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In this month's episode of Well Wisconsin Radio, ‘Living a Fulfilling Life'. We sit down with three Milwaukeeans, Ambrose Wilson-Brown, Marquayla Ellison, and Carmen Pitre, who have found their calling through the communities they are a part of, the service work they do, and their careers. We discuss how they discovered avenues to these parts of their life and ways others might find paths to a more fulfilling life for themselves. Ellastic Designs MiSpiBo Fitness Social X Milwaukee Sojourner Family Peace UN Declaration of Human Rights Project LEAD- United Way Sign up for MeQ at www.webmdhealth.com/wellwisconsin and complete a short questionnaire to begin your personalized experience. Talk to a WebMD health coach individually or sign up for group coaching today by calling 800-821-6591 The information in this podcast does not provide medical advice, diagnosis, or treatment. It should not be used as a substitution for healthcare from a licensed healthcare professional. Consult with your healthcare provider for individualized treatment or before beginning any new program.
In this episode, we sit down with Daniel Dickson, PhD who is a clinical psychologist. We discuss the complexities of sleep from insomnia to common sleep disturbances and mental health conditions, such as anxiety and depression, that can impact one's sleep. Dr. Dickson also shares practical advice for those looking to improve their sleep habits and overall well-being. Talk to a health coach individually or sign up for group coaching today by calling 800-821-6591 Sign up for MeQ at www.webmdhealth.com/wellwisconsin and complete a short questionnaire to begin your personalized experience. Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR) End the Insomnia Struggle: A Step-by-Step Guide to Help You Get to Sleep and Stay Asleep by Colleen Ehrnstrom PhD ABPP The information in this podcast does not provide medical advice, diagnosis, or treatment. It should not be used as a substitution for healthcare from a licensed healthcare professional. Consult with your healthcare provider for individualized treatment or before beginning any new program.
In this episode, we dive into the world of chronic health conditions, the leading cause of illness, disability, and death in America. We'll start by defining what a chronic condition is, explore the most common conditions, and discuss their shared risk factors. Joining us is Jillian Bodden Hoenisch, a nurse practitioner from UW Health, who shares her insights on disparities in health outcomes and advice for managing life with a chronic condition. Tune in for practical tips, lifestyle strategies, and resources to empower those navigating the complexities of chronic health management. UW Madison School of Medicine and Public Health Center for Health Disparities Research Neighborhood atlas: anyone can search it online and you can type in your zip code Your healthcare organization and your healthcare team. Ask for resources. UW Health Center for Wellness: Offers wellness consultations, health coaching, and group medical visits, amongst other things. Look for resources through your health insurance. Your county's aging and disability resource center (ADRC) Department of Health Services Advanced Care Planning Wisconsin Institute of Healthy Aging Workshop: Living Well with Chronic Conditions Talk to a health coach individually or sign up for group coaching today by calling 800-821-6591 Sign up for MeQ at www.webmdhealth.com/wellwisconsin and complete a short questionnaire to begin your personalized experience.
New research reveals managers are facing unprecedented levels of stress and burnout. MeQ co-founder Jan Bruce joins us to unpack data about manager wellbeing and shares practical strategies for building resilience in leadership roles. Discover why supporting your managers might be the most important investment your organization isn't making. Follow The Made Leader for more leadership insights and strategies. For the links mentioned, visit: https://growthsignals.co/
The REITE Club Podcast - Real Estate Investing for Canadians
Many entrepreneurs struggle with focusing on outcome goals that are ultimately out of their control, leading to feelings of imposter syndrome and a lack of confidence. But what if there's a way to shift your focus and regain control? In this episode, we explore the powerful difference between performance goals and outcome goals and how mastering this distinction can boost your confidence and propel your business forward. When you understand those things, a lot of this stuff just falls into place on its own accord. So yes, they are related because goal achievement skills are part of MEQ. - Nancy Morris In this episode, you will be able to: Mastering the Difference: Uncover the secrets to setting and achieving real estate performance and outcome goals. Conquering Imposter Syndrome: Discover how to overcome self-doubt and thrive in real estate entrepreneurship. Real Estate Investing Unveiled: Learn the proven tactics for effective and profitable real estate investment strategies. Blueprint for Success: Uncover the power of a clear and concise business plan in real estate entrepreneurship. Tech-Savvy Growth: Explore leveraging technology to scale and expand your real estate business. Tune in to listen to the full episode https://thereiteclub.com/en/podcasts Nancy Morris brings a unique perspective to the world of real estate investing with her master's degree in psychology and specialization in business psychology. As a returning guest on The REITE Club, Nancy consistently delivers valuable tips and insights for enhancing not only real estate investment businesses but also personal development. With her expertise in performance goals and outcome goals, Nancy guides entrepreneurs in overcoming imposter syndrome and developing effective strategies for real estate investing. Her emphasis on the importance of clear business plans and leveraging technology for business growth makes Nancy an invaluable resource for entrepreneurs and business professionals looking to boost their confidence and control in business management. Get in touch with Nancy Morris here: LinkedIn: https://www.linkedin.com/in/nmmorris Twitter: https://twitter.com/NancyMorris Website: http://www.nancymorris.com/ Email: Nancy@NancyMorris.com
Ce sont les consommateurs qui paieront la facture du lock-out au port de Montréal, préviennent des acteurs du milieu qui estiment que ce conflit de travail aura des conséquences catastrophiques sur l'économie dans son ensemble. Chaque jour où les activités au port sont arrêtées, des impacts économiques de près de 91 M$ se font ressentir au Québec. Entrevue avec Julie White, vice-présidente affaires publiques et porte-parole par intérim pour Manufacturiers et Exportateurs du Québec MEQ. Pour de l'information concernant l'utilisation de vos données personnelles - https://omnystudio.com/policies/listener/fr
Beaucoup de conflits de travail | Montée de l'antisémitisme | Des formations en premier soins en ligne, est-ce suffisant pour nos enfants? | Lock-out au Port de Montréal: ça va faire mal aux contribuables… | Francisation: des enseignants de la FAE en désaccord avec les décisions du gouvernement Dans cet épisode intégral du 12 novembre, en entrevue : Mathieu Laliberté, formateur de premiers soins. Julie White, vice-présidente affaires publiques et porte-parole par intérim pour Manufacturiers et Exportateurs du Québec MEQ. Mélanie Hubert, présidente de la Fédération autonome de l'enseignement FAE. Une production QUB Novembre 2024 Pour de l'information concernant l'utilisation de vos données personnelles - https://omnystudio.com/policies/listener/fr
In episode 96 of the pharmaceutical calculations podcast, Dr. Michael Danquah (michaeldanquah.com) walks you through a complex IV infusion rate problem involving potassium acetate, showing you how to accurately calculate the required flow rate in milliliters per hour (mL/hr) to deliver the desired mEq/hr.This episode was originally broadcast as a video on our YouTube channel: www.youtube.com/pharmaceuticalcalculationseasyAdditional Resources for Practice:Pharmaceutical Calculations: 1001 Questions with Answers: https://www.rxcalculations.com/shop/uncategorized/pharmaceutical-calculations-1001-questions-answers/NAPLEX Question Bank: https://www.rxcalculations.com/shop/uncategorized/gold-membership/Join Our Social Media Community:Website: http://www.rxcalculations.comForum: https://forum.rxcalculations.com/Facebook: https://www.facebbook.com/pharmaceuticalcalculationsTwitter: https://twitter.com/RxCalculationsInstagram: https://www.instagram.com/rxcalculationsYouTube: www.youtube.com/pharmaceuticalcalculationseasyAbout RxCalculations: RxCalculations helps you master pharmaceutical calculations. We make it so you never have to worry about failing an exam or compromising patient safety because of a calculations error. RxCalculations is a leading global educational service platform focused on developing top quality pharmaceutical calculations products to help prospective pharmacists and health care professionals all over the world resolve one of the biggest challenges related to their profession.Our top quality products include affordable courses, personal consults, books, video tutorials, timed quizzes and apps designed to make you an expert in solving any pharmaceutical calculations question. We also have the largest pharmaceutical calculations online question bank which has over 1000 questions covering every important calculations topic as well as step-by-step video solutions. With all these resources at your disposal we have all you need to not only master pharmacy calculations but ace every test as well as passing your board exams.
Review of the top 35 teams in the NFBC Main Event at the all star break - Tipton's MEQ update - how did the top 35 teams from last year rank at the all star break? - how did the top 35 at the all star break finish last year? - Bjorns Male Room
Research On Ghee: https://pubmed.ncbi.nlm.nih.gov/23923985/ Morning evening questionnaire (MEQ): https://reference.medscape.com/calculator/829/morningness-eveningness-questionnaire-meq Disclaimer: This episode is intended solely for educational purposes and opinions shared by the guest are his personal views. We do not seek to defame or harm any person/brand/product mentioned in the video. Our goal is to provide information to help audience make informed choices. Order 'Build, Don't Talk' (in English) here: https://amzn.eu/d/eCfijRu Order 'Build Don't Talk' (in Hindi) here: https://amzn.eu/d/4wZISO0 Subscribe to Our Other YouTube Channels:- https://www.youtube.com/@rajshamaniclips? https://www.youtube.com/@RajShamani.Shorts
JAMA. 2013;309(12):1241-1250Background Case reports as early as the 1950s suggested chelation of lead might reduce angina. The popularity of chelation accelerated around the turn of the century. Small underpowered trials of chelation were inconclusive. Mainstream medicine considered chelation unproven and potentially hazardous.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.Chelation with disodium EDTA binds divalent and some trivalent cations, including calcium, magnesium, lead, cadmium, zinc, iron, aluminum, and copper, which facilitates their urinary excretion. High dose vitamins are often co-administered with chelation.The NIH-funded Trial to Assess Chelation Therapy (TACT) trial was conducted to respond to the public health problem posed by EDTA chelation therapy: namely, that large numbers of patients could be exposed to undefined risks for unproven benefits. TACT was a double-blind placebo-controlled 2x2 factorial randomized trial enrolling 1708 patients to test chelation therapy.Patients Eligibility for TACT required patients be older than 50 years, have a creatinine of < 2 mg/dl, and have survived a previous myocardial infarction. Exclusion criteria included platelet count less than 100 000/μL, abnormal liver function, BP > 160/100 mm Hg, past intolerance to the chelation or vitamin components, chelation therapy within 5 years, coronary or carotid revascularization planned or having taken place within 6 months, cigarette smoking within 3 months, active heart failure or heart failure hospitalization within 6 months, or inability to tolerate 500-mL infusions weekly. Enrollment began in 2003 and follow-up continued until 2011. There were 134 sites; 60% of which were established chelation centers.Baseline Characteristics The median age of patients was 65 years, 18% were women and the median body mass index was 30. More than 90% of patients had had either percutaneous coronary intervention or coronary bypass surgery. Approximately 31% of patients had diabetes. Use of guideline directed medications was typical of a well-treated population of post-MI patients. Procedures The active 10-component chelation solution consisted of up to 3 g of disodium EDTA; 7 g of ascorbic acid; 2 g of magnesium chloride; 100 mg of procaine; 2500 U of unfractionated heparin; 2 mEq of potassium chloride; 840 mg of sodium bicarbonate; 250 mg of pantothenic acid; 100 mg of thiamine; 100 mg of pyridoxine; and sterile water to make up 500 mL of solution. The identical-appearing placebo solution consisted of 500 mL of normal saline and 1.2% dextrose (2.5 g total).The chelation or placebo infusions were administered through a peripheral intravenous line, weekly for the first 30 infusions, followed by an additional 10 infusions 2 to 8 weeks apart. Patient also received an oral vitamin-mineral regimen vs an oral placebo. In this review, we focus on the intention-to-treat comparison of EDTA chelation vs placebo.Endpoints The primary endpoint was a composite of death, reinfarction, stroke, coronary revascularization, or hospitalization for angina.TACT trialists had planned to enroll 2300 patients over three years with a follow-up of one year. Enrollment was slow, and with permission from the data safety monitoring board (DSMB) enrollment was decreased to 1700 patients and follow-up was extended. The resultant power was 85% to detect a 25% reduction in the primary endpoint assuming a 2.5% per year event rate in the placebo arm.Over the course of the trial, the DSMB requested 11 interim analyses of the data. Because of the increased monitoring, the level of statistical significance required for the primary endpoint was enhanced to a P value of less than 0.036.Results After a median follow-up of 55 months, a primary end point occurred in 222 (26%) of the chelation group and 261 (30%) of the placebo group (hazard ratio [HR]: 0.82 [95% CI: 0.69-0.99]; p= .035). There was no effect on total mortality (10% vs 11%, HR: 0.93, 95% CI: 0.70-1.25; p= 0.64). Myocardial infarction and coronary revascularization favored chelation (6% vs 8% and 15% vs 18%, respectively), however this did not reach statistical significance for either endpoints.Subgroup analysis revealed a potentially important heterogenous treatment effect. In patients with diabetes (about a third of patients) there was an approximate 40% reduction in the primary endpoint (HR: 0.61, 95% CI: 0.45-0.83; p= 0.002).There were no significant differences in adverse effects between the two groups.The trialists did sensitivity analyses centering on patients who withdrew from the trial or were lost to follow-up. The comparison of the 2 groups remained significant even if the percentage of events among withdrawn/lost patients in the active group was 25% higher than in the placebo group.Conclusions The results of the TACT trial surprised the cardiology community. Prior beliefs were pessimistic because heavy metals was not a proven causal factor in atherosclerosis. What's more, the majority of patients were enrolled from non-traditional medical centers.Yet the effect size was both clinically important and statistically significant. The effect size in the diabetes subgroup, which was pre-specified, was even larger and more robust statistically than the general results. In fact, there was essentially no signal of benefit from chelation in non-diabetic patients. If this was confirmed, it would be a major finding both therapeutically and scientifically, as it would have discovered heavy metal exposure as an important cause of atherosclerosis.The Journal of the American Medical Association published the manuscript along with an explanatory letter from the editors, and an accompanying editorial from Dr. Steve Nissen, which challenged the internal validity of the trial.The results of TACT did not lead to widespread adoption of chelation, but it did lead primary investigator Gervasio Lamas to seek (and obtain) funding for a TACT 2 trial to study chelation in patients with diabetes. Experts often refer to subgroup findings as “hypothesis-generating” and so it was with the TACT 1 and TACT 2 trials.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe
Greetings, and welcome back to the podcast. This episode, we are joined by Mr. Bob Dhillon - President & CEO of Mainstreet Equity - a TSX listed real estate company with a market cap of ~$2 billion.Mainstreet Equity is based in Calgary, Alberta, Canada, as at Q4 2023, assets are valued at CDN$3B+ with 17,000+ rental apartment units across western Canada (BC, AB, SK and Winnipeg). For over 22 years, Bob and Mainstreet have provided consistent, year over year, double digit returns to investors through MEQ's continued organic growth.In the 2019 Scotiabank Equity Research Daily Edge poll, MEQ led the Total Return Performance for the Canadian Listed Real Estate Sector, outperforming the TSX Real Estate Index at 89.9%. In a 20-year (2000 - 2020) stock performance comparison of the TSX, MEQ outperformed Amazon, Berkshire Hathaway and Royal Bank of Canada.Along with its healthy balance sheet success, Mainstreet is a strong and proud champion of affordable housing in western Canada.Bob is also the owner of National Payments, a Visa and MasterCard approved merchant-processing business in the financial services sector.In 2018, Bob gifted CDN$10M to the University of Lethbridge towards the creation of the Dhillon School of Business (DSB).Mr. Dhillon has been awarded numerous awards including: Appointed as Officer of the Order of Canada, the Queen Elizabeth II Platinum Jubilee Medal 2022 and Diamond Jubilee Medal, Appointed Honorary Consul General of Belize for Canada, Entrepreneur of the Year Prairies Real Estate and Construction (Ernst & Young 2015), Top 25 Canadian Immigrant Awards (Royal Bank of Canada, 2015), & Alberta's 50 Most Influential People (Alberta Venture Magazine, 2011).Mr. Dhillon sits on numerous boards including the Canada Mortgage and Housing Corporation (CMHC), Alberta Investment Management Corporation (AIMCo), Advisory Council for the Canada-India Business Council & Invest Alberta Corporation.Mr. Dhillon received a Master of Business Administration - Richard Ivey School of Business at the University of Western Ontario. Among other things, we sat down and discussed 19% interest rates, building a real estate business & why Canadian home prices are rising.Enjoy.Thank you to our sponsors.Without their support this episode would not be possible:Connate Water SolutionsGalatea TechnologiesEnergy Unitedheadracingcanada.comLearn more about each sponsor at the links above. Support the show
MEQ stands for Mindset, Emotional Intelligence and Leadership Qualities and is the foundation Dr. Sabine Charles uses to coach leaders and executives. Charles is an author, public speaker and professional certification exam tutor. Charles believes leadership is not just about vision; it's about creating a connection that inspires. She says with Leadership MEQ, her students develop the skills to lead not just with strategy, but also with heart. Charles puts her theories to the test via virtual leadership seminars and a hybrid course and gratitude and growth retreat this fall.
