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Acetazolamide Metabolic Acidosis Mechanism

Acetazolamide - Pharmapedia

Acetazolamide - Pharmapedia

Acetazolamide, sold under the trade name Diamox, is a carbonic anhydrase inhibitor that is used to treat glaucoma, epileptic seizures, benign intracranial hypertension (pseudotumor cerebri), altitude sickness, cystinuria, and dural ectasia. Acetazolamide is available as a generic drug and is also used as a diuretic. This section may be confusing or unclear to readers. Please help clarify the article; suggestions may be found on the talk page. (June 2009) This drug is a carbonic anhydrase inhibitor. Carbonic anhydrase (CA) catalyzes the forward motion of molecules in the following equation: where CA converts carbon dioxide (CO2) and water (H2O) to carbonic acid (H2CO3), which then dissociates to a hydrogen ion (H+, an acidic proton), and a bicarbonate ion (HCO3-, a basic anion). In some tissues (particularly plants), the equilibrium is such that CA can catalyze the reverse direction of the reaction. Carbonic acid inhibitors, such as acetazolamide, inhibit CA in tissue and fluid, causing less movement of carbonic acid toward CO2 production. In the kidneys, blocking CA leads to bicarbonate wasting in the tubules (alkalizes urine), loss of bicarbonate subsequently leads to a metabolic acidosis. In the meantime, H+ backs up due to acetazolamide CA inhibition in the tubule and enters the cell with Cl-, then passes into the bloodstream, creating a hyperchloremic metabolic acidosis.[1] This effect can also be used for therapeutic correction of respiratory alkalosis. Acetazolamide is often used in the treatment of various diseases. It has been used for glaucoma sufferers.[2] The drug decreases fluid formation in the eye resulting in lower intraocular pressure. In epilepsy, its main use is in absence seizures and myoclonic seizures.[3] It is also used to decrease generation of c 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 >>

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 >>

Diuretic_pharm [tusom | Pharmwiki]

Diuretic_pharm [tusom | Pharmwiki]

Diuretics are among the most commonly prescribed drugs, and play an important role in the treatment of heart failure and hypertension. They exert most of their therapeutic effects through inhibiting the reabsorption of sodium at different sites along the nephron of the kidney. Diminished reabsorption of sodium results in increased urinary loss of both sodium and water, leading to a reduction in plasma volume, and a reduction of blood pressure. Thiazide diuretics also exert an additional vasodilator effect on arterial smooth muscle by a still poorly understood mechanism. Figure 1. Overview of the transport systems in the renal nephron, and major sites of action of diuretics. ADH: antidiuretic hormone; ENaC: epithelial Na channel. Acetazolamide is the most commonly used carbonic anhydrase inhibitor (taken systemically) that affects the kidney. Figure 2. Mechanism of action of carbonic anhydrase inhibitor diuretics. Bicarbonate absorption by the proximal tubule is dependent on the activity of carbonic anhydrase (CA) which converts bicarbonate (HCO3-) to CO2 and H2O. CO2 rapidly diffuses across the cell membrane of proximal tubule cells where it is rehydrated back to H2CO3 by carbonic anhydrase. H2CO3 dissociates to HCO3- and H+ which are transported out of the cell on the basolateral side by different transporters. Bicarbonate absorption is therefore dependent on the activity of carbonic anhydrase. Inhibition of carbonic anhydrase by acetazolamide results in an increased urinary loss of bicarbonate. This also interferes with the reabsorption of Na and Cl. The basolateral Na/K ATPase (found in most epithelial cells lining the nephron) maintains a low intracellular Na concentration, which is necessary for reabsorption of Na, and in the proximatl tubule also facilitates the Continue reading >>

Carbonic Anhydrase Inhibitor

Carbonic Anhydrase Inhibitor

Acetazolamide, the prototype Carbonic Anhydrase Inhibitors, inhibits carbonic anhydrase and in doing so reduces renal bicarbonate resorption in the proximal tubule. This leads to a direct increase in urinary bicarbonate excretion and secondarily to mild increases in sodium and potassium excretion. Because of its mild effects on electrolytes acetazolamide is a largely safe drug with few adverse side effects but in consequence is rarely used for its diuretic capacity. The pharmacological effects of acetazolamide are due to its inhibitory effect on carbonic anhydrase in the proximal tubule. As discussed in Renal Bicarbonate Excretion , luminal and intracellular pools of carbonic anhydrase in the proximal tubule are critical for resorbing filtered bicarbonate and thus administration of acetazolamide results in significant increases in renal bicarbonate excretion. Because bicarbonate acts as a weak base this can lead to significant increases in urinary pH. Additionally, because bicarbonate is the primary weak base of the bicarbonate buffer , its wasting leads to a non-gap metabolic acidosis . As discussed in renal bicarbonate excretion , bicarbonate resorption utilizes a luminal Na-H+ antiporter and in consequence the net process of bicarbonate resorption is linked to sodium resorption. Given this linkage between bicarbonate and sodium resorption, acetazolamide yields significant reductions in proximal tubule sodium resorption. However, the vast majority of this sodium is resorbed by later parts of the nephron and thus urinary sodium excretion is increased only mildly. The increased distal nephron sodium delivery caused by acetazolamide results in increased potassium secretion and thus carbonic anhydrase inhibitors typically result in moderate increases of urinary potassium Continue reading >>

