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OD2 S1 > P: Anxiolytic and Hypnotic Drugs - Week 10 > Flashcards

P: Anxiolytic and Hypnotic Drugs - Week 10 Flashcards

1
Q

Name 6 forms of anxiety disorders

A
  1. Panic Disorder (PD)
  2. Obsessive Compulsive Disorder (OCD)
  3. Post-traumatic Disorder (PTSD)
  4. Phobias
  5. Generalised Anxiety Disorder
  6. Social Anxiety Disorder
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2
Q

Define Panic Disorder.

A

characterised by sudden episodes of overwhelming fear with somatic/physical symptoms (up HR, SOB, sweating)

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3
Q

Define OCD

A

compulsive and ritualistic behaviours as well as purposeless activities driven by irrational fears and thoughts (e.g. fear of contamination)

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4
Q

Define PTSD. Also Define Phobias

A

PTSD = anxiety triggered by recall of past traumatic and stressful experiences

Phobias = intense fears of objects or situations, such as fear of flying, insects or open spaces

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5
Q

Define GAD. Also define Social Anxiety Disorder.

A

Generalised Anxiety Disorder. A feeling of nervousness, tension or worry not associated with a specific event, situation or object

SAD = fear of being with and interacting with people i.e. meeting new people, public performances

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6
Q

Name 4 neurotransmitter systems that anxiety is associated with the dysregulation of

A
  • GABA
  • Serotonin
  • Noradrenaline
  • Dopamine
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7
Q

What would be the most effective therapeutic agent to treat anxiety disorders?

A

One that potentiates GABA and serotonin neurotransmission

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8
Q

What are GABA and glutamate? Where are they found in high concentrations? What do they modify? Are they potent at this?

A

They are amino acid NTs found in high concentrations in the CNS. They are extremely potent modifiers of neuronal excitability

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9
Q

In regards to GABA:
- is it inhibitory or excitatory
- What processes is it involved in? list 4 things

A

GABA is inhibitory. It is involved in memory, motor control, cognition, and consciousness

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10
Q

Name the 2 classes of GABA receptors and explain how they differ

A
  1. GABA-A receptor: is an ionotropic receptor; selectively permeable to Cl-
  2. GABA-B receptor: is a G-protein coupled receptor; inhibit Ca2+ or activate K+ channels
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11
Q

Explain how the binding of the GABA-A receptor works

A

Binding this receptor with GABA triggers the opening of a chloride ion selective pore. Increased chloride conductance (i.e. more -ve ions enter neuron) drives the membrane potential of the neuron to become more -ve and therefore less active (neuronal firing is suppressed)

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12
Q

Give another name for ionotropic

A

ligand-gated

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13
Q

Is glutamate excitatory or inhibitory? List 3 processes it is involved with?

A

Excitatory.
Involved with:
- learning + memory
- growth + development
- modulation of motor function

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14
Q

Name the 4 main receptor families for Glutamate. And state whether these receptors are ionotropic or g-protein coupled

A
  1. AMPA
  2. Kainiic acid
  3. NMDA
  4. Metabotropic

The first 3 are all ionotropic, whereas no.4 (metabotropic) is g-protein coupled

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15
Q

Describe the distribution of Serotonin in our body (3)

A

90% found in the gut
8% in platelets
1-2% in Brain + CNS

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16
Q

What is the function of Serotonin (5HT). What is it implicated in? (9)

A

It is implicated in the regulation of virtually all brain functions incl. mood, perception, anxiety, pain, sleep, temperature, appetite, neuroendocrine control, aggression

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17
Q

How many Serotonin receptors are there? Name them. Are there any subtypes?

A
  1. 5-HT1 – 5-HT7, with subtypes (A-F for 5-HT1 and A-C for 5-HT2)
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18
Q

What 2 classes of drugs can be used in the pharmacological treatment of anxiety disorders? Describe their effects (3, 2)

A
  1. Anxiolytics - relieve anxiety + tension, calm anxious/restless person without impairing consciousness (i.e. don’t induce sleep)
  2. Hypnotics - produce drowsiness, encourage onset and maintenance of a state of sleep
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19
Q

Define Insomnia. How does it differ to anxiety?

