis get Na dependent peritublar capillary glutamine scavenging too - Glutamine metabolism is pH dependent with increase with academia and decrease with alkalemia - NH4 excretion can go from 30-40 mEq/day to > 300 with severe metabolic acidosis (38 NaBicarb tabs) - Says each NH4 produces equimolar generation of HCO3 but I thought it was two bicarb for every alpha ketoglutarate?- The importance of urine pH - Though the total amount of hydrogren cleared by urine pH is insignificant, an acidic urine pH is essential for driving the reactions of TA and NH4 forward.- Regulation of renal hydrogen excretion - Net acid excretion vary inverse with extracellular pH - Academia triggers proximal and distal acidification - Proximally this: - Increased Na-H exchange - Increased luminal H-ATPase activity - Increased Na:3HCO3 cotransporter on the basolateral membrane - Increased NH4 production from glutamine - In the collecting tubules - Increased H-ATPase - Reduction of tubular pH promotes diffusion of NH3 which gets converted to NH4…ION TRAPPING - Extracellular pH affects net acid excretion through its affect on intracellular pH - This happens directly with respiratory disorders due to movement of CO2 through the lipid bilayer - In metabolic disorders a low extracellular bicarb with cause bicarb to diffuse out of the cell passively, this lowers intracellular pH - If you manipulate both low pCO2 and low Bicarb to keep pH stable there will be no change in the intracellular pH and there is no change in renal handling of acid. It is intracellular pH dependent - Metabolic acidosis - Ramps up net acid secretion - Starts within 24 hours and peaks after 5-6 days - Increase net secretion comes from NH4 - Phosphate is generally limited by diet - in DKA titratable acid can be ramped up - Metabolic alkalosis - Alkaline extracellular pH - Increased bicarb excretion - Decrease reabsorption - HCO3 secretion (pendrin) in cortical collecting tubule - Occurs in cortical intercalated cells able to insert H-ATPase in basolateral cells (rather than luminal membrane) - Normal subjects are able to secrete 1000 mmol/day of bicarb - Maintenance of metabolic alkalosis requires a defect which forces the renal resorption of bicarb - This can be chloride/volume deficiency - Hypokalemia - Hyperaldosteronism - Respiratory acidosis and alkalosis - PCO2 via its effect on intracellular pH is an important determinant of renal acid handling - Ratios he uses: - 3.5 per 10 for respiratory acidosis - 5 per 10 for respiratory alkalosis - Interesting paragraph contrasting the response to chronic metabolic acidosis vs chronic respiratory acidosis - Less urinary ammonium in respiratory acidosis - Major differences in proximal tubule cell pH - In metabolic acidosis there is decreased bicarb load so less to be reabsorbed proximally - In respiratory acidosis the increased serum bicarb increases the amount of bicarb that must be reabsorbed proximally - The increased activity of Na-H antiporter returns tubular cell pH to normal and prevents it from creating increased urinary ammonium - Mentions that weirdly more mRNA for H-Na antiporter in metabolic acidosis than in respiratory acidosis - Net hydrogen excretion varies with effective circulating volume - Starts with bicarb infusions - Normally Tm at 26 - But if you volume deplete the patient with diuretics first this increases to 35+ - Four factors explain this increased Tm for bicarb with volume deficiency - Reduced GFR - Activation of RAAS - Ang2 stim H-Na antiporter proximally - Ang2 also stimulates Na-3HCO3 cotransporter on basolateral membrane - Aldosterone stimulates H-ATPase in distal nephron - ALdo stimulates Cl HCO3 exchanger on basolateral membrane - Aldo stimulates eNaC producing tubular lumen negative charge to allow H secretion to occur and prevents back diffusion - Hypochloremia - Increases H secretion by both Na-dependent and Na-independent methods - If Na is 140 and Cl is 115, only 115 of Na can be reabsorbed as NaCl, the remainder must be reabsorbed with HCO3 or associated with secretion of K or H to maintained electro neutrality - This is enhanced with hypochloridemia - Concurrent hypokalemia - Changes in K lead to trans cellular shifts that affect inctracellular pH - Hypokalemia causes K out, H in and in the tubular cell the cell acts if there is systemic acidosis and increases H secretion (and bicarbonate resorption) - PTH - Decreases proximal HCO3 resorption - Primary HyperCard as cause of type 2 RTA - Does acidosis stim PTH or does PTH stim net acid excretion

Looking for more information on this topic? Check out the Acid-Base Disorders: Putting it all Together brick. If you enjoyed this episode, we'd love for you to leave a review on Apple Podcasts.  It helps with our visibility, and the more med students (or future med students) listen to the podcast, the more we can provide to the future physicians of the world. Follow USMLE-Rx at: Facebook: www.facebook.com/usmlerx Blog: www.firstaidteam.com Twitter: https://twitter.com/firstaidteam Twitter: https://twitter.com/mesage_hub Instagram: https://www.instagram.com/firstaidteam/ YouTube: www.youtube.com/USMLERX Learn more about Rx Bricks by signing up for a free USMLE-Rx account: www.usmle-rx.com You will get 5 days of full access to our Rx360+ program, including over 800 Rx Bricks.  After the 5-day period, you will still be able to access over 150 free bricks, including the entire collections for General Microbiology and Cellular and Molecular Biology.

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Dr. Alexis "AC" Gomez, a second year fellow at the combined MGH, Brigham and Women's, and Boston Children's nephrology program, discusses acid-base disorders with Dr. Joyce Zhou, a RTL host. She defines acid-base disorders, shares common etiologies, and offers a 5-step approach to characterizing these abnormalities.

