Metabolic acidosis hypokalemia

In acute overdose, peak serum levels > 100 pg ml may be predictive of arrhythmias and seizures. The use of sustained-release formulations and the presence of pharmacobezors in the gut may make it difficult to determine peak serum levels. Sinus tachycardia is the most common cardiac sign of theophylline toxicity. Ventricular and supraventricular tachycardia, ectopic beats, hypotension, and cardiac arrest may occur. Metabolic acidosis, hypokalemia, hypercalcemia, and hyperglycemia may be seen. Tremulousness and agitation frequently occur. Intractable seizures may occur in severe intoxications, probably secondary to adenosine receptor antagonism in the brain. Onset of seizures is a poor prognostic indicator. Persistent vomiting is commonly seen and may interfere with attempts at therapy. 

The use of CA inhibitors as diuretics is limited by their propensity to cause metabolic acidosis and hypokalemia. Their use can be indicated in patients with metabolic alkalosis and secondary hyperaldosteronism resulting for example from aggressive use of loop diuretics. Furthermore, CA inhibitors are effective dtugs to produce a relatively alkaline urine for the treatment of cysteine and uric acid stones as well as for the accelerated excretion of salicylates. Perhaps the most common use of CA inhibitors is in the treatment of glaucoma. 

Electrolytes Daily doses based on daily maintenance requirements, renal function, gastrointestinal losses, acid-base status, concomitant drug therapy, nutritional and anabolic status Pa lion I has hyponatremia, hypokalemia, hypomagnesemia, and hypophosphatemia, also has low serum bicarbonate concentration, could be component of metabolic acidosis due to sepsis... 

Prolonged use or overdose may result in electrolyte or metabolic disturbances (such as hypokalemia, hypocalcemia, and metabolic acidosis or alkalosis), as well as persistent diarrhea, vomiting, muscle weakness, malabsorption, and weight loss. 

Amiloride Blocks epithelial sodium channels in collecting tubules Reduces Na retention and wasting increases lithium clearance Hypokalemia from other diuretics reduces lithium-induced polyuria Orally active duration 24 h Toxicity Hyperkalemic metabolic acidosis... 

The cardiac arrhythmias are life-threatening, so the patient must be closely monitored, with facilities available for possible resuscitation. Drugs such as quinidine and procainamide are contraindicated, but lidocaine, propranolol, or phenytoin has been used safely and effectively. The arterial blood gas levels, pH, and electrolyte concentrations should be monitored so that metabolic acidosis or hypokalemia can be identified that would further aggravate the arrhythmias. Electrical pacing may be required if the antiarrhythmic drugs fail. Hyperpyrexia is treated by cooling. Seizures may be managed by intravenous doses of diazepam. 

Hypokalemia is a common accompaniment of the metabolic acidosis that toluene inhalation can cause (see below). However, severe hypokalemia has also been reported in the absence of acidosis (31). 

Ammonium chloride, bicarbonate, and furosemide loading tests in an epileptic man with metabolic acidosis and episodic hypokalemia taking zonisamide showed evidence of distal renal tubular acidosis (9). On reexamination 7 weeks after zonisamide had been replaced with phenytoin, the renal tubular acidosis had resolved. 

Metabolic acidosis and electrolyte disturbances. Acidic environments increase the ionization of aminoglycosides and positive cations compete with the aminoglycosides for binding sites. Consequently, metabolic acidosis and electrolyte imbalances such as hypokalemia and hyponatremia increase the binding of aminoglycosides to the phospholipid receptors on the renal tubular cells, increasing intracellular accumulation. 

Acute toxicity manifests primarily in the CNS, cardiovascular system, and gastrointestinal system. CNS signs include restlessness, tremor, nervousness, headache, insomnia, tinnitus, confusion, delirium, psychosis, and seizures. Cardiac manifestations of overdose include sinus tachycardia, various dysrhythmias, asystole, and cardiovascular collapse. Other findings include tachypnea, nausea, vomiting, hematemesis, diarrhea, and fever. Case reports also include rhabdomyolysis and pulmonary edema. Laboratory findings include metabolic acidosis, respiratory alkalosis, ketosis, hypokalemia, and hyperglycemia. The estimated lethal dose in adults is 150-200 mg kg whereas doses of 10-15mgkg ... 

The toxic events of terbutaline overdose follow its -adrenergic agonist activity. The effects of terbutaline overdose are usually mild and benign however, they can be prolonged. Cardiovascular effects are usually limited to a sinus tachycardia and widened pulse pressure. Although there may be a drop in diastolic pressure, the systolic pressure is maintained by increased cardiac output from the tachycardia. Evidence of myocardial ischemia after terbutaline overdose has been infrequently reported. Transient hypokalemia may occur, caused by a shift of extracellular potassium to the intracellular space. A transient metabolic acidosis can be seen due to increased lactate production. Restlessness, agitation, and tremors are common in terbutaline overdose. 

Whenever possible, potassium supplementation should be administered by mouth. Three salts are available for oral potassium supplementation chloride, phosphate, and bicarbonate. Potassium phosphate should be used when patients are both hypokalemic and hypophosphatemic potassium bicarbonate is most commonly used when potassium depletion occurs in the setting of metabolic acidosis. Potassium chloride, however, is the primary salt form used because it is the most effective treatment for the common causes of potassium depletion (i.e., diuretic-induced and diarrhea-induced hypokalemia). Because diarrhea and diuretics such as hydrochlorothiazide and furosemide promote net potassium and chloride losses, supplementation with potassium chloride repletes both electrolytes. Potassium chloride can be administered in either tablet or liquid formulations (Table 50-4). The liquid forms are generally less expensive however,... 

Hypokalemia, hypochloremic metabolic acidosis, elevated serum amylase... 

Toxic doses inhibits respiratory center —>4- respiration — T pC02 —> respiratory acidosis i-l pH, 4 HCCXJ, normalization of pC02) plus inhibition of Krebs cycle and severe uncoupling of oxidative phosphorylation (4- ATP) — metabolic acidosis, hyperthermia, and hypokalemia (I K+). 

Some causes of hyperkalemia and hypokalemia are listed in Table 6.1. Increases of plasma potassium may be observed following metabolic acidosis, severe tissue... 

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