Generalized anxiety disorder is characterized by excessive, uncontrollable worry about everyday life events for at least 6 months. It affects around 3-8% of people, with higher rates in women. Common comorbid disorders include social phobia, panic disorder, and OCD. Both biological and psychosocial factors contribute to its development, such as abnormalities in neurotransmitter systems like GABA and serotonin, and incorrectly perceiving threats. Treatment involves psychotherapy and medication to regulate neurotransmitter activity.
A mental health disorder characterized by feelings of worry, anxiety or fear that are strong enough to interfere with one's daily activities.
this is a detailed medical study mentioning all the aspects of anxiety disorder ,
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A mental health disorder characterized by feelings of worry, anxiety or fear that are strong enough to interfere with one's daily activities.
this is a detailed medical study mentioning all the aspects of anxiety disorder ,
please comment
thank you
Trauma and stressor-related disorders are a group of emotional and behavioral problems that may result from childhood traumatic and stressful experiences. These traumatic and stressful experiences can include exposure to physical or emotional violence or pain, including abuse, neglect or family conflict.
A presentation about depressive disorder. The presentation composed of the definition, causes, types, clinical feature, diagnosis, prognosis, treatment and prevention of depression
Trauma and stressor-related disorders are a group of emotional and behavioral problems that may result from childhood traumatic and stressful experiences. These traumatic and stressful experiences can include exposure to physical or emotional violence or pain, including abuse, neglect or family conflict.
A presentation about depressive disorder. The presentation composed of the definition, causes, types, clinical feature, diagnosis, prognosis, treatment and prevention of depression
Generalized and phobic anxiety disordernabina paneru
This slide contains information regarding Generalized and phobic anxiety disorder. This can be helpful for proficiency level and bachelor level nursing students. Your feedback is highly appreciated.
generalized anxiety disorder is very common in primary health care settings .patients usually have somatic complaints and they do not attribute these symptoms to anxiety.the doctor needs to have a high index of suspicion to be able help the patients.
A presentation about panic attacks and panic disorder. this presentation composed of the definition, causes, symptoms, diagnosis, treatment, prevention and prognosis of panic disorder.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
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The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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2. NORMAL ANXIETY
• Everyone experiences it.
• Characterized most commonly as a diffuse, unpleasant, vague
sense of apprehension, often accompanied by autonomic
symptoms such as headache, perspiration, palpitations,
tightness in the chest, mild stomach discomfort, and
restlessness, indicated by an inability to sit or stand still for long.
• The particular constellation of symptoms vary among persons.
3. Fear Vs Anxiety
• Anxiety is an alerting signal
• It warns of impending danger and
enables a person to take measures to deal with a threat
• Fear-a response to a known, external, definite, or nonconflictual
threat
• Anxiety -a response to a threat that is unknown,internal, vague, or
conflictual
5. Is Anxiety Adaptive?
• Anxiety and fear both are alerting signals and act as a warning
of an internal and external threat.
• Anxiety can be conceptualized as a normal and adaptive
response that has lifesaving qualities and warns of threats.
• It prompts a person to take the necessary steps to prevent the
threat or to lessen its consequences.
• This preparation is accompanied by increased somatic and
autonomic activity controlled by the interaction of the
sympathetic and parasympathetic nervous systems.
• Thus, anxiety prevents damage by alerting the person to carry
out certain acts that forestall the danger.
6. Stress and Anxiety
• Whether an event is perceived as stressful depends on the
nature of the event and on the person's resources,
psychological defenses, and coping mechanisms.
• All involve the ego, a collective abstraction for the process by
which a person perceives, thinks, and acts on external events
or internal drives.
• A person whose ego is functioning properly is in adaptive
balance with both external and internal worlds.
• If the ego is not functioning properly Anxiety
8. Symptoms of Anxiety
• The awareness of the physiological sensations(e.g. palpitations &
sweating)
• The awareness of being nervous or frightened
• Motor and visceral effects
• Affects thinking, perception
• Interfere with learning by lowering concentration, reducing recall,
and impairing the ability to relate one item to another that is, to
make associations.
• Confusion and distortions of perception- Not only of time & space
but also of persons and meaning of events.
• It causes significant subjective distress and /or impairment in
functioning of an impairment.
10. Epidemiology
• The anxiety disorders make up one of the most common groups
of psychiatric disorders.
• One of four persons met the diagnostic criteria for at least one
anxiety disorder
• 12-month prevalence rate of 17.7 %.
• Women > Men
(19.2 percent lifetime prevalence).
• Prevalence of anxiety disorders decreases with higher
socioeconomic status.
