Podcasts about renin

#beşerimünasebetler Öfkenizin yükseldiğinin farkına varıyor musunuz? Yönetebiliyor musunuz? Nezih Orhon araştırmalar ve önemli sonuçlarıyla NTVRadyo'da

During this presentation, Donald DiPette, MD, FACP, FAHA, on behalf Robert M. Carey, MD, reviews the role of the RAAS in normal blood pressure and salt and water homeostasis. In addition, Dr. DiPette discusses the role of the RAAS in the pathophysiology of cardiovascular disease, diabetes mellitus, and kidney disease, and he also details the pharmacologic inhibition/blockade of the RAAS.

Grönland, Kanada, PanamaTrumps Ankündigung, Grönland und den Panamakanal notfalls mit Gewalt zu annektieren und Kanada als 51. Bundesstaat an die USA anschließen zu wollen, haben international Wellen geschlagen. In Russland wird mit einer Mischung aus Besorgnis und Belustigung berichtet.Ein Kommentar von Thomas Röper.Auch in Russland war Trumps Ankündigung, Grönland und den Panamakanal notfalls mit Gewalt zu annektieren und Kanada als 51. Bundesstaat an die USA anschließen zu wollen, ein großes Thema. Um zu zeigen, wie das in Russland aufgenommen wurde, übersetze ich hier den recht langen Beitrag, der am Sonntag dazu im wöchentlichen Nachrichtenrückblick des russischen Fernsehens dazu gezeigt wurde. Er bestand aus einer langen und sehr interessanten Anmoderation im Studio und dem Bericht des russischen USA-Korrespondenten.Beginn der Übersetzung:Machtwechsel in den USA: Trump genießt es, Bidens Erbe zu zerstörenIn den USA vollzieht sich ein Wandel. Der moderne russische Denker Alexander Dugin nannte diesen Prozess auf Englisch „bro-revolution“, also „Revolution der Jungs“. Unter Trump wird all der Mist abgeschafft, über den wir lange gelacht haben, von Quoten in Unternehmen für Schwule und Lesben bis hin zu Toiletten nach Wahl, je nachdem, als wer man sich gerade fühlt. Alles von der irren Zensur in Medien und sozialen Netzwerken bis zur absurden Energiepolitik.Trumps Ziel kann klarer nicht sein: Er will Amerika handlungsfähig, gesammelt und sehr rational machen. Dazu will er sein Territorium radikal erweitern und Kanada, Grönland und Panama und vielleicht sogar Mexiko einverleiben. Er will sich einen möglichst großen Anteil an den Bodenschätzen der Welt aneignen und sich einfach bereichern. Das ist der Plan und das Werkzeug der US-Weltherrschaft für die Zukunft. Es ist schamlos.Amerika hat nicht genug Lebensraum. Dass das bei einigen sehr direkte historische Assoziationen weckt, spielt keine Rolle. Es führt direkt zum Ziel! Es gibt keine Hemmungen. Grönland gehört zu Dänemark? Lächerlich.Kanada ist Mitglied des britischen Commonwealth und das Staatsoberhaupt Kanadas ist formell der britische König Charles III, und Großbritannien ist der engste Verbündete der USA? Nach dem Tod von Elisabeth II. hat der kanadische Premierminister Karl III. schriftlich zum Staatsoberhaupt Kanadas ernannt. Aber wer in den USA würde König Charles III fragen? Und was ist für Trump ein so lächerliches Relikt wie die britische Monarchie?Amerika verändert sich wirklich, sowohl nach außen als auch im Inneren...her weiterlesen: https://apolut.net/trumps-aussenpolitische-drohungen/ Hosted on Acast. See acast.com/privacy for more information.

Dr. Centor discusses reninbngiotensin system blockade in persons with advanced chronic kidney disease with Drs. Elaine Ku and Mark Sarnak.

This episode contains short-answer questions on the renin-angiotensin-aldosterone system.Written notes can be found at https://zerotofinals.com/physiology/endocrine/reninangiotensinaldosteronesystem/ or in the Zero to Finals Endocrine System book.You can find short-answer questions, multiple-choice questions, extended-matching questions, digital flashcards, a course on how to learn medicine and the revision tracking tool at members.zerotofinals.com. The audio in the episode was expertly edited by Harry Watchman.

Müzik Habercisi podcast dizisinin bu bölümünde Michael Kuyucu, Zeki Müren'in satışta olan halılarını anlatıyor.

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances discusses a recently published original research paper on renin-angiotensin system inhibition in patients with myocardial injury complicating TAVR.

This episode covers the physiology of the renin-angiotensin-aldosterone system.Written notes can be found at https://zerotofinals.com/physiology/endocrine/reninangiotensinaldosteronesystem/ or in the endocrinology section of the 2nd edition of the Zero to Finals Medicine book.The audio in the episode was expertly edited by Harry Watchman.

Message our hosts, Kieran and Jose.We all learned about the renin-angiotensin-aldosterone system in school... Or did we? This fantastic, in-depth interview on our current understanding of the RAAS will provide a revolutionary new perspective on how we may be able to harness the maladaptive systems that are activated in heart failure for positive purposes in our patients. Join Jose and Kieran as The Animal Heartbeat welcomes Professor Marisa Ames, Board-certified veterinary cardiologist and expert on the RAAS in dogs and cats.Please check out https://www.trigdocs.com/ to find out more about The Translational RAAS Interest Group, Dr Ames' collective of interested clinicians and researchers from the fields of veterinary and human medicine.

In less than 15 minutes, Medmastery's Cardiology Digest will give you the low-down on some of the most compelling studies in cardiology that clinicians with an interest in cardiovascular health need to know about. STUDY #1: We kick things off by exploring exactly where the CHA2DS2-VASc score fits into anticoagulation decisions in patients with silent atrial fibrillation. Building on the main findings from the ARTESiA and NOAH-AFNET 6 trials, this study sparks a thought-provoking discussion on the future of risk stratification. Tune in to hear insights that could shape your clinical practice.  Lopes, RD, Granger, CB, Wojdyla, DM, et al. 2024. Apixaban versus aspirin according to CHA2DS2-VASc score in subclinical atrial fibrillation: Insights from ARTESiA. J Am Coll Cardiol. In Press, Journal Pre-proof. (https://doi.org/10.1016/j.jacc.2024.05.002) STUDY #2: Next, we break down misconceptions surrounding race and treatment efficacy in heart failure with reduced ejection fraction. This study shines a light on the impacts of renin-angiotensin system inhibition across different racial groups. See how these findings challenge the outdated genetic constructs of race, and what they mean for your approach to patient care. Shen, L, Lee, MM, Jhund, PS, et al. 2024. Revisiting race and the benefit of RAS blockade in heart failure: A meta-analysis of randomized clinical trials. JAMA. 24: 2094–2104. (https://doi.org/10.1001/jama.2024.6774) STUDY #3: Finally, we turn our focus to the V142I transthyretin gene variant, to evaluate its impacts on cardiovascular health within the U.S. Black population. This research not only highlights the need for targeted genetic screening but also raises important questions about the accessibility of costly treatments for transthyretin amyloidosis. Selvaraj, S, Claggett, B, Shah, SH,  et al. 2024. Cardiovascular burden of the V142I transthyretin variant. JAMA. 21: 1824–1833. (https://doi.org/10.1001/jama.2024.4467) Maurer, MS, Miller, EJ, Ruberg, FL, et al. 2024. Addressing health disparities—The case for variant transthyretin cardiac amyloidosis grows stronger. JAMA. 21: 1809–1811. (https://doi.org/10.1001/jama.2024.2868) Yancy, CW. 2024. Heart failure in African American individuals, Version 2.0. JJAMA. 21: 1807–1808. (https://doi.org/10.1001/jama.2024.5217) Don't miss out on this rich discussion that promises to enhance your understanding and expertise!  Learn more with these courses: Medical Treatment of Heart Failure (2 CME) Atrial Fibrillation Management Essentials (1 CME) Get a Basic or Pro account, or, get a Trial account. Show notes: Visit us at  https://www.medmastery.com/podcasts/cardiology-podcast.

TANIM Adrenal yetmezlik, adrenal bezlerin hormon üretimindeki yetersizlikle sonuçlanan klinik durumdur. Adrenal kriz ise, bu hormonların eksikliğine bağlı olarak akut şekilde gelişen ve erken teşhis edilip agresif bir şekilde tedavi edilmezse ölümcül olabilen, acil klinik bir durumdur. Hastaların öyküsünde; sıklıkla ameliyat, enfeksiyon, yanık, sepsis, travma, metabolik veya kardiyovasküler olay gibi stresin arttığı tetikleyiciler  bulunur. Klasik olarak intravenöz sıvılara ve vazopressörlere dirençli şiddetli hipotansiyon şeklinde prezente olur (Şekil 1).​1​ Bu konuyla ilgili İbrahim Sarbay tarafından yazılmış vaka sunumu ve Ddxof algoritmasına buradan ulaşabilirsiniz.   PATOFİZYOLOJİ Anatomi Adrenal bezler retroperitoneal organlardır, böbreklerin üzerinde yerleşim gösterirler. Adrenal korteks ve adrenal medulla olarak iki kısımdan oluşur. Adrenal medullada katekolaminler üretilir. Adrenal kortekste ise mineralokortikoidler (zona glomerulozada), glukokortikoidler (zona fasikulatada) ve androjenler (zona retikulozada) üretilir (Şekil 2). Sınıflandırma Adrenal yetmezlik sorunun kaynaklandığı yere göre sınıflandırılır (Şekil 3). Primer Adrenal Yetmezlik: Adrenal kortekse özgü hastalıklardan kaynaklanır. Çocuklarda primer adrenal yetmezliğin en yaygın nedeni klasik konjenital adrenal hiperplazidir. Santral Adrenal Yetmezlik: Adrenokortikotropik hormonun (ACTH) kortizol üretimini uyarmaması ile karakterizedir. Santral adrenal yetmezlik, ACTH üretimini bozan hipofiz hastalığından (sekonder adrenal yetmezlik) veya hipotalamustan kortikotropin salgılatıcı hormon (CRH) salınımındaki bozukluklardan (tersiyer adrenal yetmezlik) kaynaklanabilir. En yaygın neden, hipotalamik-hipofiz-adrenal ekseni baskılayan kronik, yüksek doz glukokortikoid tedavisinin aniden uygunsuz şekilde kesilmesidir. 2 haftanın üzerinde günlük 5 mg prednizona eş değer steroid kullanımından sonra dozun azaltılarak kesilmesi gerekir. Aldosteron sıvı ve elektrolit dengesinden sorumlu esas hormonlardan biridir. Kortikosteroidler daha çok karbonhidrat, protein ve yağ metabolizmasından sorumludur. Ayrıca glukokortikoid eksikliği, anjiyotensin I ve norepinefrine karşı vasküler yanıtın azalmasına, renin substratının sentezinin azalmasına ve prostasiklin üretiminin artmasına sebep olarak hipotansiyona katkıda bulunur.​2​ Kortikosteroidlerin temel üretimi hipotalamohipofizier aks üzerinden CRH ve ACTH hormonlarıyla düzenlenir. Mineralokortikoidlerin dengesi ise esas olarak böbreklerdeki reseptörlerle sağlanır ve Renin anjiotensin aldosteron sistemiyle yönetilir. Dolayısıyla primer adrenal yetmezlikte hem kortizol hem aldosteron eksikliği görülürken, santral adrenal yetmezlikte mineralokortikoid aktivitesi korunmuş olur.    ETİYOLOJİ Primer Adrenal Yetmezlik Otoimmün adrenalit (Adison hastalığı)İzole veya poliglandüler yetmezlikle görülebilir, HIV Enfeksiyonu (direkt etkileyebileceği gibi, dissemine sitomegalovirüs (CMV), tüberküloz, kriptokok, histoplazmozis, blastomikozis, toxoplazmozis veya pneumcystis pneumonia enfeksiyonları ile de etkileyeblir) Tüberküloz veya diğer dissemine enfeksiyonlar Metastatik kanserler (özellikle meme, akciğer) İnfiltratif hastalıklar (sarkoidoz, hemokramtozis, amiloidozis) Konjenital (adrenal hipoplazi, adrenolökodistrofi, ACTH direnci) Bilateral adrenalektomi İlaç toksisitesi (etomidat, ketokonazol, rifampisin)  Akut Durumlar Adrenal hemorajiMeningokoksemi ve diğer sepsis durumlarıAntikoagülasyon (heparin ve warfarin)Antikardiyolipin antikor sendromu Travma Santral Adrenal Yetmezlik Pitüiter Tümör (Primer veya metastatik) Pitüiter Cerrahi veya radyasyon Kronik steroid kullanımının ani kesilmesi İnfiltratif Hastalıklar (Sarkoidoz, eozinofilik granülom, tüberküloz) Travmatik beyin yaralanması Postpartum pituiter nekroz (Sheehan sendromu) Boş sella sendromu Akut DurumlarPitüiter apopleksi (pitüiter tümör içi kanama)Travmatik beyin ...

