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PHAR358 > Anxiety > Flashcards

Anxiety Flashcards

1
Q

What is anxiety?

A

a normal emotion under circumstances of threat and is thought to be part of the evolutionary fight or flight reaction of survival

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2
Q

Describe some general key points regarding anxiety.

A

a certain amount of anxiety is considered to be a normal reaction to a stressful situation
-mild-mod anxiety can help focus attention, energy, and motivation
anxiety disorders are amongst the most common mental health disorders and have high comorbidity with mood disorders
chronic anxiety associated with profound functional impairment

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3
Q

When does anxiety become disorder?

A

when it is overwhelming and affecting function & QoL by causing feelings of helplessness, confusion, and extreme worry that are out of proportion with the seriousness or likelihood of the feared event

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4
Q

What are the shared features amongst anxiety disorders?

A

excessive fear and anxiety & related behavioral disturbances

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5
Q

Differentiate fear and anxiety.

A

fear: emotional response to a real or perceived imminent threat
anxiety: anticipation of future threat

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5
Q

In general, how do anxiety disorders differ amongst themselves?

A

the types of objects or situations that induce fear, anxiety, or avoidance behavior and the associated cognitive ideation

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6
Q

How do anxiety disorders differ from developmentally normative fear?

A

by being excessive or persisting beyond developmentally appropriate periods

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7
Q

What are the core symptoms of anxiety?

A

psychological:
-fear/anxiety, worry, apprehension, difficulty concentrating
somatic (physical):
-increase HR, tremor, sweating, GI upset

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8
Q

True or false: most 1st line meds are effective for all anxiety disorders

A

true

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9
Q

Which brain regions and circuits regulate anxiety and worry?

A

amygdala: anxiety
cortico-striato-thalamo-cortical circuit: worry

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10
Q

Where is the amygdala located?

A

almond shaped brain center located near hippocampus

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11
Q

What is the role of the amygdala?

A

interpret sensory and cognitive information and determine if there will be a fear response
communicates with areas of the prefrontal cortex
-affect response=feelings of fear
-motor response = fight/flight or freeze

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12
Q

Which reciprocal connections regulate the feelings of fear?

A

the amygdala + the anterior cingulate cortex (ACC) and orbitofrontal cortex (OFC)
-may be overactivation of these circuits=feelings of fear

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13
Q

Which reciprocal connections regulate the behaviors of avoidance?

A

amygdala and periaqueductal grey (PAG)
-motor response: freeze or F/F

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14
Q

Activation of which area of the prefrontal cortex results in changes in respiration?

A

activation of the parabrachial nucleus (PBN) via the amygdala
-can also cause SOB, asthma exacerbation, etc.

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15
Q

Which reciprocal connections regulate the cardiovascular response?

A

amygdala and locus coeruleus = increased BP and HR
long term activation of this circuit may lead to increased risk of atherosclerosis, ischemia, BP/HR changes, MI, or sudden death

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16
Q

What are the symptoms of anxiety/fear associated with?

A

malfunctioning of amygdala-centered circuits

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17
Q

Which neurotransmitters are responsible for regulating amygdala-centered circuits?

A

serotonin
GABA
glutamate
NE
CRF
also voltage-gated ion channels

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18
Q

What is the CSTC linked to?

A

the prefrontal cortex

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19
Q

What is the CSTC under the control of?

A

neurotransmitters (like the amygdala)
-5HT, DA, NE, GABA, glutamate
and voltage-gated ion channels

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20
Q

Overactivation of which loop might lead to worry?

A

CSTC and the dorsolateral prefrontal cortex (DLPFC)

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21
Q

What is GABA?

A

key NT for anxiety and the role of anxiolytics
principal inhibitory NT in brain that plays a role in decreased activity of neurons

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22
Q

Which voltage-gated calcium channels are relevant to psychopharmacology?

A

N and P/Q are subtypes of VSCC

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23
Q

How do gabapentin and pregabalin work for anxiety?

A

bind to the a2S subunit of the presynaptic N and P/Q VSCC to block release of glutamate when neurotransmission is excessive (amygdala and CTSC loop) to decrease fear and worry

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24
Q

What is an option in non-responding anxiety or in combination with an AD/BZD?

A

gabapentin and pregabalin
-since different MOA

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25
Q

What is the role of serotonin in anxiety?

