anxietatea la adulti
TRANSCRIPT
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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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NORMAL VERSUS ABNORMAL ANXIETY
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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NORMAL VERSUS ABNORMAL ANXIETY
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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Epidemiology of Generalized Anxiety Disorder
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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TREATMENT OF GAD IN PRIMARY CARE
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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TREATMENT OF GAD IN PRIMARY CARE
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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TREATMENT OF GAD IN PRIMARY CARE
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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TREATMENT OF GAD IN PRIMARY CARE
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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TREATMENT OF GAD IN PRIMARY CARE
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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TREATMENT OF GAD IN PRIMARY CARE
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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TREATMENT OF GAD IN PRIMARY CARE
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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TREATMENT OF GAD IN PRIMARY CARE
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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TREATMENT OF GAD IN PRIMARY CARE
PharmacotherapyBenzodiazepines
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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TREATMENT OF GAD IN PRIMARY CARE
PharmacotherapyBenzodiazepines
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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Epidemiology of Generalized Anxiety Disorder
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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NOREPINEPHERINE & PANIC DISORDERS
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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NOREPINEPHERINE & PANIC DISORDERS
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)
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
Panic Disorder Self-Test (www.adaa.org)
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TREATMENT OF GAD IN PRIMARY CARE
Cognitive Behavior Therapy
Stress-inoculation
Reframing
Cognitive Restructuring
Relaxation Training
Progressive Relaxation
Deep breathingPositive Imagery
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TREATMENT OF GAD IN PRIMARY CARE
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
50-125 mg maintenance
12.525 mg start
100-150 mg maintenance
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Pharmacotherapy of Panic Disorder
TCA
Clomipramine
(Anafrinil)
Imipramine (Tofranil)
DOSE
5-12.5 mg start
50-125 mg maintenance
10-12.5 mg start
150-500 mg maintenance
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Pharmacotherapy of Panic Disorder
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)
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
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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PSYCHOANALYTIC MODEL OF PHOBIC
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
PSYCHOANALYTIC MODEL OF PHOBIC
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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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POST-TRAUMATIC STRESS DISORDER
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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POST-TRAUMATIC STRESS DISORDER
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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MIXED ANXIETY & DEPRESSION
SHARED SYMPTOMS
EXCESSIVE WORRY
MOTOR TENSION
EASY FATIGABILITY
DIFFICULTY CONCENTRATING
SOMATIC COMPLAINTS
MIXED ANXIETY & DEPRESSION
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MIXED ANXIETY & DEPRESSION
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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