Alcohol Drugs

Question 1

Toxicants

Answer 1

Ethanol
Methanol
Ethylene Glycol

Question 2

Antidotes

Answer 2

Disulfiram
Fomepizole
Ethanol

Question 3

Drugs for Ethanol Withdrwal

Answer 3

Diazepam

Thiamine (Vitamin B1)

Question 4

Drugs for chronic Alcoholics

Answer 4

Naltrexone

Acamprosate

Question 5

Acute methanol or ethylene glycol intoxication treatment

Answer 5

ethanol or fomepizole

Question 6

Several drugs are available to treat alcohol dependency, either through changes in

Answer 6

ethanol metabolism or through effects in the ventral tegmental area (VTA) and nucleus accumbens (NA), areas of the brain involved in the response to addictive drugs.

Question 7

The enzymes involved in conversion of alcohol are

Answer 7

alcohol dehydrogenase and aldehyde dehydrogenase

Question 8

The metabolism of ethanol, like that of phenytoin and high-­‐dose aspirin is a

Answer 8

0-­‐order process, in other words the enzymes involved in metabolism are saturated and performing at maximum capacity.

Question 9

Disulfiram is used to encourage abstinence from

Answer 9

alcohol by preventing the metabolism of acetaldehyde, thus leading to the accumulation of this normally transient intermediate.

Question 10

Accumulation of acetaldehyde gives rise to

Answer 10

a feeling of nausea and a flushing reaction of the skin.

Question 11

Although cytochrome P450 is not a major player in the metabolism of ethanol, ethanol is an important inducer of

Answer 11

CYP2E1.

Question 12

Acetaminophen is normally conjugated with either a

Answer 12

sulfate or to a glucuronide

Question 13

acetaminophen is converted through a highly reactive intermediate:

Answer 13

NAPQI, is itself rapidly conjugated and detoxified

Question 14

chronic alcoholics who have induced CYP2E1, there is a dramatically increased rate and extent of conversion to of acetaminophen to

Answer 14

NAPQI.

Question 15

In chronic alcholoics available stores of conjugate substrate to detoxify acetaminophen reactive intermediate become

Answer 15

depleted and with accumulation of NAPQI in the liver, significant hepatotoxicity occurs.

Question 16

the antidote in acetaminophen toxicity in alcoholics is

Answer 16

administration of N-­‐acetylcysteine which provides fresh conjugate substrate for the reactive intermediate to be safely detoxified.

Question 17

BAL (mg/dL) <50

Answer 17

Limited muscular incoordination

Question 18

BAL (mg/dL) 50-100

Answer 18

Pronounced incoordination

Question 19

BAL (mg/dL) 100-150

Answer 19

Mood & personality changes; intoxication over the legal limit in most states

Question 20

BAL (mg/dL) 150-400

Answer 20

Nausa, vomiting, marked ataxia, amnesia, dysarthria

Question 21

BAL (mg/dL) >400

Answer 21

Coma, respiratory insufficiency & death

Question 22

Impact of Alcohol on GABA A

Answer 22

GABA release and increase receptor density

Question 23

Impact of Alcohol on NMDA

Answer 23

Inhibition of postsynaptic NMDA receptors; with chronic use, up regulation.

Question 24

Impact of Alcohol on Dopamine

Answer 24

Increase synaptic dopamine, increase effects on ventral tegamentum/nucleus accumbens reward

Question 25

Impact of Alcohol on ACTH

Answer 25

Increase CNS and blood levels of ACTH

Question 26

Impact of Alcohol on Opoid

Answer 26

Release of B endorphins, activation of mu receptors

Question 27

Impact of Alcohol on 5-HT

Answer 27

Increase in 5-HT synaptic space

Question 28

Impact of Alcohol on Cannabinoid

Answer 28

Increase CB1 activity leading to changes in DA, GABA, glutamate activity

Question 29

Alcohols effects on CV & smooth muscles

Answer 29

CV depressant , relaxes vascular smooth muscle causing vasodilation, possible hypothermia, and increased gastric blood flow. Relaxes uterine smooth muscle.

Question 30

Since alcohol does NOT distribute into

Answer 30

adipose tissue, those with a large BMI would tend to experience higher BAL as alcohol would be excluded from that tissue compartment.