This document discusses stress, anxiety disorders, and their causes and treatment. It defines stress and describes the general adaptation syndrome model of stress involving alarm, resistance, and exhaustion stages. It also discusses types of stress including eustress and distress. Causes of stress include person-environment transactions, life events, and genetics. Treatment of anxiety disorders involves psychotherapy such as cognitive behavioral therapy to change thoughts and behaviors, as well as pharmacotherapy.

1. Stress And Anxiety
Disorders
By Heba Essawy

2. Definition Of Stress
■ Set of emotional, physical, and cognitive (i.e.,
thought) reactions to a change.
■
■
Stress as a reaction to change suggests that it is
not necessarily bad,
Could even be a good thing.

3. Causes Of Stress
When person-environment transactions to:
■ Perceive a discrepancy.
■ Whether real or not.
■ Between the demands of a situation and the
resources of the person's.
■ Either biological, psychological or social
systems

4. Stress
In medical terms:
■
■
Stress is the disruption of homeostasis through
physical or psychological stimuli.
Stressful stimuli can be mental, physiological,
anatomical or physical reactions
■ Hans Selye, defined the General Adaptation
Syndrome or GAS paradigm in 1936.

5. Types of stress
■ Richard Lazarus(1974) dividing stress into:
- Eustress and - Distress.
Eustress stress :
■ Enhances function (physical or mental,) such as
through strength training or challenging work.
Distress stress :
■ Persistent stress that is not resolved through coping
or adaptation may lead to escape anxiety or withdrawal
depression behavior.

6. Types Of Stress
Eustress, or positive stress, has the following characteristics:
■
■
■
Motivates, focuses energy
Is short-term
Is perceived as within our coping abilities
■
■
Feels exciting
Improves performance
In contrast, Distress, or negative stress, has the following characteristics:
■
■
■
■
■
■
Causes anxiety or concern
Can be short- or long-term
Is perceived as outside of our coping abilities
Feels unpleasant
Decreases performance
Can lead to mental and physical problems

7. General Adaptation Syndrome
■ Researched mainly by Hans Selye on rats
exposing animals to unpleasant or harmful stimuli
such as injections or extreme cold .
■ He found that all animals showed a series of
reactions, broken into three stages. He describes
this universal response to the stressors as the
General Adaption Syndrome or GAS in 1956.

8. Stages Of Stress
Stage one: Alarm
■
■
the body's stress response is a state of alarm.
During this stage adrenaline will be produced in order to bring about
the fight-or-flight response.
■ Activation of the HPA axis producing cortisol.
Stage two: Resistance
■
■
■
■
If the stressor persists.
Necessary to attempt means of coping with stress.
The body begins to try to adapt ,to the strains or demands of the
environment.
The body cannot keep this up , so its resources are gradually depleted.

9. Stages Of Stress
Stage three: Exhaustion
■
■
All the body's resources are depleted.
The body is unable to maintain normal function.
■ At this point the initial autonomic nervous system symptoms may
reappear
- sweating,
- raised heart rate .
If stage three is extended:
■
■
■
■
long term damage may result as the capacity of the adrenal gland.
The immune system is impaired and resulting in decompensation.
The result can manifest itself in illnesses such as
Ulcers, depression or cardiovascular problems.

10. Stages of A Stress Reaction
■ Stage 1: Recognition of environmental demand
■ Stage 2:Appraisal of the demand
■
byasking :1) Doesthis event present a threat ?
2)Dowehavethe resourcesto copewith this
event?
If webelievethat the eventis a threat , orif wewelack
the means to effectivelyrespond totheevent,
feelin
g stressed

11. Stage 3: Mobilization of the nervous
system
■ Sympathetic nervous system automatically
signals our body to prepare for action.
■ The SyNS prepares for fighting or fleeing by
triggering or activating the hypothalamic-
pituitary-adrenal axis, or HPA axis ( brain's
'stress circuit' ).

