Term
| what % of drinkers have a problem? |
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Definition
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Term
| what characterizes alcohol absorption? |
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Definition
| rapid and complete from the GI tract. empty stomach: peak levels in ~40 min. food in stomach: delays absorption. |
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Term
| what characterizes alcohol distribution? |
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Definition
| proportional to water content of tissues |
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Term
| can urine alcohol levels be used for determining level of impairment? |
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Definition
| no - can be ~130% of blood level |
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Term
| what characterizes alveolar air as a representation of blood levels? |
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Definition
| ~.05% of blood level, proportionally. this is reliable for estimating blood level. |
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Term
| what characterizes a .05 G/dL BAC (blood alcohol concentration)? |
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Definition
| euphoria/minor motor disturbances |
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Term
| what characterizes a .06 G/dL BAC? |
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Definition
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Term
| what characterizes a .08 G/dL BAC? |
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Definition
| reduced glare response (legal limit) |
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Term
| what characterizes a 0.10-0.15 G/dL BAC? |
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Definition
| significant motor incoordination |
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Term
| what characterizes a 0.20-0.30 G/dL BAC? |
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Definition
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Term
| what characterizes a 0.30-0.35 G/dL BAC? |
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Definition
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Term
| what characterizes a >0.35 G/dL BAC? |
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Definition
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Term
| what characterizes biotransformation of alcohol? |
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Definition
| 90%+ of ethanol is oxidized primarily by hepatic tissue in a zero-order process. the remainder is excreted via lungs and urine. etoh -> (alcohol dehydrogenase [rate limiting, needs NAH+]) -> acetaldehyde -> (aldehyde dehydrogenase) -> acetate -> acetyl CoA -> CO2 + H2O + 7/1 cal/g |
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Term
| what is the microsomal ethanol oxidizing system (MEOS)? |
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Definition
| this is in the hepatic smooth endoplasmic reticulum and can undergo enzyme induction. it utilizes NADPH (+O2+H+) -> NADP+ and H2O. appears to function at a fairly high BAC. in a normal adult, this biotransforms at approximately 10 mL absolute etoh/hour. in an alcoholic: slightly higher if liver function is normal (enzyme induction)/slightly lower if liver disease. |
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Term
| what is the gender difference in alcohol metabolism? |
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Definition
| (non-alcoholic) females have ~25% *less in 1st-pass metabolism of etoh and ~60% *less in gastric alcohol dehydrogenase activity. alcoholic females had only 6% of the first pass metabolism of non-alcoholic males, i.e., it was basically non-existent. |
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Term
| what are the acute CNS effects of alcohol? |
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Definition
| sedation, impaired judgment, ataxia, disinhibited behavior. reduction of cortical inhibition of subcortical centers. reduction of transmission in polysynaptic pathways of the RAS. ultimate effect influenced by both set/setting. amnesia: state-dependent learning (can only remember things learned at that level of intox.). blackout: severe-short term memory deficit, occurs during high BAC, most alcohol-induced violent behavior occurs during this state. interacts w/other CNS depressants. acute alcohol can temporarily diminish hepatic biotransformational capacity of other drugs. mechanism of alcohol's CNS depression effect not established: possible shift of cell membrane gel -> fluid or membrane more disordered. |
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Term
| what are the acute CV effects of alcohol? |
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Definition
| decreased myocardial contractility. blood vessels: vasodilation (direct - depression of vascular smooth muscle by acealdehyde/indirect - depression of medullary vasomotor center). loss of body heat: etoh ingestion in cold environment - may equal hypothermia. |
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Term
| what are the acute renal effects of alcohol? |
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Definition
| increased release of ADH from posterior pituitary (therefore diuresis can occur w/liquor shots as well as beer) |
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|
Term
| what are the acute GI effects of alcohol? |
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Definition
| low concentration: increased appetite, increased gastrin. high concentration: irritation, n/v, increased emptying time, bleeding. |
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Term
| what are the acute misc. effects of alcohol? |
|
Definition
| hypoglycemia: due to poor nutrition, depletion of hepatic glycogen, decreased gluconeogenesis. hyperuricemia. |
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|
Term
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Definition
| similar for barbiturates. hemodialysis, if needed is effective. |
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Term
| what characterizes hangover? |
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Definition
| mild form of etoh withdrawal: fatigue, vertigo, h/a (pulsating), weakness, GI irritation, dehydration. readministration of etoh can decrease some of these symptoms. |
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Term
| what are the chronic effects of alcohol abuse? |
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Definition
| tolerance, physical dependence, withdrawal syndrome, nutritional toxicity, systemic effects and skeletal muscle degeneration |
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Term
| what characterizes tolerance w/chronic alcohol abuse? physical dependence? |
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Definition
