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Pharmacology by Somebody > Deja Ch 5 Neuropharma > Flashcards

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)

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2
Q

What are the effects of benzodiazepines and barbiturates on the CNS?

A

Dose-dependent CNS depression

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3
Q

What are the different levels of CNS depression?

A

Anxiolysis, sedation, hypnosis, medullary depression, coma, and death

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4
Q

What is the mechanism of action of benzodiazepines?

A

Increased frequency of GABAergic chloride ion conductance

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5
Q

What is the mechanism of action of barbiturates?

A

Increased duration of GABAergic chloride ion conductance

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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.

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7
Q

What pharmacokinetic properties determine the clinical utility of specific benzodiazepines and barbiturates?

A

Duration of onset and duration of action

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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

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9
Q

What non-benzodiazepine anxiolytic is used in the treatment of generalized anxiety disorder?

A

Buspirone, a serotonin-1A receptor partial agonist

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10
Q

What benefits does buspirone offer compared to benzodiazepine anxiolytics?

A

Minimal side effects and decreased potential for tolerance, dependence, and abuse

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11
Q

What benzodiazepine, marketed under the trade name Librium, is often used to treat severe alcohol withdrawal?

A

Chlordiazepoxide

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12
Q

Why is chlordiazepoxide preferred in the treatment of severe alcohol withdrawal?

A

Long duration of action and parenteral administration

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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

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14
Q

Why are diazepam and lorazepam preferred in the treatment of status epilepticus?

A

Rapid onset and parenteral administration

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15
Q

Why is the phenobarbital the preferred barbiturate in the maintenance treatment of seizure disorders?

A

Long duration of action

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16
Q

Why are oxazepam, temazepam, and triazolam the preferred benzodiazepines used in the acute treatment of insomnia?

A

Short duration of action

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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)

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18
Q

What peptides are the endogenous opioids of the CNS?

A

β-endorphin, dynorphin, and enkephalin

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19
Q

What CNS receptors are preferentially activated by β-endorphin, dynorphin, and enkephalin?

A

μ-, κ-, and δ-opioid receptors, respectively

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20
Q

What are the effects of opioids on the CNS?

A

Analgesia, euphoria, sedation, and respiratory depression

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21
Q

What are the clinical indications for administration of opioids?

A

Analgesia, anesthesia, pulmonary edema, cough suppression, and diarrhea

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22
Q

Why are opioids contraindicated in pulmonary dysfunction other than pulmonary edema?

A

Opioids depress respiratory drive.

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23
Q

Why are opioids contraindicated in states of increased intracranial pressure?

A

Opioids increase cerebrovascular dilation.

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24
Q

What are common side effects of opioids?

A

Respiratory depression, constipation, miosis, hypotension, and bradycardia

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25
Q

What are the effects of chronic opioid use?

A

Pharmacodynamic tolerance (except for constipation and miosis) and physical and psychological dependence

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26
Q

Which μ-opioid receptor agonists produce the strongest analgesic effect?

A

Fentanyl, levorphanol, meperidine, and morphine

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27
Q

What is the mechanism of action of morphine-induced hypotension?

A

Peripheral histamine release

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28
Q

Why is methadone preferred in the treatment of opioid addiction?

A

Enteral administration and long duration of action

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29
Q

Which μ-opioid receptor agonists produce a moderate analgesic effect?

A

Codeine, hydrocodone, and oxycodone

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30
Q

What agents are considered mixed opioid agonist-antagonists?

A

Butorphanol, nalbuphine, and pentazocine

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31
Q

What benefits do mixed opioid agonist-antagonists offer compared to full opioid agonists?

A

Minimal respiratory depression; and decreased potential for tolerance, dependence, and abuse

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32
Q

Why do mixed opioid agonist-antagonists produce less respiratory depression, tolerance, and dependence?

A

Strong agonist activity at κ-receptor and weak agonist activity at μ-receptor

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33
Q

What antitussive opioids are used in the treatment of cough?