12. Neurochemistry of General
Adaptation Syndrome
The body reacts to stress first by releasing:
■
■
■
Catecholamine hormones.
Epinephrine and Norepinephrine
Glucocorticoid hormones, cortisol and cortisone.
■ The hypothalamic-pituitary-adrenal axis (HPA);
Involving the interactions of the hypothalamus, the pituitary gland, and
the adrenal glands.
■
■
The HPA axis is believed to play a primary role in the body's reactions
to stress by balancing hormone releases from the adrenaline-producing
adrenal medulla, and from the corticosteroid-producing adrenal cortex.
Stress can significantly affect many of the body's immune systems, as
can an individual's perceptions of, and reactions to, stress.

13. Biological Systems For Stress Reactions
■ The hypothalamus is like a thermostat that
receives inputs about the body's internal
environment.
■ If body functions are out of balance, the
hypothalamus sends messages to the ANS and
to the pituitary gland to speed up or slow down
relevant glands and organs to bring the body
back into balance at the set-point appropriate to
each system

14. Biological Systems For Stress Reactions
■ The main job of the hypothalamus is to maintain the
homeostasis as
Blood pressure,
Body temperature,
Fluid balance,
Body weight,
Sexual activity,
Sleep/wakefulness
Emotions.

15. Biological Systems For Stress Reactions
■ Some of the hormones secreted by the hypothalamus
and pituitary gland stimulate the limbic system,
■ The limbic system is heavily interconnected with the
brain's frontal cortex,
■ The limbic system and the frontal lobes work together
to make possible the appraisals or judgments regarding
whether or not a stressor is dangerous or exceeds our
coping ability
■ . The combined limbic/frontal system also influences
whether we fight, flee, or freeze in the presence of a
stressor.

16. Factors Influencing the Stress Response
Arousal Vs Anxiety
Physiological arousal is necessary to prime our bodies
for taking action.
■
■
■ If aroused increased in response to stressors, alertness
increases and attention sharpens.
Increasingly focused on the stressor itself, while other
aspects of the environment fade into the background.
Anarrowed focus of attention towards a threat is
typically adaptive, as it allows to eliminate some of the
available responses .

17. Factors affecting Arousal
■ Amount of mental energy .
■
■
Baseline level of anxiety ( level of 'trait'
anxiety),
level of anticipatory anxiety (how worried we
are in advance of an upcoming event).

18. "Yerkes-Dodson Curve".
■ A diagram suggests, increasing levels of arousal
initially improve performance, but there quickly
■
comes a point of diminishing returns.
At high levels of stress, performance ability
declines dramatically.

19. Primary and Secondary Appraisal
■ Primary Appraisal : Astressor that is perceived
as important will cause a stress reaction )"Does
this matter for me?").

20. Primary and Secondary Appraisal
■ In secondary appraisal: evaluate coping
resources (e.g., how healthy we are, how much
energy we have, whether family and friends can
help, our ability to rise to the challenge, and how
much money or equipment we have), our
available options, and the possibilities we have
for controlling our situation. If we believe that
we lack the coping resources necessary to deal
with the situation, we will perceive it as negative
stress

21. Appraisals Influence How You Feel:
The Cognitive Model
■ Beliefs (driven by appraisal process) strongly
influence subsequent mood state.
■ Having the ability and resources to handle the
stressors , mood will be generally positive

22. Cognitive Model
■ the letter "A" stands for an "Activating Event."
Activating Events are the stressors that create demands
and cause potential stress.
■ letter "B" in the equation stands for "Beliefs." We
come into the world with no preconceived.
■ letter "C" in the A+B=C equation stands for
"Consequences." Consequences refer to the feelings
that occur as a result of beliefs and self-talk in response
to the activating event.

23. Oxidative stress
Causes:
■ An imbalance between the production of reactive oxygen
and a biological system's ability to detoxify the reactive
intermediates.
■ Slow repair the resulting damage.
Oxidative stress is involved in:
■
■
■
■
Atherosclerosis.
Parkinson's disease.
Alzheimer's disease.
Prevention of ageing by induction of a process named
mitohormesis.

24. Oxidative stress
Pathophysiology :
■ All forms of life maintain a reducing environment
within the cells.
■ Reducing environment is preserved by enzymes
that maintain the reduced state through a constant
input of metabolic energy.
■ Disturbances in this normal redox state can cause
toxic effects through the production of peroxides
and free radicals that damage all components of
the cell, including proteins, lipids, and DNA.