In dieser neuen Folge sprechen wir mit Christoph Jaschke über die Außerklinische Intensivversorgung. Hierbei erfahrt ihr mehr über die Versorgungsstrukturen sowie die Situation der versorgten Menschen. Außerdem beleuchten wir gesetzliche Grundlagen und aktuelle politische Diskussionen. Viel Spaß mit der neuen Episode!Und vergiss nicht: Du machst uns einen großen Gefallen, wenn du eine Mitgliedschaft abschließt ☺️ShownotesKontakt Christoph JaschkeDeutsche Fachpflege Deutsche Interdisziplinäre Gesellschaft für außerklinische Beatmung (DIGAB) MAIK Kongress für außerklinische IntensivversorgungUN-BehindertenrechtskonventionIntensivpflege- und Rehabilitationsstärkungsgesetz (GKV-IPReG)GKV-IPReG ThinkTankVideopodcast CODY PODCASTIn eigener SacheÜbergabe Mitglied werdenNewsletter abonnierenÜbergabe bei InstagramPflegeupdate hörenIn eigener SacheÜbergabe Mitglied werdenÜbergabe bei InstagramPflegeupdate hören

Bilim insanları arasında türlerin standart bir şekilde isimlendirilmesi iletişimin kolaylaşması bakımından büyük öneme sahiptir. İşte bu nedenle, sınıflandırma bilimi olarak da bilinen "taksonomi", bir dizi kurallar bütününe sahiptir.Sınıflandırma ve isimlendirme çok önemlidir. Çünkü bilim, belirli… Seslendiren: Gülfem Akdemir

Wir sprechen über ein Thema, was wir kaum beachten: die Pflege von Menschen mit geistiger Behinderung. Dr. Stefanie Schniering von der HAW Hamburg und Tabea Zillmann sprechen über ein Projekt, welches die Gesundheitsförderung von geistig behinderten Menschen in den Fokus nimmt. Wir sprechen über systembedingte Hürden, welche Qualifikation geeignet ist für dieses Klientel und welches Ziel das Projekt verfolgt.Viel Spaß mit der neuen Episode!Und vergiss nicht: Du machst uns einen großen Gefallen, wenn du eine Mitgliedschaft abschließt ☺️ShownotesBESSER Gesund LebenEvangelisches Krankenhaus AlsterdorfNursing staff and nursing managers' experiences of using the interRAI ID instrument in assessing the service needs of persons with intellectual disabilities in housing servicesFaPP-MgB – Fallmanagement und Pflegeexpertise als Präventionsansatz für erwachsene Menschen mit geistiger Behinderung - G-BA InnovationsfondsFaPP-MgBIn eigener SacheÜbergabe Mitglied werdenNewsletter abonnierenÜbergabe bei InstagramPflegeupdate hörenIn eigener SacheÜbergabe Mitglied werdenÜbergabe bei InstagramPflegeupdate hören

Some huge fights went down over the weekend without much fanfare. The PFL vs Bellator fights were pretty amazing. I still feel a little robbed we didn't get 5 round super fights. It looks like Renin will fight Ngannou sometime this year, hopefully. UFC had a less hyped Fight Night with a handful of good fights. Jump in the chat, and let us hear your thoughts. Super Chats will get extra attention.   Main Channel: https://www.youtube.com/user/OfficialJonFitch   Fitch SMASH programs: https://jonfitch.gumroad.com   Intro to Practical Self-Defense https://jonfitch.gumroad.com/l/DOZTR   Practical Self-Defense program https://jonfitch.gumroad.com/l/Defense   More Stuff: https://linktr.ee/boilerbrawn   Sign up for the newsletter below:

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

Dr. Briggs and Brendon Neuen discuss his paper in the December issue of JASN. This article on the CREDENCE and EMPA-CKD clinical trials shows that SGLT2 inhibitors allow more consistent use of RAS blockade in patients with declining renal function.

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16:50 burç yorumları başlıyor.

Hypertension affects one third of humans. Untreated hypertension, shortens life expectancy by five years because it's a major cause of heart failure, renal failure, strokes, and coronary disease. The mortality due to hypertension has increased  more than 30% in the last three decades. And the sad fact is that hypertension is uncontrolled in the majority of hypertensive patients, but it seems there's a breakthrough treatment. Angiotensinogen is a protein, it's mainly produced by the liver. If we stop the production of Angiotensinogen in the liver, then the whole. Renin angiotensin system will be silenced. And we have the results of the study on DNA silencing available. 

iyi ki Paris ayaklandı.. Bir düzine Türk haber kanalına tutunacak dal oldu. Malûm, seçim sonrası sendromu. Patinaj döneminden geçiyorlar. Yerel seçimlere kapağı atana kadar da ‘uygun dalga' aramaya devam edecekler. Diyebilirsiniz ki, ‘seçim yayınları çok mu kaliteliydi', onda da haklısınız... Türk haber yayıncılığı “aktüel dalga” sever. İç-dış-ekonomi fark etmez. “Olay” olmalıdır. Salt nicelik arayan yayın politikaları rating-reklam gerçekliğine yaslanıyor ama öte yandan kamuoyunun canına da okuyor... Türkiye'yi de kavrayan dönüştürücü gelişmelerin dahi sebep-sonuç ilişkileri kurulamadığından köpeğin kuyruğunu yakalamaya çalışması gibi dönüp-duruyorlar... Oysa Türkiye'de bütünlüklü okumalara, nitelikli bilgiye, açıyı değil gözü değiştiren okumalara kıymet veren çok izleyici var. Dahası bu izleyici tipi zamanla diğerlerini de davet ediyor. ‘Az sonra'lardan, ‘reklamlardan sonra hemen geliyoruz'lardan daha ikna ediciler üstelik...

The following episode provides part one of sodium physiology examining how the body regulates sodium levels via the renin-angiotensin-aldosterone system.    One of my favorite lectures on this topic: https://www.youtube.com/watch?v=NMWaKdO76NQ    

You probably know that the kidneys play an important role in maintaining blood pressure within the normal range. You might also know that they do this by regulating blood volume and the degree of arterial contraction or dilation (the systemic vascular resistance). But do you know how the kidneys do this? The answer is the kidneys accomplish this primarily through a set of hormones and enzymes known together as the renin-angiotensin-aldosterone system (RAAS). In this brick, we will discuss the components, functions, and regulation of the RAAS. Renin is an enzyme released by the kidneys that ultimately causes the formation of the hormone angiotensin II (Ang II) in the body—which in turn stimulates the release of the hormone aldosterone from the adrenal cortex. Ang II and aldosterone act in a number of ways to increase blood volume and blood pressure. RAAS acts to increase sodium reabsorption in the kidney, increase vascular tone, and even stimulate antidiuretic hormone (ADH) to reabsorb more water: all of these defend our extracellular volume and blood pressure. RAAS is therefore a critical system for keeping us upright! After listening to this Audio Brick, you should be able to: Outline the renin-angiotensin-aldosterone system, including sensors, factors that control it, sources of hormone release, and the actions of each hormone. Describe the mechanisms by which the renin-angiotensin-aldosterone system regulates blood pressure. Compare and contrast tubuloglomerular feedback with the renin-angiotensin-aldosterone system. You can also check out the original brick from our Endocrine collection, which is available for free. Learn more about Rx Bricks by signing up for a free USMLE-Rx account: www.usmle-rx.com You will get 5 days of full access to our Rx360+ program, including nearly 800 Rx Bricks.  After the 5-day period, you will still be able to access over 150 free bricks, including the entire collections for General Microbiology and Cellular and Molecular Biology. *** If you enjoyed this episode, we'd love for you to leave a review on Apple Podcasts.  It helps with our visibility, and the more med students (or future med students) listen to the podcast, the more we can provide to the future physicians of the world. Follow USMLE-Rx at: Facebook: www.facebook.com/usmlerx Blog: www.firstaidteam.com Twitter: https://twitter.com/firstaidteam Instagram: https://www.instagram.com/firstaidteam/ YouTube: www.youtube.com/USMLERX Learn how you can access over 150 of our bricks for FREE: https://usmlerx.wpengine.com/free-bricks/ from our Musculoskeletal, Skin, and Connective Tissue collection, which is available for free. Learn more about Rx Bricks by signing up for a free USMLE-Rx account: www.usmle-rx.com You will get 5 days of full access to our Rx360+ program, including nearly 800 Rx Bricks.  After the 5-day period, you will still be able to access over 150 free bricks, including the entire collections for General Microbiology and Cellular and Molecular Biology.

Editor's Summary by Kirsten Bibbins-Domingo, PhD, MD, MAS, Editor in Chief of JAMA, the Journal of the American Medical Association, for the April 11, 2023, issue. Related Content: Audio Highlights

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.20.533428v1?rss=1 Authors: Xu, T., Chen, Z., Zhou, X., Wang, L., Zhou, F., Yao, D., Zhou, B., Becker, B. Abstract: The brain renin angiotensin II system plays a pivotal role in cognition and neuropathology via the central angiotensin II type 1 receptor (AT1R), yet the lack of a biologically informed framework currently impedes translational and therapeutic progress. We combined imaging transcriptomic and meta-analyses with pharmaco-resting state fMRI employing a selective AT1R antagonist in a discovery-replication design (n=132 individuals). The AT1R was densely expressed in subcortical systems engaged in reward, motivation, stress, and memory. Pharmacological target engagement suppressed spontaneous neural activity in subcortical systems with high AT1R expression and enhanced functional network integration in cortico-basal ganglia-thalamo-cortical circuits. AT1R-regulation on functional network integration was further mediated by dopaminergic, opioid and corticotrophin-releasing hormone pathways. Overall, this work provides the first comprehensive characterization of the architecture and function of the brain renin angiotensin II system indicating that the central AT1R mediates human cognition and behavior via regulating specific circuits and interacting with classical transmitter systems. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Gilbert Strang, eccrinologist, discusses the differences between glomerular and renaldamage. He also explains the role of Bowman's capsules and renin in the glomerular filtration process. Finally, he discusses the use of lube in sex and medical contexts.

In this extremely HY podcast, I discuss the renin angiotensin aldosterone system in detail and also make lots of integrations that show up as exam questions on all the USMLEs. Definitely worth a listen before you take your test. Audio Download

In dieser Folge nehmen wir das RAAS unter die Lupe. Wir klären, wie es genau abläuft und welche Hormone zum Einsatz kommen.

Join Gianmarco Meli with Renin Ratnaswamy, the head of agency partnerships at Billo as they talk about how to produce video content at scale and create videos that convert and boost sales. Renin has extensive experience in sales, product marketing, and go-to-market strategy. At Billo, he works directly with the agency helping them get the most out of the Billo marketplace to develop high-converting product videos. Here's a breakdown of what to expect in this episode:The process of creating high-converting videosIdentifying three different concept ideas to showcase your productVideo consumption; educating the consumers while entertaining themBest tips to produce high-performing videosElements that convert the best both on Amazon or social mediaWhat to avoid in post-production of video And so much more!Download the Video Production Process by Billo to guide you on how to create high-converting and noticeable videos for your online business and get more awareness.https://pixelfy.me/eNEVOy____________________________About Renin:Renin Swami, the head of agency partnerships at Billo. He has intensive experience in sales methodology, product marketing and go-to market strategy. At Billo, he works directly with the agency helping them get the most out of the Billo marketplace to create high converting product videos.  Billo is a marketplace where you can find creators who are the average consumer. Register to Billo to get $20 off on your first video! You can book a meeting with Renin on — renin@billo.app Let's Connect!You can find Jon Elder on —  LinkedInConnect with The Seller Process at — https://www.thesellerprocess.com/_____________________________Tools & Useful ResourcesBillo — Top-quality product videos. Our favorite place to create product videos for Amazon and social ads. It connects you with hundreds of video content creators that will shoot professional videos starting at 59$. Get 20$ off with code TSP20. Affiliate link click here.FBExcel — Best Automation Tools. FBAexcel offers powerful tools built entirely on Google Sheets to help you automate keyword research, PPC optimization, metrics tracking, and more. Sign up for free through the link below to get "Keyword Dominator". Affiliate link click here. 

