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Current Diagnosis and Treatment of Anxiety Disorders
Presented To –Dr. Anuja Krishnan
Presented By- Aquib Reza
MSc Biomedical Sciences
Jamia Hamdard University
Contents
Abstract
• Anxiety disorder are the most prevalent mental health condition.
• They are less visible than schizophrenia depression and bipolar disorder
• the diagnose of anxiety disorder are being continuously revised. Dimensional and
structural diagnose have been used in clinical treatment and research and both
methods have been purpose for the new classification in the diagnostic statistical
Manual of mental disorder I V (DSM-5).
• Emphasis in diagnosis has focus on neuro imaging and genetic research And
understanding of how biology stress and genetics interact to the same the symptoms
of anxiety.
• And the anxiety disorder can be effectively treated with psychopharmacological and
cognitive-behavioral intervention.
Introduction
Up to 13.3% of Americans have an anxiety disorder, making it the most common type of mental illness, disorders.
About 26 years ago, the Epidemiological Catchments Area research first made the scope of their incidence known.
The primary care physician is typically the primary assessor and treatment provider; however, it has not gained the same
respect as other significant syndromes like mood and psychotic disorders.
A significant portion of the population engages in alcohol and drug misuse. The Diagnostic and Statistical Manual of Mental
Disorders presently lists anxiety disorders,
Anxiety disorders currently included in the Diagnostic and Statistical Manual of Mental Disorders, (DSM IV-TR)
post-traumatic stress disorder (PTSD) and obsessive– compulsive disorder (OCD) have been reclassified in the separate
domains of Trauma and Stressor Related Disorders and Obsessive–Compulsive and Related Disorders, respectively
Diagnosis Dilemmas
(refer to situations in which physicians face a challenging clinical scenario.)
 Epidemiological Information Has Been Used In The Past Ten Years Or So To Try And Define More Precisely The
Limits Of The Diagnostic Categories For Anxiety Disorders.
 The Results Of This Approach Have Been Progressively Reflected From Dsm Iii To Iiir To Dsm Iv-
tr And, Finally, To Dsm-5.
 Patients With Some Disorders Such As Generalized Anxiety Disorder (Gad) And Social Anxiety
Disorder (Sad), The Presence Of Comorbidities Is A Rule Rather Than The Exception.
 During An Evaluation, The Original Diagnosis Could Be Panic Disorder, Which Goes Away After
Treatment, And Then Comes Back Later With Different Symptoms. These Symptoms Are More
Suitable For A Diagnosis Of OCD Or GAD.
 Family And Twin Studies Highlight The Significance Of Genetic Variables That May Be Common
To Many Anxiety Disorders, Depression, And Alcohol And Drug Abuse Despite Their Lack Of
Specificity.
 The Term "Spectrum" Disorders Has Emerged As A Result Of Commonalities Across Many Disorders; The Idea
Was First Created For Ocd.
 This Model, Which Has Been Broadened To Take Into Account Many Additional Spectra Like Social Anxiety,
Panic-agoraphobia, And Post-traumatic Disorders, Was Useful In Comparing Similar Reactions To
Pharmaceutical And Psychological Therapies.
 Dimensional And Categorical Diagnosis In The Dsm-iv-tr Is Usually Produced By Cross-
sectional Comparisons Of Distinct Subject Samples.
 Scientists And Physicians Have Recently Started To Recognise That The Diverse Diseases May Share Pathways
 The Model That We, For Simplicity, Call The “ABC Model Of Anxiety” Could Be Viewed As An Interaction In Space
And Time Of Alarms, Beliefs And Coping Strategies Alarms (A) Are Emotional Sensations Or Physiological
Reactions To A Trigger Situation, Sensation, Or Thought. A Well-defined Set Of Brain Circuits Rapidly Processes
Information About The Alarm.
 The Ensuing Decision To Act Is Made On The Basis Of Beliefs (B) That Rely Heavily On Previous Experiences,
Personal And Cultural Background, And The Information That Is Perceived By The Sensory Organs.
 Patients With Anxiety Disorders Appear To Process Information About A Supposedly Dangerous Situation With More
Focused Attention Compared With Individuals Without The Disorder.
 Patients With Anxiety Disorders Appear To Process Information About A Supposedly Dangerous Situation With More
Focused Attention Compared With Individuals Without The Disorder.
 Coping Strategies Can Be Considered Adaptive Or Maladaptive, Based On Their Efficacy In Reducing The Target
Anxiety.
 Leads To Coping Strategies (C), For Example, Specific Behaviors Or Mental Activity Aimed At Reducing Anxiety And
Avoiding The Perceived “Danger.”
