1
ANXIETY DISORDER
INTRO TO PSYCHOLOGY SEC A
GROUP 9
2
ANXIETY
• Anxiety defined as a subjective sense of unease ,dread or
foreboding can indicate a primary psychiatric condition
• Anxiety can be described as an uncomfortable feeling of
vague fear or apprehension accompanied by characteristic
physical sensations.
• Anxiety can produce uncomfortable and potentially
debilitating psychological (e.g., worry or feeling of threat) and
physiological arousal (e.g., tachycardia or shortness of breath).
3
CLASSIFICATION
Anxiety disorders are broadly divided into
• Generalized anxiety disorder
• Panic disorder
• Phobic disorder
• Post traumatic stress disorder
• Obsessive compulsive disorders
4
EPIDEMIOLOGY
• In general, anxiety disorders are a group of heterogeneous
illnesses that develop before age 30 and are more common
in women, individuals with social issues, and those with a
family history of anxiety and depression.
• United States, the 1-year prevalence rate for anxiety
disorders was 13.3% in persons aged 18 to 54 years and
10.6% in those over age 55 years
5
• SYMPTOMS OF ANXIETY:
• Sensitivity of noise
• Dry mouth
• Difficulty in swallowing
• Palpitations
• Restlessness ,tremor
• Gastrointestinal discomfort
• Headache
• Insomnia.
• Constriction in chest
• Poor concentration
6
PATHO PHYSIOLOGY:
GABA system:
• The role of GABA- benzodiazepine receptor complex in anxiety disorders has not been fully
characterized
• However a potential role has been implicating in panic disorders, GAD and PTSD.
• In GAD reduced temporal lobe benzodiazepine receptor are observed.
• In PTSD, cortical benzodiazepine receptor are reduced.
• In PANIC decreased GABA A binding is noted.
• Angiogenic agents – having the property of altering the binding of benzodiazepines to the
gamma amino butyric acid receptor
↓ leads to
nerve cell excitability
↓
Anxiety
7
• SEROTONIN SYSTEM :
• 5-HT is involved in the pathophysiology of
anxiety disorders.
• as abnormal regulations of serotonin release
and reuptake or abnormal responsiveness to 5-
HT signals.
8
9
Amygdala
↓
• its role includes detecting, coordinating and maintaining fearful
emotions.
• The amygdala integrates information from multiple sensory areas to
assess for threats with consideration of input regarding the context of
presenting stimulus Once a threat has been detected by the amygdala
a rapid response is coordinated.
10
NON- ADRENERGIC SYSTEM :
Locus coeruleus which is located in the brainstem
↓
Locus coeruleus is the neither primary nor epinephrine containing area of the
brain
↓
According to the noradrenergic theory of anxiety, in the presence of perceived threat,
the locus coeruleus serves as an alarm center release nor epinephrine
↓
Leads to anxiety.
• α2 adrenergic antagonist yohimbine, carbon dioxide inhalation,
caffeine,isoproterenol each of these stimuli activates a pathway leads to anxiety.
11
GENERALIZED
ANXIETY DISORDER
12
• Chronic anxiety state associated with uncontrollable worry.
• Patients with GAD have persistent, excessive, unrealistic worry
associated with muscle tension, impaired concentration and
insomnia.
• Complaints of shortness of breath, palpitations and tachycardia
are relatively rare
• Alcohol abuse and dependence are common
in GAD patient
13
Risk Factors
Factors that may increase the risk of GAD include:
 Family members with an anxiety disorder
 Increase in stress
 Exposure to physical or emotional trauma
 Unemployment, poverty
 Drug abuse
14
Diagnosis/clinical presentation
•GAD is diagnosed when an individual experiences unrealistic or
excessive anxiety and worry for a period of at least 6 months.
•Additionally, the individual must have difficult in controlling that
anxiety or worry.
•Accompanying the anxiety or worry for 6 months with 3 or more
of following symptoms: feeling tense or restless, easily fatigued ,
difficulty concentrating, irritability, and difficulty with sleep.
