diabetestalk.net

Acetazolamide Metabolic Acidosis Treatment

Metabolic Acidosis Treatment & Management: Approach Considerations, Type 1 Renal Tubular Acidosis, Type 2 Renal Tubular Acidosis

Metabolic Acidosis Treatment & Management: Approach Considerations, Type 1 Renal Tubular Acidosis, Type 2 Renal Tubular Acidosis

Metabolic AcidosisTreatment & Management Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN more... Treatment of acute metabolic acidosis by alkali therapy is usually indicated to raise and maintain the plasma pH to greater than 7.20. In the following two circumstances this is particularly important. When the serum pH is below 7.20, a continued fall in the serum HCO3- level may result in a significant drop in pH. This is especially true when the PCO2 is close to the lower limit of compensation, which in an otherwise healthy young individual is approximately 15 mm Hg. With increasing age and other complicating illnesses, the limit of compensation is likely to be less. A further small drop in HCO3- at this point thus is not matched by a corresponding fall in PaCO2, and rapid decompensation can occur. For example, in a patient with metabolic acidosis with a serum HCO3- level of 9 mEq/L and a maximally compensated PCO2 of 20 mm Hg, a drop in the serum HCO3- level to 7 mEq/L results in a change in pH from 7.28 to 7.16. A second situation in which HCO3- correction should be considered is in well-compensated metabolic acidosis with impending respiratory failure. As metabolic acidosis continues in some patients, the increased ventilatory drive to lower the PaCO2 may not be sustainable because of respiratory muscle fatigue. In this situation, a PaCO2 that starts to rise may change the plasma pH dramatically even without a significant further fall in HCO3-. For example, in a patient with metabolic acidosis with a serum HCO3- level of 15 and a compensated PaCO2 of 27 mm Hg, a rise in PaCO2 to 37 mm Hg results in a change in pH from 7.33 to 7.20. A further rise of the PaCO2 to 43 mm Hg drops the pH to 7.14. All of this would have occurred whi Continue reading >>

Metabolic Acidosis And Hyperventilation Induced By Acetazolamide In Patients With Central Nervous System Pathology

Metabolic Acidosis And Hyperventilation Induced By Acetazolamide In Patients With Central Nervous System Pathology

ACETAZOLAMIDE, a carbonic anhydrase inhibitor, is used in patients with meningeal inflammation, mild intracranial hypertension, and basal skull fractures to decrease the formation of cerebrospinal fluid (CSF). It causes mild metabolic acidosis by inhibiting the reabsorption of bicarbonate (HCO−3) ions from renal tubules. This effect has been used successfully in the treatment of patients with chronic respiratory acidosis with superimposed metabolic alkalosis 1 and central sleep apnea syndrome. 2 Life-threatening metabolic acidosis during acetazolamide therapy has been observed only in patients with renal impairment or 3 diabetes 4 and in elderly patients. 5 Severe metabolic acidosis, associated with acetazolamide, in the absence of other predisposing factors has not been reported in patients with central nervous system disease. We report three cases of severe metabolic acidosis and hyperventilation during acetazolamide therapy in normal doses in adult patients without renal impairment. A 35-yr-old man with a head injury underwent craniotomy for evacuation of a traumatic left temporal extradural hematoma. Postoperatively, the patient underwent mechanical ventilation to maintain a partial pressure of arterial carbon dioxide (Paco2) of 30–35 mmHg. On the third postoperative day, 250 mg acetazolamide administered every 8 h through a nasogastric tube was started to treat a CSF leak from the operative wound. A T-piece trial of weaning was started on the fourth postoperative day. On the fifth postoperative day, patient respiratory rate increased to 40–44 breaths/min. Arterial blood gas analysis showed metabolic acidosis resulting in compensatory hypocapnia and a normal pH (table 1). The patient was sedated and underwent artificial ventilation for the next 6 days. Attempt Continue reading >>

