Anxietatea La Adulti

8/11/2019 Anxietatea La Adulti

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ANXIETY DISORDERS IN

CHILDREN & ADULTS

THEORY

DIAGNOSISTREATMENT


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Pharmacological response to

medications designed to treat anxiety

disorders is NOT evidence or proof ofETIOLOGY.


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FEAR VERSUS ANXIETY

FEAR

OBJECTIVE

PAST EXPERIENCE

WITH STRESSOR

KNOWN PROBALITY

OF HARM

ANXIETY

SUBJECTIVE

FUTURE ORIENTED

UNKNOWN HOW ONE

WILL BE HARMED


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NORMAL VERSUS ABNORMAL ANXIETY

LEVEL OF ANXIETY

SOME LEVEL OF ANXIETY NECESSARY TOCREATE MOTIVATION

HIGH LEVELS OF ANXIETY RESULT ININTERFERENCE WITH PERFORMANCE

HIGH LEVELS OF ANXIETY RESULT IN HIGHLEVEL OF COGNITIVE & PHYSIOLOGICALAROUSAL


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JUSTIFICATION

ANY LEVEL OF ANXIETY WOULD BE

CONSIDERED ABNORMAL IF NORATIONALJUSTIFICATION EXISTS FORTHE SITUATION TO TRIGGER ANXIETY.

PERCEPTION OF THE EVENT ASTHREATENINGTO THE INDIVIDUALSSAFETY IS KEY.


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INTERFERENCE IN FUNCTIONING

ANXIETY IS ABNORMAL IF IT CAUSES ANY

IMPAIRMENT IN FUNCTIONING IN ANY LIFEAREA:

(1) SOCIAL

(2) OCCUPATIONAL(3) PHYSICAL

(4) RECREATIONAL


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PREVALENCE & INCIDENCE

OF ANXIETY DISORDERS

MOST COMMON MENTAL DISORDER IN UNITEDSTATES.

15%-TO-17% OF ADULT POPULATION SUFFERFROM 1 OR MORE ANXIETY DISORDERS.

23 MILLION HAVE ONE FORM OF THE 6 ANXIETY

DISORDERS

5% -TO-10% OF SCHOOL AGE CHILDREN HAVE

AN ANXIETY RELATED DISORDER.


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PREVALENCE & INCIDENCE

OF ANXIETY DISORDERS

26% SUFFER FROM 2 OR MOREINDEPENDENT ANXIETY DISORDERS.

19% SUFFER FROM ONLY 1 ANXIETYDISORDER.

55% SUFFERED FROM MULTIPLEDISORDERS, ONE OF WHICH HELPEDCAUSE THE OTHERS.


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ANXIETY DISORDERS

Generalized AnxietyDisorder

Panic Disorder

Obsessive-Compulsive

Disorder

Post-Traumatic Stress

Disorder

Specific Phobia

Social Phobia

Agoraphobia w/o

Panic Attacks

Agoraphobia with

Panic Attacks


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ANXIETY DISORDERS

Anxiety Disorder Due to a GeneralMedical Condition

Substance Induced Anxiety Disorder

Anxiety Disorder NOS

Mixed Anxiety-Depressive Disorder


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GENERALIZED ANXIETY DISORDER

THEORY

DIAGNOSISTREATMENT


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Epidemiology of Generalized Anxiety Disorder

One-year prevalence rate is approximately 3%

of adults.

Life-time prevalence rate approximately 5%.

25% of GAD patients present with comorbidcondition:

Depression

Panic DisorderSubstance abuse

Hypochondriasis

Personality Disorder


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Half of pts presenting for treatment report onset in

childhood or adolescence.

