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Therapeutics III > Watts Pharmacology and Pharmacotherapy of Alcohol Use/Abuse > Flashcards

Watts Pharmacology and Pharmacotherapy of Alcohol Use/Abuse Flashcards

1
Q

How is alcohol absorbed in the body?

A

-10% is absorbed from the stomach, remainder is absorbed in the intestine
-Peak absorption occurs in 30-90 minutes
-Limited by gastric emptying (slowed by food)
-Alcohol increases acid release (induces ulcers and GERD)

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2
Q

How is alcohol distributed in the body?

A

-Distributed in total body water
-Men dilute ethanol more because men have a higher body water percentage compared to women (58% men, 48% women)

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3
Q

At what rate is alcohol eliminated?

A

-Elimination is zero order at or above 10-20 mg/dl
-ADH is rate-limiting step

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4
Q

How is alcohol metabolized?

A

-90% in the liver
-Alcohol dehydrogenase (ADH)
-Microsomal ethanol oxidizing system (MEOS)
-Aldehyde dehydrogenase (ALDH)

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5
Q

How does MEOS metabolize alcohol?

A

-Only at high alcohol concentration
-Involves CYP2E1
-LOW affinity for alcohol

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6
Q

Alcohol dehydrogenase clinical pearls

A

-Enzyme is found in liver, brain and stomach
-Men express higher levels of gastric ADH

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7
Q

Fomepizole mechanism of action

A

-ADH inhibitor
-Used to treat ethylene glycol and methanol intoxication by slowing it’s conversion into formaldehyde and toxic metabolites
-Liver then has more time to further metabolize the toxic metabolites

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8
Q

Aldehyde dehydrogenase clinical pearls

A

-ALDH1B1 and ALDH2 isozymes are important for alcohol metabolism
-50% of Asians only have ALDH2
-SNP in ALDH2 reduces activity (ALDH2*2)

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9
Q

Effects of having heterozygous ALDH2*2

A

-Reduced metabolic activity
-Flushing and increased skin temp
-Can still consume alcohol

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10
Q

Effects of having homozygous ALDH2*2

A

-Deficient in the ability to metabolize acetaldehyde
-Neurotoxic
-Strong “hangover”
-Also alcoholic neuropathy

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11
Q

Disulfiram clinical pearls

A

-Irreversible inhibitor
-Effects persist up to 14 days
-Only works for people whoa re very motivated

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12
Q

Which ligand-gated ion channels does alcohol target?

A

-GABAa-receptors (allosteric activators of inhibitory neurotransmitters)
-NMDA receptor (inhibitor)
-Alpha7 nicotinic receptors

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13
Q

Which neurotransmitters does alcohol release?

A

-Opioids (enkephalin)
-Dopamine
-Serotonin, norepinephrine
-Acetylcholine
-Increases CNS and blood ACTH levels

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14
Q

What is the legal blood alcohol limit to drive in the United States?

A

-80mg% or 0.08
-This is independent of behavioral tolerance (some people can operate normally with a blood alcohol limit of 0.08)

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15
Q

Pharmacological actions of low levels of alcohol

A

-Euphoria, disinhibition
-Analgesia

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16
Q

Pharmacological actions of intermediate levels of alcohol

A

-CNS stimulation (mood swings, aggression)
-CNS depression (slurred speech, ataxia, sedation, loss of motor control, irrational behavior)

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17
Q

Pharmacological actions of high/fatal levels of alcohol

A

-Coma-death
-Respiratory paralysis
-People can survive 1000-1500 mg/dl

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18
Q

Cardiovascular effects induced by acute use of alcohol

A

-Vasodilation
-Warm, flush
-Reduced blood pressure
-Increased heart rate (decreases at high doses)

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19
Q

Cardiovascular effects induced by moderate alcohol use

A

Reduced risk of coronary disease (not worth the adverse effects associated)

20
Q

Cardiovascular effects induced by heavy/chronic use of alcohol

A

-Affects heart
-Cardiomyopathy
-Arrhythmias
-Hypertension
-Hemostasis

21
Q

Physiological effects of alcohol consumption

A

-Hypothermia (moderate in men and can be lethal in cold temps and high doses)
-Increases HCl secretion in the GI tract (alcohol is a secretagogue)
-Chronic gastritis in alcoholics
-Appetite stimulant with low doses and appetite depressant with high doses

