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2nd Year 2nd Term > MT6314 SUBSTANCE OF ABUSE > Flashcards

MT6314 SUBSTANCE OF ABUSE Flashcards

1
Q

The primary kind of alcohol which is a substance of abuse is?

A

ethyl

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2
Q

Occupies an important place in history of mankind

A

Alcohol

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3
Q

Main alcohol staple of western countries in the 19th century?

A

Beer and wine

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4
Q

Alcohol is known to be associated with?

A

acute and chronic
illnesses

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5
Q

Moderate amount of alcohol relieves and provides what?

A

relieves anxiety and provides feeling of euphoria

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6
Q

The most commonly abused drug in the world

A

Alcohol

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7
Q

continue consumption despite
suffering consequences

A

Alcohol abuse

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8
Q

inability to control drinking, devoting much time to getting and using alcohol, or recovering from its effects

A

Alcohol dependence

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9
Q

use disorders are complex; has genetic and environmental factors

A

Alcohol

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10
Q

Is ethanol water soluble?

A

Yes

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11
Q

Where does ethanol absorb rapidly in the body?

A

gastrointestinal tract

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12
Q

In fasting state, peak blood alcohol concentrations are reached within how long?

A

30mins

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13
Q

What delays alcohol absorption by slowing gastric emptying?

A

Food

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14
Q

Alcohol distribution: rapid or slow?

A

Rapid

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15
Q

Volume of distribution for ethanol approximates?

A

total body water (0.5–0.7 L/kg)

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16
Q

T or F: Women have a higher peak concentration than men

A

T

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17
Q

Why do women have a higher peak concentration than men?

A

Women have a lower total body water content and differences in first-pass metabolism

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18
Q

In CNS, concentration of ethanol rises (slowly/quickly)

A

Quickly

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19
Q

Why in the CNS, concentration of ethanol rises quickly?

A

Brain receives a large proportion of total blood flow and ethanol readily crosses biologic membranes

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20
Q

> 90% of alcohol is oxidized in? And the remainder in where?

A

the liver

remainder excreted through the lungs and in the urine

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21
Q

Excretion by the lungs can be quantified with?

A

breath alcohol tests

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22
Q

Alcohol Oxidation follows what order of kinetics?

A

zero-order kinetics

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23
Q

Typical adult can metabolize how many grams of alcohol per hour?

A

7–10 g (150–220 mmol)

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24
Q

Primary pathway for alcohol metabolism

A

Alcohol Dehydrogenase Pathway

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25
Q

Where is Alcohol Dehydrogenase Pathway mainly located?

A

Liver (main), brain, stomach

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26
Q

What about the alcohol dehydrogenase pathway affects the rate of ethanol metabolism and alters vulnerability to alcohol-abuse
disorders?

A

considerable genetic variation in ADH enzymes

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27
Q

Is metabolism by ADH greater in men or women? and why?

A

Men bec. of sex-related differences in
blood alcohol concentrations

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28
Q

The Microsomal Ethanol-Oxidizing System (MEOS) uses ____ and consists of _____

A

uses NADPH, consists
primarily of cytochrome P450 enzyme group

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29
Q

When is MEOS activity induced?

A

during chronic alcohol
consumption, also when blood levels are >100mg/dL

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30
Q

What happens in chronic alcohol consumption?

A

significant increases in ethanol metabolism and the clearance of other drugs eliminated by the cytochrome P450s that constitute the MEOS system

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31
Q

Much of the acetaldehyde formed is oxidized in the liver in a reaction is catalyzed by?

A

Aldehyde dehydrogenase (ALDH)

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32
Q

What is the product of Acetaldehyde Metabolism?

A

acetate

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33
Q

used to deter drinking by patients with alcohol dependence

A

Disulfiram

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34
Q

Acetaldehyde accumulates and causes an unpleasant reaction of facial flushing, nausea, vomiting, dizziness, and headache

A

Disulfiram + Ethanol

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35
Q

Examples of drugs that inhibit ALDH? What od these drugs do?

A

metronidazole, cefotetan, trimethoprim

Cause a disulfiram-like reaction if combined with ethanol

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36
Q

People of what descent have a genetic deficiency of ALDH?

A

East Asian descent

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37
Q

What happens to East Asians since they have deficiency in ALDH?

A

Consuming alcohol, they develop high blood acetaldehyde concentrations and experience a reaction similar to that seen with the combination of disulfiram and ethanol

Asian flush

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38
Q

What effect does alcohol have on the CNS?

A

sedation, relief of anxiety

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39
Q

At higher concentrations of alcohol, what does it cause to the CNS?

A

ataxia, impaired judgment, and
disinhibited behavior

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40
Q

Additive CNS depression occurs with concomitant ingestion of?

A

Ethanol and a variety of CNS depressants such as sedative-hypnotics, opioid agonists, and drugs that block muscarinic and H1 histamine receptors.

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41
Q

Ethanol appears to modulate the function of?

A

Signaling molecules such as the action of GABA at GABAA receptors, inhibits the ability of glutamate to activate NMDA receptors and modifying the activities of adenylyl cyclase, phospholipase C, and ion channels

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42
Q

What BAC levels leads to sedation and depression of myocardial contractility?

