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Disease in the brain > Anxiety disorders (done) > Flashcards

Anxiety disorders (done) Flashcards

1
Q

What is anxiety?

A

A feeling of unease, such as worry or fear, that can be mild or severe

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2
Q

What conditions is anxiety the main symptom of?

A
  • Generalised anxiety disorder (GAD)
  • Panic disorder
  • Obsessive compulsive disorder (OCD)
  • Post-traumatic stress disorder (PTSD)
  • Phobias
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3
Q

What are the psychological & physical symptoms of generalised anxiety disorder (GAD)?

A
  • Feeling restless of worried
  • Having trouble concentrating or sleeping
  • Dizziness or heart palpitations
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4
Q

What are the 6 things that categorise GAD?

A

1 - Excessive worry, ocurring more days than not for at least 6 months

2 - Individual finds it difficult to control the worry

3 - 3 or more of 6 the key symptoms

4 - Anxiety, worry or physical symptoms cause significant distress

5 - Disturbance not attributed to drug abuse

6 - Disturbance is not better explained by anotehr disorder

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5
Q

What are the 6 key symptoms of GAD that 3 of are required to be diagnosed?

A

1 - Restlessness or feeling keyed up or on edge

2 - Being easily fatugued

3 - Difficult concentrating or mind going blank

4 - Irritability

5 - Muscle tension

6 - Sleep disturbance

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6
Q

What is the definition of panic disorder?

A

An anxiety disorder with regular panic attacks

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7
Q

What are the characteristics of a panic attack?

A
  • Intense tymptoms that come on quickly, often for no apparent reason
  • Some symptoms overlap other health conditions (e.g. low BP)
  • Range from 1-2/month to multiple/week & usually last 5-20min
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8
Q

What are the characteristics of panic disorder?

A

1 - Palpitations
2 - Sweating
3 - Trembling or shaking
4 - Fear of dying
5 - Neausea

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9
Q

What are the 2 component of OCD?

A

Obsessions & compulsions

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10
Q

What are obsessions?

A

Unwanted/unpleasent thoughts that cause anxiety e.g. being burgled

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11
Q

What are compulsions?

A

Repetitive behaviour undertaken to supress -ive thoughts

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12
Q

What is the diagnosis for OCD?

A

Obsessions & compulsions must be time consuming & impact on day-to-day functioning

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13
Q

What are some examples of OCD obsessions?

A
  • Aggressive
  • Contamination
  • Religion
  • Self-control
  • Sexual
  • Cleanliness
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14
Q

Define PTSD:

A

An anxiety disorder caused by traumatic events

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15
Q

What are the charateristics of PTSD?

A
  • Re-lived through nightmares or flashbacks
  • Avoidance of linked memories
  • Affects 1 in 3 exposed to trauma
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16
Q

Define a phobia:

A

Overwhelming & debilitating fear of something that is often little or no actual danger

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17
Q

What are the 2 types of phobias?

A
  • Specific phobias
  • Complex phobias
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18
Q

What are specific phobias?

A

Fear of something that is normally not harmful –> cna generally be avoided/worked around

e.g. Animals (spiders), environmental (heights), situational (flying/dentist), bodily (injections)

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19
Q

What are complex phobias?

A

They are life limiting as they cannot be avoided or worked around

e.g. Agoraphobia (open spaces), Social phobia (of social performance situations, from thoughts of negative judgement or humiliation –> dread or avoidance)

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20
Q

What are the 4 types of evidence that were used to understnad anxiety?

A
  • Neuroimaging
  • Genetics
  • NTs - including treatment response
  • Neuroendocrine
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21
Q

What are the 3 main brain areas that are involved in anxiety?

A
  • PFC (prefrontal cortex)
  • ACC (anterior cingulate cortex)
  • Amygdala
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22
Q

What is the role of the PFC?

A

Involved in logical responses & reasoning to reduce anxiety

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23
Q

How does the PFC change in anxiety?

A

Anxiety can shut down the PFC –> hampers logical thinking & rationalising

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24
Q

What is the role of the anterior cingulate cortex?

A

Amplifies fear signals from the amygdala

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25
Q

How does the anterior cingulate cortex change in anxiety?

A

It malfunctions –> hyperactivating the amygdala

This amplifies -ive info, which increases anxiety

26
Q

What is the role of the amygdala?

A

Responsible for responses to fearful stimuli

27
Q

How does the amygdala change in anxiety?

A

In persistent anxiety, the amygdala increases in size - boosting response to scary stimuli

Inhibits the PFC & initiates fight-or-flight response

28
Q

What are the key brain area malfunctions that result in anxiety?

A

PFC is underactive & amygdala is overactive

29
Q

What did fMRI scans of GAD and healthy control brains show?

A

Patients w GAD showed weaker functional connectivity between the PFC & amygdala

(Dec PFC-amygdala connectivity in GAD)

30
Q

What is the heratibility of GAD?

A

Family studies show ~30% heritability; parent –> child

31
Q

Name 3 monoamines?

A

Dopamine, adrenaline & noradrenaline

32
Q

What are the 4 risk genes that have been identified with GAD?

A
  • 5-HT reuptake transporter
  • 5-HT1A receptor C1019G polymorphism
  • Monoamine oxidase A T941G polymorphism
  • Brain-derived neurotrophic factor Val66Met polymorphism
33
Q

What is the change caused by 5-HT1A receptor C1019G polymorphism in GAD?