A

Codeine and dextromethorphan

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34
Q

What opioids are used in the treatment of diarrhea?

A

Diphenoxylate and loperamide

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35
Q

What agents exhibit antagonist activity at μ-opioid receptors?

A

Naloxone, naltrexone, and nalmefene

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36
Q

What are the clinical indications for μ-opioid-receptor antagonists?

A

Acute treatment of opioid toxicity (naloxone, nalmefene) and maintenance of abstinence from alcohol (naltrexone)

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37
Q

What is the effect of opioid antagonist administration in opioid-tolerant individuals?

A

Provocation of opioid abstinence syndrome (withdrawal)

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38
Q

What is the desired effect of local anesthetics?

A

Prevention of transmission of local sensory stimuli to the CNS

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39
Q

What is the mechanism of action of the local anesthetics?

A

Inhibition of voltage-gated sodium ion channels

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40
Q

What is the site of action of local anesthetic?

A

Cytoplasm of neuronal axons

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41
Q

What chemical property influences diffusion of local anesthetic into neuronal axons?

A

Ionization status

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42
Q

Why are higher doses of local anesthetic required in acidic environments, eg, local infection and systemic acidosis?

A

Ionization of weakly basic local anesthetics impairs diffusion

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43
Q

Why do local anesthetics preferentially affect rapidly firing nerve fibers (use dependence)?

A

Preferential inhibition of open or recently inactivated ion channels

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44
Q

What physical characteristics of nerve fibers increase sensitivity to local anesthesia?

A

Smaller diameter and myelination

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45
Q

What are the two principal classes of local anesthetics?

A

Amides and esters

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46
Q

Which local anesthetics have a short duration of action?

A

Procaine and benzocaine (esters only)

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47
Q

Which local anesthetics have an intermediate duration of action?

A

Amides: lidocaine, mepivacaine, and prilocaine ; Ester: cocaine

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48
Q

Which local anesthetics have a long duration of action?

A

Amides: bupivacaine, etidocaine, and ropivacaine ; Ester: tetracaine

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49
Q

How does the metabolism of local anesthetics influence their duration of action?

A

Esters rapidly metabolized by plasma cholinesterases; amides undergo hepatic metabolism.

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50
Q

Why does administration of epinephrine increase the duration of action of local anesthetics?

A

Vasoconstriction limits local blood flow, preventing systemic redistribution.

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51
Q

What are the CNS side effects of local anesthetics?

A

Light-headedness, nystagmus, restlessness, and seizure

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52
Q

What are the cardiovascular side effects of local anesthetics?

A

Bradycardia and hypotension (especially bupivacaine) ; Tachycardia and hypertension (cocaine only)

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53
Q

What is the mechanism of action of allergic reaction to ester local anesthetics?

A

Para-aminobenzoic acid (PABA) formation

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54
Q

What is the pharmacokinetic significance of the solubility of inhalational general anesthetics?

A

Inversely proportional to duration of induction and recovery

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55
Q

How is solubility of inhalational general anesthetics quantified?

A

Blood/gas partition coefficient

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56
Q

What is the minimum alveolar concentration (MAC)?

A

Alveolar concentration of inhalational general anesthetic required to produce anesthesia in 50% of individuals

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57
Q

For what pharmacodynamic property is MAC a proxy?

A

Median effective dose (ED50)

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58
Q

What is the pharmacodynamic significance of the MAC of inhalational general anesthetics?

A

Inversely proportional to potency

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59
Q

How is the effect of anesthesia terminated?

A

Redistribution from the brain to the blood

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60
Q

Why is nitrous oxide unsuitable for single-agent anesthesia?

A

Low potency

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61
Q

What general anesthetic causes pulmonary irritation?

A

Desflurane

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62
Q

What general anesthetic is proconvulsant?

A

Enflurane

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63
Q

What general anesthetic causes hepatitis and arrhythmia?

A

Halothane

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64
Q

What general anesthetic is nephrotoxic?

