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Module 202 Theme 3 > Anxiety disorders: Clinical picture > Flashcards

Anxiety disorders: Clinical picture Flashcards

1
Q

Describe the clinical picture of acute stress reaction

A

Acute stress reaction lasts hours to 3 days
A response to exceptionally stressful events (physical/psychological)
Initial daze
Mixed and usually changing picture
Individual vulnerability

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2
Q

List some typical symptoms of acute stress

A 
Feelings of being numb or dazed
Insomnia
Restlessness
Poor concentration
Autonomic arousal
Anger/anxiety/depression
Withdrawal
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3
Q

What is adjustment disorder?

A

Wide range of emotional or behavioural symptoms
Stressor not necessarily life threatening
Out of proportion to stressor
Lasts up to 6 months

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4
Q

What is PTSD?

A

Response to exceptionally threatening or catastrophic event
… experienced ,witnessed … event that involved actual or threatened death or serious injury …. or threat to physical integrity of self or others.
… response involved intense fear, helplessness or horror …

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5
Q

List the symptoms of PTSD

A 
Re-experiencing flashbacks/nightmares
Numbness/detachment
Avoidance
Hypervigilance/startle
Insomnia
Anxiety/depression
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6
Q

Who is likely to suffer from PTSD?

A

> 50% experience a traumatic event in life
Men experience more traumatic events than women
Women more likely to develop PTSD following trauma (except rape)

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7
Q

What is the prognosis of someone with PTSD?

A

Usually immediate onset

Most recover within 1 year

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8
Q

Describe the epidemiology of stress

A

Little research into what proportion of people develop acute stress reactions to severe stress
Difficult to determine whether the different rates of acute stress disorder detected are attributable to differences in method or in the type of trauma

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9
Q

What happens to depression and substance abuse in PTSD?

A

Increases

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10
Q

Which neurotransmitters are involved in stress?

A

Catecholamines
Glucocorticoids
Serotonin
Endogenous opioids

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11
Q

Describe the clinical presentation of generalized anxiety disorder (GAD)

A

Worry & apprehension
Headache & motor tension (restless / trembling)
Autonomic hyperactivity (sweating / palpitations / dry mouth / epigastric discomfort / dizziness)

Symptoms are persistent

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12
Q

Give some psychological symptoms of generalized anxiety disorder

A 
Fearful anticipation
Irritability
Sensitivity to noise
Restlessness
Poor concentration
Worrying thoughts
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13
Q

List some physical symptoms of generalized anxiety disorder

A

Gastrointestinal
Dry mouth, difficulty swallowing, epigastric discomfort, excessive wind, frequent/loose motions
Respiratory
Tight chest, difficulty inhaling, hyperventilation
Cardiovascular
Palpitations, chest “pain”, missed beats
Genitourinary
Frequent/urgent micturition, erectile failure, dysmenorrhoea, amenorrhoea
Neuromuscular
Tremor, paraesthesia, tinnitus, dizziness, headaches, muscular aches & pains

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14
Q

Give some additional symptoms of generalized anxiety disorder

A 
Sleep disturbances
Insomnia, night terrors
Sadness
Depersonalisation
Fixation with details
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15
Q

Describe the epidemiology of generalized anxiety disorder

A

Lifetime prevalence:
8.9% (ICD-10 criteria)1
Women > men
Estimated to be 3x higher in patients in primary care clinics (indicated increased use of health care services)
High level of co-morbidity (~ 70%), especially simple phobias, social phobia, panic disorder & depression

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16
Q

Do genetics play a role in GAD?