Treatment Of Metabolic Alkalosis

Treatment Of Metabolic Alkalosis

INTRODUCTION Metabolic alkalosis is characterized by a primary rise in the plasma bicarbonate concentration, which leads to an increase in arterial pH. Two factors are required for the genesis and then maintenance of metabolic alkalosis: a process that raises the plasma bicarbonate concentration and a process that prevents excretion of the excess bicarbonate in the urine [1,2]. Treatment of metabolic alkalosis should be aimed at reversing these two factors. This topic will provide a brief overview of the pathogenesis of metabolic alkalosis followed by a discussion of how to treat affected patients. The pathogenesis of metabolic alkalosis is reviewed in more detail elsewhere. (See "Pathogenesis of metabolic alkalosis".) The etiology and evaluation of patients with metabolic alkalosis are discussed separately. (See "Causes of metabolic alkalosis" and "Clinical manifestations and evaluation of metabolic alkalosis".) OVERVIEW OF THE PATHOGENESIS The genesis and the maintenance of metabolic alkalosis are distinct processes. Initially, a process that raises the plasma bicarbonate concentration occurs, and then another process prevents excretion of the excess bicarbonate in the urine [1,2]. Factors that increase plasma bicarbonate — Several mechanisms can increase the plasma bicarbonate concentration. They include (table 1) (see "Causes of metabolic alkalosis"): Continue reading >>

Type 2 Renal Tubular Acidosis And Acetazolamide - Deranged Physiology

Type 2 Renal Tubular Acidosis And Acetazolamide - Deranged Physiology

Type 2 Renal Tubular Acidosis and Acetazolamide This form of renal tubular acidosis decreases the strong ion difference by interfering with bicarbonate resorption in the proximal tubule; the mechanism is analogous to the action of acetazolamide. Bicarbonate handling in the proximal tubule Behold, the familiar activity of carbonic anhydrase in the proximal tubule. Carbonic anhydrase converts the filtered bicarbonate into easily resorbed CO2, and then traps it again inside the cell. The filtered bicarbonate is essentialy completely reabsorbed. The concentration of chloride in the tubule is therefore expected to increase- if the bicarbonate has been reabsorbed, more chloride must remain in the tubule to maintain electroneutrality. However, the failure of carbonic anhydrase results in bicarbonate remaining trapped in the urine. This, of course, means that electroneutrality of the tubule is maintained without the excretion of any further chloride. Thus, the chloride which would otherwise be excreted, is retained. There is an excellent article which discusses the mechanisms of chloride retention in acetazolamide-intoxicated patients with metabolic alkalosis. Particularly, it contains a graph of urinary strong ion diference over time, after the administration of 500mg of acetazolamide. It looks a little like this : Causes of proximal renal tubular acidosis Isolated congenital Type 2 RTA is very rare, and would likely form a part of of a syndrome , being associated with a series of other tubular defects, or forming a part of a whole-proximal-tubule problem like Fanconi syndrome. Anong the elderly, a new onset of Type 2 RTA without any new medication changes can be due to a monoclonal gammopathy , where ligh chains selectively damage the proximal tubule. Similarly, amyloidosis Continue reading >>

7.6 Metabolic Alkalosis - Correction

7.6 Metabolic Alkalosis - Correction

Correct the primary cause of the disorder Correct those factors which maintain the disorder (esp chloride administrationin the common Cl- deficient cases) Repletion of chloride, potassium and ECF volume will promote renal bicarbonate excretion and return plasma bicarbonate to normal. Chloride administration 1 is essential for correction of chloride-depletion metabolic alkalosis and the alkalosis can be corrected with chloride even if volume depletion persists. Because of electroneutrality requirements it is not possible to give chloride alone, so 'giving chloride' is equivalent to 'giving saline' in most cases. (One exception to this is giving a dilute HCl infusion -see below) Volume administration will not correct the alkalosis unless the administered fluid contains chloride. This is not difficult though as all available ECF replacement fluids contain chloride so administering these IV fluids to correct the volume deficiency must necessarily replenish chloride. Maintenance IV fluids (eg 5% dextrose) are poor at replenishing IV volume and contain little or no chloride; they are not useful for this correction and should not be used. Mineralocorticoid excess causes renal potassium wasting. This can maintain a metabolic alkalosis even in the absence of chloride depletion. Rarely, it may be advantageous to institute treatments (eg HCl infusion; acetazolamide) that can return the bicarbonate level to normal more quickly. Rarely, it may be advantageous to institute treatments (hydrochloric acid infusion, or acetazolamide) that can return the bicarbonate level to normal more quickly. These are not routine components of management, and should not deflect attention from correcting the primary cause and from correcting a chloride deficiency, but may be useful for occasional pati Continue reading >>

Acetazolamide And Symptomatic Metabolic Acidosis In Mild Renal Failure.

Acetazolamide And Symptomatic Metabolic Acidosis In Mild Renal Failure.