15
PANIC DISORDER
16
• Panic disorder is defined by the presence of recurrent and
unpredictable panic attacks,which are distinct episodes of intense fear
and discomfort associated with a variety of physical symptoms.
SYMPTOMS :
• Palpitations
• Sweating
• Trembling or shaking
• Sensations of shortness of breath
• Chest pain or discomfort
• Nausea
• Feeling dizzy
• Fear of dying
• Paresthesias
• Chills or hot flushes.
17
• Diagnosis/clinical presentation
• A panic attack usually peaks in 10 mins and lasts no longer than 30
mins.
• A patient is diagnosed with a panic disorder when that individual
experiences repeated unexpected panic attacks and these attacks are
followed by a 1-month period of one or more: persistent concern
over future attacks
• During an attack individual will often feel like they are losing
control or dying.
18
PHOBIC
DISORDERS
19
SPECIFIC PHOBIA
A specific phobia is any kind of anxiety disorder that amounts to
an unreasonable or irrational fear related to exposure to specific
objects
20
SOCIAL PHOBIA
• Social phobia is fear of social situations where you may be
embarrassed or judged.
• Common physical symptoms include blushing,diarrhea,
sweating, and tachycardia.
21
AGAROPHOBIA
• Agorophobia is a fear of places or situations that
might cause you to panic and make you feel trapped,
helpless
22
• Phobic disorder are common ,affecting 10% of
population
• The Patients avoids phobic stimulus and this avoidance
usually impairs occupational or social functioning.
• Common phobias include fear of closed spaces (clustro
phobia), fear of blood,fear of flying.
• Patient with social phobia, in particular, have a high rate of
co-morbid alcohol abuse, as well as of other psychiatric
conditions (e.g. eating disorder)
23
POST TRAUMATIC
STRESS
DISORDERS
24
• Patients with stress disorders are at risk for the development of
other disorders related to anxiety, mood and substance abuse
(especially alcohol)
• Symptoms : nightmares, negative thinking and mood, unwanted
distressing memories of the traumatic event
• Symptoms usually begin early, within 3 months of the traumatic
incident, but sometimes they begin years afterward. Symptoms
must last more than a month
25
OBSESSIVE-COMPULSIVE
DISORDER
26
• OCD is characterized by obsessive thoughts and compulsive
behaviors that impair everyday functioning.
• Fears of contamination and germs are common as are hand
washing, counting behaviors and having check and recheck the
actions like whether a door is locked.
27
Non pharmacological treatment:
• Psychological education, short term counseling,
stress management, psychotherapy,
meditation, or exercise.
• Psychological therapy:
• Psychological therapies (talking therapies) are generally considered first
line treatments in all anxiety disorders because they provide a longer lasting
response and lower relapse than pharmacotherapy.
• The specific psychotherapy with the most supporting evidence in anxiety
disorders is cognitive behavioral therapy
28
SELECTIVE SEROTONIN REUPTAKE
INHIBITOR
• Paroxetine
• Escitalopram,
• Citalopram
• Fluoxetine
• SSRIs are the first-line treatment of GAD ,SAD, panic
disorder
• Treatment effect usually takes at least 4 weeks
29
30
• Mechanism of action:
• The SSRIs block the reuptake of serotonin, leading to increased
concentrations of the neurotransmitter in the synaptic cleft and,
ultimately,to greater postsynaptic neuronal activity
Agent Starting dose
(mg/day)
Usual dose
(mg/day)
Half life
Fluoxetine(Proxac)
Paroxetine
Sertraline
Citalopram(Celexa)
Escitalopram
10-20
10-20
25-50
10-20
5-10
20-60
20-60
50-200
20-60
10-20
7-9 days
21 hrs
24hrs
35 hrs
27-32 hrs
31
SIDE EFFECTS:
• Vivid dreams.
• Tremor.
• Nausea.
• vomiting.
• Insomnia.
• Osteopenia.
• Headache.
