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Behavioral Pharmacology > Chapter 18: Anxiety Disorders > Flashcards

Chapter 18: Anxiety Disorders Flashcards

1
Q

agoraphobia

A

Fear of public places.

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2
Q

alcohol

A

Ethyl alcohol is an organic compound that is a product of fermentation and belongs to the class of sedative–hypnotics.

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3
Q

anticipatory anxiety

A

Feeling of extreme worry over the possibility that a certain unpleasant event will occur in a particular, often public, situation.

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4
Q

anticonvulsants

A

Drugs, such as benzodiazepines, that prevent or control seizures. They are used to treat epilepsy.

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5
Q

anxiolytics

A

Drugs that alleviate feelings of anxiety in humans and that reduce anxiety-related behaviors in animals.

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6
Q

behavioral desensitization

A

Technique used to treat phobias by introducing the fear-inducing stimulus in increments, allowing the patient to maintain a relaxed feeling in its presence.

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7
Q

buspirone (Buspar)

A

Drug that stimulates 5-HT1A receptors. Symptoms include increased appetite, reduced anxiety, reduced alcohol cravings, and a lower body temperature. It is prescribed as an antianxiety medication.

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8
Q

CNS depressants

A

Large category of drugs that inhibit nerve cell firing within the central nervous system. They include sedative–hypnotics and are used to induce sleep and to treat symptoms of anxiety; include barbiturates, benzodiazepines, alcohol (all reduce neuron excitability)

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9
Q

compulsions

A

Repetitive tasks that an individual feels obligated to complete in an effort to quell the anxiety caused by obsessive thoughts.

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10
Q

general anxiety disorder

A

An anxiety disorder characterized by excessive worrying that does not have a specific cause.

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11
Q

hypnotics

A

Drugs, such as benzodiazepines, that help a patient to fall asleep and stay asleep.

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12
Q

long-acting drug

A

Drug that has low lipid solubility, taking more than an hour to reach the brain. Slow metabolism or presence of active metabolites allows for prolonged effects that persist for long periods.

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13
Q

muscle relaxants

A

Drugs, such as benzodiazepines, that reduce muscle tension in a patient.

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14
Q

obsessions

A

Worrying thoughts or ideas that an individual cannot easily ignore

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15
Q

obsessive–compulsive disorder (OCD)

A

Psychiatric anxiety disorder characterized by persistent thoughts of contamination, violence, sex, or religion that the individual cannot easily ignore, and that cause the individual anxiety, guilt, or shame, etc. and may be accompanied by compulsive repetitive behaviors.

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16
Q

panic attack

A

Feeling of extreme fear that was not preceded by a threatening stimulus.

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17
Q

panic disorder

A

Disease involving repeated attacks of extreme fear, occurring either without warning or in an environment similar to where previous panic attacks occurred.

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18
Q

phobias

A

Fears of specific objects or situations that are recognized as irrational.

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19
Q

posttraumatic stress disorder (PTSD)

A

Emotional disorder that develops in response to a traumatic event, leaving the individual feeling a sense of fear, helplessness, and terror. Symptoms include sleep disturbances, avoidance of stimuli associated with the trauma, intrusive thoughts reliving the event, and a numbing of general emotional responses. An increase in suicidal thoughts has also been observed.

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20
Q

sedative–hypnotics

A

Class of drugs that depresses nervous system activity. They are used to produce relaxation, reduce anxiety, and induce sleep.

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21
Q

short/intermediate-acting drugs

A

Drugs that are moderately lipid-soluble, reaching the brain within 20 to 40 minutes. The drugs lose effectiveness over time due to liver metabolism.

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22
Q

ultrashort-acting

A

Drugs that are highly lipid-soluble, reaching the brain within seconds when administered intravenously. They lose effectiveness quickly, as they rapidly redistribute to inactive drug depots in fat, bone, and muscle.

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23
Q

amygdaloid complex

A

structure deep within the temporal lobes; major component of several emotional processing circuits

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24
Q

components of emotional processing circuits

A

amygdala, limbic cortex, hypothalamus, hippocampus

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25
Q

what do the emotional circuits do?