11. Psychological Aspects of Anxiety
disorders
• Three major schools of psychological theory:
• Psychoanalytic Theories: Anxiety was viewed as the result of
psychic conflict between unconscious sexual or aggressive
wishes and corresponding threats from the superego or external
reality.
• Behavioural Theories: Anxiety is a conditioned response to a
specific environmental stimulus.
• Existential Theories: Persons experience feelings of living in a
purposeless universe.
12. Biological Aspects of Anxiety disorders
A) Autonomic Nervous System
Stimulation of the autonomic nervous system causes certain
symptoms cardiovascular( e.g. Tachycardia), muscular(e.g.
headache), gastrointestinal(e.g. diarrhea), and respiratory(e.g.
Tachypnea).
13. B) Neurotransmitters
• Three major neurotransmitters norepinephrine (NE), serotonin
(5HT), gamma-aminobutyric acid (GABA) are associated with
anxiety.
i)NOREPINEPHRINE (area – locus ceruleus):
• Patients may have a poorly regulated noradrenergic system with
occasional bursts of activity.
14. • Beta-adrenergic receptor agonists (e.g., isoproterenol ) and
alpha adrenergic receptor antagonists (e.g., yohimbine ) can
provoke frequent and severe panic attacks.
• Conversely, clonidine, and alpha2-receptor agonist, reduces
anxiety symptoms in some experimental and therapeutic
situations.
15. ii)Serotonin/5HT (area – locus ceruleus)
• Different types of acute stress result in increased 5-hydroxytryptamine (5-
HT) turnover in the prefrontal cortex, nucleus accumbens, amygdala, and
lateral hypothalamus.
• Effectiveness of buspirone , a serotonin 5-HT1a receptor agonist, in the
treatment of anxiety disorders also suggests the possibility of an
association between serotonin and anxiety..
• Serotonergic hallucinogens and stimulants-for example, lysergic acid
diethylamide (LSD) and 3,4-methylenedioxymethamphetamine (MDMA)---
are associated with the development of both acute and chronic anxiety
disorders.
16. iii) GABA:
• A role of GABA is supported by the undisputed efficacy of
benzodiazepines, which enhance the activity of GABA at the
GABA type A (GABA A) receptor, in the treatment of some
types of anxiety disorders.
17. C) HYPOTHALAMIC-PITUITARY-ADRENAL AXIS
• Consistent evidence indicates that many forms of psychological stress
increase the synthesis and release of cortisol.
• Excessive and sustained cortisol secretion can have serious adverse
effects, including hypertension, osteoporosis, immunosuppression,
insulin resistance, dyslipidemia, dyscoagulation, and, ultimately,
atherosclerosis and cardiovascular disease.
• Alteration of HPA axis function have been demonstrated in PTSD.
• Blunted ACTH responses to CRF have been reported in some studies
in Panic disorder.
18. D) Corticotropin-releasing hormone (CRH):
• CRH coordinates the adaptive behavioral and physiological changes
that occur
during stress.
• Hypothalamic levels of CRH are increased by stress, resulting in
activation of the HPA axis and increased release of cortisol and
dehydroepiandrosterone (DHEA)
• CRH also inhibits a variety of neurovegetative functions, such as food
intake, sexual activity, and endocrine programs for growth and
reproduction.
19. E)NEUROPEPTIDE Y:
• Evidence suggesting the involvement of the amygdala in the
anxiolytic effects of NPY via the NPY-Y1receptor.
• NPY has counterregulatory effects on (CRH) and LC-NE
systems at brain sites that are important in the expression of
anxiety, fear, and depression
• Preliminary studies in special operations soldiers under extreme
training stress indicate that high NPY levels are associated with
better performance.
20. F)GALANIN:
• It has been demonstrated to be involved in a number of physiological
and behavioral functions, including learning and memory, pain control,
food intake, neuroendocrine control, cardiovascular regulation, and,
most recently anxiety.
• galanin LC Various Cortical structures
• Hence, Galanin and NPY receptor agonists may be novel
targets for antianxiety drug development.
21. Brain Imaging Studies
• CT and MRI: occasionally show some increase in the size of cerebral
ventricles.
• fMRI studies like, PET, SPECT, and EEG - reported abnormalities in
the frontal cortex; the occipital and temporal areas; and, in a study of
panic disorder, the Parahippocampal gyrus.
23. Neuroanatomical Basis
• The locus ceruleus(NE) and the raphe nuclei(5HT) project primarily to
the limbic system and the cerebral cortex.
i) LIMBIC SYSTEM:
• Animal studies shows involvement of the limbic system in the
generation of anxiety and fear responses.
