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PHAR 358 > Anxiety > Flashcards

Anxiety Flashcards

1
Q

What does anxiety engage?

A

Flight or flight rxn of survival

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2
Q

When does anxiety become a disorder?

A

Anxiety becomes a disorder when it is overwhelming and affecting function & quality of life

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3
Q

Define Anxiety Disorders

A

Anxiety disorders include disorders that share features of excessive fear and anxiety & related behavioral disturbances

Fear is the emotional response to real or perceived imminent threat

Anxiety is anticipation of future threat

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4
Q

Describe the core sx of anxiety?

A

Psychological
Fear/anxiety, worry, apprehension, difficulty concentration

Somatic (physical)
Increase HR, tremor, sweating, GI upset

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5
Q

What are the common anxiety disorders and their classification?

A
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6
Q

What is unique about tx of anxiety disorders?

A

Most 1st line meds are effective for all anxiety d/os (disorders)

Same medications used for depression

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7
Q

How much of the population has anxiety?

A

~25% of population will have at least 1 anxiety disorder

Common for people to have more than 1 anxiety disorder.

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8
Q

Describe the pathophysiology of anxiety

A
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9
Q

How does the amagydala affect anxirty?

A

Almond shaped brain center located near hippocampus

interprets sensory and cognitive information and determines if there will be a fear response

amygdala →→→ prefrontal cortex
affect response – feelings of fear
motor response – “flight or fight” (F/F) or freezing (periaqueductal gray)

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10
Q

Purpose of CSTC

A

Controls 2nd core symptom: “worry”

linked to the pre-frontal cortex

Also under the control of neurotransmitters
Similar to the amygdala
Availability of neurotransmitters is regulated by COMT (catechol-0-methly transferase) – especially dopamine (DA)

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11
Q

GABA in ANxiety

A

key NT for anxiety and the role of anxiolytics

principal inhibitory NT in brain that plays a role in ↓ activity of neurons (amygdala, CSTC)

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12
Q

GABA Synthesis

A

stored in presynaptic vesicles
released in synapse when needed
GABA transporter back to vesicles or metabolized & inactivated by GABA transaminase

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13
Q

Voltage-sensitive calcium channels (VSCC) & α2δ ligands in Anxiety Pharamcology

A

N and P/Q are subtypes of VSCC and relevant in psychopharmacology

gabapentin & pregabalin bind to the α2δ subunit of the presynaptic N and P/Q VSCC to block release of glutamate when neurotransmission is excessive (amygdala and CSTC loop) to decrease fear and worry

since different MOA, option in non-responding anxiety patient or in combination (AD, BZD)  good for add on options

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14
Q

Sertonin and its affect in Anxiety

A

symptoms, circuits & NT for anxiety disorders overlap w/ MDD

5-HT is a key NT innervating the amygdala and CSTC
Assists with regulating fear and worry

SSRI/SNRIs block 5-HT reuptake by blocking 5-HT transporter

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15
Q

Buspirone MOA

A

buspirone is a 5-HT1A agonist effective (air quotes) only in GAD and to potentiate antidepressants

Second generation antipsychotics also have 5-HT1A agonist properties

Onset similar to AD (vs BZD) suggesting mechanism similar to AD (adaptations in neurotransmitter receptors)
Second generation

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16
Q

Noradrenergic ACtivity in ANxiety

A

NE is regulator to amygdala and to PFC/thalamus in CSTC circuits by attaching to α1 & β1 adrenergic receptors

LC ↑ autonomic activity to trigger fear, panic, anxiety and effects processing in PFC
hyperarousal (nightmares) managed with α1 blockers prazosin

fear/worry treated with NE reuptake inhibitors
symptoms can be worsened at initial dosing with SNRIs but as β1 receptors downregulate fear/worry improve long term

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17
Q

Anxiety primary Assesment (What should always be done)

A

Rule out anxiety disorders due to general medical conditions or substance use

Review substances used (caffeine, OTC use, herbal medications, recreational substances)

phenylephrine, pseudoephedrine, caffeine tabs, Midol, codeine products with caffeine

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18
Q

Anxyiolytic Medication Overview

A
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19
Q

Bupropion

A

Activating. Risk of seizures, avoid if (seizure history, head trauma, bulimia, anorexia, electrolyte disturbances)

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20
Q

Buspirone

A

Slow onset, modest efficacy. May be helpful to augment therapy in those with partial response to antidepressants. Avoid if comorbid depression.

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21
Q

Citalopram

A

Lower risk for insomnia, agitation, drug interactions compared to other SSRIs. Dose dept risk of QT prolongation.

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22
Q

Duloxetine

A

May be useful for comorbid pain. Compared to SSRIs: increased withdrawal symptoms if not tapered, increased insomnia or agitation. Avoid if liver disease or heavy ETOH use.

