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Year 2 Foundations in Clinical Practice 1 > Anxiety > Flashcards

Anxiety Flashcards

1
Q

part of the brain that processes fear

A

the amygdala

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2
Q

what is anxiety

note anxiety is not the same as fear

A

It is an unpleasant emotional state, often with inner turmoil accompanied by nervous behaviours, psychosomatic symptoms and rumination

Anxiety is not a response to a real or perceived immediate threat but rather is the expectation of future threat.

it is considered normal behaviour but when easily triggered may give rise to anxiety disorder

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3
Q

what does stress do to cortisol levels. and which part of the adrenal gland is cortisol produced from

A

raises cortisol levels

produced from the adrenal cortex

stress is a trigger to both depression and anxiety

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4
Q

some examples of anxiety and fear disorders

A

Generalised anxiety disorder (often with depression)
Social anxiety disorder (social phobia)
Specific phobic disorders (e.g. arachnophobia)
Panic attacks
Post-Traumatic Stress Disorder
Obsessive Compulsive Disorder

women are more affected in all of these than men(according to slides not me )

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5
Q

what do you know about generalised anxiety disorders

A

a chronic condition that causes excessive and uncontrollable worrying about everyday things

it is longterm

it entails anxiety about a wide range of situations

causes include childhood trauma or trauma in general , family history, stress…etc

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6
Q

some examples of phobias and their descriptions

A

Arachnophobia(fear of spiders)
Agoraphobia(fear of public places/ open spaces)
Acrophobia (fear of heights)
Claustrophobia (fear of confined places)
Social phobia (fear of social interactions)

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7
Q

panic disorder and what you know about it

A

Recurrent,sudden attacks of intense fear

Often associated with somatic symptoms, e.g.
- Tachycardia
- Sweating
- Shaking
- Shortness of breath

somatic symptoms are physical symptoms that are caused by emotional distress.

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8
Q

during stress which is released first, adrenaline or cortisol

A

adrenaline

cortisol is released after adrenaline, when the immediate stress has passed. it Increases blood sugar levels
Helps your body use fats, proteins, and carbohydrates for energy

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9
Q

the HPA axis and what happens in it

A

hypothalamic-pituitary-adrenal (HPA) axis

When the body senses a stressor, the hypothalamus releases** corticotropin-releasing hormone (CRH)** and arginine vasopressin (AVP)

These hormones travel to the pituitary gland, where they trigger the release of adrenocorticotropic hormone (ACTH)

ACTH activates the adrenal glands to produce glucocorticoids, like cortisol in humans

Glucocorticoids affect metabolism, immunity, and behavior

the HPA axis can lead to hypervigilance

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10
Q

is norepinepherine released during fight anf flight(stress)

A

yes it is, to aid adrenaline action

it is an excitatory neurotransmitter

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11
Q

the brain is mainly made up of which molecule

A

fat , makes up 60% of the brain

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12
Q

what is OCD

A

Obsessive-compulsive disorder (OCD) is a mental health condition that causes people to have unwanted, recurring thoughts and repetitive behaviors

example, people might be OBSESSED with the fear of contamination, thereby leading to COMPULSIONS like the repetitive washing of their hands

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13
Q

the amygdala is the activated part of the brain when there is fear

during anxiety what happens to levels of neuronal activity in the amygdala

A

there is increased neuronal activity

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14
Q

the lymbic system

A

The limbic system is a group of interconnected brain structures that help regulate your emotions and behavior.

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15
Q

describe PTSD

A

post-traumatic stress disorder
refers to anxiety based on the recall of past disturbing experiences

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16
Q

what does it mean to make memories “labile”, and how does this link PTSD

A

To make memories labile means to make them unstable, flexible, or susceptible to change(i.e they cacn be weakened or strengthened)

note that stored memories become labile when recalled

This process is important in PTSD therapy—if traumatic memories are made labile, they can be altered to reduce their emotional impact.