In children, Over-anxious Disorder of Childhood

Gender ratio is approximately 2-to-1 females

Course of disorder is CHRONIC but fluctuates &often WORSENS during periods of stress.

familial association


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PSYCHOANALYTIC EXPLANATION OF GAD & PANIC

DISORDERS

INTERNAL CONFLICTS ARE SOURCE OFBOTH DISORDERS

UNCONSCIOUS IMPULSES THREATEN

EXPRESSION

ANXIETY IS ALARM THAT DEFENSES AREABOUT TO BREAK DOWN.

SINCE NO FOCUS FOR DEFENSE, ANXIETYSYMPTOMS ARE RESULT OFUNSUCCESSFUL DEFENSE AGAINSTANXIETY PROVOKING IMPULSES.


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COGNITIVE THEORY OF GENERALIZED ANXIETY

DISORDER

Beck (1991) - People with GAD constantly make

unrealistic assumptions that they are in imminentdanger:

a. ANY STRANGE SITUATION SHOULD BEREGARDED AS DANGEROUS.

b. A SITUATION OR PERSON IS UNSAFE UNTILPROVEN SAFE.

c. IT IS ALWAYS BEST TO ASSUME THE WORST.

d. MY SECURITY & SAFETY DEPEND ONANTICIPATING & PREPARING MYSELF AT ALL TIMES

FOR ANY POSSIBLE DANGER.


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GABA & ANXIETYDISORDERS

Research points to a problem in feedback

system can cause fear or anxiety to gounchecked (Lloyd, 1992).

GABA is released to exert inhibitory action onexcitatory activity of neurons.

A second site on GABAAreceptor binds with

benzodiazepines.

People with GAD may have ongoing problemswith anxiety feedback system.


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GABA A Receptor with Binding Sites


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GABA & GENERALIZED ANXIETY DISORDER


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GABA & ANXIETYDISORDERS

Brain supplies of GABA too low.

May have too few GABAAreceptors.

GABA Areceptors do not readily bind

neurotransmitter.

Brain may be releasing an excess of otherchemicals reducing GABA activity at receptor

sites.


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ASSESSMENT OF GAD

SCREENING TOOLS

Anxiety Screening Questionnaire (15 items)

Primary Care Evaluation of Mental Disorders

(PRIME-MD)

Hamilton Anxiety & Depression Scale

Beck Anxiety Scale

Center for Epidemiological Studies Depression Scale

(CESD)

Hospital Anxiety & Depression Scale


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ASSESSMENT OF GAD

INTERVIEWING QUESTIONS:

During the past 4 weeks, have you been bothered by

feeling worried, tense, or anxious MOST of the

time?

Are you frequently tense, irritable, and have trouble

sleeping?

If either answered YES, further investigation is

warranted.


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TREATMENT OF GAD IN PRIMARY CARE

Treatment optionsMost efficaciously treated by

combination of CBT & Pharmacotherapy

Cognitive-Behavior Therapy

Reframing

Cognitive Restructuring

Identifying Anxiety Triggers

Cognitive RehearsalStress-Inoculation


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Pharmacotherapy

SSRI

Paroxetine (Paxil) only FDA for GAD

Fluoxetine (Prozac)

Sertraline (Zoloft)

Citalopram (Celexa)

Fluvoxamine (Luvox)

See Table 11.4 in Kaplan & Saddock for dosing.


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PharmacotherapySSRI

Advantages of SSRI

Few side effects

Not addictive/dependence liability

Treats co-morbid depression

Once daily dosing

Low sedation effect


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PharmacotherapySSRI

Disadvantages of SSRI

Patient does not experience symptom attentuation

with single dose

Several weeks to full therapeutic effects

Gastrointestinal and Sexual side-effects common


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SNRI Venaflaxine Hydrochloride (Effexor XR)

Approved by FDA

Reduces symptoms of:anxious mood

excessive motor tension

restlessness

insomnia

irritablility

poor concentration


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SNRI Venaflaxine Hydrochloride (Effexor XR)

Common side effects:

asthenia somnolence

nausea tremorconstipation abnormal ejaculation/orgasm

Patient does not experience symptom attentuation

with single dose

Several weeks to full therapeutic effects.