ReferencesWe considered the effect of a high protein diet and potential metabolic acidosis on kidney function. This review is of interest by Donald Wesson, a champion for addressing this issue and limiting animal protein: Mechanisms of Metabolic Acidosis-Induced Kidney Injury in Chronic Kidney DiseaseHostetter explored the effect of a high protein diet in the remnant kidney model with 1 ¾ nephrectomy. Rats with reduced dietary acid load (by bicarbonate supplementation) had less tubular damage. Chronic effects of dietary protein in the rat with intact and reduced renal massWesson explored treatment of metabolic acidosis in humans with stage 3 CKD in this study. Treatment of metabolic acidosis in patients with stage 3 chronic kidney disease with fruits and vegetables or oral bicarbonate reduces urine angiotensinogen and preserves glomerular filtration rateIn addition to the effect of metabolic acidosis from a diet high in animal protein, this diet also leads to hyperfiltration. This was demonstrated in normal subjects; ingesting a protein diet had a significantly higher creatinine clearance than a comparable group of normal subjects ingesting a vegetarian diet. Renal functional reserve in humans: Effect of protein intake on glomerular filtration rate.This finding has been implicated in Brenner's theory regarding hyperfiltration: The hyperfiltration theory: a paradigm shift in nephrologyOne of multiple publications from Dr. Nimrat Goraya whom Joel mentioned in the voice over: Dietary Protein as Kidney Protection: Quality or Quantity?We wondered about the time course in buffering a high protein meal (and its subsequent acid load on ventilation) and Amy found this report:Effect of Protein Intake on Ventilatory Drive | Anesthesiology | American Society of Anesthesiologists Roger mentioned that the need for acetate to balance the acid from amino acids in parenteral nutrition was identified in pediatrics perhaps because infants may have reduced ability to generate acid. Randomised controlled trial of acetate in preterm neonates receiving parenteral nutrition - PMCHe also recommended an excellent review on the complications of parenteral nutrition by Knochel https://www.kidney-international.org/action/showPdf?pii=S0085-2538%2815%2933384-6 which explained that when the infused amino acids disproportionately include cationic amino acids, metabolism led to H+ production. This is typically mitigated by preparing a solution that is balanced by acetate. Amy mentioned this study that explored the effect of protein intake on ventilation: Effect of Protein Intake on Ventilatory Drive | Anesthesiology | American Society of AnesthesiologistsAnna and Amy reminisced about a Skeleton Key Group Case from the renal fellow network Skeleton Key Group: Electrolyte Case #7JC wondered about isolated defects in the proximal tubule and an example is found here: Mutations in SLC4A4 cause permanent isolated proximal renal tubular acidosis with ocular abnormalitiesAnna's Voiceover re: Gastric neobladder → metabolic alkalosis and yes, dysuria. The physiology of gastrocystoplasty: once a stomach, always a stomach but not as common as you might think Gastrocystoplasty: long-term complications in 22 patientsSjögren's syndrome has been associated with acquired distal RTA and in some cases, an absence of the H+ ATPase, presumably from autoantibodies to this transporter. Here's a case report: Absence of H(+)-ATPase in cortical collecting tubules of a patient with Sjogren's syndrome and distal renal tubular acidosisCan't get enough disequilibrium pH? Check this out- Spontaneous luminal disequilibrium pH in S3 proximal tubules. Role in ammonia and bicarbonate transport.Acetazolamide secretion was studied in this report Concentration-dependent tubular secretion of acetazolamide and its inhibition by salicylic acid in the isolated perfused rat kidney. | Drug Metabolism & DispositionIn this excellent review, David Goldfarb tackles the challenging case of a A Woman with Recurrent Calcium Phosphate Kidney Stones (spoiler alert, many of these patients have incomplete distal RTA and this problem is hard to treat). Molecular mechanisms of renal ammonia transport excellent review from David Winer and Lee Hamm. OutlineOutline: Chapter 11- Regulation of Acid-Base Balance- Introduction - Bicarb plus a proton in equilibrium with CO2 and water - Can be rearranged to HH - Importance of regulating pCO2 and HCO3 outside of this equation - Metabolism of carbs and fats results in the production of 15,000 mmol of CO2 per day - Metabolism of protein and other “substances” generates non-carbonic acids and bases - Mostly from sulfur containing methionine and cysteine - And cationic arginine and lysine - Hydrolysis of dietary phosphate that exists and H2PO4– - Source of base/alkali - Metabolism of an ionic amino acids - Glutamate and asparatate - Organic anions going through gluconeogenesis - Glutamate, Citrate and lactate - Net effect on a normal western diet 50-100 mEq of H+ per day - Homeostatic response to these acid-base loads has three stages: - Chemical buffering - Changes in ventilation - Changes in H+ excretion - Example of H2SO4 from oxidation of sulfur containing AA - Drop in bicarb will stimulate renal acid secretion - Nice table of normal cid-base values, arterial and venous- Great 6 bullet points of acid-base on page 328 - Kidneys must excrete 50-100 of non-carbonic acid daily - This occurs by H secretion, but mechanisms change by area of nephron - Not excreted as free H+ due to minimal urine pH being equivalent to 0.05 mmol/L - No H+ can be excreted until virtually all of th filtered bicarb is reabsorbed - Secreted H+ must bind buffers (phosphate, NH3, cr) - PH is main stimulus for H secretion, though K, aldo and volume can affect this.- Renal Hydrogen excretion - Critical to understand that loss of bicarb is like addition of hydrogen to the body - So all bicarb must be reabsorbed before dietary H load can be secreted - GFR of 125 and bicarb of 24 results in 4300 mEq of bicarb to be reabsorbed daily - Reabsorption of bicarb and secretion of H involve H secretion from tubular cells into the lumen. - Thee initial points need to be emphasized - Secreted H+ ion are generated from dissociation of H2O - Also creates OH ion - Which combine with CO2 to form HCO3 with the help of zinc containing intracellular carbonic anhydrase. - This is how the secretion of H+ which creates an OH ultimately produces HCO3 - Different mechanisms for proximal and distal acidification - NET ACID EXCRETION - Free H+ is negligible - So net H+ is TA + NH4 – HCO3 loss - Unusually equal to net H+ load, 50-100 mEq/day - Can bump up to 300 mEq/day if acid production is increased - Net acid excretion can go negative following a bicarb or citrate load - Proximal Acidification - Na-H antiporter (or exchanger) in luminal membrane - Basolateral membrane has a 3 HCO3 Na cotransporter - This is electrogenic with 3 anions going out and only one cation - The Na-H antiporter also works in the thick ascending limb of LOH - How about this, there is also a H-ATPase just like found in the intercalated cells in the proximal tubule and is responsible for about a third of H secretion - And similarly there is also. HCO3 Cl exchanger (pendrin-like) in the proximal tubule - Footnote says the Na- 3HCO3 cotransporter (which moves sodium against chemical gradient NS uses negative charge inside cell to power it) is important for sensing acid-base changes in the cell. - Distal acidification - Occurs in intercalated cells of of cortical and medullary collecting tubule - Three main characteristics - H secretion via active secretory pumps in the luminal membrane - Both H-ATPase and H-K ATPase - H- K ATPase is an exchange pump, k reabsorption - H-K exchange may be more important in hypokalemia rather than in acid-base balance - Whole paragraph on how a Na-H exchanger couldn't work because the gradient that H has to be pumped up is too big. - H-ATPase work like vasopressin with premise H-ATPase sitting on endocarditis vesicles a=which are then inserted into the membrane. Alkalosis causes them to be recycled out of the membrane. - H secretory cells do not transport Na since they have few luminal Na channels, but are assisted by the lumen negative tubule from eNaC. - Minimizes back diffusion of H+ and promotes bicarb resorption - Bicarbonate leaves the cell through HCO3-Cl exchanger which uses the low intracellular Cl concentration to power this process. - Same molecule is found on RBC where it is called band 3 protein - Figure 11-5 is interesting - Bicarbonate resorption - 90% in the first 1-22 mm of the proximal tubule (how long is the proximal tubule?) - Lots of Na-H exchangers and I handed permeability to HCO3 (permeability where?) - Last 10% happens distally mostly TAL LOH via Na-H exchange - And the last little bit int he outer medullary collecting duct. - Carbonic anhydrase and disequilibrium pH - CA plays central role in HCO3 reabsorption - After H is secreted in the proximal tubule it