Podcasts about meq

The Elective Rotation: A Critical Care Hospital Pharmacy Podcast

Play Episode Listen Later Jan 29, 2024 105:56

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

god water eating goal normal worry states dark raise figure experiments salt skin points extreme rap iv progressive rice burns shock muscle serial increased hip talks damage sweat evaluation initial references gi acid gb severe bp recommend chest dry bleeding dl stomach spreads atp maternal plasma urine promotes obstetrics cerebral isbn suggests diarrhea ns glucose inability seizures electrolytes abdominal sympathetic renal elastic pulmonary lr intestinal british journal irreversible potassium impaired bun detected saline mew footnote postural anp lethargy tubular raas ringers gfr appraising nacl albumin physiologically jci feto lactic z39 hemodynamics vog dextrose renin frim obligate hgb meq isotonic colloids hco nahco3 polyuria

882: Does 10 mEq of Potassium Actually Increase Serum Potassium Levels By 0.1 mEq/L?

Play Episode Listen Later Dec 28, 2023 2:55

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.

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882: Does 10 mEq of Potassium Actually Increase Serum Potassium Levels By 0.1 mEq/L?

The Elective Rotation: A Critical Care Hospital Pharmacy Podcast

Play Episode Listen Later Dec 28, 2023 2:55

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.

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Ep 168: Critical thinking, Curiosity, and Communication w/ Dr. Sabine Charles (Charles Financial Strategies)

The Audit Podcast

Play Episode Listen Later Nov 21, 2023 34:46

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.

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Tribe Talkin' Ep 8: Best in class SaaS metrics

Transparent Venture Capital by Tribe Global Ventures

Play Episode Listen Later Oct 3, 2023 68:48

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

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Chapter Thirteen Meaning and Application of Urine Chemistries

The Litigation Psychology Podcast

Play Episode Listen Later Sep 18, 2023 91:40

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

The Litigation Psychology Podcast - Episode 178 - Expert Advice on Negotiation in Litigation

Play Episode Listen Later Aug 21, 2023 44:45

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

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Chapter Eleven, part 2: Regulation of Acid-Base Balance

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Play Episode Listen Later May 20, 2023 90:48

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 in the Face of Change with Jan Bruce at meQuilibrium

Leaders in the Trenches

Play Episode Listen Later May 11, 2023 21:53

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!

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Building a real estate empire one property at a time - Calgary - Canada's Podcast

Canada's Podcast

Play Episode Listen Later Apr 11, 2023 25:18

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

Chapter Eleven, part 1: Regulation of Acid-Base Balance

Play Episode Listen Later Feb 12, 2023 97:04

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

Chapter Ten : Acid-Base Physiology

HelixTalk - Rosalind Franklin University's College of Pharmacy Podcast

Play Episode Listen Later Dec 31, 2022 78:13

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

157 - Everything Will Be ao-K+: Potassium Formulations and Dosing for Hypokalemia

Play Episode Listen Later Nov 29, 2022 37:32

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.

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Podcast 833: NS vs LR

Emergency Medical Minute

Play Episode Listen Later Nov 28, 2022 5:16

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!

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RL 199: "It's A Wonderful World"

ASAPWeekly Rocket League Podcast

Play Episode Listen Later Nov 16, 2022 59:26

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

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13. Critical Measures of Leadership Awareness: MeQ, EmQ, and SocQ

C-Suite Intelligence

Play Episode Listen Later Nov 8, 2022 20:40

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.

ceo leadership business development emotional intelligence eq measures leadership skills business goals executive leadership meq

How Israel Stopped Syria's Nukes with Yuval Steinitz

Middle East Forum Radio

Play Episode Listen Later Oct 24, 2022 43:02

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?

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BEST way to CONVERT mEq/mL to percent strength

Pharmaceutical Calculations

Play Episode Listen Later Sep 5, 2022 6:57

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.

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Erişkin Hastada Metabolik Asidoz Yönetimi

planning principal mri mike rogers medical equipment meq

Play Episode Listen Later Jul 21, 2022 10:02

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

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Sodium Bicarb

Paramedic Drug Cards

Play Episode Listen Later Jun 17, 2022 1:03

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

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Medical Equipment Planning

SSR On Air

Play Episode Listen Later May 23, 2022 23:04

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.

Medical Equipment Planning

SSR On Air

Play Episode Listen Later May 23, 2022 23:04

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.

planning principal mri mike rogers medical equipment meq

Zehirlenmeli Hastada Eliminasyon Yöntemleri

quebec minist preschool shifted conseill meq

Play Episode Listen Later Mar 31, 2022 10:44

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 (

exchange bu vd bir ancak klasik tablo hepimizin meq meq l

ShiftED: Katherine Divolis (MEQ) on Quebec's Preschool Journey

LEARN Podcasts

Play Episode Listen Later Jan 27, 2022 27:54

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.

