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Physiology 2 > W11 - Anxiety > Flashcards

W11 - Anxiety Flashcards

1
Q

Is anxiety a normal adaptive response?

A

Anxiety can be defined as a feeling of unease (e.g. worry or fear), which can range from mild
to severe.
Anxiety can be a normal adaptive response and, in some cases, can be beneficial:

1) An innate, adaptive response…
* Fear is an adaptive response to a threatening stimuli
* Fear response comprises several components (e.g. defensive behaviours, autonomic reflexes,
increased alertness)
* Many fears are innate and species specific

2) A learned, adaptive response…
* Fears can also be learned through life experiences (e.g. not touching a hot stove)
* However, fear is not an appropriate response in all circumstances
* Fear response can occur in an anticipatory manner, sometimes independently of stimuli…

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2
Q

When does anxiety become a problem?

A

1) INTENSITY
2) CERTAIN EVENTS OR SITUATIONS

1) INTERMITTENT
2) IRRATIONAL

1) CERTAIN EVENTS OR SITUATIONS
2)CHRONIC

SOCIAL DISTURBANCES
AVOIDANCE BEHAVIOURS
INCESSANT WORRY
CONCENTRATION/MEMORY PROBLEMS

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3
Q

What are some psychological symptoms of anxiety?

A
  • Stress
  • Suspense
  • Worry
  • Foreboding
  • Uneasiness
  • Anxiety
  • Tense
  • Agitated
  • Concern
  • Fearful
  • Angst
  • Apprehension
  • Edgy
  • Nervous
  • Disquiet
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4
Q

What are some physiological symptoms of anxiety?

A

Physiological symptoms can include:
* Tachycardia
* Shortness of breath
* Excessive sweating
* Trembling or shaking
* Headache and dizziness
* Pins and needles
* Gastrointestinal disturbances
* Nausea
* Fatigue
* Insomnia

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5
Q

What can cause the symptoms of anxiety?

A

PAST EXPERIENCES
Difficult experiences in childhood, adolescence (and adulthood) are a common trigger for anxiety:

EVERYDAY LIFE AND HABITS
Current issues or problems in every day life can lead to anxiety: - Money problems and study

DIET
Some types of food and drink can trigger symptoms of anxiety (e.g. sugar, caffeine):
- Crash of blood-glucose levels can cause trembling, anxiety, heart palpitations.
- Caffeine can antagonise adenosine receptors and can lead to anxiety.

PHYSICAL AND MENTAL HEALTH
Physical health problems (e.g. chronic conditions) or mental health conditions (e.g. depression) can trigger or exacerbate anxiety…

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6
Q

What can cause the symptoms of anxiety?

A

ALCOHOL AND DRUGS
Alcohol, prescribed and recreational drugs of abuse can trigger anxiety:

  • Alcohol is a central nervous system (CNS) depressant – increases GABAergic
    neurotransmission and can block glutamatergic neurotransmission
  • Balance between GABA and glutamate crucial for optimal brain function – alcohol disrupts this balance
  • Our brain adapts to counteract this imbalance – leads to low levels of GABA and high levels of glutamate can trigger anxiety symptoms
  • Recreational drugs of abuse (e.g. psychostimulants - increase activity of CNS also disrupts balance of excitatory and inhibitory neurotransmission) can also trigger anxiety
    symptoms via mechanisms unique to a drug or class of drugs
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7
Q

What can cause the symptoms of anxiety?

A

GENETICS?
* Research has linked genetic factors to several anxiety disorders (e.g. panic disorder - GABA, Dopamine, Norepinephrine genes)

  • However, the only clear result that can be derived from genetic studies is that anxiety disorders are not based on a single gene but likely have a complex genetic basis, which can be affected by environmental factors
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8
Q

What is the pathophysiology of anxiety?

A

Hypothalamus -> CRH -> Pituitary -> ACTH -> Adrenal gland -> Cortisol

Hallmark of anxiety disorders is an inappropriate stress response either when a stressor is
not present or not immediately threatening.
The stress response is the co-ordinated reaction to threatening stimuli:
* The stress response is regulated by the hypothalamus-pituitary-adrenal (HPA) axis
* The HPA axis regulates the release of cortisol (a glucocorticoid), which contributes
to the body’s physiological response to stress

It is evident that the activation of CRH-releasing hormones of the hypothalamus play a
key role in regulating the stress response:
* Overexpressing CRH in rodent models lead to
increased anxiety-like behaviours
* Knocking out CRH receptors in rodent models
leads to less anxiety-like behaviours

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9
Q

What is the pathophysiology of anxiety? What roles does the Amygdala and Hippocampus play?

