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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

"El bicarbonato de sodio (también llamado bicarbonato sódico, hidrogenocarbonato de sodio, carbonato ácido de sodio o bicarbonato de soda) es un compuesto sólido cristalino de color blanco soluble en agua, con un ligero sabor alcalino parecido al del carbonato de sodio (aunque menos fuerte y más salado que este último), de fórmula NaHCO3. Se puede encontrar como mineral en la naturaleza o se puede producir artificialmente. La forma mineral natural es nahcolita. Es un componente del mineral natrón y se encuentra disuelto en muchos manantiales minerales."Así describe Wikipedia este milagroso compuesto químico, al que se le atribuyen todo tipo de propiedades.Y si, amigos y amigas, porque ustedes lo pidieron, decidimos hacer chistes sobre este producto. Esperamos estar a la altura de tan retadoras peticiones.

As founder of Lunya and Lahgo, Ashley Merrill is celebrating rest with intentionally crafted restwear in a simple mission: to elevate rest in people's lives. Beyond Lunya and Lahgo, Ashley is principal at impact investing firm NaHCO3, where she leverages her background in venture, technology, and the arts to invest in ways that utilize business to create opportunity and move humanity forward. Ashley is also cofounder of The Deep, a media platform that makes philosophy and personal exploration accessible through thought-provoking questions and the Chairwoman of Outdoor Voices. Both personally and professionally, she is an active supporter of organizations like SOLA, Upstream, and United Medical Corps. She is a Southern California native and resides there with her husband and their two young children. Meet My Guest: WEBSITE: Lunya.co FACEBOOK: /lunya.co LINKEDIN: /lunya-company

a befejező rész - Roland utolsó interaktív előadásával ezzel részünkről egy időre lezárjuk a témát. 2+ óra tudomány és praktikum, vízkezelő sók, mi mit csinál, mire van hatással, milyen paraméteren érdemes és melyiken nem érdemes parázni. még konkrét vízrecept készítés is van Brewfather-rel. beszélnek: Barla Roland, Mezei Krisztián, Posta Viktor, és Nyaras Tamás a "só notes" most megegyezik az epizód borítóképével, de legyen meg itt is: - kréta = chalk = CaCO3 = kalcium-karbonát  - szódabikarbóna = baking soda = NaHCO3 = nátrium-hidrogén-karbonát - gipsz = gypsum = CaSO4 = kalcium-szulfát   - útszóró só = calcium chloride = CaCl2 = kalcium-klorid   - keserűsó = epsom salt = MgSO4 = magnézium-szulfát    - konyhasó = canning salt = NaCl = nátrium-klorid

留言告訴我你對這一集的想法： https://open.firstory.me/story/ckv7ua3m13bcq0822ntuzggsy?m=comment Mandarin Lessons: https://www.yunfei.world/languages/mandarin/Book lessons with this code to get more discounts: huimin F Email: zhuimin9698@gmail.comIG@ ministar723 生詞shēngcí （Vocabulary） 1. 民宿 Mínsù 2. 太平洋 Tàipíngyáng 3. 海岸山脈Hǎi'àn shānmài 4. 淺綠色 Qiǎn lǜsè 5. 海岸Hǎi'àn 6. 海岸線Hǎi'ànxiàn 7. 徒步旅行Túbù lǚxíng 8. 體力Tǐlì 9. 水上活動Shuǐshàng huódòng 10. 不敢Bù gǎn 11. 乾爽Gānshuǎng 12. 晴天Qíngtiān 13. 出大太陽Chū dà tàiyáng 14. 選擇Xuǎnzé 15. 碳酸氫鈉: Tànsuān qīng nà:NaHCO3 16. 消除疲勞Xiāochú píláo 17. 原住民Yuán zhùmín 18. 阿美族Āměi zú 19. 卑南族Pēi nán zú 20. 氣氛Qìfēn 21. 生活步調 Shēnghuó bùdiào Powered by Firstory Hosting

