Anxiety Disorders Flashcards

1
Q

How are anxiety disorders classified in the DSM-5?

A

These disorders are characterized by: Fear = emotional response to real or perceived imminent threat. Anxiety = anticipation of future threat.

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2
Q

How are trauma and stressor-related disorders classified in the DSM-5?

A

Exposure to traumatic or stressful event is required for the diagnosis of these disorders, which are characterized by a variable combination of:

  1. Anxiety or fear
  2. Anhedonia & dysphoria
  3. Aggressiveness
  4. Dissociative symptoms.
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3
Q

How are obsessive compulsive disorders classified in the DSM-5?

A

These disorders are characterized by: Obsessions = recurrent persistent thoughts, urges, or images that are experienced as unwanted. Compulsions = repetitive behaviours or mental acts performed in response to obsessions or according to rigid rules.

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4
Q

What is a fear response?

A
Fear is an adaptive response. Reaction involves several components: 
Psychological (feelings)
Physiological (i.e. HR)
Cognitive (attention, concentration etc)
Behavioural (freezing or running away).
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5
Q

What are the anxiety disorders outlined in the DSM-5?

A

♣ Separation Anxiety Disorder – babies being separated from mums
♣ Selective Mutism – normally children display this, choosing not to speak
♣ Specific Phobia
♣ Social Anxiety Disorder (social phobia) [where do we draw the line?]
♣ Panic Disorder* (specifier for other disorders)
♣ Agoraphobia – being afraid of being in open spaces
♣ Generalized Anxiety Disorder (GAD)
♣ Substance/Medication-Induced Anxiety Disorder
♣ Anxiety Disorder due to another medical condition
♣ Other Specified Anxiety Disorder
♣ Unspecified Anxiety Disorder
*Highly comorbid but differentiated from each other.

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6
Q

What is the prevalence of anxiety disorder?

A

12 month - 18.1%. Lifetime - 28.85% (USA), 13.6% (EU).

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7
Q

What did Stahl, 2013 find?

A

Core features are anxiety and worry. Then can have a combo of other symptoms to distinguish between different anxiety disorders. For MDD, core features are depressed mood and anhedonia.

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8
Q

What are the core features of social anxiety disorder?

A

Core features are social/performance anxiety/fear and worry about exposure. This is associated with expected panic attacks and phobic avoidance/behavioural change.

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9
Q

What are the core features of GAD?

A

Core symptoms of generalised anxiety/fear and generalised worry. Associated with concentration problems, fatigue, irritability, muscle tensions, sleep deprivation.

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10
Q

What are the core features of panic disorder?

A

Core features are anticipatory anxiety/fear and worry about panic attacks. Associated with unexpected panic attacks and phobic avoidance/behavioural change.

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11
Q

What are core features of PTSD?

A

Core symptoms are anxiety/re-experiencing event and worry. Associated with arousal, lack of sleep and avoidance.

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12
Q

What are specific phobias?

A

Triggered by specific objects or situations (Blood-injury-injection phobia – does the opposite to normal phobia, as blood pressure goes down and people faint, as opposed to other phobia where heart rate increases etc.). Most common is arachnophobia. Twice as many females compared to males. Fear varies with proximity – active avoidance. Usually multiple diagnoses (on average 3 diagnoses). 75% fear more than one things/situations.

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13
Q

Why do we fear?

A

Loud noises frighten everyone, animals, heights, or separation from loved ones. J.B. Watson: Fears are learned – if we see others being afraid, we are going to learn to be afraid of it also. Exaggerated fear for not so threatening events or things.

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14
Q

What did Clark, 1986 say about panic disorder?

A

Very sensitive to their bodily functions, e.g. accurate at detecting heart rate, and wrongly misinterpret small changes (catastrophic interpretation) which causes fear and anxiety. Associated with the development of anticipatory anxiety and agoraphobia.

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15
Q

What is the heritability of anxiety disorders?

A

Panic disorder - 43%. GAD - 28%. Not highly heritable, lots of room for environmental input.

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16
Q

What are risk factors for anxiety disorders?