No Spine Alex Stein got his invertebrate body bent out of shape after Jesse posted a video about Alex's actual SCH**L SH**TER grandma. Now the Troll King is flailing around trying to figure out how to stop the POD AWFUL CULT from wreaking MAYHEM on his life. Well what does any Stein do when pressed? TIME TO GET LITIGIOUS! Alex is now initiating THE LOLSUIT 2 all because of a Twitter account impersonating him. He is not only threatening Jesse with a lawsuit for a problem solved by hitting "report" on Twitter, he also threatened to send a BOUNTY HUNTER after Jesse's parents! There's just one problem, of course... Jesse didn't make the fake Alex Stein Twitter account. But now a whole lot more people are! Davey Crocko covers Pod Awful's Primetime Feud and the Cassady Campbell conspiracy, the number of Youtube streams we are banned from goes from 109 to 110, and while the moon base is under attack, Jesse gets a surprise visit from Renin! Remember, when you live in The Glass House, don't throw Steins. https://podawful.pizza/posts/2255  Get the POD AWFTER SHOW where Jesse goes on Davey Crocko's stream to talk about Alex Stein, and confronts Davey about his nose candy! Only in the PIZZA FUND! https://podawful.pizza  VIDEO: https://youtu.be/ub0MyetGMZA RSS FEED: http://feeds.feedburner.com/podawful  YOUTUBE: http://awful.tube  DISCORD: http://podawful.com/discord  TWITTER: http://podawful.com/twitter  INSTAGRAM: http://podawful.com/instagram  DLIVE: https://dlive.tv/PodAwful  ODYSEE: https://odysee.com/@podawful:8  FACEBOOK: http://podawful.com/facebook  CULT: http://podawful.com/cult  MERCH: http://podawful.shop  http://podawful.com  #AlexStein #Lawtube #podawful Pod Awful Is an anti-podcast hosted by Jesse P-S

No Spine Alex Stein got his invertebrate body bent out of shape after Jesse posted a video about Alex's actual SCH**L SH**TER grandma. Now the Troll King is flailing around trying to figure out how to stop the POD AWFUL CULT from wreaking MAYHEM on his life. Well what does any Stein do when pressed? TIME TO GET LITIGIOUS! Alex is now initiating THE LOLSUIT 2 all because of a Twitter account impersonating him. He is not only threatening Jesse with a lawsuit for a problem solved by hitting "report" on Twitter, he also threatened to send a BOUNTY HUNTER after Jesse's parents! There's just one problem, of course... Jesse didn't make the fake Alex Stein Twitter account. But now a whole lot more people are! Davey Crocko covers Pod Awful's Primetime Feud and the Cassady Campbell conspiracy, the number of Youtube streams we are banned from goes from 109 to 110, and while the moon base is under attack, Jesse gets a surprise visit from Renin! Remember, when you live in The Glass House, don't throw Steins. https://podawful.pizza/posts/2255  Get the POD AWFTER SHOW where Jesse goes on Davey Crocko's stream to talk about Alex Stein, and confronts Davey about his nose candy! Only in the PIZZA FUND! https://podawful.pizza  VIDEO: https://youtu.be/ub0MyetGMZA RSS FEED: http://feeds.feedburner.com/podawful  YOUTUBE: http://awful.tube  DISCORD: http://podawful.com/discord  TWITTER: http://podawful.com/twitter  INSTAGRAM: http://podawful.com/instagram  DLIVE: https://dlive.tv/PodAwful  ODYSEE: https://odysee.com/@podawful:8  FACEBOOK: http://podawful.com/facebook  CULT: http://podawful.com/cult  MERCH: http://podawful.shop  http://podawful.com  #AlexStein #Lawtube #podawful Pod Awful Is an anti-podcast hosted by Jesse P-S

Episode 105: Renal Cell Carcinoma. Manpreet and Jon-Ade explain how to diagnose renal cell carcinoma. Introduction about age and kidney transplant by Dr. Arreaza and Dr. Yomi. Introduction: Too old for a new kidney?By Hector Arreaza, MD. Discussed with  Timiiye Yomi, MD.Today we will be talking about the kidneys, those precious bean-shaped organs that detoxify your blood 24/7. Amazingly, we can live normal lives with one kidney, but when the kidney function is not good enough to meet the body's demands, patients need to start kidney replacement therapy. Modern medicine has made a lot of advances with dialysis, but the perfection of a kidney has not been outperformed by any machine yet. That's why kidney transplant is the hope for many of our patients with end-stage kidney disease.The need for a kidney transplant is growing, likely due to increasing chronic diseases such as diabetes and hypertension, and also because of an increase in elderly population. About 22% of patients on the kidney transplant waiting list are over age 65. A cut-off age to receive kidney transplant has not been established across the globe. Different countries use different criteria for the maximum age for transplant. The American Society of Transplantation's guidelines states “There should be no absolute upper age limit for excluding patients whose overall health and life situation suggest that transplantation will be beneficial.” So, if your patient is older than 65 and needs a kidney, they may qualify for a transplant, and age should not be an absolute contraindication to receive it. Actually, older patients may have lower risk of rejection due to a theoretically weaker immune system. A live donor is likely to be a better option for elderly patients. A condition that would make your elderly patient a poor candidate for kidney transplant would be frailty. Common contraindications to kidney transplant include active infections or malignancy, uncontrolled mental illness, ongoing addiction to substances, reversible kidney failure, and documented active and ongoing treatment nonadherence.So, remember to take these factors into consideration when deciding if you need to refer your elderly patients for a kidney transplant, there is no such thing as being too old for a new kidney if your patient meets all the criteria for a transplant.This is Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California. Our program is affiliated with UCLA, and it's sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care physician for additional medical advice. Renal Cell Carcinoma. By Manpreet Singh, MS3, Ross University School of Medicine, and Jon-Ade Holter, MS3 Ross University School of Medicine. Moderated by Hector Arreaza, MD. Definition:Renal cell carcinoma is a primary neoplasm arising form the renal cortex. 80-85 percent of renal tumors are renal cell carcinomas followed closely by transitional cell renal cancer and Wilms tumor.  Epidemiology: In 2022, 79,000 new cases of kidney cancer were diagnosed with almost 14,000 mortalities. There is a 2:1 male to female ratio and the average age is 64 and normally 65-74. African Americans and American Indians have a higher prevalence rate compared to other racial groups. The lifetime risk for developing kidney cancer in men is about 1 in 46 (2.02%) and 1 in 80 (1.03%) in women.  Risk Factors associated with RCC: Anything that causes assault to the kidneys and affects its function would cause increased demand, injury, and inflammation. This assault can lead to cell derangement and lead to cancer. The risk factors that have been associated with RCC are smoking, obesity, HTN, family history of kidney cancer, Trichloroethylene (a metal degreaser used in large manufacturing factories), acetaminophen, and patients with advanced kidney disease needing dialysis. Patients with syndromes that cause multiple types of tumors: VHL (von Hippel-Lindau) deficiency, a tumor suppressor, gives rise to clear cell renal cell carcinoma. Familial inheritance of VHL deficiency is mostly found in patients that have RCC at a very young age, before 40 y/o. Other tumors can be found in the eye, brain, spinal cord, pancreas, and pheochromocytomas.Hereditary leiomyoma-renal cell carcinoma due to FH gene mutations causing women who have leiomyomas to have a higher risk of developing papillary RCC.Birt-Hogg-Dube (BHD) syndrome mutation in FLCN gene who develop various skin and renal tumors.Cowden syndrome is a mutation in the PTEN gene giving rise to cancers associated with breast, thyroid , and kidney cancers.Tuberous sclerosis causes benign tumors of the skin, brain, lungs, eyes, kidneys, and heart. Although kidney tumors are most often benign, occasionally they can be clear cell RCC. Screening For RCC:Screening is unnecessary because of the low prevalence of this cancer in the general population, though certain groups require annual repeat imaging via US, CT, or MRI. Inherited conditions that are associated with RCC such as VHL syndrome or Tuberous SclerosisESRD patients who have been on dialysis for 3-5 yearsFamily history of RCCPrior kidney irradiation Clinical Picture: Most patients with RCC are asymptomatic until cancer grows large enough to cause disruption of local organs, such as the kidney, bladder, or renal vein, and dysregulates other organs via metastasis. Therefore, it's important to look at other signs and symptoms caused by RCC.  The patient most likely will be an older male who presents with the classic triad of: Flank pain: caused by rapid expansion and stretching of the renal capsule.Hematuria: occurs from the invasion of the neoplasm into the collecting duct.Palpable abdominal mass: mass tends to be homogenous and mobile with respirations. Though this presents only in 9% of patients during the presentation, having physical symptoms is a sign of advanced disease and 25% of patients with these signs tend to have distant metastasis.  Anemia: normally associated with anemia of chronic disease. It precedes the disease by at least 8 months to 1 year. Males can develop varicoceles because of decreased emptying due to neoplasm obstruction. Patients normally develop varicoceles on the left due to the spermatic vein emptying in the higher resistance left renal vein, which causes backup of the blood in the pemphigus plexus. Though a right-sided varicocele should raise a higher suspicion of obstruction due to the spermatic vein draining directly into the IVC which is lower in resistance. A right-sided varicocele is seen in approximately 11 percent of patients. The paraneoplastic syndrome can also arise from RCCEpo: Erythrocytosis with symptoms of weakness, fatigue, headache, and joint pain.PTHrP: PTH-related peptide acts like PTH which gives rise to hypercalcemia with the prevalent symptoms of arthritis, osteolytic lesions, confusions, tetany, ventricular tachycardia, shortened QTc, and nausea and vomiting.Renin: overproduction from the juxtaglomerular cells can cause disarrangement of the RAAS system causing hypertension.Others also like ACTH and beta-HCG. Other disorders present include hepatic dysfunction, cachexia, secondary amyloidosis, and thrombocytosis. Workup If a patient comes in with painless hematuria, then the first test should be abdominal CT or abdominal ultrasound. A CT is more sensitive than the US but it can quickly indicate if the abdominal mass felt can be a cyst or a solid tumor.  US of kidneys should show if it's a simple cyst:-The cyst is round and sharply demarcated with smooth walls- It's anechoic – appears solid black-There is a strong posterior wall echo-Use the Bosniak classification to classify mass  Bosniak I: benign simple cyst with thin wall less than equal to 2mm, no septa or calcifications. No future workup is needed. Bosniak II: benign cyst, 3 cm diameter, requires f/u with US/CT/MRI at 6 months, 12 months, and annually for the next 5 years. Chance of malignancy: 5%.  Bosniak III: indeterminate cystic mass with thick, irregular or smooth walls. This requires nephrectomy or radiofrequency ablation. Chance of malignancy: 55%  Bosniak IV: Clearly a malignancy its grade III with enhancing soft tissue components that its independent from the wall or septum. Requires total or partial nephrectomy. Chance of malignancy 100%.  CT of the kidneys for a neoplasm should show:-Thickened irregular walls or septa -Enhancement after contrast injection are suggestive of malignancy-CT can also help detect invasion in local tissue areas such as renal vein and perinephric organs  MRI is used if the patient cannot use contrast or kidney function is poor. MRI can also evaluate the growth of the cancer. Other imaging studies:Other imaging studies that may be useful for assessing for distant metastases include bone scan, CT of the chest, magnetic resonance imaging (MRI), and positron emission tomography (PET)/CT. Treatment and staging Nephrectomy, partial or total, will be used as the initial tissue collection for pathology. If the patient is not a surgical candidate, you can also obtain a percutaneous biopsy. The nephrectomy is preferred because first, it serves as a definitive treatment option, but also it allows for definitive staging of the cancer with tumor and nodal staging. Regardless of the size, any solid mass may indicate malignancy and point towards RCC, requiring resection.   TNM staging Stage I: Tumor is 7cm across or smaller and only in the kidney with no lymph nodes or distant mets. T1N0M0 Stage IIa: Tumor size is larger than 7cm but still in the kidney but no invasion of lymph node or mets. T2N0M0 Stage IIb: Tumor is growing into the renal vein or IVC, but not into neighboring organs such as adrenals or Gerota's fascia and still lacks lymph node invasion and mets. T3N0M0.  Stage III: Tumor can be any size but has not invaded outside structures such as adrenals, though nearby lymph node invasion is present but not distant. There is no distant mets. T3N1M0. Stage IV:  The main tumor is beyond the Gerota's fascia and may grow into the adrenal gland . It may or may not spread to the lymph nodes or may not have distant mets. Stage IV also consists of any cancer that has any number of distant mets. T4 Adjuvant therapy can be done with immune therapy. Conclusion: Now we conclude our episode number 105 “Renal cell carcinoma.” This type of cancer may be asymptomatic until it is large enough to cause symptoms. Keep it on your list of differentials on patients with hematuria, flank pain, weight loss, and abnormal imaging. Keep in mind the features of simple kidney cysts vs complex cysts when assessing kidney ultrasounds. Your patient will be grateful for an early diagnosis of RCC and a prompt treatment. Even without trying, every night you go to bed being a little wiser.This week we thank Hector Arreaza, Timiiye Yomi, Manpreet Singh, Jon-Ade Holter. Thanks for listening to Rio Bravo qWeek Podcast. If you have any feedback, contact us by email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. Audio edition: Suraj Amrutia. See you next week!  Bibliography: Is There a Cut Off Age for Kidney Transplant?, Mayo Clinic Connect, Jul 18, 2017, https://connect.mayoclinic.org/blog/transplant/newsfeed-post/is-there-a-cut-off-age-for-kidney-transplant/ Atkins, Michael. “Clinical Manifestations, Evaluation, and Staging of Renal Cell Carcinoma.” UpToDate, January 21. https://www.uptodate.com/contents/clinical-manifestations-evaluation-and-staging-of-renal-cell-carcinoma American Cancer Society. “Key Statistics About Kidney Cancer”. Cancer.Org, 2022, https://www.cancer.org/cancer/kidney-cancer/about/key-statistics.html. Escudier B, Porta C, Schmidinger M, Rioux-Leclercq N, Bex A, Khoo V, Grünwald V, Gillessen S, Horwich A; ESMO Guidelines Committee. Electronic address: clinicalguidelines@esmo.org. Renal cell carcinoma: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up†. Ann Oncol. 2019 May 1;30(5):706-720. doi: 10.1093/annonc/mdz056. PMID: 30788497. https://pubmed.ncbi.nlm.nih.gov/30788497/. Gaillard, F., Bell, D. Bosniak classification system of renal cystic masses. Reference article, Radiopaedia.org. (accessed on 20 May 2022) https://doi.org/10.53347/rID-1006. Kopel J, Sharma P, Warriach I, Swarup S. Polycythemia with Renal Cell Carcinoma and Normal Erythropoietin Level. Case Rep Urol. 2019 Dec 11;2019:3792514. doi: 10.1155/2019/3792514. PMID: 31934488; PMCID: PMC6942735. https://pubmed.ncbi.nlm.nih.gov/31934488/. Leslie SW, Sajjad H, Siref LE. Varicocele. [Updated 2022 Feb 14]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK448113/. Maguire, Claire. “Understanding Endoscopic Ultrasound and Fine Needle Aspiration.” Educational Dimension, Educational Dimensions, 1 Jan. 2007, educationaldimensions.com/eLearn/aspirationandbiopsy/eusterm.php. Maller, V., Hagir, M. Renal cell carcinoma (TNM staging). Reference article, Radiopaedia.org. (accessed on 20 May 2022) https://doi.org/10.53347/rID-4699. Palapattu GS, Kristo B, Rajfer J. Paraneoplastic syndromes in urologic malignancy: the many faces of renal cell carcinoma. Rev Urol. 2002 Fall;4(4):163-70. PMID: 16985675; PMCID: PMC1475999. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1475999/.