A

Methoxyflurane

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65
Q

What potentially-fatal side effect can occur with coadministration of inhalational general anesthetics and skeletal muscle relaxants?

A

Malignant hyperthermia

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66
Q

Mutations in which calcium channel are often associated with malignant hyperthermia?

A

Ryanodine receptor

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67
Q

What agent is used in the treatment of malignant hyperthermia?

A

Dantrolene

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68
Q

What is the mechanism of action of dantrolene, a peripherally-acting spasmolytic?

A

Inhibition of ryanodine receptor- mediated calcium release from sarcoplasmic reticulum

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69
Q

What is the other potentially-fatal clinical indication for treatment with dantrolene?

A

Neuroleptic malignant syndrome

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70
Q

What pharmacokinetic properties of midazolam (benzodiazepine), thiopental, and methohexital (barbiturates) permit their use in induction and maintenance of general anesthesia?

A

Parenteral administration and short duration of action

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71
Q

What agents are used for rapid induction of anesthesia?

A

Propofol and etomidate

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72
Q

Describe the action of ketamine:

A

Dissociative amnestic and analgesic without true anesthetic properties

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73
Q

What is the “emergence reaction” associated with ketamine?

A

Excitation and disorientation on termination of anesthesia

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74
Q

Upon which receptor does ketamine act as an antagonist?

A

N-methyl-D-aspartate (NMDA) receptor

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75
Q

What is the mechanism of action of neuromuscular blockers?

A

Inhibition of motor end-plate nicotinic acetylcholine (ACh) receptors

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76
Q

What two classes of neuromuscular blockers inhibit motor end-plate nicotinic receptors?

A

Non-depolarizing competitive antagonists and depolarizing agonists

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77
Q

How do depolarizing neuromuscular blockers initially inhibit the action of endogenous ACh?

A

Decreased affinity for acetylcholinesterase (AChE) results in preferential metabolism of ACh.

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78
Q

What is the effect of decreased AChE metabolism of depolarizing blockers at the motor end-plate?

A

Persistent depolarization of the motor end-plate

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79
Q

How do muscles respond to this persistent motor end-plate depolarization?

A

With fasciculations, impairing coordinated contraction (phase I block)

80
Q

What is the effect of continuous fasciculations on muscle activity?

A

Insensitivity to endogenous ACh (phase II block)

81
Q

What effect do acetylcholinesterase (AChE) inhibitors (neostigmine, physostigmine) have on non-depolarizing neuromuscular blockers?

A

Potentiation of non-depolarizing blockade

82
Q

What effect do AChE inhibitors (neostigmine, physostigmine) have on depolarizing neuromuscular blockers?

A

Potentiation of phase I depolarization blockade, reversal of phase II desensitization blockade

83
Q

Why do mivacurium (non-depolarizing neuromuscular blocker) and succinylcholine (depolarizing neuromuscular blocker) have short durations of action?

A

Rapid metabolism by plasma cholinesterase

84
Q

Why is atracurium a safer non-depolarizing neuromuscular blocker in hepatic and renal dysfunction?

A

Undergoes spontaneous elimination

85
Q

What side effects result from muscle breakdown caused by treatment with succinylcholine?

A

Hyperkalemia and myalgia

86
Q

What centrally-acting spasmolytics are indicated for the treatment of excessive muscle tone due to CNS dysfunction, eg, cerebral palsy and multiple sclerosis?

A

Baclofen (GABAB receptor agonist) and diazepam (benzodiazepine)

87
Q

What centrally-acting spasmolytic is indicated for the treatment of excessive muscle tone due to acute muscle injury?

A

Cyclobenzaprine

88
Q

What is the mechanism of action of botulinum toxin, a peripherally-acting spasmolytic?

A

Inhibition of ACh release from presynaptic vesicles

89
Q

What hypothetical alteration in neurochemistry may be primarily responsible for the symptoms of psychotic disorders?

