diabetestalk.net

Metabolic Acidosis Pathophysiology Ppt

Pediatric Metabolic Acidosis

Pediatric Metabolic Acidosis

Author: Lennox H Huang, MD, FAAP; Chief Editor: Timothy E Corden, MD more... Metabolic acidosis is an acid-base disorder characterized by a decrease in serum pH that results from either a primary decrease in plasma bicarbonate concentration ([HCO3-]) or an increase in hydrogen ion concentration ([H+]). [ 1 ] It is not a disease but rather a biochemical abnormality. The clinical manifestations of a metabolic acidosis are nonspecific, and its differential diagnoses include common and rare diseases. (See Etiology .) Metabolic acidosis induces an increase in the excretion of urinary calcium. The increased urinary calcium excretion results mainly from the increased mobilization of calcium out of bone and the inhibition of calcium transport processes within the renal tubule. [ 2 ] The underlying disorder usually produces most of the signs and symptoms in children with a mild or moderate metabolic acidosis . (See History .) The image below depicts a flowchart for evaluating metabolic acidosis. Approach for evaluating metabolic acidosis. Untreated, severe metabolic acidosis can lead to myocardial depression, seizures, shock, and multiorgan failure. (See Pathophysiology .) Bicarbonate administration during treatment for diabetic ketoacidosis has been associated with an increased risk of cerebral edema. [ 3 ] (See Treatment .) Go to Metabolic Acidosis in Emergency Medicine and Metabolic Acidosis for complete information on these topics. A primary metabolic acidosis is a pathophysiologic state characterized by an arterial pH of less than 7.35 in the absence of an elevated PaCO2. It is created by one of three mechanisms: (1) increased production of acids, (2) decreased excretion of acids, or (3) loss of alkali. Acutely, medullary chemoreceptors compensate for a metabolic acidosis Continue reading >>

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Management Of Metabolic Acidosis

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Management Of Metabolic Acidosis

Recommendations for the treatment of acute metabolic acidosis Gunnerson, K. J., Saul, M., He, S. & Kellum, J. Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients. Crit. Care Med. 10, R22-R32 (2006). Eustace, J. A., Astor, B., Muntner, P M., Ikizler, T. A. & Coresh, J. Prevalence of acidosis and inflammation and their association with low serum albumin in chronic kidney disease. Kidney Int. 65, 1031-1040 (2004). Kraut, J. A. & Kurtz, I. Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. Am. J. Kidney Dis. 45, 978-993 (2005). Kalantar-Zadeh, K., Mehrotra, R., Fouque, D. & Kopple, J. D. Metabolic acidosis and malnutrition-inflammation complex syndrome in chronic renal failure. Semin. Dial. 17, 455-465 (2004). Kraut, J. A. & Kurtz, I. Controversies in the treatment of acute metabolic acidosis. NephSAP 5, 1-9 (2006). Cohen, R. M., Feldman, G. M. & Fernandez, P C. The balance of acid base and charge in health and disease. Kidney Int. 52, 287-293 (1997). Rodriguez-Soriano, J. & Vallo, A. Renal tubular acidosis. Pediatr. Nephrol. 4, 268-275 (1990). Wagner, C. A., Devuyst, O., Bourgeois, S. & Mohebbi, N. Regulated acid-base transport in the collecting duct. Pflugers Arch. 458, 137-156 (2009). Boron, W. F. Acid base transport by the renal proximal tubule. J. Am. Soc. Nephrol. 17, 2368-2382 (2006). Igarashi, T., Sekine, T. & Watanabe, H. Molecular basis of proximal renal tubular acidosis. J. Nephrol. 15, S135-S141 (2002). Sly, W. S., Sato, S. & Zhu, X. L. Evaluation of carbonic anhydrase isozymes in disorders involving osteopetrosis and/or renal tubular acidosis. Clin. Biochem. 24, 311-318 (1991). Dinour, D. et al. A novel missense mutation in the sodium bicarbonate cotransporter (NBCe1/ SLC4A4) Continue reading >>

