Deja Ch 5 Neuropharma Flashcards
1
Q
What amino acid derivative serves as the central nervous system’s (CNS) inhibitory neurotransmitter?
A
Gamma-aminobutyric acid (GABA)
2
Q
What are the effects of benzodiazepines and barbiturates on the CNS?
A
Dose-dependent CNS depression
3
Q
What are the different levels of CNS depression?
A
Anxiolysis, sedation, hypnosis, medullary depression, coma, and death
4
Q
What is the mechanism of action of benzodiazepines?
A
Increased frequency of GABAergic chloride ion conductance
5
Q
What is the mechanism of action of barbiturates?
A
Increased duration of GABAergic chloride ion conductance
6
Q
Why are benzodiazepines generally safer than barbiturates?
A
Barbiturate overdose is lethal, whereas benzodiazepines exhibit indirect inhibition of the GABAA at high doses.
7
Q
What pharmacokinetic properties determine the clinical utility of specific benzodiazepines and barbiturates?
A
Duration of onset and duration of action
8
Q
Why are alprazolam, clonazepam, diazepam, and lorazepam the preferred benzodiazepines used in the treatment of anxiety disorders?
A
Intermediate to long duration of action
9
Q
What non-benzodiazepine anxiolytic is used in the treatment of generalized anxiety disorder?
A
Buspirone, a serotonin-1A receptor partial agonist
10
Q
What benefits does buspirone offer compared to benzodiazepine anxiolytics?
A
Minimal side effects and decreased potential for tolerance, dependence, and abuse
11
Q
What benzodiazepine, marketed under the trade name Librium, is often used to treat severe alcohol withdrawal?
A
Chlordiazepoxide
12
Q
Why is chlordiazepoxide preferred in the treatment of severe alcohol withdrawal?
A
Long duration of action and parenteral administration
13
Q
What benefits does oxazepam offer compared to chlordiazepoxide in the treatment of severe alcohol withdrawal?
A
Renal elimination; and can be used in severe hepatic dysfunction
14
Q
Why are diazepam and lorazepam preferred in the treatment of status epilepticus?
A
Rapid onset and parenteral administration
15
Q
Why is the phenobarbital the preferred barbiturate in the maintenance treatment of seizure disorders?
A
Long duration of action
16
Q
Why are oxazepam, temazepam, and triazolam the preferred benzodiazepines used in the acute treatment of insomnia?
A
Short duration of action
17
Q
What benzodiazepine and barbiturate are used in the induction and maintenance of anesthesia?
A
Midazolam (shortest duration of action benzodiazepine) and thiopental (short duration of action barbiturate)
18
Q
What peptides are the endogenous opioids of the CNS?
A
β-endorphin, dynorphin, and enkephalin
19
Q
What CNS receptors are preferentially activated by β-endorphin, dynorphin, and enkephalin?
A
μ-, κ-, and δ-opioid receptors, respectively
20
Q
What are the effects of opioids on the CNS?
A
Analgesia, euphoria, sedation, and respiratory depression
21
Q
What are the clinical indications for administration of opioids?
A
Analgesia, anesthesia, pulmonary edema, cough suppression, and diarrhea
22
Q
Why are opioids contraindicated in pulmonary dysfunction other than pulmonary edema?
A
Opioids depress respiratory drive.
23
Q
Why are opioids contraindicated in states of increased intracranial pressure?
A
Opioids increase cerebrovascular dilation.
24
Q
What are common side effects of opioids?
A
Respiratory depression, constipation, miosis, hypotension, and bradycardia
25
What are the effects of chronic opioid use?
Pharmacodynamic tolerance (except for constipation and miosis) and physical and psychological dependence
26
Which μ-opioid receptor agonists produce the strongest analgesic effect?
Fentanyl, levorphanol, meperidine, and morphine
27
What is the mechanism of action of morphine-induced hypotension?
Peripheral histamine release
28
Why is methadone preferred in the treatment of opioid addiction?
Enteral administration and long duration of action
29
Which μ-opioid receptor agonists produce a moderate analgesic effect?
Codeine, hydrocodone, and oxycodone
30
What agents are considered mixed opioid agonist-antagonists?
Butorphanol, nalbuphine, and pentazocine
31
What benefits do mixed opioid agonist-antagonists offer compared to full opioid agonists?