25. Stress Scale
■ To measure stress according to the Holmes and Rahe
Stress Scale
■ Number of "Life Change Units" that apply to events
in the past year of an individual's life are added
■ and final score will give a rough estimate of how stress
affects health.
■ Score of 300+: At risk of illness.
■ Score of 150-299+: Risk of illness is moderate (reduced
by 30% from the above risk).
■ Score 150-: Only have a slight risk of illness.

26. Life event Life change units
■
■
■
Death of a spouse100/Divorce73/Marital separation65
Imprisonment63/Death of a close family member63/Personal injury or
illness53/Marriage50/Dismissal from work47/
Marital reconciliation45/Retirement45/Change in health of family
member44/Pregnancy40/Sexual difficulties39/
■
■
■
Gain a new family member39Business readjustment39Change in financial
state38Change in frequency of arguments35
Major mortgage32Foreclosure of mortgage or loan30Change in responsibilities at
work29Child leaving home29
Trouble with in-laws29Outstanding personal achievement28Spouse starts or stops
work26Begin or end school26Change in living conditions25Revision of personal
habits24Trouble with boss23Change in working hours or conditions20Change in
residence20Change in schools20Change in recreation19Change in church
activities19Change in social activities18Minor mortgage or loan17Change in sleeping
habits16Change in number of family reunions15Change in eating
habits15Vacation13Christmas12Minor violation of law11

27. Epidemiology Of Anxiety Disorders
■ The most common mental illness .
■ One of 4 person met the diagnosis for one
the anxiety disorders.
■ In 12- month prevalence rate of 17.1%.
■ Women have 30.5 %lifetime prevalence
more affected than men ( 19.2%).

28. Epidemiology Of Anxiety Disorder
SEX:
■ The female-to-male ratio for any lifetime anxiety disorder is 3:2.
Age
■
■
■
■
■
Most anxiety disorders begin in childhood, adolescence, and early adulthood.
Separation anxiety is an anxiety disorder of childhood .
Panic disorder in the age groups of 15-24 years and 45-54 years.
social phobia was 16 years.
The age of onset for OCD appears to be in the mid 20s to early 30s.
New-onset anxiety symptoms in older adults :
unrecognized general medical condition.
substance abuse disorder.
Major depression with secondary anxiety symptoms.
■
■
■
■

29. Classification of Anxiety Disorders
■ Anxiety due to a general medical condition
■ Substance-induced anxiety disorder
■ Generalized anxiety
■ Panic disorder
■ Acute stress disorder
■ Posttraumatic stress disorder (PTSD)
■ Adjustment disorder with anxious features
■ Social phobia
■ Obsessive-compulsive disorder (OCD)
■ Specific phobias

30. Pathophysiology
■ Anxiety disorders appear to be caused by an
interaction of biopsychosocial factors.
■
■
Genetic vulnerability.
Interaction with situations, stress, or trauma
to produce clinically significant syndromes.

31. Biological Factors
Central nervous system: The major mediators of the
■
symptoms of anxiety disorders:
Norepinephrine .
■
■
Serotonin.
Peptides, such as corticotrophin-releasing factor.
Peripherally:
■ the autonomic nervous system, especially the
sympathetic nervous system, mediates many of the
symptoms.

32. Causes of Anxiety Disorders
■ Personal environment:
- Poverty.
■
■
■
■
- Early separation from the mother.
- Family conflict.
- Critical and strict parents.
Personality.
Family dynamics.
Brain chemistry.
Genetic vulnerability .

33. Risk Factor For Anxiety
Brain chemistry:
■ Imbalance of neurotransmitters such as
serotonin, GABA, and epinephrine may
contribute to anxiety disorders.
■ Abnormalities in the stress hormone cortisol .

34. Risk Factor For Anxiety
Personality traits
■ People with anxiety disorders often view
themselves as powerless and the world as a
threatening place.
■ Pessimistic perspective can lead to low self-
confidence and poor coping skills.

35. Risk Factor For Anxiety
Heredity Factor:
■ Anxiety run in families.
■
■ People have a family history of anxiety
disorders, mood disorders, or substance .
One risk factor may be a biological vulnerability
to stress.