A

evaluate environmental stimuli, contextual cues and cognitions that have emotional relevance and initiate appropriate responses via the amygdala

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26
Q

where does the amygdala receive information from

A

sensory thalamus, sensory and association cortices, hippocampal formation

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27
Q

what does the central nucleus of the amygdala do?

A

orchestrates the components of fear: ANS activation, enhanced reflexes, increased vigilance, activation of the hypothalamic-pituitary-adrenal (HPA) axis, and others

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28
Q

why does the central nucleus of the amygdala have such widespread effects?

A

because it has connections with multiple brain areas; lateral hypothalamus- activates sympathetic nervous system; periaqueductal gray- causes freezing; locus coeruleus- initiates arousal and vigilance

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29
Q

what is the central nucleus of the amygdala essential for?

A

the fear response

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30
Q

what does the bed nucleus of the stria terminalis (BNST) do?

A

called the extended amygdala; responsible for the behavioral responses in anxiety; projects to the same areas as the amygdala but acts differently

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31
Q

response by central nucleus of the amygdala

A

is rapid

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32
Q

how does the response of the BNST differ from the central nucleus of the amygdala?

A

initiates components of the emotional response when the stimuli are less precise predictors of a potentially dangerous situation. It produces a state of sustained preparedness for an unclear danger and a prolonged period of anticipation that something unpleasant might occur; persists long after the initial stimulus is ended

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33
Q

alterations of BNST

A

chronic and unpredictable stress increases dendritic length and branching as well as volume of BNST;

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34
Q

what modulates BNST?

A

sex hormones–may explain gender differences

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35
Q

what does the amygdala help form?

A

emotional memories aka conditioned fear response; making an association between an environmental stimulus and an aversive stimulus; emotional memories are established quickly and are long lasting

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36
Q

connection between the amygdala and hippocampus?

A

contributes to the enhancement of memory consolidation through its connections with hippocampus

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37
Q

role of hippocampus in anxiety

A

reciprocal connections with the amygdala modulate emotional responses on the basis of context

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38
Q

role of PFC

A

fear extinction–learning that a cue that once predicted danger no longer does

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39
Q

corticotropin-releasing-factor

A

small neuropeptide that controls the neuroendocrine (HPA axis), autonomic, and behavioral responses to stress.

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40
Q

what activates the HPA axis?

A

the release of CRF from the hypothalamus in response to stress

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41
Q

what does CRF cause?

A

inducing the anterior pituitary to release the stress hormone adrenocorticotropic hormone (ACTH) into the blood, which in turn increases the release of glucocorticoids such as cortisol from the adrenal cortex

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42
Q

what does elevated levels of cortisol lead to?

A

a negative feedback loop by binding to receptors in the hippocampus, hypothalamus and pituitary, which inhibits HPA axis function and brings cortisol levels back to normal

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43
Q

intraventricular administration of CRF

A

stimulates the sympathetic nervous system and causes increases in plasma adrenaline and increased heart rate and blood pressure

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44
Q

effects of CRF

A

wide-ranging on feeding, GI activity, and energy balance that are consistent with preparation for dealing with environmental stressors

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45
Q

direct neuronal effects of CRF

A

strong excitatory effects;

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46
Q

where are a lot of CRF nerve endings found?

A

the amygdala

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47
Q

locus coeruleus

A

major cluster of noradrenergic cell bodies in the dorsal pons that send axons rostrally to several brain areas to increase vigilance and attention to physiologically relevant stimuli

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48
Q

reciprocal connection between the locus coeruleus and the amygdala

A

provide a mechanism for generating arousal, orienting and responding to fear evoking stimuli

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49
Q

effects of NE agonists and antagonists

A

alpha2-autoreceptor antagonist (yohimbine) increases NE release and leads to fear response; alpha2 agonist reduces NE leads to antianxiety effects

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50
Q

NE and anxiety

A

is the neurotransmitter released at the target visceral organs, including heart, during sympathetic activation. the catecholamine adrenaline released from the adrenal medulla produces widespread effects that prepare the individual to respond to danger

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51
Q

what does NE play a role in?

A

formation of emotional memories

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52
Q

is it possible to stop formation of traumatic memories?

