anxiety and anti-anxiety medications
TRANSCRIPT
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(Spielberger & Rickman, 1991)
What is anxiety?
Anxiety has been defined as an unpleasantemotional state or reaction that can bedistinguished from others, such as anger or grief, bya unique combination of experiential qualities and
physiological changes.
An anxiety state consists of feelings of tension,apprehension, nervousness, and worry, andactivation of the autonomic nervous system.
Physiological manifestations generally includeincreased blood pressure, rapid heart rate,sweating, dryness of mouth, vertigo, irregularities inbreathing, and muscular skeletal disturbances.
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(Spielberger & Rickman, 1991)
Normal VS. Abnormal
Anxiety
Anxiety is normal in any situation in which an
immediate danger may result in physical harm.
Anxiety is also a normal reaction to social-evaluative situations that pose threats to self-
esteem or psychological well-being.
Neurotic, clinical, or abnormal anxiety occurs in
situations in which there is no real physical orpsychological danger, or when the emotional
reaction is disproportionate in intensity to the
actual danger.
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(Spielberger & Rickman, 1991)
More Anxiety Definitions
State anxietyA temporal cross-sectionin the emotional stream of life of a person,consisting of tension, apprehension,
nervousness, and worry and activation(arousal) of the autonomic nervoussystem.
Trait anxietyRelatively stable individualdifferences in anxiety-proneness, that is,differences between individuals in the
tendency to perceive stressful situationsas dangerous or threatening.
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Clinical Disorders (DSM-
IV)
1. Panic disorder (PD) with or without agoraphobia
2. Agoraphobia without history of PD
3. Specific phobia
4. Social phobia
5. Obsessive-compulsive disorder (OCD)
6. Posttraumatic stress disorder (PTSD)
7. Acute stress disorder
8. Generalized anxiety disorder (GAD)
9. Anxiety disorder due to a general medical condition
10. Substance-induced anxiety disorder11. Anxiety disorder NOS
*(Formore information on diagnostic criteria and symptoms, refer towww.adaa.org andwww.nimh.nih.gov/healthinformation/anxietymenu.cfm)
http://www.adaa.org/http://www.nimh.nih.gov/healthinformation/anxietymenu.cfmhttp://www.nimh.nih.gov/healthinformation/anxietymenu.cfmhttp://www.nimh.nih.gov/healthinformation/anxietymenu.cfmhttp://www.nimh.nih.gov/healthinformation/anxietymenu.cfmhttp://www.adaa.org/ -
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Explanations of Anxiety
Psychological theories1. Freuds theory
2. Cognitive
3. Behavioral
Biological theories1. Genetics
2. Neural and neuroendocrine pathwaysinvolved in bodys normal stressresponse (fight or flight)
3. Specific action by neurotransmittersand other neurochemicals
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(Preston et al., 2005)
Neural Pathways: Fight
or Flight Response
Stressful Event
Amygdala
Hypothalamus
Pituitary
Adrenal cortex
Cortisol
Cortex
Locus coeruleus
Sympathetic
nervous system
Adrenal medulla
Thyroid
ThyroxinAdrenaline Noradrenaline
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(Preston et al., 2005)
Neuroendocrine
Pathways (Detailed)
Amygdala
HypothalamusParabrachial
Nucleus
Periaquaductal
Gray Area
Locus Coeruleus
CRF TRH
SNS
Pituitary Pituitary
ACTH TSH
Adrenal
Cortex
Thyroid
Gland
Cortisol T3 T4
Freeze,
Avoid,
Escape
(NE)*
Inc. alertness
Inc. respiration
Adrenal Medulla
NE*
Through out
the bodyAdrenaline NE*
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(Preston et al., 2005)
Gamma-aminobutyric
acid (GABA)
GABA plays a role in activating
chloride ion channels.
Chloride ions (- charge) come into thecell and hyperpolarize the cell.
This results in calming of overall
brain excitation.
(see diagram on p. 103 of Preston et al.,
2005)
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(Preston et al., 2005)
Serotonin
Excitability of locus coeruleus (LC)
also mediated by serotonin.