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23
Q

Escitalopram

A

Similar to citalopram, except QT risk is controversial.

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24
Q

Fluoxetine

A

More activating than other SSRIs. Self-tapering due to long half-life. Drug interactions (2C19, 2D6)

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25
Q

Imipramine

A

Anticholinergic; cardiotoxic in overdose. Not well tolerated.

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26
Q

Fluvoxamine

A

SSRI - Withdrawal symptoms if not tapered. Risk for drug interactions due to inhibition of CYP1A2 and 2C19.

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27
Q

Hydoxyzine

A

Useful for co-morbid insomnia. Dose-related anticholinergic effects limit clinical use.

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28
Q

Mirtazapine

A

Helpful with comorbid insomnia. Lower doses are more sedating. May increase appetite and lead to weight gain.

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29
Q

PAroxetine

A

ompared to other SSRIs more sedating, less agitation, more constipation, withdrawal symptoms if not tapered. May be associated with greater weight gain. Concern for drug interactions. Avoid in pregnancy due to cardiac septal defects.

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30
Q

Pregabalin

A

Sedation and dizziness are common. Weight gain, especially with long-term use.

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31
Q

Sertyraline

A

Compared to other SSRIs insomnia, agitation, dizziness.

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32
Q

Venlafaxine

A

Compared to other antidepressants greater risk for insomnia or agitation as well as increased blood pressure. Possible benefit for comorbid pain. Few drug interactions. Withdrawal symptoms if not tapered. Better evidence for psychological symptoms (e.g. ruminative worry of GAD).

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33
Q

GAD Prevalence and Onset

A

Ratio of women: men with GAD is 2:1

Onset usually in late adolescents or early adulthood
Cases in older adults as well

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34
Q

GAD etyiology

A

Unknown
Likely combined effect of biological and psychological factors

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35
Q

Beck’s Cognitive Triad

A

Interplay of:

Thoughts
Emotions
Behaviours

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36
Q

Causes of GAD

A
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37
Q

Medication Causes GAD

A

bupropion and norepinephrine reuptake inhibitor (STAR)

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38
Q

GAD Complexity of TX

A

GAD frequently co-occurs with other mental health disorders which complicates diagnosis and tx

Some studies have suggested up to 90% of patients with GAD present with comorbid mental disorders during their life

MDD, other anxiety disorders, substance use disorders, bipolar, sleep disorders

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39
Q

GAD comorbidities

A

GAD can also co-occur with physical health problems & may exacerbate these physical illnesses and interfere with a person’s ability to manage them:

Chronic pain
Diabetes
Cardiovascular disease
GI distress
Headache
Fatigue

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40
Q

Main Sx of GAD

A
41
Q

GAD Rating Scales

A
42
Q

GAD GOT

A
43
Q

Pharmcotherapy Initiation in Gad: When?

A

Psychotherapy + pharmacotherapy

Psychotherapy is least invasive and safest

Pharm indicated if sxs severe enough to produce fxnal disability

44
Q

Non-pharm Tx GAD

A

Reduce/avoid alcohol, caffeine, nicotine use
Avoidance of non-prescription stimulants & medications known to induce anxiety
Exercise
Psychotherapy +/- counselling
Cognitive behavioral therapy (CBT)
Relaxation techniques
Meditation, yoga
Biofeedback

45
Q

GAD TX Guidelines

A
46
Q

Non-response in GAD: What tool should be used?

A

Current data does not provide guidance as to whether it is best to increase to dose, augment, or switch when there has been a partial response to drug therapy

The Psychopharmacology Algorithm Project at the Harvard South Shore Program (PAPHSS) provides guidance

47
Q

GAD and BIpolar MAgmt

A

Avoid Ad
Quetiapine is effective for GAD and may be preffered
Consider VPA in men with mania with GAD but not in women of childbearing potential due to teratogenicity

48
Q

GAD SSRI’s

A

Paroxetine, escitalopram, sertraline all studied for GAD (others used in practice)

49
Q

SNRI’s GAD

A

Venlafaxine and duloxetine both studied for GAD

Escitalopram and venlafaxine equally effective but escitalopram better tolerated

May have increased effect for ruminative worry

50
Q

Other AD GAD

A

Imipramine and trazodone more effective than placebo but less tolerable

Open label trials showing mirtazapine to be effective

Bupropion found to have similar efficacy to escitalopram

51
Q

Benzos in GAD

A

Most often used for ACUTE anxiety 2-3 weeks until antidepressant begins to work (BRIDGE)

Long-term use not recommended due to physiological/psychological dependence

Not effective for depressive symptoms and may worsen depression (CNS depressant, can make depression sx worse)