• Two areas of the limbic system:
a)Increased activity in the septohippocampal pathway Anxiety
b)The cingulate gyrus OCD.
24. ii) CEREBRAL CORTEX
The frontal cerebral cortex and temporal cortex is connected
with the Parahippocampal region, the cingulate gyrus, and the
hypothalamus and thus may be involved in the production of
anxiety disorders.
26. • Generalized anxiety disorder is defined as excessive anxiety and worry
about several events or activities for most days during at least a 6-
month period.
• The anxiety is difficult to control, is subjectively distressing, and
produces impairment in important areas of a person's life.
28. Comorbid illnesses
• 50 to 90 % of patients with generalized anxiety disorder have
another mental disorder.
• 25 % of patients eventually experience panic disorder.
• Co morbidities viz.: social phobia, specific phobia, panic
disorder, OCD
29. ETIOLOGY
• Cause of generalized anxiety disorder is not known
• Biological and psychological factors probably work together
• Biological factors:
• Focused biological research efforts on the gamma-aminobutyric acid
and serotonin neurotransmitter systems.
• Other neurotransmitter systems in generalized anxiety disorder include
the norepinephrine, glutamate, and cholecystokinin systems.
• .
30. • Psychosocial factors
• Patients with generalized anxiety disorder respond to incorrectly and
inaccurately perceived dangers.
• Psychoanalytic school hypothesizes that anxiety is a symptom of
unresolved, unconscious conflicts.
31. DSM-5 Diagnostic Criteria for Generalized
Anxiety Disorder
A. Excessive anxiety and worry
(apprehensive expectation), occurring
more days than not for at least 6
months, about a number of events or
activities (such as work or school
performance).
B. The individual finds it difficult to
control the worry.
C.The anxiety and worry are associated
with three (or more) of the following
Restlessix symptoms (with at least
some symptoms having been present
for more days than not for the past 6
months):
Note: Only one item is required in
children.
1. Restlessness or feeling keyed up or on
edge.
2. Being easily fatigued.
3. Difficulty concentrating or mind going blank.
4. Irritability.
5. Muscle tension.
6. Sleep disturbance (difficulty falling or
staying asleep, or restless, unsatisfying
sleep).
D.The anxiety, worry, or physical
symptoms cause clinically
significant distress or impairment in
social, occupational, or
other areas of functioning.
34. COURSE AND PROGNOSIS
• Patients usually come to a clinician's attention in their 20s
• High incidence of comorbid mental disorders the clinical course
and prognosis of the disorder are difficult to predict
• Generalized anxiety disorder is a chronic condition that may
well be lifelong.
36. TREATMENT
• Behavioral approaches address somatic symptoms directly.
• Psychodynamic therapy proceeds with the assumption that anxiety can
increase with effective treatment.
• The goal of the dynamic approach may be to increase the patient's
anxiety tolerance, rather than to eliminate anxiety
37. • Pharmacotherapy
• Benzodiazepines: the drugs of choice for generalized anxiety disorder.
• Buspirone: 5-HT1A receptor partial agonist and is most likely effective in 60 to
80 percent of patients with generalized anxiety disorder.
• Disadvantage: Effect takes 2 to 3 weeks to become evident
• Venlafaxine: effective in treating the insomnia, poor concentration,
restlessness, irritability, and excessive muscle tension associated with
generalized anxiety disorder.
• Selective Serotonin Reuptake Inhibitors
• Other Drugs: Beta-adrenergic receptor antagonists may reduce the somatic
manifestations.
39. • An acute intense attack of anxiety accompanied by feelings of
impending doom is known as panic disorder.
• Comorbid conditions: most commonly agoraphobia
• Previously known as DaCosta's syndrome
41. Comorbid illnesses
• 91 % have at least one other psychiatric disorder.
• About 1/3rd have MDD before onset; 2/3rd experience during or after
the onset of MDD.
• Social anxiety disorder or social phobia
• Specific phobia
• Generalized anxiety disorder
• PTSD
• OCD
• Hypochondriasis or illness anxiety disorder, personality disorders,
and substance related disorders.
42. ETIOLOGY
• Biological Factors:
• Abnormal Regulation Of Brain Noradrenergic Systems
• Hypotheses Implicating Both Peripheral And Central Nervous System
Dysregulation.
• Major Neurotransmitter Systems: NE, 5HT, And GABA
• Postsynaptic Serotonin Hypersensitivity In Panic Disorder Local Inhibitory
• GABA-nergic Transmission in the Basolateral Amygdala, Midbrain, And
Hypothalamus can elicit anxiety-like Physiological Responses.