36. Risk factors for Anxiety
Major life stressors
■ Financial difficulties.
■
■
■
Marital problems.
Bereavement
It is important to realize that no single factor
causes an anxiety disorder.
■ The various anxiety risk factors are interrelated
and can interact with and impact one another.

37. Generalized Anxiety Disorder
Definition :
■ GAD is defined as excessive anxiety and
worry about several events or activities for
most days during at least 6- month period.
■ Worry is difficult to control and is associated
with somatic symptoms, such as muscle
tension, irritability, difficulty in sleeping and
restlessnes.

38. Generalized Anxiety Disorder
Epidemiology
■ One year prevalence range from 3 to 8%.
■
■
■
■
■
■
Male : Female is 2 : 1.
Life Time prevalence is 5-8%.
25%of all patients with anxiety is suffering GAD.
Onset : Late adolescence or early adulthood
GAD patients are seen @ primary care settings.
Separation anxiety in childhood that includes anxiety
related to going to school, is one of the precursor for adult
anxiety disorders

39. Generalized Anxiety Disorder
■
■
■
Characterized by excessive anxiety and worry.
Worrying is difficult to control.
Anxiety and worry are associated with at least 3 of the
following symptoms:
■
■
■
■
■
■
■
Restlessness or feeling keyed-up or on edge
Being easily fatigued
Difficulty concentrating or mind going blank
Irritability
Muscle tension
Sleep disturbance
Although not a diagnostic feature, suicidal ideation and completed
suicide have been associated with generalized anxiety disorder.

40. Physiological Symptoms of GAD
■ Muscle tension. - Cognitive Vigilance
Fatigue.
Restlessness.
Irritability.
- Autonomic hyperactivity
- Difficulty sleeping.
-Edginess.
■
■
■
■ Gastrointestinal discomfort or diarrhea.

41. Lab Studies
in GAD
■ CBC count .
■ Chemistry profile .
■ Thyroid function tests.
■ Urinalysis .
■ Urine drug screen.

42. Treatment Of GAD
■ The most effective treatment is the combination of
psychotherapy , pharmacotherapy and supportive
approaches.
■ Behavior Therapy
* To modify and gain control overunwanted behavior.
*The individual learns to cope with difficult situations,
often through controlled exposure to them.
* Gives the individual a sense of having control over their
life.

43. Treatment Of GAD
Cognitive Therapy
The goal of Cognitive Therapy:
■ To change unproductive or harmful thought
patterns.
■ The individual examines his feelings and learns
to separate realistic from unrealistic thoughts.
■ As with Behavior Therapy, the individual is
actively involved in his own recovery and has a
sense of control.

44. Cognitive Behavioral Therapy
■ CBT examines distortions in our ways of looking
at the world and ourselves
■
■
Negative thoughts lead to negative emotions, so
CBT aims to change those negative thoughts
before they trigger psychological difficulties.
CBT for generalized anxiety disorder involves
retraining the way you think.
■ Therapist identify automatic negative thoughts
that contribute to your anxiety.

45. Cognitive Behavioral Therapy
Education:
■
■ CBT teaches you about the cognitive, physical, and
behavioral .
Teaches you how to distinguish between helpful and
unhelpful worry.
■ An increased understanding of anxiety encourages a more
accepting and proactive response to it.
Monitoring
■
■
■
Learn to monitor anxiety, including what triggers it.
Specific things you worry about, and the severity and
length of a particular episode.
This get perspective, as well as track your progress.

46. Cognitive Behavioral Therapy
Physical control strategies:
■ Deep breathing and progressive muscle relaxation help decrease
the physical over-arousal of the “fight or flight” response that
maintains the state of fear and anxiety.
Cognitive control strategies:
■
■ Realistically evaluate and alter the thinking patterns that
contribute to anxiety
Challenge these negative thoughts, fears will begin to subside.
CBT also teaches you to test the beliefs you have about worry
itself, such as “Worry is uncontrollable” or “If I worry, bad
things are less likely to happen.”

47. Cognitive Behavioral Therapy
Behavioral strategies:
■ Instead of avoiding situations you fear.
■
■ CBT teaches to tackle them .
Start by imagining the thing you’re most afraid of.
■ By focusing on your fears without trying to avoid
or escape them.
---------→ Feeling more in control and less
anxious.