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Nonbenzodiazepine agentBuspirone (Buspar)

It is a 5-HT1A receptor partial agonist.

More effective in reducing cognitive symptoms thansomatic symptoms of GAD.

Less addictive potential associated with its use.

Indicated if patient has co-morbid substance use

disorder.


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Nonbenzodiazepine agentBuspirone (Buspar)

Patients who had used benzodiazepines are not

likely to respond to Buspirone.

Lack or absence of anxiolytic effects (muscle

relaxation & sense of well being) may be contributing

factor.

Effects take 2-to-3 weeks to become evident.


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Treatment of GAD

BENZODIAZEPINESALPRAZOLAM XANAX

CHLORDIAZEPOXIDE LIBRIUM

CLONAZEPAM KLONOPINCLORAZAPATE TRANZENE

DIAZEPAM VALIUM

LORAZEPAM ATIVAN

OXAZEPAM SERAX

PRAZEPAM CENTREX


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PharmacotherapyBenzodiazepines

Advantages

Therapeutic effect in single dose

Time to full therapeutic effect in days.

Anxiolytic effect of medications helps reduce somatic

symptoms of GAD


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Disddvantages

Impaired alertness & motor performance

High addictive or dependence liability

Does not treat co-morbid depression

Requires several doses per day

High sedation effect

Memory impairment


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Most common clinical mistake is to routinely continuetreatment INDEFINITELY.

Treatment may be minimum of 6 months-to-1 yearso consideration of other medications who seemwarranted.

Start treatment with benzodiazepine & buspirone &taper off benzodiazepine when buspirone reachesmaximum effect ( 2-to-3 weeks).


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PANIC DISORDER

THEORY

DIAGNOSISTREATMENT

E id i l f P i Di d


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Epidemiology of Panic Disorder

One-year prevalence rate is approximately

1.5% of adults.

Life-time prevalence rate approximately 3.5%.

Panic Disorder patients present with comorbid

condition:

MajorDepression GAD

Substance abuse OCD

Specific Phobia Agoraphobia

Social Phobia PTSD


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Typically onset between adolescence & mid-30s.

Females 3X more likely to have PD with agoraphobia

Males 2X more likely to have PD W/O agoraphobia

Course of disorder is CHRONIC but waxing & waning.

1stdegree biological relatives are 8 times more likelyto develop panic disorder.

If onset before age 20, 20 times more likely


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NOREPINEPHERINE & PANIC DISORDERS

Research has focused upon abnormalnorepinepherine activity in locus coeruleus.

Function of locus coeruleus is to send

messages to amygdala (limbic system) that is

known to trigger emotional reactions.

Studies have indicated that locus coerulus isinvolved in activating certain behaviors such

as increased vigilance.


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Over-activity in nordrenergic system has beenlinked to panic disorder.

Stimulation of locus coerulus in both animal &

human studies trigger panic symptoms.

Noradrenergic over-activity may be result of

fewer GABAA receptor sites and lower GABAlevels in occipital cortex of panic disorder

patients. (Malizia, 1998; Goddard, 2001)


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Anti-depressant drugs act to restoreappropriate norepinepherine activity in locus

coerulus & helps to reduce symptoms of

disorder.

80% will experience some significant

improvement.

40% reach full recovery or improve markedly;

20% show NO improvement.


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LOCUS COERULUS & PANIC DISORDER


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ASSESSMENT OF PANIC DISORDER

SCREENING TOOLS

Anxiety Screening Questionnaire (15 items)


(PRIME-MD)

Hamilton Anxiety & Depression Scale

Beck Anxiety Scale


(CESD)Hospital Anxiety & Depression Scale

Panic Disorder Self-Test (www.adaa.org)


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Cognitive Behavior Therapy

Stress-inoculation

Reframing

Cognitive Restructuring

Relaxation Training

Progressive Relaxation

Deep breathingPositive Imagery


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Pharmacotherapy

SSRI

Paroxetine (Paxil) only FDA for GAD

Fluoxetine (Prozac)

Sertraline (Zoloft)

Citalopram (Celexa)

Fluvoxamine (Luvox)

See Table 11.4 in Kaplan & Saddock for dosing.