A

Functional mesolimbic/mesocortical dopamine excess (dopamine hypothesis of schizophrenia)

90
Q

What is the mechanism of action of the typical antipsychotics?

A

Inhibition of D2 receptors of the mesolimbic/mesocortical pathways

91
Q

What is the mechanism of typical antipsychotic-associated hyperprolactinemia?

A

Inhibition of D2 receptors of the tuberoinfundibular pathway

92
Q

What are the early-onset, reversible extrapyramidal side effects associated with typical antipsychotics?

A

Dystonia, parkinsonism, and akathisia

93
Q

What is the late-onset and irreversible extrapyramidal side effect associated with typical antipsychotics?

A

Tardive dyskinesia

94
Q

How can treatment with benztropine help in distinguishing reversible and irreversible extrapyramidal side effects?

A

Reversible extrapyramidal side effects improve and tardive dyskinesia worsens with anticholinergics.

95
Q

What is the treatment for typical antipsychotic-associated tardive dyskinesia?

A

Decrease or discontinue typical antipsychotic, switch to atypical.

96
Q

Why do high-potency typical antipsychotics (haloperidol, fluphenazine) increase extrapyramidal side effects?

A

High affinity for D2 receptors inhibits dopamine activity in the nigrostriatal pathway at low doses.

97
Q

Why do low-potency typical antipsychotics (chlorpromazine, thioridazine) increase nonspecific side effects?

A

Low affinity for D2 receptors requires higher therapeutic doses.

98
Q

What nonspecific side effects associated with typical antipsychotics are attributable to anti-α-adrenergic effect?

A

Orthostatic hypotension and sexual dysfunction

99
Q

What nonspecific side effects associated with typical antipsychotics are attributable to anticholinergic effect?

A

Constipation, dry mouth, urinary retention, and visual disturbances

100
Q

What nonspecific side effects associated with typical antipsychotics are attributable to antihistamine effect?

A

Sedation and weight gain

101
Q

What potentially-fatal side effect is associated with the use of typical antipsychotics?

A

Neuroleptic malignant syndrome

102
Q

What are the symptoms of neuroleptic malignant syndrome?

A

Muscle rigidity, hyperthermia, and autonomic instability

103
Q

What is the treatment of neuroleptic malignant syndrome?

A

Dantrolene, dopamine agonists, and supportive care

104
Q

What is the mechanism of action of the atypical antipsychotics risperidone, olanzapine, quetiapine, ziprasidone, and aripiprazole?

A

5-HT2 receptor inhibition, weak D2 receptor inhibition

105
Q

What is the mechanism of action of the atypical antipsychotic clozapine?

A

5-HT2 receptor inhibition, weak D4 receptor inhibition

106
Q

What benefits do the atypical antipsychotics offer compared to the typical antipsychotics in the treatment of schizophrenia?

A

Improvement in both positive and negative symptoms and decreased extrapyramidal side effects

107
Q

What serious hematologic side effect associated with clozapine?

A

Agranulocytosis

108
Q

What electrocardiogram changes are associated with ziprasidone?

A

Prolonged QT interval and torsade de pointes

109
Q

Which atypical antipsychotic is most likely to be associated with extrapyramidal side effects?

A

Risperidone

110
Q

To what alteration in neurochemistry are symptoms of affective disorders typically attributed?

A

Functional norepinephrine and serotonin deficiency (biogenic amine theory of depression)

111
Q

What antidepressant drug class includes amitriptyline, imipramine, nortriptyline, and desipramine?

A

Tricyclic antidepressants

112
Q

What is the mechanism of action of the tricyclic antidepressants?

A

Nonselective inhibition of presynaptic norepinephrine and serotonin reuptake

113
Q

What drug class has a side effect profile similar to that of the tricyclic antidepressants?

A

Low-potency typical antipsychotics

114
Q

What side effects associated with tricyclic antidepressants are attributable to anti-α-adrenergic, anticholinergic,
and antihistamine effects?