A

50-100: sedation
>100: depression of myocardial contractility

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43
Q

What BAC levels leads to emesis and stupor?

A

200-300

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44
Q

What BAC levels leads to coma?

A

300-400

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45
Q

What BAC levels leads to respiratory depression and death?

A

> 400

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46
Q

What BAC levels leads to impaired motor function, slurred speech, ataxia?

A

100-200

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47
Q

Ethanol, in relation to smooth muscles, is also a?

A

vasodilator

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48
Q

In severe alcohol overdose, what happens to the Smooth muscles?

A

hypothermia Bec. of vasodilation

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49
Q

What augments the hypotensive effects of ethanol,
may cause severe orthostatic hypotension and syncope?

A

Flibanserin

50
Q

T or F: Ethanol also vasodilator the uterus

A

F, it relaxes it

51
Q

How does alcohol cause tissue damage?

A

Oxidative stress with depletion of glutathione, damage to mitochondria, growth factor
deregulation, potentiation of cytokine-induced injury

52
Q

What kind of tolerance facilitates GABA activity?

A

Cross-tolerance to sedative-hypnotic drugs

53
Q

What kind of dependence is seen in chronic alcohol consumption?

A

Psychological and physical

54
Q

Most common medical complication that comes with chronic alcohol consumption?

A

Liver disease

55
Q

Reduced gluconeogenesis leads to?

A

Hypoglycemia

56
Q

Progressive loss of liver function, with reversible fatty liver leads to?

A

irreversible hepatitis, cirrhosis, and liver failure

57
Q

In both sexes infected with hepatitis B or C, is hepatic dysfunction more severe in men or women?

A

Women

58
Q

Consequences of chronic alcohol consumption on the GI tract?

A

Irritation, inflammation, bleeding, and scarring of the gut wall

absorption defects and exacerbation of nutritional
deficiencies

increases the risk of pancreatitis

59
Q

Consequences of chronic alcohol consumption on the CNS?

A

Peripheral neuropathy

Wernicke- Korsakoff
syndrome

60
Q

What causes Wernicke- Korsakoff syndrome? and what is it characterized by?

A

Thiamine deficiency, along with alcohol abuse

characterized by ataxia, confusion, and paralysis of the
extraocular muscles

61
Q

How to treat Wernicke- Korsakoff syndrome? This treatment is essential to prevent?

A

Treatment with parenteral thiamine is essential to prevent Korsakoff’s psychosis: a permanent memory disorder

62
Q

Alcohol withdrawal symptoms with forced quitting/reduction causes?

A

hyperexcitability in mild cases; seizures, toxic psychosis, and delirium tremens in severe ones

63
Q

Effects of chronic alcohol consumption to the endocrine system and electrolyte balance?

A

Gynecomastia and testicular atrophy

Ascites, edema, and effusions

Alterations of whole body potassium

Severe secondary aldosteronism

Hypoglycemia

64
Q

Effects of chronic alcohol consumption to the cardiovascular system?

A

Hypertension, anemia, and dilated
cardiomyopathy

Binge drinking = arrhythmia

Modest quantities = HDL goes up

65
Q

Effects of chronic alcohol consumption to the immune system?

A

Some immune functions inhibited, some triggered

Lungs: suppressed alveolar macrophage function, inhibition of chemotaxis of
granulocytes, reduced T cells, increases mortality & morbidity of pneumonia

Liver: enhanced function of cells in immune system, increased cytokine production

66
Q

Chronic alcohol use also leads to increased risk of what cancers?

A

Cancer of the mouth, pharynx, larynx, esophagus, and liver and small increase of breast cancer in women

67
Q

What species produced by increased cytochrome P450
activity can damage DNA?

A

Acetaldehyde and reactive oxygen

68
Q

What consequence of chronic alcohol consumption has teratogenic effects?

A

Fetal alcohol syndrome

69
Q

Most commonly stem from alcohol-induced increases of drug-metabolizing enzymes

Prolonged intake without liver damage can enhance the biotransformation of other drugs

A

ALCOHOL-DRUG INTERACTIONS

70
Q

Ethanol-mediated induction of hepatic cytochrome P450 enzymes is particularly important with regard to?

A

acetaminophen
(Paracetamol)

71
Q

Chronic or acute alcohol consumption can inhibit metabolism of other drugs - decreased enzyme activity or decreased liver blood flow?

A

Acute

72
Q

Examples of drugs whose metabolisms are inhibited with acute alcohol use?

A

Phenothiazines, tricyclic antidepressants, and sedative- hypnotic
drugs

73
Q

Occurs when alcohol is combined with other CNS depressants, particularly sedative-hypnotics

A

Additive CNS depression

74
Q

What kind of drugs can be used in the management of alcohol withdrawal syndrome?