A

C to G change at position 1019 in this gene = mutation

Increases -ive feedback, dec serotonergic signalling

34
Q

What is the change caused by Monoamine oxidase A T941G polymorphism in GAD?

A

(Something about long allele)

Increases monoamine metabolism, decreases monoamine signalling

35
Q

What is the change caused Brain-derived neurotrophic factor Val66Met polymorphism in GAD?

A

Decreases BDNF activity

36
Q

What % of GAD is environmental?

A

If ~30% is inherited then ~70% is environmental

37
Q

What are some environmental risk factors for anxiety?

A
  • Childhood trauma
  • Stressful family circumstances
  • Natural disasters
38
Q

What are some examples of gene-environment interactions causing GAD?

A
  • Childhood trauma X 5-HT transporter, COMT & MAOA variants
  • Hurricane victim X neuropeptide Y variants
  • Daily life stress X 5-HT transporter variants
  • Family relationship scale X nueropeptide S receptor 1 variants
39
Q

How does GABA act in ppl with GAD & how can we use this to treat GAD?

A
  • GABA dysregulated in GAD
  • GABA A receptor downregulated in patients
  • Symptoms treated w GABA A agonists
40
Q

What are the 4 NT that can be targeted to treat GAD?

A
  • GABA
  • 5-HT
  • Corticotrophin releasing factor
  • Neuropeptides
41
Q

How can we treat GAD symptoms using 5-HT receptors?

A

SSRIs can be used to treat issues with them & inhibit serotonin reuptake

42
Q

Have treatments been found for GAD with corticotrophin releasing factor & neuropeptides?

A

Cortico –> clinical trials were unsuccessful

Neuropeptides –> patients are hypesensitive to cholecystokinin (CCK) agonists

–> unsuccessful trials investigating CCK-antagonists

43
Q

What does the HPA axis include?

A
  • Hypothalamus (in forebrain)
  • Pituitary gland (below hypothalamus)
  • Adrenal glands (above kidneys)
44
Q

What is the role of the HPA axis?

A

Work together to regulate stress reponses, mood, immune function, metabolism

45
Q

What hormones are released in the HPA axis?

A

Hypothalamus
|
|
Corticotrophin releasing hormone - CRH
|
V
Pituitary gland
|
|
Adrenocorticotropic hormone (ACTH)
|
V
Adrenal glands
|
V
Cortisol, adrenaline & noradrenaline

46
Q

how can the HPA axis cause symptoms of GAD?

A
  • Cortisol activates fight-or-flight response & inhibits CRH & ACTH release
  • This -ive feedback reduces cortisol & noradrenaline release
  • Chronic stress & GAD associated w HPA-axis dysfunction
47
Q

What needs to be considered udirng assessment for GAD?

A
  • Mental health history
  • Environemental stressors
  • Medical & drug history
  • Degree of distress & functional impairment
  • Risk of suicide
48
Q

What are the non-pharmacaological treatments of GAD?

A
  • Self help
  • Meditation & relaxation techniques (e.g. mindfulness)
  • Exercise
  • Lifestyle changes
49
Q

What are the 2 types of symptoms that are treated in GAD?

A
  • Autonomic symptoms
  • Anxiety symptoms
50
Q

What pharmacological treatments are used for the autonomic symptoms of GAD?

A

Beta-adrenoceptor antagonists –> e.g. propranolol

Can be given for experiencing inc HR that is affecting psychological symptoms

51
Q

What pharmacological treatments are used for the anxiety symptoms of GAD?

A
  • SSRIs (selective serotonin reuptake inhibitors)
  • SNRIs (serotonin & noradrenaline reuptake inhibitors
  • Atypical antidepressants
  • Benzodiazepines
52
Q

Give an example of an SNRI:

A

Venlafaxine

52
Q

Give an example of an SSRI:

A

Sertraline

(Meachanisms covered in depression lecture)

53
Q

Give examples of atypical antidepressants:

A

Vilazodone or mirtazapine

53
Q

When are benzodiazepines (BZs) used?

A

Short term use in a crisis - as they work immediately

54
Q

What are BZs used for?

A

Widely used for insomnia, epilepsy & surgical pre-medication

55
Q

What action do BZs have?

A

They enhance the effects of GABA (main inhibitory NT)

56
Q

How do BZs enhance the effects of GABA?

A
  • Bind to GABA A recpetor between the alpha & gamma subunit
  • Causes a conformational change that enhances GABA binding –> i.e. GABA A receptor positive allosteric modulator (PAM)
  • Channel opening –> Cl- influx, hyperpolarisation, red neuronal activity
57
Q

What are some problems that can occur from use of BZs?

A

Include non-responsiveness in patients

Also impair daily function as they make u DROWSY –> can’t drive or operate hearvy machinery

58
Q

List the novel treatments that are being explored:

A
  • Glutamatergics –> e.g. ketamine, riluzole, xenon
  • Neurosteroids –> e.g. aloradine
  • Cannabinoids
  • MDMA
  • L-Dopa
59
Q

What do existing treatments for GAD generally target vs novel treatments?

A

Existing –> 5-HT & GABA

Novel –> Glutamate, neurosteroids & cannabinoids

59
Q

What are some negative effects of SSRIs?

A

Can cause sexual dysfunction & weight gain

Disease in the brain (22 decks)

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