A

yes—blocking beta-adrenergic receptors right after a severe trauma; this may also disrupt already consolidated traumatic memories and associated physiological responses

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53
Q

beta blockers and emotional memories

A

they do not seem to impair declarative memory of the association of the conditioned and unconditioned stimuli but diminishes the emotional effects

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54
Q

how to benzodiazepines work?

A

NE cells in the NE locus coeruleus are excited by CRF synaptic input and are inhibited by y-aminobutryic acid (GABA) and serotonin (5-HT), as well as by stimulation of alpha2-adrenergic somatodendritic autoreceptors. benzodiazepines enhance the inhibitory function of GABA, reduced LC firing may be responsible for some of the anxiolytic effects

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55
Q

GABA

A

inhibitory amino acid neurotransmitter; modulates anxiety

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56
Q

GABAa receptor complex

A

comprises a chloride Cl- channel that when opened following GABA binding allows Cl- to enter the cell, causing hyperpolarization; several sedative hypnotics enhance function of GABA causing sedation and reduced anxiety

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57
Q

benzodiazepine binding site

A

are widely distributed and are found on many GABA complexes in the amygdala, limbic system and cerebral cortex

58
Q

benzodiazepine binding site receptor antagonist

A

flumazenil–binds to BDZ but has no effect on GABA; second group binds to BDZ sites and act as an inverse agonist by produce the opposite actions of the BDZ drugs (increased anxiety, arousal, seizures)

59
Q

beta-carboline

A

class of BDZ inverse agonists; produce extreme anxiety; acts by uncoupling GABA receptors from the Cl- channels so that GABA is less effective in causing entry of Cl- into cells leading to increased membrane excitability

60
Q

benzodiazepines and panic disorder

A

these individuals show less benzodiazepine binding in the CNS, frontal lobes (orbitofrontal cortex, medial prefrontal cortex, insula) and limbic structures involved in the anxiety neurocircuitry; they are less sensitive to BDZs

61
Q

neuroactive steroids

A

provide an additional modulatory role in anxiety; family of neurosteroids that are synthesized from cholesterol in both the central and peripheral nervous systems; are elevated by physiological stressors and have potent anticonvulsant effects

62
Q

how do neuroactive steroids work?

A

bind to a site on the GABAa receptor and potentiate the effect of GABA by increasing the duration of GABA induced chloride channel opening

63
Q

levels of neuroactive steroids in those with anxiety disorders

A

panic–baseline levels are elevated (natural self-defense); in GAD and social phobia levels are lower

64
Q

why do we think serotonin plays a role in anxiety?

A

because SSRIs, which enhance 5-HT function have an anxiolytic effect; SSRIs desensitize terminal 5-HT autoreceptors in the orbitofrontal cortex

65
Q

desensitization effect of 5-HT

A

desensitized autoreceptors indicate that more 5-HT is released to act on postsynaptic 5-HT2 receptors. If this occurs in the locus coeruleus, the enhanced serotonergic activity that gradually occurs may explain the progressive reduction in LC firing

66
Q

Differing effects of serotonin

A

tasks that require active coping (making escape)- 5-HT agonists are anxiolytic

tasks involving passive behavior– 5-HT agonists increase anxiety

67
Q

what determines the effect of 5-HT?

A

what receptor is involved, acute/chronic treatment, the specific brain regions involved in fear versus anxiety

68
Q

serotonin and fetal development

A

appropriate regulation of both pre and post natal serotonergic function is needed to prevent anatomical, functional and behavioral abnormalities; polymorphism of the promotor region of the 5-HT reuptake transporter (SERT) gene show increased emotionality and anixety

69
Q

short version of the 5-HT reuptake transporter gene

A

express fewer reuptake transporters than those with long alleles, which means that more 5-HT remains in the synapse

70
Q

what may mediate the neurodevelopmental effect of 5-HT?