A

key NT innervating the amygdala and CSTC
assists with regulating fear and worry

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26
Q

How do SSRI/SNRIs work for anxiety?

A

block 5HT re-uptake by blocking 5HT transporter
-5HT assists with regulating fear and worry

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27
Q

What is the MOA of buspirone?

A

5HT1A agonist

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28
Q

What is the use of buspirone?

A

effective only in GAD and to potentiate antidepressants

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29
Q

What is the onset of buspirone?

A

onset similar to AD suggesting mechanism similar to AD
-2 weeks or longer, not useful for acute anxiety

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30
Q

Describe the role of NE in anxiety.

A

NE is regulator to amygdala and to PFC/thalamus in CSTC circuits by attaching to the a1 and B1 adrenergic receptors
LC increases autonomic activity to trigger fear, panic, anxiety and effects processing in PFC

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31
Q

How is hyperarousal (nightmares) managed?

A

a1 blockers (prasozin)

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32
Q

How do NE reuptake inhibitors work for anxiety?

A

symptoms can be worsened at initial dosing with SNRIs but as B1 receptors downregulate fear/worry to improve long term

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33
Q

What should be evaluated for with each anxiety disorder?

A

suicidal ideation or intent

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34
Q

Which anxiolytics showed delayed onset of action?

A

serotonergic agents (SSRI, SNRI, TCA)
a2S ligands (pregabalin, gabapentin)
5HT1A agonists (buspirone, SGA)

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35
Q

Which anxiolytics showed immediate onset action?

A

benzodiazepines
beta-blockers (propranolol, atenolol)

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36
Q

Which anxiolytic agents show intermediate onset of action?

A

a1 antagonists (prazosin)

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37
Q

What are some considerations to think of for bupropion?

A

activating
risk of seizures (avoid if hx of seizures, head trauma, bulimia, anorexia, electrolyte disturbances)

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38
Q

What are some considerations to think of for buspirone?

A

slow onset, modest efficacy
maybe helpfult to augment therapy in those with partial response to antidepressants
avoid if comorbid depression

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39
Q

What are some considerations to think of for citalopram?

A

lower risk for insomnia, agitation, drug interactions compared to other SSRIs
dose dependent risk of QT prolongation

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40
Q

What are some considerations to think of for duloxetine?

A

may be useful for comorbid pain
compared to SSRIs:
-increased withdrawal sx if not tapered
-increased insomnia or agitation
avoid if liver disease or heavy EtOH use

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41
Q

What are some considerations to think of with escitalopram?

A

similar to citalopram
-except QT risk if controversial

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42
Q

What are some considerations to think of with fluoxetine?

A

more activating than other SSRIs
self-tapering due to long t1/2
drug interactions

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43
Q

What are some considerations to think of with fluvoxamine?

A

withdrawal sx if not tapered
risk for drug interactions due to inhibition of CYP1A2 and 2C19

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44
Q

What are some considerations to think of with hydroxyzine?

A

useful for comorbid insomnia
dose-related anticholinergic effects limit clinical use

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45
Q

What are some considerations to think of with imipramine?

A

anticholinergic
cardiotoxic in overdose
not well tolerated

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46
Q

What are some considerations to think of with mirtazapine?

A

helpful with comorbid insomnia
lower doses are more sedating
may increase appetite and lead to weight gain

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47
Q

What are some considerations to think of with paroxetine?

A

compared to other SSRIs
-more sedating
-less agitation
-more constipation
-withdrawal sx if not tapered
may be associated with greater weight gain
concerns for drug interactions
avoid in pregnancy due to cardiac septal effects

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48
Q

What are some considerations to think of with pregabalin?

A

sedation and dizziness are common
weight gain, especially with long term use

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49
Q

What are some considerations to think of with quetiapine?

A

concerns for metabolic ADEs
sedation
EPS

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50
Q

What are some considerations to think of with sertraline?

A

compared to other SSRIs
-insomnia
-agitation
-dizziness

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51
Q

What are some considerations to think of with venlafaxine?

A

compared to other ADs
-greater risk for insomnia or agitation
-increased BP
possible benefit for comorbid pain
few drug interactions
withdrawal sx if not tapered
better evidence for psychological sx

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52
Q

When is the onset of GAD usually seen?