 Depending On How Successfully Coping Mechanisms Reduce The Target Anxiety, They May Be Deemed Adaptive
Or Maladaptive. As These Processes Develop Over Time, A Complex Picture Of A Specific Anxiety Illness Is
Created. As A Clinical Illustration, Panic Disorder May Begin As A Devastating Initial Panic Attack Triggered By The
Brain's Warning Networks. When Combined With A Person's Personal Thoughts About The Occurrence, This Event
Stimulates Neural Pathways That Process Information About Danger And Causes Greater Concern For One's Own
Health And Safety. This Then Prompts An Effort To Specifically Lessen The Threat Of The Circumstance (Such As A
Medical Examination That Initially Relieves The Fear).
 We Have Also Found That Conceptualization Of Clinical Cases Using The Abc Model Is Particularly Helpful In
Teaching Psychiatric Residents.
 Using This Model, Residents Are Able To Understand And To Begin Administering Cognitive–behavioral Therapy
The ABC Model Of Anxiety
Interplay Between Biological and Psychological
Factors
• To Treat An Anxiety Disorder Effectively, Clinicians Should Understand How These Conditions Emerge And Which
Factors
• Are Involved In Maintaining Them.
• Cognitive Theory Assigns A Primary Importance To Abnormal Or “Catastrophic” Cognition As An Underlying
Mechanism Of All Anxiety Disorders.
• The Abc Model Focuses On The Interaction Of Information Processing And Emotional And Cognitive Processes That
Are
• Controlled By Overlapping Circuits And Compete For The Same Brain Resources.
• In Most Anxiety Disorders, Patients Usually Process Fear Inducing Information In Excessive Detail That Overwhelms
Their Ability To Appraise It Properly. They Cope By Separating The Information Into “Good” And “Bad” With No Gray
Area In Between.
• Stress
• Stress Also Plays A Major Role In The Pathology Of Anxiety Disorders.
• Ptsd Is A Condition In Which Stress Is Considered The Main Etiological Factor.
• In Other Anxiety Disorders Such As Gad And Ocd, The Role Of Stress Is Less Apparent.
• A Stressful Event Or A Persistent And Chronic Disorder Can Even Cause Secondary Biological Changes In Specific
Brain Structures.
Biological factor
• Biological Factors Are Of Primary Importance In Anxiety Disorders.
• Anxiety Disorders Can Occur In The Context Of Medical Illness And The Clinician Should
Consider An Intricate Relationship Between Medical Illnesses And Anxiety Disorders .
• Metabolic Or Autonomic Abnormalities Caused By The Illness Can Produce The Syndrome Of
Anxiety (I.E., Hyperthyroidism Sometimes Results In Panic Attacks)
• The Symptom Of Medical Illness Can Be A Trigger For Anxiety (I.E., Sensations Of Arrhythmia
Can Serve As A Trigger For A Panic Attack).
• Sometimes Medical Illness Can Mimic The Anxiety Disorder (I.E., When Perseverations In
Mental Retardation Are Mistaken For OCD)
• Medical Illness And An Anxiety Disorder Can Simply Coexist In The Same Patient .
• One Of The Most Interesting Interactions Between Medical Illness And Anxiety Disorders Is
Pediatric Autoimmune Neuropsychiatric Disorder Associated With Streptococcal Infections
(PANDAS), Which Has Been Reported In A Subset Of OCD Patients.
PHARMACOLOGICAL THERAPY
 Numerous neurotransmitters play a role in normal states and in pathological anxiety states. Each of these
systems is a
 potential target for pharmacological intervention
 few classes of medications are used in clinical practice for the treatment of anxiety.
Selective Serotonin Reuptake Inhibitors
 SSRIs, usually indicated in depression, are considered to be the first line of therapy for anxiety disorders.
 This drug class includes --
fluoxetine (Prozac, Eli Lilly), sertraline (Zoloft, Pfizer), citalopram (Celexa, Forest), escitalopram
(Lexapro, Forest), fluvoxamine (Luvox, Solvay), paroxetine (Paxil, GlaxoSmithKline), and vilazodone
(Viibryd, Forest).
Serotonin–Norepinephrine Reuptake Inhibitors
 SNRIs, which inhibit the serotonin and norepinephrine transporters
 Include venlafaxine, desvenlafaxine (Pristiq, Pfizer), and duloxetine.75 Milnacipran (Savella, Cypress/Forest) is
rarely,
 if ever, used to treat anxiety because its only FDA-approved indication is for fibromyalgia.