Chapter 47. Acidosis And Alkalosis

Chapter 47. Acidosis And Alkalosis

DuBose TD, Jr.. DuBose T.D., Jr. DuBose, Thomas D., Jr.Chapter 47. Acidosis and Alkalosis. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. Longo D.L., Fauci A.S., Kasper D.L., Hauser S.L., Jameson J, Loscalzo J Eds. Dan L. Longo, et al.eds. Harrison's Principles of Internal Medicine, 18e New York, NY: McGraw-Hill; 2012. Accessed April 22, 2018. DuBose TD, Jr.. DuBose T.D., Jr. DuBose, Thomas D., Jr.. "Chapter 47. Acidosis and Alkalosis." Harrison's Principles of Internal Medicine, 18e Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. Longo D.L., Fauci A.S., Kasper D.L., Hauser S.L., Jameson J, Loscalzo J Eds. Dan L. Longo, et al. New York, NY: McGraw-Hill, 2012, Systemic arterial pH is maintained between 7.35 and 7.45 by extracellular and intracellular chemical buffering together with respiratory and renal regulatory mechanisms. The control of arterial CO2 tension (Paco2) by the central nervous system (CNS) and respiratory systems and the control of the plasma bicarbonate by the kidneys stabilize the arterial pH by excretion or retention of acid or alkali. The metabolic and respiratory components that regulate systemic pH are described by the Henderson-Hasselbalch equation: Under most circumstances, CO2 production and excretion are matched, and the usual steady-state Paco2 is maintained at 40 mmHg. Underexcretion of CO2 produces hypercapnia, and overexcretion causes hypocapnia. Nevertheless, production and excretion are again matched at a new steady-state Paco2. Therefore, the Paco2 is regulated primarily by neural respiratory factors and is not subject to regulation by the rate of CO2 production. Hypercapnia is usually the result of hypoventilation rather than of increased CO2 production. Increases or decreases in Paco2 represent de Continue reading >>

Metabolic Acidosis: Causes, Symptoms, And Treatment

Metabolic Acidosis: Causes, Symptoms, And Treatment

The Terrible Effects of Acid Acid corrosion is a well-known fact. Acid rain can peel the paint off of a car. Acidifying ocean water bleaches and destroys coral reefs. Acid can burn a giant hole through metal. It can also burn holes, called cavities, into your teeth. I think I've made my point. Acid, regardless of where it's at, is going to hurt. And when your body is full of acid, then it's going to destroy your fragile, soft, internal organs even more quickly than it can destroy your bony teeth and chunks of thick metal. What Is Metabolic Acidosis? The condition that fills your body with proportionately too much acid is known as metabolic acidosis. Metabolic acidosis refers to a physiological state characterized by an increase in the amount of acid produced or ingested by the body, the decreased renal excretion of acid, or bicarbonate loss from the body. Metabolism is a word that refers to a set of biochemical processes within your body that produce energy and sustain life. If these processes go haywire, due to disease, then they can cause an excess production of hydrogen (H+) ions. These ions are acidic, and therefore the level of acidity in your body increases, leading to acidemia, an abnormally low pH of the blood, <7.35. The pH of the blood mimics the overall physiological state in the body. In short, a metabolic process is like a power plant producing energy. If a nuclear power plant goes haywire for any reason, then we know what the consequences will be: uncontrolled and excessive nuclear energetic reactions leading to the leakage of large amounts of radioactive material out into the environment. In our body, this radioactive material is acid (or hydrogen ions). Acidemia can also occur if the kidneys are sick and they do not excrete enough hydrogen ions out of th Continue reading >>