A

the 5-HT1a receptor

71
Q

role of DA

A

a modulatory role for DA is suggested by the significant DA projections from the VTA to the mPFC and limbic regions including the amygdala

72
Q

stress and DA

A

stress increases firing of mesocortical DA neurons and increases DA turnover in the prefrontal cortex

73
Q

DA and anxiety

A

DA projections to the amygdala from the VTA inhibit the normal descending inhibition from the mPFC and permit expression of adaptive anxiety responses. DA cells are activated by stressful and environmental stimuli. The released DA acting on D1 and D2 receptors in the amygdala reduces the inhibitory control of local GABA interneurons that are activated by the PFC. Decreasing inhibitory control increases amygdaloid activation

74
Q

trait anxiety

A

the enduring characteristic to experience anxiety in a variety of situations

75
Q

role of behavioral inhibition

A

behavioral inhibition in young children is associated with a CRF gene polymorphism and these individuals are more likely to develop social phobia and panic disorder

76
Q

early stress

A

alters the programming of the HPA axis causing a hyperactive hormonal response to challenge; changes in DNA methylation of promoter elements that control the expression of genes within the stress circuits

77
Q

epigenetic effects

A

reduced methylation of the CRF promoter region in the hypothalamus and central nucleus of the amygdala and increased methylation of the glucocorticoid receptor promoter region. These may be expected to contribute to stress circuit programming during fetal development

78
Q

Role of HPA axis activation

A

is critical for survival; excessive HPA activation leads to damaging effects on the body, including changes in brain structure and synaptic transmission. Prolonged stress and the subsequent elevation of glucocorticoids impair the function of the hippocampus by reducing neurogenesis, failing to protect cells against cell death and preventing the normal dendritic growth and elaboration that enhance synaptic connectivity

79
Q

effects of prolonged stress on hippocampus

A

synaptic structures atrophy

80
Q

brain changes in response to excessive stress

A

changes in limbic structures that comprise emotional regulation circuits, including hippocampus, amygdala, and PFC;

81
Q

effects of prolonged stress on amygdala

A

dendritic growth, increased aborization and increased spine connectivity are seen

82
Q

behavioral effects of impaired hippocampus

A

impaired hippocampus mediated learning that helps an individual to distinguish between context-appropriate and context-inappropriate emotional responding and enhanced amygdala mediated fear conditioning

83
Q

what is the medial prefrontal area responsible for?

A

extinguishing conditioning emotional responses –shows decrease in dendritic connections

84
Q

how males typically respond to danger

A

fighting or running

85
Q

how females typically respond to danger

A

engaging in social interaction such as organizing the herd and protecting the young

86
Q

differences about women

A

women have a hormonal regulation of the stress response that is distinctive from men; when estrogen levels are elevated, sensitivity to stress is greater and glucocorticoid release is increased

87
Q

neuroadaptive effect of female hormones and differences with men

A

the resistance of the female hippocampal cells to stress-induced damage suggest this

88
Q

effect of glucocorticoid levels

A

dendritic arborization in the amygdala of chronically stressed males is enhanced, and this is associated with enhanced conditioned fear acquisition; this is correlated with increased glucocorticoid levels in men but not women; although males have a greater neurobiological response to stress, their affinity to glucocorticoids in the hippocampus is almost twice as great as in females, suggesting the negative feedback that returns stress hormone levels to normal is more effective

89
Q

panic attacks

A

normal physiological response that is not regulated by appropriate feedback. It is also possible that the anxiety response is triggered too easily and may be initiated by environmental events that are not consciously processed

90
Q

what rises during a panic attack?

A

blood and urine levels of NE and ephinephrine

91
Q

what may increase susceptibility to panic disorder?

A

adrenergic dysfunction in the neurons originating in the locus coeruleus—produce widespread effects including arousal and vigilance

92
Q

brain abnormalities in panic disorder

A

small white matter lesions in the temporal lobes and enlargement of the lateral ventricles, reduction in amygdala volume, reduced hippocampal volume, reduced functioning in PFC

93
Q

pa-leng

A

morbid fear of the cold and loss of body heat

94
Q

effective treatment for phobias do what

A

reduces the hyperactivity of the amygdala, the bed nucleus of the stria terminalis, anterior cingulate cortex and insula

95
Q

brain activity in social anxiety disorder

A

increased blood flow in the amygdala during public speaking; increased activity also in other limbic areas (insula, hippocampus), which leads to anticipatory anxiety and autonomic response

96
Q

risk factors for PTSD

A

family history of psychopatholoy, they may perceive events as more traumatic than others, children with parents with PTSD have an increased risk for PTSD and also have lower than normal blood cortisol; it is possible that the normal feedback mechanism that turns off cortisol secretion is hypersensitive in PTSD

97
Q

physical brain changes in PTSD

A

reduction in hippocampus volume which may explain some of the cognitive symptoms of PTSD; unsure of causation; may represent a vulnerability factor; also, smaller less active anterior cingulate cortices and medial prefrontal cortices which inhibit the amygdala and establish extinction of conditioned emotional responses

98
Q

what do PET scans show in OCD?