48. Relaxation Techniques
■
Help to develop the ability to more effectively
cope with the stresses that contribute to anxiety.
■ as well as with some of the physical symptoms
of anxiety.
■ The techniques taught include breathing re-
training and exercise.

49. Biofeedback
What Exactly is Biofeedback?
■ Biofeedback is a self-training, mind-over-
body technique developed in the 1940s.
■ It's a method in which we consciously
control a body function that normally is
regulated automatically by the body like
skin temperature, heart rate, or blood
pressure.

50. Pharmacotherapy
■ Selective Serotonin Reuptake Inhibitors :
Citalopram
Escitalopram
Fluvoxamine
Paroxetine
Fluoxetine
Sertraline .
■ Affects the concentration serotonin linked
to anxiety disorders

51. Pharmacotherapy
Tricyclic Antidepressants (TCAs
■ Affects theconcentrationandactivityof the
neurotransmitters serotonin and norepinephrine,
chemicals in the brain thought to be linked to
anxiety disorders .

52. Pharmacotherapy
Monoamine Oxidase Inhibitors (MAOIs
■ Blocks the effect of an important brain enzyme, preventing
the breakdown of serotonin and Norepinephrine)
OtherAntidepressants
■
■ Cymbalta
Desyrel *
Effexor †
Remeron
Affects the concentration of the neurotransmitters serotonin
and/or norepinephrine, chemicals in the brain thought to
be linked to anxiety disorders

53. Pharmacotherapy
■ Azapirones (BuSpar) :Enhances the activity of
serotonin .
* Benzodiazepines: Exact mechanismunknown.
■
Some research shown to enhance the function
of gammaaminobutyric acid (GABA).
Antihistamines :Sedative effects through
blockade of histamine receptors in the brain .

54. Pharmacotherapy
Beta Blockers: Blocks receptors associated with
physiologic symptoms of anxiety.
Atypical Antipsychotics :
■ Augmentation therapy.
■ These medications may be added when
symptomsonlypartiallyrespondto another
medication to increase the overall response to
treatment

55. THANK YOU

58. Anxiety Disorders:
■ unpleasant emotional state,
■
■
■
sources of which are less readily identified.
It is frequently accompanied by physiological
symptoms
lead to fatigue or even exhaustion.

59. Panic Disorder
By Heba Essawy

60. Panic disorder
Background
Panic attacks:
■
■
■
■
■
Aperiod of intense fear in which 4 of 13 defined symptoms.
Develop abruptly and peak rapidly less than 10 minutes .
Cannot result from substance use, medical conditions, or
another psychiatric disorder .
The frequency can vary from several attacks a day to only a
few attacks a year.
Is qualified with the presence or absence of agoraphobia .

61. Panic Disorder With Agoraphobia
Agoraphobia is:
■
■
■ Anxiety toward places or situations in
which escape may be difficult or
embarrassing.
These anxiety-provoking situations are
avoided or are endured with anxiety.
Agoraphobia is not a stand-alone disorder;
it is a descriptive term .

62. DSM-IV-TR Criteria For panic
Attack
Uncoded , 4 or more symptoms
■
■
■
Palpitations, pounding heart, or accelerated heart rate
Sweating
Trembling or shaking
Sense of shortness of breath or smothering
Feeling of choking
Chest pain or discomfort
Nausea or abdominal distress
Feeling dizzy, unsteady, lightheaded, or faint
Derealization or depersonalization (feeling detached from oneself)
Fear of losing control or going crazy
Fear of dying
Numbness or tingling sensations.
Chills or hot flashes.
■
■
■
■
■
■
■
■
■
■
■

63. Diagnosis Of Panic Disorder
Diagnostic and Statistical Manual of Mental
Disorders, Fourth Edition, Text Revision:
■ Recurrent unexpected panic attacks
■ One of attacks has been followed for more than 1
month :
* subsequent persistent worry about having
another attack.
* Consequences of the attack.
* Significant behavioral changes related to the
attack.(Loosing control, having heart attack.)

