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Pharm 2 > Lecture 4 - EtOH > Flashcards

Lecture 4 - EtOH Flashcards

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1
Q

What is FDA approved for EtOH aversion?

A

Disulfiram

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2
Q

How does EtOH create a reward pathway?

A

increases dopamine in the nucleus accumbens

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3
Q

Recovering EtOHers have elevated levels of_____

A

beta endorphins

can be elevated for years despite not having EtOH

these Beta Endorphins are activating the mu opioid receptor –we think this is what causes the intense craving

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4
Q

How does naltrexone suppress the reward effects of EtOH?

A

prevents elevated beta endorphins from activating the mu opioid receptor - thus decreasing cravings

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5
Q

What are contraindications of naltrexone?

A

liver or acute hepatitis pts

heptaotoxic at high doses

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6
Q

Does combining naltrexone with disulfiram show a therapeutic advantage?

A

nope

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7
Q

What must you keep in mind when using Naltrexone with a EtOHer with opioid abuse?

A

Naltrexone can cause severe withdrawal in opioid dependent individuals

Solution: do the Narcan (Naloxone) challenge test

consider giving disulfuram instead so you don’t affect mu opioid receptor

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8
Q

For an EtOHic with opioid abuse problems and liver problems, what drug can you get them to help with EtOH aversion?

A

avoid naltrexone since it too affects the mu opioid receptors

avoid disulfiram d/t hepatotoxicity

so try acamprosate

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9
Q

FDA approved drugs for treating alcohol abuse

A

Naltrexone

Acamprosate

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10
Q

Where in the brain does Naltrexone work?

A

VTA region

reduces the reward effect of EtOH

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11
Q

How is Naltrexone administered?

A

IM monthly

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12
Q

What is the MOA of acamprosate?

A

the anticraving effect is unknown but it is an antiepileptic

increases activity of GABAa receptors
inhibits glutametergic NMDA receptors activity

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13
Q

Does combing acamprosate and disulfiram show a therapeutic advantage?

A

yes

together they have increased effectiveness over either drug alone

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14
Q

Topiramate

A

anticraving mechanism unknown
an antiepilepsy and migraine drug
NOT used to treat EtPH withdrawal sxs
reduced relapse to heavy drinking in recovering EtOHics
enhances GABAa receptor activity
inhibits glutamatergic AMPA/kainate receptor activity

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15
Q

Topiramate and Acamprosate drug class

A

antiepilepsy drugs but they are NOT used for ETOH withdrawal seizures

only used in recovery EtOHics

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16
Q

Which drug inhibits glutamatergic AMPA/kainate receptor activity?

A

Topiramate

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17
Q

Who benefits from moderate drinking?

A

older men (greater than 65y/o)

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18
Q

How can EtOH be beneficial?

A

reduce risk of heart disease (increase HDL levels)
lowers risk of DM

red wine is the best because it contains antioxidant resveratrol

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19
Q

When might you administer IV ETOH?

A

When someone has ingested methanol or ethylene glycol

EtOH saturates ADH which is used to metabolize methanol and ethylene glycol which is toxic

if Methanol gets metabolized via ADH it can cause severe acidosis and retinal damage

Ethylene glycol if metabolized by ADH can cause acidosis and nephrotoxicity

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20
Q

Fomeprizole

A

similar to EtOH, blocks ADH so it doesn’t break down Methanol or Ethylene glycol

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21
Q

What type of drug is ethanol?

A

sedative hypnotic/CNS depressant

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22
Q

Describe EtOH absorption

A

rapid and distributes to AL tissues, including placenta

slowed by prior food intake

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23
Q

How is EtOH metabolized?

A

Alcohol Dehydrogenase (ADH)
when blood ETOH level is <0.1%
ADH is found in liver and gut

> 0.1% Microsomal Ethanol Oxidizing System (P450 CYP) metabolizes ETOH

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24
Q

Where is ADH found?