22
Q

Long-term adverse effects to the liver from alcohol consumption

A

-Increase fat metabolism (promotes triglyceride synthesis from FFA)
-Fatty liver leading to cirrhosis is common in abusers
-Vitamin deficiencies; glutathione reduced leading to small intestine damage and diarrhea
-Can cause ascites, edema, effusions

23
Q

Long-term adverse effects to the blood from alcohol consumption

A

-Mild anemia
-Gastritis -> chance of blood loss
-Alcohol related folic acid deficiency

24
Q

Possible types of cancer that can occur from alcohol consumption

A

-Liver
-Along route of ingestion (mouth, larynx, esophagus, stomach)

25
Q

Important drug-drug interactions associated with alcohol

A

-CNS depressants (opioids, antipsychotics, anti-histamines, sedative-hypnotics)
-Aldehyde dehydrogenase inhibitors (disulfiram, antimicrobials (metronidazole, cephalosporins), sulfonylureas hypoglycemics (tolbutamide))
-Acetaminophen
-Aspirin

26
Q

What is the mechanism behind the interaction between alcohol and acetaminophen?

A

Upregulation of CYP2E1 leads to an increase of NAPQI toxic metabolites

27
Q

How do you treat someone who is suffering from toxicity associated with concurrent alcohol and acetaminophen use?

A

Treat with n-acetylcysteine to detoxify NAPQI

28
Q

Why can aspirin not be used with alcohol?

A

Increased ulcers and GI bleeds

29
Q

How do you manage acute alcohol intoxication?

A

-Prevent respiratory depression by keeping them awake and make sure they do not aspirate vomit

30
Q

What are signs of fetal alcohol syndrome?

A

-Facial dysmorphology
-Low birth weight
-Decreased brain size
-Mental retardation

31
Q

What are the teratogenic effects of alcohol?

A

-Fetal alcohol syndrome
-Lower testosterone and sperm quality

32
Q

Alcohol withdrawal symptoms

A

-Anxiety
-Insomnia
-Seizures/tonic-clonic convulsions
-Nausea/vomiting
-Tactile hallucinations/delirium tremens

33
Q

Treatment for alcohol withdrawal

A

-Benzodiazepines
-Phenytoin for seizures
-Electrolytes
-Alpha2-adrenergic partial agonists (clonidine, guanfacine)

34
Q

Why are alpha2-adrenergic partial agonists used for the treatment of alcohol withdrawal?

A

-Alcohol desensitizes alpha2-ARs
-Withdrawal increases NE responses

35
Q

What are examples of cues that can trigger relapse?

A

-Glass of alcohol
-Favorite bar
-Mood (stress, anxiety, depression)

36
Q

What are the three FDA approved treatments for alcoholism?

A

-Disulfiram (antabuse)
-Acamprosate (Campral)
-Naltrexone (Revia)

37
Q

Disulfiram mechanism of action

A

Aldehyde dehydrogenase inhibitor

38
Q

Disulfiram side effects

A

-Flushing
-Throbbing
-Headache
-Nausea and vomiting
-Sweating
-Hypotension
-Confusion

39
Q

What is an important counseling point regarding disulfiram?

A

Patients should be alcohol-free for 24 hours before initiating therapy

40
Q

Acamprosate mechanism of action

A

-NMDA receptor antagonist/GABA agonist
-Reduced relapse and prolonged abstinence

41
Q

Naltrexone mechanism of action

A

-Opioid receptor antagonist
-Prevents relapse and people who do relapse are in better control

42
Q

What population of patients responds better to naltrexone?

A

Patients with a mutation in the alanine118glycine gene

43
Q

Three important off-label drugs used for the treatment of alcoholism

A

-Topiramate (Topamax)
-Baclofen
-Varenicline (Chantix)

44
Q

Topiramate clinical pearls

A

-Inhibits glutamate signaling, enhances GABA signaling
-Similar in mechanism to Acamprosate
-Approved for epilepsy and migraine
-Encouraging results in two trials for alcoholism

45
Q

Baclofen clinical pearls

A

-Stimulates GABAb receptors
-Approved for treating spasticity
-Reduces anxiety and craving
-High doses reduced drinking in several small trials for alcoholism
-Not better than placebo in double blind trials

46
Q

Varenicline clinical pearls

A

-Nicotinic acetylcholine receptor partial agonist
-Approved for smoking cessation
-Human tests for alcoholism underway

Therapeutics III (42 decks)

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