[2 HOUR LONG SHOW! JOIN THE PIZZA FUND! $12 level. https://podawful.pizza/posts/2240] Jarrette and Renin are a legendary Dynamic Duo. They are best friends, autistic heroes, and cigarette reviewers. Jarrette is also the world's greatest dirty rapper (known as Ja Crispy), and a world class metal singer. Renin is a police officer, hacker, spyninja, fire alarm enthusiast... and BOUNTY HUNTER. Oh, also he's a Brony. Together they are great Youtubers, and in a scheme to get more subs, Renin has agreed to taser himself in an epic stunt. Should be simple enough for a bounty hunter to pull off, but when we got him over 100 new subscribers, Renin tried to pull a fast one on us. HE TASER SCAMMED US. Now Ja Crispy is teaming up with Pod Awful to bounty hunt the bounty hunter, and call him out on his CRIMES. PLUS: James Soren Stone has secretly been training to become a Mandalorian himself. Oh also, somehow Mini Manson showed up for the PREVIEW VERSION of the show. VIDEO: https://youtu.be/G7a9nTA8ef0 RSS FEED: http://feeds.feedburner.com/podawful  YOUTUBE: http://awful.tube  DISCORD: http://podawful.com/discord  TWITTER: http://podawful.com/twitter  INSTAGRAM: http://podawful.com/instagram  DLIVE: https://dlive.tv/PodAwful  ODYSEE: https://odysee.com/@podawful:8  FACEBOOK: http://podawful.com/facebook  CULT: http://podawful.com/cult  MERCH: http://podawful.shop  http://podawful.com  #JaCrispy #BountyHunter #podawful Pod Awful Is an anti-podcast hosted by Jesse P-S

[2 HOUR LONG SHOW! JOIN THE PIZZA FUND! $12 level. https://podawful.pizza/posts/2240] Jarrette and Renin are a legendary Dynamic Duo. They are best friends, autistic heroes, and cigarette reviewers. Jarrette is also the world's greatest dirty rapper (known as Ja Crispy), and a world class metal singer. Renin is a police officer, hacker, spyninja, fire alarm enthusiast... and BOUNTY HUNTER. Oh, also he's a Brony. Together they are great Youtubers, and in a scheme to get more subs, Renin has agreed to taser himself in an epic stunt. Should be simple enough for a bounty hunter to pull off, but when we got him over 100 new subscribers, Renin tried to pull a fast one on us. HE TASER SCAMMED US. Now Ja Crispy is teaming up with Pod Awful to bounty hunt the bounty hunter, and call him out on his CRIMES. PLUS: James Soren Stone has secretly been training to become a Mandalorian himself. Oh also, somehow Mini Manson showed up for the PREVIEW VERSION of the show. VIDEO: https://youtu.be/G7a9nTA8ef0 RSS FEED: http://feeds.feedburner.com/podawful  YOUTUBE: http://awful.tube  DISCORD: http://podawful.com/discord  TWITTER: http://podawful.com/twitter  INSTAGRAM: http://podawful.com/instagram  DLIVE: https://dlive.tv/PodAwful  ODYSEE: https://odysee.com/@podawful:8  FACEBOOK: http://podawful.com/facebook  CULT: http://podawful.com/cult  MERCH: http://podawful.shop  http://podawful.com  #JaCrispy #BountyHunter #podawful Pod Awful Is an anti-podcast hosted by Jesse P-S

Türkçe yazılan mevlid manzumelerinin arasında özel bir yere sahip olan, Süleyman Çelebi'nin aşkla kaleme aldığı Vesîlet'ün Necât (Mevlid-i Şerif) eserini Prof. Dr. Sadettin Ökten'le birlikte "Süleyman Aşk Dilin Bilir Dediler" programında hem okuyup hem de şerh ediyoruz… Süleyman Aşk Dilin Bilir Dediler'in yeni bölümünde başlıca şunlar konuşuldu; "Rahmeten lil'âlemindir Mustafa Hem şefîal müznibîndir Mustafa Vasfınî bû resme tertib ettiler Ol mübârek nûru terğib etdiler" Serdar Tuncer: Efendim hoş geldiniz, safalar getirdiniz. Süleyman Aşk Dilin Bilir Dediler... Ne diyor Süleyman Çelebi Hazretleri burada efendim? Sadettin Ökten: Alemlere rahmet diye gönderilmiştir Mustafa (s.a.v) yani zend günah demek, müznibîn günahkarlar yani insanlar hepsi günahkar. Öyle buyuruluyor zaten; "Siz günah işlemeseydiniz (ki bu mümkün değil) ben sizi yok eder günah işleyen bir ümmet yaratırdım" buyuruyor. Çünkü beşerin hali günah işlemek üzere kurgulanmıştır da bir çok beşer işlediği günahı bilmez, günahın farkında olmaz. Bu da böyle bir haldir yani beşerin bir gaflet halidir dolayısıyla Allah hepimizi bu gaflet halinden uyanmaklığımızı nasib-i müyesser buyursun inşallah. Ne yaptığımızı bilelim. Günahsa günah, sevapsa sevap. İşlemeyelim ama günahı bilelim "şefîal müznibîndir" yani ahiret gününde, hesap gününde şefaat edecek günahkarlara ama hangi günahkarlara? Müslüman günahkarlara, onu tanıyanlara... Tanımayanlara da eder de tanıyanlara edecek... Devamı videoda... Gelin, Beraber Yürüyelim...

Patrick M. Wieruszewski, PharmD, BCCCP, describes the mechanisms of the renin-angiotensin system and its interplay in vasodilatory shock, reviews emerging data surrounding the use of angiotensin II in vasodilatory shock and identifies clinical shock scenarios where angiotensin II may be of most benefit.  For more pharmacy content, follow Mayo Clinic Pharmacy Residency Programs @MayoPharmRes or the host, Garrett E. Schramm, Pharm.D., @garrett_schramm on Twitter! You can also connect with the Mayo Clinic's School of Continuous Professional Development online at https://ce.mayo.edu/ or on Twitter @MayoMedEd. 

Heart failure patients are generally multi-morbid and at risk for hyperkalemia, which makes treatment with life-saving therapies like RAASi difficult and leads to compromised medical treatment and in turn poor outcomes. This trials showed that with the use of patiromer, one can simultaneously lower the risk of hyperkalemia and increase optimal medical therapy for heart failure with reduced ejection fraction. In this interview, Javed Butler, MD MPH MBA, Anthony N. DeMaria MD, MACC, with Ioannis Mastoris, MD, MPHcand, discuss the Late Breaker: DIAMOND trial: Patiromer For The Management Of Hyperkalemia In Subjects Receiving Renin-angiotensin-aldosterone System Inhibitor Medications For Heart Failure With Reduced Ejection Fraction.

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

Prof. Murat Akova, koronavirüste hatırlatma dozu için belirlenen sürenin üç aya indirilmesini olumlu bir gelişme olarak gördüğünü açıkladı. Prof. Dr. Akova, Omicron varyantının çok hızlı bulaştığını belirterek antikorlara duyarlığının az olduğuna dikkat çekti.

CME credits: 0.50 Valid until: 15-12-2022 Claim your CME credit at https://reachmd.com/programs/cme/synergy-of-guideline-directed-medical-therapies-in-heart-failure-to-optimize-patient-outcomes/13115/ Renin-angiotensin-aldosterone system inhibition (RAASi) is the foundation of guideline-directed medical therapy (GDMT) for heart failure patients. However, due to practice gaps, a significant proportion of the population requiring its use do not experience the benefits of RAASi therapy, which is especially true for patients with comorbid conditions. Hyperkalemia is a common adverse effect of RAASi therapy that needs to be anticipated and mediated so that the optimal dosing of necessary medications can occur. Maximizing GDMT in the face of hyperkalemia remains a key clinical challenge that, if not handled properly, can result in increased morbidity and mortality. In this activity, Drs. Javed Butler, Mikhail Kosiborod, and Matthew Weir review a patient case and discuss different treatment approaches to optimize GDMT while managing hyperkalemia. Tune in to make sure you're doing all you can to improve outcomes for your patients with heart failure and comorbid conditions.

CME credits: 0.50 Valid until: 15-12-2022 Claim your CME credit at https://reachmd.com/programs/cme/synergy-of-guideline-directed-medical-therapies-in-heart-failure-to-optimize-patient-outcomes/13115/ Renin-angiotensin-aldosterone system inhibition (RAASi) is the foundation of guideline-directed medical therapy (GDMT) for heart failure patients. However, due to practice gaps, a significant proportion of the population requiring its use do not experience the benefits of RAASi therapy, which is especially true for patients with comorbid conditions. Hyperkalemia is a common adverse effect of RAASi therapy that needs to be anticipated and mediated so that the optimal dosing of necessary medications can occur. Maximizing GDMT in the face of hyperkalemia remains a key clinical challenge that, if not handled properly, can result in increased morbidity and mortality. In this activity, Drs. Javed Butler, Mikhail Kosiborod, and Matthew Weir review a patient case and discuss different treatment approaches to optimize GDMT while managing hyperkalemia. Tune in to make sure you're doing all you can to improve outcomes for your patients with heart failure and comorbid conditions.

Thanks for listening! In this episode Stan deep dives into the physiology of oliguria, with some great structures and mnemonics to really help learn this interesting but challenging topic!Here are some of the mentioned resourcesThe Covid 19 intubation video!https://youtu.be/uqKnuVfZoOgThe fantastic course by the Center for Medical Simulationhttps://harvardmedsim.orgPlease support us on our Patreonhttps://www.patreon.com/anaesthesiaAll proceeds will go to Fund a Fellow to help train anaesthetists in developing countries whilst acknowledging the work it takes to keep creating this educational resource.If you enjoyed this content please like and subscribePlease post any comments or questions below. Check out www.anaesthesiacollective.com and sign up to the ABCs of Anaesthesia facebook group for other content.Any questions please email lahiruandstan@gmail.comDisclaimer: The information contained in this video/audio/graphic is for medical practitioner education only. It is not and will not be relevant for the general public.Where applicable patients have given written informed consent to the use of their images in video/photography and aware that it will be published online and visible by medical practitioners and the general public.This contains general information about medical conditions and treatments. The information is not advice and should not be treated as such. The medical information is provided “as is” without any representations or warranties, express or implied. The presenter makes no representations or warranties in relation to the medical information on this video. You must not rely on the information as an alternative to assessing and managing your patient with your treating team and consultant. You should seek your own advice from your medical practitioner in relation to any of the topics discussed in this episode' Medical information can change rapidly, and the author/s make all reasonable attempts to provide accurate information at the time of filming. There is no guarantee that the information will be accurate at the time of viewingThe information provided is within the scope of a specialist anaesthetist (FANZCA) working in Australia.The information presented here does not represent the views of any hospital or ANZCA.These videos are solely for training and education of medical practitioners, and are not an advertisement. They were not sponsored and offer no discounts, gifts or other inducements. This disclaimer was created based on a Contractology template available at http://www.contractology.com.

01 - Atolory izao anio izao 02 - Ny herisetrafiz 3 03 - Renin-jaza mifaly 04 - Torohevitra ho an'ny Zatovovavy hanambady 02 05 - Ny vahiny eo ambavahadinao, fianarana fanampiny;

01 - Atolory izao anio izao 02 - Ny herisetrafiz 3 03 - Renin-jaza mifaly 04 - Torohevitra ho an'ny Zatovovavy hanambady 02 05 - Ny vahiny eo ambavahadinao, fianarana fanampiny;

Aydın Selcen ile Gündem Dışı: Küresel dönüşüm başlarken yerkürenin taşrası kalmayalım

In Folge 26 unserer Wissensreise lernen wir Medikamente kennen, die bei Herzerkrankungen gegeben werden. Themen sind: ACE-Hemmer, Renin-Angiotensin-Aldosteron-System, Sartane, Aldosteron-Antagonisten und Betablocker. Kurzfassungen gibt es in der nächsten Folge, da diese einfach zu lang geworden wäre. Viel Spaß beim Zuhören und Lernen ;-) Schreib mir gerne Anregung, Kritik oder einfach nur ein Hallo, auch an die Adresse: tanjaloiblhp@gmail.com. Hier kannst du mich und den Podcast unterstützen: https://steadyhq.com/wissensreise

In dieser Folge dreht sich alles um deinen Körper. Wo misst er den Blutdruck? Welche Rolle spielen deine Nierenzellen?