Today's episode is a replay of one of our earliest interviews,  all about reclaiming the art of leisure in our busy lives. We discuss the importance of downtime and why it's actually productive, while also getting real about the challenges involved in reclaiming your leisure time as both founders and as working moms. We offer tactical advice to implement more meaningful downtime into your day and discuss Lunya's new initiative Otium, which aims to promote more meaningful leisure through eating, playing, resting, contemplating, learning, resting and so much more. Learn more about Otium here.About the guest: As the founder of Lunya and Lahgo, Ashley Merrill is reinventing sleepwear for modern women and men, respectively. Both brands share a simple mission: to make people feel confidently comfortable -- at home and within themselves. Beyond her sleepwear entrepreneurship, Ashley is principal at impact investing firm NaHCO3, where she leverages her background in venture, technology, and the arts to invest in ways that leverage business to create opportunity and move humanity forward. Ashley is also CEO and co-founder of The Deep, a media platform that makes philosophy and personal exploration accessible through thought-provoking questions and content. Both personally and professionally, she is an active supporter of organizations like Girls Inc., Upstream, and United Medical Corps. She is a Southern California native and resides there with her husband and their two young children.Connect with Ashley on Instagram at @ashley_merrill Discover her modern sleepwear companies  Lunya and LahgoAbout the Host: Tiffany Paul is a mom, wife and entrepreneur, founder of The Slept Life and inventor of the Sleeper Scarf. She left her decade long corporate career in 2019 to go after her dream of being her own boss. This show is a peak inside her journey.Please stay in touch with us after the show on Instagram!@tiffanynicolepaul@dreamlifepodcast@thesleptlife

惰性/ Ready for

As founder of Lunya and Lahgo, Ashley Merrill is reinventing sleepwear for modern women and men, respectively. Both brands share a simple mission: to make people feel confidently comfortable -- at home and within themselves.  Beyond her sleepwear entrepreneurship, Ashley is Chairwoman of the Board at Outdoor Voices, a direct-to-consumer recreation label. She is also CEO and co-founder of The Deep, a media platform that makes philosophy and personal exploration accessible through thought-provoking questions and content. As principal at impact investing firm NaHCO3, where she leverages her background in venture, technology, and the arts to invest in ways that create opportunity and move humanity forward. Both personally and professionally, she is an active supporter of organizations like Girls Inc., Upstream, and United Medical Corps. She is a Southern California native and resides there with her husband and their two young children.  Shop Luyna: https://www.lunya.co/ Find out more about how you can change your conversations with The Deep: https://www.thedeep.life/products/the-deep-a-card-game