Fluids And Electrolyte Management, Part 2

Fluids And Electrolyte Management, Part 2

Etiology. Gastroenteritis is the most common cause of pediatric hypokalemia.1 Pathophysiology. Potassium is an intracellular ion whose concentration is regulated by multiple mechanisms: Alkalosis shifts potassium into cells and acidosis shifts it out. For every increase in pH by 0.1 unit, serum potassium drops by 1 mEq/L. Insulin shifts potassium into cells via a sodium-potassium ATPase pump. Potassium excretion from the kidneys is regulated by aldosterone, mineralocorticoids, antidiuretic hormone, urinary flow rate, metabolic alkalosis, and sodium delivery to the distal tubules. Specific illnesses will lower the serum potassium in different ways. Diarrhea results in the loss of potassium through the gastrointestinal tract. However, vomiting does not directly cause hypokalemia through gastrointestinal losses, but results in alkalosis secondary to the loss of gastric fluids and volume loss, and the alkalosis increases potassium excretion from the kidneys. Hypovolemia (releasing aldosterone), diuretics, genetic renal tubular disorders, and osmotic diuresis (e.g., glucosuria) all increase the secretion of potassium via the renal tubules. (See Table 2.)1,2,3 TABLE 2. ETIOLOGY OF PEDIATRIC HYPOKALEMIA2,3 Hypokalemia affects many organs since it causes cellular dysfunction. The main organs affected are the muscles (rhabdomyolysis), heart, nervous system, and kidneys. Clinical Features. History. Once hypokalemia is established, a detailed history to identify the potential cause is important. A history of diarrhea or vomiting can easily establish the cause without having to do an extensive workup. Ask about medication use and changes in enteral or parenteral formulation, such as total parenteral nutrition (TPN). Symptoms of hypokalemia typically are not seen at a serum level o Continue reading >>

Traumas Lethal Triad Of Hypothermia, Acidosis & Coagulopathy Create A Deadly Cycle For Trauma Patients

Traumas Lethal Triad Of Hypothermia, Acidosis & Coagulopathy Create A Deadly Cycle For Trauma Patients

Traumas Lethal Triad of Hypothermia, Acidosis & Coagulopathy Create a Deadly Cycle for Trauma Patients When patients are resuscitated with a fluid that doesn't contain the same clotting factors as blood, dilutional coagulopathy can occur. Photo courtesy Edmonton EMS Listthe individual components of the lethal triad of trauma. Understandthe pathophysiology that makes the lethal triad a deadly self-propogating cycle in critically ill trauma patients. Learnsimple interventions EMS providers can perform to help prevent or slow the rapid progression of the lethal triad. Acidosis:Lower than normal pH due to increased hydrogen ion concentration. Coagulation system:A temperature- and pH-dependent series of complex enzymatic reactions that result in the formation of blood clots to stop both internal and external hemorrhage. Coagulopathy:Any disorder of the blood that makes it difficult for blood to coagulate. Hypothermia:Lowered body core temperature. Lethal triad:A combination of acidosis, coagulopathy and hypothermia that usually leads to death in a patient experiencing trauma. Its 11 p.m. on a Saturday night when youre dispatched to a local nightclub for reports of a young male whos suffered multiple gunshot wounds. En route, police notify you the scene is safe and theres a single patient bleeding profusely from multiple extremity wounds. On arrival you find a 25-year-old male lying on the street in a rapidly expanding pool of blood. Hes nearly unconscious but breathing spontaneously. His skin is cool, moist and pale. His pulse is rapid and barely palpable. As you and your partner begin your rapid trauma assessment, obtain vital signs, and prepare for rapid packaging and transport to the trauma center 20 minutes away, you know this young man is on the brink of death. Despite Continue reading >>

Mala: Metformin-associated Lactic Acidosis

Mala: Metformin-associated Lactic Acidosis

By Charles W. O’Connell, MD Introduction Metformin is a first-line agent for type 2 diabetes mellitus often used as monotherapy or in combination with oral diabetic medications. It is a member of the biguanide class and its main intended effect is expressed by the inhibition of hepatic gluconeogenesis. In addition, metformin increases insulin sensitivity, enhances peripheral glucose utilization and decreases glucose uptake in the gastrointestinal tract. Phenformin, a previously used biguanide, as withdrawn from the market in the 1970’s due its association with numerous cases of lactic acidosis. Metformin is currently used extensively in the management of diabetes and is the most commonly prescribed biguanide worldwide. The therapeutic dosage of metformin ranges from 850 mg to a maximum of 3000 mg daily and is typically divided into twice daily dosing. It is primarily used in the treatment of diabetes but has been used in other conditions associated with insulin resistance such as polycystic ovarian syndrome. MALA is a rare but well reported event that occurs with both therapeutic use and overdose states. Case presentation A 22-year-old female presents to the Emergency Department after being found alongside a suicide note by her family. She was thought to have taken an unknown, but large amount of her husband’s metformin. She arrives at the ED nearly 10 hours after ingestion. She was agitated, but conversant. She reports having nausea and vague feelings of being unwell and is very distraught over the state of her critically ill husband. She has some self-inflicted superficial lacerations over her left anterior forearm. Her vital assigns upon arrival were: T 98.9 degrees Fahrenheit, HR initially 140 bpm which improved to 110 bpm soon after arrival, BP 100/50, RR 22, Continue reading >>

