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Stage 3 - Case 2 (Central Nervous System) > Lecture 3 & 4: Anxiety And Insomina Pathiophysiology, Pharmacology & Pharmaceutical Care > Flashcards

Lecture 3 & 4: Anxiety And Insomina Pathiophysiology, Pharmacology & Pharmaceutical Care Flashcards

1
Q

What is anxiety?

A
  • Anxiety is a feeling of worry, tension, or fear about potential or upcoming events, often with an imprecise or unknown threat.
  • Anxiety can manifest in various forms and intensities, affecting daily life and functioning.
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2
Q

How is anxiety different from fear?

A
  • Anxiety involves an imprecise or unknown threat, while fear involves a known or definite threat.
  • This distinction is crucial in understanding emotional responses and treatment approaches.
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3
Q

What are three types of symptoms of anxiety?

A
  • Behavioral: Avoidance behaviours, Overly attached
  • Psychological: Restlessness, Difficulty concentrating, irritability
  • Physical: Fatigue,Muscle aches, insomnia
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4
Q

Name some types of anxiety disorders.

A
  • Generalized Anxiety Disorder (GAD)
  • Panic Disorder
  • Social Anxiety Disorder.
  • Specific Phobias
  • Post traumatic stress disorder
  • Obsessive Compulsive Disorder
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5
Q

What are the first-line pharmacological treatments for anxiety?

A
  • Selective Serotonin Reuptake Inhibitors (SSRIs)
  • Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs).

These medications are often preferred due to their efficacy and safety profile.

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6
Q

What neurotransmitter systems are targeted in anxiety treatment?

A

Serotonin, noradrenaline, and GABA systems.

Targeting these systems helps regulate mood and anxiety levels.

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7
Q

What are common side effects of SSRIs?

A

Insomnia, nausea, dizziness, sexual dysfunction, serotonin syndrome (high doses) (can affect GI & CNS), hyponatraemia

Understanding side effects is important for patient management and adherence.

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8
Q

What are the advantages of benzodiazepines?

A

Quick onset of action.

This makes benzodiazepines effective for acute anxiety episodes.

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9
Q

What is the disadvantage of long-term benzodiazepine use?

A

They are highly addictive and can impair cognitive function and have withdrawal symptoms w/ long term use.

Long-term use is generally discouraged in favor of other treatment options.

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10
Q

What does Pregabalin target?

A
  • Similar effect to Benzos
  • Modulation of neurotransmitter release: Binds to alpha-2-delta subunit on voltage gated Ca2+ channels
  • Reduces release of excitatory neurotransmitters such as glutamate and norepinephrine

Pregabalin is used to treat anxiety and neuropathic pain.

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11
Q

What is insomnia?

A

Difficulty falling asleep or staying asleep, often leading to fatigue during the day.

Insomnia can significantly impact quality of life.

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12
Q

Name causes of insomnia.

A
  • Stress and psychiatric conditions like depression.
  • Other medical conditions: Alzheimers and Parkinsons
  • Medication: SSRIs & MAOIs

Identifying underlying causes is essential for effective treatment.

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13
Q

What brain circuits regulate sleep?

A
  • Wake-promoting circuits (neurons releasing serotonin, noradrenaline, dopamine, acetylcholine & histamine)
  • NREM-promoting circuits: Neurons releasing GABA in the forebrain
  • REM-promoting circuits: Neurons releasing GABA in the brainstem

The interplay of these circuits is complex and crucial for healthy sleep patterns.

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14
Q

Name some pharmacological treatments for insomnia.

A
  • Z drugs (e.g., Zolpidem) not benzos but have similar mechanisms
  • Prolonged-release melatonin.
  • Daridorexant: inhibits actions of wake promoting orexin
  • Antihistaminergic drugs

These medications target different aspects of sleep regulation.

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15
Q

What is the mechanism of action of Zolpidem?