Acetazolamide and symptomatic metabolic acidosis in mild renal failure. This article has been cited by other articles in PMC. Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (419K), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References . These references are in PubMed. This may not be the complete list of references from this article. Maren TH. Carbonic anhydrase: chemistry, physiology, and inhibition. Physiol Rev. 1967 Oct;47(4):595781. [ PubMed ] CAMPBELL DA. Diuretics and the eye. Br Med J. 1961 Aug 19;2(5250):467474. [ PMC free article ] [ PubMed ] Heuser D, Astrup J, Lassen NA, Betz BE. Brain carbonic acid acidosis after acetazolamide. Acta Physiol Scand. 1975 Mar;93(3):385390. [ PubMed ] O'Sullivan PJ, Crowley JG, Muldowney FP. A case of acetazolamide induced (Diamox) acidotic coma in polycystic renal disease. J Ir Med Assoc. 1967 Oct;60(364):382384. [ PubMed ] Higenbottam T, Ogg CS, Saxton HM. Acute renal failure from the use of acetazolamide (Diamox). Postgrad Med J. 1978 Feb;54(628):127128. [ PMC free article ] [ PubMed ] Ferry AP, Lichtig M. Gouty arthritis as a complication of acetazolamide (Diamox) therapy for glaucoma. Can J Ophthalmol. 1969 Apr;4(2):145147. [ PubMed ] NADELL J. The effects of the carbonic anhydrase inhibitor 6063 on electrolytes and acid-base balance in two normal subjects and two patients with respiratory acidosis. J Clin Invest. 1953 Jul;32(7):622629. [ PMC free article ] [ PubMed ] COUNIHAN TB, EVANS BM, MILNE MD. Observations on the pharmacology of the carbonic anhydrase inhibitor diamox. Clin Sci. 1954 Nov;13(4):583598. [ PubMed ] Epstein DL, Grant WM. Carbonic anhydrase inhibitor side effects. S Continue reading >>

Acetazolamide For Metabolic Alkalosis In Ventilated Patients

Acetazolamide For Metabolic Alkalosis In Ventilated Patients

Topf , Acetazolamide , AcidBase , Electrolytes Patients in the ICU with pulmonary disease primarily have respiratory acidosis and/or metabolic alkalosis. The respiratory acidosis is due to the primary disease and the metabolic alkalosis is due to our attempts to manage that disease, in this case with diuretics. Compensation for metabolic alkalosis is suppression of respiration to allow the carbon dioxide to accumulate reducing the change in pH. Suppressing respiration is obviously a concern in patients on the vent. One option in this situation is to treat the metabolic alkalosis. Although I have read about giving hydrochloric acid infusions, that is a bit nuts. The conventional choice is to cause a drug induce proximal (Type 2) RTA with acetazolamide. The proximal tubule reabsorbs the vast majority of filtered bicarbonate, but it does it through a complex process, where bicarbonate is metabolized to CO2 and water (catalyzed by carbonic anhydrase). The carbon dioxide diffuses into the proximal tubule cell where bicarbonate is reconstituted (again catalyzed by carbonic anhydrase) and then secreted into the circulation. So bicarbonate is destroyed in the tubules and reformed in the tubule cells. Carbonic anhydrase inhibitors slow this and cause the patient to pee bicarbonate. The loss of bicarbonate causes metabolic acidosis, or alternatively, improvement in pre-existing metabolic alkalosis. The carbonic anhydrase inhibitor of choice is acetazolamide. Other carbonic anhydrase inhibitors include Methazolamide,Dorzolamide,Brinzolamide,Topiramate. The pomegranate contains natural carbonic anhydrase activity. This is a nice theory but in February JAMA published a clinical trial to provide empiric data for this time honored strategy. This is a multi center, double-blind, paral Continue reading >>