32
TRICYCLIC ANTIDEPRESSANTS
Tertiary amine
• Imipramine
• Amitriptyline (Elavil)
• Trimipramine (Trimip)
Secondary amine
• Desipramine (Norpramin)
• Nortriptyline (Aventyl)
33
• MECHANISM OF ACTION:
• Mechanism of action of the tricyclic antidepressants (TCAs) is
that they inhibit the reuptake of the biogenic amines, mostly nor
epinephrine (NE), as well as serotonin (5HT)
• SIDE EFFECTS:
• Blurred vision, constipation, urinary retention, dry mouth,
sedation, weight gain, and orthostatic hypotension, insomnia
34
• DOSE AND ADMINISTRATION:
• IMIRAPINE:
• Initiated with 10 mg/day at bedtime and slowly increased by 10
mg every 2 to 4 days as tolerated to 75 to 100 mg/day, and then
increased by 25 mg every 2 to 4 days over a 2 to 4 week
period.
35
MONOAMINE-OXIDASE INHIBITOR
• The substrate for MAO-A enzyme is serotonin, melatonin,
epinephrine and norepinephrine
• MECHANISM OF ACTION:
• MAOIs, form stable complexes with the enzyme,causing
irreversible inactivation. This results in increased stores of nor
epinephrine, serotonin, and dopamine within the neuron and
subsequent diffusion of excess neurotransmitter into the
synaptic space.
36
• Dosing and Administration:
• The starting dose of phenelzine is 15 mg/day after the evening meal,
increasing by 15 mg/day every 3 to 4 days until a maximum dose of 45
mg/day (in two or three divided doses) is reached.
• If a patient was on an antidepressant previously, it should be discontinued
2 weeks before phenelzine is started to prevent a potential drug interaction.
ADVERSE EFFECTS:
• orthostatic hypotension
• insomnia
• weight gain,
• peripheral edema
37
BENZODIAZEPINE THERAPY
• Benzodiazepines are effective medications due to their anxiolytic
properties and may provide rapid symptom relief.
• Benzodiazepines may be most useful when used early in treatment in
combination with an antidepressant.
• Adverse effects
• Drowsiness,Sedation,Ataxia,
Disorientation,Depression,
Confusion,Irritability,Excitement
38
DRUG APPROVED
DOSAGE RANGE
(mg/day)
APPROXIMATE
EQUIVALENT
DOSE
Alprazolam(Xanax) 0.74-4 0.5
Chlordiazepoxide(Li
brium)
25-100 25
Clonazepam
(Klonopin)
1-4 0.25
39
BUSPIRONE (buspirex)THERAPY:
• Buspirone is a non benzodiazepine anxiolytic therapy
Mechanism of action:
• The anxiolytic properties of buspirone may be due to partial agonism of 5-
HT 1A –receptors by reducing the firing of serotonin neurons.
• The effectiveness of buspirone may take up to 4 weeks.
• Side effects are mild and include dizziness, nausea, and headaches, stomach
upset
• Dose :
• Initial dose -7.5mg twice daily
• With dosage increments of 5 mg/every 2-3 days as needed.
• The usual therapeutic dose of buspirone is 30-60 mg/day.
40
Selective serotonin reuptake
inhibitors
Citalopram (Celexa)
Escitalopram (Lexapro)
Fluvoxamine (Proxac)
Paroxetine (Paxil)
Sertraline (Zoloft)
DAILY DOSE
20mg/day
10mg/day
50mg/day
10-20mg/day
25-50mg/day
MAX DOSE
20-40
10-20
150-300
20-60
50-200
Serotonin-norepinephrine
reuptake inhibitor
Venlafaxine (Effexor)
75mg/day 75-225
Benzodiazepine
Clonazepam (Klonopin) 0.25mg/day 1-3
Monoamine oxidase inhibitor
Phenelzine(Nardil)
15mg q pm 60-70
Alternate agents
Buspirone (buspirex)
10mg twice per day 45-60
41
REFERENCES
• American Psychiatric Association. Diagnostic and Statistical Manual of
Mental Disorders. 5th ed., text rev., American Psychiatric Publishing, 2022.
• National Institute of Mental Health. “Anxiety Disorders.” NIMH.gov, 2023,
www.nimh.nih.gov/health/topics/anxiety-disorders.
• Craske, Michelle G., et al. “Anxiety Disorders.” Nature Reviews Disease
Primers, vol. 3, 2017, doi:10.1038/nrdp.2017.24.