Mental Health and Well-being

In Orbit: A KBR Podcast

Play Episode Listen Later Oct 5, 2021 26:00 Transcription Available

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.

mental health world mental health day meq mequilibrium

#035: 7 habits of highly resilient people

UTC Healthy You

Play Episode Listen Later Oct 5, 2021 19:28

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 puerto rico 7 habits resilient people meq mequilibrium highly resilient people

#035: What, When and Where

UTC Healthy You

Play Episode Listen Later Oct 5, 2021 11:23

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 puerto rico meq mequilibrium

Pénurie de main-d'œuvre : les coûts

Télé-Gaspé - Une télévision par et pour les gens d'ici!

Play Episode Listen Later Sep 29, 2021 19:22

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/

proulx meq

E7: A kemi mësuar nga gabimet?

Ku Ishim E Ku Po Ikim?

Play Episode Listen Later Aug 30, 2021 32:43

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.

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Episode 47. I Plead the Fifth! 5 vs 10 units of Insulin for Hyperkalemia

The Pharm So Hard Podcast: An Emergency Medicine and Hospital Pharmacy Podcast

Play Episode Listen Later Aug 6, 2021 7:27

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.

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Freely Filtered 037: The first Guideline Draft: KDIGO Hypertension Guidelines

Freely Filtered, a NephJC Podcast

Play Episode Listen Later Jul 25, 2021 90:49

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/

#35: potassium citrate (Urocit-K) | An Alkalinizing Agent for Managing Kidney Stones

Drug Cards Daily

Play Episode Listen Later Jun 14, 2021 4:20

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

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#34: potassium chloride (K-Tab) | Treatment and Management of Hypokalemia

Drug Cards Daily

Play Episode Listen Later Jun 7, 2021 9:22

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

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40 mEq doesn't fix hypokalemia

Drugs (Sometimes) Work

Play Episode Listen Later Apr 6, 2021 17:01

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."

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Preparing for the Essay Style Exam - Modified Essay Questions (MEQ)

Psych Matters

Play Episode Listen Later Mar 11, 2021 42:00

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.

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Çocuklarda Septik Şok ve Sepsis İlişkili Organ Disfonksiyonu

Play Episode Listen Later Jan 11, 2021 18:15

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

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Çocuklarda Septik Şok ve Sepsis İlişkili Organ Disfonksiyonu

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Play Episode Listen Later Jan 11, 2021 18:15

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

iv oc sd organ kb o2 yan sepsis ate sirs ssc ards ancak kili beyaz burada mmhg gks meq fio2 paco2

Pharmacy Phriday #6: Tik Tok Benadryl Challenge and Diphenhydramine Toxicity

Emergency Medical Minute

Play Episode Listen Later Jan 1, 2021 6:42

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

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IN YOUR PHASE EPISODE XII: MENTORING THE PROFESSIONAL

In Your Phase Podcast

Play Episode Listen Later Oct 31, 2020 104:34

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.

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Value of Water Series: Water Access Perspective with COPE

Talking Under Water

Play Episode Listen Later Oct 30, 2020 28:23

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.

Value of Water Series: Community Perspective with Milwaukee Water Commons

Talking Under Water

Play Episode Listen Later Oct 23, 2020 25:26

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.

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Get Coached in TRANSIT10N from Sports to Life with Joy Burke

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Play Episode Listen Later Sep 25, 2020 44:16

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!

Saying YES to your dreams with Greg Williams

Play Episode Listen Later Sep 18, 2020 42:40

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!

Transitioning from Sports to Life with Ben Sigmund

Play Episode Listen Later Sep 11, 2020 50:57

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!

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TRANSIT10N Through RELAT10NSHIP Loss with Jane Cebrynski

Play Episode Listen Later Sep 4, 2020 44:14

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!

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How to become a Certified Sports Life Coach

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Play Episode Listen Later Aug 28, 2020 56:01

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!

Leading a CHAMP10N Life with Eroni Clarke

Play Episode Listen Later Aug 21, 2020 55:02

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!

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How to Manage Your Energy for Overall Wellbeing with Helen Regan

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Play Episode Listen Later Aug 14, 2020 43:43

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

Esp: ¿Que es Mentalidad Equilibrada?

Mentalidad Equilibrada

Play Episode Listen Later Aug 1, 2020 24:16

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

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How to Be in RELAT10NSHIP with Yourself with Rory Clark

Play Episode Listen Later Jul 24, 2020 47:10

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

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Esp: Pruebas, tipos de exito y cambios de mentalidad.

Mentalidad Equilibrada

Play Episode Listen Later Jul 18, 2020 15:26

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

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How to Get Healthy with Rory Clark

Play Episode Listen Later Jul 17, 2020 41:55

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

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How to Feel Grounded in Wellbeing with Luke Sniewski