9 - General Anxiety Disorder Flashcards Preview

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Flashcards in 9 - General Anxiety Disorder Deck (31)
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1
Q

Assessment of anxiety disorders

A
  • Situational vs. anxiety disorder
  • Type of anxiety disorder
  • Psychiatric & medical disorders
  • Medication hx
  • Hx of anti-anxiety drug response
  • Duration & acuity of sx
  • Expectation of pt for recovery
  • Stressors
2
Q

Briefly describe the anatomy and NTs involved in anxiety

A
  • Brain amygdala appears key in modulating fear & anxiety
  • Px w/ anxiety disorders often show heightened amygdala response to anxiety cues
  • Major mediators = NE, serotonin, dopamine, & GABA (gamma-aminobutyric acid)
  • Autonomic NS is key
3
Q

Medications associated w/ anxiety

A
  • CNS stimulants (amphetamines, caffeine, cocaine, methylphenidate, steroids)
  • Withdrawal of CNS depressants (ethanol, anxiolytics, narcotics, sedatives)
  • Adverse effects of other meds (anticholinergics, antidepressants, antipsychotics, thyroid supplements, OTC stimulants)
4
Q

Describe the anxiety/ gut/ microbiome connection

A
  • People w/ anxiety & mood disorders are prone to GI problems
  • When GI (stomach) issues get worse, anxiety issues often do as well & vice versa
  • When GI issues get better, anxiety is often reduced
  • Evidence suggests that we can improve anxiety by improving the nature & diversity of gut flora or microbiome
5
Q

Generalized anxiety disorder (GAD) - onset, goals, recovery vs. remission

A
  • Onset sx (primary GAD) in early 20s, later onset for secondary GAD
  • Gradual onset
  • Course = chronic w/ multiple exacerbations
  • Rarely a stable condition
  • Stress/ medical health has role in persistence
  • Acute goals = reduce severity & duration of anxiety sx & improve overall function
  • Recovery = minimal or no anxiety sx, no functional impairment; feeling of “control”
  • Remission rates of 70% are achievable
6
Q

Medication choices for GAD

A
  • Antidepressant tx may start concurrently or be pending response to BZD
  • 2-4 weeks of BZD targets acute relief
  • When antidepressant tx is effective for GAD, a 12-month continuation is generally advised
7
Q

GAD goals

A
  • Short term = decrease sx (psychic sx – worrying, irritability; somatic sx – GI, fatigue, insomnia); decrease severity, duration, & frequency
  • Long term = minimize or prevent sx, improve QOL, prevent adverse effects of meds, educate pt on disorder, tx, & reduction of sx
8
Q

GAD non-pharms

A
  • Psychoeducation – short-term counseling, stress management, psychotherapy, CAM
  • Meditation, exercise, yoga, acupuncture
  • Avoid caffeine, alcohol, substances
  • Hopefully minimize prn BZD (prefer scheduled use w/ some prn)
  • CBT (cognitive behavioural therapy) very effective once realistic
9
Q

Basic principle of CBT

A
  • Helps people separate thoughts, feelings, and situations
  • We often react to perceptions of situations
  • Thought (what we think affects how we act & feel), behaviour (what we do affects how we think & feel), & emotion (what we feel affects how we think & do)
  • Helps clients identify, evaluate, & respond to their dysfunctional thoughts or beliefs
10
Q

GAD pharmacotherapy

A
  • BZD – rapid relief of acute sx of anxiety; effective, “safe” & commonly prescribed
  • Antidepressants – first-line for long-term disorder management
    • Don’t start all people immediately on antidepressants b/c take a long time to work (4 weeks)
  • Alternatives = buspirone, hydroxyzine, pregabalin, antipsychotics (SGAs)
11
Q

BZDs for GAD – onset, dosing, duration, SE

A
  • Most are equally effective as anxiolytics
  • More effective in treating somatic/autonomic sx (need antidepressants or buspirone to treat psychic sx)
  • Selection may consider – cost, onset, duration, metabolism, interactions
  • Onset – increased lipid solubility correlates w/ rapid absorption, may impact speed of onset, duration of effect, and may lengthen clearance t1/2
  • Dosing – initiation is extremely variable and must be individualized; consider weekly dose review early on; adequate therapeutic trial may require 4-week trial of very high dose (ex: 40 mg diazepam)
  • Duration – monographs suggest 2-3 weeks; shouldn’t exceed 4-6 months in general; for recurring sx = intermittent therapy in 3-4 week “pulses”
  • Adverse effects – sedation, ataxia, confusion, respiratory depression (only a concern in overdose w/ other medications, particularly opioids; not really a problem w/ single BZD overdose), CV depression, tolerance, dependence
12
Q