• “Anxiety Disorders: Symptoms and Causes.” Mayo Clinic, 2023,
www.mayoclinic.org/diseases-conditions/anxiety/symptoms-causes/syc-
20350961.
• Bandelow, Borwin, and Sophie Michaelis. “Epidemiology of Anxiety
Disorders in the 21st Century.” Dialogues in Clinical Neuroscience, vol. 17,
no. 3, 2015, pp. 327–335,
www.ncbi.nlm.nih.gov/pmc/articles/PMC4610617/.
42
GROUP MEMBERS
• OWUSU-YEBOAH NYAMEATSE
224NS01001071.
• Ofoe Jodi Teiko 224NS01001185.
• Regina Naa Momo Oye Odai
224NS01001129.
• ANYANUMEH CYNDELLA DEDE
224NS01000903.
• Adu Gyamfi Maame Akua Saahene
224NS01001229.
• Anlomegah christabel
224NS01001242.
• ANTWI RUBBEN 223NS01000764.
• AMOAH – ABABIO NOADIA YEBOAH
224NS01001218.
• Okrah Maame Akosua Boakyewaa
224NS01001168.
• Mensah Prince Adjei224NS01001200.
• Mensah Mandy Osei
224NS01001001.
• Quartey Mary 224NS01001000.
• Berniako Isaac 223NS01000887.
• Tetteh Joana 224NS01001090.
• .Okeke Nkechinyere
Adwoa224NS01001180.
• Addoko Pamela Afrah
224NS01001102.
• Dzamesi Isaac Xorse
223NS01000860.
• Tandoh Joseph
223NS01000654.
• Boakye Sabbath
223NS01000703.
• Bright Owusu Amoah
224NS01001045
43

group 9 anxiety disorder copy.bvvbhhhhpptx

  • 1.
    1 ANXIETY DISORDER INTRO TOPSYCHOLOGY SEC A GROUP 9
  • 2.
    2 ANXIETY • Anxiety definedas a subjective sense of unease ,dread or foreboding can indicate a primary psychiatric condition • Anxiety can be described as an uncomfortable feeling of vague fear or apprehension accompanied by characteristic physical sensations. • Anxiety can produce uncomfortable and potentially debilitating psychological (e.g., worry or feeling of threat) and physiological arousal (e.g., tachycardia or shortness of breath).
  • 3.
    3 CLASSIFICATION Anxiety disorders arebroadly divided into • Generalized anxiety disorder • Panic disorder • Phobic disorder • Post traumatic stress disorder • Obsessive compulsive disorders
  • 4.
    4 EPIDEMIOLOGY • In general,anxiety disorders are a group of heterogeneous illnesses that develop before age 30 and are more common in women, individuals with social issues, and those with a family history of anxiety and depression. • United States, the 1-year prevalence rate for anxiety disorders was 13.3% in persons aged 18 to 54 years and 10.6% in those over age 55 years
  • 5.
    5 • SYMPTOMS OFANXIETY: • Sensitivity of noise • Dry mouth • Difficulty in swallowing • Palpitations • Restlessness ,tremor • Gastrointestinal discomfort • Headache • Insomnia. • Constriction in chest • Poor concentration
  • 6.
    6 PATHO PHYSIOLOGY: GABA system: •The role of GABA- benzodiazepine receptor complex in anxiety disorders has not been fully characterized • However a potential role has been implicating in panic disorders, GAD and PTSD. • In GAD reduced temporal lobe benzodiazepine receptor are observed. • In PTSD, cortical benzodiazepine receptor are reduced. • In PANIC decreased GABA A binding is noted. • Angiogenic agents – having the property of altering the binding of benzodiazepines to the gamma amino butyric acid receptor ↓ leads to nerve cell excitability ↓ Anxiety
  • 7.
    7 • SEROTONIN SYSTEM: • 5-HT is involved in the pathophysiology of anxiety disorders. • as abnormal regulations of serotonin release and reuptake or abnormal responsiveness to 5- HT signals.
  • 8.
  • 9.