A
  • Binding Site: Zolpidem binds to GABA-A receptor unlike benzodiazepines, which can bind to a variety of subtypes of GABA-A receptors, zolpidem has a more selective affinity for a specific subset of GABA-A receptors that contain the alpha-1 subunit.
  • Zolpidem’s high selectivity for the alpha-1 subunit is why it has a stronger sedative effect with less impact on other cognitive functions
  • Allosteric Modulation: When binds to the alpha-1 subunit of the GABA-A receptor, it enhances the effect of GABA. This increases the opening of the chloride ion channel, allowing more chloride ions to flow into the neuron. The influx of chloride ions hyperpolarizes the neuron, making it less likely to fire.
  • This hyperpolarization results in overall CNS depression, leading to the sedative and hypnotic effects of zolpidem, which help promote sleep in individuals with insomnia.

Zolpidem enhances the effect of GABA, promoting sleep.

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16
Q

Why were barbiturates (that can be used for insomnia) replaced with benzodiazepines?

A

Barbiturates have a narrow therapeutic dosage range and a high risk of overdose.

Benzodiazepines are considered safer alternatives with a better therapeutic index.

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17
Q

What is the stress response system?

A
  • Hypothalamus releases CRH
  • Causes pituitary gland to release ACTH
  • Goes to adrenal gland (on top of kidney) and causes the release of cortisol
  • Hypothalamus responds to the level of cortisol
18
Q

What does the stress response system cause?

A
  • Mobilisation of energy
  • Increased cardio tone
  • Suppression of digestion and growth
  • Alter the immune system
19
Q

What are the different treatment strategies used in anxiety?

A
  • Changes in lifestyle (quit smoking, reduce alcohol, physical exercise)
  • Self help
  • Psychotherapy (CBT)
  • Pharmacotherapy: 6-12 months/ combination or switch
20
Q

What is second line treatment for anxiety?

A
  • Benzodiazepines
  • Pregabalin
21
Q

What are other treatments that can be used for anxiety?

A
  • Tricyclic antidepressants (TCAs)
  • 5 HT1A agonist (Buspirone)
  • Monoaminoxidase inhibitors (MAOIs)
22
Q

What is the mechanism of SSRIs

A
  • Serotonin Release: Released from presynaptic neuron. Transmit signals related to mood, anxiety, and behavior.
  • Reuptake Process: After serotonin is released into the synaptic gap, it binds to receptors on the post-synaptic neuron. Serotonin is usually reabsorbed into the presynaptic neuron via a transporter protein called the serotonin transporter (SERT) (reuptake).
  • SSRIs Block Reuptake: SSRIs work by inhibiting or blocking the serotonin transporter (SERT). This blockage reduces the reuptake of serotonin, leaving more serotonin available in the synaptic gap.
23
Q

Why do SSRIs have a delay period of 4-6 weeks?

A
  • Serotonin binds to auto receptors which stops the firing of activation of neurons
  • This inhibits further release of serotonin -> negative feedback
  • After 4-6 weeks auto receptors are desensitised and stop the negative feedback process-> affect of drug starts
24
Q

What are examples of SSRIs?

A
  • Citalopram
  • Fluoxetine
  • Paroxetine
  • Sertraline
25
Q

What are the Advantages of SSRIs?

A
  • Effective against different anxiety disorders
  • Long lasting effects
  • Less addictive than benzodiazepines
  • Potent antidepressants w/ fewer side effects
26
Q

What are the Disadvantages of SSRIs?

A
  • Delay period
  • Health issues if taken w/ other drugs (alcohol, NSAID)
  • SSRIs can increase the risk of suicidal thinking and self-harm in patients under 30.
27
Q

What is neuroplasticity?

A
  • Ability of the brain to change its activity in response to intrinsic or extrinsic stimuli by reorganising its structure, functions or connections
  • Increasing serotonin and noradrenaline may promote flexibility and make the brain more capable of changing
  • Change brain to resist anxiety more adaptable
28
Q

What is the mechanism of Benzodiazepines?