52
Q

Pregabalin/Gabapentin in GAD

A

Effective in short term GAD studies

1 trial found it is effective for use in patients stopping long term benzos (during withdrawal period)

53
Q

Buspirone GAD

A

Delayed onset of effect (2 weeks or longer), not useful for acute anxiety (misinformation here often, not a safer benzo)
Inconsistent reports of efficacy for long term use
May be more useful for patients who have not used benzos
5-HT1A partial agonist
Rarely used in clinical practice

54
Q

Hydroxyzine GAD

A

H1 and 5-HT2 antagonist
Effective in studies up to 12 weeks
2nd/3rd line due to ADEs and lack of efficacy for comorbidities
Anticholinergic, sedation (A LOT – 2nd or 3rd line)
Very rarely used in clinical practice due to lack of tolerability

55
Q

SGA’s GAD

A

3rd line due to ADEs and limited evidence (reserve them for 3rd line due to s/e)
Anxiolysis is mediated by 5-HT1A
Olanzapine, risperidone, quetiapine effective as augmenting agents

56
Q

GAD TX Timeframes SSRI’s/SNRI’s

A
57
Q

Benzodiaz MOA

A

Bind to the benzodiazepine receptors on the GABA(A) neuron

Leads to an increase in the frequency of opening of the chloride channels by increasing binding affinity for the endogenous ligand GABA

The shift in chloride ions results in hyperpolarization (a less excitable state) and stabilization

58
Q

Benzo Efficacy GAD. Which benzos?

A

Provides rapid initial relief of anxiety symptoms, but effects may not be significantly different from placebo after 4-6 weeks of treatment

Primarily effective for relieving somatic symptoms (muscle tension, changes in sleep), rather than the key psychic features (ruminative worry) that are characteristic of GAD

Magnitude of effect for GAD appears to be similar to that of cognitive therapy

RCT evidence supports the efficacy of alprazolam, bromazepam, lorazepam and diazepam in GAD

59
Q

Clonazepam in GAD?

A

While there are no RCTs evaluating the use of clonazepam in GAD, it is used extensively in clinical practice for the treatment of anxiety and it is likely that the benefits are similar to other benzodiazepines

Used as it maintains its effect within the entire dosing window (longer half-life) and avoids the peaks and troughs as seen with other benzos

60
Q

Comparison of BEnzo’s

A
61
Q

Common A/E of BEnzo’s

A

Ataxia
Dizziness, lightheadedness
Sedation & residual daytime sleepiness
Tolerance to sedation may develop (brain fog, can’t concentrated, impair coordination, confusion)
Psychomotor impairment
Agitation, irritability, confusion
Variability in the way people respond to benzos
Paradoxical responses (or in kids, brain injury  more irritable, agitated)

62
Q

Less common a/e of Benzo’s

A

Anterograde amnesia (often does not persist)
More common with lorazepam
Memory impairment
Depression, confusion, bizarre behaviour, hallucinations
Respiratory depression

63
Q

Issues with Benzodiazepines

A

Tolerance may also develop to the anxiolytic effects, necessitating dosage increases with chronic use

Psychological and physical dependence may develop with long-term use

Withdrawal symptoms can occur following discontinuation of therapy with as little as one week of use (anxiety can come back)

64
Q

Risk factors of benzo dependence

A

Risk of dependence increases with higher dose and/or longer use

Risk further increased with history of alcohol use disorder or other substance use disorders or personality disorders

65
Q

Different Benzos 9time)

A

Long Acting= good choice for tapering as less risk of withdrawal (i.e. diazepam, clonazepam), more daytime sedation
Short Acting= better hypnotic and sedative properties but more rebound anxiety (i.e. lorazepam), inter-dose withdrawal, anterograde amnesia

66
Q

Specific Benzos When???? WHich ones?

A

LOT drugs (lorazepam, oxazepam, temazepam) preferred in elderly and liver dysfunction due to no active metabolites

67
Q

Benzo Withdrawal Sx

A

sweating, tremor, nausea, vomiting, rebound anxiety, ↑ heart rate, insomnia, agitation, twitching, visual/tactile hallucinations, SEIZURES (onset within 1-2 days after BZD stopped)

68
Q

How to avoid BZD withdrawal?

A

Avoid by tapering BZD

69
Q

Withdrawal Percentages

A

30% of patients experience withdrawal if BZD stopped suddenly after 8 wks of tx.

70
Q

ow should benzo’s be taperred?

A

Use diazepam for taper (unless contraindication), conservative schedule: decrease diazepam by 10-20% q1-2weeks (often switch to diazepam; too fast of taper (trial) can have breakthorough anxiety

71
Q

Benzo Precautions

A

Substance use history (concurrent use with opioids may cause profound respiratory depression, coma, death), sleep apnea, COPD, elderly, CNS depression, pregnancy (floppy infant syndrome; possible teratogen & can precipitate withdrawal in newborns if used in 3rd trimester), clozapine-use (may lead to significant sedation, excessive salivation, and rare respiratory arrest)

72
Q

Are Benzo’s fatal?