A

liver and gut

responsible to metabolizing EtOH when it is < 0.1% in the blood

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25
What metabolized ETOH when the blood level is <0.1%?
ADH in the liver and gut
26
What metabolizes ETOH when the blood level is >0.1%?
MEOS - microsomal ethanol oxidizing system
27
What effect does Acetaldehyde have on the body?
This is what ETOH gets metabolized into it causes N/V/HA/hypotension
28
What is the pathway metabolism of EtOH?
Ethanol to acetaldehyde via ADH or MEOS (Depending on blood concentration of alcohol) then broken down via ALDH into acetate
29
What drugs can inhibit ALDH? And what is the result?
oral hypoglycemis - sulfonyureas ABX - metronidazole and some cephalosporins this means if taken with EtOH there is a risk of acetaldehyde accumulation ---disulfiram reaction --> N/V/HA/hypotension
30
What might happen if Valium is taken with EtOH?
Valium is a benzo, benzos along with tricyclic antidepressants, H1 antihistamines, and narcotics all use P450 metabolism which EtOH might out compete them for thus preventing the breakdown of these drugs and result in supra-additive CNS depression EtOH is a substrate for P450 enzymes
31
What does chronic EtOH do to enzyme activity?
``` increased expression (induction) of CYPs which can increase the likelihood of secondary drug metabolism risk of acetaminophen hepatotoxicity due to formation of highly reactive intermediate this can lead to irreversible liver damage ``` treat with N-acetylcysteine
32
What is NAC used for?
n-acetylcysteine | used to treat chronic EtOHics suspected of acetaminophen poisoning
33
How does n-acetylcysteine work?
neutralizes reactive intermediates resulting from metabolism of acetaminophen by P450 enzymes CYP2E1, CYP1A2, and CYP3A4
34
What are the units of ethanol concentration?
weight/vol g/dl (g/100ml) 0.1% = 0.1g/100ml = 100mg/100ml = 0.1g/dL
35
How much EtOH is in a "typical drink"?
15g
36
What is the volume of distribution of EtOH for males?
0. 7L/Kg | 0. 6L/kg for females
37
How can you calculate the blood EtOH % in a 70kg male who had 1 typical drink?
70kg (0.7 L/Kg) = 49L 15g (typical drink) / 49 L = 0.3 g/L = 0.03% g/100ml
38
How long does it take ADH to metabolize a single drink?
1.5 to 2 hours
39
How does the BAC differ between a a tolerant individual and a non-tolerant individual?
a tolerant user (abuser) will have a higher BAC than their corresponding clinical effect
40
What BAC is respiratory depression and death?
>500 mg/dL
41
At what BAC will the pt have abolished reflexes and possible coma?
400-500
42
What is EtOHs MOA?
enhance GABA actions at GABAa receptors inhibits glutamate activation of gulatmatergic NMDA receptors (glutamate is excitatory) NMDA receptor implicated in cognitive function, including learning and memory
43
What additional CNS effects does EtOH have in chronic alcoholics?
increases synaptic concentrations of dopamine in nucleus accumbens increase endogenous opioids in ventral tegmental area (VTA)
44
What are the 2 kinds of tolerance seen in EtOHics?
``` Metabolic tolerance (pharmocoKINETIC) induction of MEOS enzymes (upregulation) ``` Functional tolerance (pharmacoDYNAMIC) reduction of CNS sensitivity to ethanol due to adaptive changes in neurons - down regulation of GABAa receptors - up regulation of NMDA receptors - up regulation of voltage gated Ca channels
45
What affects do chronic EtOH have on the liver?
decrease gluconeogenesis hypoglycemia NAD depletion fatty accumulation in liver with eventual hepatitis and cirrhosis
46
What affects does chronic EtOH have on GI?
inflammation, bleeding, scarring | leading to absorption deficits
47
What affects does chronic EtOH have on CV?
anemia hypertension (d/t increased renin release) ventricular hypertrophy increases risk of cardiomyopathy and/or MI
48
What effects does chronic ETOH have on neoplasia?
ethanol is not a direct carinogen, acetaldehyde (its metabolite) is a carcinogen though
49
What affects does chronic EtOH have on endocrine?
altered steroid metabolism - which leads to gynectomastia, testicular atrophy, and salt retention
50
What is the most common neurological problem in alcoholics?
peripheral neuropathies
51
What causes Wernicke - Korsakoff Syndrome?
associated with thiamin deficiency resulting in encephalopathy only about 20% of these pts respond to IV thiamine recovery is slow - months to years
52
What are the sxs of Wernicke- Korsakoff syndrome?
ataxia confusion paralysis of extraocular muscles memory loss can progress to coma and death
53
What is the treatment for Wernicke- Korsakoff syndrome?
Thiamine only 20% respond to IV thiamine recovery takes months to years
54
When during pregnancy is CNS development more susceptible to ETOH?
during the first and third trimester anatomy can be affected during the second trimester
55
What is the treatment for acute intoxication?
maintain VS and prevent aspiration | IV dextrose and thiamine if Wernicke-Korsakoff is suspected
56
What determines when you will have withdrawal sxs and how severe they are?
How long you have been an abuser if you have been an abuser for years you will have sxs onset within hours
57
How do you treat life threatening seizures of chronic EtOH?
diazepam or long acting benzos ---tapper off over several weeks
58
What are the mild alcohol withdrawal symptoms?
``` anxiety insomnia tremors agitation muscle aches sweating cramping N/V/D arrhythmias ``` treat with centrally acting clonidine or peripherally acting propranolol
59
How do you treat mild alcohol withdrawal sxs?
centrally acting clonidine (decreases sympathetic outflow by activating alpha 2 adrenergic receptors in CNS) peripherally acting propranolol (decreases sympathetic outflow by blocking beta adrenergic receptors)
60
What are the severe sxs associated with alcohol withdrawal?
hallucinations DTs seizures
61
When do you use Naloxone?
if you suspect recovering EtOHic is abusing opioids perform narcan challenge test prior to treatment with naltrexone inhibits mu opioid receptors in ventral tegmental region (VTA) short acting antagonist
62
How do you treat methanol or ethylene glycol poisoning?
``` IV Ethanol or Fomepizole - to bind to ADH to prevent metabolism of methanol or ethylene glycol and Hemodialysis - to remove the poisons and Bicarb - to treat the acidosis ```
63
What is Valium used for?
aka diazepam used for severe alcohol withdrawal syndrome leading to convulsions long acting benzo that activates GABAa receptors in CNS increase affinity of endogenous GABA to GABAa receptor taper dose over weeks
64
What is the major difference between disulfiram and naltrexone?
disulfiram is aversion therapy naltrexone is anti-craving therapy both are hepatotoxic at high doses

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