Metformin-related Lactic Acidosis: Case Report - Sciencedirect

Metformin-related Lactic Acidosis: Case Report - Sciencedirect

Open Access funded by Sociedad Colombiana de Anestesiologa y Reanimacin Lactic acidosis is defined as the presence of pH <7.35, blood lactate >2.0mmol/L and PaCO2 <42mmHg. However, the definition of severe lactic acidosis is controversial. The primary cause of severe lactic acidosis is shock. Although rare, metformin-related lactic acidosis is associated with a mortality as high as 50%. The treatment for metabolic acidosis, including lactic acidosis, may be specific or general, using sodium bicarbonate, trihydroxyaminomethane, carbicarb or continuous haemodiafiltration. The successful treatment of lactic acidosis depends on the control of the aetiological source. Intermittent or continuous renal replacement therapy is perfectly justified, shock being the argument for deciding which modality to use. We report a case of a male patient presenting with metformin poisoning as a result of attempted suicide, who developed lactic acidosis and multiple organ failure. The critical success factor was treatment with continuous haemodiafiltration. Definimos acidosis lctica en presencia de pH <7.35, lactato en sangre >2.0mmol/L y PaCO2 <42mmHg. Por otro lado, la definicin de acidosis lctica grave es controvertida. La causa principal de acidosis lctica grave es el estado de choque. La acidosis lctica por metformina es rara pero alcanza mortalidad del 50%. La acidosis metablica incluyendo a la acidosis lctica puede recibir tratamiento especfico o tratamiento general con bicarbonato de sodio, trihidroxiaminometano, carbicarb o hemodiafiltracin continua. El xito del tratamiento de la acidosis lctica yace en el control de la fuente etiolgica; la terapia de reemplazo renal intermitente o continua est perfectamente justificada, donde el argumento para decidir cul utilizar ser el estado de Continue reading >>

New Findings On The Pathogenesis Of Distal Renal Tubular Acidosis

New Findings On The Pathogenesis Of Distal Renal Tubular Acidosis

The Kidney in Genetic and Rare Diseases: Review New Findings on the Pathogenesis of Distal Renal Tubular Acidosis Trepiccione F.a Prosperi F.a, b de la Motte L.R.a, b Hbner C.A.c Chambrey R.d Eladari D.e Capasso G.a, b aDepartment of Cardiothoracic and Respiratory Science, University of Campania Luigi Vanvitelli, Naples, and bBiogem S.c.a.r.l., Research Institute Gaetano Salvatore, Ariano Irpino, Italy; cInstitute of Human Genetics, Jena University Hospital, Friedrich Schiller University, Jena, Germany; dInserm U1188, Diabte athrothrombose Thrapies Runion Ocan Indien (DTROI), Universit de La Runion, and eService d'Explorations Fonctionnelles Rnales, Hpital Felix Guyon, CHU de la Runion, Saint-Denis, Ile de la Runion, France Department of Cardiothoracic and Respiratory Science University of Campania Luigi Vanvitelli E-Mail [email protected] Background: Distal renal tubular acidosis (dRTA) is characterized by an impairment of the urinary acidification process in the distal nephron. Complete or incomplete metabolic acidosis coupled with inappropriately alkaline urine are the hallmarks of this condition. Genetic forms of dRTA are caused by loss of function mutations of either SLC4A1, encoding the AE1 anion exchanger, or ATP6V1B1 and ATP6V0A4, encoding for the B1 and a4 subunits of the vH+ATPase, respectively. These genes are crucial for the function of A-type intercalated cells (A-IC) of the distal nephron. Summary: Alterations of acid-base homeostasis are variably associated with hypokalemia, hypercalciuria, nephrocalcinosis or nephrolithiasis, and a salt-losing phenotype. Here we report the diagnostic test and the underlying physiopathological mechanisms. The molecular mechanisms identified so far can explain the defect in acid secretion, but do not ex Continue reading >>

