Anxiety Disorders Flashcards
1
Q
What is Clinical Acute Stress reaction from a clinical perspective?
- symptoms
A
- a response to an exceptionally stressful event (physical/ psychological)
- this can last hours up to 3 days
- presents with an initial daze, individual vulnerability with a mixed and changing picture
- numb or dazed feeling
- Insomnia
- restlessness
- poor concentration
- autonomic aurosal
- anger/anxiety depression
- withdrawal
2
Q
What is adjustment disorder?
A
- An adverse reaction in an individual unable to cope with stressful life changes.
- the stressor is not necessarily life-threatening
- presents with a wide range of emotional or behavioural symptoms
- out of proportion to the stressor
- can last up to 6 months
3
Q
What is PTSD?
A
- response to an exceptionally threatening or catastrophic event
- could be experienced or witnessed that involved actual or threatened death or serious injury or threat to the physical integrity of self or others
- the response involved intense fear helplessness or horror
- Usually immediate onset - most recover within 1 year
- Rape victims
- 94% at 2 weeks
- 65% 1 month
- 42% at 6 months
4
Q
What are some common PTSD Symptoms
A
- Re-experienceing flashbacks/ nightmares
- Numbness/ detachment
- Avoidance
- Hypervigilance/startle
- Insomnia
- Anxiety/depression
5
Q
What Pharmacological treatment is there for PTSD?
A
- SSRIs: paroxetine; sertraline
- Other antidepressants: Tricyclic Antidepressants (TCAs)→ amitriptyline, imipramine
- Targeting specific symptoms
- Sleep disturbance: mirtazapine, levomepromazine
- Anxiety symptoms/ hyperarousal: VDZs, buspirone
- Intrusive thoughts/hostility/impulsiveness: carbamazepine, valproate, topiramate, lithium
- Psychotic symptoms/sever aggression/ agitation: antipsychotics
6
Q
What are Psychological management strategies for PTSD?
A
-
CBT
- education on the elements of PTSD, self-monitoring symptoms
- anxiety management, breathing techniques
- imaginal reliving, supportive exposure to anxiety-producing stimuli
-
Eye movement desensitization and reprocessing (EMDR)
- uses voluntary multi-saccadi eye movements → reduce anxiety
- Psychodynamic therapy
- Stress managment
- Hypnotherapy
- Supportive management
7
Q
What are risk factors for developing PTSD?
- Vulnerability factors
- Peri-traumatic factors
- Protective factors
A
- Vulnerability factors: low education Afro-Caribbean/Hispanic, female, lower social economic background, history of psychiatric problems, previous traumatic events
- Peri-traumatic factors: trauma severity, perceived life threat, peri-traumatic emotions, peri-traumatic dissociation
- Protective factors: high IQ, higher social economic class, Caucasian, male, psychopathic traits, chance to view body of dead person
8
Q
PTSD Symptoms according to ICD-10
A
Symptoms arise within 6months of the traumatic event (delayed onset occurs in ~10% of cases) with
- 2 or more ‘persistent symptoms of increased psychological sensitivity and arousal’ - not present before exposure to the stressor → difficulty falling asleep/staying asleep; irritability/ outbursts of anger; difficulty in concentrating; hypervigilance; exaggerated startle response
- Re-experiencing flashbacks/ nightmares; and in experiencing distress when exposed to circumstances resembling or associated with the stressor
- Actual or preferred avoidance of circumstances resembling or associated with the stressor
- Inability to recall, either partially or completely, some important aspects of the period of the exposure to the stressor
9
Q
What is Generalised Anxiety Disorder from a clinical perspective? (GAD)
- characteristic features
A
- persistant symptoms of anxiety that are not restricted to or strongly predominating in any particular set of circumstances
Characteristic features
- worry and apprehension
- headache & motor tension
- restless/ trembling
- autonomic hyperactivity
- sweating/ palpitations
- dry mouth
- epigastric discomfort discomfort
- dizziness
10
Q
What are the psychological symptoms of GAD?
A
- fearful anticipation
- Irritability
- Sensitivity to noise
- Restlessness
- Poor concentration
- Worrying thoughts
- Sleep disturbances: Insomnia, night terrors
- Sadness
- Depersonalisation
- Fixation with details
11
Q
Give an overview of the epidemiology of GAD
A
- greater prevalence in women than men
- ~3x higher in patients in primary care clinics
- high level of co-morbidity (~70%)
- especially simple phobias, social phobia, panic disorder & depression
12
Q
Aetiology of GAD
A
- Genetic factors play a moderate role in the prevalence of GAD
- the experience of one very important unexpected negative event was associated with 3x increase in GAD in men and women
- Disruption in early attachment forming can lead to withdrawal and depression
- a healthy parent-child relationship fosters a sense of control over events
- lack of warmth and encouragement leads to a general perception of personal inefficacy which may predispose to negative states
- overprotective coupled with a lack of warmth and responsiveness toward the child could lead to anxiety
13
Q
What are the clinical features of Panic Disorder?
psychic, somatic
A
Psychic
- Fear of losing control, going mad, fainting, dying
- derealisation, depersonalisation
Somatic
- Palpitations, tachycardia, sweating, trembling
- dyspnoea, choking, nausea, ‘butterflies’
- chest pain, urgency, dizziness, faintness, paraesthesia, chills/flushes
14
Q
What Psychological managements is used in Panic disorder?