A

usually in late adolescents or early adulthood

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53
Q

What is the etiology of GAD?

A

unknown
likely combined effect of biological and psychological factors

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54
Q

What are some drugs associated with anxiety symptoms?

A

antidepressants
-SSRI, SNRI, bupropion
corticosteroids
stimulants
-amphetamines, MPH, nicotine, caffeine, cocaine
sympathomimetics
-PSE, PE

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55
Q

What are some potential causes of GAD to keep in mind if suspecting a person has GAD?

A

medications
natural products
medical conditions
withdrawal (alcohol, sedatives, BZD)
socioeconomic (poor minority classes)
stressful event in susceptible person

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56
Q

What is the key point regarding GAD and co-morbidities?

A

GAD frequently co-occurs with other mental health disorders which complicates diagnosis and tx
-some studies suggest up to 90% of pts with GAD present with comorbidity
GAD can also co-occur with physical health problems & may exacerbate these physical illnesses and interfere with a persons ability to manage them
-pain, DM, CVD, GI, HA, fatigue

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57
Q

What are some good questions to screen someone for GAD?

A

in the past several months how frequently have you worried or been anxious about a number of things in your life?
what have you worried about?
do people tell you that you worry too much?
do you think you do?
do you have difficulty controlling your worry such that it keeps you from sleeping or makes you feel physically ill with HAs, stomach trouble, or fatigue?
when you worry do you often…feel restless? get tired easily? feel irritable? feel tense muscles? trouble sleeping?

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58
Q

What are some psychological and cognitive symptoms of GAD?

A

excessive anxiety
worries that are difficult to control
feeling on edge
poor concentration
restless
irritable
sleep disturbances

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59
Q

What are some physical symptoms of GAD?

A

fatigue
muscle tension
trembling/shaking
feeling of fullness in throat/chest
sweating
cold, clammy hands

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60
Q

What can GAD lead to in turns of impairment?

A

social, occupational or other important functional areas
poor coping skills

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61
Q

What are examples of GAD standardized rating scales?

A

GAD-7
-self rated
-screens for GAD & severity
-brief
HAM-A
-clinician rated
-brief
-assess response to treatment, assess severity of anxiety

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62
Q

What are the goals of therapy for GAD?

A

acute episode
-decrease severity and duration of anxiety symptoms
-improve overall function
long-term goals
-remission (with minimal/no anxiety sx, no functional impairment, improve QoL)
treat co-morbid conditions including SUD

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63
Q

What are the treatment principles of GAD?

A

psychotherapy + pharmacotherapy
-psychotherapy is least invasive and safest
-pharm indicated if sx severe enough to produce functional disability

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64
Q

What should be taken into consideration before initiating treatment for GAD?

A

anticipated AEs
history of prior response in patient or family member
patient preference
cost

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65
Q

What is the non-pharm treatment for GAD?

A

reduce/avoid alcohol/caffeine/nicotine
avoidance of OTC stimulants & medications known to induce anxiety
exercise
psychotherapy +/- counselling
relaxation techniques
biofeedback

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66
Q

What is the most effective psychological therapy for GAD?

A

CBT
-underused due to cost, time requirements, limited professionals
-comparable efficacy to meds in acute tx, sustained reduction in anxiety over 6-12 months

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67
Q

What is CBT?

A

identifies negative thought patterns that provoke anxiety and changes thoughts to be more positive

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68
Q

What are the 1st line treatment options for GAD as per ADAC?

A

SSRI: escitalopram, paroxetine, sertraline
SNRI: duloxetine, venlafaxine
pregabalin

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69
Q

What are the 2nd line treatment options for GAD as per ADAC?

A

BDZ (short term): alprazolam, lorazepam, diazepam
bupropion
buspirone
hydroxyzine
imipramine
quetiapine
vortioxetine

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70
Q

What is the best thing to do for GAD when there has been a partial response to pharmacotherapy?

A

current data does not provide guidance as to whether it is best to increase the dose, augment, or switch
-the PAPHSS provides guidance

71
Q

What are some key takeaways from the PAPHSS algorithm?

A

if tried an SSRI but no response can try second SSRI or duloxetine
if tried an SSRI but partial response can try augment with hydroxyzine, pregabalin, BZD (no SGA until third trial)

72
Q

Which SSRIs have been studied for GAD?