Chapter Three: How the proximal tubule is like Elizabeth Warren and other truths my friends from Boston taught me References for Chapter 3: Faisy C, Meziani F, PLanquette B et al. Effect of Acetazolamide vs. Placebo on Duration of Invasive Mechanical Ventilation among patients with chronic obstructive pulmonary disease: a randomized clinical trial. JAMA 2016 https://pubmed.ncbi.nlm.nih.gov/26836730/This randomized controlled double blinded multi-center study of acetazolamide to shorten the duration of mechanical ventilation (known as DIABLO) there was no statistically significant difference (though it may have been underpowered to do so).Salazar H, Swanson J, Mozo K, White AC, Cabda MM Acute Mountain sickness impact among travelers to Cusco, Peru J Travel Med 2012 https://pubmed.ncbi.nlm.nih.gov/22776382/ Investigators found that altitude sickness is common and alters travel plans for 1 in 5 travelers but was prescribed infrequently.Buzas GM and Supuran CT. Journal of enzyme inhibition and medicinal chemistry 2015 https://www.tandfonline.com/doi/full/10.3109/14756366.2015.1051042This review describes the use of acetazolamide to treat peptic ulcers and how it was later learned that H. pylori have carbonic anhydrase NORDIC idiopathic intracranial Hypertension Study Writing Committee. The effect of acetazolamide on visual function in patients with idiopathic intracranial hypertension and mild visual loss: the idiopathic intracranial hypertension treatment trial. JAMA 2014 https://pubmed.ncbi.nlm.nih.gov/24756514/In this multi-centered trial, acetazolamide and low sodium weight reduction diet improved mild visual loss more than diet alone. Mullens W et al. Rationale and design of the ADVOR (acetazolamide in decompensated heart failure with volume overload trial) Eur J Heart Failure 2018 https://pubmed.ncbi.nlm.nih.gov/30238574/This reference explains the rationale for this ongoing trial.Gordon CE, Vantzelfde S and Francis JM. Acetazolamide in Lithium-induced nephrogenic diabetes insipidus NEJM 2016 https://www.nejm.org/doi/full/10.1056/NEJMc1609483A case report of efficacy of acetazolamide in a patient with severe polyuria.Zehnder D et al. Expression of 25-hydroxyvitamin D-1alpha hydroxylase in the human kidney. JASN 1999 This report explores the activity in the enzyme in nephron segments and suggests that the distal nephron may play an important part in the formation of 1,25 vitamin D https://jasn.asnjournals.org/content/10/12/2465Outline: Chapter 3 - This is chapter three, kind of the first real chapter of the book- Proximal Tubule- Reabsorbs 55-60% of the filtrate - Active sodium resorption - 65% of the sodium - 55% of the chloride - 90% of HCO3 - 100% glucose and amino acids - Passive water resorption - Water resorption is isosmotic - Secretion of - Hydrogen - Organic anions - Organic cations - Anatomy - S1, S2, S3 can be differentiated by peptidases - S1 more sodium resorption and hydrogen secretion, high capacity - S2 more organic ion secretion - Cell model - Basolateral membrane - Na-K-ATPase powers all the resorption - Luminal membrane - 100 liters a day crosses the proximal tubule cells - Microvilli to increase surface area - Microvilli has brush border which has carrier proteins as well as carbonic anhydrase - Water permeable, so sodium resorption leads to water resorption - Aquaporin-1 (sounds like this transporter is unique to the proximal tubule and RBC) - HCO3 is reabsorbed early, along with Na, resulting in increased chloride concentration which passively reabsorbed via paracellular route. - Tight junction has only one strand (on freeze fracture) as opposed to 8 in distal nephron - The Na-K-ATPase - Lower activity than in the LOH and distal nephron - Maintained intracellular Na at effective concentration of 30 mmol/L - Interior of the cell is negative due to 3 sodium out and 2 K in, then K leaks back out. - 3 Na out for 2 K in - An ATP sensitive K outflow channel on the basolateral membrane - Increased ATP slows potassium eflux - The idea is if Na-K slows, ATP will accumulate and this will slow K leaving, because there is less potassium entering. - K channel is ATP sensitive, ATP antagonizes K leak. - Highly favorable ELECTROCHEMICAL gradient for sodium to flow into the cell through the luminal membrane - Must be via a channel or carrier - Cotransporters - Amino acids - Phosphate - Glucose - Called secondary active transport - Countertransporters - Only example is H excretion - Basolateral membrane - Na-3HCO3 transporter - Powered by the negative charge in the cell- Chloride resorption - Formate chloride exchanger - Formate combines with hydrogen in the lumen, becomes neutral formic acid, and is reabsorbed where the higher pH causes it to dissociate and recycle again. - Dependent on continued H+ secretion - Chloride moves across basolateral membrane thanks to Cl and KCl transporters, taking advantage of negative intracellular charge- Passive mechanisms of proximal tubule transport - Accounts for one third of fluid resorption - Mechanism - Early proximal tubule resorts most of the bicarb and less of the chloride - Tubular fluid gets a high chloride concentration - Chloride flows through the tight junction down its concentration gradient - Sodium and water follow passively behind - Water moves osmotically into intercellular space from tubular fluid even though the osmolalities are equal since chloride is an ineffective osmole, so tonicity is not the same. ****** - Argues that bicarb is primarily important solute for passive resorbtion - Acetazolamide blocks Na and chloride resorption - Similar thing happens with metabolic acidosis where less bicarb is available to drive passive resorbtion of Na and Cl - Summary - Other than Na-K-ATPase Na-H antiporter main determinant of proximal Na and water resorption - 1. Direct bicarb resorption - Preferential bicarb resorbtion proximally drives passive chloride resorption - Drives active the formate