Acetazolamide Side Effects

Acetazolamide Side Effects

Applies to acetazolamide : oral capsules, oral tablets, parenteral powder for injection Paresthesias, hearing dysfunction or tinnitus , anorexia, altered taste, nausea , vomiting , diarrhea , polyuria, drowsiness, confusion. Applies to acetazolamide: compounding powder, injectable powder for injection, intravenous powder for injection, oral capsule extended release, oral tablet Adverse reactions occurring early in therapy have included paresthesias, tinnitus, nausea, vomiting, diarrhea, and drowsiness.[ Ref ] Frequency not reported: Anaphylactic/anaphylactoid reactions including shock and fatalities[ Ref ] Frequency not reported: Blood dyscrasias such as aplastic anemia , agranulocytosis, leucopenia, thrombocytopenia , and thrombocytopenia purpura[ Ref ] Frequency not reported: Loss of appetite, electrolyte disturbances, metabolic acidosis and hypokalemia with long term therapy, hyponatremia osteomalacia with long-term therapy, hyper/ hypoglycemia [ Ref ] Frequency not reported: Skin reactions, Stevens-Johnson syndrome, toxic epidermal necrolysis , urticaria , rash including erythema multiforme[ Ref ] Frequency not reported: Nausea, vomiting, diarrhea, melena[ Ref ] Frequency not reported: Abnormal liver function, cholestatic jaundice , fulminant hepatic necrosis, hepatitis[ Ref ] Very common (10% or more): Paresthesias (up to 20%) Frequency not reported: Drowsiness, headache , dizziness , taste alteration, ataxia, flaccid paralysis, convulsions, sensory disturbances[ Ref ] Frequency not reported: Confusion, irritability, depression , excitement, reduced libido[ Ref ] Frequency not reported: Transient myopia[ Ref ] Frequency not reported: Renal colic , increased risk of nephrolithiasis , renal failure[ Ref ] Frequency not reported: Polyuria, polydipsia, crystalluria, r Continue reading >>

Use Of Acetazolamide In Copd Patients

Use Of Acetazolamide In Copd Patients

I'm a doctor in Ho Chi Minh City, Vietnam. In my department (Pulmonology), some doctors prescribe acetazolamide for the patients with COPD who have edema and chronic respiratory failure. What is the role of acetazolamide in these patients? Response from Christine Campbell Reardon, MD Some patients with chronic obstructive pulmonary disease (COPD) develop carbon dioxide (CO2) retention and hypoxemia. There are multiple factors that lead to the development of CO2 retention. One of the major factors is an alteration of ventilation and perfusion matching leading to an increase in dead space. The diaphragm may function at an anatomical disadvantage in patients with COPD. In the setting of hyperinflation caused by airflow obstruction, the diaphragm is flattened and generates less pressure than what would occur under normal circumstances. In addition, hypercapnic patients demonstrate a breathing pattern characterized by a lower tidal volume and higher respiratory rate, which increases dead space. The lower tidal volume is caused by a shorter inspiratory time rather than a decrease in respiratory drive. It had previously been thought that hypercapnic COPD patients had a blunted central respiratory drive and this was the major cause of CO2 retention. From this idea, the use of carbonic anhydrase inhibitors -- such as acetazolamide for hypercapnic COPD patients -- developed. Reversible inhibition of carbonic anhydrase results in the reduction of hydrogen ion secretion at the renal tubule and an increased renal secretion of sodium, potassium, bicarbonate, and water. Acetazolamide will block the conversion of CO2 into bicarbonate, which will acutely increase the levels of carbon dioxide in the tissues and blood. The induction of a metabolic acidosis by acetazolamide will increase Continue reading >>

Acetazolamide - Ascending Limb - Barnard Health Care

Acetazolamide - Ascending Limb - Barnard Health Care

The diuretic which is most commonly associated with the development of metabolic acidosis is acetazolamide. This diuretic acts by inhibiting the enzyme carbonic anhydrase. Given the central role that this enzyme plays in bicarbonate reabsorption in the proximal tubule, administration of this diuretic leads to the development of metabolic acidosis by disrupting the process of bicarbonate reclamation. The mechanism by which acetazolamide leads to inhibition of bicarbonate reabsorption is directly related to its ability to inhibit luminal carbonic anhydrase. This enzyme normally catalyzes the dehydration of carbonic acid (produced when filtered bicarbonate reacts with secreted hydrogen ions) to water and C02, thereby maintaining a favorable concentration gradient for further hydrogen ion secretion. The uncatalyzed dehydration of carbonic acid occurs very slowly. By inhibiting the activity of this enzyme, acetazolamide allows for the concentration of luminal carbonic acid to increase. The resultant increase in hydrogen ion concentration creates an unfavorable concentration gradient for further hydrogen ion secretion. Due to the lipid solubility of acetazolamide, inhibition of intracellular carbonic anhydrase may also contribute to the impairment in proximal bicarbonate reabsorption. Inhibition of the intracellular enzyme will decrease the supply of hydrogen ions available for the secretory process. In either case, decreased secretion of hydrogen ions will inhibit reabsorption of filtered bicarbonate. Decreased bicarbonate reabsorption in the early proximal nephron limits the development of a favorable chloride diffusion gradient which, in turn, normally creates a passive diffusion gradient for Na reabsorption in the S2 portion of proximal tubule. As a result, there is incr 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 >>