combines with HCO# to form carbonic acid. CA then dehydrates it to CO2 and H2O. (Step 2) - Constantly moving carbonic acid to CO2 and H2O keeps hydrogen combining with HCO3 since the product is rapidly consumed. - This can be demonstrated by the minimal fall in luminal pH - That is important so there is not a luminal gradient for H to overcome in the Na-H exchanger (this is why we need a H-ATPase later) - CA inhibitors that are limited tot he extracellular compartment can impair HCO3 reabsorption by 80%. - CA is found in S1, S2 but not S3 segment. See consequence in figure 11-6. - The disequilibrium comes from areas where there is no CA, the HH formula falls down because one of the assumptions of that formula is that H2CO3 (carbonic acid) is a transient actor, but without CA it is not and can accumulate, so the pKa is not 6.1. - Bicarbonate secretion - Type B intercalated cells - H-ATPase polarity reversed - HCO3 Cl exchanger faces the apical rather than basolateral membrane- Titratable acidity - Weak acids are filtered at the glom and act as buffers in the urine. - HPO4 has PKA of 6.8 making it ideal - Creatinine (pKa 4.97) and uric acid (pKa 5.75) also contribute - Under normal cinditions TA buffers 10-40 mEa of H per day - Does an example of HPO4(2-):H2PO4 (1-) which exists 4:1 at pH of 7.4 (glomerular filtrate) - So for 50 mEq of Phos 40 is HPO4 and 10 is H2PO4 - When pH drops to 6.8 then the ratio is 1:1 so for 50 - So the 50 mEq is 25 and 25, so this buffered an additional 15 mEq of H while the free H+ concentration increased from 40 to 160 nanomol/L so over 99.99% of secreted H was buffered - When pH drops to 4.8 ratio is 1:100 so almost all 50 mEq of phos is H2PO4 and 39.5 mEq of H are buffered. - Acid loading decreases phosphate reabsorption so more is there to act as TA. - Decreases activity of Na-phosphate cotransporter - DKA provides a novel weak acid/buffer beta-hydroxybutyrate (pKa 4.8) which buffers significant amount of acid (50 mEq/d).- Ammonium Excretion - Ability to excrete H+ as ammonium ions adds an important amount of flexibility to renal acid-base regulation - NH3 and NH4 production and excretion can be varied according to physiologic need. - Starts with NH3 production in tubular cells - NH3, since it is neutral then diffuses into the tubule where it is acidified by the low pH to NH4+ - NH4+ is ionized and cannot cross back into the tubule cells(it is trapped in the tubular fluid) - This is important for it acting as an important buffer eve though the pKa is 9.0 - At pH of 6.0 the ratio of NH3 to NH4 is 1:1000 - As the neutral NH3 is converted to NH4 more NH3 from theintracellular compartment flows into the tubular fluid replacing the lost NH3. Rinse wash repeat. - This is an over simplification and that there are threemajor steps - NH4 is produced in early proximal tubular cells - Luminal NH4 is partially reabsorbed in the TAL and theNH3 is then recycled within the renal medulla - The medullary interstitial NH3 reaches highconcentrations that allow NH3 to diffuse into the tubular lumen in the medullary collecting tubule where it is trapped as NH4 by secreted H+ - NH4 production from Glutamine which converts to NH4 and glutamate - Glutamate is converted to alpha-ketoglutarate - Alpha ketoglutarate is converted to 2 HCO3 ions - HCO3 sent to systemic circulation by Na-3 HCO3 transporter - NH4 then secreted via Na-H exchanger into the lumen - NH4 is then reabsorbed by NaK2Cl transporter in TAL - NH4 substitutes for K - Once reabsorbed the higher intracellular pH causes NH4 to convert to NH3 and the H that is removed is secreted through Na-H exchanger to scavenge the last of the filtered bicarb. - NH3 diffuses out of the tubular cells into the interstitium - NH4 reabsorption in the TAL is suppressed by hyperkalemia and stimulated by chronic metabolic acidosis - NH4 recycling promotes acid clearance - The collecting tubule has a very low NH3 concentration - This promotes diffusion of NH3 into the collecting duct - NH3 that goes there is rapidly converted to NH4 allowing more NH3 to diffuse in. - Response to changes in pH - Increased ammonium excretion with two processes - Increased proximal NH4 production - This is delayed 24 hours to 2-3 days depending on which enzyme you look at - Decreased urine pH increases diffusion of ammonia into the MCD - Occurs with in hours of an acid load - Peak ammonium excretion takes 5-6 days! (Fig 11-10) - Glutamine is picked up from tubular fluid but with acidosis get Na dependent peritublar capillary glutamine scavenging too - Glutamine metabolism is pH dependent with increase with academia and decrease with alkalemia - NH4 excretion can go from 30-40 mEq/day to > 300 with severe metabolic acidosis (38 NaBicarb tabs) - Says each NH4 produces equimolar generation of HCO3 but I thought it was two bicarb for every alpha ketoglutarate?- The importance of urine pH - Though the total amount of hydrogren cleared by urine pH is insignificant, an acidic urine pH is essential for driving the reactions of TA and NH4 forward.- Regulation of renal hydrogen excretion - Net acid excretion vary inverse with extracellular pH - Academia triggers proximal and distal acidification - Proximally this: - Increased Na-H exchange - Increased luminal H-ATPase activity - Increased Na:3HCO3 cotransporter on the basolateral membrane - Increased NH4 production from glutamine - In the collecting tubules - Increased H-ATPase - Reduction of tubular pH promotes diffusion of NH3 which gets converted to NH4…ION TRAPPING - Extracellular pH affects net acid excretion through its affect on intracellular pH - This happens directly with respiratory disorders due to movement of CO2 through the lipid bilayer - In metabolic disorders a low extracellular bicarb with cause bicarb to diffuse out of the cell passively, this lowers intracellular pH - If you manipulate both low pCO2 and low Bicarb to keep pH stable there will be no change in the intracellular pH and there is no change in renal handling of acid. It is intracellular pH dependent - Metabolic acidosis - Ramps up net acid secretion - Starts within 24 hours and peaks after 5-6 days - Increase net secretion comes from NH4 - Phosphate is generally limited by diet - in DKA titratable acid can be ramped up - Metabolic alkalosis - Alkaline extracellular pH - Increased bicarb excretion - Decrease reabsorption - HCO3 secretion (pendrin) in cortical collecting tubule - Occurs in cortical intercalated cells able to insert H-ATPase in basolateral cells (rather than luminal membrane) - Normal subjects are able to secrete 1000 mmol/day of bicarb - Maintenance of metabolic alkalosis requires a defect which forces the renal resorption of bicarb - This can be chloride/volume deficiency - Hypokalemia - Hyperaldosteronism - Respiratory acidosis and alkalosis - PCO2 via its effect on intracellular pH is an important determinant of renal acid handling - Ratios he uses: - 3.5 per 10 for respiratory acidosis - 5 per 10 for respiratory alkalosis - Interesting paragraph contrasting the response to chronic metabolic acidosis vs chronic respiratory acidosis - Less urinary ammonium in respiratory acidosis - Major differences in proximal tubule cell pH - In metabolic acidosis there is decreased bicarb load so less to be reabsorbed proximally - In respiratory acidosis the increased serum bicarb increases the amount of bicarb that must be reabsorbed proximally - The increased activity of Na-H antiporter returns tubular cell pH to normal and prevents it from creating increased urinary ammonium - Mentions that weirdly more mRNA for H-Na antiporter in metabolic acidosis than in respiratory acidosis - Net hydrogen excretion varies with effective circulating volume - Starts with bicarb infusions - Normally Tm at 26 - But if you volume deplete the patient with diuretics first this increases to 35+ - Four factors explain this increased Tm for bicarb with volume deficiency - Reduced GFR - Activation of RAAS - Ang2 stim H-Na antiporter proximally - Ang2 also stimulates Na-3HCO3 cotransporter on basolateral membrane - Aldosterone stimulates H-ATPase in distal nephron - ALdo stimulates Cl HCO3 exchanger on basolateral membrane - Aldo stimulates eNaC producing tubular lumen negative charge to allow H secretion to occur and prevents back diffusion - Hypochloremia - Increases H secretion by both Na-dependent and Na-independent methods - If Na is 140 and Cl is 115, only 115 of Na can be reabsorbed as NaCl, the remainder must be reabsorbed with HCO3 or associated with secretion of K or H to maintained electro neutrality - This is enhanced with hypochloridemia - Concurrent hypokalemia - Changes in K lead to trans cellular shifts that affect inctracellular pH - Hypokalemia causes K out, H in and in the tubular cell the cell acts if there is systemic acidosis and increases H secretion (and bicarbonate resorption) - PTH - Decreases proximal HCO3 resorption - Primary HyperCard as cause of type 2 RTA - Does acidosis stim PTH or does PTH stim net acid excretion