On this ID the Future, physician Howard Glicksman and host Eric Anderson dive deeper into the body's exquisite blood pressure control system, cueing off a new discovery described at Science Daily as uncovering “the location of natural blood-pressure barometers inside our bodies that have eluded scientists for more than 60 years.” According to the primary research paper at Circulation Research, “Renin-expressing cells are essential for survival, perfected throughout evolution to maintain blood pressure (BP) and fluid-electrolyte homeostasis.” How did evolution perfect the system? How did it originate the system? The paper never says. The mention of evolution appears to be little more than a de rigueur genuflection before the reigning paradigm of blind evolution. What is bearing actual fruit, according to Glicksman Read More › Source

On this ID the Future, physician Howard Glicksman and host Eric Anderson dive deeper into the body's exquisite blood pressure control system, cueing off a new discovery described at Science Daily as uncovering “the location of natural blood-pressure barometers inside our bodies that have eluded scientists for more than 60 years.” According to the primary research paper […]

On this ID the Future, physician and Evolution News writer Howard Glicksman discusses an exciting new discovery by researchers at the University of Virginia School of Medicine, described at Science Daily as uncovering “the location of natural blood-pressure barometers inside our bodies that have eluded scientists for more than 60 years.” As the article reports, “The existence of a pressure sensor inside renin cells was first proposed back in 1957. It made sense: The cells had to know when to release renin, a hormone that helps regulate blood pressure. But even though scientists suspected this cellular barometer had to exist, they couldn’t tell what it was and whether it was located in renin cells or surrounding cells.” Dr. Glicksman and Read More › Source

Gülşah uzun süredir tanıdığım, yakın bir aile dostum. İngilizce ile ilgili kendisine verilen hiçbir şey olmamasına rağmen (özel okul, yurtdışı tecrübesi vs...) kendi çabalarıyla İngilizcede iyi bir seviyeye gelip uluslararası bir firmada çalışmaya başladı ve farklı ülkelerden arkadaşlar edindi. Bu röportajımızda Gülşah bizimle hikayesini paylaşıyor. En başta çok ufak bir teknik aksaklık yaşadık, ama doğal akışı kesmemek adına yerimi değiştirip röportaja devam ettik, ve sonra da teknik açıdan da gayet akıcı bir görüşme gerçekleştirdik. İyi izlemeler.

Önemli bir işadamımız geçtiğimiz günlerde özel bir sohbetimizde, “Mücadele edilecek onca problem ve yanlışlık varken biz kendi içimizde kavga ediyoruz. Enerjimizi, sorunlarla mücadeleye değil kendi aramızdaki küçük çıkar kavgalarına harcıyoruz” demişti. Konuyu dolaylı yoldan dindar muhafazakâr kesimin kendi içindeki açmazlara ve mücadelesine de getirdi. Medyadan iş dünyasına, siyasetten, akademyaya kadar her alanda söz konusu olan “içimizde kavga” enerjimizi sömürüp tüketiyor. BÜYÜK İDEALLERİ KÜÇÜK ÇIKARLARA KURBAN ETMEK Türkiye'de 2003'ten bu yana demokrasi, insan hakları, özgürlükler başta olmak üzere ekonomi ve yaşam standartları konusunda olağanüstü bir değişim yaşanıyor. Pandemi ve öncesindeki “kur müdahalesi” olmasa şu anda refah seviyesi en yüksek ülkeler arasında ilk sıralarda yer alacaktık. Bununla birlikte “kültür” ve eğitim alanında istenen başarı elde edilememiştir. Hatta bu konuda içeriden de ciddi eleştiriler vardır. Yine de çıkılan yolda, menzil kaybı yaşanmadığına göre, gecikmeli de olsa hedeflere ulaşılabilir. Yeter ki “küçük grupların” çıkar savaşlarına “büyük idealleri” kurban etmeyelim.

You probably know that the kidneys play an important role in maintaining blood pressure within the normal range. You might also know that they do this by regulating blood volume and the degree of arterial contraction or dilation (the systemic vascular resistance). But do you know how the kidneys do this? The answer is the kidneys accomplish this primarily through a set of hormones and enzymes known together as the renin-angiotensin-aldosterone system (RAAS). In this brick, we will discuss the components, functions, and regulation of the RAAS. Renin is an enzyme released by the kidneys that ultimately causes the formation of the hormone angiotensin II (Ang II) in the body—which in turn stimulates the release of the hormone aldosterone from the adrenal cortex. Ang II and aldosterone act in a number of ways to increase blood volume and blood pressure. RAAS acts to increase sodium reabsorption in the kidney, increase vascular tone, and even stimulate antidiuretic hormone (ADH) to reabsorb more water: all of these defend our extracellular volume and blood pressure. RAAS is therefore a critical system for keeping us upright! After listening to this Audio Brick, you should be able to: Outline the renin-angiotensin-aldosterone system, including sensors, factors that control it, sources of hormone release, and the actions of each hormone. Describe the mechanisms by which the renin-angiotensin-aldosterone system regulates blood pressure. Compare and contrast tubuloglomerular feedback with the renin-angiotensin-aldosterone system. You can also check out the original brick from our Endocrine collection, which is available for free. Learn more about Rx Bricks by signing up for a free USMLE-Rx account: www.usmle-rx.com You will get 5 days of full access to our Rx360+ program, including nearly 800 Rx Bricks.  After the 5-day period, you will still be able to access over 150 free bricks, including the entire collections for General Microbiology and Cellular and Molecular Biology. *** If you enjoyed this episode, we'd love for you to leave a review on Apple Podcasts.  It helps with our visibility, and the more med students (or future med students) listen to the podcast, the more we can provide to the future physicians of the world. Follow USMLE-Rx at: Facebook: www.facebook.com/usmlerx Blog: www.firstaidteam.com Twitter: https://twitter.com/firstaidteam Instagram: https://www.instagram.com/firstaidteam/ YouTube: www.youtube.com/USMLERX Learn how you can access over 150 of our bricks for FREE: https://usmlerx.wpengine.com/free-bricks/ from our Musculoskeletal, Skin, and Connective Tissue collection, which is available for free. Learn more about Rx Bricks by signing up for a free USMLE-Rx account: www.usmle-rx.com You will get 5 days of full access to our Rx360+ program, including nearly 800 Rx Bricks.  After the 5-day period, you will still be able to access over 150 free bricks, including the entire collections for General Microbiology and Cellular and Molecular Biology.

Commentary by Dr. Valentin Fuster

Bu bölümde SpeedyMemo ve Süper Hızlı Okuma'nın sahibi Mehmet Taşhanlıgil ile hızlı okumanın bize sağlayacağı faydalardan, kitap okumanın drastik bir şekilde hayat kalitemizi artıracağından ve tabii ki nasıl daha hızlı okuyabileceğimizden bahsediyoruz. Ayrıca daha hızlı okumak için taktikler ve çalışmalar da bu bölümde!

"Yeni Fikirlere Neden Direniriz?" serisinin son bölümünde tarih bilgisinin önemini anlatıyorum. Daha Fazla İçerik: www.haddinias.net İletişim: Haddinias@ozkent.co

Back by popular demand…all two of you…the second chapter of The Clinical Physiology of Acid Base and Electrolyte Disorders. Chapter Outline- Renal Circulation and GFR - RBF is 20% of cardiac output - In terms of mL per 100 g organ weight it is 4x the liver and exercising muscle and 8x coronary blood flow! - After the glomeruli the efferent arteriole have two fates - Peritubular capillaries in the cortex - Peritubular capillaries are not necessarily associated with their parent glomeruli. Weird. - Vasa recta from juxtamedullary glomeruli in the medullaJoel Says: This seems wrong. Solute balance can be maintained down to a very low GFR. The R^2 here would be very low. Prove me wrong. - States that GFR is an important determinant of solute and water excretion. - Glomerular anatomy and function - Structure Four editions of the Bud Bible up top and a copy of Bud Light on the bottom. - Glomerulus is a tuft of capillaries - Enclosed in a capsule of epithelial cells, called Bowman's capsule - The epithelial cells of Bowman's capsule are continuous with the epithelial cells of the proximal tubule Looking at scanning EMs of the glomerulus is one of life's simple pleasures—Josh. Josh says: Look at the review in Nature Reviews Nephrology from Rachel Lennon's groupComplexities of the glomerular basement membrane - Filtration barrier - Epithelial cell (podocyte) - Epithelial cells adhere to the basement membrane via foot processes and the foot processes have slit diaphragms - Basement membrane New Super-resolution structure of the GBM: https://elifesciences.org/articles/01149 Hi res microscopy is really hi-res. Technique is call ed STORM. Melanie talks about conduits through the glomeruli. Here is a cool review: Why until just now? Undiscovered uniqueness of the human glomerulus! by L. Gabriel Navar, Owen RichfieldAm J Physiol Renal Physiol. 2018 Nov 1; 315(5): F1345–F1346. Published online 2018 Aug 15. doi: 10.1152/ajprenal.00369.2018 PMCID: PMC6293291 - Produced by both the endothelial cells and podocytes - Formed from type IV collagen - Abnormalities of type 4 collagen cause Alport - The gene coding for the alpha 5 chain is the culprit - COL4A5 - Abnormal Alpha 3 and 4 chains can also cause hereditary nephritis - Has other substances - Laminin - Nidogen - Heparin sulfate proteoglycans - Provides the negative charge - Enthothelial cell (fenestrated) - Protein excretion - Glomerular function: allow filtration of small solutes (Na and urea) while preventing filtration of larger molecules - Insulin MW 5,200 is freely filtered (upper range of freely filtered) - Preventing loss of protein prevents - Negative nitrogen balance - Development of hypoalbuminemia - Infection from loss of immunoglobulin - Size and charge selectivity of the GBM - pores are between cords of type 4 collagen - The epithelial cells and slit diaphragms matter - Macromolecules that pass through GBM can accumulate underneath the epithelial layer - Isolated GBM in invitro studies is much more permeable to than intact glomerulus - There is increased protein filtration in areas where the epithelial cells have detached from the GBM Josh really likes this figure from another Nature Reviews Nephrology paper. This one by Moeller and Chia-Gil. - Mutations in nephrin, localized to the slit diaphragm causes congenital nephrotic syndrome - Charge selectivity is important - Neutral and cationic particle are more likely to be filtered - Albumin (negative charge) is filtered 5% as well as same size neutral dextrans - In glomerular disease, while there is increased filtration of proteins there is decreased filtration of small solutes due to loss of glomerular surface areaJC says: Take a look at this research on the serving coefficient in glomerular disease. Some surprising results.Glomerular dysfunction in nephrotic humans with minimal changes or focal glomerulosclerosis - Why do people in remission have what appears to be spilling more high molecular radius particles than normal and why do patients with active MCD have lower clearance across all molecular diameters? - Other glomerular functionsJosh says: Take a look at this interesting paper by Butt et alA molecular mechanism explaining albuminuria in kidney disease - Synthetic - Epithelial cells produce GBM - Phagocytic - Remove circulating macromolecules that pass through GBM and get trapped in subepithelial spaceJosh says: The sFLT1 (soluble VEGF receptor) relationship to preeclampsia is just so cool. And here's the paper:Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsiaAnd in the NEJM: VEGF Inhibition and Renal Thrombotic Microangiopathy - Endocrine - Enthothelial cells regulate vascular tone by releasing - Prostacyclin - Endothelin - Nitric oxideJC says: Do yourself a favor and spend some time learning about extraglomerular mesangial cells with Stuart Shankland Extraglomerular origin of the mesangial cell after injury. A new role of the juxtaglomerular apparatusJoel adds, if you ever get a chance to party with Dr. Shankland, don't skip out. - Mesangial cells, two types - Intrinsic Mesangial cell - Microfilaments similar to smooth muscle - Responds to Ang2 - Regulates glomerular hemodynamics - Can release cytokines - Can respond to cytokines by proliferation - Circulating macrophages and monocytes - Phagocytic function - Clear molecules that get through the endothelial wall but cant get through the GBMJosh says, “Topf, get it right. Its Ree-nin not renin. Classic letter to JAMA. - Renin-Angiotensin System - Afferent arteriole contain specialized cells called juxtaglomerular cells - Produce prorenin which cleaved into renin - Stimuli for renin release - Hypotension - Volume depletion - Increased sympathetic activity - Renin catalyze the production of ang1 from angiotensinogen - Ang1 is catalyze to Ang2 by ACE located in the - Lung - Endothelial cells - Glomeruli itself pic.twitter.com/DaDfS7u8se— Roger Rodby (@NephRodby) February 22, 2021 - Discussion of local renin and Aniotensinogen - Explains why ACEi are useful even with low systemic renin levels and Ang2 - Actions of Ang2 - Sodium and water retention - By direct Na reabsorption in the early PT (and in the proximal tubule, water is permeable to the epithelium so every sodium reabsobed, brings a water molecule along for the osmotic ride. - Stimulates the Na-H antiporter - 40-50% of Na reabsorption in the S1 segment of the PT is due to Ang2 - By stimulation of aldosterone - Ang2 that stimulates Aldo comes from the kidney and from the adrenal gland itself - VasoconstrictionJosh talks angiotensin:Tenses the angios--love this Melanie!1961 paper from del Greco (who's endowed chair Dan Batlle has now) trying AT2 in "hopeless" patients and dialysis patients:https://jamanetwork.com/journals/jama/article-abstract/332265Great EM-crit/pulmcrit discussion here:https://emcrit.org/emcrit/deeper-vasopressors-athos-3/and caveats here:https://emcrit.org/pulmcrit/angiotensin-ii/ - Arteriolar vasoconstriction - Ang2 important for raising BP in RAS - Ang2 important in maintaining BP with volume depletion or in CHF, liver disease - Giving ACEi to cirrhosis can cause BP to dump 25 points - Regulation of GFR - Affects constriction at afferent arteriole and efferent arteriole - Mediated via thromboxane JC talks about the ATHOS trial and how there is a signal for improved outcomes especially in patients requiring renal replacement therapy.Angiotensin II for the Treatment of Vasodilatory ShockOutcomes in Patients with Vasodilatory Shock and Renal Replacement Therapy Treated with Intravenous Angiotensin II - Afferent arteriole starts bigger so reductions have less of an effect than constriction does on the narrower efferent arteriole. - This results in a fall of RBF due to increased resistance but maintaining GFR by increasing inrtaglomerular pressure. - Also stimulates prostaglandins which are vasodilator, modulating this affectJoel says: You haven't heard of the Trolly Problem? Oh you need to take 5 minutes and read this. - It can stimulate contraction of the mesangium reducing surface area of the glom reducing filtration. - It sensitizes the afferent arteriole to TG feedback so it can reduce glomerular flow in response to increased chloride detection in the TLoH. - Control of renin secretionEver wanted to know about intrarenal renin concentrations? Yeah, me neither. But JC's got you covered: Endogenous angiotensin concentrations in specific intrarenal fluid compartments of the rat. - Primarily sodium intake, increased intake results in less renin - Mediated by baroreceptors - Baroreceptors in afferent vessel wall - Cardiac and arterial baroreceptors which activate the sympathetic nervous system and catecholamines which then stimulates reninRoger says: Do your self a favor and read about Yanomamo IndiansBlood pressure and electrolyte excretion in the Yanomamo Indians, an isolated population - Cells of the macula densa in the early distal tubule which detect decreased chloride delivery - This allows loop diuretics to be particularly effective at increasing renin as they block chloride resorption - Suppression of renin in response to chloride is mediated by adenosine - Stimulation of renin in response to decreased chloride is mediated by PGE - The PGE cause local vasodilation so the kidney maintained a rich blood flow while using renin and Ang2 to cause systemic vasoconstrictionAnna's notes for the deep dive in glomerular barrierOur understanding is based on technology available at the time. Even in 1920s, there was thought that tubular reuptake of protein may be important, but studies never demonstrated this til 2007 and even then are debated. 2007 Russo, et al (and BM at IU!) showed that The normal kidney filters nephrotic levels of albumin and that failure of retrieval by proximal tubule cells is what separates proteinuria from nonproteinuria. This was countered by a study in 2009 demonstrating much lower GSC and suggesting that the high GSC in the 2007 could be the result of nonphysiologic states.Check out this 2008 debate in JASN regarding the validity of the charge model and “normal” albumin in the glomerular filtrate. Hotly debated with too many studies to cite. 2017: Lawrence et al publish their findings that the GBM and podocyte processes are sufficient and the slit diaphragm likely does not exist. They used labeled proteins and confocal microscopy to determine migration of particles through the enodthelium and GBM. They also injected NaSCN oligoclusters from the size of albumin (66kDa)up to the size of IgG dimers (300 kDa) into mice, then fixed. The size-sensitive permeation into the lamina densa of the GBM and the podocyte glycocalyx of albumin and uptake of any “escaping” albumin by the proximal tubule was also observed. This countered the common prior conception that the slit diaphragms pores are the site of albumin “capture.” For your reading pleasure the review of Clinical Physiology of Acid-Base and Electrolyte Disorders Fourth Edition in Annals of Internal Medicine

