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Pharm III Unit I > 1 Alcohol > Flashcards

1 Alcohol Flashcards

1
Q

What is the most widely used psychoactive drug in the US?

A

Alcohol!

75% of the adult population uses it

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2
Q

What is the DSM-V definition of alcohol abuse?

A

Social life of an individual is impaired for at least 1 month as a result of alcohol

14 million Americans meet criteria for alcoholism/abuse

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3
Q

What is the DSM-V definition of alcoholism?

A

The occurence of tolerance and dependence as a result of prolonged alcohol abuse

Continuous or periodic lack of control over drinking, preoccupation with alcohol, use of alcohol despite adverse consequences, and distortions in thinking, esp denial

7 million Americans are considered active alcoholics

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4
Q

What is the connection between genetics and alcoholism

A

Incidence of alcoholism is 4x higher in offspring of alcoholics

Twice as high in identical twins compared to fraternal twins

Marked increase in release of ß-endorphins in the dopamine reward pathway —> predisposition to addiction

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5
Q

Where does absorption of alcohol occur?

A

The stomach and small intestine

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6
Q

Peak blood alcohol content (BAC) occurs within _________ after the last drink and will vary between individuals

A

30-90 min

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7
Q

Alcohol is evenly distributed throughout the body and easily crosses both the _______ and _______

A

Blood-brain barrier

Placenta (fetal BAC reaches same levels as the mother’s)

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8
Q

Alcohol may acutely completely for metabolism and inhibit the breakdown of what drugs?

A

Benzos

Barbiturates

TCAs

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9
Q

Alcohol metabolism follows ______ kinetics

A

Zero order

Rate is INDEPENDENT of concentration

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10
Q

How is alcohol metabolized?

A

By alcohol dehydrogenase (ADH) to acetaldehyde

Acetaldehyde is oxidized by aldehyde dehydrogenase to acetate (requires NAD+)

When NAD+ becomes less available, Lactate and acetyl-CoA accumulate

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11
Q

In chronic alcoholics, what metabolic pathway is used to metabolize alcohol?

A

Microsomal-ethanol oxidizing system (MEOS) and CYP2E1

Chronic consumption induces both of these pathways rather than the primary ADH pathway

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12
Q

What leads to increased acetaminophen toxicity in chronic alcoholics?

A

Induction of the CYP2E1 metabolic pathway

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13
Q

What genetic things can affect how your body metabolizes alcohol?

A

Aldehyde dehydrogenase deficiency (—> Asian flush)

Women have lower levels of ADH than men

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14
Q

How does the mechanism of action differ between Disulfiram (Antabuse) and Fomepizole (Antizol)?

A

Disulfiram inhibits aldehyde dehydrogenase (leads to build up of acetaldehyde and a wicked hangover)

Fomepizole (used in methanol poisoning) inhibits alcohol dehydrogenase

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15
Q

What is the difference between pharmacokinetic and pharmacodynamic alcohol tolerance?

A

Pharmacokinetic - what your body does to the drug
• Ethanol induces CYP2E1 —> chronic uses tend to have increased ethanol metabolism

Pharmacodynamic - what the drugs do to your body
• Down-regulation of GABA receptors
• Up-regulation of NMDA receptors
• Withdrawal

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16
Q

Cross tolerance develops between alcohol and…

A

Benzos

Barbiturates

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17
Q

Alcohol is a CNS _________

A

Depressant

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18
Q

What are the two main mechanisms of action for alcohol

A

Binds to GABA-a receptor to increase Cl- influx —> enhanced inhibitory GABA transmission

Increases DA in mesolimbic pathway

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19
Q

Long-term chronic use of alcohol will ______ GABA receptors

A

Down-regulate

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20
Q

Long-term chronic use of alcohol causes ______ of NMDA receptors but also inhibits the effect of _______ on them

A

Up-regulates

Glutamate

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21
Q

Why is it so dangerous to take benzos and barbiturates together with alcohol?

A

They bind non-competitively to different sites on the GABA receptor —> synergistic inhibition

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22
Q

What are the effects of alcohol on the CNS?

A

Low concentrations —> disinhibition, decreased anxiety, mild euphoria, confidence increases, memory/concentration affected, mood swings

Increased dose —> motor function and judgement are impaired, speech slurs, and ataxia may occur

CNS depressant and sedative properties become apparent

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23
Q

Anterograde amnesia occurs as a result of…

A

Blockade of NMDA receptors

24
Q

What are the effects of alcohol on smooth muscle?

A

Vasodilator due to acetaldehyde metabolite —> hypothermia

Can also relax the uterus (used in the past to prevent premature labor)

25
Q

Effects of alcohol on the heart

A

Depression of myocardial contractility

26
Q

Effects of alcohol on the kidney

A

Decreases ADH —> diuresis

27
Q

SSx of acute alcohol toxicity

A

Emesis, stupor, coma, respiratory depression, and death

Metabolic and electrolyte disturbances

Hypothermia (from cutaneous vasodilation)

BP and CO decreased

28
Q

How do you treat acute alcohol toxicity?

