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CMOD Exam 2 > Alcohol and Smoking > Flashcards

Alcohol and Smoking Flashcards

1
Q

What is the antidote for Ethanol?

A

Disulfram

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2
Q

What is the antidote for Methanol?

A

Fomepizole

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3
Q

What is the antidote for Ethylene Glycol?

A

Ethanol

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4
Q

What are the drugs for ethanol withdrawal?

A

Diazepam and Thiamine (Vit B1)

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5
Q

What are the drugs for chronic alcoholics?

A

Naltrexone and Acamprosate

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6
Q

Describe the breakdown of ethanol:

A

It is first broken down to acetaldehyde via alcohol dehydrogenase. Acetaldehyde is then broken down to acetate via aldehyde dehydrogenase.

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7
Q

Ethanol Metabolism

A
  • Zero Order

- Very little CYP activity (some enzyme induction may occur on chronic alcoholism)

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8
Q

Disulfram

A

Used to encourage the abstinence from alcohol by preventing the metabolism of acetaldehyde, leading to its accumulation. This gives rise to a feeling of nausea and a flushing reaction of the skin.
Dose= 125-500mg/day

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9
Q

Is the activity of aldehyde dehydrogenase the same for everybody?

A

NO. There is great diversity in the functionality of this enzyme due to a number of single nucleotide polymorphic changes. An example of this is the “Asian Flush”, which occurs with even minimal EtOH consumption.

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10
Q

Can acetaldehyde be a positive reinforce?

A

YES. Research indicates that it has effects in the CNS pleasure center in the VTA. When appropriate levels are reached, reinforcement of alcohol seeking behavior may occur.
**Possible reason for high levels of alcoholism in certain populations, such as Native Americans.

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11
Q

What CYP is ethanol an important inducer of?

A

CYP2E1

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12
Q

What is significant about its induction of CYP2E1?

A

Normally, Acetaminophen is broken down into NAPQI cy CYP2E1. NAPQI is a highly toxic compound but is usually rapidly conjugated and detoxified. In the case of chronic alcoholics, the metabolism is so high that there is a dramatic increase in NAPQI. The supply of the enzyme that breaks it down is depleted so concentration builds up and leads to Tylenol toxicity.

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13
Q

What is the antidote for Tylenol toxicity?

A

Give N-Acetylcysteine, which acts as a fresh conjugate substrate for the build up of NAPQI to convert it to Cysteine and Mercaptopuric Acid.

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14
Q

Does ethanol have a specific receptor in the brain?

A

No. Rather, it modulates key pathways, including a reinforcement of the inhibitory actions of GABA and inhibition of the stimulatory actions of the glutamate system

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15
Q

What are the factors affecting BAC?

A
  1. Volume Distribution: more weight= larger total volume of distribution= lower BAL
  2. BMI: more body fat= smaller volume of distribution= higher BAL
  3. Female Gender: increased absorption, lower weight, higher % body fat
  4. Metbaolism: zero order
  5. Adaptation: behavioral and neural adaptation (more significant) and enzyme induction (less significant
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16
Q

Chronic Effects of EtOH

A
  1. LIVER: decreased gluconeogenesis= hypoglycemia; fatty liver= cirrhosis, hepatitis, and failure
  2. GI: bleeding and scarring= absorptive and nutritional deficiency
  3. CNS: peripheral neuropathy and Wernicke-Korsakoff syndrome (ataxia, confusion, ocular muscle paralysis)
  4. ENDOCRINE: gynecomastia and testicular atrophy
  5. OTHERS: mental sluggishness, apathy, impaired awareness, inability to concentrate, confusion, agitation, hallucinations
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17
Q

How is thiamine usually administered to alcoholics?

