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MT 6314 2nd Shift > 8.2 Substance of Abuse > Flashcards

8.2 Substance of Abuse Flashcards

1
Q

Generalities:

● Water soluble
● Rapidly absorbed (GI Tract)
● Primary form of Alcohol
● Rapid distribution (tissue)
● Volume of Distribution: 0.5-0.7 L/kg

A

Ethanol

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2
Q

What is the peak blood alcohol concentration in fasting state?

A

30 minutes

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3
Q

What is the peak blood alcohol concentration with food?

A

Delayed
(slow gastric emptying)

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4
Q

Metabolism of Alcohol:

What is the pathway of alcohol dehydrogenase pathway (primary)?

A
  • ADH
  • Located in liver, brain, stomach
  • Rate of metabolism
  • Vulnerability to alcohol-abuse disease
  • Occurs in more in the stomach in men
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5
Q

Metabolism of Alcohol:

What is the pathway of Microsomal Ethanol-Oxidizing System (MEOS)?

A
  • NADPH (cytochrome P450 enzyme)
  • ABL: >100 mg/dL
  • Chronic alcohol consumption (increases ethanol metabolism and clearance)
  • More toxic byproducts
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6
Q

True or False:

In acetaldehyde metabolism, much of the acetaldehyde formed is catalyzed by aldehyde dehydrogenase (ALDH).

A

True

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7
Q

What is the product of the reaction of acetaldehyde dehydrogenase?

A

Acetate

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8
Q

Acetaldehyde Metabolism:

This is used to deter drinking by patients with alcohol dependence.

A

Disulfiram

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9
Q

Acetaldehyde metabolism:

Ethanol + Disulfiram = ?

A
  • increases acetaldehyde = unpleasant reaction
  • facial flushing, nausea, vomiting, dizziness, headache
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10
Q

Acetaldehyde metabolism:

What are the other drugs that inhibit ALDH?

A
  • Metronidazole
  • Cefotetan
  • Trimethoprim
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11
Q

Acetaldehyde metabolism:

Some people of East Asian descent, have genetic deficiency of ALDH where they develop high blood acetaldehyde concentration and strongly protective against alcohol-use disorders.

A

Asian flush

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12
Q

What are the acute alcohol consumption in CNS?

A
  • Sedation, anxiety relief
  • High concentration: intoxidation or drunkenness
  • High blood conc: coma, respiratory depression, death
  • Signaling molecules effects: inc. GABA, decreased NMDA, adenylyl cyclase, PLc, ion channels
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13
Q

What are the acute aclohol consumption in the heart?

A
  • Decreased myocardial contractility
  • > 100 mgdL
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14
Q

What are the acute alcohol consumption in the smooth muscle?

A
  • Vasodilator
  • Hypothermia (marked in cold environments)
  • Fibanserin: hypotensive effects, orthostatic hypotension, syncope
  • Uterus relaxation
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15
Q

Clinical effects of blood alcohol concentration (BAC):

50-100 mg/dL

A

Sedation, subjective “high”, slower reaction times

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16
Q

Clinical effects of blood alcohol concentration (BAC):

100-200 mg/dL

A

Impaired motor function, slurred speech, ataxia

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17
Q

Clinical effects of blood alcohol concentration (BAC):

200-300 mg/dL

A

Emesis, stupor

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18
Q

Clinical effects of blood alcohol concentration (BAC):

300-400 mg/dL

A

Coma

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19
Q

Clinical effects of blood alcohol concentration (BAC):

500 mg/dL

>400 mg/dL

A

Respiratory depression, death

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20
Q

What is the tolerance, dependence in the chronic alcohol consumption?

A
  • CNS adaptation and increase rate of ethanol metabolism
  • Cross tolerance to sedative-hyptonic drugs (GABA)
  • Psychological and physical dependence
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21
Q

What are the chronic alcohol consumption in the liver?

A
  • Liver disease
  • Reduced gluconeogenesis -> hypoglycemia
  • Reversible fatty liver -> hepatitis, cirrhosis, liver failure
  • Hepatic dysfunction (sever in women)
  • Loss of function
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22
Q

What are the chronic alcohol consumption in the gastrointestinal system?

A
  • Irritation, inflammation, bleeding, and scarring absorption defects
  • Nutritional deficiencies
  • Increased risk of pancreatitis
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23
Q

What are the chronic alcohol consumption in the CNS?

