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Behavioral Pharmacology > Ch. 10 Alcohol > Flashcards

Ch. 10 Alcohol Flashcards

1
Q

acamprosate

A

Partial antagonist at NMDA receptors used for the treatment of alcoholism; blocks glutamate increase during withdrawal

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2
Q

acetaldehyde dehydrogenase (ALDH)

A

Enzyme in the liver that metabolizes the acetaldehyde intermediate formed by alcohol oxidation into acetic acid.

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3
Q

acute tolerance

A

Rapid tolerance formed during a single administration of a drug, as is the case with alcohol. ex. several of the subjective and behavioral drug effects are greater while the blood level is increasing, than decreasing even if BAC are equal

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4
Q

alcohol dehydrogenase (ADH)

A

Enzyme in the liver and stomach that oxidizes alcohol into acetaldehyde; reduces the amount of available alcohol for absorption (first pass effect)

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5
Q

alcohol poisoning

A

Toxic effects associated with the ingestion of excess alcohol, characterized by unconsciousness, vomiting, irregular breathing, and cold, clammy skin.

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6
Q

alcoholic cirrhosis

A

Condition seen in chronic alcohol abusers caused by accumulation of acetaldehyde in the liver that kills cells, stimulates scar tissue formation, and promotes cell death as scar tissue cuts off blood supplies; irreversible but can be slowed

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7
Q

alcoholic hepatitis

A

Condition seen in chronic alcohol abusers caused by accumulation of acetaldehyde in the liver and characterized by inflammation of the liver, fever, jaundice, and pain.

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8
Q

alcoholism

A

A form of substance abuse characterized by compulsive alcohol seeking and use despite damaging social and health effects.

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9
Q

behavioral tolerance

A

The reduced effectiveness of a drug administered chronically that involves learning: either instrumental or classical conditioning.

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10
Q

binge drinking

A

Consumption of five or more alcoholic drinks within a 2-hour period.

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11
Q

blackout

A

Amnesia directly associated with heavy alcohol consumption.

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12
Q

blood alcohol concentration (BAC)

A

The amount of alcohol in a given unit of blood, usually given as a percent representing milligrams of alcohol per 100 milliliters of blood.

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13
Q

case-control method

A

Technique used to identify genes associated with a disorder by comparing the genes of unrelated affected and unaffected people to determine if those who are affected are more likely to possess a particular allele.

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14
Q

CRF1 antagonist

A

A drug that binds to CRF1 receptors and produces little or no conformational change. In the presence of a CRF agonist, the agonist effect is reduced; reduces post withdrawal escalation of alcohol use, reduced binging; prevented stress-induced relapse.

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15
Q

cross-dependence

A

Withdrawal signs occurring in a dependent individual can be terminated by administering drugs in the same class; ex. sedative hypnotics and barbiturates/ benzodiazepines

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16
Q

cross-tolerance

A

Tolerance to a specific drug can reduce the effectiveness of a another drug in the same class.

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17
Q

cytochrome P450 (CYP450)

A

Class of liver enzymes, in the microsomal enzyme group, responsible for both phase 1 and phase 2 biotransformation of psychoactive drugs; convert alcohol to acetaldehyde

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18
Q

delirium tremens

A

Severe effects of alcohol withdrawal characterized by irritability, headaches, agitation, hallucinations, and confusion.

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19
Q

denial

A

Characteristic of alcoholics who insist that alcohol is not the source of their problems.

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20
Q

detoxification

A

Procedure used to treat addicted individuals in which the drug is stopped and withdrawal symptoms are treated until the abstinence syndrome has ended; e.g. substituting a benzodiazepine to prevent withdrawal until stabilized and then gradually is reduced

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21
Q

disulfiram (Antabuse)

A

A drug used to treat alcoholism by causing the buildup of toxic metabolites producing illness after alcohol intoxication; ex. inhibits ALHD the enzyme that converts acetaldehyde to acetic acid

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22
Q

enablers

A

Friends and family members who assist an alcoholic, allowing the individual to continue to function in society without getting treatment.

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23
Q

fatty liver

A

Damaging effect of alcohol characterized by the accumulation of triglycerides inside liver cells. Liver typically metabolizes fatty acids but when alcohol is present it metabolizes that leaving the fat for storage; is reversible

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24
Q

fetal alcohol syndrome (FAS)

A

The damaging developmental effects of prenatal alcohol exposure.

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25
Q

hangover

A

Effect of heavy alcohol consumption that may be a sign of withdrawal, acute toxicity, residual acetaldehyde in the body, alcohol induced gastric irritation, rebound drop in blood sugar, excess fluid loss the previous night, toxic effects from congeners (fermentation by-products).

