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Anxiety disorder Flashcards

1
Q

State whether fear is normal or pathological, time-course

A

Normal
short

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2
Q

State whether stress is normal or pathological, time-course

A

Normal if shorter, but if chronic pathological
Shorter or longer lasting

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3
Q

State whether anxiety is normal or pathological, time-course

A

pathological
Long

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4
Q

What major pathways are activated in fear, stress and anxiety?

A

HPA (Hypothalamis Pituitary Adrenal) axis
ANS

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5
Q

Outline the link between stress and inflammation

A

Won and Kim 2016: brief lab stressors (mental maths) increased natural killer cell activity.
This increase potentiated in individuals whose cardiovascular systems activate more in stress.
Therefore, people with biggest sympathetic and endocrine responses have the largest immune responses.

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6
Q

How does the HPA axis increase sympathetic tone in response to stress?

A

Stress causes paraventricular nucleus (PVN) of hypothalamus to release CRH (corticotropin releasing hormone) that projects to brainstem and spinal cord.

Locus Coeruleus (brainstem) stimulated to release noradrenaline.

Noradrenaline acts on alpha1 receptors in sym preganglionic neurones that are Gq coupled and therefore increase intracellular calcium concentration.

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7
Q

What does activation of the sympathetic nervous system cause?

A

Fight or flight response, increased heart rate, production of stress hormones, blood directed to muscles, skin opens up pores so sweat more.

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8
Q

Outline role of amygdala in limbic system

A

Acts as central node by communicating to lots of other brain regions… activates hypothalamus
Asks:
what can I see, how do I feel, do I need to remember, what action am I going to take.

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9
Q

What role does the PAG play with amygdala and where is it found?

A

Periacqueductal grey: found at base of brainstem and talks to amgdala.

Responsible for freezing and active defensive behaviours.

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10
Q

Outline role of BNST in fear and anxiety

A

Bed Nucleus Striatum terminalis: recieves amygdala.

Distinct subregions exert opposing effects on anxiety (Kim et al., 2013).

Lesions of BNST diminish anxiety but leave fear responses intact (Duval et al., 2015)

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11
Q

What are the two main types of fear?

A

1) learned or conditioned
and
2) innate or unconditioned

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12
Q

Outline circuitry involved in mediating context dependent expression of fear in response to extinguished cue. How may this relate to anxiety disorders?

A

Hippo to BLA: renewal of fear expression in response to extinguished conditioned stim.

Hippo-Infralimbic- amy: context dependent expression of fear to extinguished stim.

Deficits in circuits thought to accompany PTSD

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13
Q

What are the 3 types of validity for animal models and do all animal models need to demonstrate all three types?

A

1) face: phenotypically similar
2) construct: theory behind model (gene KO)
3) predictive: sensitive to clinically effective pharmacological agents

Only one type of validity needed.

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14
Q

State the two major types of anxiety animal experiments and how they differ.

A

Spontaneous (innate stim) causes stress, no direct pain.

Conditioned: stim paired with uncomfortable sensation.

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15
Q

Define exteroceptive and give examples of stimuli models

A

Outside body

Open field test, Elevated plus maze, Social interaction test.

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16
Q

Define interoceptive and give examples of stimuli models

A

Inside body

Caffeine induced anxiety, foot-shock induced aggression, electrical stimulation of the brain.

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17
Q

Give examples of conditioned response animal models of anxiety

A

Geller-Seifter (press lever to get food, this lever pressing delivers shock, more anxious = less food press).

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18
Q

Give examples of unconditioned response animal models of anxiety

A

Open field, elevated plus maze, social interaction, predator smell.

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19
Q

Animal: Outline the open field test

A

Anxious mouse spends more time in periphery close to walls.

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20
Q

Animal: Outline novelty supressed feeding

A

Anxious take longer to both approach and eat food.

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21
Q

Animal: Outline elevated plus maze

A

More anxious spend more time in arms of +

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22
Q

Animal: Outline social approach

A

More anxious spend more time with object than other mouse.

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23
Q

Animal: Outline light-dark test

A

More anxious mice spend longer in dark area

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24
Q

Animal: Outline fear conditioning

A

More anxious exhibit increased freeze behaviours and take longer to perform task

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25
Q

State the different ways we can test for anxiety in humans

A

Galvanic skin response: when anxious sympathetic is activated and therefore sweat more. Sweat increases skin conductance
ECG: T wave inversion sign of anxiety
Tests: such as GAD-7 that are questionaires.