    9 Amygdala ↓ • its roleincludes detecting, coordinating and maintaining fearful emotions. • The amygdala integrates information from multiple sensory areas to assess for threats with consideration of input regarding the context of presenting stimulus Once a threat has been detected by the amygdala a rapid response is coordinated.
  • 10.
    10 NON- ADRENERGIC SYSTEM: Locus coeruleus which is located in the brainstem ↓ Locus coeruleus is the neither primary nor epinephrine containing area of the brain ↓ According to the noradrenergic theory of anxiety, in the presence of perceived threat, the locus coeruleus serves as an alarm center release nor epinephrine ↓ Leads to anxiety. • α2 adrenergic antagonist yohimbine, carbon dioxide inhalation, caffeine,isoproterenol each of these stimuli activates a pathway leads to anxiety.
  • 11.
  • 12.
    12 • Chronic anxietystate associated with uncontrollable worry. • Patients with GAD have persistent, excessive, unrealistic worry associated with muscle tension, impaired concentration and insomnia. • Complaints of shortness of breath, palpitations and tachycardia are relatively rare • Alcohol abuse and dependence are common in GAD patient
  • 13.
    13 Risk Factors Factors thatmay increase the risk of GAD include:  Family members with an anxiety disorder  Increase in stress  Exposure to physical or emotional trauma  Unemployment, poverty  Drug abuse
  • 14.
    14 Diagnosis/clinical presentation •GAD isdiagnosed when an individual experiences unrealistic or excessive anxiety and worry for a period of at least 6 months. •Additionally, the individual must have difficult in controlling that anxiety or worry. •Accompanying the anxiety or worry for 6 months with 3 or more of following symptoms: feeling tense or restless, easily fatigued , difficulty concentrating, irritability, and difficulty with sleep.
  • 15.
  • 16.
    16 • Panic disorderis defined by the presence of recurrent and unpredictable panic attacks,which are distinct episodes of intense fear and discomfort associated with a variety of physical symptoms. SYMPTOMS : • Palpitations • Sweating • Trembling or shaking • Sensations of shortness of breath • Chest pain or discomfort • Nausea • Feeling dizzy • Fear of dying • Paresthesias • Chills or hot flushes.
  • 17.
    17 • Diagnosis/clinical presentation •A panic attack usually peaks in 10 mins and lasts no longer than 30 mins. • A patient is diagnosed with a panic disorder when that individual experiences repeated unexpected panic attacks and these attacks are followed by a 1-month period of one or more: persistent concern over future attacks • During an attack individual will often feel like they are losing control or dying.
  • 18.
  • 19.
    19 SPECIFIC PHOBIA A specificphobia is any kind of anxiety disorder that amounts to an unreasonable or irrational fear related to exposure to specific objects
  • 20.
    20 SOCIAL PHOBIA • Socialphobia is fear of social situations where you may be embarrassed or judged. • Common physical symptoms include blushing,diarrhea, sweating, and tachycardia.
  • 21.
    21 AGAROPHOBIA • Agorophobia isa fear of places or situations that might cause you to panic and make you feel trapped, helpless
  • 22.
    22 • Phobic disorderare common ,affecting 10% of population • The Patients avoids phobic stimulus and this avoidance usually impairs occupational or social functioning. • Common phobias include fear of closed spaces (clustro phobia), fear of blood,fear of flying. • Patient with social phobia, in particular, have a high rate of co-morbid alcohol abuse, as well as of other psychiatric conditions (e.g. eating disorder)
  • 23.
  • 24.
    24 • Patients withstress disorders are at risk for the development of other disorders related to anxiety, mood and substance abuse (especially alcohol) • Symptoms : nightmares, negative thinking and mood, unwanted distressing memories of the traumatic event • Symptoms usually begin early, within 3 months of the traumatic incident, but sometimes they begin years afterward. Symptoms must last more than a month
  • 25.
  • 26.
    26 • OCD ischaracterized by obsessive thoughts and compulsive behaviors that impair everyday functioning. • Fears of contamination and germs are common as are hand washing, counting behaviors and having check and recheck the actions like whether a door is locked.
  • 27.