Global decrease in serotonin thoughtto affect LC causing it to become
disinhibited (i.e., more sensitive to
activation)
Serotonin also hypothesized to
inhibit cellular reactivity in the
amygdala.
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(Preston et al., 2005)
Etiology of Clinical
Disorders
Primarily
psychogenic
1. GAD2. Acute stress
disorder
3. Specific
phobias4. Agoraphobia
Evidence forbiologicalfactors1. Social phobia
2. Anxietyassociated withgeneral medical
condition3. Panic disorder
- noradrenergic
hypothesis
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Anti-anxiety Medications (i.e.,
anxiolytics)
Benzodiazepines
Atypical benzodiazepines
Busipirone Antidepressants
Antihistamines
Beta blockers Clonidine
Tiagabine
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(Arikian & Gorman, 2001; Preston etal., 2005; Walsh, 1999)
Benzodiazepines
First drug of this type (Librium) created in 1957.
Mechanism: Interact with benzodiazepine receptorsand enhance the effect of GABA, increasing influx ofchloride ions.
Rapid effectwithin 30 minutes; Therapeutic effectwithin 1 week
Relatively short half-lives (see table on p. 190 ofPreston et al., 2005)
75% of users show moderate to marked
improvement in symptoms Mild and transient side effects
May become physically addictive and lead towithdrawal symptoms if discontinued abruptly.
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(Preston et al., 2005)
Atypical
Benzodiazepines
Benzodiazepine derivativesused as hypnotics.
1. Estazolam (ProSom)2. Quazepam (Doral)
3. Zolpidem (Ambien)
4. Zaleplon (Sonata)
Mechanism: Similar tobenzodiazepines.
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(Arikian & Gorman, 2001; Preston etal., 2005; Walsh, 1999)
Busipirone
Type: azapirone drug
Mechanism: Acts on 5-HT 1A receptor; thought to
balance serotonin levels by lowering them in
anxious persons. However, exact mechanismunknown.
Delayed effectTherapeutic effect within one or
two weeks.
Appears particularly effective in treatment of GAD.
Not addictive. Does not produce psychomotor impairment and
does not interact with other CNS depressants.
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(Arikian & Gorman, 2001; Preston etal., 2005; Walsh, 1999)
Antidepressants
Monoamine oxidaseinhibitors (MAO)created in mid 1950s
- MAO inhibitors not
frequentlyprescribed today dueto interaction withtyramine and theassociated foodrestrictions.
- Low therapeuticindex.
- See table on page167 of Preston et al.,2005 for drugexamples.
Cyclic drugs
- Most prescribed from
1950s 1980s
- Mechanism: Blockingreuptake of
norepinephrine,
acetylcholine, and
serotonin.
- Low therapeutic index.
- See table on page 167
of Preston et al., 2005
for drug examples.
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(Arikian & Gorman, 2001; Preston etal., 2005; Walsh, 1999)
Antidepressants (cont)
Selective serotonin reuptake
inhibitors (SSRIs)
- Introduced in 1980s- More potent than cyclic drugs.
- Long half-life.
- Bigger therapeutic index and fewer side
effects.
- See table on page 167 of Preston et al.,
2005 for drug examples.
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(Preston et al., 2005; Walsh, 1999)
Other Anti-Anxiety
Agents
Antihistamines
Mechanism: Block
histamine receptors in
the CNS associated
with anxiety and
agitation.
Rapid effectwithin
20-30 min.
May cause drowsiness,
impaired performance,and develop tolerance
to anxiolytic effects.
Beta Blockers
Mechanism: Block theeffects ofnorepinephrine at the
receptor in the brainand the peripheralnervous system.
Originally developed totreat hypertension.
Effective at reducing
physical symptoms ofanxiety (i.e., rapidheart beat, muscletension, dry mouth).
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(Preston et al., 2005)
Other Anti-Anxiety
Agents
Clonidine
Mechanism: alpha-2
adrenergic agonist;
presynaptic inhibitorof norepinephrine
release
Originally used to
treat hypertension
Tiagabine
Mechanism: GABA
reuptake inhibitor
Originally ananticonvulsant
May be useful in
treating PTSD and
PD.
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From www.healthyplace.com/Communities/Anxiety/treatment/medications.asp
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