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Pharmacotherapy of Panic Disorder

SSRI

Paroxetine (Paxil)

Fluvoxamine (Luvox)

Sertraline (Zoloft)

DOSE

5-10 mg start

20-60 mg maintenance

12.5 mg start


12.525 mg start



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TCA

Clomipramine

(Anafrinil)

Imipramine (Tofranil)

DOSE

5-12.5 mg start


10-12.5 mg start



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Benzodiazepines

Alprazolam (Xanax)

Clonazepine (Klonopin)

Lorazepam (Ativan)

DOSE

.25-.5 mg tid start

.5-2 mg tid maintenance

.25 -.5 mg bidstart

.5-2 mg bidmaintenance

25 -.5 mg bidstart

.5-2 mg bidmaintenance


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OBESSIVE-COMPULSIVE DISORDER

THEORY

DIAGNOSISTREATMENT


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OBSESSIONS

INTRUSIVE THOUGHTS WISHES THATCANNOT BE IGNORED, DISMISSED OR

RESISTED.

COMMON THEMES:

CONTAMINATION ORDERLINESS

VIOLENCE SEXUALITY


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COMMOM OBSESSIONS & COMPULSIONS


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ASSESSMENT OF OCD


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ASSESSMENT OF OCD

SCREENING TOOLS

Yale-Brown Obsessive Compulsive Scale (YBOCS)Anxiety Screening Questionnaire (15 items)


(PRIME-MD)Hamilton Anxiety & Depression Scale

Beck Anxiety Scale


(CESD)

Hospital Anxiety & Depression Scale

PSYCHOANALYTIC VIEW OFOBSESSIVE COMPULSIVE DISORDER


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OBSESSIVE-COMPULSIVE DISORDER

OCD develops when child comes to fear his own ID

impulses& uses EDMs as counter-thoughts orcompulsive actions to lessen resulting anxiety.

Three ego-defenses are common in OCD:

isolation- isolates & disowns undesirable/unwantedthoughts & experiences them as intrusions

undoing- Individual engages in acts that implicitly

cancel out their undesirable impulses.

reaction formation -Takes on lifestyle that directly

opposes their unacceptable impulses.


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SEROTONIN & OBSESSIVE-CONPULSIVE DISORDER

Serotonin plays role in operation of orbitalregion & caudate nuclei.

Low levels of serotonin disrupts functioning.

Research has found:

Reducing serotonin activity results in anincrease of OCD symptoms.

Low levels of serotonin are related to high levelsof OCD symptoms.

Increasing serotonin levels reduces symptoms.


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PHOBIC DISORDERS:SPECIFIC PHOBIA

SOCIAL PHOBIA

AGORAPHOBIA

THEORY

DIAGNOSISTREATMENT

SPECIFIC PHOBIA


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SPECIFIC PHOBIA

A. Marked & persistent fear that is excessive or

unreasonable, cued by presence or

anticipation of a specific object or situation.

B. Exposure to phobic stimulus almostinvariably provokes an immediate anxiety

response

C. Person recognizes that the fear is excessive

or unreasonable.