A

AMYGDALA
* Amygdala – role in emotion and fear response
* Stimulates HPA axis (green) to promote cortisol
release
* Amygdala hyperactivity linked to anxiety
disorders

HIPPOCAMPUS
* Hippocampus – role in learning and memory
* Supresses HPA axis (red) to prevent excessive
cortisol release
* Hippocampus underactivity linked to anxiety
disorders
Cortisol is a glucocorticoid, so the hippocampus is sensitive to circulating cortisol - important in the feedback regulation of the HPA axis.

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10
Q

What are DSM-5 2013 classification of anxiety disorders?

A

-ANXIETY DISORDERS
-OBSESSIVE-COMPULSIVE DISORDERS
-TRAUMA AND STRESSOR RELATED DISORDERS

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11
Q

What are anxiety disorders?

A

ANXIETY DISORDERS
* Generalised anxiety disorder (GAD)
* Specific phobias
* Social phobias
* Panic disorder
Other disorders include:
* Substance/medication-induced anxiety disorder
* Anxiety disorder due to a medical condition

OBSESSIVE-COMPULSIVE DISORDERS
* Obsessive-compulsive disorder (OCD)
Other disorders include:
* Body dysmorphic disorder
* Hoarding disorder
* Trichotillomania (hair-pulling disorder)

TRAUMA AND STRESSOR-RELATED DISORDERS
* Post-traumatic stress disorder (PTSD)

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12
Q

What is Generalised anxiety disorder (GAD)?

A

Generalised anxiety disorder (GAD) is characterised by an ongoing state of excessive anxiety lacking clear reason or focus.

  • Excessive anxiety and worry occurring for
    at least six months, which is difficult to
    control and impairs activities of daily
    living
  • Associated with three or more (of six)
    symptoms
  • Not attributable to a substance or
    medical condition or better explained
    by another type of anxiety disorder
  • GAD sufferers’ symptoms likely to be
    different from another person’s
    experience with GAD
    (1) Restlessness
    (2) Fatigue
    (3) Increased muscle aches or soreness
    (4) Impaired concentration
    (5) Irritability
    (6) Difficulty sleeping
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13
Q

What are specific phobias?

A

Specific phobias are extreme fears or anxieties provoked by exposure to a particular situation
or object – often leads to avoidance behaviours.
* Phobic object or situation almost always provokes immediate fear or anxiety – this is out of proportion to the actual danger posed by the object or situation
* Phobia is persistent and typically persists for at least six months, impairing activities of daily living
* Not attributable to a substance or medical condition or better explained by another type of anxiety disorder

Specific phobias:
Eg. Ornithophobia - extreme fear of birds
- Acrophobia - extreme fear of heights
- Trypanophobia - extreme fear of needles

Wide ranging
- Triskaidekaphobia - fear of number 13
- Nomophobia - fear of being without your phone

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14
Q

What are specific phobias?

A

Specific phobias are extreme fears or anxieties provoked by exposure to a particular situation
or object – often leads to avoidance behaviours.

  • Phobic object or situation almost always provokes immediate fear or anxiety – this is out of proportion to the actual danger posed by the object or situation
  • Phobia is persistent and typically persists for at least six months, impairing activities of daily living
  • Not attributable to a substance or medical condition or better explained by another type of anxiety disorder
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15
Q

What are social phobias?

A

Social phobias are characterised by significant anxiety provoked by exposure to certain types
of social or performance situations.

Eg. Social interactions, being observed, performing in front of others.

  • Social phobia may relate to one or more social situations in which the individual is exposed to possible scrutiny by others
  • Includes social interactions, being observed and performing in front of others
  • Social situations almost always provokes immediate fear or anxiety – this is out of proportion to the actual danger posed by the object or situation
  • Phobia is persistent and typically persists for at least six months, impairing activities of daily living
  • Not attributable to a substance or medical condition or better explained by another type of anxiety disorder
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16
Q

What is panic disorder?

A

Panic disorder is characterised by recurring panic attacks, without a seemingly clear cause or
trigger.
* A panic attack is an abrupt surge of intense fear or discomfort, reaching a peak within minutes
* Associated with four or more of thirteen symptoms in accordance with DSM-5:
- Include increased heart rate, sweating,
trembling/shaking, shortness of breath and fear of dying
* Individual worries about further panic attacks – can lead to a panic cycle
* Panic attacks can occur spontaneously or be a feature of a number of anxiety disorders

Panic cycle
Anxiety
Panic attack
Fear of another panic attack
More anxiety
Another panic attack
More fear
Panic cycle

17
Q

What is Obsessive compulsive disorder (OCD)?