Minimal respiratory depression; and decreased potential for tolerance, dependence, and abuse
32
Why do mixed opioid agonist-antagonists produce less respiratory depression, tolerance, and dependence?
Strong agonist activity at κ-receptor and weak agonist activity at μ-receptor
33
What antitussive opioids are used in the treatment of cough?
Codeine and dextromethorphan
34
What opioids are used in the treatment of diarrhea?
Diphenoxylate and loperamide
35
What agents exhibit antagonist activity at μ-opioid receptors?
Naloxone, naltrexone, and nalmefene
36
What are the clinical indications for μ-opioid-receptor antagonists?
Acute treatment of opioid toxicity (naloxone, nalmefene) and maintenance of abstinence from alcohol (naltrexone)
37
What is the effect of opioid antagonist administration in opioid-tolerant individuals?
Provocation of opioid abstinence syndrome (withdrawal)
38
What is the desired effect of local anesthetics?
Prevention of transmission of local sensory stimuli to the CNS
39
What is the mechanism of action of the local anesthetics?
Inhibition of voltage-gated sodium ion channels
40
What is the site of action of local anesthetic?
Cytoplasm of neuronal axons
41
What chemical property influences diffusion of local anesthetic into neuronal axons?
Ionization status
42
Why are higher doses of local anesthetic required in acidic environments, eg, local infection and systemic acidosis?
Ionization of weakly basic local anesthetics impairs diffusion
43
Why do local anesthetics preferentially affect rapidly firing nerve fibers (use dependence)?
Preferential inhibition of open or recently inactivated ion channels
44
What physical characteristics of nerve fibers increase sensitivity to local anesthesia?
Smaller diameter and myelination
45
What are the two principal classes of local anesthetics?
Amides and esters
46
Which local anesthetics have a short duration of action?
Procaine and benzocaine (esters only)
47
Which local anesthetics have an intermediate duration of action?
Amides: lidocaine, mepivacaine, and prilocaine ; Ester: cocaine
48
Which local anesthetics have a long duration of action?
Amides: bupivacaine, etidocaine, and ropivacaine ; Ester: tetracaine
49
How does the metabolism of local anesthetics influence their duration of action?
Esters rapidly metabolized by plasma cholinesterases; amides undergo hepatic metabolism.
50
Why does administration of epinephrine increase the duration of action of local anesthetics?
Vasoconstriction limits local blood flow, preventing systemic redistribution.
51
What are the CNS side effects of local anesthetics?
Light-headedness, nystagmus, restlessness, and seizure
52
What are the cardiovascular side effects of local anesthetics?
Bradycardia and hypotension (especially bupivacaine) ; Tachycardia and hypertension (cocaine only)
53
What is the mechanism of action of allergic reaction to ester local anesthetics?
Para-aminobenzoic acid (PABA) formation
54
What is the pharmacokinetic significance of the solubility of inhalational general anesthetics?
Inversely proportional to duration of induction and recovery
55
How is solubility of inhalational general anesthetics quantified?
Blood/gas partition coefficient
56
What is the minimum alveolar concentration (MAC)?
Alveolar concentration of inhalational general anesthetic required to produce anesthesia in 50% of individuals
57
For what pharmacodynamic property is MAC a proxy?
Median effective dose (ED50)
58
What is the pharmacodynamic significance of the MAC of inhalational general anesthetics?
Inversely proportional to potency
59
How is the effect of anesthesia terminated?
Redistribution from the brain to the blood
60
Why is nitrous oxide unsuitable for single-agent anesthesia?
Low potency
61
What general anesthetic causes pulmonary irritation?
Desflurane
62
What general anesthetic is proconvulsant?
Enflurane
63
What general anesthetic causes hepatitis and arrhythmia?
Halothane
64
What general anesthetic is nephrotoxic?
Methoxyflurane
65
What potentially-fatal side effect can occur with coadministration of inhalational general anesthetics and skeletal muscle relaxants?
Malignant hyperthermia
66
Mutations in which calcium channel are often associated with malignant hyperthermia?
Ryanodine receptor
67
What agent is used in the treatment of malignant hyperthermia?
Dantrolene
68
What is the mechanism of action of dantrolene, a peripherally-acting spasmolytic?
Inhibition of ryanodine receptor- mediated calcium release from sarcoplasmic reticulum
69
What is the other potentially-fatal clinical indication for treatment with dantrolene?