A

Environmental and genetic factors (interaction). Across anxiety disorders. Negative Affect (Neuroticism) is believed to be a risk factor. Childhood experiences (exception GAD) – is it just one experience or continuous exposure?Panic disorders - smoking and stressors preceding the 1st panic attack. Sexual dimorphism – lots more women than men (COMT gene). Heritability varies, i.e. 61% agoraphobia, SAD 2-6x greater risk for first degree relatives.

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17
Q

What is COMT?

A

Degrades dopamine in the prefrontal cortex. Has different variations - Met or Val alleles. Met (low activity COMT thus more DA in the PFC) - makes them more susceptible to worry and be diagnosed with anxiety disorder. Women are more likely to carry this. Val (high activity of COMT thus less DA in the PFC) - able to battle anxiety and survive a stressor.

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18
Q

What are BDNF polymorphisms?

A

Allele Val66Met has been associated with increased risk for anxiety disorders (Yu et al 2009). Atypical activity in frontal cortex and amygdala. Impaired extinction of conditioned fear memory
Harrisberger et al 2015 - Meta-analysis: confirmed that neuropsychiatric patients had smaller hippocampal volumes compared to healthy controls, regardless of the genotype – doesn’t seem to be related.

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19
Q

What is the phenotype of anxiety?

A

Have fear aspect – panic, phobia. Fear is amygdala-centred, quick to respond. And have worry aspect – anxious misery, apprehensive expectation, obsessions. This involves cortio-striato-thalamo-cortical circuits. Hippocampus – we remember where we were when we had fearful response. Increases cortisol levels, makes our heart beat fast etc. – can lead to health problems if chronic. Amygdala communicates and has to do with autonomic nervous system – can increase heart rate which can lead to problems e.g. heart disease, hypertension, arrhythmia, and sudden death. Respiratory fear response in the Parabrachial Nucleus – leads to Bronchospasm: ‘fast’ breathing. Increase breathing because we may need to run away (flight).

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20
Q

What structures are involved in anxiety?

A

¥ Amygdala – involved in aggression and emotional memory. Increased activity. Increases in dendrites, BDNF (opposite of hippocampus and PFC)
¥ Hippocampus – involved in episodic memory and declarative memory. Decreased functioning and volume. Decreases in dendrites, in sptial memory and working memory (decrease in volume)
¥ Prefrontal cortex – involved in working memory and fear extinction. Decreased functioning and volume.

21
Q

What is the treatment of anxiety?

A

Psychotherapy: CBT especially for specific phobias i.e. Systematic Desensitisation, Alternative therapies.
Pharmacotherapy: Barbiturates, Benzodiazepines, SSRIs, SNRIs, Buspirone, etc.

22
Q

What are animal tests of anxiety?

A

Elevated plus maze – can choose to walk in sheltered or open arm. If anxious, they may run in the middle (in the open, panic).
Open field test – large box, place them in the middle, see where they choose to go. If around the edges, they are more anxious than those in the centre.
Defensive burying test – do movements with front paws to move bedding around.
Light—Dark box – depending on which one they choose to go to shows how anxious.

23
Q

How is γ-aminobutyric acid GABA involved?

A

Synthesized from glutamate via the enzyme glutamic acid decarboxylase (GAD). Released normally during inhibitory neurotransmission. Its actions are terminated with the help of its transporter (GAT) or the enzyme GABA transaminase (GABA-T).

24
Q

What are different types of GABA?

A

Three major types of receptors: GABAA, GABAB and GABAC – A and C is ionotropic, B is metaotropic. Each type has various subtypes and differential distribution in the brain. Anxiety drugs such as barbiturates and benzodiazepines bind this receptor – bind to the GABA a receptor. It has 5 subunits that form a channel which takes things from outside to inside the cell. Depending on the subunit, the different combination of subunits alters its function.

25
Q

What are benzodiazepines?