    27 Non pharmacological treatment: •Psychological education, short term counseling, stress management, psychotherapy, meditation, or exercise. • Psychological therapy: • Psychological therapies (talking therapies) are generally considered first line treatments in all anxiety disorders because they provide a longer lasting response and lower relapse than pharmacotherapy. • The specific psychotherapy with the most supporting evidence in anxiety disorders is cognitive behavioral therapy
  • 28.
    28 SELECTIVE SEROTONIN REUPTAKE INHIBITOR •Paroxetine • Escitalopram, • Citalopram • Fluoxetine • SSRIs are the first-line treatment of GAD ,SAD, panic disorder • Treatment effect usually takes at least 4 weeks
  • 29.
  • 30.
    30 • Mechanism ofaction: • The SSRIs block the reuptake of serotonin, leading to increased concentrations of the neurotransmitter in the synaptic cleft and, ultimately,to greater postsynaptic neuronal activity Agent Starting dose (mg/day) Usual dose (mg/day) Half life Fluoxetine(Proxac) Paroxetine Sertraline Citalopram(Celexa) Escitalopram 10-20 10-20 25-50 10-20 5-10 20-60 20-60 50-200 20-60 10-20 7-9 days 21 hrs 24hrs 35 hrs 27-32 hrs
  • 31.
    31 SIDE EFFECTS: • Vividdreams. • Tremor. • Nausea. • vomiting. • Insomnia. • Osteopenia. • Headache.
  • 32.
    32 TRICYCLIC ANTIDEPRESSANTS Tertiary amine •Imipramine • Amitriptyline (Elavil) • Trimipramine (Trimip) Secondary amine • Desipramine (Norpramin) • Nortriptyline (Aventyl)
  • 33.
    33 • MECHANISM OFACTION: • Mechanism of action of the tricyclic antidepressants (TCAs) is that they inhibit the reuptake of the biogenic amines, mostly nor epinephrine (NE), as well as serotonin (5HT) • SIDE EFFECTS: • Blurred vision, constipation, urinary retention, dry mouth, sedation, weight gain, and orthostatic hypotension, insomnia
  • 34.
    34 • DOSE ANDADMINISTRATION: • IMIRAPINE: • Initiated with 10 mg/day at bedtime and slowly increased by 10 mg every 2 to 4 days as tolerated to 75 to 100 mg/day, and then increased by 25 mg every 2 to 4 days over a 2 to 4 week period.
  • 35.
    35 MONOAMINE-OXIDASE INHIBITOR • Thesubstrate for MAO-A enzyme is serotonin, melatonin, epinephrine and norepinephrine • MECHANISM OF ACTION: • MAOIs, form stable complexes with the enzyme,causing irreversible inactivation. This results in increased stores of nor epinephrine, serotonin, and dopamine within the neuron and subsequent diffusion of excess neurotransmitter into the synaptic space.
  • 36.
    36 • Dosing andAdministration: • The starting dose of phenelzine is 15 mg/day after the evening meal, increasing by 15 mg/day every 3 to 4 days until a maximum dose of 45 mg/day (in two or three divided doses) is reached. • If a patient was on an antidepressant previously, it should be discontinued 2 weeks before phenelzine is started to prevent a potential drug interaction. ADVERSE EFFECTS: • orthostatic hypotension • insomnia • weight gain, • peripheral edema
  • 37.
    37 BENZODIAZEPINE THERAPY • Benzodiazepinesare effective medications due to their anxiolytic properties and may provide rapid symptom relief. • Benzodiazepines may be most useful when used early in treatment in combination with an antidepressant. • Adverse effects • Drowsiness,Sedation,Ataxia, Disorientation,Depression, Confusion,Irritability,Excitement
  • 38.
    38 DRUG APPROVED DOSAGE RANGE (mg/day) APPROXIMATE EQUIVALENT DOSE Alprazolam(Xanax)0.74-4 0.5 Chlordiazepoxide(Li brium) 25-100 25 Clonazepam (Klonopin) 1-4 0.25
  • 39.
