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Pharmaco > Class 6- anxiety > Flashcards

Class 6- anxiety Flashcards

1
Q

COMMON CORE OF ANXIETY DISORDERS

A

The amygdala is responsible for the physiological reactions of fear and anxiety.
Cortico-cortical loops are responsible for the «worry».
The hippocampus is important in the formation of affective memory. It also contributes to the genesis of
anxiety symptoms

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2
Q

AMYGDALA Hyperactivity =

A

Physiological reactions of fear and anxiety

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3
Q

CORTICO-CORTICAL LOOPS Hyperactivity =

A

Worry

Ruminations

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4
Q

TREATMENT OF ANXIETY

CHOOSE ACCORDING TO :

A
  • Patient preferences
  • Motivation and ability to engage in treatment
  • Severity of the disease
  • Availability of psychological treatments
  • Previous response to treatment
  • Comorbidities
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5
Q

NON-PHARMACOLOGICAL

MEASURES

A
  • Stress Management Strategies
  • Avoid caffeine or alcohol consumption
  • Avoiding the use of substances that can cause anxiety
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6
Q

THERAPEUTIC ARSENAL

A 
v Antidepressants
v Benzodiazepines
v Antipsychotics
v Anticonvulsants
v Buspirone
v Prazosin
v Hydroxyzine
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7
Q

ANTIDEPRESSANTS

A

q Selective serotonin reuptake inhibitors (SSRIs)
q Serotonin and norepinephrine reuptake inhibitors (NSRI)
q Bupropion
q Mirtazapine
q Tricyclic antidepressants (ATC)
q Monoamine oxidase inhibitors (IMAO)
Not all antidepressants have the official indication of all anxiety disorders, but they are well studied and used in a clinic

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8
Q

ANTIDEPRESSANTS

MECHANISM OF ACTION (IN ANXIETY)

A
  • Serotonin is an inhibitory neurotransmitter in some anatomical structures, including the cerebral cortex and limbic system including the amygdala and hippocampus;
  • Antidepressants increase inhibitory serotonin discharges to the amygdala;
  • This will also slow down the activity of all anxiety-causing brain structures that have a relay in the amygdala
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9
Q

ANTIDEPRESSANTS

* AT THE BEGINNING OF THE TREATMENT *

A
  • Decrease in neuronal discharges secondary to stimulation of 5-HT1A receptors
  • Anxiety can be increased at the beginning of treatment
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10
Q

5-HT1A RECEPTOR

A
  • Pre-synaptic receptor

* Brake on serotonin release

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11
Q

SSRI – POST SYNAPTIC EFFECT

A
  • Selective inhibition of 5-HT recapture via SERT receptor inhibition
  • ↑ 5-HT amount in synapse
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12
Q

SSRI – PRESYNAPTIC EFFECT

A

• ↑ 5-HT to bind to 5-HT1A presynaptic receptors
• Brake on 5-HT release
• After a while: “downregulation” of 5-HT1A receptors
• Decrease in the “brake” on the 5-HT release = ↑ 5-HT
This delay before ‘downregulation’ is said to be due to anxiety at the beginning of treatment

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13
Q

ANTIDEPRESSANTS DOSES

A
  • The same as in the treatment of depression
  • OCD is an exception
  • requires > 30% dose
  • requires longer pharmacological trials
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14
Q

DELAY OF ACTION ANTIDEPRESSANTS

A

4 – 8 weeks

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15
Q

BENZODIAZEPINES CLINICAL INDICATIONS

A 
o Anxiety
o Insomnia
o Agitation
o Epilepsy
o Alcohol weaning
o Catatonia
o Dystonia
o Late dyskinesia
o And several others.
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16
Q

BENZODIAZEPINES CLINICAL INDICATIONS ANXIETY

A
  • Acute anxiety or agitation
  • Adjuvant at the beginning of treatment to overcome the time frame of action of antidepressants (2 - 3 weeks)
  • Used in the majority of anxiety disorders
    • Avoid using them in OCD and PTSD
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17
Q