exchanger for chloride resorption- Neurohormonal influence - AT2 drives a lot of Na resorption, primarily in S1 segment - Does not have a net effect on H-CO3 movement - Dopamine antagonizes sodium resorption - Blocks both Na-K-ATPase and - Na H antiporter- Capillary uptake - Starlings. Again - Low hydraulic pressure due to glomerular arteriole - High plasma on oncotic pressure from loss of the filtrate - The two together promote resorption - There maybe movement from interstitial back into tubular fluid (back diffusion) conflicting data- Glomerular tubular balance - The fractional tubular reabsorption remains constant despite changes in GFR (tubular load) - It is essential the GFR is matched by resorption - The rise in capillary osmotic pressure with increased GFR via increased filtration fraction is one mechanism of GT balance - Glomerular tubular balance os one of three mechanisms that prevents fluid delivery from exceeding the resorptive capacity of the tubules - GT balance - TG feedback - Autoregulation - GT balance can be altered if patients are volume overloaded or depleted - Closes this section with a story of a kid born without a brush border - Primacy of sodium in proximal tubule activity - Discusses bicarb resorbtion - There is no Tm for Bicarb as long as volume overload is prevented, in rats can rise over 60! - If you give NaHCO3 you get volume overload and the Tm I about 60 - Glucose - S1 and S2 have high capacity, low affinity glucose resorption - S3 has high affinity 2 Na fo every glucose - Tm glucose is 375 mg/min - For a GFR of 125t that comes out to 300mg/dL - 125 ml/min * 3mg/ml (300 mg/dL) = 375 mg/min - Functionally this is 200 mg/dL due to splay - Urea - Only 50-60 of filtered urea is excreted - Calcium Loop and distal tubule - Phosphate - 3Na-Phosphate high affinity transporters late in proximal tubule - three types of Na-Phos transporters, type 2 are the most important - regulated by PTH and plasma phosphate - PTH suppresses Phos resorption -Metabolic acidosis also reduces phosphate resorption (good to have phosphate in the tubule to soak up H+ - Decreased tubular pH converts HPO42- to H2PO4- which has lower affinity for phosphate binding site - Mg Loop and distal tubule - Uric AcidWhy do I love acetazolamide?- I love the proximal tubule- Many uses- Often forgottenMOA- Inhibit carbonic anhydraseMain effects- Renal: less bicarb reabsorption (ie less H secretion) à more distal Na/bicarb delivery à hypokalemic metabolic acidosis- Brain: reduce CSF production, reduce ICP/IOP, aqueous humor- Pulm: COPDNotes- Tolerance develops in 2-3 days- Sulfonamide derivative- Highly protein bound, eliminated by kidneys Source: Buzas and upuran, JEIMC, 2016S Data:1968 - High altitudeHigh altitude usually results in respiratory alkalosisAcetazolamide – lessens symptoms of altitude sickness (insomnia, headache) which occur because of periodic breathing/apnea1979- NEJM study took 9 mountaineers asleep at 5360 meters à improvement in sleep, improved SaO2 from 72 to 78.7 mmHg, reduce periodic breathing, increased alveolar ventilation (pCO2 change from 37 mmHg to 30.8mm Hg)1950s - Seizures/migrainesCAI reduces pH (more H intracellularly), K movement extracellularly à hyperpolarization and increase in seizure thresholdWeak CAI (Topamax, zonisamide) but not though to be important mechanism of antiseizure effect (topamax enhances inhibitory effect of GABA, block voltage dependent Na and Ca channels)Pulmonary/COPDThought to help with the metabolic alkalosis and as a respiratory stimulant to increase RR, TV, reduce ventilator timeIn 2001 Cochrane review – no difference in clinical outcomes, but did reduce pH and bicarb minimallyDIABLO study (RCT) on ventilated COPD patients – no difference in median duration of mechanical ventilation despite correction of metabolic alkalosisHigh altitude erythropoiesis (Monge disease)First described in 1925 via Dr. Carlos Monge Medrano (Peruvian doctor), seen in people living > 2500-3000 meters (more common in South America than other high altitude areas)Usually chronic altitude sickness with HgB > 21 g/dL + chronic hypoxemia, pHTNAcetazolamide – reduces polycythemia because induces a met acidosis à increases ventilation and arterial PPO2 and SaO2 à blunts erythropoiesis and reduces HCT and improves pulmonary vascular resistanceGI ulcersWhen H2 and PPI available, less useHistory: 1932 – observed alkaline tide, presumed existence of gastric CA (demonstrated in 1939)Acetazolamide was used to inhibit acid secretion in 1960s, ulcer symptoms, with reversible metabolic acidosis, BUT lots of SE (electrolyte losses, used Na/K/Mg salts to help, renal colic, headache, fatigue, etc)Later found H. Pylori encodes for two different CasHelps to acclimatize to acidic environmentBasically, the Ca changes CO2 into H+ and HCO3They also have a urease which produces NH3The NH3 binds with H+, leaving an alkaline environment for them to live inInhibition of CA with acetazolamide is lethal for pathogen in vitro1940sFound there was CA in pancreasThought acetazolamide to reduce volume of secretions from NGT (output from exocrine pancreas) Source: Human Anatomy at Colby Blog Diuretic resistanceIf develop hyperchloremic metabolic alkalosis, short course of acetazolamide + spironolactone (b/c need distal Na blockage) à can helpMay help with urine alkalization (ie uric acid stone) but increases risk of calcium phosphate stonesADVOR trial acetazolamide in HF exacerbation in Belgiumuse may help to prevent new episode, lower total diuretic doseCSF reduction (pseudotumor cerebri)Reduces CSF by as much as 48% when > 99.5% of CA in choroid plexus is inhibitedNORDIC trial (acetazolamide v. placebo) – improvement in visual symptoms especially if advanced papilledema, and reduced opening pressure)Side note also used off label to help with increased ICP and CSF leaks, as alternative to VP shunts, repeat LPs, etc Source: Eftekari et al, Fluid Barriers CNS, 2019.