 SNRIs are typically used after failure or inadequate response to an SSRI. They are used in place of augmentation
to SSRIs because the combination of these two drug classes may result in serotonin syndrome.
Benzodiazepines
 Benzodiazepines were widely used in the past to treat anxiety
conditions, they are no longer considered to be first-line therapies
because of the risks associated with their chronic use. physiological and
psychological dependence.
 • potential fatalities upon withdrawal.
 • impaired cognition and coordination.
 • a potentially lethal overdose when they are mixed with alcohol or
opioids.
 • inhibition of memory encoding, which can interfere with the efficacy of
concomitant psychotherapy.
 For these reasons, the use of benzodiazepines is often restricted to the
short-term treatment of acute anxiety or as therapy for refractory anxiety
after failed trials of several other drugs.
 Note, some subgroups of patients do well with low doses of
TREATMENT STRATEGIES
 During the 1990s, mainstream psychological and pharmacological treatments of
anxiety disorders were developed and tested, leading to an initial algorithm that is
similar for all major anxiety disorders.
The typical algorithm, adapted from Roy- Byrne et al.
 A general principle with SSRIs is to “start low and go slow,” starting with
approximately half the dose of that used for depression and slowly titrating the dose
upward, with no more than a once-weekly change in the dosage.
 Benzodiazepines are generally avoided except in acute states or treatment-resistant
chronic conditions.
 Based on clinical experience, generally recommend continuing treatment until the
patient has achieved marked symptom reduction for at least 6 months.
 In the later stages of anxiety treatment, GABA-ergic antiepileptic drugs and atypical
antipsychotic agents may be tried.
 Anxiety disorders are treatable. The development of better algorithms and the
identification of effective treatments . However, more study has to be done to integrate
our knowledge of the molecular processes underlying anxiety with current therapeutic
techniques in order to better predict and increase therapy response.
 Dynamic models of anxiety, like the ABC model, can help us better understand the
interconnections between the systems responsible for the onset and maintenance of
anxiety symptoms throughout time, as well as between the biological and psychological
factors influencing them.
 In order to distribute currently useful medications in real healthcare settings, such as
primary care, and to inform the public through media channels, we need to design
better delivery systems. We should continue to test alternate methods of treating and
preventing anxiety disorders in order to help people whose anxiety is resistant to
conventional medications .
 we must consider the patient's perspectives on mental illness and deal with their
responses early on in the therapeutic process. The treatment of worried people will be
improved by all of these approaches.
CONCLUSION
Thank You

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anxiety ppt.pptx

  • 1. Current Diagnosis and Treatment of Anxiety Disorders Presented To –Dr. Anuja Krishnan Presented By- Aquib Reza MSc Biomedical Sciences Jamia Hamdard University
  • 3. Abstract • Anxiety disorder are the most prevalent mental health condition. • They are less visible than schizophrenia depression and bipolar disorder • the diagnose of anxiety disorder are being continuously revised. Dimensional and structural diagnose have been used in clinical treatment and research and both methods have been purpose for the new classification in the diagnostic statistical Manual of mental disorder I V (DSM-5). • Emphasis in diagnosis has focus on neuro imaging and genetic research And understanding of how biology stress and genetics interact to the same the symptoms of anxiety. • And the anxiety disorder can be effectively treated with psychopharmacological and cognitive-behavioral intervention.
  • 4. Introduction Up to 13.3% of Americans have an anxiety disorder, making it the most common type of mental illness, disorders. About 26 years ago, the Epidemiological Catchments Area research first made the scope of their incidence known. The primary care physician is typically the primary assessor and treatment provider; however, it has not gained the same respect as other significant syndromes like mood and psychotic disorders. A significant portion of the population engages in alcohol and drug misuse. The Diagnostic and Statistical Manual of Mental Disorders presently lists anxiety disorders, Anxiety disorders currently included in the Diagnostic and Statistical Manual of Mental Disorders, (DSM IV-TR) post-traumatic stress disorder (PTSD) and obsessive– compulsive disorder (OCD) have been reclassified in the separate domains of Trauma and Stressor Related Disorders and Obsessive–Compulsive and Related Disorders, respectively
  • 5. Diagnosis Dilemmas (refer to situations in which physicians face a challenging clinical scenario.)  Epidemiological Information Has Been Used In The Past Ten Years Or So To Try And Define More Precisely The Limits Of The Diagnostic Categories For Anxiety Disorders.  The Results Of This Approach Have Been Progressively Reflected From Dsm Iii To Iiir To Dsm Iv- tr And, Finally, To Dsm-5.  Patients With Some Disorders Such As Generalized Anxiety Disorder (Gad) And Social Anxiety Disorder (Sad), The Presence Of Comorbidities Is A Rule Rather Than The Exception.  During An Evaluation, The Original Diagnosis Could Be Panic Disorder, Which Goes Away After Treatment, And Then Comes Back Later With Different Symptoms. These Symptoms Are More Suitable For A Diagnosis Of OCD Or GAD.  Family And Twin Studies Highlight The Significance Of Genetic Variables That May Be Common To Many Anxiety Disorders, Depression, And Alcohol And Drug Abuse Despite Their Lack Of Specificity.  The Term "Spectrum" Disorders Has Emerged As A Result Of Commonalities Across Many Disorders; The Idea Was First Created For Ocd.  This Model, Which Has Been Broadened To Take Into Account Many Additional Spectra Like Social Anxiety, Panic-agoraphobia, And Post-traumatic Disorders, Was Useful In Comparing Similar Reactions To Pharmaceutical And Psychological Therapies.  Dimensional And Categorical Diagnosis In The Dsm-iv-tr Is Usually Produced By Cross- sectional Comparisons Of Distinct Subject Samples.  Scientists And Physicians Have Recently Started To Recognise That The Diverse Diseases May Share Pathways
  • 6.