FORMULATIONS BENZODIAZEPINES

A
  • Tablet (e.g. lorazepam)
  • Sublingual tablet (e.g. lorazepam SL)
  • Capsule (e.g. temazepam)
  • Solution for injection
  • Diazepam, lorazepam, midazolam
  • For psychiatric emergencies
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18
Q

MECHANISM OF ACTION BENZODIAZEPINES

A

GABAA RECEPTOR AGONIST

  • In the absence of GABA, there is no effect
  • Simultaneous use of the receptor by benzodiazepines AND GABA produces potentiation
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19
Q

GABAA RECEPTOR

A
  • Includes several sub-units
  • Benzodiazepines are mainly linked to sub-units α, β and γ

Example of effect by sub-unit:
• α1 : sedation
• α2 : anxiolytic
• α 5 : anterograde amnesia

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20
Q

Oral absorption BENZODIAZEPINES

A
  • Well absorbed (lipophils)

* Effect appears 30 minutes to 2 hours after taking

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21
Q

Distribution BENZODIAZEPINES

A

• Go through the BBB (lipophiles)

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22
Q

Metabolism BENZODIAZEPINES

A

• Many generate active metabolites, which can accumulate and cause more side effects

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23
Q

do not produce active metabolites

A
  • LOT * : metabolised by glucuronoconjugation, do not produce active metabolites and their elimination is not affected by liver function - good choices in the elderly
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24
Q

Clonazepam Onset of action Half-life Duration of action

A

Intermediate 20 to 80 h Intermediate

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25
Q

Diazepam Onset of action Half-life Duration of action

A

Rapid > 100 h Long

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26
Q

Lorazepam Onset of action Half-life Duration of action

A

Intermediate 10 to 20 h Intermediate

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27
Q

good choice for reg dose not PRN

A

Temazepam low onset intermediate duration

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28
Q

‘POPULAR’ CHOICES benzo

A

v Glucoronoconjugated benzodiazepines : better for the elderly or those with liver failure
• Lorazepam
• Oxazepam
• Temazépam

v Clonazépam: directly targets rumination
v Alprazolam

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29
Q

INTRODUCING TREATMENT benzos

A

üUse the smallest dose possible

üSeparate into several takes during the day

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30
Q

Precautions / Contraindications benzos

A
  • Sleep apnea
  • Severe respiratory disorder
  • Substance abuse disorder
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31
Q

SIDE EFFECTS benzos

A 
• Drowsiness, sedation
• Weakness
• Ataxia
• Dizziness
• Light-headed feeling
• Dry mouth
• Headache
• Confusion, disorientation
• Tachycardia, palpitations
• Anterograde amnesia 
Generally few side effects if used in the short term at an adequate dose
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32
Q

MANAGEMENT OF SIDE EFFECTS benzos

A

« Hangover » effect
• Administer a shorter-acting BZD

Paradoxical effect
• Especially children, elderly, behavioral disorder, borderline personality disorder, autistic
• Stop immediately!

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33
Q

Benzos Long-term use leads to

A

a reduction in the synthesis of certain sub-unit= Loss of efficacy or tolerance

34
Q

WITHDRAWAL benzos

A

Cessation or decrease= The “brake” is cut = Release of excitatory neurotransmitters Withdrawal symptoms

35
Q

WITHDRAWAL SYMPTOMS benzos

A
  • Muscle stiffness
  • Weakness
  • Gastrointestinal disorders
  • Paresthesia
  • Influenza-like
  • Visual/olfactory disorders
  • Tachycardia
  • Anxiety
  • Agitation
  • Insomnia
  • Depersonalization
  • Cognitive disorders
  • Delirium/ hallucinations
  • Depression
36
Q