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26
Q

induction

A
  1. Increase in liver enzymes specific for drug metabolism in response to repeated drug use. (metabolic tolerance) 2. Process that establishes psychostimulant sensitization by activating glutamate NMDA receptors and, in some cases, D1 receptors.
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27
Q

linkage study

A

Method used to locate genes responsible for a disorder, such as alcoholism or schizophrenia, by comparing similarities in the genetic loci of families with affected members.

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28
Q

metabolic tolerance

A

Type of tolerance to a drug that is characterized by a reduced amount of drug available at the target tissue, often as a result of more-rapid drug metabolism. It is sometimes also called drug disposition tolerance.

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29
Q

microsomal ethanol oxidizing system (MEOS)

A

The cytochrome P450 enzyme CYP 2E1 that metabolizes ethanol and many other drugs; MEOS activity increases after chronic alcohol consumption; converts ethanol to acetaldehyde

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30
Q

nalmefene

A

A dual κ/μ-opioid antagonist effective in reducing lever pressing for alcohol in rodent studies, particularly in alcohol-dependent animals.

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31
Q

naltrexone

A

A μ-receptor antagonist that reduces consumption and craving in some alcoholic individuals, perhaps by reducing the positive feeling caused by alcohol.

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32
Q

nor-binaltorphimine

A

A selective κ-opioid antagonist. Because it reduces the self-administration of alcohol only in animals dependent on alcohol, a role for the κ receptor in alcohol abuse is suspected.

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33
Q

pharmacodynamic tolerance

A

Type of tolerance formed by changes in nerve cell functions in response to the continued presence of a drug.

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34
Q

pharmacotherapeutic treatment

A

Method of disease treatment that uses drugs to modify a clinical condition; includes making alcohol ingestion unpleasant and reducing its reinforcing qualities

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35
Q

physical dependence

A

Developed need for a drug, such as alcohol or opioids, by the body as a result of prolonged drug use. Termination of drug use will lead to withdrawal symptoms (abstinence).

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36
Q

psychosocial treatment programs

A

Counseling programs that involve educating the user, promoting behavioral change and alleviating problems caused by drug use.

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37
Q

tolerance

A

Decreased response to a drug as a direct result of repeated drug exposure.

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38
Q

Wernicke–Korsakoff syndrome

A

Symptom of thiamine deficiency characterized by confusion, disorientation, tremors, poor coordination, ataxia, and in later stages, short-term memory loss; progressive but can stop degeneration with massive doses of B1; cell loss in medial thalamus and mammillary bodies of hypothalamus

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39
Q

Types of alcohol

A

ethyl alcohol, methyl alcohol, isopropyl alcohol

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40
Q

Ethyl Alcohol

A

beverage; two carbon atoms, a H, and -OH

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41
Q

Methyl alcohol

A

highly toxic if consumed because it metabolizes into formic acid and formaldehyde; causes blindness, coma, death

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42
Q

Isopropyl alcohol

A

rubbing alcohol; dangerous to consume

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43
Q

How is ethyl alcohol formed?

A

fermentation—yeast cells convert each sugar molecule into two molecules of alcohol and two of carbon dioxide—continues until the concentration of alcohol is about 15%

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44
Q

Distillation

A

requires heating the fermented mixture to the point where the alcohol boils off in steam leaving some of the water behind. the alcohol vapor passes through a series of cooling tubes (still) and condenses to be collected as hard liquor

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45
Q

why do we easily feel the effects of alcohol?

A

cannot be ionized and mixes easily mixes with water, is not high in lipid solubility and is easily absorbed from the GI tract and diffused into the body

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46
Q

how is alcohol absorbed into the body?

A

10% stomach, 90% GI tract; small molecules move across membrane barriers by passive diffusion from the higher concentration on one side (GI tract) to that lower concentration on the other (blood)

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47
Q

pyloric sphincter

A

muscle that regulates the movement of material from stomach to intestine

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48
Q

what speeds up movement of material into the intestine

A

carbonation

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49
Q

how is alcohol excreted?

A

95% is metabolized by the liver before being excreted as carbon dioxide and water (urine) and 5% is excreted by the lungs

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50
Q

does the rate of alcohol metabolism vary depending on how much is in the blood?

A

no–oxidation is constant over time; average rate is about 1-1.5 oz of 80 proof alcohol per hour

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51
Q

what happens when you have the inactive form of acetaldehyde dehydrogenase (ALDH)?