64. Pathophysiology Of Panic :
Biological
Serotonergic model:
■ 5HT system or one of its subsystems may
play a role in the pathophysiology of panic
■
disorder,
Exaggerated postsynaptic receptor
response to synaptic serotonin.
■ Recent studies report subsensitivity of
5HT1A receptors.

65. Pathophysiology Of Panic : Bio.
■ Catecholamine model :
* Increased sensitivity to adrenergic CNS
■
discharges, with hypersensitivity of presynaptic
alpha-2 receptors.
Locus ceruleus model:
*Increased local discharge resulting in adrenergic
neuron stimulation.
*Affects hypothalamic-pituitary-adrenal axis,
which can respond abnormally to clonidine in
patients with panic disorder.

66. Pathophysiology Of Panic : Bio.
Panic inducing substances → Respiratory stimulation →shift
acid- base balance
■ Sodium Lactates :focuses on symptom production by
postulated aberrant metabolic activity induced by lactate.
■ Carbon dioxide (False suffocation hypothesis): explains
panic phenomena by hypersensitive alarm system by↑ co2
and Lactate activate asphyxia monitor @ brain stem
receptors.
■ Bicarbonate.
Act through neurotransmitters include yohimbine , α2-
adrenergic , mCPP, cholecystokinine
■

67. Pathophysiology Of Panic : Bio.
■ GABA model: postulates decreased inhibitory
receptor sensitivity, with a resultant excitatory
effect.
■ The neuroanatomic model:
* Mediated by a "fear network" in the brain that
involves the amygdala, the hypothalamus, and the
brainstem centers.
*Cortical atrophy @ rt. Temporal lobe
■ The genetic hypothesis :MZ>DZ.
Definable genetic loci ??

68. Pathophysiology Of Panic : Bio.
■ Mitral valve prolapse:
Heterogeneous disorder.
Prolapsed one leaflets. Mid-
Systolic click.

69. Psychological Factors
■ Cognitive- Behavioral Theories:
- Learned from parental behavior
- through classic conditioning
■ Psychoanalytic Theories:
- Unsuccessful defense against anxiety.
- Agoraphobia due to
* loss of a parent in childhood and history of
separation anxiety.
* Parental separation in childhood.
*Death of the parent before 10ys.

70. Demographic Data
■ Prevalence : 1.5-5%for panic disorder.
3-5.6% for panic attacks.
■ Race: * African Americans presenting with somatic
symptoms .
■
■
* seeking help in medical settings.
Sex: One-month prevalence women:men, 0.7%: 0.3%
(1: 2-3 folds) .
Age : * Bimodal distribution.
* Highest incidence in late adolescence .
* Second peak in the mid 30s.

71. Patterns of Panic Attacks
■
■
■
■
Unexpected panic attacks have no known precipitating cue
→ panic disorder without agoraphobia.
Situationally bound (cued) panic attacks recur predictably
in temporal relationship to the trigger →specific phobia-
type diagnosis.
Situationally predisposed panic attacks are more likely to
occur in relation to a given trigger, with inability to escape
→ panic disorder with agoraphobia.
Use of caffeine, alcohol, nicotine, or other substances can
trigger or potentiate panic attacks.

72. Comorbidities Of Panic
■
■
Panic disorder often coexists with mood disorders.
Alcohol and other substance use disorders are a sequelae
of panic disorder
Medical conditions :
■
■
■
■
■
■
■
Mitral valve prolapse.
Hypertension.
Cardiomyopathy .
Chronic obstructive pulmonary disorder,
Irritable bowel syndrome.
Migraine headache.

73. Pharmacothearapy
■ Selective serotonin reuptake inhibitors (SSRIs) are
generally used as first-line agents.
followed by tricyclics.
■
■
■
■
*Benzodiazepines can achieve long-term control but
should be reserved for patients with refractory panic
disorder.
Fluoxetine (Prozac) can be used at very low starting
doses.
*Paroxetine (Paxil) has a more sedating effect, potentially
making its potential aggravation of anxiety better tolerated
initially. Drug alter metabolism of cytochrome P-450 -2D.