Metabolic Acidosis Nclex Review Notes

Metabolic Acidosis Nclex Review Notes

Are you studying metabolic acidosis and need to know a mnemonic on how to remember the causes? This article will give you a clever mnemonic and simplify the signs and symptoms and nursing interventions on how to remember metabolic acidosis for nursing lecture exams and NCLEX. In addition, you will learn how to differentiate metabolic acidosis from metabolic alkalosis. Don’t forget to take the metabolic acidosis and metabolic alkalosis quiz. This article will cover: Metabolic acidosis simplified Lab values expected with metabolic acidosis Causes of metabolic acidosis Signs and symptoms of metabolic acidosis Nursing interventions for metabolic acidosis Lecture on Metabolic Acidosis Metabolic Acidosis Metabolic Acidosis in Simple Terms: a metabolic problem due to the buildup of acid in the body fluids which affects the bicarbonate (HCO3 levels) either from: increased acid production (ex: DKA where ketones (acids) increase in the body which decreases bicarbonate) decreased acid excretion (ex: renal failure where there is high amount of waste left in the body which causes the acids to increase and bicarb can’t control imbalance) loss of too much bicarb (diarrhea) When this acidic phenomena is taking place in the body other systems will try to compensate to increase the bicarb back to normal. One system that tries to compensate is the respiratory system. In order to compensate, the respiratory system will cause the body to hyperventilate by increasing breathing through Kussmaul’s respirations. Kussmaul respirations are deep, rapid breathes. The body hopes this will help expel CO2 (an acid) which will “hopefully” increase the pH back to normal. Lab values expected in Metabolic Acidosis: HCO3: decreased <22 Blood pH: decreased <7.35 CO2: <35 or normal (may be normal b Continue reading >>

Subacute Ruminal Acidosis

Subacute Ruminal Acidosis

(Chronic ruminal acidosis, Subclinical ruminal acidosis) By Ingrid Lorenz, DMV, DMVH, DECBHM, Lecturer in Bovine Medicine, School of Agriculture, Food Science and Veterinary Medicine, University College Dublin Ruminant animals are adapted to digest and metabolize predominantly forage diets; however, growth rates and milk production are increased substantially when ruminants consume high-grain diets. One consequence of feeding excessive amounts of rapidly fermentable carbohydrates in conjunction with inadequate fiber to ruminants is subacute ruminal acidosis, which is characterized by periods of low ruminal pH that resolve without treatment and is rarely diagnosed. Dairy cows, feedlot cattle, and feedlot sheep are at risk of developing this condition. Ruminal pH fluctuates considerably during a 24hr period (typically between 0.51 pH units) and is determined by the dynamic balance between the intake of fermentable carbohydrates, buffering capacity of the rumen, and rate of acid absorption from the rumen. In general, subacute ruminal acidosis is caused by ingestion of diets high in rapidly fermentable carbohydrates and/or deficient in physically active fiber. Subacute ruminal acidosis is most commonly defined as repeatedly occurring prolonged periods of depression of the ruminal pH to values between 5.6 and 5.2. The low ruminal pH is caused by excessive accumulation of volatile fatty acids (VFAs) without persistent lactic acid accumulation and is restored to normal by the animals own physiologic responses. The ability of the rumen to rapidly absorb organic acids contributes greatly to the stability of ruminal pH. It is rarely difficult for peripheral tissues to utilize VFAs already absorbed from the rumen; however, absorption of these VFAs from the rumen can be an importa Continue reading >>