A

occurs in approximately 10% of asians; drinking even small amounts of alcohol produce high levels of acetaldehyde, causing intense flushing, nausea, vomiting, tachycardia, headache, sweating, dizziness, confusion; genetic marker for low alcoholism

52
Q

do the enzymes that break down alcohol also break down other drugs?

A

Yes–when alcohol is consumed with the other drugs that are broken down by microsomal ethanol oxidizing systems (MEOS) they compete for the same enzyme molecules—alcohol consumption may lead to high and potentially dangerous levels of other drugs

53
Q

Types of tolerance

A
  1. acute tolerance
  2. metabolic tolerance (increases P450 liver microsomal enzymes)
  3. pharmacodynamic tolerance
  4. behavioral tolerance
54
Q

what significantly relates to behavioral tolerance?

A

classical conditioning; in a novel environment tolerance is significantly less

55
Q

signs of hangover

A

nausea and perhaps vomiting, dry mouth, fatigue, malaise

56
Q

abstinence syndrome

A

caused by withdrawal from repeated drinking over months or years; tremor, intense anxiety, high blood pressure, rapid heart rate, excessive sweating, rapid breathing, nausea, vomiting,

57
Q

CNS effects of alcohol

A

low doses: feel less anxious, relaxed, reduced social inhibition, self-perception and judgment are somewhat impaired, confident, memory problems based on expectation, may enhance performance on tasks
high doses: possible amnesia of events (blackout), slurred speech, impaired fine-motor skills, delayed reaction time, reductions in attention, increased sedation, drowsiness, impaired judgment and emotional control,

58
Q

alcohol and sleep

A

with increasing doses mild sedation deepens and produces sleep—suppresses REM and withdrawal after repeated use increases REM that may interfere with normal sleep patterns and produce nightmares

59
Q

what leads to brain damage?

A

interaction of factors: high levels of alcohol, elevated acetaldehyde, liver deficiency, inadequate nutrition—B1 deficiency (critical for brain glucose metabolism), leads to cell death

60
Q

brain damage from drinking

A

enlarge ventricles; extensive shrinkage of brain tissue (smaller mass; mostly in frontal lobes); shrinkage of medial temporal lobe structures (hippocampus, cholinergic cells of basal forebrain); cerebellar cell loss,

61
Q

what is the damage to frontal lobes responsible for?

A

personality changes; apathy, disinhibition, diminished executive functioning

62
Q

what is tissue shrinkage in medial temporal lobe structures (hippocampus, cholinergic cells of basal forebrain) responsible for?

A

memory disturbance; failure to remember recent events or form new memories

63
Q

what is cerebeller cell loss responsible for?

A

ataxia and incoordination of lower limbs

64
Q

what may play a role in the brain changes?

A

glutamate induce hyperexcitability of neurons during abstinence

65
Q

types of effects alcohol has on the body

A 
cardiovascular
renal-urinary 
reproductive
gastrointestinal
liver
66
Q

Cardiovascular system effects

A

dilation of peripheral blood vessels, brings them closer to skin–> makes people flushed and warm (means heat is being lost from body);

67
Q

can alcohol have positive effects on the cardiovascular system?

A

vasodilation may improve cognitive function in older adults by aiding in circulation; a low to moderate dose may reduce the risk of heart disease by increasing good and decreasing bad cholesterol; reduce incidence of stroke and blood clots

68
Q

renal-urinary effects

A

produce larger volumes of urine that is more dilute than normal; loss of fluids caused by reduced secretion of antidiuretic hormone

69
Q

sexual response

A

expectation plays a large part; Male: low doses enhanced arousal a small extent and higher doses reduced sexual response; Female: physiological measures decreased with increasing alcohol, but subjective arousal increased

70
Q

effects of chronic alcohol use on sex

A

Men: may become impotent, atrophy of testicles, reduced sperm production, shrinkage of prostate and seminal vesicles
Women: disrupted overian function, menstrual disorders

71
Q

gastrointestinal tract effects

A

increases salivation and secretion of gastric juices–> may explain the increase in appetite and aid in digestion; irritates stomach lining; inflammation of the stomach and esophagus; diarrhea, inhibits utilization of proteins, reduces absorption and metabolism of vitamins and minerals

72
Q

diagnostic signs of FAS

A
  1. mental retardation and other developmental delays
  2. low birthweight
  3. neurological problems (irritability, hypersensitivity to sound, poor sleep patterns, attentional deficits)
  4. distinctive craniofacial malformations (small head, small wide-set eyes, drooping eyelids, short upturned nose, thin upper lip, flattening of the vertical groove between the nose and lip)
  5. other physical abnormalities (cardiac defects; failure of kidney development; undescended testes; skeletal malformations in fingers and toes)
73
Q

J shaped relationship

A

among maternal alcohol consumed and scores on hyperactivity, emotional difficulties, and conduct problems—children whose mothers were light drinkers (1-2 drinks per week or per occasion) showed fewer problems than those whose mothers were totally abstinent.