A

sertraline, paroxetine, escitalopram
-others used in practice

73
Q

Which SNRIs have been studied for GAD?

A

duloxetine
venlafaxine

74
Q

What is the evidence for mirtazapine in GAD?

A

open label trials have shown it to be effective
-low evidence but can be helpful

75
Q

What is the role of benzos for GAD?

A

for acute anxiety for 2-3 weeks until antidepressants start to work

76
Q

Is long term use of benzos recommended for GAD?

A

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

77
Q

Do benzos have a role in depression?

A

not effective for depressive symptoms and may worsen depression

78
Q

In which patients might buspirone be more useful in?

A

patients who have not used benzos

79
Q

What is the MOA of hydroxyzine?

A

H1 and 5HT2 antagonist

80
Q

Why is hydroxyzine used 2nd/3rd line for GAD?

A

due to ADEs and lack of efficacy for comorbidities

81
Q

What are the side effects of hydroxyzine?

A

anticholinergic
sedation

82
Q

Why are SGAs 3rd line for GAD?

A

due to ADEs and limited evidence

83
Q

Which SGAs are effective as augmenting agents in GAD?

A

quetiapine
olanzapine
risperidone

84
Q

What is the onset of symptom relief with SSRI/SNRIs for GAD?

A

2-4 weeks
-maximal response: 12 weeks

85
Q

What is the treatment duration of GAD with SSRIs/SNRIs?

A

12-24 months

86
Q

What is the MOA of benzodiazepines?

A

bind to the BZD receptors on the GABAa neuron
-leads to an increase in the frequency of opening of 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

87
Q

Describe the efficacy of benzodiazepines.

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 sx (muscle tension, change in sleep) rather than key psychic features that are characteristic of GAD
magnitude of effect for GAD appears to be similar to that of cognitive therapy

88
Q

Which benzos have RCTs supporting their efficacy in GAD?

A

alprazolam
bromazepam
diazepam
lorazepam
while there are no RCTs evaluating the use of clonazepam in GAD, it is used extensively in clinical practice for the treatments of anxiety and it is likely that the benefits are similar to other benzos

89
Q

Why is clonazepam often used in clinical practice for GAD even though it has no RCTs evaluating its use?

A

maintains its effect within the entire dosing window (longer t1/2) and avoids the peaks and troughs seen with other benzos

90
Q

Which benzos are longer acting?

A

clonazepam (t1/2 20-80h)
diazepam (t1/2 100h)
good choice for tapering as less risk of withdrawal, more daytime sedation

91
Q

Which benzo has a quick on and quick off?

A

alprazolam

92
Q

In general, what is the onset of benzos?

A

~20-60 min

93
Q

What are the adverse effects of benzos?

A

ataxia
dizziness, lightheadedness
sedation & residual daytime sleepiness
-tolerance to sedation may develop
psychomotor impairment
agitation, irritability, confusion
-variability in the way people respond to benzos
-paradoxical responses

94
Q

What are some less common adverse effects of benzos?

A

anterograde amnesia
-more common with lorazepam
depression, confusion, bizarre behavior, hallucinations
respiratory depression

95
Q

What might occur to the anxiolytic effects of benzos when used chronically?

A

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

96
Q

What might occur with long-term use of benzos?

A

psychological and physical dependence

97
Q

What increases the risk of dependence on benzos?

A

higher dose and/or longer use
-risk further increased with hx of AUD/SUD or personality disorders

98
Q

When do withdrawal symptoms appear from benzos?

A

can occur following dc of therapy with as little as one week of use

99
Q

Which benzo is short acting?

A

lorazepam
-better hypnotic and sedative properties but more rebound anxiety, inter-dose withdrawal, anterograde amnesia

100
Q

What is the benefit of the LOT drugs? What are they?

A

lorazepam, oxazepam, temazepam
preferred in elderly and liver dysfx as no active metabolites

101
Q

What are the withdrawal symptoms of benzos?

A

sweating
tremor
NV
rebound anxiety
increased HR
insomnia
agitation
twitching
visual/tactile hallucinations
*SEIZURES (ONSET WITHIN 1-2 DAYS AFTER BZD STOPPED)

102
Q

How can the withdrawal symptoms of benzos be avoided?