74. Cognitive and behavioral
psychotherapy
Cognitive therapy :
■
■
Understand false beliefs/distortions .
Provides information about panic attacks.
Behavioral therapy ;
■ Involves sequentially greater exposure of the patient to
anxiety-provoking stimuli; over time, the patient becomes
desensitized to the experience.
Relaxation techniques :
■Control patients' levels of anxiety.
Respiratory training
■ Control hyperventilation during panic attacks.

75. Specific Phobia
■ An excessive fear of a specific object,
circumstance , or situation.
■ Specific phobia is a strong , persistent fear of
an object or situation.
■ Person with specific phobia may anticipate
harm ( bitten by dog, fainting).

76. Social phobia
■ Intense, irrational and persistent fear of being
criticized or negatively evaluated by others.
■ Feared social or performance situations typically
provoke an immediate anxious reaction ranging
from diffuse apprehension to situational panic.
■ To meet the diagnostic criteria for this disorder,
the symptoms must be severe enough to cause
significant distress or disability .

77. Diagnostic Criteria for Social Phobia
■ A. Amarked and persistent fear of one or more social or performance
situations in which the person is exposed to unfamiliar people or to
possible scrutiny by others.
The individual fears will be humiliating or embarrassing.
note: In children, there must be evidence of the capacity for age-
appropriate social relationships with familiar people and the anxiety
must occur in peer settings, not just in interactions with adults.
■ B. Exposure to the feared social situation almost invariably provokes
anxiety, which may take the form of a situationally bound or
situationally predisposed panic attack.
note: In children, the anxiety may be expressed by crying, tantrums,
freezing, or shrinking from social situations with unfamiliar people

78. Diagnostic Criteria for Social Phobia
■C. The person recognizes that the fear is excessive or unreasonable.
NOTE: In children, this feature may be absent.
■ D. The feared social or performance situations are avoided or else are
endured with intense anxiety or distress.
■ E. The avoidance, anxious anticipation interferes significantly with the
person's normal routine, occupational (academic) functioning .
■
■
F. In individuals under 18years of age, the duration is at least six
months.
G. The fear or avoidance is not due to the direct physiologic effects of a
substance (e.g., a drug of abuse, a medication) or a general medical
condition and is not better accounted for by another mental disorder .

79. Diagnostic Criteria for Social Phobia
■ H. If a general medical condition or another
mental disorder is present, the fearin Criterion Ais
unrelated to it; (e.g., the fear is not of stuttering,
trembling in Parkinson's disease or exhibiting
abnormal eating behavior in anorexia nervosa or
bulimia nervosa.)
■ Specifyif:
Generalized: if the fears include most social
situations (also consider the additional diagnosis
of avoidant personality disorder).

80. Common Fears in Social Phobia
■ Public speaking or performing.
■ Making "small talk.
*Small group discussion.
*Asking questions in groups.
*Being introduce.
*Meeting or talking with strangers.
*Being assertiveness.

81. Common Fears in Social Phobia
■ Being watched doing something (e.g.,
eating, writing).
*Attending social gatherings
*Using the telephone
*Using public restrooms
*Interacting with "important" people
*Indirect evaluation (e.g., test taking)

82. Epidemiology
■ lifetime prevalence rate of 13.3 percent .
■
■
■
One-year prevalence rate of 7.9 percent.
It s the third most prevalent psychiatric
disorder, following substance abuse and
depression.
Fears of public speaking or performing are
most prevalent.

83. Onset of social phobia
■
■
Occurs between 11and 19 years of age.
Onset after age 25 is rare, until some new social or
■
occupational demand forces these persons into
social encounters that trigger the syndrome.
(e.g., meeting new people, public speaking,
promotion).
Slightly more females than males have social
phobia.

84. Comorbidity Of social phobia
* One half of patients with have comorbid mental,
drug or alcohol problems.
■ 70% had comorbid major depression.
■ Up to 16 %of patients who present with social
phobia have alcohol abuse problems.
■
■ Patients presenting for treatment of substance
abuse meet the criteria for social phobia.
longitudinal data show that social phobia
precedes approximately 70 percent of these
comorbid condition.