  • 7.  The Model That We, For Simplicity, Call The “ABC Model Of Anxiety” Could Be Viewed As An Interaction In Space And Time Of Alarms, Beliefs And Coping Strategies Alarms (A) Are Emotional Sensations Or Physiological Reactions To A Trigger Situation, Sensation, Or Thought. A Well-defined Set Of Brain Circuits Rapidly Processes Information About The Alarm.  The Ensuing Decision To Act Is Made On The Basis Of Beliefs (B) That Rely Heavily On Previous Experiences, Personal And Cultural Background, And The Information That Is Perceived By The Sensory Organs.  Patients With Anxiety Disorders Appear To Process Information About A Supposedly Dangerous Situation With More Focused Attention Compared With Individuals Without The Disorder.  Patients With Anxiety Disorders Appear To Process Information About A Supposedly Dangerous Situation With More Focused Attention Compared With Individuals Without The Disorder.  Coping Strategies Can Be Considered Adaptive Or Maladaptive, Based On Their Efficacy In Reducing The Target Anxiety.  Leads To Coping Strategies (C), For Example, Specific Behaviors Or Mental Activity Aimed At Reducing Anxiety And Avoiding The Perceived “Danger.”  Depending On How Successfully Coping Mechanisms Reduce The Target Anxiety, They May Be Deemed Adaptive Or Maladaptive. As These Processes Develop Over Time, A Complex Picture Of A Specific Anxiety Illness Is Created. As A Clinical Illustration, Panic Disorder May Begin As A Devastating Initial Panic Attack Triggered By The Brain's Warning Networks. When Combined With A Person's Personal Thoughts About The Occurrence, This Event Stimulates Neural Pathways That Process Information About Danger And Causes Greater Concern For One's Own Health And Safety. This Then Prompts An Effort To Specifically Lessen The Threat Of The Circumstance (Such As A Medical Examination That Initially Relieves The Fear).  We Have Also Found That Conceptualization Of Clinical Cases Using The Abc Model Is Particularly Helpful In Teaching Psychiatric Residents.  Using This Model, Residents Are Able To Understand And To Begin Administering Cognitive–behavioral Therapy
  • 8. The ABC Model Of Anxiety
  • 9. Interplay Between Biological and Psychological Factors • To Treat An Anxiety Disorder Effectively, Clinicians Should Understand How These Conditions Emerge And Which Factors • Are Involved In Maintaining Them. • Cognitive Theory Assigns A Primary Importance To Abnormal Or “Catastrophic” Cognition As An Underlying Mechanism Of All Anxiety Disorders. • The Abc Model Focuses On The Interaction Of Information Processing And Emotional And Cognitive Processes That Are • Controlled By Overlapping Circuits And Compete For The Same Brain Resources. • In Most Anxiety Disorders, Patients Usually Process Fear Inducing Information In Excessive Detail That Overwhelms Their Ability To Appraise It Properly. They Cope By Separating The Information Into “Good” And “Bad” With No Gray Area In Between. • Stress • Stress Also Plays A Major Role In The Pathology Of Anxiety Disorders. • Ptsd Is A Condition In Which Stress Is Considered The Main Etiological Factor. • In Other Anxiety Disorders Such As Gad And Ocd, The Role Of Stress Is Less Apparent. • A Stressful Event Or A Persistent And Chronic Disorder Can Even Cause Secondary Biological Changes In Specific Brain Structures.