The duration and severity of withdrawal symptoms depend on the : benzos

A
  • Half-life
  • Potency
  • Exposition
37
Q

Short-to-middle half-life benzos withdrawal

A
  • Peak: 2-3 days
  • Duration: 7-10 days
  • Moderate intensity
38
Q

Long half-life benzos withdrawal

A
  • Peak: 7-10 days
  • Duration: 17-21 days
  • Low intensity
39
Q

RULE OF THUMB benzos withdrawal

A

25 % reduction in dose per week until 50 % of the dose is reached, then reduce dose by 1/8 every 4 – 7 days

40
Q

Therapy > 8 weeks : taper benzos

A

slow taper over 2 – 3 weeks

41
Q

benzos Therapy > 6 months : slow taper over

A

4 – 8 weeks

42
Q

benzos Therapy > 1 year : slow taper over

A

2 – 4 months

43
Q

BENZODIAZEPINES TAPER

THERAPEUTIC GOALS

A
  1. Complete cessation
  2. Avoid the onset of withdrawal symptoms
  3. Prevent the rebound effect
44
Q

BENZODIAZEPINES TAPER

HOW TO TAPER : 1st

A
  1. Lunch
  2. Dinner
  3. Morning
  4. Bedtime
45
Q

TAPER – LONG VERSION benzos

A

SUBSTITUTION TO DIAZEPAM (VALIUMTM)
o Long-acting benzodiazepine : fewer rebound or withdrawal symptoms
o Smaller doses, more practical formulation for the final steps
• Half a 2 mg tablet = 1 mg
o Tapering over about 20 weeks
o Increased chances of success
• It’s better to go too slowly than too fast

46
Q

TAPER – ELDERLY benzos

A

SUBSTITUTION TO OXAZEPAM (SERAXTM)
o Intermediate half-life
o No pharmacokinetic alteration in the elderly
o Find the equivalent dose and then remove 2,5 mg
• ¼ of 10 mg tablet per month until the end

47
Q

Taper benzol monitor

A 
BENZODIAZEPINES WITHDRAWAL
SYMPTOMS QUESTIONNAIRE
SCORE
o > 20 = change strategy
o increase in 3-point score = change strategy
48
Q

INTERACTIONS benzos

A
  • Plasma protein binding (e.g. diazepam)
  • Cytochrome P450 3A4 mainly
  • Increased drowsiness
  • Alcohol
  • Antihistamines
  • Opiates
  • Some antidepressants
  • Some antipsychotics
49
Q

– ATYPICAL ANTIPSYCHOTICS

MECHANISM OF ACTION

A

Anxiolysis is thought to be mediated by 5-HT1A receptor agonism

50
Q

CLINICAL USE IN ANXIETY– ATYPICAL ANTIPSYCHOTICS

A

v Evidence for monotherapy is sparse
• Quetiapine XR
v Some evidence as augmenting agents
• Risperidone, olanzapine, aripiprazole

51
Q

PREGABALINE MECHANISM OF ACTION

A
  • Does not act on GABA, but decreases neuronal activity and neurotransmission
  • Antiepileptic, anxiolytic and analgesic properties
52
Q

CLINICAL USE IN ANXIETY PREGABALINE

A

v TAG and social anxiety

v Sometimes allows long-term benzodiazepines to be taper

53
Q

DELAY OF ACTION PREGABALINE

A

Rapid effect vs antidepressants

about 1 week

54
Q

SIDE EFFECTS PREGABALINE

A
  • Dizziness
  • Drowsiness
  • Peripheral edema
  • Dry mouth
  • Constipation
55
Q

BUSPIRONE MECHANISM OF ACTION

A
  • Partial agonist of 5-HT1A receptors

* Slowing electrical impulses in amygdala

56
Q

CLINICAL USE IN ANXIETY BUSPIRONE

A

v Unlike benzodiazepines, is not useful if used in single or occasional doses
v Mixed effect, poorly constructed clinical studies