A

Management of respiratory depression**

Prevent emesis

Rehydrate

29
Q

Why do we get hangovers after too much alcohol?

A

Buildup of acetaldehyde

Dehydration

Beginning of withdrawal

30
Q

If seizures occur with acute alcohol toxicity, how do you treat?

A

Lorazepam (Ativan) - benzo

Phenytoin (Dilantin) - anticonvulsant

31
Q

Effects of alcohol on liver and GI tract

A

Gastritis and pancreatitis

Liver disease is the most common medical complication**

Metabolism of alcohol lowers glutathione —> oxidative stress and tissue damage

Fatty liver —> fibrosis —> cirrhosis

Alcoholic hepatitis

Liver cancer

32
Q

When is liver cancer most likely to occur for alcoholics?

A

About 10 years after you stop consuming alcohol - because the liver is attempting to heal itself

33
Q

Most common deficiencies for alcoholics

A

Folate and THIAMINE

34
Q

CNS effects of chronic alcohol abuse

A

Wernicke-Korsakoff syndrome due to thiamine deficiency

Korsakoff’s psychosis (chronic disabling memory loss)

Peripheral neuropathy

35
Q

What is Wernicke-Korsakoff syndrome?

A

Paralysis of eye muscles

Ataxia

Confusion

Coma

Death

Due to thiamine deficiency

36
Q

CV effects of chronic alcohol abuse

A

Cardiomyopathy due to direct toxic effects of acetaldehyde

Arrhythmias - binges can lead to atrial and ventricular

Hypertension

Increased risk of stroke, CHD

37
Q

Chronic alcohol abuse increases the carcinogenicity of …

A

Tobacco

38
Q

Effect of chronic alcohol abuse on sexual function

A

Testicular atrophy

Impotence

Gynecomastia

39
Q

Effects of chronic alcohol abuse on immune system

A

Increased respiratory infections

40
Q

Effects of chronic alcohol abuse on skeletal muscle

A

Atrophy

41
Q

What is fetal alcohol syndrome?

A

Alcohol crosses the placenta —> teratogenic

Microcephaly, mental retardation, poor coordination, flattened face, joint abnormalities, heart defects, and impaired immune system

42
Q

Chronic alcohol use may ______ metabolism of phenytoin and oral hypoglycemics

A

Increase

43
Q

Acute use of alcohol may inhibit the breakdown of what drugs?

A

Benzos

Barbiturates

Phenothiazines

TCAs

44
Q

What is the most effective way to treat alcoholism?

A

A combination of pharmacological and psychosocial treatments

Drugs + AA

45
Q

What are the four drugs used to treat alcohol addiction?

A

Naltrexone (ReVia)

Acamprosate (Campari EC)

Disulfiram (Antabuse)

Topiramate (Topamax)

46
Q

MOA for Naltrexone (ReVia)

A

Opioid receptor antagonist - blocks the ability of alcohol to stimulate the reward pathway

Reduces cravings and decreases the rate of relapse by 50%

47
Q

What is the most important caution to keep in mind with Natrexone?

A

Large doses may cause liver damage - do not use in patients with liver failure

48
Q

MOA for Acamprosate (Campral EC)

A

Structural analogue of GABA

Restores the normal balance of GABA and glutamate —> decreases craving and likelihood of relapse

Excreted by the kidneys so NO liver toxicity

49
Q

MOA for Disulfiram (Antabuse)

A

Inhibits aldehyde dehydrogenase —> acetaldehyde build up (so really really bad hangover)

Long duration of action

Effects can be severe - vomiting, sweating, CP, hypotension, vertigo, blurred vision, shock

Dangerous and NOT recommended

50
Q

What is the MOA for Topiramate (Topamax)?

A

Anticonvulsant drug that decreases cravings and increases abstinence in recovering alcoholics

We don’t really understand the MOA though 🤷‍♀️🤷‍♀️🤷‍♀️

51
Q

Alcohol withdrawal can begin within ______ and last ______

A

6-8 hours

7-10 days

52
Q

What are the SSx of alcohol withdrawal?

A

Mild —> anxiety, irritability, insomnia, nausea, tachycardia

Severe —> hallucinations, delirium and tremors (DTs), seizures, arrhythmias, hypotension

53
Q

How to treat alcohol withdrawal

A

Restore electrolyte imbalances (hydration)

Maybe thiamine

To prevent seizures —> Diazepam (Valium) or Chlordiazepoxide (Librium)

To treat seizures that are already occurring —> Lorazepam (Ativan)

54
Q

SSx of methanol poisoning

A

Symptoms include visual disturbances “like being in a snowstorm”

Formaldehyde may be smelled on the breathe (b/c it’s metabolized by ADH to toxic aldehydes and oxalates)

Transient CNS excitation followed by depression, then severe metabolic acidosis

Bradycardia, coma, seizures, followed by cessation of respiration

55
Q

Treatment for methanol poisoning

A

Support respiration, lavage, alkalization for acidosis, dialysis

FOMEPIZOLE (Antizol) - an alcohol dehydrogenase inhibitor to prevent production of toxic metabolites

May also use ethanol if no Fomepizole

Pharm III Unit I (9 decks)

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