While we all breathe, few of us are conscious of it and the impact that it has on our performance and health. This is unfortunate because how you breathe is an important factor and most of you reading this have one or more breathing dysfunctions. One of the most common is Overbreathing. This is where you breathe more than is necessary to meet your metabolic needs, breathing in more Oxygen (O2) and breathing out more Carbon Dioxide (CO2) than is necessary. While this may not seem like a big deal, chronic Overbreathing can cause some health and performance problems. So how do you know if you suffer from Overbreathing? Well, the easiest way to tell is to check to see how many breaths you take in a minute. Anything over 10 breaths per minute is Overbreathing, with 6-8 breaths per minute being optimal. If you Overbreathe at rest then odds are really high that you do it while working hard as well. And this means that you chronically Overbreathe, which impacts a few things. First, it is metabolically inefficient. Each breath you take requires energy and so the fewer breaths you take to meet your body's need for oxygen the less overall energy that you will use. This is helpful from both a health and a performance standpoint. Second, Overbreathing disrupts the natural levels of the gasses in your blood. This creates a new internal environment for your body to react and adapt to. While taking in more O2 might seem like the right idea, especially during periods of high effort, the flip side is that you are also blowing off more CO2. Again, this may seem like a good idea on the surface but doing so causes some different problems. In the short term, your body needs CO2 to offload oxygen from red blood cells. Called The Bohr Effect, this means that you need CO2 present in the blood to get oxygen to working muscles. Blowing off more than is needed means that you have less CO2 to unlock oxygen, which means that it takes longer to get it where it is needed. In the long run, chronic Overbreathing and blowing off too much CO2 also causes your body to adapt in some less-than-optimal ways. One way that it adapts is by lowering the set point for when you trigger the “I can't catch my breath” feeling that we all dread so much. This is caused by rising levels of CO2 and your body's tolerance to it - the more it can tolerate the harder you can work before triggering that feeling. When you chronically breathe out too much CO2, especially at rest or during your daily activities, then you create a new, lower set point for your body to trigger that feeling. Your body adapts to the lower levels of CO2 by becoming less tolerant and more sensitive to it, which is the opposite of what we want on the trail. The other way that your body adapts to chronically lowered levels of CO2 is to break down bicarbonate to maintain blood pH balance. Your body requires a strict Acid/ Base balance in the blood and Overbreathing creates a shift in that balance that your body has to react to. By breaking down the bicarbonate that is in the blood your body keeps the pH level balanced, however this comes at a price. You now have less bicarbonate available to buffer lactic acid and the acidic environment created by hard efforts. This means you are less able to deal with this environment and your ability to push hard is diminished.  So while it may not seem like a big deal, Overbreathing creates both short- and long-term problems that affect your health and performance. The good news is that it isn't hard to fix and just requires some time and attention. The main thing you can do is to shift to nose breathing and become more conscious of your breathing. Check in on your breathing throughout the day and make sure you aren't mouth breathing or Overbreathing. By simply doing these two things you will make a big impact. You can also spend some time each day doing Breathwork, which is just a way to help you slow down your breathing while creating a higher CO2 environment for your body to adapt to. Something as simple as breathing in to a 4 count and out to a 6 count for 5 minutes can start you in the right direction. As a side note, Breathwork is basically a form of meditation, which has been shown to have its own benefits for focus, stress levels and health. There is also a lot of science behind these practices now, making them more mainstream and less fringe than in the past. If you care about your health and fitness then you have to include breathing as part of your overall focus. Ignoring it while spending time and energy on things like cardio and strength training is not only holding you back but potentially having a negative impact on your health. Everything you do starts with your breathing and so spending some time and energy on optimizing it only makes sense. Until next time… Ride Strong, James Wilson MTB Strength Training Systems p.s. I know how important breathing is to your health and performance, which is why I created the Guide To Better Breathing For MTB. In this 40 page manual you'll learn everything you need to know to understand what makes up optimal breathing and how you can apply it to your daily life, your workouts and your rides. It's the only breathing guide made by a rider for fellow riders and is guaranteed to help improve your health, performance and mindset. Sure, there's a lot of great free info out there about breathing but if you want to cut out the guesswork around what to do and how to get started, plus having it explained in a MTB specific context, then click the link below to get your copy of the Guide To Better Breathing For MTB.  Click Here To Get You Copy Of The Guide To Better Breathing For MTB  

