Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Information from the clinical laboratory can contribute in several ways to the evaluation and management of the acute consequences of alcohol ingestion. If a blood alcohol analysis is not available, measurement of serum osmolality can be helpful. An elevated ethanol level can explain central nervous system depression. Evidence of acute or chronic alcohol use can explain atypical responses to various drugs. Severe acidosis in association with an increased anion gap may suggest ingestion of other toxic volatiles, such as methanol or ethylene glycol. Alcoholic ketoacidosis, also associated with a large anion gap, may occur in the absence of measureable alcohol or positive test for ketones.
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PMID:Acute toxicology of ethanol ingestion. Role of the clinical laboratory. 700 69

Although hypophosphatemia is relatively uncommon, it may be seen in anywhere from 20% to 80% of patients who present to the ED with alcoholic emergencies, diabetic ketoacidosis (DKA), and sepsis. Severe hypophosphatemia, as defined by a serum level below 1.0 mg/dL, may cause acute respiratory failure, myocardial depression, or seizures. Because hypophosphatemia is not as often treated by ED physicians, becoming familiar with a single intravenous phosphate solution and specific guidelines for phosphate repletion are essential. One mL of the most commonly available phosphate solution (K2PO4) contains 4.4 meq of potassium and 3 mmol (93 mgs) of phosphate. Administering K2PO4 at a rate of 1 mL per hour is almost always a very safe and appropriate treatment for hypophosphatemia. This article provides guidelines for phosphate therapy in hypophosphatemic ED patients including those in DKA, those presenting with alcohol-related complaints including alcoholic ketoacidosis and patients with acute exacerbation of asthma and chronic obstructive pulmonary disease.
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PMID:Hypophosphatemia in the emergency department therapeutics. 1091 39

(1) Many diabetic patients, like the rest of the population, enjoy alcoholic drinks. We conducted a review of the literature for information on the possible risks of alcohol consumption for diabetic patients, based on our standard in-house methodology. (2) Many of the data we found are not very convincing, because alcohol consumption was not properly taken into account. Nevertheless, they provide some useful pointers for diabetic patients. (3) Most wines and spirits do not contain sugar. However, some alcoholic beverages contain sugar and can affect glycaemic control. (4) Light consumption of alcohol seems to have a favourable effect on the vascular complications of diabetes. Drinking one standard unit a day (about 10 grams of alcohol) seems to be an acceptable amount. (5) Alcohol consumption can cause episodes of severe hypoglycaemia in diabetic patients, sometimes occurring several hours later. Fasting, sustained physical exercise and malnutrition are precipitating factors. (6) Alcohol can provoke ketoacidosis, which should not be confused with diabetic ketoacidosis. Alcoholic ketoacidosis requires rehydration but not insulin. (7) Studies of alcohol withdrawal in patients with peripheral and vegetative neuropathies, severe foot lesions, erectile disorders, liver disease or depression have provided conflicting results. However, in practice, it seems better to recommend abstinence in patients with these conditions, as alcohol is an aggravating factor.
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PMID:Diabetes and alcohol: distinctive interactions. 1863 Mar 89