BZD drug interactions

A
  • CNS depressants increase sedation; alcohol increases BZD levels?
  • Increased BZD levels – CYP 3A4 inhibitors (erythromycin, fluvoxamine, other SSRIs), grapefruit juice, amiodarone, ketoconazole
  • Decreased BZD levels – carbamazepine, rifampin, smoking
13
Q

BZD withdrawal – sx, incidence, prevention

A
  • Common sx = anxiety, insomnia, restlessness, irritability (most often the sx that the BZD was originally being used to treat)
  • Less frequent = nausea, blurred vision, depression
  • Rare = confusion, paranoid delusion, hallucination, seizures (depends on how much they were taking & how abruptly they stop)
  • Increased incidence of sx if regularly used for > 3-4 months, “higher” doses used for long period (> 15 mg diazepam equivalent), sudden cessation of med, short-acting BZD used (t1/2 < 20 h), previous hx of dependence on drugs or alcohol
  • 2/3 of people will have some sx on withdrawal from sustained ingestion
  • Prevention – limit duration & dose of BZD tx when realistic to 2-3 weeks
    • For longer-term use – decrease dose 10-25% every 3-7 days; very high doses taper over 6 months
    • If difficulty withdrawing, switch to longer half-life agent (ex: diazepam)
14
Q

BZD pt education

A
  • What it is used for & what sx will be treated
  • Anticipated duration of tx
  • Potential adverse effects
  • Drug interactions w/ CNS depressants
  • Don’t decrease, increase, or d/c suddenly w/o consultation w/ HCP
15
Q

GAD – antidepressants

A
  • First line for long term tx
  • More effective than BZD in treating psychic sx (apprehension, worry)
  • Onset of meaningful anxiety response 2-6 weeks
  • Duration if responsive = at least 12 months
  • No clear “first choice” of agent; can use SSRIs, SNRIs, or TCAs
16
Q

Buspirone - MOA, advantages, SE

A
  • 5-HT 1A partial agonist – binds to pre- & post-synaptic receptors to serotonergic transmission (increase 5-HT)
  • Effective agent for chronic, persistent anxiety
  • Advantages:
    • No abuse, dependence, withdrawal sx
    • No interaction w/ alcohol
    • Fewer CNS side effects than BZDs
    • Fewer GI effects than SSRI
  • More helpful w/ psychological sx than physical
  • Delayed onset; maximal effect in 4-6 weeks (huge challenge to pt adherence)
  • Efficacy maintained at least 1 year
  • Adverse effects = dizziness, nausea, headache, nervousness
  • Less overall evidence than w/ SSRIs +/- BZD
17
Q

Buspirone drug interactions

A
  • Increased buspirone levels (verapamil, diltiazem, erythromycin)
  • Increased levels of cyclosporine & haloperidol
18
Q

Panic disorder

A
  • Usually a relapsing, remitting disorder
  • Index attacks from “out of the blue”
  • Only about 60-80% achieve full remission w/ SSRI & BZD tx
  • Relapse is common
  • Worry & behaviour change can be major functional impacts, & the targets for long-term management
19
Q

Medical conditions associated w/ panic disorder

A
  • Hypo/hyperthyroidism
  • Asthma
  • “Excessive” intake of caffeine or stimulants
  • Withdrawal from alcohol or other CNS depressants
20
Q

Panic attack sx

A
  • Abrupt development of at least 4 sx
    • Intense fear, “sense of doom”
    • Palpitations, pounding heart, high HR
    • Sweating, trembling, shaking
    • Sensation of SOB or smothering
    • Feeling of choking
    • Chest pain or discomfort
    • Feeling dizzy, lightheaded or faint
21
Q

Panic disorder goals of tx

A
  • Decrease frequency of panic attacks, level of anticipatory anxiety, level of phobic avoidance, physical sx w/ attacks
  • Avoid substances that may precipitate panic attacks (caffeine, drugs of abuse, non-Rx stimulants)
22
Q