A

tapering

103
Q

Which benzos are good for tapering?

A

diazepam or clonazepam
-decrease 10-20% q1-2wks

104
Q

What are some precautions for benzos?

A

SUD (esp opioids=increased risk of resp dep)
sleep apnea
COPD
elderly
CNS depression
pregnancy
clozapine-use (sedation, excessive salivation, resp arrest)

105
Q

What is the risk of benzo use in pregnancy?

A

floppy infant syndrome
-possible teratogen and can precipitate withdrawal in newborns if used in 3rd trimester

106
Q

Are benzos commonly fatal on their own?

A

rarely
-increased risk with alcohol, opioids, barbiturates

107
Q

What is the benzo antidote?

A

flumazenil
-reverses hypnotic-sedative effect of BZD but clinically use is limited due to risk of causing seizures in BZD dependent patients

108
Q

What do people with panic disorder experience?

A

seemingly out of the blue panic attacks that interfere with their daily lives
-they often live in fear of their next panic attack and might have anxiety about situations that could set one off

109
Q

Differentiate panic attacks and panic disorder.

A

panic attacks:
-a distinct period of intense fear and discomfort when 4 or more sx develop suddenly and achieve a peak within 10 min
-chills/flushing, GI, increased HR, sweating, fear of dying, feeling of unreality, trembling, SOB, feeling of choking, chest pain, numbness, dizzy
panic disorder:
-recurrent unexpected attacks with at least 1 of the attacks being followed by 1 month or or longer with at least one of the following: concern of having another attack, being anxious of the implications of an attack, maladaptive behavior change to avoid attacks

110
Q

Describe some key points about the epidemiology of panic disorder.

A

rates increase during adolescents and peak during adulthood
-lower rates <14yrs and >64yrs
females 2: males 1
untreated is chronic but waxing and waning
high rates of social, occupational, and physical disability; economic costs; highest # of hospitalizations among anxiety disorders

111
Q

What is the etiology and risk factors for panic disorder?

A

mixture of biological and psychological factors along with some environmental factors
-personality types
-temperamental
-environment (ex: abuse history, smoking)
-genetic and physiological
-medications (as per GAD)

112
Q

What are some comorbidities that might be seen with panic disorder?

A

other anxiety disorders
depression
bipolar
alcohol use disorder
higher rates of suicide attempts and suicidal ideation
medical comorbidities
-asthma, COPD, arrhythmia, hyperthyroid, Cushings, IBS, dizziness, pheochromocytoma

113
Q

Describe the clinical presentation of a panic attack.

A

psychological:
-depersonalization, derealization, fear of losing control/dying/going crazy
physical:
-sweating, trembling, tachycardia, chills, dizziness, chest pain, feeling of choking, abdominal distress, hot flashes, nausea, paresthesias, SOB

114
Q

Describe the clinical course of panic disorder.

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 patients have unremitting & chronic course

115
Q

What do most patients with panic disorder require and why?

A

long-term treatment to achieve remission, prevent relapse, and reduce risks associated with comorbidity

116
Q

What are the predictors of a chronic course of panic disorder?

A

long duration of illness
comorbidity with other mood, anxiety, personality disorders
excessive sensitivity to the physical sx of anxiety

117
Q

What are the treatment principles for panic disorder?

A

initiate tx with meds or psychotherapy
-evidence does not support superiority of either or combo
-augment with CBT if ongoing sx despite pharm
1st line pharmacotherapy: SSRI or venlafaxine
-BZD for residual anxiety and/or rapid sx control
2nd line pharmacotherapy:
-TCA: similar efficacy but less well tolerated
-augment with BZD or SGA
3rd line pharmacotherapy:
-phenelzine (if not responded to anything else)

118
Q

How does the effectiveness of CBT compare to pharmacotherapy for panic disorder?

A

comparable effectiveness

119
Q

What are the 1st and 2nd line treatment options for panic disorder according to APA?

A

1st line:
-SSRI: citalopram, escitalopram, fluoxetine, fluvoaxmine, paroxetine, sertraline
-SNRI: venlafaxine, duloxetine
2nd line:
-TCA: clomipramine, imipramine
-BZD: alprazolam, clonazepam

120
Q

Which SSRIs are most effective for panic disorder?