FDA 批准血管紧张素II用于休克病人低血压的治疗NEJM 秋水仙碱在慢性冠心病患者中的疗效Circulation 心脏内源性干细胞和心肌细胞增殖的争论、谬误和进展血管紧张素II（angiotensin II）2017年12月，FDA批准合成人血管紧张素II用于治疗分布性休克患者。《ATHOS-3研究：血管紧张素II治疗血管舒张性休克的3期临床研究》New England Journal of Medicine，2017年8月 (1)血管舒张性休克的患者对高剂量的血管收缩剂反应差，而且会增加死亡率。此研究的目的是评价这类患者使用血管紧张素II的疗效。研究纳入需要大剂量血管收缩药物维持血压的、血管舒张性休克的患者344人（去甲肾上腺素用量>0.2μg/kg/min或等剂量的血管收缩药），随机分入血管紧张素II治疗组和安慰剂组。用药3小时后，血压升高10mmHg或平均血压升高至75mmHg的患者，干预组达到69.9%，安慰剂组只有23.4%（P0.2）或高血压显著升高的情况（P>0.2）。结论：卡那单抗虽然可降低主要心血管事件发生率，但这些获益与血压变化无关。《COLCOT研究：小剂量秋水仙碱治疗心肌梗死的疗效和安全性》New England Journal of Medicine，2019年11月 (6)秋水仙碱是一种口服的，有效的抗炎药物，是用于治疗痛风和心包炎。研究的目的是评价秋水仙碱抗炎治疗近期心肌梗死患者对缺血性心血管事件的影响。研究招募了急性心肌梗死30天内的患者共4745人，随机分到秋水仙碱 0.5mg qd组或安慰剂。平均随访22.6个月后，秋水仙碱组和安慰剂组分别有5.5%和7.1%的患者出现主要终点事件（心血管原因死亡、心脏骤停复苏、心肌梗死、卒中或因心绞痛紧急住院导致冠状动脉血运重建）（P = 0.02）。与安慰剂相比，秋水仙碱心血管原因死亡的风险比0.84，心脏骤停风险比0.83，心肌梗死风险比为0.91；能显著降低卒中的风险达74%，同时能显著降低心绞痛住院再次血运重建的风险达50%。两组最常见的不良事件是腹泻，发生率没有差异，最严重的不良事件是肺炎，发生率分别为0.9%和0.4%（P = 0.03）。结论：在近期心肌梗死患者中，每天0.5 mg的秋水仙碱比安慰剂显著降低缺血性心血管事件的风险。《COLCOT研究：秋水仙碱治疗起始时间与心肌梗死后心血管预后的关系》European Heart Journal，2020年8月 (7)这项COLCOT研究的分析，纳入了4661例患者，按照启动秋水仙碱治疗距离急性心肌梗死的时间可分为三个亚组，8天组。平均随访22.7个月后，8天组没有统计学意义（风险比 0.96和0.82）。不仅如此，3天内启动秋水仙碱治疗的患者，心绞痛住院血运重建术的风险显著降低（风险比 0.35）、再次血运重建风险显著降低（风险比 0.63），而且所有的复合心血管死亡、心脏骤停、心肌梗死或卒中的风险均显著降低（风险比 0.55，P < 0.05)。结论：心肌梗死后，患者应尽早在医院内给予秋水仙碱治疗。《LoDoCo2研究：秋水仙碱在慢性冠心病患者中的疗效》New England Journal of Medicine，2020年8月(8)秋水仙碱的抗炎作用可降低近期心肌梗死患者发生心血管事件的风险，但对慢性冠心病患者的证据有限。这项随机、对照、双盲试验中，招募5522名慢性冠心病患者，随机分配至秋水仙碱0.5mg qd组或安慰剂组，平均随访时间为28.6个月。主要终点事件（心血管死亡、自发心肌梗死、缺血性卒中或缺血驱动的冠状动脉血运重建）在秋水仙碱组和安慰剂组的发生率分别为6.8%和9.6%（P < 0.001)。次要终点事件（心血管死亡、自发心肌梗死、缺血性卒中）在秋水仙碱组和安慰剂组的发生率分别为4.2%和5.7%（P = 0.007）。秋水仙碱组的自发性心肌梗死或缺血驱动的冠脉血运重建的复合终点、心血管死亡或自发性心肌梗死的复合终点、缺血驱动的冠脉血运重建和自发性心肌梗死的发生率也显著降低。秋水仙碱组的非心血管疾病死亡发生率高于安慰剂组（风险比 1.51）。结论：秋水仙碱可以显著降低慢性冠心病患者发生心血管事件的风险。小羽点评：冠心病发病机制复杂，不仅限于胆固醇内膜浸润，也是免疫系统的全身和局部激活驱动的血管壁的慢性炎症的结果，最终导致斑块破裂或侵蚀、血栓形成、心肌梗死。在广泛使用他汀类药物后，仍有大量患者出现复发，反映了残留炎症并没有被充分控制。现在抗炎药物治疗成为热点，但是否能上升到一线治疗的地位，我们拭目以待。心脏干细胞修复技术《综述：心脏内源性干细胞和心肌细胞增殖的争论、谬误和进展》Circulation，2020年7月 (9)在过去的十年里，许多类型的心脏干细胞（CSCs）从实验室到临床研究，但并有什么确切的治疗效果。有关干细胞示踪的基础研究开始质疑心脏干细胞的基础生物学和作用机制，挑战心脏干细胞的起源和存在。除了心脏干细胞在心脏再生中的潜在作用外，现有心肌细胞的增殖得到了更多的关注。中国科学院研究人员发表的这篇综述评估了过去和现在关于心脏干细胞和心肌细胞增殖的研究的方法和技术方面，也讨论了潜在局限性。作者认为未来的研究方向：（1）由于缺乏常驻CSC存在的证据，内源性心肌细胞增殖频率又非常低，如何促进心肌细胞增殖可能是未来一个重要的研究领域；（2）除了诱导心肌细胞增殖外，还可以考虑其他替代方法，比如通过过表达特定转录因子、或小分子诱导的方式，使成纤维细胞原位重新编程成为心肌细胞，如此使心肌细胞再生同时减少瘢痕形成；（3）人胚胎干细胞或诱导多潜能细胞来源的心脏祖细胞和心肌细胞已成功移植到大型动物模型中，并已证实了移植细胞在宿主心肌内的存活和心脏功能的改善；（4）即使没有直接的心肌细胞再生，促进新血管形成的方法，如通过移植能够分泌血管生长因子的间充质干细胞，或减轻心肌梗死后炎症损伤等方法，来改善心肌存活率、减少疤痕形成；（5）双重干细胞疗法协同改善心肌损伤后心脏功能和血管新生，如人类诱导性多潜能干细胞来源的心肌细胞和间充质干细胞，或人类胚胎干细胞来源的心外膜细胞和心肌细胞；（6）含有生长因子或多种心脏细胞类型的心外膜贴片，也被证明可以改善心肌梗死后的心脏功能和新生血管；（7）通过RNA修饰心外膜祖细胞后产生的血管内皮生长因子A可以使血管再生增强；最后，作者认为，由于内源性假定心脏干细胞的错误，因此，为达到心脏修复和再生的最终目标，应该将更多的精力和资源投入到更有前途的方向上是很重要的。《综述：对胚胎干细胞在心脏修复中的作用的评价》European Heart Journal，2020年7月 (10)尽管胚胎干细胞（ESCs）具有分化为心肌细胞的能力，胚胎干细胞或胚胎干细胞来源的细胞的移植仍面临着一些非常棘手的问题：（1）移植物排斥反应，通过药物诱导免疫抑制本身就是一种疾病；（2）心律失常，研究发现在灵长类动物中移植人类胚胎干细胞来源的细胞会导致危及生命的心律失常，而这种心律失常的发生与剂量无关；（3）恶性肿瘤，在当代临床研究中，对恶性肿瘤等灾难性影响的耐受限度为零。尽管胚胎干细胞分化成肿瘤的可能性非常低，但不是完全没有可能，特别是移植细胞的数量级在十亿的时候；（4）长期再生能力，虽然胚胎干细胞和胚胎干细胞来源的细胞被吹捧为具有长期再生能力，但干细胞示踪技术显示这些细胞在移植后迅速消失，没有长期移植或再生的证据；（5）越来越多的证据表明胚胎干细胞的作用是通过旁分泌机制来发挥的，尚没有开展或启动胚胎干细胞来源细胞在心血管疾病中的临床对照试验；作者最后对未来发展的方向做了预估：（1）成年细胞已用于数千名心脏病患者，没有显著的副作用，其结果令人鼓舞，值得进行II期和III期试验。（2）人诱导的多潜能干细胞提供类似胚胎干细胞的多能性，而不需要终身免疫抑制。《COVID-19患者中使用秋水仙碱治疗对心脏、炎症指标及临床预后的影响》JAMA Network Open，2020年6月 (11)研究旨在比较秋水仙碱和标准化治疗对心脏、炎症指标及临床预后的影响。在105例随机临床试验中，秋水仙碱干预组在常规治疗的基础上，首剂1.5mg，如果没有观察到胃肠道不良反应则60分钟后再给0.5mg，维持剂量为0.5mg qd（体重60kg）直至出院或满21天。对照组的主要临床终点、临床恶化率高于秋水仙碱组，而且对照组患者出现恶化比较快。两组高敏肌钙蛋白浓度无差异，但秋水仙碱组患者D-二聚体的增幅较小。结论：秋水仙碱对COVID-19由一定的治疗作用。参考文献1.Khanna A, Ostermann M, Bellomo R. 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Hypertension. 2020;75(2):477-82.6.Tardif JC, Kouz S, Waters DD, Bertrand OF, Diaz R, Maggioni AP, et al. Efficacy and Safety of Low-Dose Colchicine after Myocardial Infarction. N Engl J Med. 2019;381(26):2497-505.7.Bouabdallaoui N, Tardif JC, Waters DD, Pinto FJ, Maggioni AP, Diaz R, et al. Time-to-treatment initiation of colchicine and cardiovascular outcomes after myocardial infarction in the Colchicine Cardiovascular Outcomes Trial (COLCOT). Eur Heart J. 2020.8.Nidorf SM, Fiolet ATL, Mosterd A, Eikelboom JW, Schut A, Opstal TSJ, et al. Colchicine in Patients with Chronic Coronary Disease. New England Journal of Medicine. 2020.9.He L, Nguyen NB, Ardehali R, Zhou B. Heart Regeneration by Endogenous Stem Cells and Cardiomyocyte Proliferation. Circulation. 2020;142(3):275-91.10.Wysoczynski M, Bolli R. A realistic appraisal of the use of embryonic stem cell-based therapies for cardiac repair. Eur Heart J. 2020;41(25):2397-404.11.Deftereos SG, Giannopoulos G, Vrachatis DA, Siasos GD, Giotaki SG, Gargalianos P, et al. Effect of Colchicine vs Standard Care on Cardiac and Inflammatory Biomarkers and Clinical Outcomes in Patients Hospitalized With Coronavirus Disease 2019: The GRECCO-19 Randomized Clinical Trial. JAMA Network Open. 2020;3(6):e2013136-e.