• Patients With Panic Disorder are Sensitive to The Anxiogenic Effects Of
Yohimbine.
43. Panic-Inducing Substances: Panicogens
• Carbon dioxide (5 to 35 percent mixtures)
• Sodium lactate, and bicarbonate
• Neurochemical panic-inducing substances that act through specific
neurotransmitter systems include yohimbine, an a2-adrenergic receptor
antagonist; mCPP, m-caroline drugs; GABA-B receptor inverse agonists;
flumazenil, a GABA-B receptor antagonist; cholecystokinin; and caffeine,
Isoproterenol.
• Respiratory panic-inducing substances may act initially at the
peripheral cardiovascular baroreceptors and relay their signal by vagal
afferents to the nucleus tractus solitarii and then on to the nucleus
paragigantocellularis of the medulla.
44. Brain Imaging
• MRI: Temporal lobes, particularly
the hippocampus and the amygdala.
• PET: Dysregulation of cerebral blood flow, cerebral
vasoconstriction, which may result in CNS symptoms, such as
dizziness, and in peripheral nervous system symptoms that may
be induced by hyperventilation and hypocapnia.
45. Genetic Factors
• First-degree relatives of patients with panic disorder have a
four- to eightfold higher risk for panic disorder than first-degree
relatives of other psychiatric patients.
46. Psychosocial Factors
• Psychoanalytic theories- panic attacks as arising from an unsuccessful defense
against anxiety-provoking impulses.
• Panic attacks is likely to involve the unconscious meaning of stressful events
• The pathogenesis of the panic attacks may be related to neurophysiological
factors triggered by the psychological reactions.
• Panic attacks are correlated neurophysiologically with the locus ceruleus, the
onset of panic is generally related to environmental or psychological factors.
• Stressful life events (particularly loss)
• Childhood physical and sexual abuse.
• Before the therapy, the patients responded to panic attack induction with lactate.
After successful cognitive therapy, lactate infusion no longer
produced a panic attack.
47. DIAGNOSIS
• Panic Attacks
• A panic attack is a sudden period of intense fear or apprehension that may
last from minutes to hours.
48. DSM-5 Diagnostic Criteria for Panic Disorder
A. Recurrent unexpected panic attacks. A panic attack is
an abrupt surge of intense fear or intense discomfort
that reaches a peak within minutes and during which
time four (or more) of the following symptoms occur:
Note: The abrupt surge can occur from a calm state or
an anxious state.
1. Palpitations, pounding heart, or accelerated heart
rate.
2. Sweating.
3. Trembling or shaking.
4. Sensations of shortness of breath or smothering.
5. Feelings of choking.
6. Chest pain or discomfort.
7. Nausea or abdominal distress.
8. Feeling dizzy, unsteady, light-headed, or faint.
9. Chills or heat sensations.
10.Paresthesias (numbness or tingling sensations).
11.Derealization (feelings of unreality) or
depersonalization (being detached from one-self).
12.Fear of losing control or "going crazy.“
13.Fear of dying.
Note: Culture-specific symptoms (e.g., tinnitus, neck
soreness, headache, uncontrollable screaming or
crying) may be seen. Such symptoms should not
count as one of the four required symptoms.
B. At least one of the attacks has been followed by 1
month
(or more) of one or both of the following:
1. Persistent concern or worry about additional
panic
attacks or their consequences (e.g., losing
control, having a heart attack, "going crazy").
2. A significant maladaptive change in behavior
related
to the attacks (e.g., behaviors designed to
avoid having
panic attacks, such as avoidance of exercise
or unfamiliar situations).
49. CLINICAL FEATURES
• First panic attack is often completely spontaneous, although panic
attacks occasionally follow excitement, physical exertion, sexual
activity, or moderate emotional trauma.
• The attack often begins with a 10-minute period of rapidly increasing
symptoms. The major mental symptoms are extreme fear and a
sense of impending death and doom.
• Patients often try to leave whatever situation they are in to seek help.
The attack generally lasts 20 to 30 minutes and rarely more than an
hour.
• Between attacks, patients may have anticipatory anxiety about
having
another attack.
50. CLINICAL FEATURES
• Somatic concerns of death from a cardiac or respiratory problem may
be the major focus of patients' attention.
• Hyperventilation can produce respiratory alkalosis and other
symptoms. The age-old treatment of breathing into a paper bag
sometimes helps because it decreases alkalosis.
54. COURSE AND PROGNOSIS
• Panic disorder, in general, is a chronic disorder, although its course is
variable.
• About 30 to 40 percent - symptom free at long-term follow-up,
• About 50 percent - have symptoms that are sufficiently mild not
to affect their lives significantly,
• About 10 to 20 percent continue to have significant symptoms.