Get a free nursing lab values cheat sheet at NURSING.com/63labs   What is the Lab Name for Osmolality Lab Values? Osmolality   What is Osmolality in terms of Nursing Labs? Osmolality is a measure of the particles in solution. The size, shape, and charge of the particles do not impact the osmolality   What is the Normal Range for Osmolality? 261 – 280 mOsm/kg   What are the Indications for Osmolality? Monitor: Electrolyte balance Acid-Base balance Hydration Evaluate function of antidiuretic hormone.   What would cause Increased Levels of Osmolality? Dehydration Azotemia Hypercalcemia Hyperosmolar Hyperglycemia Syndrome (HHS) Hypernatremia Diabetes Insipidus Hyperglycemia Mannitol therapy Uremia Severe pyelonephritis Shock Ketosis     What would cause Decreased Levels of Osmolality? Hyponatremia Syndrome of Inappropriate Antidiuretic Hormone (SIADH) Overhydration

References for Chapter 10We did not mention many references in our discussion today but our listeners may enjoy some of the references below. Effects of pH on Potassium: New Explanations for Old Observations - PMC although the focus of this article is on potassium, this elegant review by Aronson and Giebisch reviews intracellular shifts as it relates to pH and K+.Josh swooned for Figure 10-1 is this right? Which figure was it? which shows the relationship between [H+] and pH. You can find this figure in the original reference from Halperin ML and others, Figure 1 here. Factors That Control the Effect of pH on Glycolysis in Leukocytes Here's Leticia Rolon's favorite Henderson-Hasselbalch calculator website: ​​Henderson-Hasselbalch Calculator | Buffer Solutions [hint! for this site, use the bicarbonate (or “total CO2”) for A- and PCO2 for the HA] There's also a cooking tab for converting units! Fundamentals of Arterial Blood Gas Interpretation - PMC this review published posthumously from the late but beloved Jerry Yee and his group at Henry Ford Hospital, explores the details and underpinnings of our understandings of arterial blood gas interpretation (and this also addresses how our colleagues in clinical chemistry measure total CO2 - which JC referenced- but JC said “machine” and our colleagues prefer the word “instrument.”)Amy went deep on bicarbonate in respiratory acidosis. Here are her refs:Sodium bicarbonate therapy for acute respiratory acidosisSodium Bicarbonate in Respiratory AcidosisBicarbonate therapy in severe metabolic acidosisEffect of Intravenous Sodium Bicarbonate on Ventilation, Gas Exchange, and Acid-Base Balance in Patients with Chronic Pulmonary InsufficiencyBicarbonate Therapy in Severe Metabolic Acidosis | American Society of Nephrology this review article from Sabatini and Kurtzman addresses the issues regarding bicarbonate therapy including theoretical intracellular acidosis. Bicarbonate in DKA? Don't do it: Bicarbonate in diabetic ketoacidosis - a systematic review Here's a review from Bushinsky and Krieger on the effect acidosis on bone https://www.sciencedirect.com/science/article/abs/pii/S0085253822002174Here is the primary resource that Anna used in here investigation of meat replacements Nutritional Composition of Novel Plant-Based Meat Alternatives and Traditional Animal-Based MeatsWe enjoyed this paper that Dr. Rose references from the Journal of Clinical Investigation 1955 in which investigators infused HCl into nephrectomized dogs and observed changes in extracellular ions. https://www.jci.org/articles/view/103073/pdWe wondered about the amino acids/protein in some available meat alternatives they are explored in this article in the journal Amino Acids: Protein content and amino acid composition of commercially available plant-based protein isolates - PMC and you may enjoy this exploration of the nutritional value of these foods: Full article: Examination of the nutritional composition of alternative beef burgers available in the United StatesOutlineChapter 10: Acid-Base Physiology - H concentration regulated tightly - Normal H+ is 40 nm/L - This one millionth the concentration of Na and K - It needs to be this dilute because H+ fucks shit up - Especially proteins - Cool foot note H+ actually exists as H3O+ - Under normal conditions the H+ concentration varies little from normal due to three steps - Chemical buffering by extracellular and intracellular bufffers - Control of partial pressure of CO2 by alterations of alveolar ventilation - Control of plasma bicarbonate by changes in renal H+ excretion - Acid and bases - Use definition by Bronsted - Acid can donate protons - Base can accept protons - There are two classes of acids** - Carbonic acid H2CO3 - Each day 15000 mmol of CO2 are generated - CO2 not acid but combines with water to form carbonic acid H2CO3 - CO2 cleared by the lungs - Noncarbonic acid - Formed from metabolism of protein. Sulfur containing AA generate H2SO4. Only 50-100 mEq of acid produced from these sources. - Cleared by the kidneys - Law of Mass Action - Velocity of reaction proportional to the product of the concentrations of the reactants - Goes through mass action formula for water - Concludes that water has H of 155 nanoM/L, more than the 40 in plasma - Says you can do the same mass experiment for every acid in the body - Can do it also for bases but he is not going to. - Acids and Bases can be strong or weak - Strong acids completely dissociate - Weak acids not so much - H2PO4 is only 80% dissociated - Weak acids are the principle buffers in the body - Then he goes through how H is measured in the blood and it becomes clear why pH is a logical way to measure. - Then there is a lot of math - HH equation - Derives it - Then uses it to look at phos. Very interesting application - Buffers - Goes tot he phosphate well again. Amazing math describing how powerful buffers can be - Big picture the closer the pKa is to the starting pH the better buffer, i.e. it can absorb lots of OH or H without appreciably changing pH - HCO3 CO2 system - H2CO3 to H + HCO3 has a PKA of 2.72 but then lots of Math and the bicarb buffer system has a pKa of 6.1 - But the real power of the bicarb buffer is that it is not a sealed system. The ability to ventilate and keep CO2 constant increases the buffering efficiency by 11 fold and the ability to lower the CO2 below normal increases 18 fold. - Isohydric principle - There is only one hydrogen ion concentration and since that is a critical part of the buffer equation, all buffer eq are linked and you can understand all of them by understanding one of them. So we just can look at bicarb and understand the totality of acid base. - Bicarb is the most important buffer because - High concentration in plasma - Ability for CO2 to ventilate - Other buffers include - Bone - Bone is more than just inorganic reaction - Live bone releases more calcium in response to an acid load than dead bone - More effect with metabolic acidosis than respiratory acidosis - Hgb - Phosphate - Protein

In this episode, we review the high-yield topic of Acid-Base Disorders from the Renal section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets --- Send in a voice message: https://anchor.fm/medbulletsstep1/message

In this episode, Anil Harrison, MD, speaks with Paul Shiu, DO, about 3 patient case presentations with mixed acid-base disorders, including concomitant metabolic acidosis and metabolic alkalosis.

In deze aflevering van Intensief de Podcast bespreek ik samen met Thomas Smits alles omtrent vocht toediening en fluid responsiveness. Thomas is IC-verpleegkundige en verplegingswetenschapper en heeft tijdens zijn studie veel expertise opgedaan over het bepalen van fluid responsiveness en zal deze expertise met ons delen. We bespreken de o.a. volgende onderwerpen:Wat is fluid responsiveness en het Frank-Starling principe?Waarom geven we vocht aan onze IC-patiënten?Waarom moeten we vocht als medicijn gaan zien?Waarom zijn tachycardie, hypotensie, een lage CVD en een hoog lactaat slechte tekenen  voor fluid responsiveness? En wat zijn dynamische en statische parameters?Wat is een fluid challenge en een passive leg raise?Hoe kan je de beademingsmachine gebruiken om fluid responsiveness te bepalen?Waarom moeten we vocht met een drukzak toedienen en niet met een infuuspomp?Wat zijn de nieuwste technieken en hoe ziet de toekomst eruit?Bronnen:CV Physiology | Frank-Starling MechanismFluid responsiveness in acute circulatory failure | Journal of Intensive CareFluid challenges in intensive care: the FENICE studyIV Fluid Overload: Don't Drown your Patients!Ventricular Pressure-Volume Relationship: Preload, Afterload, Stroke Volume, Wall Stress & Frank-Starling's law – ECG & ECHOHypotension: Differential Diagnosis – emupdatesTachycardia DDx • LITFL • CCC Differential DiagnosisWill This Hemodynamically Unstable Patient Respond to a Bolus of Intravenous Fluids? | Acid Base, Electrolytes, Fluids | JAMA | JAMA NetworkNoninterventional follow‐up vs fluid bolus in RESPONSE to oliguria—The RESPONSE trial protocol and statistical analysis plan Fluid Bolus in Resuscitation: Pressure Bag vs. 999ml/hr on the IV PumpPrediction of fluid responsiveness. What's new?Hoeveel zout mag ik eten? | VoedingscentrumBalanced Crystalloids Versus Saline in Critically Ill Adults: A Systematic Review and Meta-analysisEffect of a fluid bolus on cardiovascular collapse among critically ill adults undergoing tracheal intubation (PrePARE): a randomised controlled trial Effect of Fluid Bolus Administration on Cardiovascular Collapse Among Critically Ill Patients Undergoing Tracheal Intubation (PREPAREBedankt voor het luisteren!Volg @intensiefdepodcast op InstagramVragen? intensiefdepodcast@gmail.com

In this episode, Dr Harrison speaks with Paul Shiu, MD, about the order and disorder of acid-base basics, including the interpretation of arterial blood gasses (ABGs) and the various respiratory and metabolic disorders that cause abnormality in ABGs.