Diuretics Flashcards | Quizlet

Diuretics Flashcards | Quizlet

what part of the nephron does Acetazolamide work on? -decreases aqueous humor formation by sodium bicarbonate blockade for glaucoma treatment -works on choroid plexus to decrease cerebrospinal fluid formation what is the Acetazolamide related drug that is used for glaucoma? why does acetazolamide cause metabolic acidosis? because it gets rid of bicarbonate in the urine what kind of emergency would acetazolamide be used for? someone who swallowed too much asprin; acetazolamide traps acidic substances Acetazolamide does not have direct effects, so what mechanism in the kidney does this drug take advantage of? why is Acetazolamide not used as diuretic? b/c tachyphylaxis; the effects quickly wear off what is a contraindication of acetazolamide? what substance will rise in the serum when taking acetazolamide that would cause hepatic encephalopathy? Acetazolamide b/c of phophaturia and calciuria, K+ loss and CNS effects like drowsiness and parasthesia reduce intracranial and intraocular pressure and maintains tubular flow what are some of the adverse effects of mannitol? causes extracellular volume causing pulmonary edema and CHF Why are loop diuretics called high ceiling diuretics? *Furosemide* along with bumetanide torsemide, ethacrynic acid inhibition of the coupled Na+/K+/Cl- transport system in the thick ascending limb which part of the loop of henle does the Furosemide work on? In what kind of conditions would you use Furosemide? -someone with oliguria and has acute renal failure -forced diuresis when person has toxins in body (also given with mannitol) what is a good drug when a patient presents with pulmonary edema? what do you want to monitor when you are giving Furosemide to somone? what is the mechanism of action of the Furosemide and other loop diuretics? it bloc Continue reading >>

Drug-induced Metabolic Acidosis

Drug-induced Metabolic Acidosis

Go to: Introduction Metabolic acidosis is defined as an excessive accumulation of non-volatile acid manifested as a primary reduction in serum bicarbonate concentration in the body associated with low plasma pH. Certain conditions may exist with other acid-base disorders such as metabolic alkalosis and respiratory acidosis/alkalosis 1. Humans possess homeostatic mechanisms that maintain acid-base balance ( Figure 1). One utilizes both bicarbonate and non-bicarbonate buffers in both the intracellular and the extracellular milieu in the immediate defense against volatile (mainly CO 2) and non-volatile (organic and inorganic) acids before excretion by the lungs and kidneys, respectively. Renal excretion of non-volatile acid is the definitive solution after temporary buffering. This is an intricate and highly efficient homeostatic system. Derangements in over-production, under-excretion, or both can potentially lead to accumulation of excess acid resulting in metabolic acidosis ( Figure 1). Drug-induced metabolic acidosis is often mild, but in rare cases it can be severe or even fatal. Not only should physicians be keenly aware of this potential iatrogenic complication but they should also be fully engaged in understanding the pathophysiological mechanisms. Metabolic acidosis resulting from drugs and/or ingestion of toxic chemicals can be grouped into four general categories ( Figure 2): Some medications cannot be placed into one single category, as they possess multiple mechanisms that can cause metabolic acidosis. In suspected drug-induced metabolic acidosis, clinicians should establish the biochemical diagnosis of metabolic acidosis along with the evaluation of respiratory compensation and whether there is presence of mixed acid-based disorders 2, then convert the bioche Continue reading >>

Pathogenic Mechanism, Prophylaxis, And Therapy Of Symptomatic Acidosis Induced Byacetazolamide.

Pathogenic Mechanism, Prophylaxis, And Therapy Of Symptomatic Acidosis Induced Byacetazolamide.

1. J Investig Med. 2002 Mar;50(2):125-32. doi: 10.2310/6650.2002.31297. Pathogenic mechanism, prophylaxis, and therapy of symptomatic acidosis induced byacetazolamide. Filippi L(1), Bagnoli F, Margollicci M, Zammarchi E, Tronchin M, Rubaltelli FF. (1)Department of Critical Care Medicine, University of Florence, Careggi Hospital, Italy. [email protected] BACKGROUND: Acetazolamide, a noncompetitive carbonic anhydrase inhibitor, canproduce symptomatic acidosis and bone marrow suppression by a mechanism that isstill unknown. This presentation occurs in the elderly, patients with renal orliver failure, people with diabetes, and newborns. The objective of this studywas to understand the pathogenic mechanism of these adverse effects and topropose a possible prophylaxis and therapy.METHODS: Four human clinical cases were studied, and one animal experiment wasperformed. Four preterm newborns with posthemorrhagic ventricular dilationdeveloped severe metabolic acidosis after treatment with acetazolamide. Theacidosis suddenly disappeared after a packed red blood cell transfusion.Metabolic studies were performed in one patient and in newborn guinea pigstreated with 200 mg/kg acetazolamide.RESULTS: Acetazolamide can produce severe lactic acidosis with an increasedlactate-to-pyruvate ratio, ketosis with a lowbeta-hydroxybutyrate-to-acetoacetate ratio, and a urinary organic acid profiletypical of pyruvate carboxylase deficiency. The acquired enzymatic injuryresulting from the inhibition of mitochondrial carbonic anhydrase V that providesbicarbonate to pyruvate carboxylase can produce tricarboxylic acid cycle damage. We demonstrate that the dramatic disappearance of metabolic acidosis andnormalizing metabolism after blood transfusion were due to the citrate contained in the pack Continue reading >>