A

no evidence of differential efficacy between SSRIs

121
Q

Describe the efficacy of SNRIs for panic disorder.

A

venlafaxine:
-no comparative trials to SSRIs but better than placebo
duloxetine:
-open label study demonstrated anxiolysis

122
Q

Describe the efficacy of TCAs for panic disorder.

A

efficacy comparable to SSRIs but less well tolerated
clomipramine and imipramine most studied
useful for intolerance or ineffectiveness to SSRI/SNRI

123
Q

Describe the evidence for mirtazapine in panic disorder.

A

open label study found it equal to fluoxetine in decreasing panic attacks

124
Q

When is phenelzine used for panic disorder?

A

when SSRIs, SNRIs, and TCAs have not been effective

125
Q

What is the role of benzos for panic disorder?

A

2nd line after failed several trials of antidepressants
do not use monotherapy if comorbid depression
avoid if hx of SUD
limited data supports combo BZD + SSRI in during first few weeks for rapid sx relief

126
Q

What is the role of benzos for panic attacks?

A

NOT an effective strategy as the onset of the benzo will occur after the panic attack

127
Q

What is the onset for antidepressants in panic disorder?

A

most patients with PD are hypersensitive to medication AE at initiation (anxiety, agitation, irritability)
reduction of panic attack frequency, anticipatory anxiety, and avoidance may take 3-4 wks
full remission may take 6 months of longer if significant avoidance

128
Q

What is the onset for benzos in panic disorder?

A

hours for autonomic sx of anxiety, full benefit may take 4-6 wks

129
Q

Describe important treatment timeframes for panic disorder.

A

acute tx duration: 1-3 months
-alter tx if no response in 6-8 wks
maintenance tx duration: 12 months
-if residual sx continue then continue tx
-factors to consider before stopping: motivation to stop, ongoing stressors, duration of stability
tapering duration: 4-6 months
-slow to reduce relapse risk

130
Q

Describe the epidemiology of SAD.

A

higher rates in females than males
median age of onset: 13 years
-prevalence decreases with age
associated with increased school dropouts and decreased QoL, well-being, employment, SES, and productivity
only ~50% seek tx and usually after 15-20yrs of sx

131
Q

What are the risk factors for SAD?

A

combo of environmental and genetic risk factors

132
Q

Describe the comorbidity often seen with SAD.

A

70-80% have concurrent anxiety, depression, and SUD
females report greater # of social fears and comorbid depressive, bipolar, and anxiety disorders
comorbid MDD higher in older adults
males more likely to fear dating, have oppositional defiant disorder or conduct disorder, and use alcohol or recreational drugs to relieve sx of disorder
substances may be used to self-medicate for social fears but sx of intoxication or withdrawal may be a source of further social fear

133
Q

Describe some of the signs and symptoms of SAD.

A

fears:
-embarrassment/humiliation
-being scrutinized by others
feared situations:
-public speaking
-eating/drinking in front of others
-using public washrooms
-interacting with authority figures
-talking with strangers
physical symptoms:
-diarrhea
-butterflies
-trembling
-tachycardia
-sweating
-blushing
types:
-generalized: fear and avoidance of a wide range of situations
-nongeneralized: fear is limited to one or two situations

134
Q

What are some non-pharm treatments for SAD?

A

CBT: education, exposure, cognitive restructuring
-treatment for at least 12 weeks
-individual treatment more effective than group treatment
-similar efficacy to pharmacotherapy for acute tx
-effects may last 6-12+ months
social skills training

135
Q

What are the treatment principles for SAD?

A

1st line: individual CBT or SSRI
-if both declined: interpersonal therapy
if little or no response try alt SSRI or venlafaxine
limited evidence to support augmentation with buspirone, clonazepam or SGA in partial response
phenelzine can be used in treatment refractory patients

136
Q

What are the 1st line treatment options for SAD according to the Canadian Anxiety Guidelines 2014?

A

SSRI: escitalopram, paroxetine, sertraline, fluvoxamine
SNRI: venlafaxine
pregabalin
CBT
fluoxetine is 3rd line

137
Q

What is the role of propranolol and atenolol in SAD?

A

performance situations

138
Q

Describe the evidence for SSRIs in SAD.

