Alcohol Flashcards

1
Q

Alcohol- MOA

A

Increases duration of GABA channel opening and acts at GABA/ Cl.
Acts on other NT’s receptors, and disrupts membrane fluidity

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2
Q

Alcohol absorption

A

passive diffusion in stomach but mostly in the SI.

Affected by food, gastric rate, and concentration

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3
Q

Alcohol distribution and BAC

A

Distributes through all of the body water

BAC therefore depends on BW: M vs F, young vs old, weight, dehydration

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4
Q

What BAC corresponds to psychomotor impairment

A

.1

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5
Q

what BAC is the legal limit

A

.08

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6
Q

What happens at BAC .3-.4%

A

alcohol becomes as strong as a surgical anesthetic

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7
Q

What order kinetics is alcohol metabolism?

Why?

A

zero order- alcohol metabolism is independent of concentration and time
Even a small amount of alcohol saturate the receptors

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8
Q

What system/s metabolize alcohol

A

Both in liver
alcohol dehydrogenase system
CYPP450 (microsomal) ethanol oxidizing system- this system causes lots of drug interactions

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9
Q

Describe the alcohol dehydrogenase pathway

A

EtOH –> acetaldehyse via (Alcohol dehydrogenase
acetaldehyde –> acetate via aldehyde dehydrogenase
Acetate is broken down to CO2 and Water via metabolism which provides calories –> dec appetite –> nutrient deficiencies

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10
Q

CNS side effects of alcohol

A

dec inhibitions
reduces REM sleep
respiratory depression
coma/death- linear slope from anesthesia to death

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11
Q

Process of alcohol intoxication that leads to death

A

Inhibitions dec –> Anxiolytic –> sedation –> hypnosis –> anesthesia –> respiratory depression –> coma –> death
most alcohol related deaths are from the respiratory depression

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12
Q

Non CNS effects of Alcohol

A

cutaneous vasodilation resulting in flushing and feelings of warmth but actually heat loss. At higher doses leads to HTN, cardiomyopathy, arrhythmias, and can be fatal
Inhibits ADH –> diuretic
moderate amounts improve lipid profile
Appetite- large amounts suppress apetite –> nutrient deficiencies ie Korsakoff and wernicke (thiamin and niacin)
Liver- dose dependent toxicity- fatty change leads to hepatitis, cirrhosis, and hepatic failure
pancreatitis can be fatal
Gout exacerbation
Hyperestrogenemia
Emesis and other GI issues
Fetal alcohol syndrome

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13
Q

Alcohol and drug interactions- mechanism

A

in the beginning it is a CYP450 inducer dec drugs metabolized by this system.
As liver damage progresses that system slows down

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14
Q

Signs of Fetal Alcohol syndrome

A

microcephaly
mental retardation
abnormal- face, joints, and heart

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15
Q

Alcohol tolerance

A

pharmacokinetic tolerance= more efficiently metabolized
pharmacodynamic tolerance= less sensitive to the drug
Behavioral tolerance= learn how to not act drunk when you are

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16
Q

What two issues are caused by B1 deficiency

A

Thiamine deficiency results in Wernikes and Korsakoff encephalopathy

17
Q

Wernikes encephalopathy

A

reversible

ataxia, opthalmoplegia, confusion

18
Q

Korsakoff encephalopahty

A

Irreversible

apathy, antero and retrograde amnesia, confabulations

19
Q

What are the signs of hyperestrogenemia

A

gynecomastia

Testicular shrinkage

20
Q

Emesis issues with alcohol

A

Mallor Weiss tear
Boerhaave syndrome
aspiration
GERD

21
Q

Withdrawal- alcohol

A

starts 6-24 hours after last drink
last 5 days
characterized by irritability, insomnia, tachycardia, palpitations, hallucinations, delirium, tremors, grand mal seizures, arrhythmias
seizures and arrhythmias can be deadly

22
Q

Alcohol withdrawal treatment

A

benzos- diazepam, lorazepam, oxazepam- work on same receptor. oxazepam and lorazepam are not dependent on hepatic metabolism (preferred bc alcoholics may have liver damage.
phenytoin- control seizures
betablockers, clonidine- control autonomic effects
vitamins and thiamine for nutrient deficiencies

23
Q

do you give antipsychotics in alcohol withdrawal

A

NO!, inc seizures

24
Q

Drugs to give after alcohol withdrawal has subsided and now patient is focused on kicking the addiction

A

Disulfram –> block acetaldehye dehydrogenase causing a buildup of acetaldehyde –> flushing, HA, N/V, hepatotoxicity
Naltrexone- long acting opiod agonist- reduces cravings, cause hepatotoxicity
Acamprosate- dec cravings to help maintain abstinence, may act on GABA receptors. Less potential for hepatotixicity.
Naltrexone + acamprosate work well together and are better than either one alone