Acetazolamide - An Overview | Sciencedirect Topics

Acetazolamide - An Overview | Sciencedirect Topics

Acetazolamide is a carbonic anhydrase inhibitor that causes a metabolic acidosis that increases the stimulus to breathe while lowering the arterial Pco2 apneic threshold.133 Jeffrey K. Aronson, in Side Effects of Drugs Annual , 2011 Acetazolamide causes a metabolic acidosis, which is usually mild, but can be associated with hypokalemia. In nine subjects who took acetazolamide 250mg or placebo every 8hours for 3days in a double-blind, randomized, crossover design, metabolic acidosis due to acetazolamide was accompanied by a rise in ventilation, a substantial fall in PaCO2, and a parallel leftward shift of the ventilatory CO2 response curve [27c]. Acetazolamide shifted the concentrationeffect curve relating hypoxic sensitivity to arterial hydrogen ion concentration to the left, without altering its slope, showing that it did not affect the interaction of O2 and CO2. There was no specific inhibitory effect of acetazolamide on hypoxic sensitivity. In a 9-year-old girl recombinant human growth hormone 6mg/week caused idiopathic intracranial hypertension (pseudotumor cerebri), which was treated with acetazolamide [28A]. After 4days the dose was increased to 30mg/kg/day, and 2days later she developed a severe metabolic acidosis, with a pH of 7.29. There has been a previous report of metabolic acidosis in a 1-year-old girl who took 5001250mg of acetazolamide [29A]. Jean-Pierre Guignard MD, in Nephrology and Fluid/Electrolyte Physiology: Neonatology Questions and Controversies (Second Edition) , 2012 Acetazolamide increases the urinary excretion of HCO3, Na+, and K+, promoting alkaline diuresis with consequent systemic metabolic acidosis. Acetazolamide may be useful to alkalinize the urine when necessary, such as when chemotherapy is given. Acetazolamide can also be used to ass Continue reading >>

Normal Anion Gap Metabolic Acidosis

Normal Anion Gap Metabolic Acidosis

Home | Critical Care Compendium | Normal Anion Gap Metabolic Acidosis Normal Anion Gap Metabolic Acidosis (NAGMA) HCO3 loss and replaced with Cl- -> anion gap normal if hyponatraemia is present the plasma [Cl-] may be normal despite the presence of a normal anion gap acidosis -> this could be considered a ‘relative hyperchloraemia’. Extras – RTA, ingestion of oral acidifying salts, recovery phase of DKA loss of bicarbonate with chloride replacement -> hyperchloraemic acidosis secretions into the large and small bowel are mostly alkaline with a bicarbonate level higher than that in plasma. some typical at risk clinical situations are: external drainage of pancreatic or biliary secretions (eg fistulas) this should be easily established by history normally 85% of filtered bicarbonate is reabsorbed in the proximal tubule and the remaining 15% is reabsorbed in the rest of the tubule in patients receiving acetazolamide (or other carbonic anhydrase inhibitors), proximal reabsorption of bicarbonate is decreased resulting in increased distal delivery and HCO3- appears in urine this results in a hyperchloraemic metabolic acidosis and is essentially a form of proximal renal tubular acidosis but is usually not classified as such. hyperchloraemic metabolic acidosis commonly develops during therapy of diabetic ketoacidosis with normal saline oral administration of CaCl2 or NH4Cl is equivalent to giving an acid load both of these salts are used in acid loading tests for the diagnosis of renal tubular acidosis CaCl2 reacts with bicarbonate in the small bowel resulting in the production of insoluble CaCO3 and H+ the hepatic metabolism of NH4+ to urea results in an equivalent production of H+ REASONS WHY ANION GAP MAY BE NORMAL DESPITE A ‘HIGH ANION GAP METABOLIC ACIDOSIS’ 1. Continue reading >>