A

high levels of metabolic activity in the basal ganglia and other brain areas

99
Q

neurobiological model of OCD

A

abonormalities in a neural loop connecting the basal ganglia (caudate and globus pallidus), frontal lobe, thalamus, and anterior cingulate cortex

100
Q

what is different in the brains of OCD?

A

the caudate–an area that normally helps sequence and elaborate behavior; may lead to stereotyped behavior and perseveration

101
Q

role of anterior cingulate cortex in OCD

A

dysfunction in OCD may be responsible for reduced response inhibition and inflexible behavior. Increased neural activity of the anterior cingulate cortex is linked with compulsive behavior

102
Q

why do SSRIs sometimes help OCD?

A

they enhance the activity of the serotonergic neurons of the raphe nuclei and this interrupts the neural loop by inhibiting cell firing in the caudate

103
Q

effect of drugs that reduce anxiety

A

produce a calm and relaxed state with drowsiness and mental clouding, incoordination, prolonged reaction time.
higher doses- induce sleep
highest doses- coma, death

104
Q

primary method of action of anxiety drugs

A

primary mechanism of action involved enhancing GABA transmission. GABA is the major inhibitory neurotransmitter and thus has receptors on most cells in CNS

105
Q

what does the GABAa receptor complex do?

A

regulates the Cl- channel that increases Cl- current into the cell to move the membrane potential farther away from the threshold for firing

106
Q

GABA agonists

A

inhibit cell firing

107
Q

how to barbiturates and benzodiazepines work?

A

they have binding sites as part of the GABAa receptor complex and enhance the inhibitory effects of GABA

108
Q

what happens when BDZs bind to their modulatory sites on the GABAa complex?

A

they enhance the effects of GABA by increasing the number of times the channel opens. in the absence of GABA, the benzodiazepines have no effect on Cl- channel opening. Presence of BDZ alters the physical state of the receptors, increasing the receptor affinity for GABA so that GABA opens the channels more easily

109
Q

drugs that bind most readily to the BDZ receptor

A

clinically effective at low doses

110
Q

how do barbiturates work?

A

increase affinity of GABAa receptor for GABA; they increase the duration of the opening of GABA-activated Cl- channels rather than the number of openings; they directly open the Cl- channel without GABA

111
Q

BNST

A

nucleus of the stria terminalis– secondary pathway that carries more of a behavioral response to anxiety; separate from amygdala but responds similarly

112
Q

inverse agonist

A

effect is opposite that of an agonist beta-caboline (uncouples GABA from Cl- channels to make GABA less effective—> increase in anxiety)

113
Q

what have benzodiazeptines replaced?

A

barbiturates

114
Q

structure of barbiturates

A

all have a similar ring structure but vary in length and complexity which determines differences in lipid solubility

115
Q

ultrashort-acting barbiturates

A

pentothal and evipal; are highly lipid soluble and readily penetrate into the brain and put an individual to sleep within 10 to 20 seconds

116
Q

short/intermediate acting barbiturates

A

are moderately lipid soluble and take longer to reach significant brain levels; produce relaxation and sleep in about 20-30 minutes and last about 5-8 hours; termination depends more on liver metabolism than redistribution; most likely to be abused

117
Q

long acting barbiturates

A

have poor lipid penetration; onset takes 1+ hours, prolonged action for 10-12 hours; used to treating seizures

118
Q

side effects of barbiturates

A

induce sleep but reduce REM; cognitive side effects (mental clouding, loss of judgment, slowed reflexes); high doses (intoxication, staggering, jumbled speech, impaired thinking, coma, death);

119
Q

barbiturates and tolerance

A

when used repeatedly barbiturates increase the number of liver microsomal enzymes which enhances drug metabolism, producing lower blood levels (metabolic tolerance) and reduced effectiveness

120
Q

what shows the greatest tolerance in barbiturates?