A
- CBT - behavioural methods
- treat phobic avoidance by exposure
- relaxation, control of hyperventilation
- CBT - cognitive methods
- teaching about bodily responses to anxiety
- modification of thinking errors
- Psychodynamic psychotherapy: emotion focused treatment where feelings are explored
15
Q
What is the Pharmacological management for Panic Disorder?
A
- SSRI’s: citalopram (20-30mg), escitalopram (5-10mg), paroxetine (10-40mg), sertraline (50-200mg)
- Second line would be other classes of drugs listed below
- if txt is successful continue for 12-18months before trial tapered discontinuation over 2-4 months
- may continue for ~1 yr before considering second trail discontinuation
- SNRI’s, TCA’s, MAOI’s not licensed in the UK
- BDZs [not recommended by NICE]: used with caution due to risk of dependency, used for severe, frequent, incapacitating symptoms
16
Q
What are potential aetiologies of Panic Disorder?
A
- Exaggerated post synaptic receptor response to 5-HT
- Increased adrenergic activity, with hypersensitivity of presynaptic alpha-2 receptor → affects HPA axis increasing firing rate
- Decreased GABA receptor sensitivity → decreased inhibitory response in presence of BDZs → increased excitatory effect
- CCK-pentagastrin model: pentagastrin induces panic in a dose dependent fashion in people with panic disorder
17
Q
What are comorbidities of Panic disorder?
A
- Agoraphobia
- other anxiety related disorders
- Alcohol or substance missuse
- Bipolar affective disorder
- Medical conditions (CVS, resp)
18
Q
What are the potential differential instead of Panic Disorder?
A
- Endocrine
- Hypoglycaemia
- Phaeocromocytoma
- Carcinoid
- Cardiovascular
- Arrythmia
- Respiratory
- Asthma
- COPD
- Drugs
- Neurological
- Seizures
- Vestibular
19
Q
What is the management for Social Phobia?
A
- Psychological: CBT (individual or group) is first line with ()SSRI’s/MAOIs); may be better for preventing relapses
- includes relaxation techniques, social skills training, integrated exposure methods, cognitive reconstruction
- Pharmacological
- SSRIs - escitalopram 10mg/daily, sertraline 25mg/day increase to 50mg/day after a week max of 200mg/day
- MAOIs - phenelzine (unlicensed) -more effective
- RIMAs, BDZ
20
Q
What is Social Phobia?
A
- symptoms of incapacitating anxiety that are not 2y to delusional or obsessive thoughts and are restricted to particular social situations → desire to escape or avoidance
- this can reinforce ideas of social inadequacy
21
Q
What is the management for Agoraphobia?
A
- Pharmacological
- Antidepressants ad in panic disorder
- BDZs in short-term use
- Psychological
- Behavioural: exposure techniques, relaxation training, anxiety management
- Cognitive: teaching about bodily responses associated with anxiety, education about panic disorders, modification of thinking errors
22
Q
What is Agoraphobia from a clinical perspective?
A
- Anxiety in a specific context
- away from home
- in crowds
- in situations, they cannot easily leave
- Presents with anxiety symptoms & panic attacks
- anxious cognitions about fainting and loss of control are common
- Avoidance is common
23
Q
Describe the genetic and environmental aetiology of Panic Disorder
-Genetic Predisposition
A
- increased risk in 1st degree relatives (7x)
- increased concordance in monozygotic twins
- modest inheritability suggested by family & twin studies
- at least 50% environmental influences
- seperation/loss
- relationship difficulties/ new relationships
- Traumatic early life events
- early parental seperation
- traumatic childhood event - 3 fold)
- early sexual abuse (<5 years of age)
24
Q
What is the lifetime prevalence of having a simple/ specific phobia?
A
12.5%
25
Q
What is the Management for simple/ specific phobias?
A
- Psychological
- Behavioral therapy is the 1st line
- aims to reduce fear response via Wolpe’s systematic desentization w/ relaxation and graded exposure
- Cognitive therapy
- education/anxiety management, coping skills/ strategies and cognitive restructuring
- Behavioral therapy is the 1st line
- Pharmacological: generally not used except in sever cases to reduce fear/avoidance
- BDZs - diazepam - allows patient to engage in behavior
- may reduce efficacy of behavioral therapy by inhibiting anxiety during exposure
26
Q
What is the biological aetiology of specific phobia?