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 >>

Mechanisms Of Action Of Acetazolamide In Prophylaxis And Treatment Of Acute Mountain Sickness

Mechanisms Of Action Of Acetazolamide In Prophylaxis And Treatment Of Acute Mountain Sickness

What are the 3 major classes of high altitude disease? 1)Acute mountain sickness (10% at 3500m, 75% at 4500) What are the multitude of systemic effects that make acteozolamide effective besides inducing metabolic acidosis (inducing chemoreceptors to respond more to hypoxic stimuli at high altitude? -Improvements in ventilation through, tissue respiratory acidosis -improvements in sleep quality from carotid body CA inhibition What are the two hypothesis that causes of AMS? ;What is the problem with these hypothesis?What is the agreement of symptoms caused by? 1) Hypoxia-mediated mild cerebral edema and increased cranial pressure; brain morphological changes don't correlate with symptoms of AMS 2)Vasogenic Edema: rupture of blood brain barrier, Free radical damage barrier function under hypoxic conditions don't support pathophysiology of AMS -HYPOXIA not hypobaria. Oxygen therapy also effective treatment Ambiguity of causes of AMS,but what is the relative agreement of symptoms? What txt is consistent with this? caused predominantly by hypoxia and not hypobaria --oxygen therapy is an effective treatment for AMS How did acetazolamide significantly increased minute ventilation by 50%? Mechanism is still poorly understood. due to predominantly to increase in TV not due to frequency Improves arterial PO2 and oxyhemoglobin saturation (during sleep increased from 72%-79%. What is the most commonly cited explanation for drug enhancement? At high altitude, reduced barometric pressure and partial pressure of PIO2=>hypoxemia which drives minute ventilation. Hyperventilation causes respiratory alkalosis->leads to symptoms of AMS acetozolamide generates metabolic acidosis and reduce the limit of increased ventilation reduce the effects of alkalosis and improve AMS Hypercapnia ventila Continue reading >>

Acetazolamide - An Overview | Sciencedirect Topics

Acetazolamide - An Overview | Sciencedirect Topics

Acetazolamide is a useful prophylactic agent in several channelopathies and may be useful in children with FHM1. 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]. Domenic A. Sica, in Side Effects of Drugs Annual , 2008 Acetazolamide is used to reduce the frequency of attacks of ataxia in patients with episodic ataxia type 2. However, the metabolic acidosis that acetazolamide causes can result in nervous system complications (5A). A 49-year-old man with episodic ataxia type 2 responded to acetazolamide 250mg qds. However, during an attack of ataxia he developed gaze-evoked nystagmus, positional nystagmus, dysarthria, and aggravated gait Continue reading >>

Carbonic Anhydrase Inhibitor

Carbonic Anhydrase Inhibitor

Demetrius Ellis, in Smith's Anesthesia for Infants and Children (Eighth Edition) , 2011 This carbonic anhydrase inhibitor causes sodium bicarbonate diuresis and a reduction in total body bicarbonate stores. Its effectiveness is limited by the development of hyperchloremic metabolic acidosis. The bicarbonaturia induces phosphaturia, whereas the metabolic acidosis increases calcium excretion (Lemman et al., 1967; Beck and Goldberg, 1973). Both factors are responsible for renal stone formation and nephrocalcinosis during prolonged use of acetazolamide. It can cause severe K+ wasting, especially during the acute bicarbonaturic phase. Therapeutically, acetazolamide may be effective in the chronic treatment of glaucoma, in alkalinization of the urine, in the treatment of acute mountain sickness, to stimulate ventilation in central sleep apnea, to reduce endolymph formation in Meniere's disease, and in the treatment of refractory hydrocephalus (Conger and Falk, 1977; Vogh, 1980; Greene et al., 1981; Brookes et al., 1982; White et al., 1982; Maren, 1987). Clodagh M. Ryan MB, BCh, BAO, MD, T. Douglas Bradley MD, in Murray and Nadel's Textbook of Respiratory Medicine (Sixth Edition) , 2016 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 One small 6-day randomized trial demonstrated a modest (38%) reduction in the AHI in heart failure patients with CSR-CSA in association with reductions in daytime sleepiness and fatigue.134 Theophylline is an adenosine antagonist that stimulates central respiratory drive and augments cardiac contractility. In a 5-day randomized trial involving 15 patients with heart failure and CSR-CSA, theophylline reduced the AHI but did 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 >>

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