A

mood changes and sedation

121
Q

what barbiturate effects do not show tolerance?

A

the lethal respiratory-depressant action of the drug

122
Q

barbiturate physical dependence

A

significant physical dependence—termination after long term use produces a potentially fatal rebound hyperexcitability withdrawal syndrome

123
Q

benzodiazepines

A

target anxiety without producing excessive sedation; has a low incidence of tolerance, a less severe withdrawal syndrome than barbiturates, and a very safe therapeutic index

124
Q

structure of benzodiazepines

A

all have a similar structure but the choice of a particular one depends primarily on the speed of onset and the duration of drug action, which is determined by the drugs lipid solubility

125
Q

what determines benzodiazepines duration of action?

A

1-differences in their method of biotransformation

2- extent of redistribution to inactive depots such as skeletal muscle and fat

126
Q

how do long acting benzodiazepines work?

A

they undergo several metabolic steps to produce multiple active metabolites that may have half-lives of 60 hours or longer

127
Q

benzodiazepines and surgery

A

useful for presurgical anesthesia during which the patient is conscious but is less aware of his surroundings; can be used for rapid onset of relaxation and deep sleep during brief surgical procedures (short half life = recovery in a few hours); sleep aid/ date rape drug

128
Q

benzodiazepines and reducing anxiety

A

relieve the sense of worry and fearfulness and physical symptoms

129
Q

longer acting benzodiazepines

A

useful hypnotics– shorten the time needed to fall asleep and increase duration of sleep time and reduce the number of nighttime wakings; all sleep medications may cause reduced alertness the next day and rebound insomnia

130
Q

what else can benzodiazepines be used for?

A

muscle relaxants, anticonvulsants, preventing alcohol/ barbiturate withdrawal symptoms

131
Q

advantage of benzodiazepines over other sedative hypnotics

A

high therapeutic index; overdose is extremely rare; safer than barbiturates because they don’t increase liver enzymes; reduced tolerance and fewer drug interactions; lower probability of physical dependence and abuse; much less reinforcing

132
Q

high doses of benzodiazepines can produce what?

A

disorientation, cognitive impairment, amnesia, a paradoxical increase in aggressiveness, irritability, anxiety, over dose is rare except if taken in combination with other CNS depressants; chronic use/dependence can occur; abstinence syndrome–though not life threatening;

133
Q

symptom of benzodiazepine abstinence syndrome

A

insomnia, restlessness, headache, anxiety, mild depression, subtle perceptual distortions, muscle pain, twitches, panic, delirium, seizures

134
Q

benzodiazepines partial agonists

A

bind readily to benzodiazepine modulatory sites but produce less of an effect; relieve anxiety with reduced side effects, less sedation and muscle relaxation than benzodiazepines, enhanced safety— BUT in humans clinical efficacy was not maintained over time–no practical utility

135
Q

subunit selective drugs

A

drugs may be developed to act selectively on GABAa receptors with distinct alpha subunits isoforms

136
Q

second generation anxiolytics

A

buspirone

137
Q

buspirone

A

has significant anxiolytic actions though it is much less effective in reducing the physical symptoms of anxiety than the cognitive aspects of worry and poor concentration

138
Q

advantages of buspirone

A

usefulness in treating depressing that often accompanies anxiety; not accompanied by sedation, confusion, mental clouding; does not enhance the CNS depressant effects of alcohol; no rebound withdrawal syndrome

139
Q

disadvantages of buspirone

A

takes several weeks before anxiolytic effects are seen; does not show cross tolerance or cross dependence with benzodiazepines or sedative hypnotics and thus cant be used to help with alcohol withdrawal; lacks the hypnotic effects to treat insomnia;

140
Q

how does buspirone work?

A

does not enhance GABA function but instead acts as a partial agonist at 5-HT1a receptors; down regulation of the 5-HT receptors may be responsible for the delayed onset o action

141
Q

SSRIs

A

have been found to be effective in reducing OCD symptoms possibly by blocking 5-HT function by blocking reuptake of the monoamine

142
Q

tricyclic antidepressants and MAOIs

A

also seen as effective in treating some anxiety disorders although side effects are often troublesome

Behavioral Pharmacology (11 decks)

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