A

Is a common clinical manifestation of anxiety but NOT a disease entity

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20
Q

Name 5 Benzodiazepine anxiolytics. Describe their naming convention, what is similar about all their names?

A
  • Alprazolam
  • Diazepam
  • Loraepam
  • Nitrazepam
  • Oxazepam

Note they all end in ‘pam’

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21
Q

What is the mechanism of action for Benzodiazepine Anxiolytics?

A

they potentiate the effects of GABA on GABA-A receptors by binding to benzodiazepine (BZ) site

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22
Q

How can we classify Benzodiazepine Anxiolytics? Rank the 5 drugs in terms of this classification

A

Classify based on half-life
Long = Diazepam
Medium = Alprazolam
Intermediate = Oxazepam
Short = Lorazepam
Ultra-short = Midazolam

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23
Q

List 5 common adverse effects of Benzodiazepine Anxiolytics

A
  1. confusion (esp. older people) (+ memory impair)
  2. drowsiness + impaired coordination
  3. long-lasting hangover effects
  4. tolerance + dependence
  5. suppression of REM sleep
24
Q

How big is the therapeutic window for Benzodiazepine Anxiolytics?

A

Wide therapeutic window (good safety margin)

25
Q

How do Benzodiazepine Anxiolytics affect CV and respiratory system? (3)

A

In healthy consumers: little effect
In pathological states: can cause CVS + respiratory depression
If taken in excess with alcohol or other CNS depressants: lethal

26
Q

Name 3 other CNS depressants. Should you take them in conjunction with Benzodiazepine Anxiolytics?

A
  • opioids
  • anticonvulsants
  • TCA

No you absolutely should not

27
Q

Describe the pharmacokinetics of Benzodiazepine Anxiolytics, in terms of:
A: Absorption level and form of administration
B: What is necessary for clearance?
C: What drugs they interact with and is this good or bad (2)

A

A: Good absorption after oral administration
B: Metabolic transformation (or “biotransformation”) to hydrophilic metabolites is necessary for clearance of this drug
C: Mood stabilisers and SSRIs = reduce the elimination of benzodiazepines. Therefore is BAD and should not be given together

28
Q

Are drug interactions common or rare for Benzodiazepines?

A

common

29
Q

What determines the level of absorption for benzodiazepines?

A

the lipophilicity of the drug

30
Q

What are 4 warnings/precautions for the use of benzodiazepines?

A
  1. do not mix with alcohol
  2. more addictive than heroin
  3. increased risk of falls in older people
  4. can cross placenta + enter breast milk in pregnancy + lactation
31
Q

Why shouldn’t you mix benzodiazepines with alcohol?

A

Leads to additive CNS depression and then death

32
Q

How should you consider the increased risk of falls in older people when taking benzodiazepines? (3)

A

Should “Start low and Go Slow” i.e. start at a low dose of benzodiazepines and then slowly increase. Decrease dose if drowsiness and confusion occur

33
Q

What are the typical withdrawal symptoms for benzodiazepines? (3)

A
  • anxiety + restlessness; shakes
  • rebound insomnia (worse than pre-treatment)
  • weakness, orthostatic hypotension, generalized seizures
34
Q

What are the consequences of a couple of weeks of continuous benzodiazepine use? (2)

A

Tolerance and dependence

35
Q

What is the recommendation for how patients should stop taking benzodiazepines?

