TAILIEUCHUNG - Chapter 048. Acidosis and Alkalosis (Part 8)

Methanol (See also Chap. e34) The ingestion of methanol (wood alcohol) causes metabolic acidosis, and its metabolites formaldehyde and formic acid cause severe optic nerve and central nervous system damage. Lactic acid, ketoacids, and other unidentified organic acids may contribute to the acidosis. Due to its low molecular weight (32 Da), an osmolar gap is usually present. Metabolic Acidosis: Treatment This is similar to that for ethylene glycol intoxication, including general supportive measures, fomepizole or ethanol administration, and hemodialysis. Isopropyl Alcohol Ingested isopropanol is absorbed rapidly and may be fatal when as little as 150 mL of rubbing alcohol, solvent, or de-icer is. | Chapter 048. Acidosis and Alkalosis Part 8 Methanol See also Chap. e34 The ingestion of methanol wood alcohol causes metabolic acidosis and its metabolites formaldehyde and formic acid cause severe optic nerve and central nervous system damage. Lactic acid ketoacids and other unidentified organic acids may contribute to the acidosis. Due to its low molecular weight 32 Da an osmolar gap is usually present. Metabolic Acidosis Treatment This is similar to that for ethylene glycol intoxication including general supportive measures fomepizole or ethanol administration and hemodialysis. Isopropyl Alcohol Ingested isopropanol is absorbed rapidly and may be fatal when as little as 150 mL of rubbing alcohol solvent or de-icer is consumed. A plasma level 400 mg dL is life threatening. Isopropyl alcohol differs from ethylene glycol and methanol in that the parent compound not the metabolites causes toxicity and acidosis is not present because acetone is rapidly excreted. Alcohol Toxicity Treatment Isopropanol alcohol toxicity is treated by watchful waiting and supportive therapy IV fluids pressors ventilatory support if needed and occasionally hemodialysis for prolonged coma or levels 400 mg dL. Renal Failure See also Chaps. 273 and 274 The hyperchloremic acidosis of moderate renal insufficiency is eventually converted to the high-AG acidosis of advanced renal failure. Poor filtration and reabsorption of organic anions contribute to the pathogenesis. As renal disease progresses the number of functioning nephrons eventually becomes insufficient to keep pace with net acid production. Uremic acidosis is characterized therefore by a reduced rate of NH4 production and excretion primarily due to decreased renal mass. HCO3- rarely falls to 15 mmol L and the AG is rarely 20 mmol L. The acid retained in chronic renal disease is buffered by alkaline salts from bone. Despite significant retention of acid up to 20 mmol d the serum HCO3 does not decrease further indicating participation .

• Y học thường thức
• Acidosis and Alkalosis
• bệnh học và điều trị
• bài giảng bệnh học
• tài liệu học ngành y
• Harrisons Internal Medicine
• Respiratory acidosis
• Respiratory alkalosis
• Metabolic acidosis
• Arterial blood gas interpretation
• Metabolic alkalosis
• Compensatory mechanisms
• BMC Pharmacology and Toxicology
• Airway surface liquid pH
• Airway blood flow
• Blood gases
• Case examples
• medical books
• pharmacology
• epidemiologic
• Obstetrics
• anatomy
• Preventing Morbidity
• Multidisciplinary Care
• Handbook of blood gas
• Base interpretation
• Buffer systems
• Carbon dioxide levels
• Gas exchange
• The non invasive monitoring
• Clinical approach
• Diagnose acid–base disorders
• Drinking binge yesterday