A

Orthostatic hypotension, sexual dysfunction, constipation, dry mouth, urinary retention, visual disturbances, sedation, and weight gain

115
Q

What are the symptoms of tricyclic antidepressant toxicity?

A

Coma, convulsion, cardiotoxicity (three Cs), mydriasis, and hyperthermia

116
Q

How is tricyclic antidepressant toxicity best treated?

A

Cyproheptadine or benzodiazepines for seizure, anti-arrhythmics, and supportive care

117
Q

What antidepressant drug class includes amoxapine, bupropion, maprotiline, trazodone, mirtazapine, nefazodone, and venlafaxine?

A

Heterocyclic antidepressants

118
Q

Which heterocyclic antidepressant is most likely to be associated with priapism and sedation?

A

Trazodone

119
Q

Which heterocyclic antidepressants are most likely to be associated with seizure and cardiotoxicity?

A

Amoxipine and maprotiline

120
Q

Which heterocyclic antidepressant is most likely to be associated with extrapyramidal side effects?

A

Amoxipine

121
Q

Which heterocyclic antidepressants are associated with cytochrome P450 enzyme inhibition?

A

Nefazodone and venlafaxine

122
Q

Which heterocyclic antidepressant is used in the treatment of nicotine addiction?

A

Bupropion

123
Q

What antidepressant drug class includes citalopram, fluoxetine, fluvoxamine, paroxetine, and sertraline?

A

Selective serotonin reuptake inhibitors (SSRIs)

124
Q

What is the mechanism of action of the SSRIs?

A

Selective inhibition of presynaptic serotonin reuptake

125
Q

What are the common side effects of SSRIs?

A

Anxiety, insomnia, nausea, and sexual dysfunction

126
Q

What are the symptoms of SSRI toxicity?

A

Agitation, confusion, coma, muscle rigidity, hyperthermia, seizure, and autonomic instability

127
Q

How is SSRI toxicity best treated?

A

Cyproheptadine or benzodiazepine for seizure, and supportive care

128
Q

What antidepressant drug class includes phenelzine, tranylcypromine, and isocarboxazid?

A

Monoamine oxidase (MAO) inhibitors

129
Q

What is the mechanism of action of the MAO inhibitors?

A

Nonselective inhibition of metabolism of serotonin, norepinephrine, and dopamine by MAO-A and MOA-B

130
Q

What are the common side effects of MAO inhibitors?

A

Orthostatic hypotension, insomnia, and weight gain

131
Q

What drugs can provoke a hypertensive crisis when coadministered with MAO inhibitors?

A

Indirect-acting sympathomimetics (cocaine, amphetamine) and tyramine (red wine, aged cheese)

132
Q

What are the symptoms associated with serotonin syndrome?

A

Muscle rigidity, hyperthermia, autonomic instability, and seizure

133
Q

Coadministration of which drugs is associated with serotonin syndrome?

A

SSRIs, tricyclic antidepressants, MAO inhibitors, meperidine, and/or dextromethorphan

134
Q

What drugs are indicated in the first-line treatment of bipolar disorders?

A

Lithium, valproic acid, and olanzapine

135
Q

What is the mechanism of action of lithium in the treatment of bipolar disorders?

A

Inhibition of neuronal phosphoinositide recycling

136
Q

Why are atypical antipsychotics and/or benzodiazepines indicated in the initial treatment of bipolar disorders?

A

Lithium has slow onset of action.

137
Q

What hematologic side effect is associated with lithium?

A

Leukocytosis

138
Q

What reversible renal side effect is associated with lithium?

A

Nephrogenic diabetes insipidus

139
Q

Why does the plasma concentration of lithium have to be monitored regularly?

A

Lithium has a narrow therapeutic index.

140
Q

What is the therapeutic index?

A

Ratio of the median toxic (TD50) or lethal (LD50) dose to the median effective dose (ED50)

141
Q

What alteration of neurochemistry is responsible for the symptoms of parkinsonism and Parkinson disease?