FDA 批准血管紧张素II用于休克病人低血压的治疗NEJM 秋水仙碱在慢性冠心病患者中的疗效Circulation 心脏内源性干细胞和心肌细胞增殖的争论、谬误和进展血管紧张素II（angiotensin II）2017年12月，FDA批准合成人血管紧张素II用于治疗分布性休克患者。《ATHOS-3研究：血管紧张素II治疗血管舒张性休克的3期临床研究》New England Journal of Medicine，2017年8月 (1)血管舒张性休克的患者对高剂量的血管收缩剂反应差，而且会增加死亡率。此研究的目的是评价这类患者使用血管紧张素II的疗效。研究纳入需要大剂量血管收缩药物维持血压的、血管舒张性休克的患者344人（去甲肾上腺素用量>0.2μg/kg/min或等剂量的血管收缩药），随机分入血管紧张素II治疗组和安慰剂组。用药3小时后，血压升高10mmHg或平均血压升高至75mmHg的患者，干预组达到69.9%，安慰剂组只有23.4%（P0.2）或高血压显著升高的情况（P>0.2）。结论：卡那单抗虽然可降低主要心血管事件发生率，但这些获益与血压变化无关。《COLCOT研究：小剂量秋水仙碱治疗心肌梗死的疗效和安全性》New England Journal of Medicine，2019年11月 (6)秋水仙碱是一种口服的，有效的抗炎药物，是用于治疗痛风和心包炎。研究的目的是评价秋水仙碱抗炎治疗近期心肌梗死患者对缺血性心血管事件的影响。研究招募了急性心肌梗死30天内的患者共4745人，随机分到秋水仙碱 0.5mg qd组或安慰剂。平均随访22.6个月后，秋水仙碱组和安慰剂组分别有5.5%和7.1%的患者出现主要终点事件（心血管原因死亡、心脏骤停复苏、心肌梗死、卒中或因心绞痛紧急住院导致冠状动脉血运重建）（P = 0.02）。与安慰剂相比，秋水仙碱心血管原因死亡的风险比0.84，心脏骤停风险比0.83，心肌梗死风险比为0.91；能显著降低卒中的风险达74%，同时能显著降低心绞痛住院再次血运重建的风险达50%。两组最常见的不良事件是腹泻，发生率没有差异，最严重的不良事件是肺炎，发生率分别为0.9%和0.4%（P = 0.03）。结论：在近期心肌梗死患者中，每天0.5 mg的秋水仙碱比安慰剂显著降低缺血性心血管事件的风险。《COLCOT研究：秋水仙碱治疗起始时间与心肌梗死后心血管预后的关系》European Heart Journal，2020年8月 (7)这项COLCOT研究的分析，纳入了4661例患者，按照启动秋水仙碱治疗距离急性心肌梗死的时间可分为三个亚组，8天组。平均随访22.7个月后，8天组没有统计学意义（风险比 0.96和0.82）。不仅如此，3天内启动秋水仙碱治疗的患者，心绞痛住院血运重建术的风险显著降低（风险比 0.35）、再次血运重建风险显著降低（风险比 0.63），而且所有的复合心血管死亡、心脏骤停、心肌梗死或卒中的风险均显著降低（风险比 0.55，P < 0.05)。结论：心肌梗死后，患者应尽早在医院内给予秋水仙碱治疗。《LoDoCo2研究：秋水仙碱在慢性冠心病患者中的疗效》New England Journal of Medicine，2020年8月(8)秋水仙碱的抗炎作用可降低近期心肌梗死患者发生心血管事件的风险，但对慢性冠心病患者的证据有限。这项随机、对照、双盲试验中，招募5522名慢性冠心病患者，随机分配至秋水仙碱0.5mg qd组或安慰剂组，平均随访时间为28.6个月。主要终点事件（心血管死亡、自发心肌梗死、缺血性卒中或缺血驱动的冠状动脉血运重建）在秋水仙碱组和安慰剂组的发生率分别为6.8%和9.6%（P < 0.001)。次要终点事件（心血管死亡、自发心肌梗死、缺血性卒中）在秋水仙碱组和安慰剂组的发生率分别为4.2%和5.7%（P = 0.007）。秋水仙碱组的自发性心肌梗死或缺血驱动的冠脉血运重建的复合终点、心血管死亡或自发性心肌梗死的复合终点、缺血驱动的冠脉血运重建和自发性心肌梗死的发生率也显著降低。秋水仙碱组的非心血管疾病死亡发生率高于安慰剂组（风险比 1.51）。结论：秋水仙碱可以显著降低慢性冠心病患者发生心血管事件的风险。小羽点评：冠心病发病机制复杂，不仅限于胆固醇内膜浸润，也是免疫系统的全身和局部激活驱动的血管壁的慢性炎症的结果，最终导致斑块破裂或侵蚀、血栓形成、心肌梗死。在广泛使用他汀类药物后，仍有大量患者出现复发，反映了残留炎症并没有被充分控制。现在抗炎药物治疗成为热点，但是否能上升到一线治疗的地位，我们拭目以待。心脏干细胞修复技术《综述：心脏内源性干细胞和心肌细胞增殖的争论、谬误和进展》Circulation，2020年7月 (9)在过去的十年里，许多类型的心脏干细胞（CSCs）从实验室到临床研究，但并有什么确切的治疗效果。有关干细胞示踪的基础研究开始质疑心脏干细胞的基础生物学和作用机制，挑战心脏干细胞的起源和存在。除了心脏干细胞在心脏再生中的潜在作用外，现有心肌细胞的增殖得到了更多的关注。中国科学院研究人员发表的这篇综述评估了过去和现在关于心脏干细胞和心肌细胞增殖的研究的方法和技术方面，也讨论了潜在局限性。作者认为未来的研究方向：（1）由于缺乏常驻CSC存在的证据，内源性心肌细胞增殖频率又非常低，如何促进心肌细胞增殖可能是未来一个重要的研究领域；（2）除了诱导心肌细胞增殖外，还可以考虑其他替代方法，比如通过过表达特定转录因子、或小分子诱导的方式，使成纤维细胞原位重新编程成为心肌细胞，如此使心肌细胞再生同时减少瘢痕形成；（3）人胚胎干细胞或诱导多潜能细胞来源的心脏祖细胞和心肌细胞已成功移植到大型动物模型中，并已证实了移植细胞在宿主心肌内的存活和心脏功能的改善；（4）即使没有直接的心肌细胞再生，促进新血管形成的方法，如通过移植能够分泌血管生长因子的间充质干细胞，或减轻心肌梗死后炎症损伤等方法，来改善心肌存活率、减少疤痕形成；（5）双重干细胞疗法协同改善心肌损伤后心脏功能和血管新生，如人类诱导性多潜能干细胞来源的心肌细胞和间充质干细胞，或人类胚胎干细胞来源的心外膜细胞和心肌细胞；（6）含有生长因子或多种心脏细胞类型的心外膜贴片，也被证明可以改善心肌梗死后的心脏功能和新生血管；（7）通过RNA修饰心外膜祖细胞后产生的血管内皮生长因子A可以使血管再生增强；最后，作者认为，由于内源性假定心脏干细胞的错误，因此，为达到心脏修复和再生的最终目标，应该将更多的精力和资源投入到更有前途的方向上是很重要的。《综述：对胚胎干细胞在心脏修复中的作用的评价》European Heart Journal，2020年7月 (10)尽管胚胎干细胞（ESCs）具有分化为心肌细胞的能力，胚胎干细胞或胚胎干细胞来源的细胞的移植仍面临着一些非常棘手的问题：（1）移植物排斥反应，通过药物诱导免疫抑制本身就是一种疾病；（2）心律失常，研究发现在灵长类动物中移植人类胚胎干细胞来源的细胞会导致危及生命的心律失常，而这种心律失常的发生与剂量无关；（3）恶性肿瘤，在当代临床研究中，对恶性肿瘤等灾难性影响的耐受限度为零。尽管胚胎干细胞分化成肿瘤的可能性非常低，但不是完全没有可能，特别是移植细胞的数量级在十亿的时候；（4）长期再生能力，虽然胚胎干细胞和胚胎干细胞来源的细胞被吹捧为具有长期再生能力，但干细胞示踪技术显示这些细胞在移植后迅速消失，没有长期移植或再生的证据；（5）越来越多的证据表明胚胎干细胞的作用是通过旁分泌机制来发挥的，尚没有开展或启动胚胎干细胞来源细胞在心血管疾病中的临床对照试验；作者最后对未来发展的方向做了预估：（1）成年细胞已用于数千名心脏病患者，没有显著的副作用，其结果令人鼓舞，值得进行II期和III期试验。（2）人诱导的多潜能干细胞提供类似胚胎干细胞的多能性，而不需要终身免疫抑制。《COVID-19患者中使用秋水仙碱治疗对心脏、炎症指标及临床预后的影响》JAMA Network Open，2020年6月 (11)研究旨在比较秋水仙碱和标准化治疗对心脏、炎症指标及临床预后的影响。在105例随机临床试验中，秋水仙碱干预组在常规治疗的基础上，首剂1.5mg，如果没有观察到胃肠道不良反应则60分钟后再给0.5mg，维持剂量为0.5mg qd（体重60kg）直至出院或满21天。对照组的主要临床终点、临床恶化率高于秋水仙碱组，而且对照组患者出现恶化比较快。两组高敏肌钙蛋白浓度无差异，但秋水仙碱组患者D-二聚体的增幅较小。结论：秋水仙碱对COVID-19由一定的治疗作用。参考文献1.Khanna A, Ostermann M, Bellomo R. Angiotensin II for the Treatment of Vasodilatory Shock. N Engl J Med. 2017;377(26):2604.2.Bellomo R, Forni LG, Busse LW, McCurdy MT, Ham KR, Boldt DW, et al. Renin and Survival in Patients Given Angiotensin II for Catecholamine-Resistant Vasodilatory Shock. A Clinical Trial. Am J Respir Crit Care Med. 2020;202(9):1253-61.3.Silvain J, Kerneis M, Zeitouni M, Lattuca B, Galier S, Brugier D, et al. Interleukin-1beta and Risk of Premature Death in Patients With Myocardial Infarction. J Am Coll Cardiol. 2020;76(15):1763-73.4.Everett BM, MacFadyen JG, Thuren T, Libby P, Glynn RJ, Ridker PM. Inhibition of Interleukin-1beta and Reduction in Atherothrombotic Cardiovascular Events in the CANTOS Trial. J Am Coll Cardiol. 2020;76(14):1660-70.5.Rothman AM, MacFadyen J, Thuren T, Webb A, Harrison DG, Guzik TJ, et al. Effects of Interleukin-1beta Inhibition on Blood Pressure, Incident Hypertension, and Residual Inflammatory Risk: A Secondary Analysis of CANTOS. Hypertension. 2020;75(2):477-82.6.Tardif JC, Kouz S, Waters DD, Bertrand OF, Diaz R, Maggioni AP, et al. Efficacy and Safety of Low-Dose Colchicine after Myocardial Infarction. N Engl J Med. 2019;381(26):2497-505.7.Bouabdallaoui N, Tardif JC, Waters DD, Pinto FJ, Maggioni AP, Diaz R, et al. Time-to-treatment initiation of colchicine and cardiovascular outcomes after myocardial infarction in the Colchicine Cardiovascular Outcomes Trial (COLCOT). Eur Heart J. 2020.8.Nidorf SM, Fiolet ATL, Mosterd A, Eikelboom JW, Schut A, Opstal TSJ, et al. Colchicine in Patients with Chronic Coronary Disease. New England Journal of Medicine. 2020.9.He L, Nguyen NB, Ardehali R, Zhou B. Heart Regeneration by Endogenous Stem Cells and Cardiomyocyte Proliferation. Circulation. 2020;142(3):275-91.10.Wysoczynski M, Bolli R. A realistic appraisal of the use of embryonic stem cell-based therapies for cardiac repair. Eur Heart J. 2020;41(25):2397-404.11.Deftereos SG, Giannopoulos G, Vrachatis DA, Siasos GD, Giotaki SG, Gargalianos P, et al. Effect of Colchicine vs Standard Care on Cardiac and Inflammatory Biomarkers and Clinical Outcomes in Patients Hospitalized With Coronavirus Disease 2019: The GRECCO-19 Randomized Clinical Trial. JAMA Network Open. 2020;3(6):e2013136-e.