Metabolic Acidosis Nursing Management And Interventions - Nurseslabs

Metabolic Acidosis Nursing Management And Interventions - Nurseslabs

Metabolic Acidosisis an acid-base imbalance resulting from excessive absorption or retention of acid or excessive excretion of bicarbonate produced by an underlying pathologic disorder. Symptoms result from the bodys attempts to correct the acidotic condition through compensatory mechanisms in the lungs , kidneys and cells. Metabolic acidosis is characterized by normal or high anion gap situations. If the primary problem is direct loss of bicarbonate, gain of chloride, or decreased ammonia production, the anion gap is within normal limits. If the primary problem is the accumulation of organic anions (such as ketones or lactic acid), the condition is known as high anion gap acidosis. Compensatory mechanisms to correct this imbalance include an increase in respirations to blow off excess CO2, an increase in ammonia formation, and acid excretion (H+) by the kidneys, with retention of bicarbonate and sodium . High anion gap acidosis occurs in diabetic ketoacidosis ; severe malnutrition or starvation, alcoholic lactic acidosis; renal failure; high-fat, low-carbohydrate diets/lipid administration; poisoning, e.g., salicylate intoxication (after initial stage); paraldehyde intoxication; and drug therapy, e.g., acetazolamide (Diamox), NH4Cl. Normal anion gap acidosis is associated with loss of bicarbonate form the body, as may occur in renal tubular acidosis, hyperalimentation, vomiting/ diarrhea , small-bowel/pancreatic fistulas, and ileostomy and use of IV sodium chloride in presence of preexisting kidney dysfunction, acidifying drugs (e.g., ammonium chloride). This condition does not occur in isolation but rather is a complication of a broader problem that may require inpatient care in a medical-surgical or subacute unit. Use of carbonic anhydrase inhibitors or anion-exchan Continue reading >>

Blood Gas Analysis--insight Into The Acid-base Status Of The Patient

Blood Gas Analysis--insight Into The Acid-base Status Of The Patient

Acid-Base Physiology Buffers H+ A- HCO3- CO2 Buffers H+ A- CO2 Cells Blood Kidney Lungs Fluids, Electrolytes, and Acid-Base Status in Critical Illness Blood Gas Analysis--Insight into the Acid-Base status of the Patient The blood gas consists of pH-negative log of the Hydrogen ion concentration: -log[H+]. (also, pH=pK+log [HCO3]/ 0.03 x pCO2). The pH is always a product of two components, respiratory and metabolic, and the metabolic component is judged, calculated, or computed by allowing for the effect of the pCO2, ie, any change in the pH unexplained by the pCO2 indicates a metabolic abnormality. CO +H 0ºº H CO ººHCO + H2 2 2 3 3 - + CO2 and water form carbonic acid or H2CO3, which is in equilibrium with bicarbonate (HCO3-)and hydrogen ions (H+). A change in the concentration of the reactants on either side of the equation affects the subsequent direction of the reaction. For example, an increase in CO2 will result in increased carbonic acid formation (H2CO3) which leads to an increase in both HCO3- and H+ (\pH). Normally, at pH 7.4, a ratio of one part carbonic acid to twenty parts bicarbonate is present in the extracellular fluid [HCO3-/H2CO3]=20. A change in the ratio will affect the pH of the fluid. If both components change (ie, with chronic compensation), the pH may be normal, but the other components will not. pCO -partial pressure of carbon dioxide. Hypoventilation or hyperventilation (ie, minute2 ventilation--tidal volume x respitatory rate--imperfectly matched to physiologic demands) will lead to elevation or depression, respectively, in the pCO2. V/Q (ventilation/perfusion) mismatch does not usually lead to abnormalities in PCO2 because of the linear nature of the CO2 elimination curve (ie, good lung units can make up for bad lung units). Diffus Continue reading >>