A

Dopamine deficiency and/or ACh excess in the striatum

142
Q

What is the mechanism of action of L-dopa?

A

Synthetic precursor converted to dopamine by DOPA decarboxylase.

143
Q

How does coadministration of carbidopa increase the potency of L-dopa?

A

Inhibition of peripheral conversion of L-dopa to dopamine

144
Q

What chemical property of carbidopa is responsible for preferential inhibition of peripheral L-dopa metabolism?

A

Poor lipid solubility prevents diffusion across blood-brain barrier.

145
Q

What other peripheral enzyme inhibitors enhance the potency of L-dopa?

A

Entacapone and tolcapone

146
Q

What is the mechanism of action of entacapone?

A

Inhibition of peripheral conversion of L-dopa to 3-O-methyldopa by catecholamine-O-methyltransferase (COMT)

147
Q

To what drug class do the antiparkinson medications bromocriptine and pergolide belong?

A

Ergot alkaloids

148
Q

What are the symptoms of ergotism toxicity (St. Anthony’s fire)?

A

Disorientation, hallucination, convulsion, muscle cramps, and dry gangrene of extremities

149
Q

What drug of abuse is an ergot alkaloid?

A

Lysergic acid diethylamide (LSD)

150
Q

Why is selegiline, a selective MAO-B inhibitor, an effective treatment for parkinsonism?

A

MAO-B is CNS-specific and preferentially metabolizes dopamine

151
Q

What is the mechanism of action of antiparkinsonian agents benztropine and trihexyphenidyl?

A

Inhibition of the striatum muscarinic anticholinergic receptors

152
Q

What alteration in neurochemistry is the basis for current therapeutics in Alzheimer disease?

A

Functional cortical and hippocampal ACh deficiency

153
Q

What class of drug is indicated in the treatment of mild to moderate Alzheimer disease?

A

AChE inhibitors, eg, rivastigmine, donepezil, galantamine, and tacrine

154
Q

What is the mechanism of action of the AChE inhibitors in the treatment of Alzheimer disease?

A

Increased concentration of synaptic terminal ACh

155
Q

What other enzyme is inhibited by rivastigmine and tacrine?

A

Butyrylcholinesterase

156
Q

What drug class is indicated in the treatment of moderate to severe Alzheimer disease?

A

NMDA antagonists (memantine)

157
Q

What is the mechanism of action of the NMDA antagonists in the treatment of Alzheimer disease?

A

Inhibition of glutaminergic NMDA calcium conductance

158
Q

What is tolerance?

A

Habituation to the physiologic effects of a drug

159
Q

What are the pharmacodynamic effects of tolerance?

A

It decreases efficacy and larger doses are required to achieve the same effect.

160
Q

What is dependence?

A

A physiologic and/or psychologic state characterized by compulsive substance use

161
Q

What are the effects of alcohol intoxication?

A

Increased sociability and impairment of motor, cognitive, and memory function

162
Q

What is the mechanism of action of alcohol intoxication?

A

Incompletely understood, GABAergic and generalized CNS depression

163
Q

How is alcohol metabolized?

A

Via a two-step process with zero- order kinetics and a toxic intermediate

164
Q

What is the first step in metabolism of alcohol?

A

Conversion of alcohol to acetaldehyde by cytoplasmic alcohol dehydrogenase

165
Q

What is the second step in metabolism of alcohol?

A

Conversion of acetaldehyde to acetate by mitochondrial aldehyde dehydrogenase

166
Q

What are the effects of acetaldehyde toxicity?

A

Nausea, vomiting, hyperventilation, tachycardia, chest pain, and dyspnea

167
Q

What agent used in the treatment of alcohol dependence inhibits aldehyde dehydrogenase causing acetaldehyde accumulation?

A

Disulfiram

168
Q

What is the mechanism of action of benzodiazepine in the treatment of alcohol dependence?