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17
Q

Obsessive-compulsive disorder (OCD) and post-traumatic stress disorder (PTSD) are closely related to anxiety disorders, which some may experience at the same time, along with depression, true or false

A

true

note that it is important to be treated for both OCD and PTSD if one is indicated in a patient, as they often occur together

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18
Q

treatment options in anxiety

A

Cognitive and Behavioural Therapy
Pharmacological
Alternative treatments

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19
Q

there is reduced PFC stimulation in anxiety disorders, true or false

A

true, research has shown this

note the amygdala is regulated by the PFC, so reduced PFC stimulation leads to dysregulation , which could lead to amygdala overactivation, leading tgo anxiety disorders

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20
Q

some effects of the amygdala being overactivated

A

exaggerated fear response

hypervigilance

persistent negative thoughts and excessive worry

poor emotional regulation…etc

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21
Q

what happens if an individual experiences anxiety, and avoids it

what abt if it is not avoided

A

it continuously worsens over time

it will worsen in the early stages, them plateau, and eventually the levels decrease to normal

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22
Q

what is tehe aim of cognitive behavioural therapy, and how long does it take to seee any benefits

A

focuses on identifying, understanding, and changing thinking and behavior patterns. it ensures patients are actively involved in their own treatments

12-16weeks. note that the duration is dependent on the individual.

note consistency is required for this treatment option to work

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23
Q

some CBTs used in anxiety
treatment

A

exposure therapy

acceptance and commitment therapy

Eye movement desensitization and reprocessing (EMDR)

24
Q

describe exposure therapy

A

a form of CBT, it is a process for reducing fear and anxiety responses by phenomena like sensitization and
extinction

A person is gradually exposed to a feared situation or object, learning to become less sensitive over time
This type of therapy has been found to be particularly effective for obsessive-compulsive disorder and phobia