A

IV or IM

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18
Q

More Chronic Effects of EtOH

A
  1. CV:HTN, anemia, dilated cardiomyopathy, arrhythmias with binge drinking
  2. NEOPLASIA: GI cancer increased in alcoholics
  3. IMMUNE SYSTEM: enhanced inflammation in the liver and pancreas but reduced immune responses in other tissues
    * **Chronic Alcoholics are susceptible to infectious pneumonia
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19
Q

What is the beneficial effect of modest alcohol consumption?

A

Increased HDL which may protect against chronic heart disease

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20
Q

Fetal Alcohol Syndrome

A

Alcohol crosses the placental barrier and levels in fetal blood reflect those in maternal blood. Since the fetus is unable to metabolize the drug, especially in the first trimester when critical organogenesis is occurring, defects occur.

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21
Q

What are the characteristics of FAS?

A

Intrauterine growth retardation, microcephaly, poor coordination, midfacial underdevelopment, minor joint abnormalities, congenital heart defects, and subtle neurologic deficits

22
Q

How would you treat an intoxicated patient?

A
  1. Monitor ABC vitals
  2. Thiamine (given before dextrose)
  3. Dextrose
  4. Correct Electrolyte Issues
23
Q

How would you treat a withdrawing patient?

A
  1. BNZ Sedative (Diazepam unless there are concerns over impaired hepatic function then lorazepam is given)
  2. Thiamine
  3. Correct Electrolyte Issues
24
Q

What are some of the symptoms of a withdrawing patient?

A

Insomnia, tremor, anxiety, rarely seizure and DTs, diarrhea, arrhythmias

25
Q

Describe the Pharmacokinetic interactions of EtOH:

A

Increased teratogenicity through metabolism changes and increased absorption of with compartment

26
Q

Describe the Pharmacodynamic interactions of EtOH on the body?

A
  1. Additive CNS depression actions with drugs
  2. Increases toxicity of Acetaminophen
  3. Increased risk of bleeding with NSAIDs and anticoagulants
  4. Increased risk of hypoglycemia in diabetics n medication
27
Q

Naltrexone

A

mu opioid antagonist that is thought to decrease drinking through a decrease in feelings of with reward with alcohol and/or decrease in cravings
**Dose= 50mg/day

28
Q

Acamprosate

A

weak NMDA antagonist and activator of GABAa receptors that may decrease mild protracted abstinence syndromes with a decrease in the feelings of a “need” for alcohol

29
Q

Methanol or Ethylene Glycol Poisoning

A

Alcohol Dehydrogenase converts both of these substances into their toxic counterpart. Therefore, administration of Fomepizole, which inhibits alcohol dehydrogenase, will results in decreased converstion and ultimately increased renal elimination of the unchanged substance. Alternatively, ethanol can be administered as a competitive inhibitor.

30
Q

Nicotine

A

A highly addictive psychoactive agent that rapidly gains access to the CNS following uptake from the alveoli. It then interacts with nicotine specific receptors in the brain and gives rise to the physical dependence and many symptoms experienced by smokers during withdrawal.

31
Q

What are some of the symptoms of nicotine withdrawal?

A

depressed mood, insomnia, irritability, frustration, anger, anxiety, difficulty concentrating, restlessness, increased appetite or weight gain

32
Q

Describe the delivery of nicotine with the use of cigarettes, oral snuff, and chewing tobacco:

A

All three give a rapid increase in nicotine in the brain with longer sustainability in the non cigarette products.

33
Q

How do addictive substances work?

A

They modulate dopamine levels by one of a number of processes, including ion channel modulation and also activation of G-protein coupled receptors and by modulation of amine transporter processes.

34
Q

Describe the addictiveness of nicotine:

A

High levels of dopamine are responsible for it.
Less than cocaine.
More than alcohol or benzos.
On par with opiates.

35
Q

Describe nicotine addiction:

A

Nicotine initially acts on both the GABA receptors, which transmits an acute nicotine reward signal from the VTA to the TPP, and Dopamine receptors, which transmits an acute nicotine aversion signal from the VTA to the nucleus accumbiens. As time goes on, the GABA receptor becomes desensitized and the dopamine receptor is primarily employed. This causes the adverse feelings that stimulate the desire for more nicotine to overcome the desensitization of the GABA pathway.