A
  • Peripheral neuropathy
  • Wernicke-Korsakoff syndrome: thiamine deficiency
  • Withdrawal symptoms (delirium tremens)
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24
Q

What are the acute alcohol consumption in the endocrine system and electrolyte balance?

A
  • Gynecomastia
  • Testicular atrophy
  • Disorders of fluid and electrolyte balance
  • Alteration of whole body potassium
  • Severe secondary aldosteronism
  • Hypoglycemia: hepatic gluconeogenesis
  • Cortisol, GH: fluid and electrolyte imb
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25
Q

What are the chronic alcohol consumption in the cardiovascular system?

A
  • Hypertension
  • Anemia
  • Dilated cardiomyopathy
  • Arrhythmia (binge)
  • Increase HDL (moderate)
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26
Q

What are the acute alcohol consumption in the immune system in the lungs?

A
  • Macrophage
  • Chemotaxis of granulocytes
  • Reduced number of T cells
27
Q

What are the acute alcohol consumption in the immune system in the liver?

A
  • Innate immune system (Kupffer cells, hepatic stellate)
  • Increase cytokine prod
28
Q

What are the increased risks of cancer in acute alcohol consumption?

A
  • Increased P450 activity = damaged DNA
  • Cancer mouth, pharynx, larynx, esophagus, liver
  • Small risk of breast cancer
  • Changes in folate metabolism and growth-promoting effects of chronic inflammation
29
Q

What are the fetal alcohol syndrome in chronic alcohol consumption?

A
  • Mental retardation
  • Growth deficiency
  • Microencephaly
  • Underdevelopment of midface region
  • Congenital heart defect
30
Q

Alcohol drug interaction:

  • Ethanol induction of Hepatic P450 enzyme
  • Increase hepatoxicity risk
  • Increase P450 mediated conversion: reactive hepatotoxic metabolites
A

Acetaminophen

31
Q

Alcohol drug interaction:

  • Inhibit metabolism of drugs
  • Decreased enzyme activity
  • Decreased liver blood flow
A

Phenothiazines, TCA, Sedative-hypnotics
+Acute alcohol use

32
Q

Alcohol drug interactions:

Addictive CNS depression

A

Sedative-hypnotics

33
Q

Alcohol drug interaction:

Potentiates effects of many non-sedative drugs

A

Vasodilators/Oral Hypoglycemic agents

34
Q

True or False:

In managing acute alcohol intoxication, it should prevent respiratory depression and asipiration of vomitus.

A

True

35
Q

In managing acute alcohol intoxication, what is considered fatal in blood alcohol concentration?

A

> 400 mg/dL

36
Q

What is needed to manage hypoglycemia and ketoacidosis in acute alcohol intoxication?

A

Glucose

37
Q

What is needed as prophylaxis against Wernicke-Korsakoff syndrome?

A

Thiamine and Vit B1

38
Q

True or False:

In managing alcohol withdrawal, the discontinuance would lead to insomnia, tremor, anxiety, delirium and delirium tremens.

A

True

39
Q

What are the long-acting (tapering effect) sedative-hypnotic drug replaced for alcohol?

A
  • Chlordiazepoxide
  • Diazepam

Both are benzodiazepines.

40
Q

What is are the short-acting (convert to water soluble) sedative-hypnotic drug replaced for alcohol?

A

Lorazepam and Oxazepam

Both are benzodiazepines.

41
Q

Determine what drug in treating alcoholism:

  • Long-acting opioid antagonist, blocks μ-opioid receptors
  • Reduces the rate of relapse to either drinking or alcohol dependence
  • Reduces craving for alcohol, especially with high adherence
  • Dose-dependent hepatotoxicity, used with caution if with abnormal serum aminotransferase activity
  • Not given with disulfiram to avoid hepatotoxicity
A

Naltrexone

42
Q

Determine what drug in treating alcoholism:

  • Molecular effects including actions on GABA, glutamate, serotonergic noradrenergic, and dopaminergic receptors
  • Weak NMDA-receptor antagonist and a GABAA-receptor activator
  • Widely distributed and is eliminated renally
  • Does not appear to participate in drug-drug interactions
  • Most common adverse effects are gastrointestinal
  • Should not be given to patients with severe renal impairment
A