  • 10. Biological factor • Biological Factors Are Of Primary Importance In Anxiety Disorders. • Anxiety Disorders Can Occur In The Context Of Medical Illness And The Clinician Should Consider An Intricate Relationship Between Medical Illnesses And Anxiety Disorders . • Metabolic Or Autonomic Abnormalities Caused By The Illness Can Produce The Syndrome Of Anxiety (I.E., Hyperthyroidism Sometimes Results In Panic Attacks) • The Symptom Of Medical Illness Can Be A Trigger For Anxiety (I.E., Sensations Of Arrhythmia Can Serve As A Trigger For A Panic Attack). • Sometimes Medical Illness Can Mimic The Anxiety Disorder (I.E., When Perseverations In Mental Retardation Are Mistaken For OCD) • Medical Illness And An Anxiety Disorder Can Simply Coexist In The Same Patient . • One Of The Most Interesting Interactions Between Medical Illness And Anxiety Disorders Is Pediatric Autoimmune Neuropsychiatric Disorder Associated With Streptococcal Infections (PANDAS), Which Has Been Reported In A Subset Of OCD Patients.
  • 11. PHARMACOLOGICAL THERAPY  Numerous neurotransmitters play a role in normal states and in pathological anxiety states. Each of these systems is a  potential target for pharmacological intervention  few classes of medications are used in clinical practice for the treatment of anxiety. Selective Serotonin Reuptake Inhibitors  SSRIs, usually indicated in depression, are considered to be the first line of therapy for anxiety disorders.  This drug class includes -- fluoxetine (Prozac, Eli Lilly), sertraline (Zoloft, Pfizer), citalopram (Celexa, Forest), escitalopram (Lexapro, Forest), fluvoxamine (Luvox, Solvay), paroxetine (Paxil, GlaxoSmithKline), and vilazodone (Viibryd, Forest). Serotonin–Norepinephrine Reuptake Inhibitors  SNRIs, which inhibit the serotonin and norepinephrine transporters  Include venlafaxine, desvenlafaxine (Pristiq, Pfizer), and duloxetine.75 Milnacipran (Savella, Cypress/Forest) is rarely,  if ever, used to treat anxiety because its only FDA-approved indication is for fibromyalgia.  SNRIs are typically used after failure or inadequate response to an SSRI. They are used in place of augmentation to SSRIs because the combination of these two drug classes may result in serotonin syndrome.
  • 12. Benzodiazepines  Benzodiazepines were widely used in the past to treat anxiety conditions, they are no longer considered to be first-line therapies because of the risks associated with their chronic use. physiological and psychological dependence.  • potential fatalities upon withdrawal.  • impaired cognition and coordination.  • a potentially lethal overdose when they are mixed with alcohol or opioids.  • inhibition of memory encoding, which can interfere with the efficacy of concomitant psychotherapy.  For these reasons, the use of benzodiazepines is often restricted to the short-term treatment of acute anxiety or as therapy for refractory anxiety after failed trials of several other drugs.  Note, some subgroups of patients do well with low doses of
  • 13. TREATMENT STRATEGIES  During the 1990s, mainstream psychological and pharmacological treatments of anxiety disorders were developed and tested, leading to an initial algorithm that is similar for all major anxiety disorders. The typical algorithm, adapted from Roy- Byrne et al.  A general principle with SSRIs is to “start low and go slow,” starting with approximately half the dose of that used for depression and slowly titrating the dose upward, with no more than a once-weekly change in the dosage.  Benzodiazepines are generally avoided except in acute states or treatment-resistant chronic conditions.  Based on clinical experience, generally recommend continuing treatment until the patient has achieved marked symptom reduction for at least 6 months.  In the later stages of anxiety treatment, GABA-ergic antiepileptic drugs and atypical antipsychotic agents may be tried.
  • 14.  Anxiety disorders are treatable. The development of better algorithms and the identification of effective treatments . However, more study has to be done to integrate our knowledge of the molecular processes underlying anxiety with current therapeutic techniques in order to better predict and increase therapy response.  Dynamic models of anxiety, like the ABC model, can help us better understand the interconnections between the systems responsible for the onset and maintenance of anxiety symptoms throughout time, as well as between the biological and psychological factors influencing them.  In order to distribute currently useful medications in real healthcare settings, such as primary care, and to inform the public through media channels, we need to design better delivery systems. We should continue to test alternate methods of treating and preventing anxiety disorders in order to help people whose anxiety is resistant to conventional medications .  we must consider the patient's perspectives on mental illness and deal with their responses early on in the therapeutic process. The treatment of worried people will be improved by all of these approaches. CONCLUSION