A

Yes they play a modest role

Five fold increase in 1st degree relatives
Shared heritability for GAD and mood disorders

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17
Q

Describe the cause of generalized anxiety disorder and state the evidence for each neurotransmitters involvement

A

Effects of stress apparently mediated through cortisol – some evidence exists for abnormalities in the HPA axis

Benefit from SSRIs and venlafaxine suggests a role for serotonin, but there is no direct evidence for this

Noradrenergic pathways associated with fear, arousal & stress response; role in persistent anxiety states implicated but unclear

γ-Aminobuyric acid (GABA) has a role & benzodiazepine-type agonists are clearly effective

Several studies found an association with stressful / traumatic life events
The experience of even one very important unexpected negative event was associated with a 3x ↑ in GAD in men and women

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18
Q

Give some examples of Specific stressors associated with ↑ risk of GAD:
relationships

A

Early parental death
Rape
Combat
Chronically dysfunctional marital and family

19
Q

What is attachment theory?

A

Parents or other consistent caregivers serve important function in a child’s development
They provide a protective and secure base from which the child can operate
Disruption leads to anxious apprehension and dependency
Severe disruption leads to withdrawal and depression

Overprotection coupled with a lack of warmth and responsiveness toward the child could lead to anxiety

20
Q

Describe agorpahobia

A

Anxiety in 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

21
Q

Give the epidemiology of panic

A

Panic attacks: 7-9% of the population
Panic disorder:1.5-2.5% lifetime prevalence
Onset has two peaks: 15-24 & 45-54

22
Q

State some risk factors of panic

A

Widowed, divorced or separated individuals in cities
Limited education, early parental loss & physical/sexual abuse
Females > males
Agoraphobia is especially prevalent in females – 75% of the sample with extensive avoidance
Males – longer duration but less agoraphobia and depression

23
Q

Is there a genetic predisposition to panic?

A

Increased risk in 1st degree relatives ~ 7 fold
Increased concordance in all but one monozygotic twin study
Modest inheritability suggested by family & twin studies
At least 50% environmental influences

24
Q

Describe some environmental factors contributing to the cause of panic

A

Precipitating events in 60-96% of cases
Separation / loss
Relationship difficulties
New responsibilities

Traumatic early life events
Early parental separation
Traumatic childhood event – 3 fold increase
Early sexual abuse (<5 years of age)

25
Q

Describe some biological models of the aetiology of panic

A

Panic attacks may be triggered in the locus coeruleus
↑ firing associated with ↑ CO2 etc

Noradrenergic agents (yohimbine & isoproterenol) stimulate attacks in sufferers

SSRIs are effective but contradictory findings regarding the role of serotonin

γ-Aminobuyric acid (GABA) has a role:
Benzodiazepine agonists are clearly effective
Benzodiazepine antagonist (flumazenil) aggravates attacks

Cholecystokinin causes panic attacks in animals & pentagastrin causes attacks in panic disorder patients

26
Q

Describe the clinical picture of specific phobias

A

Inappropriate anxiety in the presence of one or more particular objects or situations
Characterised by adding the name of the stimulus (e.g. Spider Phobia)
Avoid jargon (e.g. Arachnophobia)

27
Q

List some subtypes of specific phobias

A

Blood, injection, injury – a specific case?
Animals & Insects
Aspects of the natural environment (e.g. heights)
Situational (e.g. flying)
Other (e.g. dental/medical procedures, choking, etc.).

28
Q

Describe some responses of specific phobias

A

Individuals with blood–injection–injury phobias exhibit a biphasic anxiety reaction:
Initial short-lived sympathetic arousal
Followed by parasympathetic arousal
May result in vasovagal syncope
The subjective experience tends to disgust and repulsion rather than pure apprehension
In other subtypes, exposure to the phobic stimulus evokes intense anxiety that may meet the criteria for a situationally bound panic attack
There is extreme apprehension and desire to escape or avoid the phobic stimulus

29
Q

Describe the epidemiology of specific phobias

A

> 80% experience at least one lifetime psychiatric disorder (odds ratio 5x)
Lifetime prevalence: 11.3%
Mean age of onset: 15 years
Animal phobias onset age 7
Blood phobias onset age 9
Claustrophobia onsets age 20
Women > men (blood–injection–injury phobia did not differ)

30
Q

Give the evidence for genetic involvement in the cause of specific phobias

A 
All Specific Phobias: evidence for genetic transmission
31% of 1st degree relatives affected
Animal phobias: 
monozygotic 26%
Dizygotic 11%
31
Q