74
Q

ingestion during time of conception

A

significantly increases the risk of teratogenic effects and within the first 3 weeks the fetus may not survive

75
Q

ingestion during the 4-9th weeks

A

produces most severe formative damage and severe mental retardation

76
Q

ingestion during later pregnancy

A

causes slowed growth

77
Q

why is alcohol damaging to fetuses?

A

not entirely known–hormone like substances called prostaglandins ares suspected of mediating teratogenic effects because inhibitors of prostaglandins, such as aspirin, reduce alcohol-induced birth defects in animals. Also, ethanol acting on both glutamate and y-aminobutyric acid (GABA) neurons may trigger significant cell death in the developing brain

78
Q

Why are animal models important?

A
  1. some of the common human correlates of heavy alcohol use can be eliminated (e.g. psychiatric disorders)
  2. can use methods inappropriate for humans
  3. genetic manipulations are possible
  4. serve as screening tools for treatment strategies
79
Q

nonspecific actions

A

depend on its ability to move into membranes, changing the fluid character of the lipids that make up the membrane

80
Q

specific actions

A

interacts with specific sites on particular proteins

81
Q

what neurotransmitters does alcohol act on?

A

glutamate; GABA; Dopamine; opioid systems

82
Q

effects on NMDA (glutamate) receptor

A

is a ligand gated channel that allows positively charged ions (Ca+ and Na+) to enter and cause localized depolarization.

83
Q

what does glutamate action at NMDA receptors cause?

A

associative learning and has a role in the damaging effects of excessive glutamate activity (excitotoxicity) which happens with prolonged seizures after stroke

84
Q

NMDA role in alcohol effects

A
  1. memory loss
  2. rebound hyperexcitability associated with the abstinence syndrome after long term use
  3. NMDA mediated excitotoxicity associated with alcoholic brain damage
85
Q

does alcohol activate or inhibit glutamate neurotransmission?

A

inhibits by reducing the effectiveness of glutamate at the NMDA receptor

86
Q

effects of glutamate antagonists (alcohol)

A

impairs learning and memory; reduces glutamate release in hippocampus (deficits in spatial memory);

87
Q

neuroadaptations related to repeated use of alcohol

A

increase in the number of NMDA receptors (up-regulation) in response to reduce glutamate activity; occurs in the hippocampus and cerebral cortex

88
Q

glutamate and withdrawal

A

correlation between the magnitude of glutamate output during withdrawal and the intensity of abstinence signs; elevated glutamate activity during withdrawal causes excessive calcium influx–> cell death

89
Q

glutamate and birth defects

A

drinking during 3rd trimester can impair NMDA receptors and decrease glutamate release in baby; may disrupt brain development; may lead to impairments in learning and memory

90
Q

GABA

A

a major inhibitory amino acid neurotransmitter; binds to the GABAa receptor complex and opens the chloride (Cl-) channel, allowing Cl- to enter the cell to hyperpolarize the membrane; sedative-hypnotic drugs enhance the effects of GABA at the GABAa receptor by binding to their modulatory sites on the receptor complex

91
Q

how does alcohol modulate GABA function?

A

directly by GABAa receptors and indirectly by stimulating GABA release

92
Q

does alcohol act on all GABAa receptors?

A

no; GABAa receptors that are highly sensitive to alcohol have an alpha subunit along with alpha4 or alpha6 subunits and are located extrasynaptically

93
Q

what are the extrasynaptic receptors for GABA responsible for?

A

behavioral and subjective effects produced by low or moderate amounts of drinking; reinforcing effects of oral ethanol

94
Q

nucleus accumbens & GABA receptors

A

reducing receptors in the shell altered alcohol intake bc shell is associated with self-administration of drugs of abuse

95
Q

repeated alcohol exposure and GABA

A

reduces GABAa mediated Cl- flux; becomes down-regulated to compensate for initial GABA enhancing effects of alcohol and may contribute to the appearance of toolerance and withdrawal bc of GABA mediated inhibition

96
Q

what does DA play a major role in?

A

the reinforcement and motivational mechanisms underlying behaviors that are vital to survival

97
Q

explain the DA pathway

A

begins in the ventral tegmental area (VTA) of the midbrain and courses rostrally to the limbic structures, including the nucleus accumbens (NAcc) and the central nucleus of the amygdala

98
Q

why the nucleus accumbens important?