A

Bind GABA receptors with 1,2,3,5 but not 4 and 6. Depending on the composition of the pentamer they can induce sleep (α1 subunits), anxiety (α2 subunits) and muscle relaxation. Half-life ranges from 4-15hrs (oxazepam) up to 30-40hrs (Diazepam) – can be short lasting or long-lasting, so not recommended for long-term use. If sedate too much, can have problems remembering things etc. (as you are inhibiting the brain). Potential for dependency after chronic use – antidepressants instead. SE: memory impairments and excessive sedation. Flumazenil – short-acting antagonist to benzos to reverse overdose. Benzodiazepines are allosteric agonists of the gaba a receptor. That is, they allosterically modulate the binding site for GABA, thus increasing the opening frequency of the GABAA channel. Will allow chloride axons to enter the cell, and therefore have more inhibition. Can’t open the channel alone.

26
Q

What are the different benzodiazepine binding GABA A receptor distributions?

A

a1 - everywhere high in cortex (60% of brain). a2 - everywhere (but less) - limbic structures hippocampus, amygdala striatum, spinal cord. This is where the anti-anxiety effects take place. a3 - reticular activating structures brain stem basal forebrain, spinal cord. a5 - hippocampus, spinal cord.

27
Q

What are barbiturates?

A

Barbiturates act in two ways. They allosterically modulate the binding site for GABA, thus increase the duration of the GABAA channel opening. Furthermore, they directly open the channel.

28
Q

What is the anxiolytic effect of GABAergic drugs?

A

Inhibit fear responses and the worry through inhibition in the dorsal lateral prefrontal cortex by taking medication.

29
Q

What is an inhibitory GABAergic interneuron?

A

Depending on where GABA receptor is, can have inhibitory effects, but if inhibiting gaba inerneuron, it means the neuron downstream is active even more.

30
Q

What is the adrenergic system?

A

Noradrenergic (norepinephrine) hyperactivity in anxiety. Locus coeruleus – excessive output which triggers autonomic overdrive and symptoms of anxiety & fear - nightmares, hyperarousal, flashbacks and panic attacks
How to tackle this effect: NE Reuptake Inhibitors – eventually downregulate and desensitize postsynaptic NE receptors and reduce symptoms of fear and worry. Alpha 2δ ligands also have anxiolytic effects in SAD and PD. Block calcium channels.

31
Q

What is buspirone?

A

Partial agonist of 5HT1A receptor (serotonin receptor) and inhibitor of presynaptic α2 receptors. Lacks sedating and muscle relaxant effects
SSRIs can also be used, but in greater doses than that used for depression.

32
Q

What is PTSD?

A

Introduced in 1980 (‘shell shock’) – unique in that it is determined by a single environmental event. First entered in DSM3. 1/3 of Vietnam Veterans suffered from PTSD. Growing understanding of the disorder.

33
Q

What are trauma and stressor-related disorders in the DSM-5?

A

♣ Reactive Attachment Disorder
♣ Disinhibited Social Engagement Disorder
♣ Post-Traumatic Stress Disorder (PTSD)
♣ Acute Stress Disorder – 3 days-1 month after traumatic event happened, if goes beyond this diagnosed with PTSD
♣ Adjustment Disorder – adjusting to new situation that is stressful, usually goes away within 6 month
♣ Other Specified Trauma and Stressor-Related Disorder
♣ Unspecified Trauma and Stressor-Related Disorder.

34
Q

How is PTSD diagnosed? (A)

A

Exposure to actual or threatened death, serious injury or sexual violence (direct, witnessing, learning that it occurred to someone else, repeated or extreme exposure to aversive details of the traumatic event i.e. first responders).

35
Q

How is PTSD diagnosed? (B)

A

Presence of intrusion symptoms (memories, dreams, flashbacks, distress).

36
Q

How is PTSD diagnosed? (C)

A

Avoidance of stimuli associated with the traumatic events (avoid memories or people or situations that may remind the stressful event).

37
Q

How is PTSD diagnosed? (D)

A

Negative alterations in cognitions and mood associated with the traumatic events (memory of the traumatic event may be bad, negative beliefs about oneself, distorted cognitions about the cause or consequences of the event, diminished interest in participation in activities, inability to experience positive symptoms).

