Acidosis chronic

Chronic salicylism presents clinically in a similar fashion to the acute situation, although it is often associated with a delay in diagnosis, and a higher morbidity and mortality. Chronic salicylism is more often associated with pronounced hyperventilation, dehydration, pulmonary edema, renal failure, coma, seizures, and acidosis. Chronic salicylism can occur at serum salicylate levels as low as 15mgdl. ... 

For patients with bladder drainage, enteric conversion may be required for refractory problems, such as dehydration, metabolic acidosis, chronic urethritis caused by trypsinogen derivation, urinary tract infections, and recurrent reflux pancreatitis. This uivolves an anastomosis between the graft duodenal segment and the recipient small bowel. 

These actions on electrolyte transport, in the kidney and in other tissues e.g., colon, salivary glands, and sweat glands), appear to account for the physiological and pharmacological activities that are characteristic of mineralocorticoids. Thus, the primary features of hyperaldosteronism are positive Na balance with consequent expansion of extracellular fluid volume, normal or slight increases in plasma Na+ concentration, hypokalemia, and alkalosis. Mineralocorticoid deficiency, in contrast, leads to Na+ wasting and contraction of the extracellular fluid volume, hyponatremia, hyperkalemia, and acidosis. Chronically, hyperaldosteronism can cause hypertension, whereas aldosterone deficiency can lead to hypotension and vascular collapse. 

The regulation of NHE2 is multifactorial. Chronic exposure to nitric oxide and gamma-interferon decrease NHE2 activity, whereas metabolic acidosis and chronic stimulation with epidermal growth factor (EGF) increase activity. 

Metformin is contraindicated in patients with heart failure, renal disease, hypersensitivity to metformin, and acute or chronic metabolic acidosis, including ketoacidosis. The drug is also contraindicated in patients older than 80 years and during pregnancy (Pregnancy Category B) and lactation. 

Stimulation of basolateral Na /H exchanger transport activity in LLC-PK] cells during chronic metabolic acidosis is accompanied by a parallel increase in NHE-1 transcript abundance [80]. Chronic metabolic acidosis also increases the abundance of Na /H exchanger transcripts in rat renal cortices [81] and SV40-transformed mouse proximal tubule cells [82]. 

Chronic or large ingestions of propylene glycol have been associated with the development of hyperosmolar anion-gap metabolic acidosis, renal dysfunction, hemolysis, cardiac arrhythmias, and seizures. 

Contraindicated in patients who are anuric or uremic or have chronic respiratory acidosis or salicylate toxicity... 

Rarely, may lead to a small rise in PC02 in patients with chronic respiratory acidosis ° If alkalosis persists or if pH > 7.6 or HC03 >45 mEq/L... 

Chronic respiratory acidosis i Increased3 Increased0 AHCO3- = 0.35 x ARiCC V ... 

It is critical to differentiate acute and chronic respiratory acidosis, as the acute form is often a medical emergency that requires intubation and mechanical ventilation, whereas the chronic form is typically a stable condition. The blood gases in Case Study 2 came from a patient with advanced emphysema who is a "C02 retainer" due to ineffective ventilation. Because this patient s disease is chronic, the elevated PaC02 developed very slowly and allowed for metabolic compensation. 

Severe, acute respiratory acidosis produces a variety of neurologic abnormalities. Initially these include headache, blurred vision, restlessness, and anxiety. These may progress to tremors, asterixis, somnolence, and/or delirium. If untreated, terminal manifestations include peripheral vasodilation leading to hypotension and cardiac arrhythmias. Chronic respiratory acidosis is typically associated with cor pulmonale and peripheral edema. 

The goals of therapy in patients with chronic respiratory acidosis are to maintain oxygenation and to improve alveolar ventilation if possible. Because of the presence of renal compensation it is usually not necessary to treat the pH, even in patients with severe hypercapnia. Although the specific treatment varies with the underlying disease, excessive oxygen and sedatives should be avoided, as they can worsen C02 retention. 

Factors that can predispose patients to developing metabolic bone disease include deficiencies of phosphorus, calcium, and vitamin D vitamin D and/or aluminum toxicity amino acids and hypertonic dextrose infusions chronic metabolic acidosis corticosteroid therapy and lack of mobility.35,39 Calcium deficiency (due to decreased intake or increased urinary excretion) is one of the major causes of metabolic bone disease in patients receiving PN. Provide adequate calcium and phosphate with PN to improve bone mineralization and help to prevent metabolic bone disease. Administration of amino acids and chronic metabolic acidosis also appear to play an important role. Provide adequate amounts of acetate in PN admixtures to maintain acid-base balance. 

Respiratory acidosis Acidosis caused by retention of carbon dioxide due to a respiratory abnormality (e.g., chronic obstructive lung disease). 

Like ketoacidosis, respiratory acidosis can also upset the acid-base balance in the body. Respiratory acidosis occurs when the lungs cannot remove enough carbon dioxide from the body. This may be due to severe lung diseases such as chronic asthma, emphysema, or bronchitis, or it could be caused by mechanical restrictions to the emptying of the lung due to scoliosis (curvature of the spine) or severe obesity. 

There are two types of respiratory acidosis. One type, called chronic respiratory acidosis, forms over a long period of time. The body can adjust to this type of respiratory acidosis by signaling the... 

GSH-S deficiency is a more frequent cause of GSH deficiency (HI7), and more than 20 families with this enzyme deficiency have been reported since the first report by Oort et al. (05). There are two distinct types of GSH-S deficiency with different clinical pictures. In the red blood cell type, the enzyme defect is limited to red blood cells and the only clinical presentation is mild hemolysis. In the generalized type, the deficiency is also found in tissues other than red blood cells, and the patients show not only chronic hemolytic anemia but also metabolic acidosis with marked 5-oxoprolinuria and neurologic manifestations including mental retardation. The precise mechanism of these two different phenotypes remains to be elucidated, because the existence of tissue-specific isozymes is not clear. Seven mutations at the GSH-S locus on six alleles—four missense mutations, two deletions, and one splice site mutation—have been identified (S14). 

The major manifestation of chronic metabolic acidosis is bone demineralization with the development of rickets in children and osteomalacia and osteopenia in adults. 

In a patient with chronic respiratory acidosis (e.g., chronic obstructive pulmonary disease), treatment is essentially similar to that for acute respiratory acidosis with a few important exceptions. Oxygen therapy should be initiated carefully and only if the Pao2 is less than 50 mm Hg because the drive to breathe depends on hypoxemia rather than hypercarbia. 

Respiratory and metabolic acidosis can develop in patients with cardiorespiratory arrest, with chronic lung disease and shock, and with metabolic acidosis and respiratory failure. 

Metabolic alkalosis and respiratory acidosis can occur in patients with chronic obstructive pulmonary disease and respiratory acidosis who are treated with salt restriction, diuretics, and possibly glucocorticoids. 

A chronically iU patient on long-term (home) parenteral nutrition develops metabolic acidosis, a grayish pallor, scaly dermatitis, and alopecia (hair loss). These symptoms subside upon addition of the B vitamin biotin to the alimentation fluid. 

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