Today's episode is all about reclaiming the art of leisure in our busy lives. We discuss the importance of downtime and why it's actually productive, while also getting real about the challenges involved in reclaiming your leisure time as both founders and as working moms. We offer tactical advice to implement more meaningful downtime into your day and discuss Lunya's new initiative Otium, which aims to promote more meaningful leisure through eating, playing, resting, contemplating, learning, resting and so much more. Learn more about Otium here. About the guest: As the founder of Lunya and Lahgo, Ashley Merrill is reinventing sleepwear for modern women and men, respectively. Both brands share a simple mission: to make people feel confidently comfortable -- at home and within themselves. Beyond her sleepwear entrepreneurship, Ashley is principal at impact investing firm NaHCO3, where she leverages her background in venture, technology, and the arts to invest in ways that leverage business to create opportunity and move humanity forward. Ashley is also CEO and co-founder of The Deep, a media platform that makes philosophy and personal exploration accessible through thought-provoking questions and content. Both personally and professionally, she is an active supporter of organizations like Girls Inc., Upstream, and United Medical Corps. She is a Southern California native and resides there with her husband and their two young children.Connect with Ashley on Instagram at @ashley_merrill  Discover her modern sleepwear companies  Lunya and Lahgo About the Host: Tiffany Paul is a mom, wife and entrepreneur, founder of The Slept Life and inventor of the Sleeper Scarf. She left her decade long corporate career in 2019 to go after her dream of being her own boss. This show is a peak inside her journey.Stay in touch with us after the show on Instagram!@dreamlifepodcast@thesleptlife@tiffanynpaulIf you enjoyed this episode, please write a review! It really helps a new show like ours get visibility. If you screenshot your review and DM us @dreamlifepodcast we'll send you a $10 credit towards Tiffany's online sleep marketplace The Slept Life.