Neuroleptic malignant syndrome
70
What pharmacokinetic properties of midazolam (benzodiazepine), thiopental, and methohexital (barbiturates) permit their use in induction and maintenance of general anesthesia?
Parenteral administration and short duration of action
71
What agents are used for rapid induction of anesthesia?
Propofol and etomidate
72
Describe the action of ketamine:
Dissociative amnestic and analgesic without true anesthetic properties
73
What is the "emergence reaction" associated with ketamine?
Excitation and disorientation on termination of anesthesia
74
Upon which receptor does ketamine act as an antagonist?
N-methyl-D-aspartate (NMDA) receptor
75
What is the mechanism of action of neuromuscular blockers?
Inhibition of motor end-plate nicotinic acetylcholine (ACh) receptors
76
What two classes of neuromuscular blockers inhibit motor end-plate nicotinic receptors?
Non-depolarizing competitive antagonists and depolarizing agonists
77
How do depolarizing neuromuscular blockers initially inhibit the action of endogenous ACh?
Decreased affinity for acetylcholinesterase (AChE) results in preferential metabolism of ACh.
78
What is the effect of decreased AChE metabolism of depolarizing blockers at the motor end-plate?
Persistent depolarization of the motor end-plate
79
How do muscles respond to this persistent motor end-plate depolarization?
With fasciculations, impairing coordinated contraction (phase I block)
80
What is the effect of continuous fasciculations on muscle activity?
Insensitivity to endogenous ACh (phase II block)
81
What effect do acetylcholinesterase (AChE) inhibitors (neostigmine, physostigmine) have on non-depolarizing neuromuscular blockers?
Potentiation of non-depolarizing blockade
82
What effect do AChE inhibitors (neostigmine, physostigmine) have on depolarizing neuromuscular blockers?
Potentiation of phase I depolarization blockade, reversal of phase II desensitization blockade
83
Why do mivacurium (non-depolarizing neuromuscular blocker) and succinylcholine (depolarizing neuromuscular blocker) have short durations of action?
Rapid metabolism by plasma cholinesterase
84
Why is atracurium a safer non-depolarizing neuromuscular blocker in hepatic and renal dysfunction?
Undergoes spontaneous elimination
85
What side effects result from muscle breakdown caused by treatment with succinylcholine?
Hyperkalemia and myalgia
86
What centrally-acting spasmolytics are indicated for the treatment of excessive muscle tone due to CNS dysfunction, eg, cerebral palsy and multiple sclerosis?
Baclofen (GABAB receptor agonist) and diazepam (benzodiazepine)
87
What centrally-acting spasmolytic is indicated for the treatment of excessive muscle tone due to acute muscle injury?
Cyclobenzaprine
88
What is the mechanism of action of botulinum toxin, a peripherally-acting spasmolytic?
Inhibition of ACh release from presynaptic vesicles
89
What hypothetical alteration in neurochemistry may be primarily responsible for the symptoms of psychotic disorders?
Functional mesolimbic/mesocortical dopamine excess (dopamine hypothesis of schizophrenia)
90
What is the mechanism of action of the typical antipsychotics?
Inhibition of D2 receptors of the mesolimbic/mesocortical pathways
91
What is the mechanism of typical antipsychotic-associated hyperprolactinemia?
Inhibition of D2 receptors of the tuberoinfundibular pathway
92
What are the early-onset, reversible extrapyramidal side effects associated with typical antipsychotics?
Dystonia, parkinsonism, and akathisia
93
What is the late-onset and irreversible extrapyramidal side effect associated with typical antipsychotics?
Tardive dyskinesia
94
How can treatment with benztropine help in distinguishing reversible and irreversible extrapyramidal side effects?
Reversible extrapyramidal side effects improve and tardive dyskinesia worsens with anticholinergics.
95
What is the treatment for typical antipsychotic-associated tardive dyskinesia?
Decrease or discontinue typical antipsychotic, switch to atypical.
96
Why do high-potency typical antipsychotics (haloperidol, fluphenazine) increase extrapyramidal side effects?
High affinity for D2 receptors inhibits dopamine activity in the nigrostriatal pathway at low doses.
97
Why do low-potency typical antipsychotics (chlorpromazine, thioridazine) increase nonspecific side effects?
Low affinity for D2 receptors requires higher therapeutic doses.
