VC - Anxiety Flashcards

1
Q

What are the biological pathways associated with Depression and Anxiety?

A

Depression: Mood pathway
Anxiety: Fear pathway

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2
Q

What is the definition focus for Depression vs. Anxiety?

A

Depression: Symptoms and duration of time are reported

Anxiety: Symptom classification and self-reporting

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3
Q

What brain pathways are involved in Depression and Anxiety?

A

Depression: Circuit level connectivity

Anxiety: Circuit level connectivity (including the amygdala)

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4
Q

What is the primary transmitter pathway associated with Depression and Anxiety?

A

Depression: Monoamines
Anxiety: GABA

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5
Q

What is the molecular target in the treatment of Depression and Anxiety?

A

Depression: Transmitter transporter

Anxiety: Inhibitory GABA receptor

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6
Q

What are the clinical confounds associated with treating Depression vs. Anxiety?

A

Depression: Side effects

Anxiety: Withdrawal and addiction

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7
Q

How is fear (4) distinguished from anxiety (3)?

A

Fear
* Physiological response
* Adaptive survival mechanism
* Context-appropriate

Anxiety
* Pathological
* Maladaptive response
* Context-inapproriate; responds to neutral/ambiguous cues

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8
Q

What is the physiological response in fear (5)?

A
  • Hyper-arousal
  • Increased heart rate
  • Heightened sensory awareness
  • Fight-or-flight response
  • Enhanced metabolic readiness
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9
Q

What are the symptoms of anxiety as a pathophysiological state (6)?

A
  • Increased heart rate
  • Decreased salivation
  • GI disturbances
  • Hypervigilance
  • Heightened startle response
  • Autonomic symptoms
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10
Q

What are the similarities between fear and anxiety (5)?

A
  • Both involve learning mechanisms and can be acquired through direct experience or observational learning.
  • Each uses neuromodulatory pathways and involves cognitive processing.
  • Both activate the autonomic nervous system, leading to physiological responses like increased heart rate and heightened alertness.
  • Memory systems influence both, affecting how past experiences shape responses.
  • Can lead to behavioral modification as individuals adapt or avoid perceived threats.
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11
Q

What are examples of anxiety disorders (9)?

A
  • Panic attack,
  • Agoraphobia
  • Panic disorder
  • Specific phobia
  • Social phobia
  • OCD
  • PTSD
  • Acute stress disorder
  • Generalised anxiety disorder
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12
Q

What are animal models used in fear/anxiety research?

A

Fear Conditioning: Context and signal-based fear responses (e.g., freezing, heart rate measurement)

Purpose: To mimic human responses and assess fear circuits via contextual and sensory cues

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13
Q

Explain context conditioning in fear response.

A

Unsignaled Conditioning: An animal is placed in a blue box and receives an electric shock, causing a fear response. When placed in a different (purple) cage, no fear response occurs.

Signaled Conditioning: A bell rings right before an electric shock, creating an association between the sound and the shock. Later, even in a cage without shocks, the bell alone triggers a fear response.

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14
Q

How does the amygdala contribute to fear response (4)?

A
  • Integrates information to create emotional response
  • Links with hypothalamus, hippocampus, orbital cortex, etc
  • Supports associative learning in fear circuitry
  • There are both negative and positive modulations of the core fear centre
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15
Q

What roles do the Orbital cortex, Hippocampus, Central amygdala and Striatum play in fear and anxiety responses?

A
  • Orbital Cortex: Involved in choice behavior and emotional memory
  • Hippocampus: Responsible for learning and spatial memory
  • Central Amygdala and Bed Nucleus of the Stria Terminalis: Controls autonomic responses and attention
  • Striatum: Associated with avoidance behavior
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16
Q

What is the preferred treatment order for anxiety (5)?

A
  1. SSRIs (increase serotonin)
  2. Tricyclic antidepressants (increase serotonin, noradrenaline)
  3. Benzodiazepines (GABA potentiation)
  4. Anticonvulsants (e.g., valproate)
  5. Monoamine oxidase inhibitors (increase serotonin; less favored)

Drug treatment now commonly supported by Cognitive Behavioural Therapies encompassing relaxation approaches.

17
Q

How do benzodiazepines function (5)?

A
  • Act on GABA receptors as allosteric modulators
  • Increase chloride influx, causing membrane hyperpolarization
  • Affect GABA channels only when GABA is bound
  • Agonists increase flux (anxiolytic)
  • Inverse agonists decrease flux (anxiogenic)
18
Q

What are the successes (4) and limitations (3) of benzodiazepines (BZ)?

A

Successes:
* Rapid-acting: Provides quick relief, unlike SSRIs which take 8-12 weeks.
* Acts as an anxiolytic, sedative, hypnotic, and muscle relaxant through different GABA receptor types.
* Broad receptor expression: Affects GABA receptors throughout the brain, including in the amygdala.
* High efficacy with limited toxicity compared to barbiturates.

Limitations:
* Can cause amnesia with prolonged use.
* Tolerance and withdrawal issues, leading to dependence.
* Primarily used for short-term or acute treatment.

Often tapered off gradually and combined with SSRIs for long-term management.

19
Q

What are some non-drug therapies for anxiety (4)?

A

Psychoanalysis: Explores unconscious mind (mixed evidence)

Mindfulness: Focus on present; meditation affects brain state (mixed outcomes)

Cognitive Behavioral Therapy: Organizes thought processes (evidence of brain activity changes)

Family Therapy: Addresses life events and social context (variable outcomes)