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SPECIFIC PHOBIA

.Animal Type

Natural Environment Type (heights,

storms, water)

Blood Injection Injury type

Situational Type (airplanes, elevators,

enclosed places)

AGE OF ONSET OF PHOBIA


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AGE OF ONSET OF PHOBIA

PSYCHOANALYTIC MODEL OF PHOBIC


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REACTIONS

PHOBIAS ARE EXPRESSIONS WISHES/FEARS WHICH ARE UNACCEPTABLE TOEGO

UNCONSCIOUS CONFLICT IS DISPLACEDTO EXTERNAL OBJECT OR SITUATION

PHOBIA IS LESSTHREATENING TOPERSON THAN THE RECOGNITION OF THEUNCONSCIOUS IMPULSE



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REACTIONS

PHOBIA IS ONLY A SYMPTOM OF UNDERLYINGCONFLICT.

LEVEL OF PHOBIC FEAR INDICATES

STRENGTH OF CONFLICT.

ONCE UNDERLYING CONFLICT IS DISPLACED

ONTO EXTERNAL SITUATION, CONFLICTCAN BE CONTROLLED SIMPLY THROUGH

AVOIDANCE.


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SOCIAL PHOBIA

LIFE TIME PREVALENCE 11% MALES

15% FEMALES

ONSET IN ADOLESCENCE

COMMON IN FAMILIES WHO:

USE SHAME AS CONTROL TECHNIQUE

STRESS IMPORTANCE OF OPINIONS OF

OTHERS


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SOCIAL PHOBIA


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SOCIAL PHOBIA

PERFORMANCE

EXCESSIVE ANXIETY OVER ACTIVITIES

PLAYING INSTRUMENT

SPEAKING IN PUBLIC

EATING IN RESTAURANTUSING PUBLIC RESTROOM


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LIMITED INTERACTIONAL

EXCESSIVE FEAR ONLY IN SPECIFICSOCIAL or VOCATIONAL SITUATIONS

ex. INTERACTING WITH AUTHORITY FIGUREGOING OUT ON A DATE

SOCIAL PHOBIA

SOCIAL PHOBIA


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SOCIAL PHOBIA

GENERALIZED

EXTREME ANXIETY DISPLAYED INMOST SOCIAL SITUATIONS

MAY RESULT IN AVOIDANCE OF ALLSOCIAL INTERACTION


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AGORAPHOBIA

Anxiety about being in places or situations fromwhich:

escape might be difficult (or embarrassing)

ORhelp may not be available in the event of having

an unexpected or situationally predisposedPanic Attack or panic like symptoms.

AGORAPHOBIA


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AGORAPHOBIA

Agoraphobic fears typically involve characteristicclusters of situations that include:

being outside home alone

being in a crowd or standing in line

being on bridge

traveling in bus, train, or automobile.

AGORAPHOBIA


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AGORAPHOBIA

LIFE TIME PREVALENCE 5% OFMALES & 12% OF FEMALES.

DEVELOPS IN 50% OF PANICDISORDERS

FAMILY & TWIN STUDIES INDICATE 3-TO-5 TIMESGREATER RISK FORPANIC DISORDER/ AGORAPHOBIATHAN IN GENERAL POPULATION

POST-TRAUMATIC STRESS DISORDER IN


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AFFECTS 1/2 OF VICTIMS BY AGE 8

SOME MAY HAVE BEEN BORN WITHTENDENCY TOWARDS EXTREME SHYNESS

1-IN-5 DEMONSTRATED CONSISTENT FEAR &DISTRESS IN NOVEL SITUATIONS AS EARLYAS 8 WEEKS OF AGE.

DISORDER THOUGHT TO OCCUR MOREOFTEN IN FEMALES BUT MALES

CHILDREN


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POST-TRAUMATIC STRESS DISORDER

MUST EXPERIENCE TRAUMATIC EVENT

INTRUSIVE RE-EXPERIENCING OF

EVENT(DREAMS, FLASHBACKS, IMAGES,

THOUHGTS, RECOLLECTIONS)

AVOIDANCE OF STIMULI ASSOCIATEDWITH EVENT

PERCENTAGE OF INDIVIDUALS DX WITH PTSD


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PERCENTAGE OF INDIVIDUALS DX WITH PTSD

POST TRAUMATIC STRESS DISORDER


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NUMBING OF RESPONSIVENESS TO THE

WORLD & RESTRICTION OF AFFECT

SYMPTOMS OF INCREASED AROUSAL

EXAGGERATED STARTLE REACTION

HYPERVIGILANCE

DIFFICULTY CONCENTRATING

INSOMINIANIGHTMARES

POST TRAUMATIC STRESS DISORDER


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PTSD can occur at any age even childhood.