Urine Ammonium, Metabolic Acidosis And Progression Of Chronic Kidney Disease

Urine Ammonium, Metabolic Acidosis And Progression Of Chronic Kidney Disease

Urine Ammonium, Metabolic Acidosis and Progression of Chronic Kidney Disease Pourafshar N.a · Pourafshar S.a · Soleimani M.b,c aDepartment of Medicine at University of Virginia, Charlottesville, VA, USA bDepartment of Medicine, University of Cincinnati, Cincinnati, OH, USA cDepartment of Medicine Services, Veterans Medical Center, Cincinnati, OH, USA The metabolism of a typical Western diet generates 50–100 mEq of acid (H+) per day, which must be excreted in the urine for the systemic acid-base to remain in balance. The 2 major mechanisms that are responsible for the renal elimination of daily acid under normal conditions are ammonium (NH4+) excretion and titratable acidity. In the presence of systemic acidosis, ammonium excretion is intensified and becomes the crucial mechanism for the elimination of acid. The impairment in NH4+ excretion is therefore associated with reduced acid excretion, which causes excess accumulation of acid in the body and consequently results in metabolic acidosis. Chronic kidney disease (CKD) is associated with the impairment in acid excretion and precipitation of metabolic acidosis, which has an adverse effect on the progression of CKD. Recent studies suggest that the progressive decline in renal ammonium excretion in CKD is an important determinant of the ensuing systemic metabolic acidosis and is an independent factor for predicting the worsening of kidney function. While these studies have been primarily performed in hypertensive individuals with CKD, a closer look at renal NH4+ excretion in non-hypertensive individuals with CKD is warranted to ascertain its role in the progression of kidney disease. The elimination of acid (H+) by kidney is the most crucial step in the maintenance of systemic acid-base homeostasis [ 1 , 2 ]. The rena Continue reading >>

Metabolic Acidosis |authorstream

Metabolic Acidosis |authorstream

Automatically changes to Flash or non-Flash embed The presentation is successfully added In Your Favorites . This Presentation is Public Favorites: ynm DDUH NEW DELHI 64 1 ACID - BASE BALANCE By Dr Y.N MAURYA M.B.B.S, D.C.H Medical Officer Deen Dayal Upadhyay Hospital Govt. of NCT New Delhi- 64 ynm DDUH NEW DELHI 64 2 SOME NORMAL VALUES pH --- 7.35-7.45HCO3 --- 22-26 mmol/LPaCO2 --- 35-45 mmHgPaO2 --- 60-100 mmHgALBUMIN-- 45.5 g/dlNa+ --- 135-145 mmol/LK+ --- 3.5-5.5 mmol/LCa+2 --- 1.12-1.23 mmol/LCl --- 98-106 mmol/L[H+] at pH 7.4 --- 40 nmol/L ynm DDUH NEW DELHI 64 3 Why pH 7.357.45 is necessary ? FOR OPTIMAL FUNCTIONING OF CELLULAR ENZYMES & METABOLIC PROCESSES : ynm DDUH NEW DELHI 64 4 FOR OPTIMAL FUNCTIONING OF CELLULAR ENZYMES & METABOLIC PROCESSES WHICH pH SHOULD BE MAINTAINED ? : ynm DDUH NEW DELHI 64 5 WHICH pH SHOULD BE MAINTAINED ? INTRACELLULAR OR EXTRACELLULAR INTRACELLULAR pH SHOULD BE MAINTAINED : ynm DDUH NEW DELHI 64 6 INTRACELLULAR pH SHOULD BE MAINTAINED IS IT INTRACELLULAR pH WHICH MEASURED NORMALY ? : ynm DDUH NEW DELHI 64 7 IS IT INTRACELLULAR pH WHICH MEASURED NORMALY ? NORMALY MEASURED pH IS EXTRACELLULAR pHBECAUSE INTRACELLULAR pH PARALLELS EXTRACELLULAR pH & LATER IS EASY,SO IT IS EXTRACELLULAR pH WHICH IS NORMALY MEASURED NORMAL PHYSIOLOGY OF ACID- BASE BALANCE : ynm DDUH NEW DELHI 64 8 NORMAL PHYSIOLOGY OF ACID- BASE BALANCE MAINTAINENCE OF EXTRACELLULAR pH & BUFFER : ynm DDUH NEW DELHI 64 9 MAINTAINENCE OF EXTRACELLULAR pH & BUFFER WHAT IS BUFFER ? . SUBSTANCES THAT ATTENUATE CHANGE IN pH.THESE ARE WEAK ACIDS OR WEAK BASES. ARE 50% DISSOCIATED AT IT'S pK (diss. Constant)BEST BUFFERS HAVE pK CLOSE TO 7.4 ynm DDUH NEW DELHI 64 10 IMPORTANT BUFFERS ? BICARBONATE BUFFER H++ HCO3 == H2O+ CO2 ( pK 6.1 ) ? NON-BICARBONATE BUFFERS 1. ALBUMIN ( PK 6 Continue reading >>

More in ketosis