A

Rarely fatal alone but may be fatal when taken in combination with alcohol, opioids, barbiturates (strong CNS depressants).

73
Q

Benzo ANtidote and Use

A

Benzo antidote –> Flumazenil

Reverses hypnotic-sedative effect of BZD but clinically use is limited due to risk of causing seizures in BZD dependant patients

74
Q

WHICH AD in Preganncy?

A

Sertraline, Citalopram

75
Q

Define a panic attack?

A

A distinct period of intense fear or discomfort when 4 or more symptoms develop suddenly and achieve a peak within 10 minutes:

76
Q

Define Panic Disorder

A

Recurrent unexpected panic attacks with at least 1 of the attacks being followed by a month or longer of at least 1 of the following:

  • constant concern about having another attack
  • being anxious about the implications of the attack or its consequences (e.g., losing control, having a heart attack)
  • maladaptive change in behavior designed to avoid having panic attacks
77
Q

Panic Disorder Genders and Onset. WHat type of disorder?

A

Females 2: Males 1

Rates increase during adolescents (especially in females) and peak during adulthood

Median age at onset is 20-24 years
If untreated disorder is chronic but waxing and waning (periods of stability; periods of debilitation)

78
Q

Which anxiety disoder has the highest number of clinical visists?

A

Panic Disorder

79
Q

Panic Disoder Commorbidities

A

Other anxiety disorders
Depression
10-65%
In 1/3 of patients the depression precedes panic disorder
Bipolar disorder
Alcohol use disorder
Higher rates of suicide attempts and suicidal ideation
Medical comorbidities (lead to disruption in catecholamines, neurotransmitters)
Dizziness, cardiac arrhythmias, hyperthyroidism, asthma, COPD, IBS, Cushing’s syndrome, pheochromocytoma

80
Q

Charcteristic Sx of PD

A
81
Q

PD Clinical Course

A

Panic attacks vary in frequency and intensity
Wax and wane over time and in response to stressors
1/3 of patients achieve remission
1/5 of patients have unremitting & chronic course

Most patients require long-term treatment to achieve remission, prevent relapse, & reduce risks associated with co-morbidity

82
Q

Predictors of Chronic Course PD

A

Long duration of illness
Comorbidity with personality, mood, other anxiety disorders
Excessive sensitivity to physical symptoms of anxiety

83
Q

Rating Scales PD

A
84
Q

Treatment of PD

A
85
Q

Pharmacotx PD

A
86
Q

Benzo’s PD

A

2nd line after several trials of antidepressants have failed

Do not use as monotherapy if comorbid depression (will not treat mood disorder)

Avoid if history of substance/alcohol use disorder

Limited data support combo BZD + SSRI during first 1st few weeks of treatment for rapid symptom relief

BZDs are NOT an effective strategy to treat an acute panic attack because the onset of BZD will typically occur after the panic attack

87
Q

AD Onset of ACtion In PD

A

Most patients with PD are hypersensitive to medication ADEs at initiation and this can lead to activation (early worsening of anxiety, agitation, irritability)

Reduction of panic attack frequency, anticipatory anxiety, and avoidance may start within first 3-4 weeks

For patients with significant avoidance, full remission may take up to 6 months or longer

88
Q

Benzo’s Onset PD

A

Onset within hours for autonomic symptoms of anxiety, full benefit may take 4-6 weeks

89
Q

PD Tx Timelines

A
90
Q

SAD Age of Onset

A

Median age of onset: 13 years

75% have an age at onset between 8-15 years
Onset can occur in early childhood (may follow a stressful or humiliating experience, e.g. being bullied)
Prevalence decreases with age

Higher rates in females than males

91
Q

Most strong predictor of SAD?

A

Unemployment is a strong predictor of persistence of SAD

92
Q

SAD Tx Seeking

A

Only ~50% of patients with SAD seek treatment and usually only after 15-20 years of symptoms

93
Q

Characteristic Sx of SAD

A
94
Q

Rating Scales for SAD

A
95
Q

Non-Pharm TX SAD

A
96
Q

SAD TX

A
97
Q

SAD TX 1st Line

A
98
Q

Beta-Blockers SAD

A

ay be used for performance related SAD
Decreases tremor, palpitations, blushing
Dosing
Propranolol 10-80mg or atenolol 25-50mg 1-2 hour before performance
Give test dose to assess tolerability
Contraindications: cardiogenic shock, sinus bradycardia, cardiac failure, bronchial asthma, known hypersensitivity

99
Q

SAD Tx Timelines

A

PHAR 358 (4 decks)

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