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat coming to you from Children's Healthcare of Atlanta/Emory University School of Medicine and I'm Rahul Damania from Cleveland Clinic Children's Hospital. We are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let's get into our episode: In today's episode, we discuss about a 12-year-old male with lethargy after ingestion. Here's the case presented by Rahul: A 12-year-old male is found unresponsive at home. He was previously well and has no relevant past medical history. The mother states that he was recently in an argument with his sister and thought he was going into his room to “have some space.” The mother noticed the patient was in his room for about 1 hour. After coming into the room she noticed him drooling, minimally responsive, and cold to the touch. The patient was noted to be moaning in pain pointing to his abdomen and breathing fast. Dark red vomitus was surrounding the patient. The mother called 911 as she was concerned about his neurological state. With 911 on the way, the mother noticed a set of empty vitamins next to the patient. She noted that these were the iron pills the patient's sister was on for anemia. EMS arrives for acute stabilization, and the patient is brought to the ED. En route, serum glucose was normal. The patient presents to the ED with hypothermia, tachycardia, tachypnea, and hypertension. His GCS is 8, he has poor peripheral perfusion and a diffusely tender abdomen. He continues to have hematemesis and is intubated for airway protection along with declining neurological status. After resuscitation, he presents to the Pediatric ICU. Upon intubation, an arterial blood gas is drawn. His pH is 7.22/34/110/-6 — serum HCO3 is 16, and his AG is elevated. To summarize key elements from this case, this patient has: Lethargy and unresponsiveness after acute ingestion. His hematemesis is most likely related to his acute ingestion. And finally, he has an anion gap metabolic acidosis, as evidenced by his low pH and low HCO3. All of these salient factors bring up the concern for acute iron ingestion! In today's episode, we will not only go through acute management pearls for iron poisoning, but also go back to the fundamentals, and cover ACID BASE disorders. We will break this episode down into giving a broad overview of acid base, build a stepwise approach, and apply our knowledge with integrated cases. We will use a physiologic approach to cover this topic! Pradip, can you give us a quick overview of some general principles when it comes to tackling this high-yield critical care topic? Absolutely, internal acid base homeostasis is paramount for maintaining life. Moreover, we know that accurate and timely interpretation of an acid–base disorder can be lifesaving. When we conceptualize acid base today, we will focus on pH, HCO3, and CO2. As we go into each disorder keep in mind to always correlate your interpretation of blood gasses to the clinical status of the patient. Going back to basic chemistry, can you comment on the relationship between CO2 and HCO3? Yes, now this is a throwback. However, we have to review the Henderson–Hasselbalch equation. The equation has constants & logs involved, however in general this equation shows that the pH is determined by the ratio of the serum bicarbonate (HCO3) concentration and the PCO2, not by the value of either one alone. In general, an acid–base disorder is called “respiratory” when it is caused by a primary abnormality in respiratory function (i.e., a change in the PaCO2) and “metabolic” when the primary change is attributed to a variation in the bicarbonate concentration. Now that we have some fundamentals down, let's move into definitions. Can you define acidemia and alkalemia and comment on how...

Neben relationalen Datenbanken gibt es noch eine ganz andere Welt: NoSQL.Doch wofür steht eigentlich NoSQL? Kein SQL? Not Only SQL? Was ist eigentlich die Geschichte hinter dem Hype? Warum wurde diese Art von Datenbanken erfunden? Wofür sind diese gut? Folgen NoSQL Datenbank auch dem ACID-Concept? Was ist Eventual Consistency? Und was sind Neo4J, M3, Cassandra, und Memcached für Datenbanken? Eine Episode voller Buzzwords … Hoffen wir auf ein Bingo.Bonus: Warum Wolfgang keinen Manta fährt und ob Andy bald mit einem Ferrari zum einkaufen fährt.Feedback an stehtisch@engineeringkiosk.dev oder via Twitter an https://twitter.com/EngKioskLinksACID: https://de.wikipedia.org/wiki/ACIDBASE: https://db-engines.com/de/article/BASECAP-Theorem: https://de.wikipedia.org/wiki/CAP-TheoremEventual Consistency: https://de.wikipedia.org/wiki/Konsistenz_(Datenspeicherung)#Verteilte_SystemeMichael Stonebraker / The End of an Architectural Era (It's Time for a Complete Rewrite): http://nms.csail.mit.edu/~stavros/pubs/hstore.pdfMongoDB: https://www.mongodb.com/Presto: https://prestodb.io/SAP HANA: https://www.sap.com/germany/products/hana.htmlRedis: https://redis.io/Neo4J: https://neo4j.com/M3: https://m3db.io/InfluxDB: https://www.influxdata.com/VictoriaMetrics: https://victoriametrics.com/Cassandra: https://cassandra.apache.org/Memcached: https://memcached.org/MySQL: https://www.mysql.com/de/MySQL Memcached Plugin: https://dev.mysql.com/doc/refman/5.6/en/innodb-memcached.htmlSprungmarken(00:00:00) Intro(00:00:53) Wolfgangs Auto, Entlastungspaket in Deutschland(00:03:23) Heutiges Thema: NoSQL Datenbanken und CO2-Einsparung durch Datenbank-Optimierungen(00:07:20) Was ist anders zur Episode 19 (Datenbanken) und ist NoSQL überhaupt noch ein Thema?(00:08:39) Was verstehen wir unter dem Begriff NoSQL und woher kommt es eigentlich?(00:15:58) Tip: Für Side Projects besser vertikal anstatt horizontal skalieren(00:16:50) NoSQL: Speziellere Lösungen mit Fokus auf Einfachheit und Benutzerfreundlichkeit(00:18:38) Braucht man heute noch Datenbank-Administratoren (DBA)?(00:21:13) Der Job des klassischen System-Administrator ist weiterhin relevant(00:23:15) Gibt es wirklich keine Datenbank-Schemas in der NoSQL-Welt?(00:27:23) Schema-Lose Möglichkeit in relationalen Datenbanken und Arbeit in die Datenbank oder Software auslagern(00:30:53) NoSQL hat die ACID-Properties aufgeweicht und warum ACID nachteilig für die Skalierung ist(00:33:28) Das NoSQL BASE Akronym(00:36:15) Der Client muss die Datenbank ordentlich nuzten um ACID-Garantien zu bekommen(00:41:35) Was bedeutet eigentlich NoSQL? Kein SQL? Not Only SQL?(00:43:38) Haupt-Speicher Datenbanken und was SAP damit zu tun hat(00:48:02) Was ist Neo4J für eine Datenbank und welcher Use-Case kann damit abgedeckt werden?(00:50:49) Was ist M3 für eine Datenbank und welcher Use-Case kann damit abgedeckt werden?(00:53:06) Was ist Cassandra für eine Datenbank und welcher Use-Case kann damit abgedeckt werden?(00:54:20) Was ist Memcached für eine Datenbank und welcher Use-Case kann damit abgedeckt werden?(00:58:44) OutroHostsWolfgang Gassler (https://twitter.com/schafele)Andy Grunwald (https://twitter.com/andygrunwald)Engineering Kiosk Podcast: Anfragen an stehtisch@engineeringkiosk.dev oder via Twitter an https://twitter.com/EngKiosk