A

DA; the shell belongs to a network of structures called the extended amygdala, which is involved in integrating emotion with hormonal responses and sympathetic nervous system activity; the core is associated with the striatum, which modulates movement

99
Q

nucleus accumbens role in substance abuse

A

supplying primary reinforcing qualities that lead to repeated drug use and the incentive or motivation for the drug

100
Q

chronic use and DA

A

withdrawal dramatically reduces the firing rate of DA in nucleus accumbens and reduction in DA metabolites

101
Q

impact of down regulation of DA

A

responsible for negative emotional signs characteristics of withdrawal from many abused substances

102
Q

is DA solely responsible for reinforcing effects?

A

no—when mesolimibic terminals are destroyed it does not abolish self-administration

103
Q

opioids

A

family of neuropeptides that have opiate-like effects modulate pain, mood, feeding, reinforcement, and response to stress; contribute to reinforcing effects (possibly by modulating DA); craving

104
Q

what effect does alcohol have on opioids?

A

enhances endogenous opioid activity, increases endogenous opioid release from the brain and the pituitary gland and increases blood levels of opioids

105
Q

chronic alcohol use and opioids

A

reduces gene expression, making less of the peptides available for release; reduced brain levels of endorphin

106
Q

what regulates DA release in mesolimbic neurons?

A

opioid cells in the VTA and NAcc

107
Q

opioid antagonists

A

e.g. naloxone and naltrexone compete for endogenous opioid receptors significantly reduce alcohol self-administration; u-opioid receptor mice fail to administer alcohol

108
Q

abstinence and opioids

A

in alcoholics abstinence increased the u-receptors and the number of receptors was positively correlated with scores on a drinking scale—as u-receptors increased so did craving scores

109
Q

relapse and opioids

A

activation of opioids may impair executive control leading to an increased probability of relapse

110
Q

essential features of alcoholism

A

compulsive alcohol seeking and use despite damaging health and social consequences

111
Q

three areas that contribute to vulnerability to alcoholism

A
  1. neurobiological
  2. psychological
  3. sociocultural
112
Q

psychological factors

A

response to stress (symptomatic drinking–> to relieve stress); anxiety; stress early in life; family history (greater cortisol release during stress); novelty seeking

113
Q

acute versus chronics stress

A

acute stress reduces alcohol intake where as chronic stress increases it

114
Q

does alcohol reduce stress?

A

it can relieve stress under some conditions but alcohol increases the function of brain and endocrine stress systems, making alcohol itself an additional stressor that may lead to further alcohol use; withdrawal increases anxiety

115
Q

chemical links to alcohol increasing stress

A

acute alcohol administration elevates levels of the stress hormones corticotropin-releasing factor (CRF), adrenocorticotropic hormone (ACTH), and glucocorticoids (cortisol) & withdrawal of alcohol after several weeks of chronic administration produces more anxious behavior in rodents

116
Q

neurobiological factors

A

genetic vulnerability (close relatives are at a 3-7x greater risk); genes explain 50-60% of variance of risk; heritability is 38%; low sensitivity to alcohol;

117
Q

genes associated with alcoholism

A

chromosome 11p close to genes for the D4 dopamine receptor and tyrosine hydroxylase, an enzyme needed for DA and NE synthesis; chromosome 4p near the gene for the GABAa receptor complex

118
Q

Cloninger Subtype I

A

after 25; male and female; moderate genetic influence; high environmental; high use as an escape; low use to feel good; low novelty seeking; infrequent inability to control; frequent guilt/fear about drinking; infrequent aggressive/antisocial; infrequent inability to stop

119
Q

Cloninger Subtype II

A

before 25; male; high genetic influence; low environmental; low use as an escape; high use to feel good; high novelty seeking; frequent inability to control; infrequent guilt/fear about drinking; frequent aggressive/antisocial; frequent inability to stop

120
Q

social & cultural

A

mold changing attitudes about drinking as well as the definition of problem drinking

121
Q

community reinforcement approach

A

assumes that environmental contingencies (rewards and punishers) are powerful in encouraging drinking behavior but that they can be modified to become powerful reinforcers of nondrinking as well

122
Q

u-opioid agonists

A

increase alcohol consumption

123
Q

u-antagonists

A

decrease self-administration

124
Q

k-opioid receptors

A

have a role in the development of alcohol dependence and withdrawal induced alcohol consumption; becomes up-regulated during consumption

125
Q

what may improve abstinence rates?

A

blocking u receptor reinforcement and k receptor induce anhedonia

126
Q

most effective treatment?

A

medical management with either naltrexone or CBI

Behavioral Pharmacology (11 decks)

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