A

Gradual dose reduction over around 2 months

36
Q

What is Buspirone? How does it differ from benzodiazepines? (2)

A

Buspirone is a non-bensodiazepine anxiolytic drug with selective anxiolytic effects but a different pharmacological profile compared to benzodiazepines.
Buspirone:
- relieves anxiety without causing marked sensitive/hypnotic effects and euphoria
- lacks muscle relaxant and anticonvulsive properties

37
Q

Describe the mechanism of action for Buspirone. How does this compare to other anxiolytics? (2)

A
  • is a partial agonist at 5-HT1A, and also has affinity for D2 receptors
  • is completely different from other anxiolytics: b/c it has no direct effects on GABA-A
38
Q

Where in the body does Buspirone appear to have no affect on D2?

A

In the basal ganglia (i.e. in subcortical areas of the brain)

39
Q

In regards to Buspirone:
A: Describe how liable this drug is to abuse
B: how long may its anxiolytic effects take to become established? What does this infer?
C: Describe the speed of absorption after oral administration

A

A: Minimal abuse liability: no rebound anxiety or withdrawal syndrome
B: anxyiolytic effects may take 3-4 weeks to become established (therefore this drug is not useful for acute anxiety states)
C: Rapid absorption

40
Q

What are the adverse effects of Buspirone? Compared to other anxiolytics? (2)

A
  • less psychomotor impairment and does not affect driving [that’s good!]
  • dizziness, headache, GI upset [that’s bad!]
41
Q

What type of metabolism does Buspirone undergo?

A

Extensive first-pass hepatic metabolism

42
Q

What condition might slow the clearance of Buspirone?

A

Liver dysfunction

43
Q

Name 2 short acting benzodiazepine hypnotics and 2 short-acting relating compounds

A

benzodiazepine hypnotics:
- Lorazepam
- Temazepam
Related compounds:
- Zopiclone
- Zolpidem

44
Q

Describe the pharmacodynamics of Benzodiazepine Hypnotics

A

enhance GABA transmission by binding to a “BZ” site within GABA-A receptor; this is complex and not completely understood.

45
Q

What are the roles of the 3 BZ sites?

A

BZ1 = mediates hypnotic effects (sleep)
BZ2 = mediates muscle relaxant effects (motor function)
BZ3 = mediates anxiolytic effects

46
Q

What are the adverse effects of Benzodiazepine Hypnotics? (2)

A

Broken sleep (particularly with temazepam)
suppress REM sleep; rebound insomnia (after abrupt cessation)

47
Q

Describe the mechanism of action for Zoplicone and Zolpidem (2)

A

Increase GABA transmission by selective binding to BZ1; lacks binding at BZ2 or BZ3

48
Q

Does Sopiclone and Zolpidem suppress REM sleep?

A

No

49
Q

How do the adverse effects of Zopiclone and Zolpidem differ from benzodiazepines? (4)

A

Zopiclone and Zolpidem can cause hallucinatory and/or psychotic features and sleep-related events such as sleep walking and sleep driving

50
Q

List 5 other prominent adverse effects of Zoplicone and Zolpidem

A

binge eating + weight gain
QT interval changes
drowsiness
dizziness
confusion

51
Q

What is a QT interval?

A

The time in ECG between from the beginning of the QRS complex, representing ventricular depolarisation, to the end of the T wave, resulting from ventricular repolarisation

52
Q

Describe the Pharmacokinetics of Zopiclone and Zolpidem (2)

A

Rapid sleep onset may be delayed by food; undergoes lipid metabolism

53
Q

In what scenarios may the pharmacokinetics of Zopiclone and Zolpidem be altered? (3)

A

Older people and clients with renal or hapatic disease

54
Q

Are SSRIs and SNRIs (antidepressants) approved for anxiety disorder treatment?

A

Yes. For all anxiety disorders

55
Q

What is the advantage of antidepressants over benzodiazepines?

A

Antidepressants no not carry the risk of dependance and tolerance that occur with the benzodiazepines

56
Q

What type of antidepressant is a first line treatment for PTSD?

A

SSRIs

57
Q

What form of anxiety disorder is quetiapine useful for?

A

Generalised Anxiety Disorder (GAD)

OD2 S1 (47 decks)

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