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26
Q

What is the neural circuitry that underlies anxiety?

A

Duval et al., 2015: There is no common circuit for all diff types of anxiety.

E.g. hyperactivation of hippocampus implicated in PTSD (hypo also in PTSD) and social anxiety disorder. But hippo plays more than one role so most likely involved in different processes in both.

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27
Q

State differential neurocircuitry associated with GAD

A

Duval et al., 2015: hypoactivation of ACC, PFC when percieved threat.
Hyperarousal to emotion due to ineffective PFC processing.

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28
Q

State differential neurocircuitry associated with OCD

A

Duval et al., 2015: CSTC

Cortex underactive so stay locked in loop.

Greater activation of direct pathway than neurotypical and hypo of indirect

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29
Q

State differential neurocircuitry associated with SAD

A

Duval et al., 2015: hyperacativation of limbic system esp, amygdala in response to social stim.
Disfunction between corticolimbic.
Hyperactivation of insula and PFC in response to social emotion.

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30
Q

State differential neurocircuitry associated with PD

A

Duval et al., 2015: hyperactivation of fear network, brainstem and hypothalamus (though panic symptoms).
Hyper insula - bodily sensations.

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31
Q

State differential neurocircuitry associated with PTSD

A

Duval et al., 2015: hyperactivation of lateral and BLA for fear consolidation and expression.
Hyper insula
Hypo ACC and PFC which leads to insufficient regulation of limbic.

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32
Q

What is the ACC and role in anxiety?

A

Anterior Cingulate cortex (part of limbic cortex).

Emotional processing: conflict monitoring, error detection.

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33
Q

What is PFC and role in anxiety?

A

Prefrontal cortex

When PFC hypo or not efficient amygdala takes on bigger role (bad as less regulation)

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34
Q

Outline function of the Cortico-striatal-thalamo-cortical pathway and state anxiety disorder it has been implicated in

A

brain circuit that controls movement execution, habit formation and reward. Hyperactivity = OCD

Radulescu et al., 2017

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35
Q

State lifetime prevalence, symptoms and prognosis of GAD

A

LP: 5.1%
Symptoms: 3 or more of (restlessness, fatigue, concentration difficulties, irritability, muscle tension, sleep disturbances.
Prognosis: ~70% recover

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36
Q

What does GAD stand for and give medical definition

A

Generalised anxiety disorder: excessive worry occuring more days than not for at least 6 months.

Generalised Anxiety Disorder Questionnaire (GAD-7) is how diagnosed

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37
Q

State treatments used for GAD

A

Drug: SSRI and BDZ (BDZ are effective and provide rapid relief but are not prescribed for use over 4 weeks due to concern about withdrawal). BDZ slowly withdrawn and only SSRI remains after.
TCAs and MAOis

Other: CBT

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38
Q

What does PD in anxiety stand for and state medical definition

A

Panic disorder: discrete period of intense fear or discomfort in which symptoms develop abruptly and peak within 10 minutes. 4 or more panic attacks in period of four weeks.

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39
Q

State lifetime prevalence, symptoms and prognosis of PD

A

LP: 3.5%
Symptoms: palpatations, sweating, trembling, shortness of breath, naseua or abdominal pain, depersonalisation, numbness or tingling.
Prognosis: 25-45% improve

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40
Q

State treatments used for PD

A

Drug: SSRI and Alprazolam only (BDZ with short half life) Other BDZ are effective only at high doses and therapeutic effect slower.
Also treated with antidepressants: TCAs, MAOi (phenelzine)
Other: Exposure

NB: evidence shows treatments with longest duration of effect in decending order…
CBT, Self help, pharmacological

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41
Q

When does PD most frequently first occur?

A

Early 20’s

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42
Q

How many times more likely is it for women to suffer from PD and why?

A

2.5X

Progesterone: converted in brain to allopregnanolone which enhances function of GABA A thus acting as anxiolytic via allosteric modulation and increases CL-
In PMS, decreased progesterone which mimicked in rats by BDZ abrupt withdrawal.
More alpha 4 subunit encoding therefore subunit expression changes. less inhibition of amygdala. (Smith et al., 1998)

Furthermore, as oestrogen drops in some women so does serotonin…

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43
Q

Outline co-morbidity of GAD, major depression, and panic disorder

A

GAD: 2.6X more likely major D, 5.2X more likely panic disorder.