You’ve heard Marc Merrill’s incredible story of founding Riot Games, creator of League of Legends. You’ve heard Ashley Merrill’s inspiring story of launching Lunya. In this episode, Marc and Ashley are BACK on the show - this time, together! - to share how they did it while building a family, the tough challenges they faced along the way (in both business as well as their relationship), and much more.Marc and Ashley also give us some updates on what’s next for them, their new project “The Deep,” their advice for couples (especially husband & wife founders), and their bold predictions for the 2020s.This is one of our most insightful and interesting conversations yet! You definitely don’t want to miss this!SUBSCRIBE TO TFH NEWSLETTER & STAY UPDATED > http://bit.ly/tfh-newsletterFOLLOW TFH ON INSTAGRAM > http://www.instagram.com/thefounderhourFOLLOW TFH ON TWITTER > http://www.twitter.com/thefounderhourINTERESTED IN BECOMING A SPONSOR? EMAIL US > partnerships@thefounderhour.com

Episode 33 features Ashley Merrill as we talk about how you can DO IT ALL - be a good wife, mama, and business woman. Ashley Merrill is a founder and CEO of Lunya, principal at investment firm NaHCO3, wife, and mother of two. She’s living the new female archetype, debunking the myth that women can’t be successful at home and work at the same time. Ashley worked for a VC at a young age, then later at a tech company where she hired her mom. For the past six years has been running her own fashion tech business notorious for their provocative ads and has recently launched her investment fund with her husband. This episode is sponsored by Drink Copper Cup, the best TUMERIC latte maker on the market! --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app