57
Q

DELAY OF ACTION BUSPIRONE

A

• A few weeks

58
Q

SIDE EFFECTS BUSPIRONE

A
  • Dizziness, nausea, headache
  • No sedative effect
  • No addiction or withdrawal
  • Interesting in patients with respiratory disorder, as it does not cause respiratory depression
  • High dropout rate in studies (ineffective?)
59
Q

PRAZOSIN MECHANISM OF ACTION

A
  • Antagonist of alpha1-adrenergic receptors

* Antihypertensive drug

60
Q

SIDE EFFECTS PRAZOSIN

A
  • Hypotension
  • Nausea
  • Drowsiness
  • Headache
61
Q

HYDROXYZINE MECHANISM OF ACTION

A

H1 receptor antagonist (antihistaminic)

62
Q

CLINICAL USE IN ANXIETY HYDROXYZINE

A

GAD

63
Q

DELAY OF ACTION HYDROXYZINE

A
  • 30 minutes for sedative effect

* Longer-term effect is uncertain

64
Q

SIDE EFFECTS HYDROXYZINE

A
  • Anticholinergic effects
  • Cognitive function
  • Constipation
  • Blurred vision
  • Sedation
65
Q

Medications RISK factors GAD

A

• Toxicity (e.g. anticholinergics,
corticosteroids, bronchodilatators)
• Withdrawal (e.g. alcohol, benzodiazepines)
• Stimulants, thyroid hormone, etc.

66
Q

Drugs with an anxiolytic effect ???? NE release

A

decrease

67
Q

Drugs that reduce anxiety and produce sedation target ???? receptor

A

GABAa

68
Q

Abnormalities in serotonergic functioning occur through release and uptake at the

A
  • Presynaptic autoreceptors (5-HT1A/1D)
  • Serotonin reuptake transporter site
  • Postsynaptic receptors (5-HT1A, 5-HT2A, 5-HT2C)
69
Q

GAD, panic, PTSD, SAD Continue treatment for at least ??? following response to treatment, then reassess

A

1 year

70
Q

panic If discontinuation of treatment is considered, do it over

A

4 to 6 months

71
Q

PATHOPHYSIOLOGY PTSD

A

ALPHA1 ADRENERGIC POST-SYNAPTIC
RECEPTORS: Over-activation of these receptors to
activate symptoms related to PTSD, especially those related to sleep (nightmares)
ALPHA2 ADRENERGIC POSTSYNAPTIC
RECEPTORS: Involved in cognitive processes and
response to stimuli

72
Q

FIRST LINE TREATMENT: NIGHTMARES & INSOMNIA

A
  • Non-pharmacological measures
73
Q

PTSD PSYCHOTIC SYMPTOMS

• x% of patients

A

40

74
Q

PHARMACOLOGICAL TREATMENT : PTSD

A
  1. SSRIs or SNRIs to treat PTSD (psychotic symptoms may be related to it)
  2. Flash-back, hypervigilance, dissociation and paranoia can respond to anticonvulsants
  3. Atypical antipsychotic
75
Q

SAD pathophys

A

NE
• Involved especially if performance-related anxiety
DA
• Dysfonction
• Decreased ability to bind to D2 receptors 5-HT
• Hypersensitivity of 5-HT2 receptors

76
Q

performance-related anxiety

A

USING BETA BLOCKERS?
• Possibly useful if performance-related anxiety
• Decrease in tremors, palpitations and blushing
e.g. propranolol 10 mg 2 hours before performance (watch out for bradycardia!)

77
Q

SAD when discontinue, taper over

A

3 - 4 months

78
Q

PATHOPHYSIOLOGY OCD

A

Abnormalities in the transmission of 5-HT, DA and glutamate

79
Q

WHAT ABOUT BENZODIAZEPINES? OCD

A

No

80
Q

Recommended long-term treatment after OCD

A

2 to 4 relapses

81
Q

A treatment duration of ???? is generally

recommended before considering a cessation of treatment

A

12 to 24 months

Pharmaco (11 decks)

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