MD: 26.5X more likely panic

Panic: 9.4X more likely MD

44
Q

What is agoraphobia and how does it relate to panic disorder

A

extreme or irrational fear of entering open or crowded places, of leaving one’s own home, or of being in places from which escape is difficult.

95% of patients with panic disorder will develop.

45
Q

State lifetime prevalence, symptoms and prognosis of PTSD

A

LP: 6.2-8.2% men 13-20.4% women (Byrant, 2019)
Symptoms: re-experiencing trauma (flashbacks or nightmares), avoidancen(decreased participation) hyperarousal and emotional numbness ( agression, hypervigilance, difficulty sleeping, problems concentrating)
Prognosis: Over 50% leave ‘clinical’ class

46
Q

What does PTSD stand for, give definition

A

Post Traumatic Stress Disorder: Diagnosed when person experiences symptoms for at least one month following event.

NB: symptoms may not appear until several months or years after event.

47
Q

What types of events lead to PTSD?

A

Exposure to actual or threatened death, serious injury or sexual violation.

48
Q

State lifetime prevalence, symptoms and prognosis of OCD

A

LP: 2.5%
Symptoms: Obsessive thoughts (unwanted and unpleasant, repeatedly enters mind) and compulsive behaviours (repetitive behaviour or mental act that you feel you need to carry out to temporarily relive unpleasant feelings)
Prognosis: 60% improve within a year

49
Q

Define OCD

A

Obsessive compulsive disorder: no test for OCD diagnosed after asked about symptoms.

50
Q

State lifetime prevalence and prognosis of specific phobias

A

LP: 11.3%
Prognosis: reduction common but loss of phobia rare

51
Q

State lifetime prevalence and prognosis of social phobias

A

LP: 13.3%
Prognosis: 75% replapse on drug withdrawal

52
Q

Give evidence via animal models that anxiety disorders are disorders of synaptic plasticity

A

McEwen, 2000: chronic restraint stress caused apical dendrites of pyramidal ca3 cells in rats to atropy.

Wang et al., 2020: Mice experience maternal stress early in life have decreased post synaptic density in hippocampus later in life. Greater anxiety scores in open field test etc

Issue with experiment is that MS stress group also recieved chronic restraint. So combo…

53
Q

Outline animal experiment on effect of progesterone on anxiety

A

Hantsoo and Epperson 2020: progesterone exposure and rapid withdrawal upregulated expression of alpha 4 subunit in rats.

Increased alpha 4 associated with increased anxiety

54
Q

How is BDNF implicated in synaptic plasticity

A

BDNF (brain derived neurotropic factor)

Mahan and Ressler (2012): single nucleotide polymorphism (SNP) found in brains of humans and alters BDNF stability and release. SNP humans show greater recruitment of amygdala. KI mice showed increase anxiety, impaired NMDA plasticity. BDNF binds to TrkB and activates, ras/erk pathway. (inhib of erk shown to prevent ampar insertion).

Braham and Messaoudi (2005):TrkB is localised to glutamatergic NMDARs and enhances function.

55
Q

Give evidence of structural and functional plasticity in anxiety

A

Stress reduces spine density and impairs LTP in the PFC and hippocampus pyramidal neurons (Rosenkranz et al., 2010

56
Q

Give clinical/human evidence for plasticity in anxiety

A

Hippocampus stress-induced shrinkage of hippocampal neurons in rodents and reduced volume in depressed human patients.

However, inconsistency in volume in amygdala where diff studies show increase, decrease and no change in volume (Christoffel, 2011)

57
Q

Give general molecular structure of BDZs

A

Contain aromatic rings

58
Q

Outline the structure of a GABA A receptor

A

Pentameric transmembrane ionotropic receptor that opens to cause Cl- influx.

5 subunits (2 alpha1, 2 beta1 and gamma2) most common around ion channel pore.

59
Q

Where is BDZ site on GABA AR?

A

on most common found gamma2 and alpha1

60
Q

How do BDZ impact GABA A? name one

A

Increases frequency of channel opening: causes GABA dose-response curve to shift to left.

This means less GABA needed to produce same response.

diazepam

61
Q

If alpha1 subunit of GABA A is eliminated what effect is eliminated?