55. Treatment
1)Pharmacotherapy
• Alprazolam and paroxetine are the two drugs approved by the (FDA) for the
treatment of panic disorder.
• superiority of the SSRIs and Clomipramine over the benzodiazepines, MAOis,
and tricyclic and tetracyclic drugs
• Clonazepam can be prescribed for patients who anticipate a situation in
which panic may occur (0.5 to 1 mg as required).
56. Treatment
2) Psychotherapy
Cognitive and Behavior Therapies
a)Instruction about false belief –Pts tendency to misinterpret mild
body sensations as …
b) information about panic attacks- explanations that Panic
attacks are time limited and not life threatening
59. • Involves the fear of social situations, including situations that
involve scrutiny or contact with strangers.
• Persons with social anxiety disorder are fearful of embarrassing
themselves in social situations (i.e. Social gatherings, oral
presentations, meeting new people).
• Social anxiety Vs Specific Phobia- Social anxiety which is the intense
and persistent fear of an Object or situation.
• May have specific fears about performing specific activities such as
eating or speaking in front of others etc..
60. EPIDEMIOLOGY
• Lifetime prevalence- 3 to 13 %
• 6-month prevalence is about 2 to 3 per 100 persons
• Females > males
• Onset - 5 to 35 years
61. Etiology
• Children with a trait characterized by a consistent pattern of behavioral
inhibition.
• Children of parents affected with panic disorder and may develop into
severe shyness as the children grow older.
• Parents of persons with social anxiety disorder, as a group, were less
caring, more rejecting, and more overprotective of their children than
were other
parents.
62. Neurochemical factors
• Two specific neurochemical hypotheses:
i)Adrenergic theory – Performance phobias
Increased NE or Epinephrine both centrally & peripherally or
Sensitive to normal level of Adrenergic stimulation
ii)Dopaminergic activity- MAOIs more effective than TCA i.e.
suggests dopamine dysfunction
• SPECT scan –Decreased striatal dopamine reuptake site
density
63. Genetic factors
• First-degree relatives of persons with social anxiety disorder are
about three times more likely to be affected with social anxiety
disorder
64. Comorbid illnesses
• Persons with social anxiety disorder may have
-a history of other anxiety disorders
-mood disorders
-substance-related disorders
-and bulimia nervosa
65. DSM-5 Diagnostic Criteria for Social
Anxiety Disorder
A. Marked fear or anxiety about one or more
social situations in which the individual is
exposed to possible scrutiny by others.
Examples include social interactions (e.g.,
having a conversation, meeting unfamiliar
people), being observed (e.g., eating or
drinking), and performing in front of others
(e.g., giving a speech).
Note: In children, the anxiety must occur in
peer settings and just during interactions with
adults.
B. The individual fears that he or she will act in a
way or show anxiety symptoms that will be
negatively evaluated (i.e., will be humiliating
or embarrassing; will lead to rejection or
offend others).
C. The social situations almost always provoke
fear or anxiety.
Note: In children, the fear of anxiety may be
expressed by crying, tantrums, freezing,
clinging, shrinking, or failing to speak in social
situations.
D. The social situations are avoided or endured
with intense fear or anxiety.
E. The fear of anxiety is out of proportion to the
actual threat posed by the social situations
and to the sociocultural context.
F. The fear, anxiety, or avoidance is persistent,
typically lasting for 6 months or more
Specify if:
Performance only: If the fear is restricted to
speaking or performing in public
67. COURSE AND PROGNOSIS
• Onset in late childhood or early adolescence.
• Typically chronic
• Although Pts whose symptoms do remit tend to stay well.
68. Treatment
Both psychotherapy and pharmacotherapy.
A)Pharmacotherapy
-SSRIs the first-line treatment
-Benzodiazepines
-venlafaxine
-Buspirone as add on with SSRI.
• In severe cases-Irreversible MAOIs such phenelzine
Reversible MAOIs such moclobemide &
Brofaromine
69. Treatment
• In case of performance situations
- Beta-blocker viz. atenolol & propranolol
- Short or intermediate acting BZDs viz. Lorazepam or Alprazolam
Shortly before exposure to a phobic stimulus.
B)Psychotherapy
A combination of behavioral and cognitive methods- including cognitive
retraining, desensitization, rehearsal during sessions, and a range of
homework assignments.
70. • References-
1) Kaplan & Sadock’s SYNOPSIS OF PSYCHIATRY 11th edition
Page no.387-417
2) Neeraj Ahuja Textbook of Psychiatry…