98
What nonspecific side effects associated with typical antipsychotics are attributable to anti-α-adrenergic effect?
Orthostatic hypotension and sexual dysfunction
99
What nonspecific side effects associated with typical antipsychotics are attributable to anticholinergic effect?
Constipation, dry mouth, urinary retention, and visual disturbances
100
What nonspecific side effects associated with typical antipsychotics are attributable to antihistamine effect?
Sedation and weight gain
101
What potentially-fatal side effect is associated with the use of typical antipsychotics?
Neuroleptic malignant syndrome
102
What are the symptoms of neuroleptic malignant syndrome?
Muscle rigidity, hyperthermia, and autonomic instability
103
What is the treatment of neuroleptic malignant syndrome?
Dantrolene, dopamine agonists, and supportive care
104
What is the mechanism of action of the atypical antipsychotics risperidone, olanzapine, quetiapine, ziprasidone, and aripiprazole?
5-HT2 receptor inhibition, weak D2 receptor inhibition
105
What is the mechanism of action of the atypical antipsychotic clozapine?
5-HT2 receptor inhibition, weak D4 receptor inhibition
106
What benefits do the atypical antipsychotics offer compared to the typical antipsychotics in the treatment of schizophrenia?
Improvement in both positive and negative symptoms and decreased extrapyramidal side effects
107
What serious hematologic side effect associated with clozapine?
Agranulocytosis
108
What electrocardiogram changes are associated with ziprasidone?
Prolonged QT interval and torsade de pointes
109
Which atypical antipsychotic is most likely to be associated with extrapyramidal side effects?
Risperidone
110
To what alteration in neurochemistry are symptoms of affective disorders typically attributed?
Functional norepinephrine and serotonin deficiency (biogenic amine theory of depression)
111
What antidepressant drug class includes amitriptyline, imipramine, nortriptyline, and desipramine?
Tricyclic antidepressants
112
What is the mechanism of action of the tricyclic antidepressants?
Nonselective inhibition of presynaptic norepinephrine and serotonin reuptake
113
What drug class has a side effect profile similar to that of the tricyclic antidepressants?
Low-potency typical antipsychotics
114
What side effects associated with tricyclic antidepressants are attributable to anti-α-adrenergic, anticholinergic,
and antihistamine effects?
Orthostatic hypotension, sexual dysfunction, constipation, dry mouth, urinary retention, visual disturbances, sedation, and weight gain
115
What are the symptoms of tricyclic antidepressant toxicity?
Coma, convulsion, cardiotoxicity (three Cs), mydriasis, and hyperthermia
116
How is tricyclic antidepressant toxicity best treated?
Cyproheptadine or benzodiazepines for seizure, anti-arrhythmics, and supportive care
117
What antidepressant drug class includes amoxapine, bupropion, maprotiline, trazodone, mirtazapine, nefazodone, and venlafaxine?
Heterocyclic antidepressants
118
Which heterocyclic antidepressant is most likely to be associated with priapism and sedation?
Trazodone
119
Which heterocyclic antidepressants are most likely to be associated with seizure and cardiotoxicity?
Amoxipine and maprotiline
120
Which heterocyclic antidepressant is most likely to be associated with extrapyramidal side effects?
Amoxipine
121
Which heterocyclic antidepressants are associated with cytochrome P450 enzyme inhibition?
Nefazodone and venlafaxine
122
Which heterocyclic antidepressant is used in the treatment of nicotine addiction?
Bupropion
123
What antidepressant drug class includes citalopram, fluoxetine, fluvoxamine, paroxetine, and sertraline?
Selective serotonin reuptake inhibitors (SSRIs)
124
What is the mechanism of action of the SSRIs?
Selective inhibition of presynaptic serotonin reuptake
125
What are the common side effects of SSRIs?
Anxiety, insomnia, nausea, and sexual dysfunction
126
What are the symptoms of SSRI toxicity?
Agitation, confusion, coma, muscle rigidity, hyperthermia, seizure, and autonomic instability
127
How is SSRI toxicity best treated?
Cyproheptadine or benzodiazepine for seizure, and supportive care
128
What antidepressant drug class includes phenelzine, tranylcypromine, and isocarboxazid?
Monoamine oxidase (MAO) inhibitors
129
What is the mechanism of action of the MAO inhibitors?
