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| 50 % of ppl > _ years old drink alcohol |
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| alcohol abuse is linked to _ diseases |
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is alchol depedence considered a disease? why? |
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yes its a deviation from normal body characterisitcs |
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| its not how much or frequency of drinking, its if you have a - |
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| compulsion to drink (WHEN you drink) |
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| does alcoholism have genetics? |
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| what are some genes leading to alcoholism-3 |
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| env factros that increase risk of alcoholism-2 |
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urban residence religious background |
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| with alcoholism the main problems are devlopment os what issues?-2 |
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| social problems wiht alcoholism:2 |
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| medical complications with alcoholism-4 |
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malnutrition/thiamine def cardiomyopahty pancreatitis liver disease |
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| ethanol is what class of agent |
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| CNS depressant ;sedative/hypnotic |
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| alcohol affetcs what NTs?-2 |
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| Alcohol on GABA-A recpt increase what ions?-3 |
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| alcohol acting on GABA A recptors decrease what ions-2 |
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| allosteric modulator of GABA A results in-3 |
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| hypnotic, sedation, anxiolysis, |
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| the motor incoordination from alcohol is result of what? |
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| the direct opening of a GABA A recpt cna lead to?-2 |
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| the cognitive impairment by alcohl is done by inhibiting what recptors-2 |
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| inhibit NMDA and kainate recpts (glut) |
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| how many grams of alcohol are in a 12 oz beer |
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| a typical beer will increase blood alcohol level to what? |
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| what is a lethal blood alcohol level? |
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| what is he absoprtion for alcohol in GI? |
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Definition
| rapid in stomach and small intestine |
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| what can delay gastric empyting with alcohol? |
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Definition
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| what is the enzyme that inactivates alcohol? -2 |
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Definition
alcohol dehydrogenanse aldehyde dehydrogenase |
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| what med inhibits alcohol dehydogenase ? |
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| peak conc of alcohol is within- |
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| whcih enzyme converts alchol to acetaldehyde |
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| acetaldehyde is converted to _ which then is metab to -2 |
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| alcohol elimination follow what order kinetics? |
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| max rate of alcohol eliminationis- |
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blood alcohol decreases at rate of _ per hour? so how long for one beer? |
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alchol is broken down by which CYP? *only improtant wiht chronic exposure bc of enzyme induction |
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| if pt has low acitvity of this enzyme they are prone to flushing when drinking |
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| at larger doses blood alchol conc fallas linearly with time or log of blood alcohol? |
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| alcohol primarily effects what? |
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| loss of ocnciousness form alcohol is at what percent |
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chronic alcoholism increases _ which damages hepatocytes? this this leads to what? |
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acetaldehyde fat accum (fatty liver) -> cirrhosis |
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| bc alcohol is a source of calories, it causes what chronically? |
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| mal ingestion of proteins/vitamins like thaimine |
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| only chronic high intake of alcohol is damaging to brain, what are the diseases?-3 |
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Definition
wernicke enceph thaimine def korsakow |
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with light to moderate consuption alcohol cna reduce-3 when does it change? |
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Definition
CAD, ischemic stroke, total mortality 33g/d it now increases mortality |
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| with light to moderate alcohol it can increasE _ and reduce _ |
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| how do you get hepatotoxicity from alcohol? |
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| NADH + acetylCoA-> TGs->fatty liver->cirrhosis |
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| does alcoholism cause dehydration |
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| 1/1000 babies have fetal alcohol syndrome |
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| acute alcohol withdrawl= hangover, wht are th sypmtoms-3 |
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| headache, nauseau, dry moouth |
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| chronic alcohlism withdrawal symtpoms-3 |
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| what drug class is good fro managing symtpoms of alchol withdrawal (like tremor/seizure) |
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| treatment for severe alcohol withdrawla should be done where-2 |
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| treatment for preventiuon of alcoholism replase is drugs + _ |
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| what are the drugs for alcoholism prevention-2 |
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MOA of disulfuram so if the eprson drinks alcohol it causes-3 |
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inhibit aldehyde dehydrogenase flushing, headahce, chest pain |
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| which med has compliance issues |
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naltrexone MOA what does it do? |
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anatag of opioid recpt reeduces craving by attenuating effects of alcohol |
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| semi-synthetic opiate from morphine? |
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| semi-synthetic opiate from codine?-2 |
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| semi-synthetic opiate from thebaine?-2 |
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| opiods increase DA in the _, this acitavtes the _ |
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VTA-> nucelus accumbens pleasure pathway |
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| how do opioids increase DA?-2 |
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decrease releas eof GABA decrease stimulation of GABA |
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| what NT regulates DA release? |
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| opioids accum in hgihly perfused organs like brain, kidney, liver* |
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| no tolerance devlopes for what opioids effects-3 |
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miosis constipation convulsions |
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| primary withdrwal symtoms of opiod withdrwal occur when |
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| secdonary withdrwal of opioids occurs when |
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| what are some symptoms of opiod withdrwal |
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muscle aches/fever runny nose N/V/D |
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| the new opioid with stong hallucinogenic prooperties is ? |
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| what opioid works on the K opioid recptors |
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| what are the recpotrs for marijuana |
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| periphery (includes testes) |
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| at high levels marijuana localizes where-2 |
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hippocampus cerebral cortex |
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| at moderate levels marijuana localizes where-3 |
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spinal cord hypothalmus amygadala |
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| at hgih levels of marijuana what is the effect? |
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| marijuana interacts with what systems |
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marijuana inhibits release of-3 this affects? -3 |
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glut, DA, GABA learning, movement, memory |
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| what is the most widely used illict drug? |
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what is the susntance in marijuana that is the cannibinoid agonsit? how much does a joint have? |
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what is the active marijuana metab? inactive? |
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11-hydroxy THC (mroe active than regular THC) 11-nor-carboxy THC |
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| how long can nor-carboxy THC be detected for? |
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| does marijuana have abuse potention? |
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marijuana has increased _ effects it also increases-2 |
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postivie subjective heart rate, food intake |
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| in acute marijuana smokers what are negative effects |
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| anxiety, paranoia, hallucinations |
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| meddicla marijuana can be used for-4 |
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gluacoma pain appetie stimualnt chemo induced nausea |
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| upon chronic use of marijuana there cna be what type fo depednence? |
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| when is the only time there are marijuana withdrwal symtpoms? |
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| can marijuana affect fetus? |
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