A

Obsessive compulsive disorder (OCD) is characterised by compulsive, ritualistic behaviour
driven by irrational anxiety.

Obsessions - Recurrent, intrusive thoughts, images, ideas or impulses

Compulsions -Repetitive behaviours or mental acts that are performed to reduce anxiety associated with the obsessions

  • Obsessions and compulsions are time consuming (e.g. over an hour per day), impairing activities of daily living
  • Not attributable to a substance or medical condition or better explained by another type of anxiety disorder
18
Q

What is Post-traumatic stress disorder (PTSD)?

A

Post-traumatic stress disorder (PTSD) is characterised by distress triggered by the recall of past traumatic experiences.

  • Disturbances persist for at least one-month, impairing activities of daily living
  • Not attributable to a substance or medical condition
  • Triggered by exposure to certain situations – actual or threatened death, serious injury or sexual violence
  • Exposure may be direct, as a witness or learning that a close family member or friend experience the traumatic event
  • Associated with one or more intrusion symptoms:
  • Include recurrent intrusive memories, nightmares, dissociative reactions (e.g. flashbacks) and psychological and physiological distress at exposure to cues resembling the traumatic event
  • Disturbances persist for at least one-month, impairing activities of daily living
  • Not attributable to a substance or medical condition
19
Q

What are the anxiety disorder treatment?

A

PSYCHOLOGICAL
Cognitive behavioural therapy(CBT)

PHARMACOLOGICAL
Anxiolytics

20
Q

What are Anxiolytics?

A

Anxiolytics are a class of drugs used to treat anxiety disorders.
Anxiolytic drug classes include (but are not limited to):
1. BENZODIAZEPINES - GABAA receptor
modulators

  1. 5-HT1A RECEPTOR AGONISTS - 5-HT1A receptor agonists
  2. B -NORADRENERGIC RECEPTOR ANTAGONISTS - B -noradrenergic receptor antagonists
21
Q

How does GABAA receptor: a key target of anxiolytics work?

A

Ligand-gated Cl- channel:

Pentameric structure:
Six a subtypes (a 1–6)
Three B subtypes (B 1-3)
Three Y subtypes (Y1-3)
Also δ ε π θ subunits
2α 2β γ most common configuration

The location of the GABAA receptor is post-synaptic and GABAA is terminated upon reuptake via GABA transporter (GAT).

GABA activity terminated upon reuptake by
GABA reuptake transporter (GAT) GATGAT

Multiple binding sites:

*Agonists/antagonists e.g. GABA - binds between a and B subunits.
*Benzodiazepine binding site - binds between a and Y
*Channel blockers e.g. picrotoxin - poison toxin that can be used as a CNS stimulant is a non-competitive antagonist functioning to block GABAA
*Channel modulators e.g. GA - general anaesthetics are GABAA channel modulators serving to increase GABAA channel openings.

*Allosteric modulators e.g. barbiturates - can be used to treat epilepsy and once used to treat anxiety are no longer recommended due to their addiction and dependency potential, bind at the B subunit of receptor.

22
Q

What is do Benzodiazepines do?

A

Benzodiazepines are a class of GABAA receptor positive allosteric modulators.
* Benzodiazepines bind to a distinct regulatory site on GABAA receptors
* Benzodiazepines stabilise the GABAA receptor binding site for GABA in the open configuration

increase GABA affinity

Potentiating effects of a benzodiazepine
on GABA responses

  • Benzodiazepines therefore increases GABA affinity for its binding site and produces a general enhancement of its neuroinhibitory actions
  • Benzodiazepines are therefore classed as positive allosteric modulators.

Potentiating effects of a benzodiazepine
is restricted to GABA responses

  • Benzodiazepines are “cleaner” compounds compared to the barbiturates – do not activate other receptors (e.g. glycine, glutamate receptors)
23
Q

What is the duration of action of Benzodiazepine?

A

Midazolam - Ultrashort (< 6 hours) - Anaesthetic

Lorazepam Short - (12-18 hours) - Anxiolytic, hypnotic, anti-convulsant

Alprazolam Medium - (24 hours) -Anxiolytic

Diazepam - Long (24-48 hours) - Anxiolytic, anti-convulsant

Benzodiazepines (unlike 5-HT1A agonists and anti-depressants) act quickly and are useful for patients who need acute treatment that can be taken “as needed”.

24
Q

What role do Barbiturates and benzodiazepines have in addiction?

A

Barbiturates and benzodiazepines can be associated with unwanted side-effects (e.g.
amnesia) and can induce tolerance and withdrawal symptoms.