OutlineChapter 14- Hypovolemic States- Etiology - True volume depletion occurs when fluid is lost from from the extracellular fluid at a rate exceeding intake - Can come the GI tract - Lungs - Urine - Sequestration in the body in a “third space” that is not in equilibrium with the extracellular fluid. - When losses occur two responses ameliorate them - Our intake of Na and fluid is way above basal needs - This is not the case with anorexia or vomiting - The kidney responds by minimizing further urinary losses - This adaptive response is why diuretics do not cause progressive volume depletion - Initial volume loss stimulates RAAS, and possibly other compensatory mechanisms, resulting increased proximal and collecting tubule Na reabsorption. - This balances the diuretic effect resulting in a new steady state in 1-2weeks - New steady state means Na in = Na out - GI Losses - Stomach, pancreas, GB, and intestines secretes 3-6 liters a day. - Almost all is reabsorbed with only loss of 100-200 ml in stool a day - Volume depletion can result from surgical drainage or failure of reabsorption - Acid base disturbances with GI losses - Stomach losses cause metabolic alkalosis - Intestinal, pancreatic and biliary secretions are alkalotic so losing them causes metabolic acidosis - Fistulas, laxative abuse, diarrhea, ostomies, tube drainage - High content of potassium so associated with hypokalemia - [This is a mistake for stomach losses] - Bleeding from the GI tract can also cause volume depletion - No electrolyte disorders from this unless lactic acidosis - Renal losses - 130-180 liters filtered every day - 98-99% reabsorbed - Urine output of 1-2 liters - A small 1-2% decrease in reabsorption can lead to 2-4 liter increase in Na and Water excretion - 4 liters of urine output is the goal of therapeutic diuresis which means a reduction of fluid reabsorption of only 2% - Diuretics - Osmotic diuretics - Severe hyperglycemia can contribute to a fluid deficit of 8-10 Iiters - CKD with GFR < 25 are poor Na conservers - Obligate sodium losses of 10 to 40 mEq/day - Normal people can reduce obligate Na losses down to 5 mEq/day - Usually not a problem because most people eat way more than 10-40 mEq of Na a day. - Salt wasting nephropathies - Water losses of 2 liters a day - 100 mEq of Na a day - Tubular and interstitial diseases - Medullary cystic kidney - Mechanism - Increased urea can be an osmotic diuretic - Damage to tubular epithelium can make it aldo resistant - Inability to shut off natriuretic hormone (ANP?) - The decreased nephro number means they need to be able to decrease sodium reabsorption per nephron. This may not be able to be shut down acutely. - Experiment, salt wasters can stay in balance if sodium intake is slowly decreased. (Think weeks) - Talks about post obstruction diuresis - Says it is usually appropriate rather than inappropriate physiology. - Usually catch up solute and water clearance after releasing obstruction - Recommends 50-75/hr of half normal saline - Talks briefly about DI - Skin and respiratory losses - 700-1000 ml of water lost daily by evaporation, insensible losses (not sweat) - Can rise to 1-2 liters per hour in dry hot climate - 30-50 mEq/L Na - Thirst is primary compensation for this - Sweat sodium losses can result in hypovolemia - Burns and exudative skin losses changes the nature of fluid losses resulting in fluid losses more similar to plasma with a variable amount of protein - Bronchorrhea - Sequestration into a third space - Volume Deficiency produced by the loss of interstitial and intravascular fluid into a third space that is not in equilibrium with the extracellular fluid. - Hip fracture 1500-2000 into tissues adjacent to fxr - Intestinal obstruction, severe pancreatitis, crush injury, bleeding, peritonitis, obstruction of a major venous system - Difference between 3rd space and cirrhosis ascities - Rate of accumulation, if the rate is slow enough there is time for renal sodium and water compensation to maintain balance. - So cirrhotics get edema from salt retension and do not act as hypovolemia - Hemodynamic response to volume depletion - Initial volume deficit reduced venous return to heart - Detected by cardiopulmonary receptors in atria and pulmonary veins leading to sympathetic vasoconstriction in skin and skeletal muscle. - More marked depletion will result in decreased cardiac output and decrease in BP - This drop in BP is now detected by carotid and aortic arch baroreceptors resulting in splanchnic and renal circulation vasoconstriction - This maintains cardiac and cerebral circulation - Returns BP toward normal - Increase in BP due to increased venous return - Increased cardiac contractility and heart rate - Increased vascular resistance - Sympathetic tone - Renin leading to Ang2 - These can compensate for 500 ml of blood loss (10%) - Unless there is autonomic dysfunction - With 16-25% loss this will not compensate for BP when patient upright - Postural dizziness - Symptoms - Three sets of symptoms can occur in hypovolemic patients - Those related to the manner in which the fluid loss occurs - Vomiting - Diarrhea - Polyuria - Those due to volume depletion - Those due to the electrode and acid base disorders that can accompany volume depletion - The symptoms of volume depletion are primarily related to the decrease in tissue perfusion - Early symptoms - Lassitude - Fatiguability - Thirst - Muscle cramps - Postural dizziness - As it gets more severe - Abdominal pain - Chest pain - Lethargy - Confusion - Symptomatic hypovolemia is most common with isosmotic Na and water depletion - In contrast pure water loss, causes hypernatremia, which results in movement of water from the intracellular compartment to the extracellular compartment, so that 2/3s of volume loss comes from the intracellular compartment, which minimizes the decrease in perfusion - Electrolyte disorders and symptoms - Muscle weakness from hypokalemia - Polyuria/poly dips is from hyperglycemia and hypokalemia - Lethargy, confusion, Seizures, coma from hyponatremia, hypernatremia, hyperglycemia - Extreme salt craving is unique to adrenal insufficiency - Eating salt off hands ref 18 - Evaluation of the hypovolemic patient - Know that if the losses are insensible then the sodium should rise - Volume depletion refers to extracellular volume depletion of any cause, while dehydration refers to the presence of hypernatremia due to pure water loss. Such patients are also hypovolemic. - Physical exam is insensitive and nonspecific - Finding most sensitive and specific finding for bleeding is postural changes in blood pressure - I don't find this very specific at all! - Recommends laboratory confirmation regardless of physical exam - Skin and mucous membranes - Should return too shape quickly - Elastic property is called Turgur - Not reliable is patients older than 55 to 60 - Dry axilla - Dry mucus membranes - Dark skin in Addison's disease Frim increased ACTH - Arterial BP - As volume goes down so does arterial BP - Marked fluid loss leads to quiet korotkoff signs - Interpret BP in terms of the patients “normal BP” - Venous pressure - Best done by looking at the JVP - Right atrial and left atrial pressure - LV EDP is RAP + 5 mmHg - Be careful if valvular disease, right heart failure, cor pulmonare, - Figure 14-2 - Shock - 30% blood loss - Lab Data - Urine Na concentration - Should be less than 25 mmol/L, can go as low as 1 mmol/L - Metabolic alkalosis can throw this off - Look to the urine chloride - Figure 14-3 - Renal artery stenosis can throw this off - FENa - Mentions that it doesn't work so well at high GFR - Urine osmolality - Indicates ADH - Volume depletion often associated with urine osm > 450 - Impaired by - Renal disease - Osmotic diuretic - Diuretics - DI - Mentions that severe volume depletion and hypokalemia impairs urea retension in renal medulla - Points out that isotonic urine does not rule out hypovolemia - Mentions specific gravity - BUN and Cr concentration - Normal ratio is 10:1 - Volume depletion this goes to 20:1 - Serum Na - Talks about diarrhea - Difference between secretory diarrhea which is isotonic and just causes hypovolemia - And osmotic which results in a lower electrolyte content and development of hypernatremia - Talks about hyperglycemia - Also can cause the sodium to rise from the low electrolyte content of the urine - But the pseudohyponatraemia can protect against this - Plasma potassium - Treatment - Both oral and IV treatment can be used for volume replacement - The goal of therapy are to restore normovolemia - And to correct associated acid-base and electrolyte disorders - Oral Therapy - Usually can be accomplished with increased water and dietary sodium - May use salt tablets - Glucose often added to resuscitation fluids - Provides calories - Promotes intestinal Na reabsorption since there is coupled Na and Glucose similar to that seen in the proximal tubule - Rice based solutions provide more calories and amino acids which also promote sodium reabsorption - 80g/L of glucose with rice vs 20 g/L with glucose alone - IV therapy - Dextrose solutions - Physiologically equivalent to water - For correcting hypernatremia - For covering insensible losses - Watch for hyperglycemia - Footnote warns against giving sterile water - Saline solutions - Most hypovolemic patients have a water and a sodium deficit - Isotonic saline has a Na concentration of 154, similar to that of plasma see page 000 - Half-isotonic saline is equivalent to 550 ml of isotonic saline and 500 of free water. Is that a typo? - 3% is a liter of hypertonic saline and 359 extra mEq of Na - Dextrose in saline solutions - Give a small amount of calories, otherwise useless - Alkalinizing solutions - 7.5% NaHCO3 in 50 ml ampules 44 mEq of Na and 44 mEq of HCO3 - Treat metabolic acidosis or hyperkalemia - Why 44 mEq and not 50? - Do not give with calcium will form insoluble CaCO3 - Polyionic solutions - Ringers contains physiologic K and Ca - Lactated Ringers adds 28 mEq of lactate - Spreads myth of LR in lactic acidosis - Potassium chloride - Available as 2 mEq/mL - Do not give as a bolus as it can cause fatal hyperkalemia - Plasma volume expanders - Albumin, polygelastins, hetastarch are restricted to vascular space - 25% albumin can pull fluid into the vascular space - 25% albumin is an albumin concentration of 25 g/dL compare to physiologic 4 g/dL - Says it pulls in several times its own volume - 5% albumin is like giving plasma - Blood - Which fluid? - Look at osmolality, give hypotonic fluids to people with high osmolality - Must include all electrolytes - Example of adding 77 mEw of K to 0.45 NS and making it isotonic - DI can be replaced with dextrose solutions, pure water deficit - Case 14-3 - Diarrhea with metabolic acidosis - He chooses 0.25 NS with 44 mEq of NaCl and 44 NaHCO3 - Talks about blood and trauma - Some studies advocate delaying saline until penetrating trauma is corrected APR about to. Keep BP low to prevent bleeding. Worry about diluting coagulation factors - Only do this if the OR is quickly available - Volume deficit - Provides formula for water deficit and sodium deficit - Do not work for isotonic losses - Provides a table to adjust fluid loss based on changes in Hgb or HCTZ - Says difficult to estimate it from lab findings and calculations - Follow serial exams - Serial urine Na - Rate of replacement - Goal is not to give fluid but to induce a positive balance - Suggests 50-100 ml/hr over what is coming out of the body - Urine - Insensibles 30-50 - Diarrhea - Tubes - Hypovolemic shock - Due to bleeding - Sequesting in third space - Why shock? - Progressive volume depletion leads to - Increased sympathetic NS - Increased Ang 2 - Initially this maintains BP, cerebral and coronary circulation - But this can decrease splanchnic, renal and mucocutaneous perfusion - This leads to lactic acicosis - This can result in intracellular contents moving into circulation or translocation of gut bacteria - Early therapy to prevent irreversible shock - In dogs need to treat with in 2 hours - In humans may need more than 4 hours - Irreversible shock associated with pooling of blood in capillaries - Vasomotor paralysis - Hyperpolarization of vascular smooth muscle as depletion of ATP allows K to flowing out from K channels opening. Ca flows out too leading to vasodilation - Glyburide is an K-ATP channel inhibitor (?) caused increased vasoconstriction and BP - Pluggin of capillaries by neutrophils - Cerebral ischemia - Increased NO generation - Which Fluids? - Think of what is lost and replace that. - Bleeding think blood - Raise the hct but not above 35 - Acellular blood substitutes, looked bad at the time of this writing - Di aspirin cross linked hemoglobin had increased 2 and 28 day mortality vs saline - Colloids sound great but they fail in RCTs - SAFE - FEAST - Points out that saline replaces the interstitial losses why do we think those losses are unimportant - Pulmonary circulation issue - Pulmonary circulation is more leaky so oncotic pressure less effective there - Talks about the lungs be naturally protected from pulmonary edema - Rate of fluid - 1-2 liters in first hour - Suggests CVP or capillary wedge pressure during resuscitation - No refs in the rate of fluid administration section - Lactic acidosis - Points out that HCO can impair lactate utilization - Also states that arterial pH does not point out what is happening at the tissue level. Suggests mixed-venous sample.ReferencesJCI - Phenotypic and pharmacogenetic evaluation of patients with thiazide-induced hyponatremia and a nice review of this topic: Altered Prostaglandin Signaling as a Cause of Thiazide-Induced HyponatremiaThe electrolyte concentration of human gastric secretion. https://physoc.onlinelibrary.wiley.com/doi/10.1113/expphysiol.1960.sp001428A classic by Danovitch and Bricker: Reversibility of the “Salt-Losing” Tendency of Chronic Renal Failure | NEJMOsmotic Diuresis Due to Retained Urea after Release of Obstructive Uropathy | NEJMIs This Patient Hypovolemic? | Cardiology | JAMAAnd by the same author, a textbook: Steven McGee. 5th edition. Evidence-Based Physical Diagnosis Elsevier Philadelphia 2022. ISBN-13: 978-0323754835The clinical course and pathophysiological investigation of adolescent gestational diabetes insipidus: a case report | BMC Endocrine DisordersSensitivity and specificity of clinical signs for assessment of dehydration in endurance athletes | British Journal of Sports MedicineDiagnostic performance of serum blood urea nitrogen to creatinine ratio for distinguishing prerenal from intrinsic acute kidney injury in the emergency department | BMC NephrologyThe meaning of the blood urea nitrogen/creatinine ratio in acute kidney injury - PMCLanguage guiding therapy: the case for dehydration vs volume depletion https://www.acpjournals.org/doi/10.7326/0003-4819-127-9-199711010-00020?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmedValidation of a noninvasive monitor to continuously trend individual responses to hypovolemiaReferences for Anna's voice of God on Third Spacing : Shires Paper from 1964 (The ‘third space' – fact or fiction? )References for melanie's VOG:1. Appraising the Preclinical Evidence of the Role of the Renin-Angiotensin-Aldosterone System in Antenatal Programming of Maternal and Offspring Cardiovascular Health Across the Life Course: Moving the Field Forward: A Scientific Statement From the American Heart Association2. excellent review of RAAS in pregnancy: The enigma of continual plasma volume expansion in pregnancy: critical role of the renin-angiotensin-aldosterone systemhttps://journals-physiology-org.ezp-prod1.hul.harvard.edu/doi/full/10.1152/ajprenal.00129.20163. 10.1172/JCI107462- classic study in JCI of AngII responsiveness during pregnancy4. William's Obstetrics 26th edition!5. Feto-maternal osmotic balance at term. A prospective observational study