85. Drugs Used in Treating Social
Phobia
MAOIs
■ Phenelzine (Nardil) 45 to 90 mg / day
■Tranylcypromine (Parnate) 40 to 60 mg / day
SSRIs
■ Fluoxetine (Prozac)
■ Paroxetine (Paxil)
■ Sertraline (Zoloft)
■ Fluvoxamine (Luvox)
■ Citalopram (Celexa)
10 to 100 mg / day..
20 to 60 mg / day
50 to 200 mg / day
50 to 150 mg / day
40 mg / day

86. Drugs Used in Treating Social
Phobia
Benzodiazepines
■ Alprazolam (Xanax)
■ Lorazepam (Ativan)
2 to 10 mg / day
2 to 6 mg /day
■ Clonazepam (Klonopin) 1to 3 mg / day
Nonbenzodiazepine, azaspirone
■ Buspirone (Buspar) 35 to 60 mg / day
Beta blockers
■ Propranolol (Inderal) 40 mg as needed

87. Components of Cognitive Behavior
Therapy for Social Phobia
■
■
Anxiety management skills
May involve controlled breathing, relaxation exercise
Social skills training
verbal and nonverbal skills that facilitate social effectiveness,
■
■
such as initiating and maintaining conversation, making
appropriate eye contact .
Cognitive restructuring
Involves learning to identify, challenge and change fearful
thinking that overestimates social threat, underestimates one's
ability to manage social demands and catastrophizes the
consequences of social miscues
Gradual exposure to feared situations
Involves gradual reentry into feared social situations to reduce
the anxiety that they engender

88. THANK YOU

89. THANK YOU

93. Lab Studies in GAD
Initial lab studies might be limited to the following:
■ CBC count .
■ Chemistry profile.
■ Thyroid function tests.
■ Urinalysis .
■ Urine drug screen.

94. Pharmacotherapy
■ Sertraline -- First drug approved by FDA for PTSD. May be
effective in reducing some symptoms in at least some patients.
Adult Dose :
Pediatric Dose:
Contraindications:
50-200 mg PO qd .
Not established
Documented hypersensitivity.
■
■
■
■ Interactions; Increases toxicity of MAOIs, diazepam and
warfarin, due to inhibition of cytochrome P-450 enzymes .
Pregnancy : not established.
■
■ Precautions Caution in preexisting seizure disorders, recent
myocardial infarction, unstable heart disease, and hepatic or renal
impairment

95. Paroxetine
■
■
– For PTSD, causing reduction in reexperiencing,
numbing/avoidance, and hyperarousal.
Adult Dose starting dose: 20 mg/d PO; if indicated,
may be increased in 10-mg increments at intervals >1
wk; doses from 20-50 mg are effective .
■ Pediatric Dose:
■ Contraindications:
Not established.
MAOIs or thioridazine.
■ Precautions: Caution in history of seizures, mania,
renal disease, and cardiac disease; the CR product
should not exceed 50 mg/d for elderly, debilitated, or
severely renally or hepatically impaired persons

96. Paroxetine
■ Interactions : Avoid alcohol, tryptophan, and
thioridazine; avoid within 14 d of MAOIs; may
inhibit metabolism of TCAs;
- May change concentrations with plasma-bound
drugs; hyperreflexia, weakness, and incoordination
have been reported ;
- Monitor theophylline; caution with lithium,
digoxin, diuretics, cimetidine, phenobarbital,
warfarin, phenytoin, quinidine, and drugs
metabolized by CYP-450 2D6 (eg, type 1C
antiarrhythmics, phenothiazines, antidepressants)
■ Pregnancy : - not established.

97. Phenelzine
for symptoms of panic disorders.
Adult Dose starting dose: 1 tab (15 mg) PO tid; lower starting doses are
advised in patients sensitive to medications (ie, the 7% of the population who
are slow metabolizers)
Pediatric Dose: Not established
Contraindications : Documented hypersensitivity; alcoholism,
congestive heart failure, and pheochromocytoma.
Interactions :Co administration with foods containing tyramine can increase
blood pressure; concurrent use with tryptophan should be approached with
caution because serotonin syndrome may result; may enhance therapeutic and
toxic response of meperidine, and concomitant administration of these drugs
should be avoided.
Pregnancy - not established.
Precautions: monitor for postural hypotension; convulsion .