Raad ChowdhuryNicole ShmidtSrikanth BathiniSharmi HaquePhysiology and pathophysiology of the calcium-sensing receptor in the kidney | American Journal of Physiology-Renal Physiology. American Journal of Physiology-Renal Physiology. Published 2020. https://dx.doi.org/10.1152%2Fajprenal.00608.2009Rondon H, Badireddy M. Hyponatremia. PubMed. Published 2020. https://www.ncbi.nlm.nih.gov/books/NBK470386/Asonitis N, Kassi E, Kokkinos M, Giovanopoulos I, Petychaki F, Gogas H. Hypercalcemia of malignancy treated with cinacalcet. Endocrinology, Diabetes & Metabolism Case Reports. 2017;2017. doi:10.1530/edm-17-0118Ayus JC, Moritz ML. Misconceptions and Barriers to the Use of Hypertonic Saline to Treat Hyponatremic Encephalopathy. Frontiers in Medicine. 2019;6. doi:10.3389/fmed.2019.00047Schrier RW, Gross P, Gheorghiade M, et al. Tolvaptan, a Selective Oral Vasopressin V2-Receptor Antagonist, for Hyponatremia. New England Journal of Medicine. 2006;355(20):2099-2112. doi:10.1056/nejmoa065181Sood L, Sterns RH, Hix JK, Silver SM, Chen L. Hypertonic saline and desmopressin: a simple strategy for safe correction of severe hyponatremia. American Journal of Kidney Diseases: The Official Journal of the National Kidney Foundation. 2013;61(4):571-578. doi:10.1053/j.ajkd.2012.11.032Burton David Rose. Clinical Physiology of Acid-Base and Electrolyte Disorders. Mcgraw-Hill; 2020.LeGrand SB, Leskuski D, Zama I. Narrative Review: Furosemide for Hypercalcemia: An Unproven yet Common Practice. Annals of Internal Medicine. 2008;149(4):259. doi:10.7326/0003-4819-149-4-200808190-00007Campbell OM. Women in White Coats : How the First Women Doctors Changed the World of Medicine. Park Row Books; 2022.Cheungpasitporn W, Suksaranjit P, Chanprasert S. Pathophysiology of vomiting-induced hypokalemia and diagnostic approach. The American Journal of Emergency Medicine. 2012;30(2):384. doi:10.1016/j.ajem.2011.10.005

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Welcome to our episode on the ever-tricky acid base disturbances! Here we delve deep into metabolic and respiratory acidoses and alkaloses, providing you with common clinical scenarios AND useful approaches to these problems. Enjoy!

This week, Rob and Zach will be teaching you everything you need to know about Acid Base Disorders & ABG InterpretationWe will be discussing:Definition of Acidosis and AlkalosisComplicationsCompensation MechanismsABG InterpretationTo follow along with Notes & Illustrations for our podcasts please become a member on our website! https://www.ninjanerd.org/podcast/acid-base-disorders-abg-interpretationFollow us on:YouTube: https://www.youtube.com/ninjanerdscienceInstagram: https://www.instagram.com/ninjanerdlecturesFacebook: https://www.facebook.com/NinjaNerdLecturesTwitter: https://twitter.com/ninjanerdsciDiscord: https://discord.com/invite/3srTG4dngWTikTok: https://www.tiktok.com/@ninjanerdlecturesSupport the show (https://paypal.me/ninjanerdscience)

Looking for more information on this topic? Check out the Acid-Base Disorders: Putting it All Together brick. If you enjoyed this episode, we'd love for you to leave a review on Apple Podcasts.  It helps with our visibility, and the more med students (or future med students) listen to the podcast, the more we can provide to the future physicians of the world. Follow USMLE-Rx at: Facebook: www.facebook.com/usmlerx Blog: www.firstaidteam.com Twitter: https://twitter.com/firstaidteam Instagram: https://www.instagram.com/firstaidteam/ YouTube: www.youtube.com/USMLERX Learn how you can access over 150 of our bricks for FREE: https://usmlerx.wpengine.com/free-bricks/ from our Musculoskeletal, Skin, and Connective Tissue collection, which is available for free. Learn more about Rx Bricks by signing up for a free USMLE-Rx account: www.usmle-rx.com You will get 5 days of full access to our Rx360+ program, including nearly 800 Rx Bricks.  After the 5-day period, you will still be able to access over 150 free bricks, including the entire collections for General Microbiology and Cellular and Molecular Biology.

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Aya, Abe, and Hunt talk Ascending Tubule, Connecting Acid-Base with Kidneys, and Concentration Gradients

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We are so privileged to interview Professor David Story. Professor David Story is foundation chair of Anaesthesia and Deputy Director of the Centre for Integrated Critical Care at the University of Melbourne. He is a part-time staff anaesthetist at the Austin Hospital in Melbourne where his clinical work is predominantly perioperative care for sicker adults including for liver transplantation.His research includes perioperative outcomes and models of care; applied physiology including acid-base disorders; environmental aspects of anaesthesia; He studied medicine at Monash University and also graduated with a bachelor of medical sciences on exercise at high altitude. David received his FANZCA in 1997. His doctorate from the University of Melbourne (2004) is on simplifying the Stewart approach to acid-base disorders.Besides being on a number of important committees, He was an examiner in the ANZCA primary exam for 12 years. Here are some of the resources mentioned. The Stewart approach apphttps://www.abgst.altervista.orgA couple of Prof Story's Articles:Stewart Acid-Base: A Simplified Bedside Approachhttps://emcrit.org/wp-content/uploads/2016/05/27140683_-Stewart-Acid-Base_-A-Simplified-Bedside-Approach.pdfBench-to-bedside review: a brief history of clinical acid-basehttps://pubmed.ncbi.nlm.nih.gov/15312207/Please support us on our patreonhttps://www.patreon.com/anaesthesiaAll proceeds will go to fund a fellow to help train anaesthetists in developing countries.and check us out on iTunes at https://podcasts.apple.com/au/podcast/anaesthesia-coffee-break/id1540682318Or spotify athttps://open.spotify.com/show/0rnOhhB9IGqgBmgPyNy91s?si=C2uKucgjRomqxWyXvEkKzg&dl_branch=1If you enjoyed this content please like and subscribePlease post any comments or questions below. Check out www.anaesthesiacollective.com and sign up to the ABCs of Anaesthesia facebook group for other content.Any questions please email abcsofanaesthesia@gmail.comDisclaimer: The information contained in this video/audio/graphic is for medical practitioner education only. It is not and will not be relevant for the general public.Where applicable patients have given written informed consent to the use of their images in video/photography and aware that it will be published online and visible by medical practitioners and the general public.This contains general information about medical conditions and treatments. The information is not advice and should not be treated as such. The medical information is provided “as is” without any representations or warranties, express or implied. The presenter makes no representations or warranties in relation to the medical information on this video. You must not rely on the information as an alternative to assessing and managing your patient with your treating team and consultant. You should seek your own advice from your medical practitioner in relation to any of the topics discussed in this episode' Medical information can change rapidly, and the author/s make all reasonable attempts to provide accurate information at the time of filming. There is no guarantee that the information will be accurate at the time of viewingThe information provided is within the scope of a specialist anaesthetist (FANZCA) working in Australia.The information presented here does not represent the views of any hospital or ANZCA.These videos are solely for training and education of medical practitioners, and are not an advertisement. They were not sponsored and offer no discounts, gifts or other inducements. This disclaimer was created based on a Contractology template available at http://www.contractology.com.