The Elective Rotation: A Critical Care Hospital Pharmacy Podcast
Show notes at pharmacyjoe.com/episode882. In this episode, I'll discuss the change in serum potassium after supplementation. The post 882: Does 10 mEq of Potassium Actually Increase Serum Potassium Levels By 0.1 mEq/L? appeared first on Pharmacy Joe.
The Elective Rotation: A Critical Care Hospital Pharmacy Podcast
Show notes at pharmacyjoe.com/episode882. In this episode, I ll discuss the change in serum potassium after supplementation. The post 882: Does 10 mEq of Potassium Actually Increase Serum Potassium Levels By 0.1 mEq/L? appeared first on Pharmacy Joe.
This week, our guest is Dr. Sabine Charles, Chief Executive Officer at Charles Financial Strategies and Chief Internal Auditor at Touro University. In this episode, Dr. Charles explores a diverse range of subjects related to enhancing emotional intelligence within the internal audit profession. The discussion spans topics such as distinguishing between EQ and MEQ, cultivating relationship skills from a CAE perspective, and effectively communicating in a remote setting. Be sure to connect with Dr. Charles on LinkedIn. AuditBoard and internal Audit 360 – Webinar: Rising to the Audit Analytics Challenge: How to Prioritize Efficiency, Accuracy, and Value (1 CPE) Also, be sure to follow us on our new social media accounts on LinkedIn, Instagram, and TikTok. Also be sure to sign up for The Audit Podcast newsletter and to check the full video interview on The Audit Podcast YouTube channel. * This podcast is brought to you by Greenskies Analytics, the services firm that helps auditors leap-frog up the analytics maturity model. Their approach for launching audit analytics programs with a series of proven quick-win analytics will guarantee the results worthy of the analytics hype. Whether your audit team needs a data strategy, methodology, governance, literacy, or anything else related to audit and analytics, schedule time with Greenskies Analytics.
In this episode of Tribe Talkin; we discuss: The Instacart's IPO, and where IPO's fit as an exit option. Trends we are seeing in the pricing of secondary share sales. Issues around minority shareholder oppression following action against Sleeping Duck. The challenges with selling a business with an earn out structure and why they often don't deliver for the entrepreneur. Why early stage businesses should stay away from traditional bank debt. What can be learnt from Meta's rollout of Threads. MEQ raising $6m for its AI enabled meat tech, and what we are seeing in AI. Tail winds occurring for AgTech and feedback we often get from investors. The Top 100 innovators list released by the Australian, with a few shout outs. What best in class SaaS metrics look like from the following report: https://chartmogul.com/reports/saas-growth-report/2023/ We'd appreciate a review and a rating of the podcast while you're here :) hello@tribeglobal.vc
ReferencesJC mentioned that the diagnostic accuracy of 24 hour urine collection increases with more collections! Metabolic evaluation of patients with recurrent idiopathic calcium nephrolithiasisWe didn't refer to a particular study on sodium intake and the 24 hour urine but this meta-analysis Comparison of 24‐hour urine and 24‐hour diet recall for estimating dietary sodium intake in populations: A systematic review and meta‐analysis - PMC 24‐hour diet recall underestimated population mean sodium intake.Anna looking up ace i and urinary sodium Effects of ACE inhibition on proximal tubule sodium transport | American Journal of Physiology-Renal PhysiologyThe original FENa paper by Espinel: The FeNa Test: Use in the Differential Diagnosis of Acute Renal Failure | JAMA | JAMA NetworkSchreir's replication and expansion of Espinel's data: Urinary diagnostic indices in acute renal failure: a prospective studyHere's a report from our own JC on the Diagnostic Utility of Serial Microscopic Examination of the Urinary Sediment in Acute Kidney Injury | American Society of NephrologyJC shared his journey regarding FENa and refers to his recent paper Concomitant Identification of Muddy Brown Granular Casts and Low Fractional Excretion of Urinary Sodium in AKIAnd Melanie's accompanying editorial Mind the Cast: FENa versus Microscopy in AKI : Kidney360 (with a great image from Samir Parikh)JC referenced this study from Schrier on FENa with a larger series: Urinary diagnostic indices in acute renal failure: a prospective studyNonoliguric Acute Renal Failure Associated with a Low Fractional Excretion of Sodium | Annals of Internal MedicineUrine sodium concentration to predict fluid responsiveness in oliguric ICU patients: a prospective multicenter observational study | Critical Care | Full TextA classic favorite: Acute renal success. The unexpected logic of oliguria in acute renal failure Marathon runners had granular casts in their urine without renal failure. Kidney Injury and Repair Biomarkers in Marathon RunnersCute piece from Rick Sterns on urine electrolytes! Managing electrolyte disorders: order a basic urine metabolic panelThe Urine Anion Gap: Common Misconceptions | American Society of NephrologyThe urine anion gap in context CJASNExcellent review from Halperin on urine chemistries (including some consideration of the TTKG): Use of Urine Electrolytes and Urine Osmolality in the Clinical Diagnosis of Fluid, Electrolytes, and Acid-Base Disorders - Kidney International ReportsRenal tubular acidosis (RTA): Recognize The Ammonium defect and pHorget the urine pH | SpringerLinkOutlineChapter 13- New part: Part 3, Physiologic approach to acid-base and electrolyte disorders - Do you remember the previous two parts? - Renal physiology - Regulation of water and electrolyte balance- Chapter 13: Meaning and application of urine chemistries - Measurement of urinary electrolyte concentrations, osmolality and pH helps diagnose some conditions - There are no fixed normal values - Kidney varies rate of excretion to match intake and endogenous production - Example: urine Na of 125/day can be normal if patient euvolemic on a normal diet, and wildly inappropriate in a patient who is volume depleted. - Urine chemistries are: - Useful - Simple - Widely available - Usually a random sample is adequate - 24-hour samples give additional context - Gives example of urinary potassium, with extra renal loss of K, urine K should be < 25, but if the patient has concurrent volume deficiency and urine output is only 500 mL, then urine K concentration can appropriately be as high as 40 mEq/L - Table 13-1 - Seems incomplete, see my notes on page 406 - What is Gravity ARF?- Sodium Excretion - Kidney varies Na to maintain effective circulating volume (I'd say volume homeostasis) - Urine Na affected by RAAS and ANP - Na concentration can be used to determine volume status - Urine Na < 20 is hypovolemia - Says it is especially helpful in determining the etiology of hyponatremia - Calls out SIADH and volume depletion - Used 40 mEq/L for SIADH - Also useful in AKI - Where differential is pre-renal vs ATN - In addition to urine Na (and FENa) look at urine osmolality - Again uses 40 mEq/l - Mentions FENa and urine osmolality - Urine Na can estimate dietary sodium intake - Suggests doing this during treatment of hypertension to assure dietary compliance - 24 hour urine Na is accurate with diuretics as long as the dose is stable and the drugs are chronic - Diuretics increase Na resorption in other segments of the tubule that are not affected by the diuretic - Points to increased AT2 induced proximal Na resorption and aldosterone induced DCT resoprtion - In HTN shoot for less than 100 mEq/Day - Urine Na useful in stones - Urine uric acid and urine Ca can cause stones and their handling is dependent on sodium - Low sodium diet can mask elevated excretion of these stone forming metabolites - 24-hour Na > 75 and should be enough sodium to avoid this pitfall - Pitfalls - Low urine sodium in bilateral renal artery stenosis or acute GN - High urine sodium with diuretics, aldo deficiency, advanced CKD - Altered water handling can also disrupt this - DI with 10 liters of urine and urine sodium excretion of 100 mEq is 10 mEq/L but in this case there is no volume deficiency - Opposite also important, a lot of water resorption can mask volume deficiency by jacking up the urine sodium - Advises you to use the FENa - THE FENA - < 1% dry - >2-3% ATN - It will fail with chronic effective volume depletion - Heart failure, cirrhosis, and burns - Suggests that tubular function will be preserved in those situations - Also with contrast, rhabdo, pigment nephropathy - Limitations - Dependent on the amount of Na filtered - Goes through the math of a normal person with GFR of 125/min and Na of 150 has filtered sodium of 27,000/day so if they eat 125-250 mEq their FENa will be 600-800 - Urine osm < plasma osm in face of hypernatremia indicates renal water loss due to lack of or resistance to ADH - In ATN urine OSM < 400 - In pre-renal disease it could be over 500 - Specific but not sensitive due to people with CKD who are unable to concentrate urine- Specific gravity - Plasma is 8-10% igher than plasma so specific gravity is 1.008 to 1.010 - Every 30-35 mOsm/L raises urine Osm of 0.001 - so 1.010 is 300-350 mOsm/L H2O - Glucose raises urine specific gravity more than osmolality - Same with contrast - Carbenicillin- pH - Normally varies with systemic acid-base status - PH should fall before 5.3 (usually below 5.0) with systemic metabolic acidosis - Above 5.3 in adults and 5.6 in children indicate RTA - PH goal 6.0-6.5 - Separate individual RTAs through FR of HCO3 at various serum HCO3 levels - Also can monitor urine pH to look for success in treating metabolic alkalosis - Look for pH > 7 - In treatment of uric acid stone disease - Want to shift eq: H + urate – uric acid to the left because urate is more soluble - PH goal 6.0-6.5
Bill Mitchell, Founding Partner, Cruser & Mitchell joins Bill Kanasky, Jr., Ph.D. to discuss negotiation in litigation. Bill Mitchell shares his philosophy on managing litigation and comments on the lack of focus on the negotiation phase of litigation vs. the outsized focus on trial, when fewer than 1% of cases go to trial. Bill talks about mistakes that he sees defense attorneys making including not identifying the leverage point for every case and not being an open communicator and engaging in open discussions with opposing counsel. Bill Mitchell discusses his approach when dealing with plaintiff attorneys who are not willing to negotiate and how important communication is in those situations. Lastly, Bill talks about timing for negotiations, parachuting in on cases, and how he handle multiples co-defendants. Watch the video of this episode: https://www.courtroomsciences.com/r/mEq
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
Getting team alignment is crucial to the success of any organization, particularly in the face of change. As organizations experience change, it is essential to have a cohesive team that can adapt and work collaboratively towards shared goals. Today's guest is Janesse Bruce, Founder, and CEO at meQuilibrium. Inc Magazine ranked her company #2813 on the 2022 Inc 5000 list. meQuilibrium (meQ) is the #1 global digital resilience solution to build workforce well-being and performance. Their mission is to make any workforce a workforce for growth. In this episode, Jan talks about getting team alignment in the face of change. She also talks about resilience and over-communicating. Join us as we explore different approaches to getting team alignment, including communication strategies, creating shared vision and values, and team-building exercises. Tune in to discover the secrets of getting team alignment and build a strong foundation for your team's success. Get the show notes for Getting Team Alignment in the Face of Change with Jan Bruce at meQuilibrium Click to Tweet: Listening to a fantastic episode on Growth Think Tank with #JanBruce featuring your host @GeneHammett https://bit.ly/gttJanBruce #GettingTeamAlignment #GeneHammettPodcast #GHepisode989 #meQ #digitalresilience Give Growth Think Tank a review on iTunes!
