Alcohol - pharmacology b. 2
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62 terms
Terms | Definitions |
|---|---|
 Ethanol is a small ... | water soluble molecule |
| Ethanol is rapidly absorbed in the ... | GI tract |
| Peak blood alcohol concentration during fasting is reached in ... | 30 minutes (delayed in presence of food) |
| Volume of distribution of ethanol ... | 0.5-0.7 L/kg (approximately total body water) |
| Ethanol has rapid distribution with tissue levels approximating ... | blood concentration |
| Two reasons that ethanol concentration in the CNS rises quickly ... | high blood flow and the ability of ethanol to cross membranes |
| Ethanol is metabolized ... | more than 90% in the liver |
| Aside from the liver, ethanol is metabolized/excreted via ... | lungs or urine |
| The rate of ethanol oxidation follows ... | zero-order kinetics (independent of time and concentration) |
| The typical adult can metabolize ... | 7-10 g of ethanol per hour, or 1 'drink' |
| Two metabolic pathways of ethanol ... | Alcohol Dehydrogenase Pathway (AD) and Microsomal Ethanol Oxidizing System (MEOS) |
| Most ethanol metabolism under normal conditions follows this pathway ... | Alcohol dehydrogenase pathway |
| The alcohol dehydrogenase pathway needs this to work ... | NAD+ |
| In the ADH pathway, NAD+ removes this from ethanol to make this ... | a proton / acetaldehyde |
| This population could experience polymorphism of ADH pathway, leading to an increased risk of this ... | Asian / alcoholism |
| In addition to the liver, alcohol dehydrogenase can also occur here ... | brain and stomach (smaller amounts) |
| ADH metabolism appears to contribute to ... | metabolic disorders (chronic alcoholism) and lactic acidosis/hypoglycemia (acute alcohol poisoning) |
| The only time that the MEOS pathway is active ... | when the levels of ethanol in the system are extremely high |
| The MEOS pathway has a high ___ meaning a low ___ for ethanol ... | Km / affinity |
| The MEOS pathway requires this cofactor to work ... | NADPH |
| The main metabolic enzymes that use the MEOS pathway are ... | CYP 2E1, 1A2 and 3A4 |
| At this blood level or lower, the MEOS system does little ethanol metabolism ... | 100 mg/dL or lower |
| The MEOS system is induced with ... | chronic alcohol consumption |
| Other effects of the MEOS system ... | increase in clearance of other drugs eliminated by CYP450s, increased generation of toxic byproducts (toxins and free radicals) |
| The damage associated with chronic alcohol consumption in the liver is caused by ... | toxins and free radicals freed up in the MEOS pathway of metabolism |
| Both the ADH and MEOS pathways end up with the same metabolite ... | acetaldehyde |
| Acetaldehyde is oxidized primarily in the liver by ... | aldehyde dehydrogenase |
| Aldehyde dehydrogenase requires this cofactor to work ... | NAD+ (again) |
| The product of acetaldehyde oxidization is ... | acetate |
| Fomepizole | drug used to inhibit NAD+ |
| Fomepizole indications | used in treating methanol (cleaners) and ethylene glycol (antifreeze) poisoning |
| The main symptom of methanol poisoning is ... | visual disturbance (snow storm) |
| Another way to treat methanol/ethylene glycol poisoning is with ... | ethanol |
| Disulfiram | drug used to deter alcoholism by inhibiting ALDH, leading to an accumulation of acetaldehyde |
| Disulfiram causes ... | flushing, throbbing headache, nausea, vomiting, sweating, hypotension and confusion |
| Disulfiram symptoms occur ... | within a few minutes of alcohol ingestion and last ~30 minutes to several hours |
| Disulfiram administration ... | takes 12 hours for full action and elimination is slow, so it may persist for days |
| A genetic deficiency of ALDH activity in Asian population is characterized by the ... | Asian glow |
| The Asian Glow is caused by ... | accumulation of acetaldehyde that triggers a histamine release |
| Ethanol in the CNS can be useful for ... | sedation and anxiety relief |
| At higher concentrations in the CNS, ethanol leads to ... | slurred speech, ataxia, impaired judgement and disinhibited behavior, and at high concentrations coma, respiratory depression and death |
| In most of the US, a blood level above ___ for adults is sufficient for DWI ... | 80-100 mg/dL |
| Alcohol affects a number of membrane proteins, but the two key ones are ... | glutamate (excitatory) and GABA (inhibitory) |
| Ethanol's effect on glutamate ... | inhibits cation channel opening associated with NMDA subtype, possibly responsible for the 'blackouts' |
| Ethanol's effect on GABA | enhanced action of the neurotransmitter at the A subtype |
| Ethanol's effect on the heart ... | significant depression of myocardial contractility |
| Ethanol's effect on smooth muscle ... | it is a vasodilator, so it relaxes the uterus and could cause hypothermia |
| Chronic consumption of alcohol can lead to ... | induction of certain CYPs, enhancing metabolism of other drugs (like acetaminophen) |
| Acute consumption of alcohol can lead to ... | inhibition of metabolism (decreased enzyme activity level) of drugs like phenothiazines, TCAs and sedative-hypnotics |
| Tactics in treating acute alcohol intoxication ... | prevention of respiratory depression or aspiration of vomit; metabolic alterations such as treating hypoglycemia/ketosis with glucose, Wernicke-Korsakoff with thiamin and dehydration with electrolytes |
| Drug treatment for detoxification in severe cases of alcoholism involves ... | substituting a long-acting sedative-hypnotic drug for the alcohol / gradually reduce (taper) the dose of the long acting drug |
| The long-acting sedative-hypnotic drug used in place of alcohol in withdrawals ... | benzodiazepine class |
| Symptoms of alcohol withdrawal ... | Anxiety, insomnia, tremors, seizures, visual hallucinations (days 0-4) and delirium tremens (days 2 through 8) |
| After detoxification, this is the primary treatment for alcohol dependence ... | psycosocial therapy |
| Three drugs approved for treatment of alcohol dependence ... | Naltrexone / Acamprosate / Disulfiram |
| Naltrexone | long-acting opioid receptor antagonist that blocks the effects of alcohol at opioid receptors |
| Naltrexone's efficacy | in short-term trials, showed reduced cravings and reduced rate of relapse, but in longer trials, failed to show evidence of efficacy |
| Naltrexone's dosing ... | QD PO or IM Q4weeks |
| Patients taking naltrexone need to be free of ... | opioids (you could induce opioid withdrawals) |
| Acamprosate | drug that has many molecular effects including actions on GABA, glutamate, serotonergic, noradrenergic and dopaminergic receptors |
| Acamprosate MOA | weak NMDA-receptor antagonist and GABAa-receptor activator |
| Acamprosate dosing | 1-2 enteric coated tablets TID (poorly absorbed, widely distributed with renal elimination) - watch for GI issues and rash |
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