In this episode, we review the high-yield topic of Acid-Base Differential Diagnosis from the Renal section. --- Send in a voice message: https://anchor.fm/medbulletsstep1/message

Today we will be covering the importance of fluid in the body and how the electrolyte you consume can affect your health. This is kind of an introduction to pathophysiology, but you will also be coving these topics in your physiology class. This is a very important topic to discuss before going into the diseases that are talked about in pathophysiology because a lot of what is discussed here is related to how the body is going to function and balance electrolytes in disease-states. Afterward, I will cover acid-base imbalances on a surface level understanding, just as an introduction. I really encourage you to look up the pathways in your own time to get a better understanding of how the body compensates for a pH imbalance! Sources: 1. Hubert RJ, VanMeter KC. Gould's Pathophysiology for the Health Professions. 6th ed. St. Louis, MO; Elsevier. 2018.

A quick, problem-based review of the high-yield topics covering the STEP 2 Electrolytes and Acid/Base subject matter. --- Support this podcast: https://anchor.fm/usmle/support

Welcome to Electrolytes/Acid-Base Part 2. Don't forget to check out our website to download your free BINGO sheet in order to get guaranteed free merchandise. Have a wonderful day. Cheer! --- Support this podcast: https://anchor.fm/usmle/support

2021 is off to a great start with our first episode covering all things electrolytes/acid-base. We have plenty of things in store for you all, such as practice exams and interactive videos, so keep in touch via our website (buzzwordsmed.com) and socials. This episode covers some complex, high-yield topics, primarily on electrolyte management. Stay tuned for part 2 where we finish off electrolytes and dive into Acid-Base. Cheers! --- Support this podcast: https://anchor.fm/usmle/support

ABG & Fluids

On this episode of humanOS Radio, I speak with Lynda Frassetto. Lynda is a Professor Emeritus of Medicine in the Division of Nephrology at UCSF. During her research career, she and her colleagues investigated regulation of acid-base balance in both healthy and older people, as well as dietary influences on acid-base balance.  In particular, she has explored how the ratios of potassium to sodium, as well as base to chloride, differ in the modern diet versus the ancestral diet, and how these changes may be linked to greater risk of chronic disease as we get older.  Anthropological evidence suggests that ancient hominids consumed far less sodium and far more potassium, and specifically more potassium alkali salts (primarily from wild plants). The reduction in potential base in the modern diet increases the net systemic acid load, and this in turn may take a physiological toll in myriad ways. Chronic acid load appears to play a role in osteoporosis, hypertension, cardiovascular disease, and even age-related decline in growth hormone secretion. Naturally, lots of questions emerge from this idea. Which nutritional components determine whether a diet is net acid-producing? And what can we do about it on an individual basis? Should we take potassium supplements to rectify the imbalance? Could restoring a healthy sodium to potassium ratio be a hidden anti-aging tool? To learn about how you can live a more alkaline life, check out the interview!

Pathopharmacology lecture

In this episode, we cover the following topics: In this new series, we are discussing database consistency models explained in three acts. This episode is "Act III: Eventual consistency saves the web (circa early 2000s)". We explain eventual consistency and the motivation behind the philosophy. The BASE acronym stands for three key properties of a distributed system that utilizes eventual consistency. We define and explain these BASE attributes: Basically available Soft state Eventual consistency We share the story of Werner Vogel's keynote at re:Invent 2018, where he outlined the reasons why DynamoDB was created. In particular, DynamoDB allows for an eventual consistency data model. Interestingly, the DynamoDB story closely parallels what happened when Chris was at Microsoft. It just happened at least 6 years earlier. We then wrap up everything we have learned about ACID, CAP, and BASE by providing some guidelines on when to choose ACID vs. BASE systems. Detailed Show NotesWant the complete episode outline with detailed notes? Sign up here: https://mobycast.fm/show-notes/Support Mobycasthttps://glow.fm/mobycastEnd SongWhisper In A Dream (Feathericci Remix) by UskmatuMore InfoFor a full transcription of this episode, please visit the episode webpage.We'd love to hear from you! You can reach us at: Web: https://mobycast.fm Voicemail: 844-818-0993 Email: ask@mobycast.fm Twitter: https://twitter.com/hashtag/mobycast Reddit: https://reddit.com/r/mobycast

In this episode, we cover the following topics: In this new series, we are discussing database consistency models explained in three acts. This episode is "Act II: The arrival of the Internet creates new challenges (circa 1998)". Problems with building large scale-out systems led to the "discovery" of the CAP theorem (by Eric Brewer of Inktomi). We explain what the CAP theorem postulates and break it down in understandable terms. The three properties of the CAP theorem are consistency, availability and partition tolerance. What exactly is meant by "partition tolerance"? A key implication of the CAP theorem is that must choose your priorities. As a system scales, it cannot be both available and consistent. We discuss Physalia, a technology developed by AWS for making Elastic Block Service (EBS) more resilient. The design of Physalia was inspired by the principles of the CAP theorem. We then take a personal story detour that is (mostly) related to the CAP theorem. It turns out, Eric Brewer and Chris share a common experience during the first Internet bubble. Detailed Show NotesWant the complete episode outline with detailed notes? Sign up here: https://mobycast.fm/show-notes/Support Mobycasthttps://glow.fm/mobycastEnd SongDisruption by Miquel SallaMore InfoFor a full transcription of this episode, please visit the episode webpage.We'd love to hear from you! You can reach us at: Web: https://mobycast.fm Voicemail: 844-818-0993 Email: ask@mobycast.fm Twitter: https://twitter.com/hashtag/mobycast Reddit: https://reddit.com/r/mobycast

In this episode, we cover the following topics: In this new series, we are discussing database consistency models explained in three acts. This episode is "Act I: Transaction processing (circa 1973)". We start with the motivation behind talking about database soup - why are ACID, CAP, and BASE important to understand? We define transaction processing and its origins. What exactly is a "transaction"? Transactions are governed by ACID semantics. We define and explain the four characteristics of the ACID acronym:: Atomicity Consistency Isolation Durability The computer scientist, Jim Gray, came up with the idea of ACID semantics in the late 1970's. We discuss some of the history behind this, along with a bizarre and tragic ending to his story. We also share a personal story about another important player in transaction processing, Phil Bernstein. Detailed Show NotesWant the complete episode outline with detailed notes? Sign up here: https://mobycast.fm/show-notes/Support Mobycasthttps://glow.fm/mobycastEnd SongTalcum by Lost LakeMore InfoFor a full transcription of this episode, please visit the episode webpage.We'd love to hear from you! You can reach us at: Web: https://mobycast.fm Voicemail: 844-818-0993 Email: ask@mobycast.fm Twitter: https://twitter.com/hashtag/mobycast Reddit: https://reddit.com/r/mobycast