Bob Dhillon is the Founder, President & CEO of Mainstreet Equity Corp, based in Calgary, Alberta, Canada. Mainstreet is publicly traded on the Toronto Stock Exchange (TSX:MEQ). As of Q1 2023, assets were valued at close to CDN$3B and MEQ reported its 23rd year of consistent, year-over-year, double-digit returns through its continued organic growth. Year-to-date holdings currently consist of 16,802+ apartments across western Canada (British Columbia, Alberta, Saskatchewan, and Winnipeg, Manitoba). Along with its healthy balance sheet success, Mainstreet is a strong and proud champion of affordable housing. In 2018, Bob gifted CDN$10M to the University of Lethbridge towards the creation of the Dhillon School of Business (DSB). Bob's strong belief that education and entrepreneurship are the engines of national prosperity, along with his strong desire to give back to the province that provided him with so many opportunities, motivated his decision to make this substantial and transformative contribution. One of the primary areas of study at DSB is a world-class research and emerging technologies. Bob is also very proud of the fact that DSB was the first post-secondary institution in Canada to mandate an indigenous studies course requirement. Bob is also the owner of National Payments, a Visa and MasterCard-approved merchant-processing business in the financial services sector. Entrepreneurs are the backbone of Canada's economy. To support Canada's businesses, subscribe to our YouTube channel and follow us on Facebook, Instagram, LinkedIn and Twitter. Want to stay up-to-date on the latest #entrepreneur podcasts and news? Subscribe to our bi-weekly newsletter
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
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
HelixTalk - Rosalind Franklin University's College of Pharmacy Podcast
In this episode, we review the management of a patient with hypokalemia, including both inpatient and outpatient supplementation with potassium chloride supplements and what dosage forms are available for potassium repletion. Key Concepts Most diets will provide sufficient potassium to avoid hypokalemia. Hypokalemia usually occurs due to drug therapy (such as diuretics) or GI losses from severe vomiting or diarrhea. In patients with chronically low potassium, supplements are dosed to increase dietary intake of potassium by about 20-40 mEq per day. For acute repletion, 10 mEq of potassium should increase serum potassium by about 0.1 mEq/L. Over-the-counter potassium (as potassium gluconate) contains a very small amount of potassium (2.5 mEq). Potassium chloride powders and liquids (like salt substitutes) taste terrible and are poorly tolerated. Most patients will replete potassium via slow-release tablets (Klor-Con or Klor-Con M) or via potassium chloride IV infusions. Most IV fluids do not contain any potassium at all (or very little potassium). Patients receiving these IV fluids who are NPO will eventually become hypokalemic. Certain maintenance fluids do contain potassium – most patients will receive about 40 mEq of potassium per day with these IV fluids.
Contributor: Travis Barlock, MD Educational Pearls: Normal Saline (NS) contains 154 mEq of both Sodium (Na) and Chloride (Cl), and has a pH of 5.5 Normal Na and Cl in adult humans are about 140 mEq/L and 103 mEq/L. respectively Excess negative charge resulting from hyperchloremia is managed via bicarbonate excretion leading to loss of base Overall, administration of NS drives metabolic acidosis Lactated Ringers (LR) contains 130 mEq of Na and 109 mEq Cl, and has a pH of 6.5 LR components are closer to physiologic levels thus may generally be a more efficacious fluid choice NS is still frequently given in scenarios where there is concern for increased intracranial pressure or existing hypochloremic alkalosis from emesis. ReferencesLi H, Sun SR, Yap JQ, Chen JH, Qian Q. 0.9% saline is neither normal nor physiological. J Zhejiang Univ Sci B. 2016;17(3):181-187. doi:10.1631/jzus.B1500201 Lehr AR, Rached-d'Astous S, Barrowman N, et al. Balanced Versus Unbalanced Fluid in Critically Ill Children: Systematic Review and Meta-Analysis. Pediatr Crit Care Med. 2022;23(3):181-191. doi:10.1097/PCC.0000000000002890 Self WH, Semler MW, Wanderer JP, et al. Saline versus balanced crystalloids for intravenous fluid therapy in the emergency department: study protocol for a cluster-randomized, multiple-crossover trial. Trials. 2017;18(1):178. Published 2017 Apr 13. doi:10.1186/s13063-017-1923-6 Semler MW, Self WH, Wanderer JP, et al. Balanced Crystalloids versus Saline in Critically Ill Adults. N Engl J Med. 2018;378(9):829-839. doi:10.1056/NEJMoa1711584 Summarized by Kirsten Hughes, MS4 | Edited by John Spartz, MD, & Erik Verzemnieks, MD In an effort to promote diversity, equity, and inclusion in Emergency Medicine, The Emergency Medical Minute is proud to present our 2nd annual Diversity and Inclusion Award. We support increasing the representation of underrepresented groups in medicine and extend this award to individuals applying to emergency medicine residencies during the 2022-2023 cycle. For information on award eligibility and the application process, visit https://emergencymedicalminute.com/edi-award/ Donate to EMM today!
Patreon: https://www.patreon.com/ASAPWeekly Zodiak22 Too Much Space Chaos Maker Space Bear Franc FluxAwsomniss Caleb Razz Digital Toast PaintAUROOOOOOOOOOOOOOOOOOK YaboiHuntee Yung slugTopics:All teams qualedMesi predicts the right team (EU Invitational)and is awesome pog,World Chumps missing Fall Major, Eu 2-5 shaky compared to NA 2-5Chrsor hits GC 2 ;)Pwr coming back after shaky start to split (who? xD jkjk)Prof missing major cuz baby yayyayayyayayayayayayayayayayayayay (next prodigy rokt leeg player?)Yes this ^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^Major matchups out, seeding based on Worlds placements for each regionBlueberry is the BEST fruit no contest, fight meQ and ASupport this podcast at — https://redcircle.com/asapweekly-rocket-league-podcast/donationsAdvertising Inquiries: https://redcircle.com/brandsPrivacy & Opt-Out: https://redcircle.com/privacy
There are three levels of leadership awareness that are critical for any leader, or aspiring leader: self-awareness (MeQ), one-to-one leadership (EmQ), and one-to-many leadership (SocQ), which includes the broader social context and environment. Taylor Griffin and Courtney Hamilton discuss why today's “social economy” compels leaders to develop a more nuanced awareness toward various stakeholders and audiences, both within the company and without.
Continuing the Middle East Forum's intense focus on the Israeli strike on a Syrian nuclear plant in 2007 – see the MEQ articles by Ori Wertman and Ehud Barak - Yuval Steinitz will explain his fascinating and hitherto untold story of his battle with the IDF establishment to push it to take steps against Syria's acquiring a nuclear weapons capability. How did that battle play out? How are its implications relevant today?
In episode 49 of the pharmaceutical calculations podcast, you will learn the best way to convert mEq per mL to percent strength using an important question asked by a viewer. This episode was originally broadcast as a video on our YouTube channel: www.youtube.com/pharmaceuticalcalculationseasy Additional Resources for Practice: Pharmaceutical Calculations: 1001 Questions with Answers: https://www.rxcalculations.com/shop/uncategorized/pharmaceutical-calculations-1001-questions-answers/ NAPLEX Question Bank: https://www.rxcalculations.com/shop/uncategorized/gold-membership/ Join Our Social Media Community: Website: http://www.rxcalculations.com Forum: https://forum.rxcalculations.com/ Facebook: https://www.facebook.com/pharmaceuticalcalculations Twitter: https://twitter.com/RxCalculations Instagram: https://www.instagram.com/rxcalculations YouTube: www.youtube.com/pharmaceuticalcalculationseasy About RxCalculations: RxCalculations helps you master pharmaceutical calculations. We make it so you never have to worry about failing an exam or compromising patient safety because of a calculations error. RxCalculations is a leading global educational service platform focused on developing top quality pharmaceutical calculations products to help prospective pharmacists and health care professionals all over the world resolve one of the biggest challenges related to their profession. Our top quality products include affordable courses, personal consults, books, video tutorials, timed quizzes and apps designed to make you an expert in solving any pharmaceutical calculations question. We also have the largest pharmaceutical calculations online question bank which has over 1000 questions covering every important calculations topic as well as step-by-step video solutions. With all these resources at your disposal we have all you need to not only master pharmacy calculations but ace every test as well as passing your board exams.
Bu yazımda acil serviste takip ettiğimiz hastalarda sık karşılaştığımız bir durum olan metabolik asidoz sebepleri ve yönetimini özetlemeyi amaçladım. Ayrıca sık gözlenen klinik durumlardaki tedavi önerilerini derlemeye çalıştım. İyi okumalar dilerim. Metabolik asidoz vücuttaki hidrojen iyonlarının arttığı ve bikarbonatın azaldığı bir süreç olarak tabir edilebilir. Bu süreç sadece kan gazı sonuçlarında pH değerine bakarak açıklanmamalıdır. Metabolik asidozda vücuttaki kompansasyona bağlı olarak pH değeri düşük, normal veya yüksek saptanabilir. Kan pH değerinin
Class: Electrolyte replacement /Alkalizing AgentMOA: Counteracts existing acidosisIndications: Acidosis, Drug intoxications (barbiturates, salicylates, methyl alcohol)Contraindications: Metabolic alkalosis, hypocalcemiaSide effects: metabolic alkalosis, hypernatremia, injection site reaction, sodium and fluid retention, peripheral edema.Dosing Metabolic acidosis during cardiac arrest Adult:1 mEq/kg slow IV/IO may repeat at 0.5 mEq/kg in 10 minsPedi:SAA
On this episode of SSR On Air, Mike Rogers and Debbie Heitzman, Principal, talk about the ins and outs of medical equipment planning. From the ground floor to the top, our MEQ team plans for every piece of equipment, like thermometers, MRI machines, mortuary fridges, and even disco balls! Learn more about our growing team across the nation and how they stay up to date on the latest technologies in equipment.
On this episode of SSR On Air, Mike Rogers and Debbie Heitzman, Principal, talk about the ins and outs of medical equipment planning. From the ground floor to the top, our MEQ team plans for every piece of equipment, like thermometers, MRI machines, mortuary fridges, and even disco balls! Learn more about our growing team across the nation and how they stay up to date on the latest technologies in equipment.