Algorithm for panic disorder tx

A
  • BZD targets acute relief
  • SSRI or venlafaxine 1st line, most often started concurrently w/ BZD
  • 12-24 months duration should follow a favourable response to antidepressant tx
23
Q

BZD for panic disorder

A
  • Advantages –> rapid onset (1-2 weeks; continued improvement over 4-6 weeks), no tolerance to anti-panic effect, favourable side effect profile
  • Disadvantages –> sedation, dependence, abuse, withdrawal sx
  • Increased dose in comparison to tx of GAD
24
Q

Antidepressants for panic disorder

A
  • SSRIs first choice tx for panic disorder
  • Advantages –> no abuse or dependence, antidepressant activity (many people have both anxiety & depression), alter underlying mechanisms not just sx control
  • Disadvantages –> delayed onset (3-5 weeks, up to 8-12 weeks), “mild” hyperstimulation (anxiety, insomnia, jitteriness, irritability), sleep disturbance, sexual disturbances
  • Tx duration after good response = 12-24 months then taper over 4-6 months
  • Combination tx (BZD & antidepressant)
    • Rapid onset if needed
    • Greater adherence w/ combo
    • Ideal if supervised tapering of BZD after response, but may be challenging to take BZD away
25
Q

Obsessive compulsive disorder

A
  • Compulsions = repetitive, intentional behaviour or mental progressions in response to an obsession and/or according to rigid rules; may not be realistically connected w/ obsession; behaviours or thinking aimed at preventing some dread event or situation
  • Common examples = checking, cleaning/ washing, counting, repeating, hoarding/ collecting
  • DSM -V definition = presence of either obsession +/- compulsions (most px have both), time consuming > 1 h/day, impairment in functioning
  • Both serotonin & dopamine implicated in pathogenesis
  • Antipsychotics may have a role in augmentation, esp. if partial response to SRI, tics, concurrent Tourette’s
26
Q

OCD tx

A
  • Identify specific targets (sx)
  • Serotonin critical for anti-obsessional effects
  • Clomipramine (more serotonin specific than SSRIs), SSRIs, CBT, CBT + meds
  • Response – obsessions more responsive than compulsions, sx often reduced by 40-60% w/ a single agent, complete control quite rare …
  • *Instead of increasing dose of BZD, we increase dose of antidepressants
27
Q

Caution w/ clomipramine

A
  • TCA
  • TCA side effect profile (antihistaminic, alpha-adrenergic, antimuscarinic)
  • Serotonin side effects
  • Very high cardiac toxicity in overdose
  • Seizure risk, especially at high dose
  • Cautiously decrease dose during maintenance tx
  • Monitor serum levels, QT interval (especially at higher doses or w/ other QT-impacting meds)
28
Q

PTSD

A
  • May anticipate following a horrific life event (ex: assault, sexual assault, motor vehicle accident)
  • High incidence of another mental health disorder (80% meet depression or anxiety criteria)
  • May lie very deep until “reawakened” by experience, stressors, or sensory “déjà vu”
  • Re-experiencing, hyperarousal, avoidance
  • High incidence of EtOH or substance abuse/ dependence
  • High suicide attempt rate (~20% if no improvement in sx)
  • NT imbalance may impact 1 or more of NE, glutamate, DA, GABA, or serotonin
29
Q

Benefits of prazocin for nightmares

A
  • Alpha-1 antagonist, crosses BBB
  • Non-sedating
  • Reduces nightmares & disturbed arousals
  • Benefits on suicidality are uncertain
30
Q

PTSD tx

A
  • Initially, focus on presenting sx w/ pharm & non-pharm approaches
  • Psychotherapy including CBT, psychoeducation
  • Antidepressants – SSRIs, SNRIs, TCAs, mirtazapine
  • Target is decrease of hyperarousal, re-experience, avoidance/ numbing
  • Antidepressants – 12-week trial/ 12-month maintenance supported by evidence
  • Dosing similar to that for depression appears appropriate
31
Q

Describe accumulation of BZDs

A
  • Accumulation – consider t1/2 of parent and metabolite
    • Lorazepam and alprazolam –> less accumulation w/ multiple dosing
    • Lorazepam and oxazepam –> favoured metabolism (glucuronide); preferred for elderly (not diazepam b/c long half-life so will accumulate)