25
describe acceptance and commitment therapy(ACT)
uses strategies of acceptance and mindfulness as a way to cope with unwanted thoughts, feelings, and sensations. ACT imparts skills to accept these experiences, place them in a different context
26
describe how eye movement desensitization and reprocessing works
The person recalls the traumatic memory in detail While recalling the memory, they follow a back-and-forth movement or sound with their eye The person then pays attention to shifts in how they experience the memory ## Footnote EMDR directly linked to REM sleep and memory consolidation effective for PTSD, panic attacks, other phobias
27
EMDR is directly linked to REM sleep and memory consolidation, true or false
true
28
name some pharmacological treatments for anxiety
Benzodiazepines ((alprazolam, clonazepam, diazepam, and lorazepam) ) SSRIs (citalopram, escitalopram, fluoxetine, paroxetine, and sertraline) SNRIs( Serotonin-Norepinepherine Reuptake Inhibitors ) (venlafaxine and duloxetine) Tricyclic Antidepressants (amitriptyline, imipramine, and nortriptyline)
29
Benzodiazepines should be used longterm for anxiety, true or false
false, they should be used short term ## Footnote Long-term use may require increased doses to achieve the same effect, which may lead to problems related to tolerance and dependence
30
how do SSRIs work in anxiety
SSRIs relieve symptoms by blocking the reuptake of serotonin by certain neurons. This leaves more serotonin available which improves mood. SSRIs (citalopram, escitalopram, fluoxetine, paroxetine, and sertraline) generally produced fewer side effects when compared with tricyclic antidepressants.
31
how do SNRIs work in anxiety treatment
SNRI (venlafaxine and duloxetine) possess a dual mechanism of action: they increase the levels of both serotonin and norepinephrine by inhibiting their reabsorption.
32
first line treatment for generalised anxiety disorders
SNRIs
33
which between benzodiazepines and tricyclic antidepressants are preferred anti-depressants and why
tricyclic antidepressants preferred, as they cause much less dependence compared to benzodiazepines
34
how do benzodiazepines work in anxiety treatment
they promote relaxation and reducing muscular tension and other physical symptoms of anxiety.
35
name the neutranmitters implicated in anxiety
Gamma-Aminobutyric acid (GABA) ➢ Serotonin ➢ Noradrenaline ➢ Dopamine ➢ Corticotrophin-releasing hormone
36
what is meant by fear response
A "fear response" in anxiety refers to the physical and physiological reactions the body experiences when perceiving a threat, even if it's not immediately present, essentially preparing the body to "fight or flight" by activating the autonomic nervous system, which can manifest as symptoms like increased heart rate, rapid breathing, muscle tension, and sweating; this response is closely linked to anxiety as it often arises from worries about potential future dangers, not just immediate threats like in a typical fear reaction.
37
how does the body react to fear response
As a feedback system, inhibitory neurons release GABA Receiving neurons are signalled to stop firing The neuronal inhibition is perceived as “staying calm” ## Footnote GABAergic neurotransmission
38
the role of GABA in anxiety
GABA is an inhibitory neurotransmitter in the nervous system and its receptors are on most CNS cells, it exerts widespread inhibitory effects via the GABA A receptor, which is a **chloride channel **
39
during anxiety, what happens to the rate at which neurons fire APs
Key neurons in the brain and body fire more rapidly , creating a state of excitability throughout the brain and body.
40
MoA of Barbiturates
Enhance GABAA action by increasing affinity of GABAA receptor for GABA, Increasing the duration of the opening of GABA activated chloride channel they also Directly open chloride channel without GABA ## Footnote Barbiturates largely replaced by Benzodiazepines due to their side effects
41
the flow of chloride ions through the cell membrane creates inhibitory effects, true or false
true
42
some adverse effects of barbiturates
Altered sleep pattern(falling asleep more rapidly ) Cognitive effects like mental clouding, impaired thinking, slowed reflexes.. increased microsomal enzymes in the liver(can have numeroud effects , like making patient more tolerant to the drug, and reducing the effectiveness of the drug) ## Footnote increased microsomal enzymes in the liver causes a more rapid breakdown of the drug/active metabolite
43
MoA of benzodiazepines
they target the GABA A receptor, by binding **allosterically** to it, increasing it's affinity for GABA. Increases probabilty of chloride channel opening Note that they have no affinity for the GABA binding sites, which is why theu bind allosterically
44
list some therapeutic uses for benzodiazepines
Reduction of anxiety and aggression Sedation - improvement of insomnia, E.g. nitrazepam is most widely used, with fewer negative side effects * Muscle relaxation and in loss of motor coordination * Suppression of convulsions (antiepileptic effect), e.g. clonazepam
45
some major adverse effects of benzodiazepines
**acute overdose can cause respiratory and cardiovascular depression(just like barbiturates), so can be used for suicide** side effects like anterograde amnesia(similar for barbs. as well), drowsiness, confusion...etc patient might build tolerance to it
46
advantages of benzos. over barbs.
benzos do not induce liver enzymes, and have less reaction with alcohol relative to barbs
47
name the neurotransmitters that benzos reduce the release of
Noradrenaline Serotonin Dopamine
48
which serotonin receptor is heavily implicated in anxiety
5-HT1A receptor
49
what role does serotonin play in anxiety ## Footnote think about the normal serotonin functions and apply that to this
Low serotonin levels lead to increased amygdala reactivity, making individuals more prone to anxiety. Low serotonin impairs PFC regulation of emotions and fear extinction, allowing anxiety to take over. Low serotonin leads to higher cortisol levels, which worsens anxiety symptoms Serotonin plays a role in neuroplasticity, helping the brain "unlearn" fears through exposure, guess what low levels do haha. This is why SSRIs are used in anxiety treatment etc..
50
MoA of Buspirone
**They are Serotonin 5-HT1A receptor partial agonists( need absolutely to remember this)** Also dopamine D2, a1, and a2-adrenergic receptor antagonists
51
advantages of buspirone
Desensitizes 5-HT1A autoreceptors, increasing 5-HT transmission Significant anxiolytic action used to treat GAD, panic disorder and OCD Minimal severe side effects and no fatalities have been reported; thus * No sedation, confusion or mental clouding * Does not enhance CNS depressant effect of alcohol or other CNS depressants * Little or no potential of recreational use or dependence * No rebound withdrawal syndrome ## Footnote Autoreceptors are part of a **negative feedback loop **in signal transduction
52
disadvantages of buspirone
takes quite long to be effective(long onset time Less effective in reducing physical symptoms of anxiety than the cognitive aspects of worry and poor concentration Lack of hypnotic effects - Necessary to treat insomnia Has no muscle relaxant effect and does not control seizures
53
are barbiturates still in used for anxiety
no
54
the link between levels of noradrenaline and anxiety
**increased **NA levels linked to PTSD, and therefore anxiety
55
name of the cells that produce NA (noradrenaline) IN THE BRAIN
Locus coeruleus(LC) cells
56
alpha 2 receptors inhibit NA release, true or false ## Footnote think about how this might be beneficial in anxiety
true
57
name some drugs that target NA release, used in anxiety
Clonidine(an alpha2 autoreceptor agonist)-decreases presynaptic calcium levels, leading to NA release inhibition beta blockers like Propranolol- reduces physical symptoms of anxiety ## Footnote beta blockers directly block NA effects

Year 2 Foundations in Clinical Practice 1 (22 decks)

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