Eliminasyon kelime anlamı olarak; eleme, yok etme, ortadan kaldırma, bir maddenin biyoransformasyondan sonra vücut dışına atılmasıdır. Hepimizin bildiği üzere vücudumuz dışarıdan aldığı maddeleri üriner, fekal, pulmoner ve sekresyonlar yolu ile elimine eder. Sınırlı sayıda yöntem ile zehirlenme durumlarında, eliminasyonu artırarak ksenobiyotiklerin vücuttan uzaklaştırılmalarını hızlandırabiliriz. Ancak bu yöntemlerin klinik pratikte kullanımları sınırlıdır ve tüm zehirlenme çeşitlerinde de kullanılmamaktadır (Tablo-1). Korporeal (Vücut içi) yöntemler Ekstrakorporeal (Vücut dışı) yöntemler Üriner alkalinizasyon Hemodiyaliz Tekrarlayan doz aktif kömür Hemoperfüzyon Zorlu diürez Hemofiltrasyon Metal şelasyonu Sürekli Renal Replasman Tedavileri Serebrospinal sıvı replasmanı Plazmaferez, Exchange transfüzyon Reçineler (Prusya mavisi, kolestiramin, kolestipol, kayeksalat) Karaciğer destek araçları Tablo-1. Eliminasyonu artırıcı yöntemler Bu yazımızda klinik pratikte sık uygulanan eliminasyonu artırıcı yöntemleri sizlere sunmayı amaçladık. Üriner Alkalinizasyon Zayıf asit yapıdaki ksenobiyotiklerin eliminasyonunu arttırmak için asidik olan idrar pH'ının (pH:4-5) alkalileştirilmesi esasına dayanan bir yöntemdir. Bu yöntemin en sık uygulandığı ajanlar ise Salisilatlar, Fenobarbital ve Metotreksat'dır. Bu zayıf asitler, alkali idrar pH'ında iyonize hale gelerek renal tübüllerden reabsorbsiyona uğramadan idrarla atılırlar. Alkalinizasyonda, idrarın hedef pH'ını 7-8'e çıkarmak için intravenöz sodyum bikarbonat (1-2 mEq/kg hızlı iv bolus ve idame iv infüzyonu) uygulanır. Bu esnada dikkat edilmesi gereken en önemli noktalar; serum pH'nın 7.5'i geçmemesi, serum potasyum seviyesinin 4 mEq/L'nin altına düşmemesidir1. Tekrarlayan Doz Aktif Kömür Aktif kömür, dekontaminasyon yöntemi dışında enterohepatik sirkülasyona giren ajanların eliminasyonunu artırmak amacıyla 0.5 g/kg dozunda ve her 6 saate bir, toplam 4 kez olacak şekilde oral yolla veya nazogastrik tüpten uygulanır. Böylece aktif kömür, ilacın veya toksinin enterohepatik dolaşımını engelleyerek sistemik dolaşıma tekrar karışmasını önler ve serum konsantrasyonunu düşürür. Tekrarlayan doz aktif kömür uygulamasının endike olduğu durumlar arasında Karbamazepin, Amitriptilin, Siklosporin, Dapson, Digitoksin, Nadolol, Nortriptilin, Fenobarbitaller, Siklopeptid içeren mantar zehirlenmeleri yer alır. Unutulmaması gereken dekontaminasyon amaçlı aktif kömür uygulamasının kontrendike olduğu her durum tekrarlayan doz aktif kömür uygulaması için de geçerlidir2,3. Ekstrakorporeal Yöntemler The Extracorporeal Treatments in Poisoning - EXTRIP çalışma grubu, 30'dan fazla uluslararası derneği temsil eden çeşitli alanlardan uzmanların işbirliğiyle (tıbbi/klinik toksikoloji, nefroloji, farmakoloji, yoğun bakım, acil tıp) zehirlenmelerde özellikle hemodiyaliz endikasyonları ve diğer ekstrakorporeal tedavi yöntemleri ile ilgili çeşitli önerileri kılavuz şeklinde yayınlamaktadır ve bu önerileri güncellemektedir. Hemodiyaliz Hemodiyaliz keşfedildiğinden bu yana 100 yılı aşkın süredir klinikte kullanılmaktadır ve zehirlenmelerde en sık kullanılan ekstrakorporeal tedavi yöntemidir. Çünkü hemodiyaliz, toksini dolaşımdan uzaklaştırmanın yanısıra asit-baz ve elektrolit bozukluklarının hızlı düzeltilmesi ve böbrek fonksiyonlarının bozuk olduğu durumlarda ultrafiltrasyon ile volüm yükünün azaltılması gibi destek tedavisi amaçlı da kullanılmaktadır. Klasik hemodiyaliz sırasında, kan ve ters akımlı diyalizat, yarı geçirgen bir zar (diyalizör) ile ayrılır. Ksenobiyotikler daha sonra membran boyunca kandan diyalizata konsantrasyon farkı esasına dayanarak difüze olur. Kan, geçici bir diyaliz kateterinin bir lümeninden pompalanır, makineden geçirilir ve ikinci lümenden venöz dolaşıma geri döndürülür. Bir maddenin hemodiyaliz ile kandan uzaklaştırılabilmesi için molekül ağırlığının küçük (
In the most recent ShiftED podcast I had the great privilege of talking with preschool educator/consultant Katherine Divolis, currently working as Conseillère en éducation préscolaire, at Ministère de l'Éducation et de l'Enseignement Supérieur du Québec (MEQ). We had a rich conversation about the newly revised preschool program that was just launched in the last school year which is currently being implemented across the province.
October 10 is World Mental Health Day. To mark the occasion, hosts Joanna Bedford and Lubna Salim are joined in this episode by Rebecca Clements, client success director at meQuilibrium, an app-based platform that helps users build resilience, face change and uncertainty, and manage stress through personalized action plans. Listen along as they discuss how supporting employee mental health and well-being is an absolute must for modern companies, as well as some of the helpful techniques for managing stress offered on the meQ app.
DJ and JT talk with Dr. Andrew Shatte, co-founder of meQuilibrium, an app that is designed to help you discover simple techniques to build your resilience and shift your response to stressful situations. Note: All U.S.-based employees (excluding Puerto Rico) are eligible for meQ. If you are a union-represented employee, aspects of your benefits may be covered by your union contract.
DJ and JT talk with Dr. Andrew Shatte, co-founder of meQuilibrium, an app that is designed to help you discover simple techniques to build your resilience and shift your response to stressful situations. Note: All U.S.-based employees (excluding Puerto Rico) are eligible for meQ. If you are a union-represented employee, aspects of your benefits may be covered by your union contract.
Véronique Proulx, présidente-directrice générale de Manufacturiers et Exportateurs du Québec (MEQ), nous parle des coûts liés à la pénurie de la main-d'œuvre et des solutions proposées par son organisme. https://meq.ca/
Hey miq, së pari ju kërkojmë ndjesë për mungesën e gjatë dhe së dyti e kemi treguar në këtë episod cfarë kemi qenë duke bëre. Meqë periudhë vere e gjakun e kemi në lëvizje më së shumti, vendosëm të flasim se sa kemi mësuar ne nga gabimet.
The Pharm So Hard Podcast: An Emergency Medicine and Hospital Pharmacy Podcast
Introduction Insulin with dextrose is an effective method to lower potassium levels quickly in acute hyperkalemia Literature shows ranges of potassium reduction by 0.5-1.0 mEq after administration of a single dose. Patients with renal insufficiency and end-stage renal disease (ESRD) have a higher incidence of hypoglycemia after treatment with insulin for hyperkalemia due to: Reduced […] The post Episode 47. I Plead the Fifth! 5 vs 10 units of Insulin for Hyperkalemia appeared first on The Pharm So Hard Podcast.
The Filtrate:Joel TopfSwapnil HiremathNayan AroraSophie AmbrusoJoshua WeismanEditorJoel TopfShow Notes:Soccer star Christian Eriksen 'was gone' after on-field cardiac arrest, doctor says (NBC News)120-sided Die. This was covered in Wired Magazine. Respect. https://www.wired.com/2016/05/mathematical-challenge-of-designing-the-worlds-most-complex-120-sided-dice/ Nephrologists that played D&D: https://twitter.com/kidney_boy/status/1398660927680036865?s=20 Doctors that played D&D (i.e. control group): https://twitter.com/kidney_boy/status/1398661170328899586?s=20 Average sodium intake among Americans is 3,400 mg (147 mEq of Na per day). Sodium and the Dietary Guideline Factsheet (PDF)DASH Sodium Diet Trial https://www.nejm.org/doi/10.1056/NEJM200101043440101 The PURE Trial as discussed by NephJC and as seen in the NEJMFormulas to Estimate Dietary Sodium Intake From Spot Urine Alter Sodium-Mortality Relationship https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.119.13117 The Taiwan Nursing Home study: https://pubmed.ncbi.nlm.nih.gov/16762939/ Peruvian Cluster RCT of sodium reduction in Nature (oooh!) https://www.nature.com/articles/s41591-020-0754-2 DASH Diet in CKD https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4957723/ A comparison of treating metabolic acidosis in CKD stage 4 hypertensive kidney disease with fruits and vegetables or sodium bicarbonate https://pubmed.ncbi.nlm.nih.gov/23393104/ ACCORD https://www.nejm.org/doi/full/10.1056/nejmoa1001286 Kidney Damage Biomarkers and Incident CKD During Blood Pressure Reduction: A Case-Control Study within SPRINT https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6953744/ Association of Urinary Biomarkers of Inflammation, Injury, and Fibrosis with Renal Function Decline: The ACCORD Trial https://pubmed.ncbi.nlm.nih.gov/27189318/ Lake Wobegon https://en.wikipedia.org/wiki/Lake_Wobegon SPRINT https://www.nejm.org/doi/full/10.1056/nejmoa1511939 Effect of Intensive vs Standard Blood Pressure Control on Probable Dementia https://jamanetwork.com/journals/jama/fullarticle/2723256 Characterizing Frailty Status in the Systolic Blood Pressure Intervention Trial https://pubmed.ncbi.nlm.nih.gov/26755682/ Syncope, Hypotension, and Falls in the Treatment of Hypertension: Results from the SPRINT Randomized Clinical Trial https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8045467/ The USPSTF recommends screening for hypertension in adults 18 years or older with office blood pressure measurement (OBPM). The USPSTF recommends obtaining blood pressure measurements outside of the clinical setting for diagnostic confirmation before starting treatment. https://www.uspreventiveservicestaskforce.org/uspstf/recommendation/hypertension-in-adults-screening Concordance Between Blood Pressure in the Systolic Blood Pressure Intervention Trial and in Routine Clinical Practice https://pubmed.ncbi.nlm.nih.gov/33044494/
There are two commonly used forms of potassium. Potassium chloride (to treat hypokalemia) and potassium citrate (as an alkalinizing agent). Unlike potassium chloride, potassium citrate is also measured in “mg” in addition to “mEq”. It comes in a 5 mEq (540 mg), 10 mEq (1080 mg), and 15 mEq (1620 mg) strength ER tablet. The main indication for potassium citrate in in the management of kidney stones. In mild-moderate treatment you initiate 15 mEq PO bid or 10 mEq PO tid with a max dose of 100 mEq per day. Since potassium citrate is an alkalinizing agent the way it works is it makes urine less acidic. It raises the pH of urine to 6-7 which will help rid uric acid from the body. The reduction of uric acid helps manage gout and kidney stones. Since potassium citrate is a known GI irritant it is recommended to take the tablets whole with a glass of water to remain upright after taking it with food or at least within 30 minutes of a meal or snack. Go to DrugCardsDaily.com for my episode show notes which will contain a drug summary, quiz, and a link to FREE drug card sheets. SUBSCRIBE on Spotify or Apple Podcasts or search for us on your favorite place to listen to podcasts. I will go over the Top 100-200 Drugs as well as throwing in some recently released drugs that peak my interest. Also, if you'd like to say hello, suggest a drug, or leave any constructive feedback on the show I'd really appreciate it! Leave a voice message at anchor.fm/drugcardsdaily or message us through twitter @drugcardsdaily --- Send in a voice message: https://anchor.fm/drugcardsdaily/message
There are two most commonly used versions of potassium. Potassium chloride (supplementation) or potassium citrate (alkalinizing agent). Potassium chloride, also known as K-Tab or Klor-Con, is an electrolyte supplementation used in treating and preventing Hypokalemia (low potassium). Potassium is an essential cation that is needed for the conduction of nerve impulses in the heart, brain, and muscle. Unlike most drugs, potassium is not measured in “mg'' and is measured in “mEq” or milliequivalents. Potassium chloride comes in multiple dosage forms such as an ER capsule and tablet, a powdered packet, oral solution, and also as an intravenous solution. When the IV solution is used a major concern is for extravasation, which is when plasma escapes from the extracellular space and forms blisters on the patient. If this occurs the drug hyaluronidase is injected as 5 separate 0.2-0.3 mL injections along with applying a cold compress and elevating the extremity. Another important note for the IV solution is that it is never administered as IV push and the solution must be diluted prior to administration. Go to DrugCardsDaily.com for my episode show notes which will contain a drug summary, quiz, and a link to FREE drug card sheets. SUBSCRIBE on Spotify or Apple Podcasts or search for us on your favorite place to listen to podcasts. I will go over the Top 100-200 Drugs as well as throwing in some recently released drugs that peak my interest. Also, if you'd like to say hello, suggest a drug, or leave any constructive feedback on the show I'd really appreciate it! Leave a voice message at anchor.fm/drugcardsdaily or message us through twitter @drugcardsdaily --- Send in a voice message: https://anchor.fm/drugcardsdaily/message
Electrolytes are among the drugs we use in the hospital setting. And like any drug, we're better when we truly understand what we are using them to treat. In this episode, we tackle one of the most common electrolyte abnormalities in hospitalized patients....hypokalemia, and we discuss why it makes no sense to say that we treated our patients hypokalemia with 40 mEq of potassium. Understanding why requires understanding how our body shifts around and stores potassium. Join me in this podcast as we figure it out and learn why it makes no sense to say, "I repleted my hypokalemic patient with 40 mEq of potassium."
In this episode of Psych Matters, Associate Professor Stephen Parker, Dr Catherine Maud, Dr Karen Freier and Dr Roth Trisno share their own personal insights and opinions on how to prepare for Modified Essay Questions exam and are not necessarily the views of the Committee for examinations and the College.The Essay-style exam is a summative assessment and a Fellowship requirement of the RANZCP Fellowship Program.It is set at the standard expected at the end of Stage 3 and assesses the application of knowledge and the capacity for critical thinking.Disclaimer: This podcast is provided to you for information purposes only and to provide a broad understanding of various training and/or assessment topics. The podcast may represent the views of the speakers and not necessarily the views of The Royal Australian and New Zealand College of Psychiatrists ('RANZCP'). The podcast is not to be relied upon as formal advice or as a substitute for preparation. By accessing The RANZCP's podcasts you also agree to the full terms and conditions of the RANZCP's Website.