Metabolic Acidosis; Non-gap

Metabolic Acidosis; Non-gap

Non-gap metabolic acidosis, or hyperchloremic metabolic acidosis, are a group of disorders characterized by a low bicarbonate, hyperchloremia and a normal anion gap (10-12). A non-gapped metabolic acidosis fall into three categories: 1) loss of base (bicarbonate) from the gastrointestinal (GI) tract or 2) loss of base (bicarbonate) from the kidneys, 3) intravenous administration of sodium chloride solution. Bicarbonate can be lost from the GI tract (diarrhea) or from the kidneys (renal tubular acidosis) or displaced by chloride. A. What is the differential diagnosis for this problem? Proximal renal tubular acidosis: (low K+) Distal renal tubular acidosis: (low or high K+) Prostaglandin Inhibitors, (aspirin, nonsteroidal anti-inflammatory drugs, cyclooxygenase 2 inhibitors) Adrenal insufficiency (primary or secondary) (high K+) Pseudoaldosteronism, type 2 (Gordon's syndrome) B. Describe a diagnostic approach/method to the patient with this problem. Metabolic acidosis can be divided into two groups based on anion gap. If an anion gap is elevated (usually greater than 12), see gapped metabolic acidosis. Diagnosis of the cause of non-gapped metabolic acidosis is usually clinically evident - as it can be attributed to diarrhea, intravenous saline or by default, renal tubular acidosis. Occasionally, it may not be clear whether loss of base occurs due to the kidney or bowel. In such a case, one should calculate the urinary anion gap. The urinary anion gap (UAG) = sodium (Na+)+K+- chloride (Cl-). Caution if ketonuria or drug anions are in the urine as it would invalidate the calculation. As an aid, UAG is neGUTive when associated with bowel causes. Non-gapped metabolic acidosis can further be divided into two categories: 1. Historical information important in the diagnosis of Continue reading >>

Acetazolamide In The Treatment Of Sickle Cell Anemia

Acetazolamide In The Treatment Of Sickle Cell Anemia

, Volume 28, Issue11 , pp 460462 | Cite as Acetazolamide in the treatment of sickle cell anemia Acetazolamide was tried in a dosage of 7 mg. per kg. of body weight in 8 cases of sickle cell anemia in the hope that as a potent carbonic anhydrase inhibitor it will prevent deoxygenation of the haemoglobin, intravascular thrombosis and subsequent destruction of the red cells. Sodium bicarbonate and potassium chloride were given to all the cases as well, to prevent metabolic acidosis and hypokalemia. The therapy not only did not produce any beneficial effect and prevent a hemolytic crisis, but possibly even produced increased destruction of the red cells so that three of the cases became very severely anemic during the course of the therapy and expired. Acetazolamide is thus not suitable for treatment of cases of sickle cell anemia. Sickle Cell AnemiaSickle CellMetabolic AcidosisAcetazolamidePotassium Chloride These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. From the Department of Pediatrics, Medical College and Hospital, Nagpur. This is a preview of subscription content, log in to check access Unable to display preview. Download preview PDF. Charmot, G. andReynaud, R.Quoted bySantos andLehmann. Google Scholar Conley, J. R., Martin, M. B. andRecinos, A. Jr.Quoted bySpregue andPaterson. Google Scholar Edington, G. M.B. M. J.,2: 957, 1953. Google Scholar Ferguson, A. D., Carrington, H. T. andScott, R. B.Quoted bySpregue andPaterson. Google Scholar Grek, I. J. andFindlay, M.Quoted byEdington. Google Scholar Griffiths, F. E. D.Lancet,2: 20, 1955. CrossRef Google Scholar Hilkovitz, G.B. M. J.,2: 266, 1957. CrossRef Google Scholar Hughes, J. G., Diggs, L. W. andGillespie, Continue reading >>

Acetazolamide: Mechanism Of Action

Acetazolamide: Mechanism Of Action

Home / ABA Keyword Categories / A / Acetazolamide: mechanism of action Acetazolamide is a reversible inhibitor of the carbonic anhydrase enzyme that results in reduction of hydrogen ion secretion at the renal tubule and an increased renal excretion of sodium, potassium, bicarbonate, and water. It can be used as a diuretic or to treat glaucoma as it prevents excessive build up of aqueous humor. It also inhibits carbonic anhydrase in the central nervous system to minimize abnormal and excessive discharge from CNS neurons. Acetazolamide can be administered to patients with a metabolic alkalosis to promote retention of hydrogen ions at the level of the renal tubule. Mechanism of action: for the reduction of Intraocular pressure Acetazolamide inactivates carbonic anhydrase and interferes with the sodium pump, which decreases aqueous humor formation and thus lowers IOP. Systemic effects however include increased renal loss of sodium, potassium, and water secondary to the drugs renal tubular effects. Arterial Blood gases may show a mild hyperchloremic metabolic acidosis. Continue reading >>

More in ketosis