    39 BUSPIRONE (buspirex)THERAPY: • Buspironeis a non benzodiazepine anxiolytic therapy Mechanism of action: • The anxiolytic properties of buspirone may be due to partial agonism of 5- HT 1A –receptors by reducing the firing of serotonin neurons. • The effectiveness of buspirone may take up to 4 weeks. • Side effects are mild and include dizziness, nausea, and headaches, stomach upset • Dose : • Initial dose -7.5mg twice daily • With dosage increments of 5 mg/every 2-3 days as needed. • The usual therapeutic dose of buspirone is 30-60 mg/day.
  • 40.
    40 Selective serotonin reuptake inhibitors Citalopram(Celexa) Escitalopram (Lexapro) Fluvoxamine (Proxac) Paroxetine (Paxil) Sertraline (Zoloft) DAILY DOSE 20mg/day 10mg/day 50mg/day 10-20mg/day 25-50mg/day MAX DOSE 20-40 10-20 150-300 20-60 50-200 Serotonin-norepinephrine reuptake inhibitor Venlafaxine (Effexor) 75mg/day 75-225 Benzodiazepine Clonazepam (Klonopin) 0.25mg/day 1-3 Monoamine oxidase inhibitor Phenelzine(Nardil) 15mg q pm 60-70 Alternate agents Buspirone (buspirex) 10mg twice per day 45-60
  • 41.
    41 REFERENCES • American PsychiatricAssociation. Diagnostic and Statistical Manual of Mental Disorders. 5th ed., text rev., American Psychiatric Publishing, 2022. • National Institute of Mental Health. “Anxiety Disorders.” NIMH.gov, 2023, www.nimh.nih.gov/health/topics/anxiety-disorders. • Craske, Michelle G., et al. “Anxiety Disorders.” Nature Reviews Disease Primers, vol. 3, 2017, doi:10.1038/nrdp.2017.24. • “Anxiety Disorders: Symptoms and Causes.” Mayo Clinic, 2023, www.mayoclinic.org/diseases-conditions/anxiety/symptoms-causes/syc- 20350961. • Bandelow, Borwin, and Sophie Michaelis. “Epidemiology of Anxiety Disorders in the 21st Century.” Dialogues in Clinical Neuroscience, vol. 17, no. 3, 2015, pp. 327–335, www.ncbi.nlm.nih.gov/pmc/articles/PMC4610617/.
  • 42.
    42 GROUP MEMBERS • OWUSU-YEBOAHNYAMEATSE 224NS01001071. • Ofoe Jodi Teiko 224NS01001185. • Regina Naa Momo Oye Odai 224NS01001129. • ANYANUMEH CYNDELLA DEDE 224NS01000903. • Adu Gyamfi Maame Akua Saahene 224NS01001229. • Anlomegah christabel 224NS01001242. • ANTWI RUBBEN 223NS01000764. • AMOAH – ABABIO NOADIA YEBOAH 224NS01001218. • Okrah Maame Akosua Boakyewaa 224NS01001168. • Mensah Prince Adjei224NS01001200. • Mensah Mandy Osei 224NS01001001. • Quartey Mary 224NS01001000. • Berniako Isaac 223NS01000887. • Tetteh Joana 224NS01001090. • .Okeke Nkechinyere Adwoa224NS01001180. • Addoko Pamela Afrah 224NS01001102. • Dzamesi Isaac Xorse 223NS01000860. • Tandoh Joseph 223NS01000654. • Boakye Sabbath 223NS01000703. • Bright Owusu Amoah 224NS01001045
  • 43.

Editor's Notes

  • #6 GABA circuits are integrally involved in anxiety.
  • #26 gns and symptoms: The symptoms of OCD, which are the obsessions and compulsions, may vary. Obsessions – are repeated thoughts, urges, or mental images that cause anxiety. Common symptoms include: Fear of dirt or contamination by germs Fear of causing harm to another or to themselves. Excessive doubt and the need for constant reassurance Compulsions – are repetitive behavior that a person with OCD feels urge to do in response to an obsessive thoughts. Repeatedly bathing, showering, or washing hands Refusing to shake hands or touch doorknobs Repeatedly checking things, such as locks or stoves Eating foods in a specific order