| enzymatic (biotransformational): not very significant. cellular: very significant. degree of tolerance proportional to amount consumed per day and duration of consumption. occurs in social and alcoholic drinkers. physical dependence occurs as tolerance develops. |
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Term
| what characterizes withdrawal w/chronic alcohol abuse? |
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Definition
| degree related to amount and duration of ethanol abuse. BAC does not have to reach zero. mild: begins w/in 6-8 hrs after last drink - anxiety, irritability, sweating, insomnia (rebound REM), hyperreflexia, tremors, vomiting. severe: occurs ~24 hrs after last drink/peaks @ 24-48, disorientation, visual hallucinations, delirium tremens (global confusion, auditory/visual/tactile hallucinations, ANS hyperactivity: mydriasis, sweating, tachycardia, and seizures: tonic-clonic. |
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Term
| how is alcohol withdrawal treated? |
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Definition
| BZDs for agitation, phenytoin if seizures are likely. medical emergency: 5-10% chance of death. |
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Term
| what characterizes possible nutritional toxicity effects with chronic alcohol abuse? |
|
Definition
| folic acid deficiency (megaloblastic anemia), iron deficiency, niacin deficiency, and peripheral neuropathy (axonal degeneration of motor nerves, paresthesias, related to thiamine deficiency). |
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|
Term
| can chronic alcohol abuse cause skeletal muscle degeneration? |
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Definition
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|
Term
| what characterizes CV effects w/chronic alcohol abuse? |
|
Definition
| cardiomyopathy (fatty infiltration of the myocardium, fibrosis replacement of functional tissue), dilation of blood vessels around eyes/nose, HTN at 3+ drinks/day, elevation in high-density lipoproteins (appears to reduce CAD), reduction in low-density lipoproteins (also appears to reduce CAD). |
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Term
| what characterizes liver effects w/chronic alcohol abuse? |
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Definition
| initially: alcoholic fatty liver, which is reversible, but can progress to alcoholic hepatitis: cell damage, necrosis w/inflammation, jaundice, and fibrosis. 80% of hepatitis pts have at least a 5 yr of of heavy alcohol intake. portal cirrhosis: fibrosis extends to portal tracts. |
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Term
| what characterizes hematological effects w/chronic alcohol abuse? |
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Definition
| hemolytic anemia and thrombocytopenia |
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Term
| what characterizes CNS effects w/chronic alcohol abuse? |
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Definition
| wernicke-korsakoff syndrome. wernicke's encephalopathy: early phase, related to thiamine deficiency (cerebellar ataxia, confusion/disorientation, polyneuropathy). korsakoff's psychosis: later continuation of the syndrome - poor short term memory (similar to alzheimer's). tx: thiamine IV. |
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|
Term
| what are common cancers associated w/alcohol abuse? |
|
Definition
| esophagus, pharynx, larynx, liver, and pancreas |
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Term
| what is fetal alcohol syndrome? |
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Definition
| this occurs reliably with approximately 2.5 ounces of absolute alcohol per day. low IQ, smaller birth weight, length, head circumference, facial defects (hypoplasia of the maxilla and short palpebral fissures), atrial septal defect, and poor muscle coordination. increased rates of spontaneous abortion. |
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Term
| what is the most effective and best chance for complete/permanent recovery from chronic alcoholism? |
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Definition
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|
Term
| what is pharmacologic tx for chronic alcoholism? |
|
Definition
| disulfiram, acamprosate and naltrexone |
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Term
| what characterizes disulfiram as pharmacologic tx for chronic alcoholism? |
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Definition
| disulfiram inhibits aldehyde dehydrogenase (level can be 5-10x > than from same amount of alcohol ingested without disulfiram). accumulation of acetaldehyde causes: garlic-like aftertaste, n/v, weakness/confusion, impotence, extreme vasodilation (flushing of skin, severe h/a, hypotension/tachycardia - all may be severe). |
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Term
| when is disulfiram contraindicated? |
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Definition
| in pts w/severe myocardial dz or coronary occlusion. pts need to abstain from alcohol for up to 14 days following last dose. |
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Term
| what are drug interactions w/disulfiram? |
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Definition
| reduces biotransformation of phenytoin (may need to lower dose) as well as BZDs (longer acting) and oral anticoagulants. |
|
|
Term
| what other drugs can produce a disulfiram-like reaction? |
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Definition
| sulfonamide oral hypoglycemics and metronidazole |
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Term
| what characterizes acamprosate as pharmacologic tx for chronic alcoholism? |
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Definition
| this acts to reduce central glutamate levels. some data show that a persistent hyperglutamatergic state contributes to pathogenesis of alcoholism & contributes to hyperactivity occurring during withdrawal. reduces symptoms of protracted withdrawal, e.g., insomnia, anxiety, restlessness, and dysphoria. |
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Term
| what characterizes naltrexone as pharmacologic tx for chronic alcoholism? |
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Definition
| naltrexone is a narcotic antagonist which decreases etoh-induced increased blood flow in the R prefrontal cortex (likely via etoh-induced release of endorphins w/in the frontal cortex-thalamus-limbic system loop). most commonly reported effect of naltrexone: decrease in alcohol use, fewer drinks per day, alcoholic beverages tasted less pleasant, experienced less of a 'high' from alcohol, improved compliance with treatment program, reduced relapse, lower dropout rate, longer time to relapse, and more successful in coping with relapse when it occurred. |
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