Nonselective inhibition of metabolism of serotonin, norepinephrine, and dopamine by MAO-A and MOA-B
130
What are the common side effects of MAO inhibitors?
Orthostatic hypotension, insomnia, and weight gain
131
What drugs can provoke a hypertensive crisis when coadministered with MAO inhibitors?
Indirect-acting sympathomimetics (cocaine, amphetamine) and tyramine (red wine, aged cheese)
132
What are the symptoms associated with serotonin syndrome?
Muscle rigidity, hyperthermia, autonomic instability, and seizure
133
Coadministration of which drugs is associated with serotonin syndrome?
SSRIs, tricyclic antidepressants, MAO inhibitors, meperidine, and/or dextromethorphan
134
What drugs are indicated in the first-line treatment of bipolar disorders?
Lithium, valproic acid, and olanzapine
135
What is the mechanism of action of lithium in the treatment of bipolar disorders?
Inhibition of neuronal phosphoinositide recycling
136
Why are atypical antipsychotics and/or benzodiazepines indicated in the initial treatment of bipolar disorders?
Lithium has slow onset of action.
137
What hematologic side effect is associated with lithium?
Leukocytosis
138
What reversible renal side effect is associated with lithium?
Nephrogenic diabetes insipidus
139
Why does the plasma concentration of lithium have to be monitored regularly?
Lithium has a narrow therapeutic index.
140
What is the therapeutic index?
Ratio of the median toxic (TD50) or lethal (LD50) dose to the median effective dose (ED50)
141
What alteration of neurochemistry is responsible for the symptoms of parkinsonism and Parkinson disease?
Dopamine deficiency and/or ACh excess in the striatum
142
What is the mechanism of action of L-dopa?
Synthetic precursor converted to dopamine by DOPA decarboxylase.
143
How does coadministration of carbidopa increase the potency of L-dopa?
Inhibition of peripheral conversion of L-dopa to dopamine
144
What chemical property of carbidopa is responsible for preferential inhibition of peripheral L-dopa metabolism?
Poor lipid solubility prevents diffusion across blood-brain barrier.
145
What other peripheral enzyme inhibitors enhance the potency of L-dopa?
Entacapone and tolcapone
146
What is the mechanism of action of entacapone?
Inhibition of peripheral conversion of L-dopa to 3-O-methyldopa by catecholamine-O-methyltransferase (COMT)
147
To what drug class do the antiparkinson medications bromocriptine and pergolide belong?
Ergot alkaloids
148
What are the symptoms of ergotism toxicity (St. Anthony's fire)?
Disorientation, hallucination, convulsion, muscle cramps, and dry gangrene of extremities
149
What drug of abuse is an ergot alkaloid?
Lysergic acid diethylamide (LSD)
150
Why is selegiline, a selective MAO-B inhibitor, an effective treatment for parkinsonism?
MAO-B is CNS-specific and preferentially metabolizes dopamine
151
What is the mechanism of action of antiparkinsonian agents benztropine and trihexyphenidyl?
Inhibition of the striatum muscarinic anticholinergic receptors
152
What alteration in neurochemistry is the basis for current therapeutics in Alzheimer disease?
Functional cortical and hippocampal ACh deficiency
153
What class of drug is indicated in the treatment of mild to moderate Alzheimer disease?
AChE inhibitors, eg, rivastigmine, donepezil, galantamine, and tacrine
154
What is the mechanism of action of the AChE inhibitors in the treatment of Alzheimer disease?
Increased concentration of synaptic terminal ACh
155
What other enzyme is inhibited by rivastigmine and tacrine?
Butyrylcholinesterase
156
What drug class is indicated in the treatment of moderate to severe Alzheimer disease?
NMDA antagonists (memantine)
157
What is the mechanism of action of the NMDA antagonists in the treatment of Alzheimer disease?
Inhibition of glutaminergic NMDA calcium conductance
158
What is tolerance?
Habituation to the physiologic effects of a drug
159
What are the pharmacodynamic effects of tolerance?
It decreases efficacy and larger doses are required to achieve the same effect.
160
What is dependence?
A physiologic and/or psychologic state characterized by compulsive substance use
161
What are the effects of alcohol intoxication?
Increased sociability and impairment of motor, cognitive, and memory function
162
What is the mechanism of action of alcohol intoxication?
Incompletely understood, GABAergic and generalized CNS depression
163
How is alcohol metabolized?