A
- MZ:DZ = 25.9%:11% for animal phobia in twin studies
- situational phobia is roughly equally suggesting a role played by the environment
37
Q
Review this picture and how Amygdala plays a role in emotion
- effect of lesions in the amygdala
A
- HPA: Hypothalamus-pituitary- adrenal axis
- lesions in the amygdala can cause loss of fear
38
Q
Which key areas from this overview of how the amygdala emotional activity causes fear
A
key areas affected are the
- lateral hypothalamus –> sympathetic activation –> tachycardia, galvanic skin response, paleness, pupil dilation, blood pressure elevation
- ventral tegmental area/ locus coerulus/ dorsal lateral tegmental nucleus –> activation of DA, NE and ACh –>behavioural and EEG arousal, increased vigilance
- periventricular nucleus –> ACTH release –> corticosteroid release (stress response)
39
Q
How does fearful stimuli elicit a stress response?
A
- sensory info channelled to the amygdala
- amygdala excites locus coeruleus (LC) + hypothalamus –> acute stress response
- HPA axis s also activated
- H releases CRH: corticotropin-releasing hormone
- P releases ACTH: adrenocorticotropin hormone
- A releases cortisol
- LC releases NE, which triggered “fight or flight” response
- HPA axis s also activated
40
Q
Explain the Push-pull regulation of the HPA axis
A
- Amygdala stimulates the HPA axis which releases cortisol
- the Hippocampus inhibits the activity of the HPA axis, less cortisol is released
- cortisol acts as positive feedback to increase the dysregulation activity the hippocampus has on the HPA
42
Q
What is the effect of stress on the brain?
A
- causes cell death in the hippocampus
- loss of pyramidal cells
45
Q
What does this scan suggest about GABAergic dysfunction in anxiety disorders?
A
- Patients with PD have fewer benzodiazepine binding sites
- (it was radiolabeled with Flumazenil - which also indicates BSD binding sites)
- therefore this suggests PD patients lack sufficient inhibitory control in cortical and limbic regions to prevent inappropriate fear responses and subsequent panic attakcs
46
Q
What role does the serotonergic system play in anxiety?
A
- SSRIs used in treatment (Fluoxetine/ Prozac)
- prolong the action of 5-HT in the synapse
- Buspirone
- also acts as a partial agonist
- works on somatodendritic 5-HT receptors
- symptomatic changes are seen after weeks of treatment
47
Q
How does antidepressant treatment affect neuroplasticity?
A
- produces an overall trophic effect due to increased BDNF gene expression
- increased 5-HT and NE availability at receptors
- leads to increased Adenylate cyclase and increased Ca2+ dependant kinases
- increased AC –> increased cAMP –> increased c-AMP dependent kinase
- increased kinase activity –> increased CREB activity which increases gene expression
- reversal of stress-induced changes may restore normal brain function (hence several weeks until symptomatic changes are seen)
48
Q
How do the serotonergic systems and the norepinephrine systems relate to panic disorder?
A
- Serotonergic systems and Norepinephrine systems project diffusely through the brain and are thought to have opposing functions.
- NE release stimulates arousal and alertness
- 5-HT inhibits Norepinephrine (NE) release
- Opposing functions in various brain areas
- amygdala
- hippocampus
- hypothalamus
- A shifted balance between the pathways to NE may be manifested in Panic Attacks - fear responses to inappropriate stimuli
- SSRIs, by increasing 5-HT release, will push balance back
49
Q
The Indirect and Direct pathways and its relation to OCD
A
- D1- direct pathway that facilitates movement (red)
- controls previously learned behaviour so they become automatic and can be executed
- D2- indirect pathway that inhibits movement (black)
- suppresses these behaviours allowing the person to switch to more adaptive behaviour (behavioural flexibility)
- overactivity of the direct pathway may lead to the compulsive behaviours without being able to switch them off
- GPe = external segment of the globus pallidus;
- GPi = internal segment of the globus pallidus;
- SNc = substantia nigra pars compacta;
- STN = subthalamic nucleus.
50
Q
What is the best treatment for OCD?
A
- Benzodiazepines
- good immediate effect but patients can develop tolerance –> potential abuse and anxiety during withdrawal
- SSRI
- fluoxetine
- can initially act as an anxiogenic
-
Clomipramine
- a tricyclic antidepressant (TCA)
best to combine BZD and SSRI and taper of BZD when tolerance starts to build and the SSRI starts taking effect
51
Q
How does caudate hyperactivity relate to OCD?
A
- The caudate sends GABAergic inhibitory projections to the globus pallidus (GP),
- which sends inhibitory projections to the thalamus,
- which then projects to the OFC.
- It’s possible that OCD involves disinhibition which leads to activity reverberating in this circuit.
after pharmaco- and psychotherapy interventions in OCD PET scans show decreased caudate activity