36
Q

Varenicline (Chantix)

A
  • Best agent
  • Partial agonist of the a4b2 nicotinic ACh receptor that blocks the effect of additional nicotine challenge while causing release of mesolimbic dopamine
  • Most common adverse effect is nausea
  • Depression, suicidal ideation, and emotional lability have been reported
37
Q

Bupropion (Wellbutrin SR)

A
  • Less effective than Chantix but better than nicotine replacement therapy
  • NorEpi and dopamine reuptake inhibitor
  • Decreases cravings and withdrawal symptoms while interacting with pathways underlying addiction (thought to reduce depressive symptoms of nicotine withdrawal)
  • adverse events include insomnia, dry mouth and nausea
  • Suicidal ideation has been seen in patients without previous psychiatric disorders.
38
Q

Clonidine (Catapres)

A
  • Oral antihypertensive drug
  • Oral dosing or patch delivery
  • Blocks cravings, anxiety, restlessness, tension, and hunger
  • Sedative effect, therefore has potential utility for agitated, anxious ex smokers
  • Side effects include sedation, dry mouth, and dizziness
39
Q

Mecamylamine (Inversine)

A
  • Nicotine antagonist (ganglionic blocker)
  • Fallen out of favor because of the widespread actions that it has on the sympathetic and parasympathetic nervous systems.
  • Common side effects are orthostatic hypotension, fatigue, sedation, constipation, dry mouth
  • **Has best utility when used with NRT
  • **Contraindicated in coronary and renal insufficiency, glaucoma, and uremia
40
Q

Naltrexone (ReVia)

A
  • Opiate Antagonist

- Has utility in treating other forms of addiction but is not favorable in respect to smoking cessation.

41
Q

Nicotine Replacement Therapy

A
  • Levels attained are high enough to prevent withdrawal symptoms but low enough and not rapid enough to produce dependence.
  • Allows gradual tapering off of consumption
42
Q

What forms does NRT come in?

A
  • Gum, patch, lozenge are sold without prescription.

- Nasal spray and oral vapor inhaler are available via Rx.

43
Q

What form of NRT produces the most constant nicotine blood level?

A

Patch

44
Q

Nicotine Patch

A
  • 12 week course with step down titration
  • Side effects include application sites reactions, headaches, cold and flu like symptoms
  • Caution is advised on those with CV disease, diabetes, moderate hepatic impairment, ulcers, and uncontrolled hyperthyroidism
  • *Smoking on patches increases the risk of CV events
45
Q

Nicotine Gum

A

-2mg doses (no more the 24/day)
-12 week course
-Avoid eating or drinking 15 minutes prior to gum
Side effects include jaw pain and orthodontal problems
**Addiciton may be transferred to the gum

46
Q

Nicotine Inhaler Spray

A
  • Inhaler= 12 week course
  • Nasal Spray= minimum 3 month course
  • Side effects include localized irritation in mouth or nostrils, headaches, nausea, heartburn, hicups
47
Q

Which of the NRTs is the best?

A

They all produce comparable benefits. The spray/ inhaler may actualaly be best but the database for information is much smaller than that for gum and the patch.

48
Q

Are there potential harms of quitting smoking?

A

The act of quitting can have potential harmful effects for those who are quitting that are concurrently taking Rx/OTC meds. This would be most problematic during the early stages of quitting and should be monitored.

49
Q

What effects does smoking have while pregnant?

A

Produces growth restriction, preterm delivery, and stillbirth.

50
Q

How should you approach treatment of a smoking pregnant woman?

A

First try psychological intervention. Oral NRT can be considered next. There is no evidence for the safety of nonNRT smoking cessation products during pregnancy.

CMOD Exam 2 (7 decks)

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