Acil Bakışıyla Surviving Sepsis Campaign Pediatrik Kılavuzu Sepsis, pediatrik yaş grubunda, tanınmasının oldukça önemli olduğu bir klinik durumdur. SSC tarafından Şubat 2020’de yayımlanan, çocuklarda sepsis ve septik şok yönetimine kanıta dayalı öneriler getiren bu kılavuzu acilci bakışıyla gözden geçirmek istedim. Kılavuzun tamamına buradan1 ulaşabilirsiniz. İyi okumalar. Sepsis, dünya genelinde pediatrik popülasyon için önde gelen bir morbidite ve mortalite nedenidir. Dünya çapında yılda 22/100000 çocuk sepsis vakası ve 100000 canlı doğumda 2202 yenidoğan sepsis vakası görülmektedir, bu sayılar toplamda 1,2 milyon/yıl çocukluk çağı sepsis vakasına tekabül etmektedir. 18 yaşın altında hastanede yatan tüm hastaların %4'ünden fazlasında ve çocuk yoğun bakım ünitelerine kabul edilen hastaların yaklaşık %8'inde sepsis görülür ve mortalite hastalığın şiddetine ve çocuğun risk faktörlerine bağlı olarak %4 ila %50 arasında değişmektedir. Sepsise bağlı ölümlerin çoğu ilk 48 ila 72 saat içinde meydana gelmektedir, birçoğu refrakter şok ve/veya çoklu organ disfonksiyonu ile ilişkilidir. Sepsis Tanımı Burada çocuklarda sepsis tanımıyla ilgili bir parantez açmamız gerekiyor. 2016’da Sepsis 3.0 ile erişkinlerde sepsis tanımında sepsis ve septik şok tanımları geçerliliğini korurken SIRS (Sistemik İnflamatuvar Yanıt Sendromu) ile ciddi sepsis tanımları günlük pratiğimizden çıkmıştı. Ancak bu değişiklikler şimdilik erişkin hastalar için geçerlidir. Çocuklar için mevcut tanımlar ise şu şekildedir:2Enfeksiyon: Herhangi bir patojen ile gelişen şüpheli ya da kanıtlanmış enfeksiyon durumu ya da yüksek olasılıkla enfeksiyon ilişkili gelişen bir klinik sendromSIRS: Aşağıdakilerden 2 ya da daha fazlasının olması (biri beyaz küre sayısı ya da ateş olmalı)1. Ateş >38,5 oC ya da 19,5 ya da 17,5 ya da 22>15,5 ya da 18>13,5 ya da 14>11,5 ya da
Acil Bakışıyla Surviving Sepsis Campaign Pediatrik Kılavuzu Sepsis, pediatrik yaş grubunda, tanınmasının oldukça önemli olduğu bir klinik durumdur. SSC tarafından Şubat 2020’de yayımlanan, çocuklarda sepsis ve septik şok yönetimine kanıta dayalı öneriler getiren bu kılavuzu acilci bakışıyla gözden geçirmek istedim. Kılavuzun tamamına buradan1 ulaşabilirsiniz. İyi okumalar. Sepsis, dünya genelinde pediatrik popülasyon için önde gelen bir morbidite ve mortalite nedenidir. Dünya çapında yılda 22/100000 çocuk sepsis vakası ve 100000 canlı doğumda 2202 yenidoğan sepsis vakası görülmektedir, bu sayılar toplamda 1,2 milyon/yıl çocukluk çağı sepsis vakasına tekabül etmektedir. 18 yaşın altında hastanede yatan tüm hastaların %4'ünden fazlasında ve çocuk yoğun bakım ünitelerine kabul edilen hastaların yaklaşık %8'inde sepsis görülür ve mortalite hastalığın şiddetine ve çocuğun risk faktörlerine bağlı olarak %4 ila %50 arasında değişmektedir. Sepsise bağlı ölümlerin çoğu ilk 48 ila 72 saat içinde meydana gelmektedir, birçoğu refrakter şok ve/veya çoklu organ disfonksiyonu ile ilişkilidir. Sepsis Tanımı Burada çocuklarda sepsis tanımıyla ilgili bir parantez açmamız gerekiyor. 2016’da Sepsis 3.0 ile erişkinlerde sepsis tanımında sepsis ve septik şok tanımları geçerliliğini korurken SIRS (Sistemik İnflamatuvar Yanıt Sendromu) ile ciddi sepsis tanımları günlük pratiğimizden çıkmıştı. Ancak bu değişiklikler şimdilik erişkin hastalar için geçerlidir. Çocuklar için mevcut tanımlar ise şu şekildedir:2Enfeksiyon: Herhangi bir patojen ile gelişen şüpheli ya da kanıtlanmış enfeksiyon durumu ya da yüksek olasılıkla enfeksiyon ilişkili gelişen bir klinik sendromSIRS: Aşağıdakilerden 2 ya da daha fazlasının olması (biri beyaz küre sayısı ya da ateş olmalı)1. Ateş >38,5 oC ya da 19,5 ya da 17,5 ya da 22>15,5 ya da 18>13,5 ya da 14>11,5 ya da
Contributor: Ruben Marrero-Vasquez, PharmD Educational Pearls: ACEP and FDA have both issued warnings about the viral Tik Tok Benadryl (diphenhydramine) challenge where individuals voluntarily overdose on diphenhydramine which can cause fatal toxicity Diphenhydramine is typically dosed at 0.5-1 mg/kg in pediatric patients Q4-6 PRN and carries a fatal dose of 20-40 mg/kg but anywhere from 3-5x recommended dose does can cause toxicity Diphenhydramine toxicity causes both central and peripheral anticholinergic toxicity Central anticholinergic toxicity symptoms: delirium, agitation, combativeness, confusion, restlessness, hallucinations, ataxia, tremor and seizures Peripheral anticholinergic toxicity symptoms: tachycardia, dry flushed skin, dry mucus membranes, thick secretions, dilation of pupils, urinary retention, and decreased bowel sounds Pneumatic to help you remember anticholinergic toxidrome: Red as a beet Dry as a bone Blind as a bat Mad as a hatter Hot as a hare Full as a flask Management typically only requires supportive care, agitation from central anticholinergic delirium can be hardest aspect to treat, IV benzodiapines are first line treatment to control and may require large doses to prevent rhabdomyolysis and hyperthermia Diphenhydramine toxicity has been associated with blockade of sodium and potentially potassium channels increasing risk of arrhythmia and seizures. Cardiac changes can include: QRS widening, myocardial depression, QT prolongation and torasades-type ventricular tachycardia. Wide QRS complexes indicate delayed ventricular depolarization caused by sodium channel blockade, bolus of sodium bicarbonate can be used dosed 1-2 mEq/kg followed by continuous infusion Prolonged QT: restoration of low serum potassium and magnesium to high normal range Benzodiazipines should be used as first line therapy for toxin induced seizures Don’t use fosphenytoin or phenytoin sodium channel blockers as they can worsen cardiac conduction References Su M, Goldman M. Anticholinergic Poisoning. UpToDate. https://www.uptodate.com/contents/anticholinergic-poisoning?search=diphenhydramine overdose&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1. Published October 6, 2020. Accessed December 26, 2020. Summarized by Mason Tuttle
On this week's episode we look over a GT that happened in Span this past weekend. We also talk shop on anti-MEQ necon lists for John. As always be sure to like and subscribe. Let us know what you like and what you'd like to see in a review. You can check out our weekly Sunday Stream games alternating between AoS and 40k On our Twitch and on our Facebook and Youtube.
In this special episode of Talking Under Water, One Water, One Podcast, hosts Bob Crossen, Lauren Del Ciello and Katie Johns share the final interview in the four-part Value of Water Series. The series aims to share diverse voices and perspectives on solving water access, equity and affordability issues starting with the role of one water before digging into the utility perspective, a community group perspective and finally a perspective from the ground floor on water access. In this episode, Lauren interviews Carmen George, research & MEQ manager for the Community Outreach & Patient Empowerment (COPE) program. The program is a partnership with the Navajo Nation Community Health Representative Outreach Program to improve the lives of those living with chronic diseases in Navajo Nation. The program has also been significantly involved in water access issues in the community, especially in light of current circumstances. Lauren and Carmen discuss COPE’s mission and barriers to clean drinking water access. Additionally, the conversation digs into the role of education in long-term change for water access and use, as well as how the “one water” approach can be a sustainable, long-term method to meet these access and education obstacles.
In this special episode of Talking Under Water, One Water, One Podcast, hosts Bob Crossen, Lauren Del Ciello and Katie Johns share the third interview in the four-part Value of Water Series. The series aims to share diverse voices and perspectives on solving water access, equity and affordability issues starting with the role of one water before digging into the utility perspective, a community group perspective and finally a perspective from the ground floor on water access. In this episode, Katie interviews Kirsten Shead and Brenda Coley, co-executive directors of the Milwaukee Water Commons.They talk about the efforts of the Milwaukee Water Commons and water equity in the city of Milwaukee and beyond. The series will conclude next week, Oct. 30, with an interview between Lauren and Carmen George, research & MEQ manager for the Community Outreach & Patient Empowerment (COPE) program discussing water access. The TUW hosts are committed to elevating conversations surrounding issues of water access, equity and affordability and the role of one water in driving change. We encourage you to reach us at talkingunderwater@sgcmail.com to share your thoughts and start a dialogue.
CONVERSAT10N: How can Sports Life Coaching impact your life? In this episode of 10 Talks, head Sports Life Coach, Carlette Patterson introduces us to newly certified Sports Life Coach, Joy Burke who shares the powerful impact that sports life coaching made on her life. Joy’s Stats:2020 Patterson Sports Ventures CHAMP10N Sports Life Coach Certification2014 Arizona State University Master of Communications and Advocacy2010-2014 Division 1 (Arizona State University ) Women’s Basketball team member2014-2019 Professional Basketball Player2015 Denmark, Champion2015-2019 Australia (earned MVP and Female athlete of year)Represented Chinese Taipei on multiple occasions 2015 FIBA Asia Championships - Wuhan, China2017 FIBA Asia Championships - Bangalore, India2018 Asian Games - Jakarta, IndonesiaAre you a college or professional athlete wondering what sports life coaching could do for you as you transition out of your sport? Transitioning from sports to life is a process that Joy has not only experienced, but is now passionate about coaching others through. Joy shares all the ups and downs of her sports career from the high of the recruitment process to the rigors and stress of training while managing a packed schedule. Listen to Joy’s excitement for sharing what she has learned with others and how coaching you for your life is just as important as coaching an athlete is for their sport.Our hope is that you will be inspired and encouraged to go for the life you want. Check out our MeQ™ courses available at MeQ10.com! Remember, Sports Life Coaching is for EVERYONE, so if you would like to Get Coached or sign up for any of our other courses, go to www.lifetrainingacademy.com. Enjoy the CONVERSAT10N!
CONVERSAT10N: Have you ever dreamt of accomplishing something big and wondered how to get there? Are you the coach of a team, a CEO, or even starting your own business and looking for inspiration? In this week’s episode of “10 Talks”, Carlette has an impactful conversation with Greg Williams, Head Equestrian coach at Auburn University with an impressive set of accomplishments: Since the 2002-03 season, the Auburn Tigers have totaled six national titles (2006, 2011, 2013, 2016, 2018, 2019), five Hunt Seat national titles (2008, 2011, 2013, 2018, 2019), one Western national title (2018), three Southeastern Conference titles (2016, 2019, 2020), and three Southern Equestrian championships (2004, 2010, 2011). Greg’s student-athletes have combined for 90 All-America accolades since the 2010-11 season and have totaled 101 All-SEC and Freshman All-SEC selections.Auburn continued its unbeaten streak in 2019-20, finishing the shortened season with a 13-0 mark. The squad was named the outright SEC champion and had 12 All-America honors. The 2019 squad took Auburn’s success to a new level, becoming the first program in the sport’s history to go unbeaten with an 18-0 markIn this powerful conversation you’ll hear how Greg turned his passion for horses into 6 national equestrian titles for Auburn with 90 All-American athletes. You’ll hear how he accomplished creating a true team atmosphere out of a traditionally individual sport and how he and his team worked to build the program from the ground up! Literally ... the team of girls built the arena! Greg will also share some of his winning strategies for successful leadership.Our hope is that you will be inspired and encouraged to go for the life you want. Check out our MeQ™ courses available at MeQ10.com! Remember, Sports Life Coaching is for EVERYONE, so if you would like to Get Coached or sign up for any of our other courses, go to www.lifetrainingacademy.com. Enjoy the CONVERSAT10N!
CONVERSAT10N: How do professional athletes TRANSIT10N from sport to life? In this episode of “10 Talks'' Carlette's guest is retired New Zealand professional soccer player, Ben Sigmund. Ben’s international soccer career for New Zealand began in 2000. He also played professionally for the Wellington Phoenix for many years and capped off his career representing New Zealand in the 2010 FIFA World Cup in South Africa. He shares with us the powerful story of his athletic journey and all it’s ups and downs including giving it all up for a few years. You’ll hear how after some drinks in a pub, Ben did some soul searching and decided to do whatever it took to make a comeback to professional soccer. Ben shares the personal struggles he fought through to get himself back into the sport. He also talks about the real emotional pressure he felt, the loneliness, and eventually the faith he found to be a role model for youth watching their beloved game of soccer.Our hope is that you will be inspired and encouraged to go for the life you want. Check out our MeQ™ courses available at MeQ10.com! And, if you would like to Get Coached or sign up for any of our other courses, go to www.lifetrainingacademy.com. Enjoy the CONVERSAT10N!