A
  • GABA is the primary inhibitory neurotransmitter in the brain, meaning it reduces neuronal excitability and dampens overall brain activity & binds to GABA receptors.
    The main subtype GABA-A receptor for Benzo action.
  • Allosteric Modulation: Benzodiazepines don’t directly activate GABA-A receptors, they bind to a specific site on the GABA-A receptor (a site distinct from where GABA itself binds) in a process called allosteric modulation. This enhances the effect of GABA (receptor more responsive to GABA)
  • Increased Chloride Ion Influx: Causes the receptor to open and allows chloride ions (Cl-) to flow into the neuron. This influx of chloride ions hyperpolarizes the neuron, making it less likely to fire an action potential (a signal). stronger inhibition of neuronal activity, which produces the calming and sedative effects associated with benzodiazepines.
  • Resulting Effects:
    – Anxiolysis: Reduction of anxiety due to decreased activity in regions of the brain involved in stress and fear (e.g., the amygdala).
    – Sedation and Hypnotic Effects: Depresses CNS.
    – Muscle Relaxation: Reduce muscle tone
    – Anticonvulsant Effects: controlling seizures.
29
Q

What are tricyclic antidepressants also antagonists of?

A
  • Various serotonin receptors
  • a1 adrenergic receptors
  • Histamine receptor
  • Muscarinic cholinergic receptor
30
Q

What are the main side effects of tricyclic antidepressants?

A
  • Dry mouth
  • Sedation
  • Weight gain
  • Constipation
  • Dizziness
  • Heart rhythm problems
31
Q

What are some treatment strategies for insomnia?

A
  • Changes in sleep patterns and/or lifestyle
  • Tackle stress/ anxiety
  • Psychotherapy (CBT)
  • Pharmacotherapy (short term less than 3 months)
32
Q

What are some risk factors for insomnia?

A
  • Stress
  • Caffeine
  • Sleep hygiene (mindfulness, position)
33
Q

Why is diazepam not the most appropriate choice for short term insomnia and name some councelling points?

A
  • Diazepam is a long-acting benzodiazepine, increasing the risk of daytime hangover effects. Short-acting benzodiazepines like temazepam, lormetazepam, or loprazolam are preferred for insomnia to minimize this risk.
  • Risk in pregnant women (lipohilic drug (penetrate brain)
  • Short term course (addictive)
  • Risk in elderly (risk of falls and lightheadedness)
34
Q

What are 2 over the counter remedies for insomnia?

A
  • Antihistamines like diphenhydramine (found in Nytol) repeated requests indicate chronic, medication interactions
  • Valerian root extract, which has mild sedative effects.
35
Q

What are 3 characteristics of General Anxiety Disorder (GAD)

A
  • GAD is characterized by disproportionate, pervasive, and uncontrollable worry
  • a range of somatic, cognitive, and behavioral symptoms
  • varying severity.
36
Q

What are some complications of untreated GAD?

A
  • reduced quality of life
  • impaired social and occupational functioning
  • comorbidities like depression
  • increased risk of suicidal ideation and attempts.
37
Q

How do you diagnosis GAD

A
  • International Diagnostic Criteria (DSM-V/ ICD-10)
  • Physical symptoms
  • Risk factors
  • GAD-7 (7 questions & count score)
38
Q

What is Step 1 of treatment of GAD

A
  • Assess severity
  • Mental health history
  • Active monitoring
39
Q

What is Step 2 of the treatment of GAD

A
  • Low intensity psychological interventions (CBT)
40
Q

What is Step 3 & 4 of the treatment of GAD

A
  • High intensity CBT
  • Drug therapy: 1st line SSRI/ SNRI
  • Review every 2-4 weeks
41
Q

What are examples of SNRIs and name some side effects?

A
  • Duloxetine and Venlafaxine
  • Caution in a range of conditions: bleeding disorders, history of seizures
  • Adverse effects: Nausea, dizziness, dry mouth

Stage 3 - Case 2 (Central Nervous System) (10 decks)

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