EtOH Use and Abuse Flashcards

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1
Q

Pt is experiencing symptoms of EtOH withdrawal. What do you give them, from a pharm standpoint? How will they help?

A

Benzos
- relax the agitated pt

Thiamine
- bc chronic alcoholics are generally malnourished and need thiamine to metabolize glucose.

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2
Q

Pt is experiencing acute methanol or ethylene glycol intoxication. What two drugs can you give them to treat this? How do they work?

A

EtOH for methanol
Fomepizole for ethylene glycol

both - inhibit alcohol dehydrogenase –> can’t convert methanol/ethylene glycol to their toxic metabolites.

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3
Q

Disulfram prevents the action of this enzyme, resulting in an accumulation of this metabolite of EtOH that causes flushing and nausea.

What population’s enzyme deficiency mimics this?

A

–I Aldehyde dehydrogenase —> accu. of acetaldehyde –> nausea/flushing

Asian flush due to deficiency of aldehyde dehydrogenase

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4
Q

In what population is CYP metabolism of EtOH important?

A

Alcoholics.

In mild-moderate drinkers, CYPs do NOT metabolize EtOH

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5
Q

Some alcoholics find accumulation of acetaldehyde pleasurable. How is this possible?

A

Acetaldehyde accumulation in the periphery is unpleasant but pleasurable in the ventral tegmental area (VTA) where it reinforces alcohol seeking behavior. A polymorphism of aldehyde dehydrogenase causes this.

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6
Q

How does EtOH lead to toxic effects of acetaminophen?

How do you treat this toxicity?

A

EtOH induces CYP2E1
—> more production of NAPQI (toxic!)

N-acetylcysteine–> produces fresh substrate Glutathione to accelerate metabolism of NAPQI
—> cysteine and mercaptopuric acid conjugates (non-toxic)

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7
Q

What are the non-toxic metabolites of Tylenol?

A

Sulfate conjugate

Glucuronide conjugate

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8
Q

Who is more at risk for Tylenol toxicity, acute drinkers or chronic alcoholics?

A

Chronic alcoholics, bc they have baseline elevations of CYP2E1 that quickly converts acetaminophen—> NAPQI

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9
Q

Describe the physiological effects on a pt w/ a BAL (mg/dL) of:

A

limited muscular incoordination

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10
Q

Describe the physiological effects on a pt w/ a BAL (mg/dL) of:
50-100

A

Pronounced incoordination

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11
Q

Describe the physiological effects on a pt w/ a BAL (mg/dL) of:
100-150

A

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

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12
Q

Describe the physiological effects on a pt w/ a BAL (mg/dL) of:
150-400

A

Nausea, vomiting, marked ataxia, amnesia, disarthria

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13
Q

Describe the physiological effects on a pt w/ a BAL (mg/dL) of:
>400

A

Coma, respiratory insufficiency, death

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14
Q

What impact does EtOH have on:

GABAa?

A

GABA release, ^ receptor density

- hence sedation/depression!

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15
Q

What impact does EtOH have on:

NMDA?

A

Inhibition of postsynaptic NMDA receptors
Chronic use leads to upregulation —> seizures, CNS overstimulation during withdrawal

Initial inhibition leads to BLACKOUTS

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16
Q

What impact does EtOH have on:

Dopamine?

A

^ synaptic DA, ^ effects on VTA/nucleus accumbens reward

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17
Q

What impact does EtOH have on:

ACTH?

A

^ CNS and BV levels of ACTH

18
Q

What impact does EtOH have on:

Opioid receptors?

A

Release of B endorphins. Activation of mu receptors.

19
Q

What impact does EtOH have on:

5-HT?

A

^ in 50HT synaptic space

20
Q

What impact does EtOH have on:

Cannabinoids?

A

^ CB1 activity

–> changes in DA, GABA, Glutamate activity

21
Q

EtOH leads to CV depression or elevation in function?

How does this happen?

A

Depression

  • relaxes vascular SM
  • incr. gastric BF
  • possible hypothermia
22
Q

More weight = incr/decr in BAL?

A

lower BAL

23
Q

Higher BMI = incr/decr in BAL?

A

Higher, bc EtOH will not distribute into adipose tissue

24
Q

Female gender = incr/decr in BAL?

Why?

A

Incr
Females absorb more EtOH from gut.
Generally they have lower weights.
Higher % body fat in women.

25
Q

Chronic EtOH consumption leads to liver dysfunction that results in hypoglycemia. What is going on here?

A

Inhibits gluconeogenesis (done by liver!)

26
Q

How does chronic EtOH consumption lead to endocrine dysfunction?

A

Decr. corticosteroid synthesis–> endocrine dysfunction

27
Q

What cardiac effects can very high BALs resulting from acute binge drinking cause?

A

Arrythmias

28
Q

Chronic alcoholics are more susceptible to this type of infection:

A

Pneumonia

29
Q

Fetal alcohol syndrome is characterized by:

A
intrauterine growth retardation
microcephaly
poor coordination
midfacial underdevelopment
minor joint abnormalities
-congenital heart defects/subtle neurologic deficits also reported
30
Q

Pt comes into your ED obviously EtOH intoxicated. What is your course of action?

A

ABCs
Thiamine THEN Dextrose
Correct electrolyte issues

31
Q

Describe the pharmacokinetic issues that alcohol presents, as they pertain to interactions with other drugs in general.

A

EtOH increases teratogenicity of concurrent drugs with such effects through changes in metabolism.

EtOH increases absorption of both itself and concurrent drugs.

32
Q

Describe the effect EtOH has on bleeding risks involved with NSAIDs and anticoags.

A

Increases bleeding risk associated w/ NSAIDs and anticoagulants

33
Q

What influence does EtOH have on diabetics on medications for diabetes?

A

Incr. risk of hypoglycemia

34
Q

What drugs are known to have disulfram-like effects?

A

Sulfonylureas, Cefotetan, ketoconazole, procarbazine

35
Q

How does Naltrexone work?

A

It is a u opioid antagonist. Decr. desire for EtOH by decr. reward felt. Good for addicts!

36
Q

How does acamprosate work?

A

Weak NMDA antagonist, and GABAa activator. Decr. “need” for alcohol in people withdrawing.

37
Q

The reward centers targeted by EtOH are found where in the brain?
Does EtOH directly stimulate these areas?

A

The corticomesolimbic dopaminergic pathway- extends from VTA to nucleus accumbens

EtOH INDIRECTLY stimulates the VTA-NA through the release of other NTs: opioids, 5-HT, glutamate, GABA, and ACh.

38
Q

Both ethylene glycol and methanol are known to have this toxic effect:

A

acidosis

SEVERE in methanol

39
Q

In addition to acidosis, ethylene glycol also causes:

A

nephrotoxicity

40
Q

In addition to acidosis, methanol also causes:

A

retinal damage. And is metabolized to formaldehyde which will be smelled on the pt’s breath when they present.