A

many RCTs support use to improve anxiety, avoidance sx, and disability
meta-analyses found the odds 3x > than placebo

139
Q

What should be kept in mind regarding dosing with SSRIs in SAD?

A

generally flat dose response curve
-few pts respond to higher doses

140
Q

Describe the evidence for venlafaxine in SAD.

A

effective for pts who fail to respond to SSRIs
improves social function, performic, some fear factors

141
Q

Describe the evidence for anticonvulsant use in SAD.

A

pregabalin and gabapentin found to be effective in small RCTs

142
Q

Describe the evidence for beta-blocker use in SAD.

A

may be used for performance related SAD
decreases tremor, palpitations, and blushing

143
Q

How should beta-blockers be dosed for SAD?

A

1-2 hours before performance
give test dose to assess tolerability

144
Q

Describe important treatment timeframes for SAD.

A

onset of sx relief: 6-8 wks
-as early as 3 wks with venlafaxine
treatment duration: 1+ yrs
tapering duration: 3-4 months (slow to decrease relapse risk)

145
Q

Describe the epidemiology of PTSD.

A

lifetime prevalence of traumatic experiences: 50-90%
PTSD prevalence: 8-9%
-2x more women than men
most people are resilient

146
Q

What are some risk factors for PTSD?

A

trauma severity
lack of social support
life stress

147
Q

Summarize some key points regarding the pathophysiology of PTSD.

A

reconsolidation of memories:
-memory traces are potentially vulnerable to modification
alert, safe, interested:
-moderate lvls of catecholamines weakening the amygdala
stressed:
-high lvls of catecholamines strengthening the amygdala
insufficient glucocorticoids at time of trauma:
-enhances SNS activation that enhances consolidation of traumatic memory

148
Q

What are the 3 dimensions of PTSD once trauma has occured?

A
  1. re-experiencing the event with distressing dreams, flashbacks, recollections, psychological and physical distress
  2. persistent avoidance of stimuli that might invite memories or experiences of the trauma
  3. increased arousal
149
Q

Describe the comorbidity seen with PTSD.

A

75-80% have other psychiatric disorder (many have > 3)
-MDD (worsens prognosis, decreased tx response)
-SUD/AUD
-anxiety
-psychosis
-bipolar
-personality dysfx
increased rates of medical comorbidities
-CVD, respiratory, autoimmune

150
Q

What is the core of PTSD treatment?

A

trauma-focused psychotherapy

151
Q

What are the limitations of trauma-focused psychotherapy?

A

resources
high drop out rates
30-50% have residual sx

152
Q

What are the goals of therapy in PTSD?

A

symptom reduction:
-decrease intrusive thoughts and images
-decrease avoidance of trauma related stimuli
-decrease mood symptoms (negative thoughts)
-decrease hyperarousal/reactivity
improve:
-sleep, QoL, and participation in non-pharm tx
minimize:
-AEs and comorbidities

153
Q

What are the 1st line treatment options for PTSD according to the Canadian Anxiety Guidelines 2014?

A

SSRI: fluoxetine, paroxetine, sertraline’
SNRI: venlafaxine
prasozin: trauma related nightmares

154
Q

Which agents are NOT recommended for PTSD according to the Canadian Anxiety Guidelines 2014?

A

alprazolam, clonazepam
citalopram
DVP

155
Q

What is the role of benzos in PTSD?

A

should be relatively contraindicated
-lack of efficacy
-potential for harm (worse severity, worse outcomes, development of aggression/depression/SUD)

156
Q

What are important timeframes to keep in mind with treatment of PTSD?

A

onset of sx relief: 2-8 wks
maximal response: 12 wks
tx duration: 12-24 months

157
Q

What is OCD?

A

OCD is defined by the relationship between obsessions and compulsions
-obsession: unwanted, intrusive thoughts/images/urges that trigger intensely distressing feelings
-compulsion: behaviors an individual engages in to attempt to get rid of the obsession and/or decrease distress
when a person with OCD have obsessions which cause anxiety, they do a compulsion to relieve that anxiety

158
Q

Describe the epidemiology of OCD.

A

more common in individuals with other psychiatric disorders
females slightly more affected than males
mean age of onset 19.5 years

159
Q

What is the pathophysiology of OCD?