38
Q

How is PTSD diagnosed? (E)

A

Marked alterations in arousal and reactivity associated with the traumatic events (irritable behavior, reckless or self-destructive behavior, hypervigilance, problems with concentration and sleep).

39
Q

What are clinical features of PTSD?

A

1) Re-experiencing – memories (“frozen memories” – reliving the memory), thoughts, images, nightmares
2) Avoidance – emotional numbing where the person is unable to feel a range of emotions, amnesia, behavioral avoidance, cognitive avoidance (distractions)
3) Arousal symptoms – exaggerated startle response, irritability, hypervigilance
* Accompanying emotions such as sadness, anger, guilt, shame.

40
Q

What is Horowitz’s theory?

A

We have a natural tendency to make everything understandable, and integrate life experiences into our existing schemas. If something happens that is so traumatic and beyond what we expect, it is hard for us to integrate this into our schemas. There is an oscillation (trying to move on), but can’t because there is a constant battle to integrate. Then either have successful integration or incomplete resolution, which is PTSD (it is there unresolved).

41
Q

What is the prevalence of PTSD?

A

Overall prevalence: 7-8% (women 10.4% vs men 5%). Rates following exposure to a traumatic event 15% (for rape it is higher. 70-80% of PTSD patients have an additional diagnosis such as psychosis, anxiety disorder, & depression. In combat veterans, depression, GAD and substance abuse are frequently co-diagnosed. A history of psychological or behavioral problems are predictive of PTSD following trauma. Social support seems to be a protective factor – better outcome, more internal focus of control and a more internal and controllable attributional style for positive events. Internal and controllable attributions for disaster-related events seem to be associated with poorer outcome.

42
Q

What are cognitive biases in PTSD?

A

Some studies did find greater interference for words related to the trauma than people without PTSD to those same words. Stroop task (John Ridley Stroop, 1935). Emotional Stroop – give attention to stimuli that triggers memory of traumatic event.

43
Q

Why does the propensity of people to develop PTSD vary?

A

Predisposing factors, such as personality, childhood experiences, genetic vulnerability. Strongest contribution is genetic but still 5-10% of those affected by a traumatic event will develop PTSD. Vietnam Twin Registry: MZ conc higher than DZ. Serotonin transporter allele (l vs s). GxE interaction s allele contributed to PTSD only when traumatic exposure was severe and there was lack of social support.

44
Q

What do neuroimaging and brain structures in PTSD patients show?

A

Consistent findings regarding volume: decreased volume of hippocampus, decreased volume also of the amygdala and Insula. Question of which one came first. Consistent findings regarding activity: Increased response of amygdala and decreased response of mPFC and hippocampus. dACC and insult are hyperactive and thus support the learning of fear memories.

45
Q

What does the HPA axis show in PTSD patients?

A

Hypersensitivity of HPA axis. GR sensitivity - lower levels of cortisol in PTSD patients.

46
Q

What is extinction (PTSD)?

A

Conditioned emotional responses are important for survival. If the CS (i.e. the tone) is present by itself, extinction occurs (not forgetting). ¥ The expression of the CR is inhibited and not removed – ventro-medial Prefrontal Cortex (vmPFC)
Ð Lesions in the vmPFC impair extinction
Ð Stimulation of this region inhibits conditioned emotional responses
Ð Modulates the expression of fear
¥ mvPFC (activates AMY) and Hippocampus (Context)
¥ Output depends on which system is stronger
¥ Renewal may happen if old fear is presented in a new context (extinction is context specific)
Need to generalize extinction to other settings.

47
Q

What is reconsolidation?

A

Consolidation – thought to be permanent, but - Emotional memories can be weakened or erased upon retrieval – Reconsolidation makes it labile – can lose it/change it around. Beta blockers and opioids can disrupt reconsolidation and reduce the chances of PTSD after trauma.

48
Q

How are beta blockers used for PTSD?

A

Adrenergic blockade i.e propranolol. Developed for cardiac arrhythmias (for acute symptoms as in panic attack). Adrenaline increases HR and cardiac output.