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pharm III exam 1 > alcohol > Flashcards

alcohol Flashcards

1
Q

alcohol (ethanol and methanol) are metabolized by what 3 things

A
  • ADH: alcohol dehydrogenase
  • MEOS
  • CYP2E1
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2
Q

alcohol metabolism follows what order kinetics? Is rate dependent on concentration?

A
  • zero order
    • 10 g/ hr
  • rate is independent of concentration
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3
Q

describe the pathway of metabolism of alcohol

A
  • Alcohol (ethanol and methanol) is metabolized in the GI tract and liver by alcohol dehydrogenase (ADH) to acetaldehyde.
  • Acetaldehyde is oxidized by aldehyde dehydrogenase to acetic acid.
    • Oxidation requires a cofactor, NAD+
  • Since the available NAD+ is used for alcohol metabolism, there is less available for other enzymes requiring NAD+
    • Lactate increases, the TCA cycle is inhibited, and acetyl-CoA accumulates.
    • This supports fatty acid synthesis, storage and accumulation of triglycerides, formation of ketones and contributes to lactic acidosis.
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4
Q

chronic consumption of alcohol induces

A
  • Microsomal-ethanol oxidizing system (MEOS) (CYP450s)
  • CYP2E1
    • thus increasing metabolism. Increased metabolism may account for the greater tolerance of chronic drinkers
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5
Q

chronic consumption of alcohol induces CYP2E1, this increases toxicity to what drug

A

acetaminophen

  • therapeutic amounts of acetaminophen can cause hepatotoxicity in alcoholics, increasing conversion of acetaminophen to a toxic metabolite
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6
Q

Aldehyde dehydrogenase deficiency is commonly seen in what patient population? What is the effect?

A
  • acetaldehyde can accumulate in people with a mutation in ADH, especially those of Asian descent, leading to facial flushing, headache and nausea when alcohol is consumed.
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7
Q

do women or men have lower levels of ADH

A

women

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8
Q

MOA of Disulfiram

A

acts by inhibiting aldehyde dehydrogenase, producing very unpleasant and possibly dangerous effects with alcohol

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9
Q

MOA of Fomepizole

A

inhibits alcohol dehydrogenase

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10
Q

Tolerance in chronic drinkers is due to down regulation of receptors and up-regulation of receptors. What does this lead to when a chronic drinker stops drinking?

A
  1. GABA
  2. NMDA
  3. severe withdrawl
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11
Q

In chronic alcoholic drinkers, cross tolerance is seen with

A
  • barbiturates
  • benzodiazepines
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12
Q

Alcohol has what effect on CNS

A

CNS depressant

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13
Q

alcohol binds to what receptor? Binding increases influx of . What is the overall effect?

A
  1. GABAA receptor
  2. increases Cl- influx
  3. enhance inhibitory GABA transmission
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14
Q

Alcohol inhibits the effect of glutamate on the . These receptors are involved in learning and memory, and generation of seizure activity.

A

NMDA receptor

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15
Q

Alcohol increases in the mesolimbic pathway

A

dopamine

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16
Q

What are the effects of alcohol on the CNS at low concentrations and at increased doses

A
  • low concentration: alcohol may have some stimulant-like effect. It inhibits inhibitory pathways (disinhibition). Memory, concentration, and rational thought are affected. Confidence, mood
  • Increased dose: inhibit excitatory pathways -> motor function and judgment impaired, speech clurs, ataxia
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17
Q

anterograde amnesia (blackouts) occur due to blockage of what receptors

A

NMDA receptors

18
Q

effects of alcohol on smooth muscle

A
  • Ethanol is a vasodilator, and large amounts can cause hypothermia due to vasodilation
  • Ethanol also relaxes the uterus, and has been used intravenously to prevent premature labor.
19
Q

effects of alcohol on the heart

A

depression of myocardial activity

20
Q

effects of alcohol on the kidney

A
  • decreases antidiuretic hormone thus producing a diuretic effect
21
Q

Treatment of severe intoxication includes what two main goals

A
  • management of respiratory depression
  • preventing aspiration of vomitus.
22
Q

hangovers are due to

A
  • buildup of acetaldehyde
  • dehydration
  • withdrawal
23
Q

What medications can be given if seizures occur during acute alcohol toxicity

A
  • Lorazepam (ativan): benzodiazepine
  • Phenytoin (dilantin): anticonvulsant
24
Q

Lorazepam (ativan) falls in what drug class

A

benzodiazapine

25
Q

what is the most common medical complication from chronic alcohol abuse

A

liver disease

  • fatty liver -> fibrosis -> cirrhosis
26
Q

chronic alcohol abuse causes malnutrition due to deficiencies in

A
  • folate
  • thiamine
27
Q

wernicke-Korsakoff syndrome

A
  • paralysis of eye muscles, ataxia, confusion, coma and death
    • Associated with thiamine deficiency but vary rare in absence of alcoholism
28
Q

Korsakoff’s psychosis

A

chronic disabling memory loss associated with chronic alcohol abuse

29
Q

effects of chronic alcohol abuse on cardiovascular system

A
  • cardiomyopathy: due to direct toxic effect of acetylaldehyde
  • arrhythmias
  • htn
30
Q

MOA of Naltrexone

A
  • opioid receptor antagonist
  • blocks ability of alcohol to stimulate the reward pathway
  • reduces craving
31
Q

MOA of Acamprosate

A
  • structural analog of GABA
  • restores normal balance of GABA and glutamate
    • ​decreases craving and likelihood of relapse
32
Q

Acamprosate is excreted by

A
  • kidneys
33
Q

adverse effects of Naltrexone

A
  • liver damage
  • CI: liver failure
34
Q

Chlordiazepoxide (Librium®) is used in alcohol withdrawal to

A
  • Used to prevent seizures and DTs
  • tapers the withdrawal symptoms
35
Q

Lorazepam is used in alcohol withdrawal to

A
  • used to treat seizures
36
Q

Use of Diazepam (Valium®) in alcohol withdrawal

A
  • Used to prevent seizures and DTs
  • tapers the withdrawal symptoms
37
Q

primary symptoms of methanol poisoning

A
  • visual disturbances “like being in a snowstorm”
  • metabolic acidosis
38
Q

methanol is metabolized by alcohol dehydrogenase to and

A
  • aldehydes (toxic)
  • oxalates
39
Q

MOA of Fomepizole (Antizol®)

A

alcohol dehydrogenase inhibitor that decreases the conversion of methanol and ethylene glycol to aldehydes

40
Q

use of Fomepizole (Antizol®)

A

methanol poisoning

pharm III exam 1 (11 decks)

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