A

not well understood
possibly related to abnormalities in:
-serotonin neurotransmission
-dopamine transmission
-glutamate

160
Q

What is the etiology/risk factors for OCD?

A

mix of genetics and environment
-pregnancy
-1st degree relative
-environment
-PANDAS
-temperamental

161
Q

Describe the clinical course of OCD.

A

commonly 1st present to physician other than psychiatrist
> 50% have sudden onset of symptoms
onset often occurs after a stressful event
usually a delay of 5-10yrs before tx as patients keep sx secret
if untreated, course is chronic with waxing and waning sx
1/3 have depression, suicide is a risk for all patients

162
Q

Describe the comorbidity seen with OCD.

A

males more likely to have comorbidities
suicidal thoughts occur at some point in ~50% of pts, suicide attempts are reported in 25%
MDD and bipolar common
anxiety disorder
tic disorder
triad of OCD, tic disorder, and ADHD can also be seen in children

163
Q

What are some indicators of a good prognosis for OCD?

A

good social & occupational adjustment
presence of precipitating event
episodic nature of the symptoms

164
Q

What are some indicators of a poor prognosis for OCD?

A

acting on compulsions
bizarre compulsions
delusional beliefs
childhood onset
need for hospitalization
comorbid depression
comorbid personality disorders

165
Q

What are some signs and symptoms of OCD?

A

obsessions
-fear of contamination
-unwanted sexual or aggressive thoughts
-doubts
-need for symmetry
-concerns about throwing away something valuable
compulsions:
-washing, cleaning
-checking, pray, asking for reassurance
-repeated checking behaviors
-hoarding
-ordering/arranging/balancing until “just right”

166
Q

What is an example of a standardized rating scale for OCD?

A

Yale-Brown Obsessive Compulsive Scale (Y-BOCS)
-clinician rated
-measures overall severity of obsessions/compulsions

167
Q

Describe the treatment approach to OCD.

A

1st line is CBT or SSRI
-combo tx can be considered
-trial 1st line pharmacotherapy x 12wks and CBT x 13 weekly sessions before concluding inadequate response
-sx reduction often takes 6-8 wks (up to 10-12 wks)
if little or no response try alt SSRI or venlafaxine
clomipramine is recommended after failure of 2 SSRIs
augmentation:
-consider in pts with partial response as 40% of pts will have a decrease in Y-BOCS of 25% in 4 wks

168
Q

What is the non-pharm treatment for OCD?

A

CBT
-as effective as pharmacotherapy
-more effective for compulsions vs obsessions
-guidelines suggest it should be offered to all patients
deep brain stimulation
radio frequency wave surgery

169
Q

What are the 1st and 2nd line treatment options for OCD according to the Canadian Anxiety Guidelines 2014?

A

1st line:
-SSRI: escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline
-SNRI: venlafaxine
-adj: aripiprazole, risperidone
2nd line:
-clomipramine, citalopram, mirtazapine

170
Q

Describe the evidence for SSRIs in OCD.

A

40-60% response rate
higher doses produced increased responses
similar efficacy to clomipramine but more tolerable

171
Q

Describe the evidence for venlafaxine in OCD.

A

large RCT found as effective as paroxetine

172
Q

Describe the evidence and key points for clomipramine in OCD.

A

mean Y-BOCS score typically decreased by 40%
equal or slightly more effective than SSRIs (less effective if comorbid depression)
metabolized hepatically
fluvoxamine, paroxetine, and fluoxetine inhibit metabolism

173
Q

Describe the evidence for SGA augmentation in OCD.

A

meta-analysis of SGA + AD found efficacy for risperidone but not quetiapine or olanzapine
results for aripiprazole and haloperidol are mixed
1/3 of AD-resistant OCD pts benefited from augmentation

174
Q

Describe some key monitoring parameters for OCD.

A

acute phase: weekly x 4 wks then biweekly, once stable q1-2mo
assessment of response:
-Y-BOCS used to evaluate obsessive and compulsive sx
-tx goals should be individualized
encourage pts to keep a sx diary
-date and content of obsessions and compulsions
-time spent carrying out compulsion

175
Q

Describe important OCD treatment timeframes.

A

onset of sx relief: 2-4 wks
maximal response: 10-12 wks
tx duration: 1-2 yrs
-experts recommend tx should be indefinite in most

PHAR358 (20 decks)

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