CONVERSAT10N: Are you going through a period of TRANSIT10N? All of us do at many different times in our lives. Change, no matter how big or small, can affect every DIMENS10N of your life and how you navigate through the transition can impact you for years to come. In this episode of 10 Talks, Carlette introduces you to one of the Life Training Academy’s own Sports Life Coaches, Jane Cebrynski. Jane was going through a major life change when she met Carlette. Through Sports Life Coaching, Jane not only got coached, she also found INSPIRAT10N to become a coach and is now launching her own TRANSIT10N Coaching program at the Life Training Academy. Listen in to the CONVERSAT10N as Jane shares with us her journey and how she hopes to help others through their own TRANSIT10NS. Our hope is that you will be inspired and encouraged to go for the life you want and get coached as you go through any of life’s many TRANSIT10NS. Also, check out our MeQ™ courses available at MeQ10.com! And, if you would like to Get Coached, become a certified Sports Life Coach™, or sign up for any of our other courses, go to www.lifetrainingacademy.com. Enjoy the CONVERSAT10N!
CONVERSAT10N: What is the Certified Sports Life Coach training like? In today’s episode of 10 Talks, you’ll hear the newest graduating class of Certified Sports Life Coaches reflect on the process, what they learned, and how they plan on using their new CERTIFICAT10NS. You’ll hear how this diverse group from all over the world started out as strangers and soon became a team as they supported each other through the certification process. You’ll also hear about their G.I.V.E.H.O.P.E. project called “365 G.I.V.E.H.O.P.E.” and how you can contribute to the project! Our hope is that you will be inspired and encouraged to go for the life you want and to invest in your own wellbeing. Check out our MeQ™ courses available at MeQ10.com! And, if you would like to Get Coached, become a certified Sports Life Coach, or sign up for any of our other courses, go to www.lifetrainingacademy.com. Enjoy the CONVERSAT10N!
CONVERSAT10N: What do wellbeing and a traditional tribal war dance have in common? In this episode of 10 Talks, head Sports Life Coach, Carlette Patterson talks with Eroni Clarke, former international rugby player for the New Zealand All Blacks. Eroni will explain to us the history of the haka which is the Maori tribal war challenge performed by the All Blacks before every match immediately prior to kick-off. The captivating story of the haka parallels some fundamentals of wellbeing. Listen as Carlette and Eroni talk about applying the haka’s lessons to life including unity, the power of team and asking for help. As a bonus, you’ll hear Eroni’s journey to become an All Black which began as a dream at the tender age of 7. Our hope is that you will be inspired and encouraged to go for the life you want and to invest in your own wellbeing. Check out our MeQ™ courses available at MeQ10.com! And, if you would like to Get Coached or sign up for any of our other courses, go to www.lifetrainingacademy.com. Enjoy the CONVERSAT10N!
CONVERSAT10N: Would you like to consistently perform at a high level in all dimensions of your life? The number of hours in a day is fixed, but personal energy levels are not. Managing your energy is a skill that, with intention and practice, can be mastered. Listen as Head Sports Life Coach Carlette Patterson and CHAMP10N guest and Master Sports Life Coach Helen Regan talk about the MeQ™ Skill, Energy Management. You’ll learn some Winning Strategies to use your 24 Golden Nuggets as efficiently as possible so that you have enough energy for all dimensions of your life (Personally, Professionally, and Philanthropically) while living your “10” life.Our hope is that you will be inspired and encouraged to go for the life you want. Check out our MeQ™ courses available at MeQ10.com! And, if you would like to Get Coached or sign up for any of our other courses, go to www.lifetrainingacademy.com. Enjoy the CONVERSAT10N!MeQ™ Skills: Energy Management, Winning Strategies, Performance Barriers, Actions to Change, Rest and Recovery, Joy Breaks, Rituals and Routines, Stats, Give Hope
Especial: Hoy hay nuevos cambios en MEQ y en este episodio quiero explicarles que es mentalidad equilibrada, para que puedan tener una referencia continua si es que dudan y puedan escucharlo cuando quieran, empezaremos hablando de lo que es la felicidad, y de procurar hacer los momentos felices los mas seguidos posibles y si es posible ni notar los negativos.Mentalidad equilibrada es paz, estar en el punto de balance y a pesar de que nos vamos al extremo en algo, la idea es regresar y en el proceso no afectar, ni dañar la vida de otros. Vivir como un verdadero ecosistema. En este episodio tambien daremos ejemplos de la vida y del equilibro entre la salud, amor y riqueza, los limites que son necesarios tener, porque los extremos nos pueden hacer mucho daño y cuando pasas ese umbral, ese limite, no será tan fácil retornar.Discutremos sobre el control y llevar una vida plena, cual es nuestro objetivo, y como vamos a agregar un granito de arena en cada capitulo, de este podcast, que llevará tu vida a un nivel diferente y extraordinario. ¿Que cambios crees que se necesita tener? ¿Cuales son las esas reglas que nos frenan? Sigue tu destino y no permitas que esas reglas te quiten poder para lograrlo. Mantener el equilibrio no es facil y por ese mismo motivo vale la pena. Haz que tu vida pase de normal a extraordinaria, el poder está a tu alcance, tu decisión… tomarlo Síguenos en todas las redes como Mentalidad EquilibradaInstagram Facebook Twitter No te olvides de escuchar los anteriores episodios en la página web o en cualquiera de tus plataformas favoritas:www.mentalidadequilibrada.com
CONVERSAT10N: Want to actually go for the life you want? Life is like a game of football; as you are advancing toward your goal there are plenty of people and obstacles attempting to tackle you and take you out of the game. In this episode of 10 Talks, The Life Training Academy’s Head Sports Life Coach™, Carlette Patterson is back with Rory Clarke for another CONVERSAT10N in our series on RELATIONSHIPS. This powerful discussion about self identity is loaded with plenty of fun moments and winning strategies that will have you rethinking your relationship with yourself. Remember to check out our website, lifetrainingacademy.com to get coached as well as meq10.com to enroll in any of our MeQ™ courses. MeQ™ Skills: Winning Strategies, Performance Barriers, Joy Breaks, Stats, Unconditional Love
Haremos cambios en MEQ y ahora probaremos con algunas cosas nuevas para poder manejar la idea del podcast en una forma un poco mas interesante, hablaremos del tipo de éxito, pondremos ejemplos de como algunas personas mezclan la idea de éxito para ir al extremo de usar esas dos palabras diciendo SIEMPRE o NUNCA, no debemos poner a todos en la misma bolsa y no es mucha diferencia entre pensar asi y llegar al odio o racismo. Dejemos los estereoptipos exagerados y las formas de generalizar. Tambien hablaremos de como brindamos ayuda y como podemos hacer para crear una mejor forma de conectar con las personas, tambien mencionaremos de que no hay una regla que aplique a todo pero si hay técnicas que pueden ayudar mas a uno que a otros. No te olvides de compartir el episodio si te gusto y si quieres equilibrar tu vida sigue el podcastHaz que tu vida pase de normal a extraordinaria, el poder está a tu alcance, tu decisión… tomarlo Sígueme en todas las redes como Mentalidad EquilibradaInstagram Facebook Twitter No te olvides de escuchar los anteriores episodios en la página web o en cualquiera de tus plataformas favoritas:www.mentalidadequilibrada.com
CONVERSAT10N: Did you know that if you live to be 65, chances are you’ll live to be 90? Would you like to learn some winning health strategies to get you there? A lot of us don’t take much time learning about our physical well being until later in life. The good news is, most medical issues can be reversed quickly once we take control and become the manager of our own health. Listen in as Carlette continues her Relat10nship series with Rory Clark. In this conversat10n, you’ll learn some powerful winning strategies for your physical health. And remember, if you’d like to get coached, go to lifetrainingacademy.com or if you’d like to register for any of our MeQ™ courses, go to meq10.com. Enjoy the conversat10n!MeQ™: Winning Strategies, Performance Barriers, My Support Team, Rituals and Routines, Joy Breaks
CONVERSAT10N: Would you like to feel more grounded and centered when life throws you a curveball? This week Carlette welcomes back Luke Sniewski to launch The Life Training Academy’s newest MeQ™ course on Wellbeing. Luke will introduce you to his book “A Million Ways to Live” and the 6 principles of life that wellbeing is grounded in. Carlette and Luke will also talk about stillness which is the warm up to the practice of wellbeing. You’ll also hear some of the performance barriers to wellbeing as well as some actions to change. Please visit our website lifetrainingacademy.com to get coached. And, to enroll in our new MeQ™ Wellbeing course go to meq10.com Enjoy the conversation!MeQ™ Skills: Winning Strategies, Performance Barriers, Actions to Change
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.29.178160v1?rss=1 Authors: Rahmati, N., Normoyle, K. P., Glykys, J., Dzhala, V. I., Lillis, K. P., Kahle, K. T., Raiyyani, R., Jacob, T., Staley, K. J. Abstract: Developmental, cellular, and subcellular variations in the direction of neuronal Cl- currents elicited by GABAA receptor activation have been frequently reported, and we found a corresponding variance in the reversal potential (EGABA) for individual interneurons synapsing on a single pyramidal cell. These findings suggest a corresponding variance in the cytoplasmic concentration of Cl- ([Cl-i]). We determined [Cl-]i by: 1) two-photon imaging of the Cl- sensitive, ratiometric fluorescent protein SuperClomeleon (sCLM); 2) Fluorescence Lifetime IMaging (FLIM) of the Cl- sensitive fluorophore MEQ; and 3) electrophysiological measurements of EGABA. These methods collectively demonstrated stable [Cl-]i microdomains in individual neurons in vivo. Fluorometric and electrophysiological estimates of local [Cl-]i were highly correlated. [Cl-]i microdomains persisted after pharmacological inhibition of cation-chloride cotransporters (CCCs) but steadily decreased after inhibiting the polymerization of the anionic macromolecule actin. These studies highlight the existence of functionally significant neuronal Cl- microdomains that modify the impact of GABAergic inputs. Copy rights belong to original authors. Visit the link for more info
O tema deste episódio é a energia solar: como funcionam os painéis capazes de captar a energia do sol, qual a Química por trás destes painéis e também como se faz para armazenar (ou estocar) a energia solar para uso posterior. Notas do episódio: https://pubs.rsc.org/en/content/articlelanding/2019/TA/C9TA04905C#!divAbstract https://onlinelibrary.wiley.com/doi/full/10.1002/cplu.201900330 https://estudogeral.sib.uc.pt/bitstream/10316/15328/1/Mestrado_Julia%20Valente.pdf http://www.cienciaviva.pt/docs/celulafotovoltaica.pdf https://recipp.ipp.pt/bitstream/10400.22/7667/1/DM_ManuelVilarica_2010_MEQ.pdf https://www.ufsj.edu.br/portal2-repositorio/File/coqui/TCC/Monografia-TCC-Leticia_M_C_Bernardes-20151.pdf http://static.sites.sbq.org.br/rvq.sbq.org.br/pdf/v7n1a08.pdf https://books.google.com.br/books?hl=pt-BR&lr=&id=M4diDwAAQBAJ&oi=fnd&pg=PP3&dq=energia+solar&ots=z3j1d87aZR&sig=WFD65_ghRyjzgtGvq3HOO0nlTmk#v=onepage&q=energia%20solar&f=false http://www.scielo.br/scielo.php?pid=S0102-47442004000200010&script=sci_arttext&tlng=pt http://solar.fc.ul.pt/i1.pdf Celula … Continue lendo EP.41: Energia solar, células fotovoltaicas e a ‘estocagem de luz’ →
La litiasis renal es una patología frecuente que produce en ocasiones trastornos importantes de la salud. Puede ser silente y dar alteraciones de la estructura renal si no se detecta y elimina a tiempo. En caso de que la litiasis se desprenda y ocupe la vía urinaria puede producir dilatación de esta vía y el temido cólico nefrítico (en un intento de expulsar este objeto que impide el drenaje normal de la orina).Las recomendaciones para cualquier paciente litiásico de oxalato son las siguientes 4:- Oxalatos: 40 a 50 mg/día.- Proteína: normalizar la ingesta a 0,8 a 1,0 g/kg de peso corporal/día.- Calcio: normalizar la ingesta de 800 mg/día para los hombres; 1.200 mg/día para las mujeres (equilibrar a lo largo del día).- Fluidos: 12 a 16 vasos para producir un volumen de orina de 2,5 L.- Sodio: menor consumo de 100 a 150 mEq/día (2.300 a 3.450 mg/día).- Calorías: Nivel para mantener peso saludable.- Vitaminas/suplementos minerales (vitamina B no es nociva, la vitamina C debe limitarse a la ingesta dietética de referencia).
La litiasis renal es una patología frecuente que produce en ocasiones trastornos importantes de la salud. Puede ser silente y dar alteraciones de la estructura renal si no se detecta y elimina a tiempo. En caso de que la litiasis se desprenda y ocupe la vía urinaria puede producir dilatación de esta vía y el temido cólico nefrítico (en un intento de expulsar este objeto que impide el drenaje normal de la orina).Las recomendaciones para cualquier paciente litiásico de oxalato son las siguientes 4:- Oxalatos: 40 a 50 mg/día.- Proteína: normalizar la ingesta a 0,8 a 1,0 g/kg de peso corporal/día.- Calcio: normalizar la ingesta de 800 mg/día para los hombres; 1.200 mg/día para las mujeres (equilibrar a lo largo del día).- Fluidos: 12 a 16 vasos para producir un volumen de orina de 2,5 L.- Sodio: menor consumo de 100 a 150 mEq/día (2.300 a 3.450 mg/día).- Calorías: Nivel para mantener peso saludable.- Vitaminas/suplementos minerales (vitamina B no es nociva, la vitamina C debe limitarse a la ingesta dietética de referencia).