A

sedation

62
Q

If gamma2 subunit of GABA A is eliminated what effect is eliminated?

A

anxiolytic

63
Q

How do barbituates impact GABA A? name one

A

Increase length of time cl- (chloride) pore stays open. Shifts dose-response curve to the left and increases maximal possible response.

Pentobarbital

64
Q

How do steriods impact GABA A? name one

A

Potentiate actions of GABA via increasing opening frequency and lifetime.

allopregnanaolone

65
Q

The lower the Ki…

A

The greater the binding affinity

66
Q

How does affinity relate to therapeutic dose for BDZ

A

The greater the affinity (the lower the Ki value) the lower the therapeutic dose.

67
Q

State other properties of BDZ use other than anxiolytic

A

Sedation, anti-epileptic, amnesia, can cause loss of inhibitions

68
Q

State and explain reasons that BDZ are used as anxiolytics instead of barbituates.

A

1) Barbituates have low therapeutic index (LD50/ED50 as low as 3:1 whereas BDZ 1:300), therefore high risk overdose.
2) Barb causes respiratory depression
3) Barb shows rapid tolerance and convulsions upon withdrawal
4) Barb induce liver microsomal enzymes which modify the blood level of other drugs.

69
Q

Name an antagonist for BDZs and state why this is useful

A

Flumazenil: can reverse effects (if for some lethal too high dose)

Note flumazenil has a short half-life and multiple use is often required in benzodiazepine overdose

70
Q

Outline how OCD is managed

A

Drug: SSRIs
Other: CBT

often offered in combo

71
Q

Outline how specific phobias are treated

A

Behaviour therapy but if immediate help is required (for help in air travel) BDZs can be used.

72
Q

Outline how social phobia is treated

A

Beta-blockers as the symptoms are peripheral rather than central (propranolol drug of choice)

73
Q

Define insomnia

A

sleep disorder characterised by difficulty falling or staying asleep

74
Q

Describe obstructive sleep apnea

A

Partly or complete blockage of upper airway when asleep. So continuously wake up due to lack of oxygen.

75
Q

Describe central sleep disorder

A

Lower brainstem dysfunction causes you to wake up regularly during sleep.

76
Q

Describe hypersomnia

A

Trouble staying awake during the day

77
Q

Describe parasomnia

A

Disruptive sleep disorders that can occur during arousals from REM sleep or partial arousals from non-REM sleep. Include nightmares, night terrors, sleepwalking, confusional arousals etc.

78
Q

Describe REM sleep disorder

A

Paralysis that usually occurs in REM sleep is absent allowing person to act out his or her dreams

79
Q

Describe narcolepsy

A

Suddenly fall asleep at innappropriate times, neurological disorder

80
Q

Outline when circadian rhythm sleep disruptions occur

A

Time zone changes, pre-menopause and AD or Parkinson’s

81
Q

Outline lifestyle changes to treat imsomnia

A

Go to bed and get up same time everyday, avoid caffeine and alcohol in evening, avoid naps, if you cannot sleep get up and occupy yourseld until you feel sleepy.

82
Q

Outline drugs used to treat imsomnia

A

Hypnotics:
Short acting BDZs and Z (Zolpidem, selective for alpha1 containing subunits.
Zopiclone: non selective adn longer half life
Zaleplon: v short half life selectivity same as Zolpidem

83
Q

BDZ can be used as both an anxiolytic and a hypnotic: explain

A

Higher dose = sedative as greater receptor activation (80%).

anxiolytic only 30% receptor activation recquired.

84
Q

Why do we want the time course of hypnotics and anxiolytics to be different

A

Hypnotics: we want short time course so can wake up

Anxiolytic: long time course

84
Q

Why do we want the time course of hypnotics and anxiolytics to be different

A

Hypnotics: we want short time course so can wake up

Anxiolytic: long time course

85
Q

State molecular structure of hypnotic BDZs

A

Multiple phenyl rings

86
Q

Outline drug interactions of BDZs

A

When combined with CNS depressants will exacerbate sedative effects and leads to decreases in psychomotor performance.

CNS: antidepressants, narcotic analgesics, antipsychotics, antihistamines, alcohol.

Can be life threatening in combo.

87
Q

Outline PTSD treatment

A

Drug: antidepressants (sertraline etc used for adults).