Give some psychological theories of specific phobias

A

Psychoanalytic approach: Symptoms related to unresolved unconscious conflicts
Classical conditioning: phobias are learned through association of negative experience with an object or situation
Marks’ ‘preparedness’ theory maintains that commonly feared objects are those that historically threatened the survival of the individual or the species
Large number of studies suggest that phobias may be acquired via observational learning

32
Q

Give the clinical picture of social phobia

A

Inappropriate anxiety in:
Situations where the person is observed
Situations where there is potential for criticism
Leads to avoidance of trigger situations
Eating in public
Dinner parties
Committees, seminars, public speaking

33
Q

What are the symptoms of social phobia?

A

Anticipatory anxiety
Feeling anxious
Blushing
Trembling (observed writing is a problem)
Relieved by alcohol (potential for abuse)

34
Q

What is the epidemiology of social Phobia?

A

Possibly as high as 7% of primary care patients
Lifetime risk 2.4 – 13.3% depending upon the definition of “caseness”
81% at some time meet the criteria for another psychiatric disorder (very high comorbidity)
Onset usually early in life
1st peak before age 5
2nd peak between 11 – 15
Presentation unusual after age 30
Women > men, but men more likely to present

35
Q

Give the aetiology of social phobia

A

Both genetics and environmental factors contribute, with genetics contributing < ⅓ of the variance in the transmission
16% of relatives of probands vs 5% of relatives of controls
Monozygotic > dizygotic

36
Q

Give the clinical picture of OCD

A 
Obsessional thoughts / images
Words, ideas, beliefs and/or images
Recognised as own
Intrude forcibly into the mind
They are resisted
Compulsions reduce anxiety
Cleaning/checking
Precision – ‘just right'
Obsessional impulses
Urges to perform acts
Obsessional rituals
Magic words or numbers
Desire to complete acts (e.g. hand washing)
37
Q

What are the symptoms of OCD?

A

Contamination – washing
Compulsions – the need to act on the obsessions
Doubts - checking

38
Q

What is the epidemiology of OCD?

A

Several researchers have reported lifetime prevalence of 2-3%
This rate has been confirmed across different cultures

Men = women
Some reports suggest a slight female predominance
During adolescence, boys > girls. 
Mean age of onset is ~ 20 years of age. 
Prevalence 2-3%
39
Q

Describe the co-morbidity of OCD

A

Major depressive episode: ~67% lifetime prevalence
↑ lifetime risk for:
alcohol disorders
social phobia
specific phobia
panic disorder
eating disorders
Schizophrenia
tic disorders (~ 40% in juvenile OCD)
↑ prevalence of Tourette’s syndrome in relatives
Unclear relationship between OCD & obsessive–compulsive personality disorder (OCPD), but it appears that OCPD is not a prominent risk factor for OCD

40
Q

Which neurotransmitters are involved in OCD? Give the evidence

A

Serotonin dysregulation:
Evidence from efficacy of various serotonergic drugs

Dopamine dysfunction:
Evidence from abundance of OCD symptoms in basal ganglia disorders
The therapeutic benefits from co-administration of dopamine blockers and SSRIs in a subset of patients with OCD and tic disorders

41
Q

Describe the genetics of OCD

A

Monozygotic&raquo_space; dizygotic

First-degree relatives of patients with childhood-onset OCD have a higher than expected incidence of OCD

42
Q

What is learning theory of OCD?

A

Obsessions are conditioned stimuli: when a relatively neutral stimulus is coupled with an anxiety-provoking stimulus, it produces anxiety when presented alone
Compulsions reduce anxiety and the patient repeats them and learns them in order to avoid anxiety
Avoidance strategies are learned and become fixed

43
Q

What is dynamic theory of OCD?

A

Obsessional Neurosis first described by Freud

The disorder was thought to result from a regression from the Oedipal Phase to the Anal Phase

Module 202 Theme 3 (11 decks)

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