A

Withdrawal seizure treatment and prophylaxis via GABA-A receptor activation

169
Q

What is the mechanism of action of naltrexone in the treatment of alcohol dependence?

A

Reduces cravings via opioid receptor inhibition

170
Q

What are the symptoms of acute alcohol withdrawal?

A

Agitation, tremor, insomnia, nausea, vomiting, diarrhea, arrhythmia, delirium tremens, and potentially-fatal seizure

171
Q

What is the treatment for acute alcohol withdrawal?

A

Thiamine, benzodiazepine taper, clonidine, and propranolol for hyperadrenergic state

172
Q

What other CNS depressants are frequently abused?

A

Benzodiazepines and barbiturates

173
Q

What are the symptoms of CNS depressant withdrawal?

A

Agitation, delirium, insomnia, and potentially-fatal seizure

174
Q

What drugs are indicated in the treatment of CNS depressant withdrawal?

A

Long-acting benzodiazepine to suppress acute symptoms, tapering dose

175
Q

What drugs are indicated in the treatment of CNS depressant toxicity?

A

Flumazenil for benzodiazepine toxicity

176
Q

What is the mechanism of action of CNS stimulants?

A

Increased synaptic terminal concentration of dopamine, norepinephrine, and serotonin

177
Q

What are the symptoms of CNS stimulant intoxication?

A

Euphoria, anxiety, insomnia, anorexia, tachycardia, hypertension, and mydriasis

178
Q

What are the symptoms of CNS stimulant withdrawal

A

Depression, fatigue, increased sleep, and increased appetite

179
Q

What are the symptoms of CNS stimulant toxicity?

A

Arrhythmia, MI, cardiovascular, hallucination, paranoia, hyperthermia, seizure, and death

180
Q

What drugs are indicated in the treatment of CNS stimulant toxicity

A

Benzodiazepine and antipsychotic agents

181
Q

What are the symptoms of opioid intoxication?

A

Euphoria, analgesia, cough suppression, miosis, and constipation

182
Q

What are the symptoms of opioid withdrawal?

A

Mydriasis, diarrhea, rhinorrhea, lacrimation, diaphoresis, and yawning

183
Q

What drugs are indicated in the treatment of opioid withdrawal?

A

Methadone, LAAM, buprenorphine, and clonidine

184
Q

What are the symptoms of opioid toxicity?

A

Nausea, vomiting, sedation, respiratory depression, bradycardia, hypotension, coma, and death

185
Q

What drugs are indicated in the treatment of opioid toxicity?

A

Naloxone and naltrexone

186
Q

What is the mechanism of action of cannabis (marijuana, hashish) intoxication?

A

Cannabinoid (CB1 and CB2) receptor activation

187
Q

What are the symptoms of cannabis intoxication?

A

Euphoria, disinhibition, perceptual changes, conjunctival injection, dry mouth, and increased appetite

188
Q

What is the mechanism of action of hallucinogens (LSD, mescaline, psilocybin) intoxication?

A

Serotonin receptor activation

189
Q

What are the symptoms of hallucinogen intoxication?

A

Perceptual changes and synesthesia

190
Q

What are the symptoms of hallucinogen withdrawal?

A

No physiologic dependence

191
Q

What is the mechanism of action of phencyclidine (PCP; “angel dust”)?

A

NMDA receptor antagonist

192
Q

What are the symptoms of PCP intoxication?

A

Agitation, nystagmus, rigidity, decreased response to pain, hyperacusis, paranoia, and violent behavior

193
Q

What is the mechanism of action of 3,4-methylenedioxymethamphetamine (MDMA; “ecstasy”) intoxication?

A

Increased synaptic terminal concentration of serotonin

194
Q

What are the symptoms of MDMA intoxication?

A

Euphoria, disinhibition, and perceptual changes

195
Q

What are the symptoms of inhalant (glue, solvents) toxicity?

A

Motor and cognitive impairment and multiple organ dysfunction

Pharmacology by Somebody (25 decks)

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