In Part 2 of #meQ, Mindy Caterina and Garrett Jamieson break down the evidence of Lucy DeCoutere and S.D., the remaining two witnesses/complainants in the Jian Ghomeshi trial. Afterward, we discuss the fallout: how the media and campus movements treated Jian Ghomeshi's lawyer, Marie Henein, and Lucy DeCoutere's response to an article Jian Ghomeshi wrote years after the trial.Finally, we ask if this trial created an opportunity to examine different ways of approaching sexual assault in Canada. We've talked about how and why the current system is the way it is. Is it the best tool to address this difficult issue? Could there be another way forward? Brighter minds than ours will figure out these answers. We just hope we can contribute to making this an informed conversation!Useful Links:Maclean's article that focused on the appearance of Jian Ghomeshi's defence team (discussed in this podcast episode)"Let Justice Speak" - a defence lawyer discusses the opposition to Jian Ghomeshi's defence lawyer, Marie Henein, speaking at university campusesEpisode website: https://lawlawlandshow.com/episode-8-meq-unpacking-the-jian-ghomeshi-trial-part-2-of-2
I detta avsnitt tar vi upp lite info infor er tentamen! Vad forvantar vi oss att ni kan? Hur gar MEQ till? Vi pratar ocksa lite om hur det kanns att kugga och vilken matsack som ar bast!
Summary Working 9 to 5 may not be the best way for everyone to maximise their productivity. In this episode we look at the science of chronotypes, and how leaders can use our natural sleep/wake cycles to get the best out of their people. Transcript Hello and welcome to episode 29 of the Leadership Today Podcast where each week we tackle one of today’s biggest leadership challenges. Today we are talking about chronotypes and the perils of working 9 to 5. As you wade into research about patterns in daily productivity, focus and sleep, you find a wealth of information, often confusing and sometimes contradictory. So let’s start with the basics. Chronotypes are used to categorise people based on their sleep/wake cycles across a 24 hour period. There are three main chronotypes - morning, intermediate and evening types. These follow a normal distribution, so 50% of people are classed as intermediate types. But even these intermediate types can have a preference towards morning or evening. Your chronotype impacts when you best exercise, concentrate, eat and sleep - it’s not just a learned preference, it has a biological basis. Hormones are part of that biological basis. For example, the hormone melatonin starts being produced in greater levels by the pineal gland as a person approaches sleep, it peaks during the night, and then more rapidly declines towards waking time. Another hormone, cortisol, follows an opposing pattern - rising as morning approaches, peaking later in the morning, then tapering off towards evening. Cortisol is typically classed as a stress hormone, and you’ve probably only heard bad things about it. But, in moderation, it has a number of positive benefits relating to concentration, energy levels, and positive mood. Peaks in melatonin typically vary by around four hours between morning and evening types. A morning type could have a melatonin level at 7pm that an evening type doesn’t reach until 11pm. Some research has even seen ranges in melatonin peaks of up to ten hours. You can imagine the impact of forcing morning and evening types to go to sleep or wake at the same time. Yet so often our business hours are a compromise between these two types - 9 to 5. I’m definitely a morning person, and that has become even clearer now I have greater flexibility over my day. This morning preference has also become more pronounced as I age, but more on that soon. In contrast, I remember a participant on a leadership program with a quite different chronotype to me. She really struggled with the program’s 8.30am start time, which was an hour earlier than when she usually got to work. She wasn’t particularly sharp in the morning. While others were asking questions and engaging in activities, this participant took a while to warm up. However, at the very point when most people were fading in the afternoon, this person came into their own - they were asking questions, engaging with activities and were much more physically animated. During a break I asked what her perfect work day would look like if she had absolute freedom to choose. It turns out her perfect work day would be 11am to 7.30pm. In fact she had even suggested these work hours to her manager. This would allow her to get up around 9.30am, and still have time to get to the gym before work. But most of her fellow team members were working 8.30am to 5pm, and her manager thought an 11am start would be too extreme. They ended up negotiating a compromise of 9.30am to 6pm, but it was common for her to work an extra hour or two at the end of the agreed work day when she felt particularly sharp and focused. Interestingly she did work her preferred hours when she worked from home - no one noticed any difference and she felt great. I wonder how much those compromised hours are costing her and the business. The impact of having people working outside their preferred hours is much like crossing time zones - having to wake consistently earlier, or later than our natural biological rhythms. This wreaks havoc on our bodies and health. Even one hour shifts for daylight saving changes mess with our biological clocks, and you can even see the impact of that in mental health and crime statistics. Sleep wake cycles are also linked to age. Teenagers need more sleep, and tend to shift towards later sleep and wake times, achieving what’s known as “peak lateness” at 19 years old. Given this, the optimal school day for most teenagers should start around 10am or even later. As we age, we tend to shift more towards the morning. For example, men on average shift from evening to morning types around 40 years of age. So older workers may prefer an earlier start, but there is a very broad distribution of preferences at any age. As a leader there are a number of ways in which we can take chronotypes into account to support both individuals and the business: Ask individuals - if they could pick their perfect work hours, what would they be? It’s important to not set up an expectation that you can automatically provide these hours, but it’s a great question to gain additional information that could impact rosters and work times. Assess and raise awareness about chronotypes - The Center for Environmental Therapeutics has an online version of the often-used Morning Evening Questionnaire (or MEQ) which can help people to identify their chronotype. I’ve included a link to the questionnaire in the show notes (http://www.cet-surveys.com/index.php?sid=61524). Provide flexibility - encourage people to trial different work hours when they are working at home. Just be aware that, like jet lag, it takes a few days to adjust into a new rhythm. Communicate - like any other diversity in the workplace, there is a risk of misunderstanding. Make sure you communicate when people are trialing new hours so people don’t think the other types are being lazy by either leaving earlier or arriving later than usual. Focus on outputs - measure what people deliver, not how long it takes them or the process. This will provide people with greater flexibility over how they produce results. And chronotypes aren’t just about how you lead others, they’re also important for managing yourself. Here are some things to try if you’re struggling with your sleep/wake cycle: Complete the assessment - find out what your preferred chronotype is. Negotiate work time experiments. Sometimes managers are concerned about making large changes and what that might mean for them and the team they manage. Turning this into experiments may give them more confidence. Even if your new work hours are a complete failure, they can always change back. Go with consistent sleep times - go to bed and wake up at the same times every day. It makes a huge difference in really establishing those rhythms. Make sure you get plenty of light in the morning and not much at night - get outdoors in the morning so your brain and body can synch with sunlight cues, and avoid screens at night. In winter consider bright lights in morning and dimmer lighting in the evenings. Sleep is really tightly linked with diet and exercise, so improvements in these will also help the quality of our sleep. Read up - there are two really interesting books that I highly recommend around these topics: Why we sleep: The new science of sleep and dreams. By Matthew Walker. It includes some fascinating science, and there’s a particularly great narrator on the audio book - in fact I’ve fallen asleep while listening to that book on more than one flight. When: The scientific secrets of perfect timing. By Daniel Pink. Daniel has a fantastic ability to consolidate a broad range of scientific research together with entertaining stories focused on decision making and chronotypes. Well I hope you found the content in this episode helpful. As always it would be great if you could share the podcast with your friends and work colleagues, and please make contact via the leadership.today website if you have any feedback or questions. See you next week. Research Find out your type by taking the Morning Evening Questionnaire by the Center for Environmental Therapeutics: http://www.cet-surveys.com/index.php?sid=61524 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4868668/ - Emotion. 2016 Jun; 16(4): 431–435. Published online 2016 Mar 7. Positive upshots of cortisol in everyday life Lindsay T. Hoyt,1,* Katharine H. Zeiders,2 Katherine B. Ehrlich,3 and Emma K. Adam3,4,* https://www.psychologytoday.com/au/blog/the-land-nod/201301/changing-night-owl-lark https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0178782
¡Emprender SÍ! El Podcast Episodio 07 Mujeres Emprendedoras de Querétaro Amigo emprendedor, tu mente puede poseer cualidades extraordinarias pero, lo cierto es que varias mentes valiosas y bien enfocadas siempre te ayudarán a ampliar la visión que has fijado para tu emprendimiento. En este sentido, Mujeres Emprendedoras de Querétaro, MEQ, por sus siglas, se ha convertido en un importante punto de apoyo para muchas mujeres que han escuchado ese poderoso llamado interno a emprender. En entrevista privada para ¡Emprender Sí! El Podcast, Blanca Villeda y Nayeli Ramírez, líderes de MEQ, conversaron con Eric Solano en el parque, tal como escucharán, sobre su dinámica de trabajo, casos exitosos y, ¿por qué no?, también algunos errores naturales del emprendimiento. ¡Emprender Sí! El Podcast, es producido en la ciudad de Querétaro, México, por Eric Solano para ICONEMA COMMUNICATION & FILMS. Todos los derechos reservados. ¡Emprender Sí! El Podcast, está dirigido a todas las personas de habla hispana que ya emprendieron algún negocio o están pensando en hacerlo. ¡Genérate más! Puedes descargar / escuchar más episodios de ¡Emprender Sí! El Podcast, en: Ivoox: https://mx.ivoox.com/es/27720098 iTunes: https://itunes.apple.com/mx/podcast/emprender-sí-el-podcast/id1428833739?mt=2 Facebook: http://ow.ly/Gp7K30m42Fo Youtube: http://ow.ly/3sbr30m42Vs Suscríbete a nuestro canal: https://www.youtube.com/iconema_sub_confirmation=1 Búsquenos también en Linkedin: https://www.linkedin.com/in/iconemacf/ Canción a la mitad de este episodio: Every Kind Of People, de Ana Popovic En Spotify: https://open.spotify.com/track/7emJRv7wSOfoDQAR122qNn?si=1m6SHsFmRwaLI9kOFycnRA En iTunes: https://itunes.apple.com/mx/album/can-you-stand-the-heat/628144875 Canal oficial en Youtube: https://www.youtube.com/user/anapopovicband/videos Muchas gracias por escuchar ¡Emprender Sí! El Podcast. Atentamente, Eric Solano, director general y agente de medios de comunicación en ICONEMA COMMUNICATION & FILMS. ¡Genérate más!
The Editorial Committee of Australasian Psychiatry hopes to engage trainees by providing practice Modified Essay Questions (MEQ) and providing some guidance as to how best to answer these questions. These questions also serve as a good refresher for established clinicians.
This week we discuss the presentation and treatment of hypokalemia. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_61_0_Final_Cut.m4a Download Leave a Comment Show Notes Take Home Points Hypokalemia has a wide variety of presentations ranging from generalized weakness, to paralysis, to cardiac arrhythmia or cardiac arrest. When you discover hypokalemia, be sure to check and EKG. Think about underlying causes of hypokalemia, because it is rarely a solo event. Treat with oral potassium supplementation of 40-60 orally every 4-6 hours for mild hypokalemia and 10-20 mEq/hour IV for severe or symptomatic hypokalemia. Additional Reading LITFL: Hypokalemia LITFL: Hypokalemic Periodic Paralysis Core EM: Hypokalemia Read More
This week we discuss the presentation and treatment of hypokalemia. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_61_0_Final_Cut.m4a Download Leave a Comment Show Notes Take Home Points Hypokalemia has a wide variety of presentations ranging from generalized weakness, to paralysis, to cardiac arrhythmia or cardiac arrest. When you discover hypokalemia, be sure to check and EKG. Think about underlying causes of hypokalemia, because it is rarely a solo event. Treat with oral potassium supplementation of 40-60 orally every 4-6 hours for mild hypokalemia and 10-20 mEq/hour IV for severe or symptomatic hypokalemia. Additional Reading LITFL: Hypokalemia LITFL: Hypokalemic Periodic Paralysis Core EM: Hypokalemia Read More
This week we discuss the presentation and treatment of hypokalemia. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_61_0_Final_Cut.m4a Download Leave a Comment Show Notes Take Home Points Hypokalemia has a wide variety of presentations ranging from generalized weakness, to paralysis, to cardiac arrhythmia or cardiac arrest. When you discover hypokalemia, be sure to check and EKG. Think about underlying causes of hypokalemia, because it is rarely a solo event. Treat with oral potassium supplementation of 40-60 orally every 4-6 hours for mild hypokalemia and 10-20 mEq/hour IV for severe or symptomatic hypokalemia. Additional Reading LITFL: Hypokalemia LITFL: Hypokalemic Periodic Paralysis Core EM: Hypokalemia Read More
Steve Cash isn't just an incredible author of the Meq trilogy, he's also been a painter, poet, and founding member of the rock group The Ozark Mountain Daredevils. Del Rey editor-in-chief Betsy Mitchell sat down with the multi-talented author to talk about his latest book, the concluding novel in the Meq trilogy, THE REMEMBERING. They also touch on Steve's other passions: painting and rock 'n' roll.Hey, our music changed! We're featuring two songs from Steve and his group in this week's podcast. Be sure to keep an eye on our feed, as we'll also be sending these out in their entirety for you to listen to later on in the week. All songs appear by permission of Steve Cash and are not for resale. Intro music: If You Want to Get to Heaven - The Ozark Mountain Daredevils (live). Outro music: The Vine and the Rose - The Ozark Mountain Daredevils (live). Suvudu: http://www.suvudu.com/