In today's podcast, I review the pathophysiology of the Renin Angiotensin Aldosterone System (RAAS). Let's Review!

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.15.340935v1?rss=1 Authors: Ma, S., Henderson, J. A., Shen, J. Abstract: Renin is a pepsin-like aspartyl protease and an important drug target for the treatment of hypertension; despite three decades' research, its pH-dependent structure-function relationship remains poorly understood. Here we employed the continuous constant pH molecular dynamics (CpHMD) simulations to decipher the acid/base roles of renin's catalytic dyad and the conformational dynamics of the flap, which is a common structural feature among aspartyl proteases. The calculated pKa's suggest that the catalytic Asp38 and Asp226 serve as the general base and acid, respectively, in agreement with experiment and supporting the hypothesis that renin's neutral optimum pH is due to the substrate-induced pKa shifts of the aspartic dyad. The CpHMD data confirmed our previous hypothesis that hydrogen bond formation is the major determinant of the dyad pKa order. Additionally, our simulations showed that renin's flap remains open regardless of pH, although a Tyr-inhibited state is occasionally formed above pH 5. These findings are discussed in comparison to the related aspartyl proteases, including beta-secretases 1 and 2, capthepsin D, and plasmepsin II. Our work represents a first step towards a systematic understanding of the pH-dependent structure-dynamics-function relationships of pepsin-like aspartyl proteases that play important roles in biology and human disease states. Copy rights belong to original authors. Visit the link for more info

Egolarımız ne kadar büyük? Bu videoda yapılmış olan bir çalışmadan yola çıkarak kendi egolarımız ile en kısa biçimde yüzleşmenin yolu olan imzalarımızdan bahsettim. Elbette ki ilgili çalışmayı okuduğunuzda konunun daha çok narsisizm ile iligli olduğunu görecekseniz. Ancak videoda iki kavram arasında gidip geliyorum :). Videoda bahsettiğim makalenin ism: "Narcissism is a Bad Sign: CEO Signature Size, Investment, and Performance" ve linki: https://link.springer.com/article/10.... Kanalımızın gelirleri her ay sizlerin belirlemiş olduğu bir hayır kurumuna bağışlanmaktadır. Bağış miktarını arttırabilmemize katkı sağlamak ve gelecek videolardan haberdar olmak için linke tıklayarak abone olabilirsiniz: https://www.youtube.com/channel/UCFH3... Kanalımızı diğer sosyal medya hesaplarından takip etmek isterseniz linkler aşağıda yer alıyor. ilgili hesaplarda da olabildiğince faydalı paylaşımlar yapma çabamız devam ediyor, takip ederek bizlere destek verebilirsiniz:) : Instagram: https://www.instagram.com/akademiklink/ Twitter: https://twitter.com/istatistikvean1 Facebook: https://www.facebook.com/AkademikLink...

In this episode, Zach talks to Gus Houghtaling, Director of Sales at Renin, whose e-commerce strategy is largely tied to learning what new products perform well that they can then bring to actual brick and mortar stores E-commerce is typically seen as a way to grow sales and get closer to the customer. But there's actually a key benefit to selling online that most people don't think about and it applies to in-store sales as well.

Joining Suzanne this week are authors David Agredano and Kenny Campbell, along with business strategist Keziah Robinson and Pam Gockley , who is Executive Director/Founder at The Camel Project: Certified Cognitive Behavioral Therapy (CBT) Practitioner. “Reinhardt's Inferno” is a new "Epic Choice Adventure" series by David Agredano. Upon a small, rural world known as Narsei, an evil spreading beyond the boundaries of the universe has come at last. Armies of horrific beasts once thought to be myths and legends are now manifest throughout the land, their violent determination seemingly preordained. Yet, all is not lost.Awakening within the bowels of a deranged prison, captured princes Renin and Feldir Reinhardt are given a one chance opportunity at freedom. Vera Sin, a determined, mysterious elf wielding incredible arcane powers offers them her aid, and little else. A member of a rumored secret society, the Daelinloch, she hides her true identity, and her own true mission. Having no other options, however, the two warrior princes try their luck with the elven sorceress, embarking on an epic journey to discover the origin of the evil that has encompassed their land. Their only starting information is a strange summons by a powerful demon overlord to the north, beckoning them to travel to his realm. “When You Wish Upon a Stone” is the first children's published by Kenny Campbell and it's about having a precious stone and wondering what wishes could come true and where you could travel and what things could you see!?! It's a beautiful children's book for ages 4- 10, so if you have grandbabies, this is right up your alley! Keziah Robinson, CFA is a business strategist, coach, and investor with over 15 years of experience working with CEOs, founders & executive leadership across multiple industries. She is the founder of Cassia Partners, an independent advisory firm with expertise in early stage startups, pivots/turnarounds, and intrapreneurial corporate initiatives. Keziah's tailored approach incorporates elements of design thinking and behavioral science. Pam Gockley maintains a wide range of business commitments, from the Vigilant and Gockley Associates family of businesses, to her active role as a leader in many business women's organizations. She focuses on transitioning businesses in Customer Service, Sales, and Marketing, teaching her trademarked Reputation Factor™ strategy. She is a sought-after keynote speaker for business groups, corporations, colleges and non-profit organizations.  

Commentary by Dr. Valentin Fuster

High fructose consumption is associated with metabolic syndrome, but the mechanisms are not well understood. Listen as Associate Editor Fabio Recchia (Temple University and Scuola Superiore Sant'Anna) interviews lead author An Huang (New York Medical College) and content expert Zsolt Bagi (Medical College of Georgia) about the new study by Froogh et al, which used an animal model to test the hypothesis that a high fructose diet elicits a chymase-dependent increase in angiotensin II production and oxidative stress. In this technical tour de force of a podcast, we unpack the complexities of EET as a protective factor against oxidative stress. Listen as our experts discuss metabolic syndrome in the context of COVID-19, as well as the potential clinical translation of chymase and soluble epoxide hydrolase as therapeutic targets for the treatment of metabolic syndrome.   Ghezal Froogh, Sharath Kandhi, Roopa Duvvi, Yicong Le, Zan Weng, Norah Alruwaili, Jonathan O. Ashe, Dong Sun, An Huang The contribution of chymase-dependent formation of ANG II to cardiac dysfunction in metabolic syndrome of young rats: roles of fructose and EETs Am J Physiol Heart Circ Physiol, published April 2, 2020. DOI: doi.org/10.1152/ ajpheart.00633.2019

With Dr Gabriela Kuster & Dr Qian Zhou, University of Basel - Switzerland Link to paper

Emerging information about how SARS-CoV-2 virus infects cells has led to speculation that NSAIDs and ACE inhibitors/angiotensin receptor blockers (ARBs) may worsen clinical disease. Infectious disease physician Carlos del Rio, MD, of Emory University explains the concerns and their clinical implications.

Emerging information about how SARS-CoV-2 virus infects cells has led to speculation that NSAIDs and ACE inhibitors/angiotensin receptor blockers (ARBs) may worsen clinical disease. Infectious disease physician Carlos del Rio, MD, of Emory University explains the concerns and their clinical implications.

Commentary by Dr. Valentin Fuster

In this episode I cover the pathophysiology, causes, investigations and management of hyperaldosteronism.If you want to follow along with written notes on hyperaldosteronism go to zerotofinals.com/hyperaldosteronism or find the endocrinology section in the Zero to Finals medicine book.This episode covers the pathophysiology, causes, investigations and management of hyperaldosteronism. We specifically look at the renin-angiotensin-aldosterone system, renal artery stenosis and aldosterone antagonists. 

Hayır Demeyi Öğrenin by Korkusuz Dişi Lider by Meltem Bozçal

MYM Podcast - Renal Physiology Part 1 Renin and Angiotensin Youtube Video : https://youtu.be/K3cXs4lOprc Ready to cut your study time in half? Join Our MYM Membership! Start your first month 50% off when you use the code : MYMpodcast https://masteryourmediccourses.thinkific.com

Did you know that our kidneys control our blood pressure? It does this so it can continually create 180 litres of filtered blood every day to keep us healthy! The system that the kidneys use to control blood pressure is called the renin angiotensin aldosterone system (RAAS) - it's a big name but easy to learn! Many patients with hypertension manage their blood pressure by taking medications that act upon this system! Join Dr. Matt & Dr. Mike in this episode to explore this clinically important system! 

Der primäre Hyperaldosteronismus (PHA) ist die häufigste Ursache einer sekundären Hypertonie. Ausgehend von den Beobachtungen, dass eine aberrante Rezeptorexpression bei dem pathophysiologisch ähnlichen Krankheitsbild des ACTH-unabhängigen Cushing-Syndroms durchaus häufig vorkommt, wurde in dieser Studie untersucht, ob bei dem PHA ebenso abnorme Rezeptoren vorkommen und welche Rolle diese in der Pathophysiologie der Erkrankung spielen. So könnten neben der Spironolactontherapie und der Adrenalektomie alternative Therapieansätze (z.B. durch Blockade dieser Rezeptoren) eröffnet werden. An der Studie nahmen 12 Patienten mit einem gesicherten PHA und 12 gesunden Kontrollpersonen teil. Die Studienteilnehmer wurden mittels eines Dreitagestestprotokolls biochemisch auf das Vorliegen einer aberranten Rezeptorexpression in der Nebenniere untersucht. Folgende Stimulationen wurden durchgeführt: Orthostasetest, Mahlzeit-Test, ACTH-, GnRH-, TRH-, Glukagon-, AVP- und MCP-Stimulation. Hiermit wurde insgesamt auf 11 potentielle adrenal exprimierte Rezeptoren untersucht. In Plasma wurden Aldosteron, Cortisol, Renin und ACTH bestimmt. Die Auswertung erfolgte mittels deskriptiver Statistik, wobei nur ein Aldosteronanstieg über 50% über dem Ausgangswert als positiv gewertet wurde. Die Ergebnisse zeigten, dass aberrante Rezeptoren sowohl bei PHA-Patienten, als auch bei Gesunden vorkommen. Eine Reaktion auf GnRH und TRH war ausschließlich bei Erkrankten nachzuweisen, so dass wir davon ausgehen, dass diese Rezeptoren krankheitsspezifisch für den PHA sein könnten. GIP-Rezeptoren konnten weder bei den Patienten noch bei den Probanden nachgewiesen werden und spielen somit keine Rolle für das Aldosteronhaushalt. Die restlichen Rezeptoren (ACTH, AVP, MCP, Glukagon) wurden sowohl bei Patienten als auch bei Probanden nachgewiesen und scheinen somit nicht PHA bezogen zu sein. Schlussendlich konnten wir unsere Hypothese bestätigen - aberrante Rezeptoren kommen bei PHA-Patienten vor und sind teilweise krankheitsspezifisch, so dass eine selektive Blockade dieser Rezeptoren als Therapieansatz durchaus denkbar wäre.

Host: Gary Kohn, MD Guest: Thomas Wang, MD Cardiologist Dr. Tom Wang of the Harvard Medical School talks about the broad distribution of Vitamin D receptors and the implications for cardiovascular and renal disease risk.

Audio Journal of Cardiovascular Medicine Direct Renin Inhibitor Combined with Angiotensin Receptor Blockade Gives Additional Blood Pressure Lowering REFERENCE: Abstract 405-12, American College of Cardiology New Orleans SUZANNE OPARIL, University of Alabama, Birmingham A combination of two antihypertensive agents has given improved blood pressure control in a study with nearly 2000 patients reported to the ACC meeting in New Orleans by a group from the University of Alabama at Birmingham. Suzanne Oparil presented findings on the use of the direct rennin inhibitor, aliskiren, combined with the angiotensin receptor blocker, valsartan. She explained to Peter Goodwin how this “dual renin system blockade” gave enhanced blood pressure lowering in patients with mild to moderate hypertension who were followed with ambulatory monitoring.

The role of the atrial natriuretic factor and of the main counteracting sodium-retaining principle, the renin-aldosterone system, in acute volume regulation of cirrhosis of the liver has been investigated. Central volume stimulation was achieved in 21 patients with cirrhosis, 11 without and 10 with ascites, and 25 healthy controls by 1-hr head-out water immersion. Immersion prompted a highly significant (p

Fri, 1 Jan 1988 12:00:00 +0100 https://epub.ub.uni-muenchen.de/5769/1/5769.pdf Wernze, H.; Paumgartner, Gustav; Jüngst, Dieter; Schnizer, W.; Gerzer, R.; Arendt, Rainer M.; Gerbes, Alexander L.