Anxiety and Anti-Anxiety Medications

8/2/2019 Anxiety and Anti-Anxiety Medications

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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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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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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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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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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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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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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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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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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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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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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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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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Anxiety and Anti-Anxiety Medications

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