Other: CBT, group therapy, eye movement desensitisation, reprocessing (EMDR)

88
Q

Outline EMDR

A

Subjects make specific eye movements (thought to decrease negative emotion) while talking about memory. Faster than regular talking.

Lack of longterm research and some people believes promotes dissociation.

Some see reliving as making new memories as synaptic plasticity.

89
Q

Why do anxiolytic drugs target GABA receptors

A

Low levels of GABA implicated in anxiety disorders.

Deactivation of enzyme needed for GABA synthesis = loss of anxiolytic BZD effects. (Nuss 2015)

90
Q

Name neurosteroids and impact on anxiety

A

Serotonin: decreases via activation of serotonin

Allopregnanolone: enhances function of GABA AR, increases channel opening frequency and lifetime

Pregnenolone sulfate (note E): acts as antagonist to GABA AR.

91
Q

Outline mechanism of action of SSRIs

A

Selective Serotonin Reuptake Inhibitors inhibit the serotonin transporter (SERT), increased 5-HT in synaptic cleft.

92
Q

List side effects SSRIs and state why they have less side effects than TCAs and MAOis.

A

SE: weight changes, dizziness, sexual dysfunction

As no effect on dopamine, noradrenaline, histamine etc. SSRIs are specific.

93
Q

Outline mechanism of action of tricyclic antidepressants

A

Acts on different neurotransmitter pathways:
1) block serotonin reuptake
2) block noradrenaline reuptake.
3) decrease 2-adrenoreceptor sensitivity as competitive antagonists to acetylcholine, acetylcholine decreases release into presynapse. (alpha1,2 and histaminergic receptors).
4) reduce Beta1 sensitivity, connected to K, therefore, less K influx and more hyperpol.

1 and 2 = antidepressant

94
Q

Describe mechanism of action of MAOi’s and state what acronym stands for

A

Monoamine oxidase inhibitors: block action fo monoamine oxidase enzyme which breaks down (noradrenaline, serotonin, dopamine and tyramine). Thus, increasing level in brain, increased response from above transmitters.

95
Q

Describe mechanism of action of propanolol

A

beta-adrenoreceptor 1 and 2 antagonist.

When above receptors activated, increased cAMP which leads to increased contractability of muscle fibres in heart

96
Q

Give evidence for antihistamines as an axiolytic

A

h1R antagonist improved anxiety in open field test.

97
Q

Outline how cannabis is regarded as both an axioltyic and an anxiogenic

A

THC: anxiogenic
CBD: anxiolytic

However, low dose CBD (4mg) increased intoxicating effects of THC whereas high (400mg) decreased.

Conversely…biphasic effect: low dose cannabinoids interact with cortical glutamergic CB1 receptor terminals = anxiolytic
At higher doses… interacts with CB1 receptors on GABAergic terminals = anxiogenic.

98
Q

Why are TCAs only used for severe anxiety

A

Low therapeutic index (prone to overdose).

Side effects: block of acetylcholine. dry mouth.
slight blurring of vision, constipation, problems passing urine.
drowsiness.
dizziness.
weight gain.

This is due to block of choline receptors.

99
Q

Why can MAOis be used to treat parkinson’s?

A

Decreased DA in PD, so….

blocking enzyme increases DA therefore good.

100
Q

Why have MAOis been replaced?

A

increase blood pressure therefore have to be on strict diet.

Possibility of serotonin syndrome.

101
Q

How does histamine receptor block anxiolytic?

A

Histamines = inflammatory therefore anxiogenic

Antihistamines = anti-inflam, sedative and have anxiolytic effect

102
Q

Outline HPA activation in stress

A

Hypothalamus activated by amygdala and signals to pituitary by releasing CRH (corticotrophin releasing hormone).

Pituitary release ACTH (adrenocorticotropic releasing hormone).

ACTH causes adrenal gland to release cortisol.

There are feedback loops ie (when cortisol released less ACTH and CRH released).

103
Q

Theory behind PTSD?

A

At time of trauma: surge in number of stress hormones = strong associative learning event.

Byrant, 2019

104
Q

Volumetric brain changes in PTSD?

A

Kuhn et al.,
MRI on soldiers before and after deployment.

findings: no diff in hippocampus (smaller predisposes), reduction in ACC, mPFC, thalamus (extinction learning) that persist.

Issues: few women sampled, no soldiers developed PTSD, childhood etc.

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