Who is Ashley? As founder of clothing companies Lunya and Lahgo, Ashley Merrill is reinventing sleepwear for modern women and men, respectively. Both brands share a simple mission: to make people feel confidently comfortable inside — inside their homes and inside themselves. Beyond her sleepwear entrepreneurship, Ashley is principal at impact investing firm NaHCO3, where […]

Merry Xmas! This weeks post was inspired by a recent unexpected case of severe hyperkalaemia in a severe pre-eclamptic - I have put together a fictitious case which is a little more severe in order to illustrate the principles of managing hyperkalaemia - I hope you enjoy & take it easy over Xmas! CASE HISTORY (*A fictitious patient history ) Your pager goes off - code blue medical labour ward! On arrival you are told the patient for whom the code was called has just arrived following an urgent transfer from another hospital. She presented to their service at 31 weeks with a headache, BP 190/100, proteinuria and mildly raised creatinine. She was diagnosed with severe pre-eclampsia, given labetalol, nifedipine and then transferred. She now appears confused with the following vital signs: HR 33/min, BP 74/55, SpO2 92%, RR 17/min (*Image courtesy www.lifeinthefastlane ) An immediate venous blood gas shows the following result: Na 139, K 8.4, pH 7.23, pCO2 37, pO2 63, Lactate 1.8 How are you going to manage this patient?   Immediate Standard Mgmt 1 - Is it real? Common causes of high potassium includes hemolysis of red cells from the sampling and handling process.  Always do an ECG whilst awaiting a repeat result - if the patient is compromised and the ECG is abnormal / consistent with hyperkalaemia then assume it is real and don't delay your treatment! The quickest way to get a repeat sample is usually a VBG this usually only takes a few minutes and will also give you the glucose and pH - important values to know for both mgmt and diagnosis. 2 - Prevent an arrhthymia Immediate mgmt - stabilise the cardiac membrane with intravenous calcium. Most guidelines recommend calcium if there are ECG changes or the absolute K level is over 7mmol/L. *Calcium chloride has 3 times more calcium than calcium gluconate. 3 - Shift K intracellularly a) Insulin / Glucose. Usual dose 10units actrapid + 25-50ml 50% Dextrose Stimulates Na/K/ATPase Give glucose to prevent hypoglycaemia' Lowers K by 0.5 -1 mmol/L per hour b) Salbutamol 20mg neb Good choice if the patient is bradycardic (common in severe hyperK) Stimulates Na/K/ATPase also c) NaHCO3 (if acidotic) When acidosis exists H+ is exchanged for intracellular K+ Makes sense to consider NaHCO3 if acidosis is present 50-100ml of NaHCO3 8.4% 4 - Eliminate K from the body (usually renal) - Enhance renal elimination - diuretics (e.g. frusemide), K free crystalloid (if indicated - saline) or both! - Dialysis - institute early in patients with complete renal failure -  GI exchange resins (eg resonium) most guidelines now consider they have no role in the acute management. 5 - Identify and treat the cause! - You need to address this issue to stop if from recurring! Usually multiple factors combine to lead to hyperkalaemia. Fix reversible causes especially drugs! Don't rely on your memory - get their medication chart out then google all the known drugs that can cause hyperkalaemia! Drugs Known to Cause / Contribute to hyperkalaemia (either impair excretion or promote transcellular shift) ACE inhibitors / AT2 antagonists Spironolactone / Amiloride NSAIDs Beta blockers (see discussion below) Trimethoprim Heparin Pentamidine Suxamethonium Renal dysfunction - almost always there is a degree of renal impairment preventing excretion of the excess K load. Make sure you aren't missing important reversible causes - e.g. obstruction (consider USS renal tract urgently).  Cell release (eg hemolysis, tumour lysis, trauma or extensive surgical injury). In our O& G patients this includes widespread tissue injury especially after major surgery or perhaps chemotherapy. BUT This is a pregnant woman with PET - renal impairment, acidosis, hemolysis, transfusion - these are common events in our pregnant patients. Cardiac Arrest Secondary to Hyperkalaemia

Core questions:   Define DKA. List 6 potential triggers of DKA. Describe the pathophysiology of DKA. (Fig 118.1) How is DKA managed in children? In adults? What are the epidemiologic risk factors for cerebral edema in DKA? What are signs and symptoms of cerebral edema? How do you manage a pt with DKA and suspected cerebral edema? List 5 complications of DKA management List five common serious infections in diabetics and how they are managed. How does hypoglycemia classically present? List 10 causes of hypoglycemia Describe the treatment of hypoglycemia What is the definition of hyperglycemic, hyperosmolar state? Contrast DKA and HHS (Table 118.2) What is the pathophysiology of HHS? How is HHS managed?   WiseCracks:   Why are urine ketones less sensitive for DKA than serum ketones? When do you give NaHCO3 to a patient with DKA? What is euglycemic DKA? What is the differential diagnosis of hypoglycemia in a patient who does not have DM? What would you add to the differential diagnosis in a pt who has DM?    