In anxiety disorders labelled Symptomatic:
- There is an imbalance between major inhibitory neurotransmitter GABA and major excitatory neurotransmitter glutamate.
- GABA is often low
- Barbiturates/Benzodiazepines can be prescribed to act as positive allosteric modulators to stabilise the receptors binding site for GABA in the open configuration.
- Increases GABA affinity for binding site and produces a general enhancement of GABA neuroinhibitory reactions.
- Can suppress symptoms of anxiety in some individuals.
- Over time, individuals can develop Tolerance. There is a gradual escalation of dose needed to produce the required effects.
- In part, this is due to the trafficking and insertion of additional glutamate receptors to the cell membrane.
- Serves to restore initial imbalance.
- Individual needs to take a higher dose of benzodiazepines to address new imbalance.

  • If they were to suddenly decrease inhibitory GABA neurotransmission coupled with increased excitatory glutamate neurotransmission. -> leads to heightened anxiety, tremor, dizziness, convulsions
25
Q

What does serotonin do?

A

Serotonin (5-HT) is a neurotransmitter in the peripheral nervous system (PNS) and in the central nervous system (CNS).
* Serotonin activates G-protein coupled receptor sub-types (5-HT1 - 5-HT7), with the exception of a ligand-gated ion channel (5-HT3)

FUNCTION
Important roles in sleep and wakefulness, in
addition to mood and emotional behaviours

DRUG TARGET
A key drug target for depression (e.g. SSRI’s) and
anxiety disorders (e.g. 5-HT1A agonists)

26
Q

What do 5-HT1A receptor agonists do?

A

5-HT1A receptor agonists (e.g. buspirone) are a class of drugs primarily used to treat
generalised anxiety disorder (GAD).

  • Buspirone’s side-effects are less troublesome than benzodiazepines – include dizziness, nausea and headache
  • Buspirone activates 5-HT1A auto-receptors – this inhibits 5-HT release
  • Buspirone also inhibits the activation of noradrenergic neurons – decreases arousal reactions
  • However, a delay of several days before
    anxiolytic effects are seen…
27
Q

What is Buspirone and SSRI?

A

Buspirone:
Activates 5-HT1A auto-receptors – decrease 5-HT
release = Generalised anxiety disorder (GAD)

SSRI’s
Block serotonin re-uptake transporter (SERT) -
more 5-HT available = Long-term anxiety and depression

STOP = If selective serotonin re-uptake inhibitors (SSRIs) are used for long-term anxiety states, how can buspirone be used for generalised
anxiety disorder (GAD)?!?

28
Q

What are the mechanisms of action for Buspirone?

A
  • Buspirone is a 5-HT1A receptor agonist
  • 5-HT1A receptors are auto-inhibitory and, therefore, buspirone initially inhibits 5-HT release
  • However, if buspirone is taken over a period of time (e.g. weeks), buspirone can induce desensitisation of auto-inhibitory 5-HT1A receptors - this can lead to downregulation
    of 5-HT1A receptors
  • The desensitisation and downregulation of 5-HT1A receptors ultimately results in heightened excitation of serotonergic neurons and enhanced 5-HT release
  • Supresses the symptoms of anxiety in generalised anxiety disorder (GAD) – not effective against phobias
29
Q

What does noradrenaline do?

A

Noradrenaline is a neurotransmitter in the peripheral nervous system (PNS) and in the central nervous system (CNS).

  • Noradrenaline activate G-protein coupled receptor subtypes – a -noradrenergic and B -noradrenergic receptors

FUNCTION
* Noradrenaline is the major neurotransmitter
of the sympathetic nervous system (e.g.
cardiovascular tone)
* Noradrenaline also has roles in attention,
arousal and sleep and wakefulness

DRUG TARGET
A drug target for peripheral manifestations of
anxiety (e.g. B -noradrenergic receptor
antagonists)

30
Q

What do B -noradrenergic receptors antagonists do?

A

B -noradrenergic receptor antagonists (e.g. propranolol) are a class of drugs that can be used
to treat some forms of anxiety.

Main effects of receptor activation:
B1:
Increase cardiac rate
Increase cardiac force

B2:
Bronchodilation
Vasodilation
Relaxation of visceral smooth
muscle
Hepatic glycogenolysis
Muscle tremor

  • B -noradrenergic antagonists reduce some of the peripheral manifestations of anxiety
  • Include tachycardia, sweating, gastrointestinal problems and tremor
  • Effectiveness dependent on blocking peripheral
    sympathetic responses (“fight or flight”) rather than CNS effects
  • Propranolol is non-selective between B1 and B2
    noradrenergic receptors
  • Accordingly, find abuse in some sports like darts requiring a steady hand (reduce tremor) and the performing arts (reduce stage fright).

Physiology 2 (39 decks)

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