A

Long-acting sedative-hypnotic drug replaced for alcohol (Benzodiazepines preferred- chlordiazepoxide, diazepam)

Shorter-acting benzodiazepines- lorazepam and oxazepam

75
Q

Useful in alcoholic patients with liver disease

A

lorazepam and oxazepam

76
Q

Built in tapering effect where active metabolites may accumulate

A

Long-acting sedative-hypnotic drug replaced for alcohol

77
Q

Main DRUG TREATMENTS OF ALCOHOLISM

A

Naltrexone
Acamprosate
Disulfiram

78
Q

Nicotine & Caffeine effects (common)

A

cardiovascular, respiratory, and neoplastic disease with smoking

addiction and dependence

79
Q

Causes respiratory paralysis

A

Nicotine

80
Q

Seen in small children who ingest nicotine gum, nicotine patches or vaping solutions

A

Severe nicotine toxicity

81
Q

Characterized by excessive CNS stimulation with tremor, insomnia, and nervousness; cardiac stimulation and arrhythmias

A

Acute toxicity for both nicotine and caffeine

82
Q

Nicotine is the selective agonist of?

A

nicotinic acetylcholine receptor

83
Q

Nicotine is slowly or quickly absorbed?

A

Slowly

84
Q

Partial agonist action at α4β2 nicotinic receptors

A

Varenicline

85
Q

Effects of varenicline?

A

may impair the capacity to drive, associated with suicidal ideation

86
Q

antidepressant is approved for nicotine cessation therapy

A

Bupropion

87
Q

When is Bupropion most effective?

A

when combined with behavioral therapies

88
Q

agonist at cannabinoid receptors, used off-label in smoking cessation

A

Rimonabant

89
Q

Caffeine is a member of what family?

A

methylxanthine

90
Q

Effects of caffeine on the heart?

A

Has positive chronotropic and inotropic effects on the heart

91
Q

Antidote to caffeine withdrawal?

A

Esmolol a short-acting β blocker

92
Q

Inhibits caffeine metabolism

A

Quinolone

93
Q

What treatment of alcoholism: long acting opioid antagonist, blocks u-opioid receptors

A

Naltrexone

94
Q

What treatment of alcoholism: Can cause dose-dependent hepatotoxicity, used with caution if with abnormal serum aminotransferase activity

A

Naltrexone

95
Q

T or F: Naltrexone is usually taken with disulfiram

A

F, if taken together, will result in hepatotoxicity

96
Q

What treatment for alcoholism: Has actions on GABA, glutamate, serotonergic, noradrenergic, and dopaminergic receptors

A

Acamprosate

97
Q

What treatment for alcoholism: A weak NMDA-receptor antagonist and a GABAA-receptor activator.

A

Acamprosate

98
Q

What treatment for alcoholism: Should not be given to patients with severe renal impairment

A

Acamprosate

99
Q

What treatment for alcoholism: Inhibits aldehyde dehydrogenase, acetaldehyde accumulates

A

Disulfiram

100
Q

Disulfiram inhibits the metabolism of?

A

Phenytoin
Oral anticoagulants
Isoniazid

101
Q

What type of alcohol: Used in industrial production of synthetic organic compounds and as a constituent of many commercial solvents, also in windshield-washing products

A

Methanol/methyl alcohol/wood alcohol

102
Q

Methanol/methyl alcohol/wood alcohol is oxidized to?

A

formaldehyde, formic acid, and CO2

103
Q

Methanol can also cause poisoning from?

A

Accidental ingestion

104
Q

Methanol is absorbed well in the?

A

Skin
Respiratory
GI

105
Q

Treatment for methanol poisoning?

A

Respiration support

106
Q

Modalities of treatment for severe methanol poisoning?

A

Suppression of metabolism by alcohol dehydrogenase to toxic products

Hemodialysis

Alkalinization

107
Q

alcohol dehydrogenase inhibitor

A

Fomepizole

108
Q

higher affinity than methanol for alcohol dehydrogenase saturation reduces formate production

A

Intravenous ethanol

109
Q

Used as heat exchangers, in antifreeze formulations, and as industrial solvents

A

Ethylene glycol

110
Q

Stages of overdose of ethylene glycol?

A

transient excitation followed by CNS depression (first few hours after ingestion)

severe metabolic acidosis (after 4-12 hours)

delayed renal insufficiency

111
Q

Treatment to ethylene glycol overdose?

A

fomepizole, ethanol, and hemodialysis

112
Q

Alcohol has an additive sedative effect with?

A

Sedative-hypnotics

113
Q

Alcohol additive vasodilator effect with?

A

Hypoglycemic agents

114
Q

Alcohol additive anti-platelet action with?

A

Aspirin

115
Q

Ethylene glycol toxicity is retarded by?

A

Fomepizole or IV ethanol

116
Q

Alcohol-drug interactions have the induction of?

A

SER

117
Q

What treatment for alcohol: NMDA antagonist

A

Acamprosate

118
Q

What treatment for alcohol: Opioid antagonist

A

Naltrexone

119
Q

What treatment for alcohol: 5-HT3 antagonist

A

Ondansetron

120
Q

What treatment for alcohol: Aldehyde dehydrogenase antagonist

A

Disulfiram

121
Q

What treatment for alcohol: Mainly targets CNS NTA system

A

Naltrexone

2nd Year 2nd Term (38 decks)

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