Core questions:   Define DKA. List 6 potential triggers of DKA. Describe the pathophysiology of DKA. (Fig 118.1) How is DKA managed in children? In adults? What are the epidemiologic risk factors for cerebral edema in DKA? What are signs and symptoms of cerebral edema? How do you manage a pt with DKA and suspected cerebral edema? List 5 complications of DKA management List five common serious infections in diabetics and how they are managed. How does hypoglycemia classically present? List 10 causes of hypoglycemia Describe the treatment of hypoglycemia What is the definition of hyperglycemic, hyperosmolar state? Contrast DKA and HHS (Table 118.2) What is the pathophysiology of HHS? How is HHS managed?   WiseCracks:   Why are urine ketones less sensitive for DKA than serum ketones? When do you give NaHCO3 to a patient with DKA? What is euglycemic DKA? What is the differential diagnosis of hypoglycemia in a patient who does not have DM? What would you add to the differential diagnosis in a pt who has DM?    

这里没有专家  只有一群奋斗在教育一线的老师分享「家庭教育」与「孩子学习」相关内容文|嘉津老师分享  科科整理记忆力虽然是一个词，但它其实包含了：背诵、复习、分类三个环节。如果孩子的记忆力不好，想提高又无从下手，我建议就从这三个环节入手。下面我会给出一些判断标准供孩子定位自己的问题，并且根据问题结合我自身的经验给出相应的建议。记忆的第一个环节▼背诵如果孩子背很多遍还是记不住，问题就出在背诵环节，我建议从3个方面来改善。1背诵的时候一定要出声不仅是英语和语文，数理化也是，读出来的时候，其实是眼睛看了一遍，嘴读了一遍，自己读出的声音又被自己耳朵听到，通过三次的加强，记忆效果就会好很多。我上高一的时候，我们学校的一个高三学长从不上晚自习，也不回家，就跑到楼顶上大声背诵今天学的内容，这个学长成绩一直很好，每次考试都是年级前几名。2一定要在理解的基础上进行记忆比如在背英语课文的时候，你不理解这段话的意思，不明白每句话之间的逻辑关系，你就很难背下来。即时背下来，也是丢三落四。3利用思维导图来帮助记忆我个人非常推崇这个方法。这里的思维导图是一个泛概念，它包括：流程图、树状图和矩阵图。流程图：适用于先后顺序比较明显的内容。初中的时候，老师要求我们背”侯氏制碱法“，书上是一大段的文字描述：要制纯碱，先制得溶解度较小的NaHCO3。再利用碳酸氢钠不稳定性分解得到纯碱等等……总之非常长的一段，我当时背了很久都背不下来，后来我发现这块内容有明显的先后顺序，要怎么样，先怎么样，再怎么样。我就画了一个图，用箭头标注顺序，然后看着图背，很快就完了，后来才知道我画的那个图叫流程图。图|嘉津老师的流程图树状图：对文科和理科的记忆都有帮助。举个简单的例子：化学会讲物质的分类，物质可以分为纯净物和混合物，纯净物又可以继续细分。类似这种知识用树状图进行记忆，效果就会非常好。文科知识也可以用树状图来记忆，比如：我背一道政治大题，通常会先看答案有几段，每一段有几句话，每句话的关键词是什么，然后用树状图表示出来。利用树状图来记忆，有一个好处，就是不容易遗漏。图|嘉津老师的树状图矩阵图：这个方法非常适合背历史。学古代史的时候，我会画矩阵图来帮助记忆，纵轴按照时间顺序写上朝代，横轴写上朝代持续的时间，定都于哪里，开国皇帝是谁，又发生了那些著名的战争。空闲的时候，我还会放下书，把矩阵图默背一下，有忘的知识马上拿起书看，这就是矩阵图的用法。图|嘉津老师的矩阵图记忆的第二环节▼复习如果孩子背的快，忘的也快，这就是复习环节存在问题。针对这个问题，分享一个我自己的方法。对于当天学习的文科知识，我会当晚复习一遍，周末复习一遍，然后月底再复习一遍。按照这个规律复习，我背过的东西，很少会忘。对于理科知识，因为需要记忆的内容很少，我就把主要的精力集中到错题的复习上，依然是按照上面介绍的复习规律，当天，当周，当月来进行。依我的个人的经验而言，复习最好按照一定的规律进行，并且长期坚持。记忆的第三环节▼分类如果孩子有过这样的经历：一看答案，恍然大悟，拍着自己脑袋说“哎呀，这个我明明知道的，当时怎么没想起来！”这就说明，孩子在背诵的时候没有把内容系统的分类，就像是一堆东西堆放在箱子里，你想找点什么都很难。所以记忆也是需要分类、归类整理的。知识也是如此，做好分类，才能灵活运用。那么如何做好分类呢？首先你要给知识打上标签，然后按照标签进行分类。比如下面这些四字短语：依依惜别、依依不舍、离愁别绪、爱别离苦。它们共同的标签就是：送别。如果题目要求写关于送别的四字短语，你就能根据“送别”这个标签从大脑中提取出一连串的四字短语。对于一些用以上方法都记不住的知识点，那这里再分享一个万用大法：肌肉记忆法除了上面的脑力记忆外，还有一种有关体力的记忆法。家长们会觉得奇怪，这记忆都是靠大脑，怎么出来的体力记忆呢？这里说的体力记忆其实指的就是肌肉记忆法。比如做广播体操，下一个动作是什么？怎么记住动作？还比如自行车，这些都属于肌肉记忆，那么肌肉记忆能应用到平时的学习吗？下面这件事，孩子一定做过：比如上面说过的“大声读”就可以配合肌肉记忆。如果你不相信，那就试着用英文从1-10快速读出来，然后再从10到1快速读出来，是不是不太顺利？因为这就是嘴部的肌肉记忆记住了1-10的英文阅读，当把他们变换顺序的时候，就突然不那么顺利了，这就是肌肉记忆。如果在平时的学习中有的内容实在是记不住，就可以运用大声读来促进肌肉记忆。当然这种方法是在你是在记不住而且理解困难的知识点上。最后，用一句话来总结今天的内容。如果孩子的记忆力不好，想提高又无从下手，我建议从记忆力的3个环节：背诵、复习、分类入手，逐一进行分析，定位自己的问题，然后针对性地解决。实在记不住的内容，就可以用肌肉记忆法来协助解决。中国教育，鱼龙混杂你的朋友圈需要一个懂教育的人科科就想做这样一个“人”科科是谁？科科代表的是一群懂教育的人他们不是教育专家是奋斗在教育一线的一群人 长按二维码 识别后关注我们

Matériel : support résistant au feu, lunettes et gants de protection Produits chimiques : sable, éthanol, pastilles de NaHCO3 (du bicarbonate de sodium) et sucre glace Procédure expérimentale : un cône de sable est formé sur le support réfractaire (ou assiette en porcelaine). Trois pastilles sont placés sur le somment du cône, et au moins 5 ml d'éthanol sont ajoutés et allumés. Après la combustion de l'alcool, des masses noires émergent du « volcan », qui ressemblent à des serpents vivants en croissance. Elles sont de taille d'un doigt et peuvent atteindre 1 mètre. Explication : le sucre fondu et le gaz libéré du bicarbonate de sodium produisent une masse extrêmement volumineuse. Une partie du sucre brûle sous carbonisation, et l'ensemble forme le serpent grandissant. Elimination des déchets : tout peut partir à la poubelle H.W. Roesky et W. Möckel, « Chemical Curiosities », page 20, 1996, Copyright Wiley-VCH Verlag GmbH and Co. KGaA. Traduit de l'anglais avec permission.

Cast Iron Cornbread - Ever wonder what that large piece of metal next to the stovetop is. Well, it's called a cast iron skillet and is it ever a wonder tool in the kitchen. Watch it in action as we tackle the Firehouse tradition that is Cornbread. In this episode we discuss NaHCO3, evaporating water and voiceovers cost the show money. For this episodes recipe and more, please visit www.thefirehousechef.com.