In young people, the response may beexpressed as agitated behavior.

Most young people with PTSD avoid thingsthat remind them of what happened.

Many have physical symptoms as well, such asstartling easily.

PTSD IN CHILDREN

ETIOLOGICAL FACTORS


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ETIOLOGICAL FACTORS

Certain PREMORBIDpersonality profiles& attitudes are more likely to developPTSD.

Pre-morbid personality or psychologicaldifficulties are associated with increaserisk & more severe ASD & PTSD

symptoms:poor interpersonal relationships

external locus of control

pessimism

ETIOLOGICAL FACTORS


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ETIOLOGICAL FACTORS

NATURE & QUALITY OF SOCIAL SUPPORT

SYSTEM

Person with a strong social support system after atraumatic event less likely to develop an extendeddisorder.

If feels loved/accepted/valued, will be more likely

to recover.

Societal support for appears to be important inlessening severity & duration of symptoms.

ETIOLOGICAL FACTORS


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ETIOLOGICAL FACTORS

DEGREE OF EXPOSURE & SUBJECTIVEEXPERIENCE OF THREAT PLAYS CRITICALROLE IN DEVELOPMENT OF PTSD & ASD.

DURATION OF THE EXPOSURE

LEVEL OF INVOLVEMENT

SALIENCE

DEGREE OF HARM EXPERIENCED

MIXED ANXIETY & DEPRESSION


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SHARED SYMPTOMS

EXCESSIVE WORRY

MOTOR TENSION

EASY FATIGABILITY

DIFFICULTY CONCENTRATING

SOMATIC COMPLAINTS



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ANXIETY

SHORTNESS OF

BREATH

CHEST PAIN

NERVOUSNESS

IRRITABILITY

BURNING STOMACH DIFFICULTY FALLING

ASLEEP

DEPRESSION

DEPRESSED MOOD

ANHEDONIA

WEIGHT LOSS ORGAIN

SUICIDALTHOUGHTS

EARLY MORNINGAWAKENING

C O S C


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MEDICATIONS THAT REDUCE ANXIETY

AZASPIRONES

BUSPRIONE BUSPAR

BETA BLOCKERS

PROPANOLOL INDERAL

ATENOLOL TENORMIN

ANXIETY DISORDERS IN PRIMARY CARE:

GUIDELINES


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GUIDELINES

RECOGNIZE ANXIETY AS CAUSE OF PTs

PRESENTING SYMPTOMS:

LOOK FOR MULTIPLE SYMPTOMS

GREATER # OF PHYSICAL SYMPTOMS, MORE

LIKELY ANXIETY D/O PRESENT

GREATER # OF SOMATOFORM SYMPTOMS,

MORE LIKELY ANXIETY D/O PRESENT

ANXIETY DISORDERS IN PRIMARY CARE: GUIDELINES


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RECOGNIZE ONLY A SMALL NUMBER OF PTS WITH

ANXIETY SYMPTOMS ARE A RESULT OF GENERAL

MEDICAL CONDITION.

LOOK FOR ANXIETY IN OTHER LIFE AREAS

LOOK FOR TRIGGERS OR AVOIDANCE

(TIME/PLACE/SETTING/CONTEXT)

LOOK FOR MULTIPLE SYMPTOMS

LOOK FOR SOMATOFORM SYMPTOMS

EPIDEMIOLOGY = APPEARS IN YOUNGER PT-->

LESS RISK FOR ILLNESS


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