Via a two-step process with zero- order kinetics and a toxic intermediate
164
What is the first step in metabolism of alcohol?
Conversion of alcohol to acetaldehyde by cytoplasmic alcohol dehydrogenase
165
What is the second step in metabolism of alcohol?
Conversion of acetaldehyde to acetate by mitochondrial aldehyde dehydrogenase
166
What are the effects of acetaldehyde toxicity?
Nausea, vomiting, hyperventilation, tachycardia, chest pain, and dyspnea
167
What agent used in the treatment of alcohol dependence inhibits aldehyde dehydrogenase causing acetaldehyde accumulation?
Disulfiram
168
What is the mechanism of action of benzodiazepine in the treatment of alcohol dependence?
Withdrawal seizure treatment and prophylaxis via GABA-A receptor activation
169
What is the mechanism of action of naltrexone in the treatment of alcohol dependence?
Reduces cravings via opioid receptor inhibition
170
What are the symptoms of acute alcohol withdrawal?
Agitation, tremor, insomnia, nausea, vomiting, diarrhea, arrhythmia, delirium tremens, and potentially-fatal seizure
171
What is the treatment for acute alcohol withdrawal?
Thiamine, benzodiazepine taper, clonidine, and propranolol for hyperadrenergic state
172
What other CNS depressants are frequently abused?
Benzodiazepines and barbiturates
173
What are the symptoms of CNS depressant withdrawal?
Agitation, delirium, insomnia, and potentially-fatal seizure
174
What drugs are indicated in the treatment of CNS depressant withdrawal?
Long-acting benzodiazepine to suppress acute symptoms, tapering dose
175
What drugs are indicated in the treatment of CNS depressant toxicity?
Flumazenil for benzodiazepine toxicity
176
What is the mechanism of action of CNS stimulants?
Increased synaptic terminal concentration of dopamine, norepinephrine, and serotonin
177
What are the symptoms of CNS stimulant intoxication?
Euphoria, anxiety, insomnia, anorexia, tachycardia, hypertension, and mydriasis
178
What are the symptoms of CNS stimulant withdrawal
Depression, fatigue, increased sleep, and increased appetite
179
What are the symptoms of CNS stimulant toxicity?
Arrhythmia, MI, cardiovascular, hallucination, paranoia, hyperthermia, seizure, and death
180
What drugs are indicated in the treatment of CNS stimulant toxicity
Benzodiazepine and antipsychotic agents
181
What are the symptoms of opioid intoxication?
Euphoria, analgesia, cough suppression, miosis, and constipation
182
What are the symptoms of opioid withdrawal?
Mydriasis, diarrhea, rhinorrhea, lacrimation, diaphoresis, and yawning
183
What drugs are indicated in the treatment of opioid withdrawal?
Methadone, LAAM, buprenorphine, and clonidine
184
What are the symptoms of opioid toxicity?
Nausea, vomiting, sedation, respiratory depression, bradycardia, hypotension, coma, and death
185
What drugs are indicated in the treatment of opioid toxicity?
Naloxone and naltrexone
186
What is the mechanism of action of cannabis (marijuana, hashish) intoxication?
Cannabinoid (CB1 and CB2) receptor activation
187
What are the symptoms of cannabis intoxication?
Euphoria, disinhibition, perceptual changes, conjunctival injection, dry mouth, and increased appetite
188
What is the mechanism of action of hallucinogens (LSD, mescaline, psilocybin) intoxication?
Serotonin receptor activation
189
What are the symptoms of hallucinogen intoxication?
Perceptual changes and synesthesia
190
What are the symptoms of hallucinogen withdrawal?
No physiologic dependence
191
What is the mechanism of action of phencyclidine (PCP; "angel dust")?
NMDA receptor antagonist
192
What are the symptoms of PCP intoxication?
Agitation, nystagmus, rigidity, decreased response to pain, hyperacusis, paranoia, and violent behavior
193
What is the mechanism of action of 3,4-methylenedioxymethamphetamine (MDMA; "ecstasy") intoxication?
Increased synaptic terminal concentration of serotonin
194
What are the symptoms of MDMA intoxication?
Euphoria, disinhibition, and perceptual changes
195
What are the symptoms of inhalant (glue, solvents) toxicity?
Motor and cognitive impairment and multiple organ dysfunction