Acamprosate

43
Q

Determine what drug in treating alcoholism:

  • Inhibits ALDH, acetaldehyde accumulate
  • Flushing, throbbing headache, nausea, vomiting, sweating, hypotension, and confusion occur effects may last 30 minutes to several hours
  • Rapidly and completely absorbed from the gastrointestinal tract
  • Slow elimination, and action may persist for several days
  • Inhibits the metabolism of many other therapeutic agents
  • Inhibits the metabolism of: Phenytoin, oral anticoagulants, and isoniazid
  • Should not be administered with medications that contain alcohol
  • Can cause small increases in hepatic transaminases
A

Disulfiram

44
Q

Determine what drug in treating alcoholism:

  • Used in industrial production of synthetic organic compounds and as a constituent of many commercial solvents, also in windshield-washing products
  • Poisonings from accidental ingestion
  • Visual dysfunction, GI distress, shortness of breath, loss of consciousness, and coma
  • Absorbed through the skin, respiratory or GI tract and distributed in body water
  • Oxidized to formaldehyde, formic acid, and CO2
  • Susceptibility of humans to methanol toxicity is due to metabolism to formate and formaldehyde
A

Methanol/methyl alcohol/wood alcohol

45
Q

Determine what drug in treating alcoholism:

Alcohol dehydrogenase inhibitor

A

Fomepizole

46
Q

Determine what drug in treating alcoholism:

higher affinity than methanol for alcohol dehydrogenase saturation reduces formate production

A

Intravenous ethanol

47
Q

Determine what drug in treating alcoholism:

  • Used as heat exchangers, in antifreeze formulations, and as industrial solvents
  • Young children and animals are attracted by the sweet taste
  • Ingested intentionally as an ethanol substitute or in attempted suicide
  • Relatively harmless, eliminated by the kidney, metabolized to toxic aldehydes and oxalate
  • Fomepizole, ethanol, hemodialysis
A

Ethylene glycol

48
Q

What are the effects of nicotine & caffeine?

A
  • High incidence of cardiovascular, respiratory, and neoplastic disease with tobacco smoking
  • May cause addiction and dependence
49
Q

What are the acute toxicity of nicotine & caffeine?

A
  • excessive CNS stimulation with tremor
  • insomnia
  • nervousness; cardiac stimulation and arrhythmias
50
Q

What are the toxicity in nicotine?

A

Respiratory paralysis

51
Q

True or False:

Ingestion of nicotine gum, nicotine patches or vaping solutions has severe nicotine toxicity in small children.

A

True

52
Q

Identify if Nicotine or Caffeine:

Selective agonist of the acetylcholine receptor.

A

Nicotine

53
Q

Identify if Nicotine or Caffeine:

The withdrawal is mild, involved irritability, anxiety and sleep problems.

A

Nicotine

54
Q

Identify if Nicotine or Caffeine:

Among the most addictive drugs, relapse after attempted cessation is common.

A

Nicotine

55
Q

Identify if Nicotine or Caffeine:

Member of the methylxanthine family, and has as the most marked central nervous system effects.

A

Caffeine

56
Q

Identify if Nicotine or Caffeine:

Cause mild cortical arousal with increased alertness and deferral of fatigue, and has positive chronotropic and inotropic effects on the heart.

A

Caffeine

57
Q

Identify if Nicotine and Caffeine:

The withdrawal causes lethargy, irritability, and headache.

A

Caffeine

58
Q

Identify if Nicotine or Caffeine:

Antidote: Esmolol (short-acting β blocker).

A

Caffeine

59
Q

Identify if Nicotine or Caffeine:

Intake during nursing is moderately safe.

A

Caffeine

60
Q

Identify if Nicotine or Caffeine:

Quinolone antibiotics inhibit its metabolism.

A

Caffeine

61
Q

Identify drugs when treating nicotine:

A partial agonist action at α4β2 nicotinic receptors and may impair the capacity to drive, associated with suicidal ideation.

A

Varenicline

62
Q

Identify drugs when treating nicotine:

An antidepressant is approved for nicotine cessation therapy. Most effective when combined with behavioral therapies.

A

Bupropion

63
Q

Identify drugs when treating nicotine:

Agonist at cannabinoid receptors, used off-label in smoking cessation.

A

Rimonabant

MT 6314 2nd Shift (8 decks)

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