Anxiety D/O Flashcards
primary neurotransmitter in fear
norepinephrine
primary neurotransmitter in anxiety
gamma-aminobutyric acid benzodiazepine system
what is anxiety
response to a threat that is unknown, vague, internal or a response to an indirect threat such as a loss of people or things that represent security
neural circuit of fear and anxiety
- a threatening stimulus is integrated into an image linked to a place and time
- activated memory traces of prior experiences
- incorporate the emotional tone of previous experience
- then trigger an appropriate response
the stimuli from the sensory system is transmitted to the thalamus to the amygdala
Short loop in fear and anxiety
- direct pathway from thalamus to amygdala
- emotional input is based on fragments of information and precedes conscious appraisal of the stimuli based on integrated perceptions of objects and events
- short loop jump starts the fear system and therefore it will process info arriving later with info from cortex
long loop
- sensory info is first processed in sensory cortex then to amygdala, hypothalamus, and brain stem that is involved in emotional behavioral and somatic responses to anxiety and fear
- long loop regulates the response of amygdala (whether to continue or stop response)
- amygdala gets info from short loop directly therefore anxiety may involve imbalance of the control over the long loop over the short loop
GAD criteria
has to last for atleast 6 months is accompanied by hyper vigilance and multiple somatic sx substantial impairment worry about every day things degree of worry is out of proportion
GAD epidemiology and etiology
- occurs in women more than men
- usually around age of 20
- associated with more psych co-morbidities
- fam hx; hx of abuse/trauma; a medical illness; smoking; seperated/divorces/widowed
- genetic 22-37%;
GAD theories
Frued (conflict between id/ego/superego); insecure attachment patterns; biological (structural abnormalities of occipital, basal ganglia, limbic system, hippocampus, brain stem, frtonal cortex); impairment of cognitive functioning (ppl will view ambiguous info as threatening or negative, pay more attention to potential threats, pessimistic)
GAD and co-morbidities
MDD; substance abuse; cluster c avoidant personality sx; OCD; IBS; HA
differential dx
- high level worriers: have more control over their worry than GAD, usually onset is after 35 and GAD is 20;
- med dx
GAD tx
- CBT: greatest effects are achieved after 6months of wkly therapy; long term effects maintained in half of pts; Good
- SSRIs SNRIs first line
a. Buspar-Sa1 agonist; effective in a lot of pts with GAD
BUT NOT IF THEY have been on BZD before
less effective in tx somatic but good at psychological sx
No antidepressant effect
first choice if hx of substance abuse; pulmonary disease;
those who operate heavy equipment - BZD effective in acute phase; strongest effect on hyper vigilance and somatic sx; less effective in relieving sx of dysphoria/depression; w/drawal sx;
- wellbutrin is NOT effective in GAD
- venlafaxine and duloxetine are approved for GAD and considered first line tx about 70% response rate; good with somatic sx;
- fluoxetine may increase anxiety but paroxetine and sertraline do not
- beta blockers good for palpitations, sweating tremors; performance anxiety take 2 hours before event
SAD definition
response to a threat to social status or reputation
fear of social performance or in social situation
SAD in children
associated with failing grade
in adolescents can see dropping out of school, not graduating, increased risk for alcohol abuse
SAD epidemiology and etiology
- more in women, those who have not married, and those who never completed high school
- western society may have fear of embarrassing self but in Japan more fear of offending others and AA fear of failing/evaluation
- pattern with first degree relatives; some genetic influence; infants with inhibited personality are at risk;
Theories of SAD
- developmental theories: parents who are distant and rejecting have children who are shy and socially w/drawn (maternal depression; nervousness and irritability) (insecure attachment patters or inhibited temperment lack opportunities and support to develop social skills)
- biological basis: high concentrations of carbon dioxide, caffeiene or cholecystokinin that stimulates release of cortisol and ACTH hormones, patients with SAD and panic disorders have more intense reactions to controls
SAD tx
- exposure therapy; CBT;
- for generalized SAD: SSRIs and SNRIs considered first line; venlafaxine is good;
- second line pharm: BZD, mirtazapine;
- NOT effective is bupropion and TCAs;
- combined therapy with pharm is best, pharm see improve faster and CBT is longer lasting
- non-generalized SAD: beta blockers like metropolis or atenolol and propranolol or BZD are first choice; decrease autonomic distress; take two hours before performance
- social skills training; relaxation techniques
N-methyl-D-aspartate (NMDA receptor agonist
D-cycloserine
- ATB to tx TB
- has effects in brain and helps to overcome phobias
Panic disorder definition
manifestation of an underlying constitutional vulnerability for anxiety, probably a genetic vulnerability; expressed in panic attacks that are key feature; presence of attacks occur frequently and with some regularity; impair social and occupational functioning;
sx: can’t catch their breath, dizzy light headed or faint; feel like they are about to die; events act as triggers
characteristic of panic attack
sudden onset of intense fear
feeling of terror, sense of doom
palpitations, pounding heart, sweating, nausea, dizzy, light headed
fear of dying, fear of loosing control, going crazy
derealization (things aren’t real)
depersonalization (feel that one is detached)
last about 5-20 minutes
occur with or without agroaphobia
panic d/o epidemiology and etiology
occur more often in women
women more likely to have agoraphobia with it
men more likely to use alcohol
more common in never married ppl, less in those who completed college
child hood of SAD
genetics first degree high
panic d/o theories
developmental theories: behavioral inhibition, an attribute to genetically influenced temperament, may be defined as an increased state of arousal and inhibition of behavior in the face of new, unfamiliar or challenges; inhibited temperament (colic in infant, irritability, shyness, fearfulness, constrict behavior in new situations; higher heart rate; agoraphobia; fear of separation like in children is linked to social phobia)
attachment theory: controlling domineering parent; quarrels and violent behavior between parents; threats of abandoment of child or being rejected for being bad; over protective parents
biological: abnormalities in structure (amygdala); carbon dioxide hypersensitivity (dysregulated respiratory control; irregular breathing)
chemical basis/serotonergic dysregulation: important areas lacking serotonin
Stages of panic d/o
stage 1 sub-panic stage: tachycardia, light headedness; SOB
2 panic attacks start with fear of loss of control, freezing, or flight
3 hypochondriasis; pt fears panic sx are related to physical illness
4 anticipatory anxiety for future attacks
5 phobic avoidance
-may become depressed, abuse alcohol; impair relationships, social, occupational, SI
panic d/o co-morbidities
medical: hypothyroidism, cardiac px, resp px, chronic fatigue syndrome; joint hyper mobility and mitral valve prolapse (mitral valve prolapse increased in those with joint hyper mobility and panic d/o)
psychiatric: MDD, SAD, GAD, PTSD, OCD, alcohol abuse; increased risk SI
panic d/o tx
- SSRI’s first line
- BZD can be added
- some pt with panic d/o are very sensitive to medications so have to warn about the side effects so the will be compliant (HA, nausea, irritability, palpitations, dizzy, sweating, tremors; decrease after 2 weeks; start low and go slow; increase every 1 to 2 weeks; 8-12 weeks full treatment could take;
- FDA approved: paroxetine, sertraline, fluoxetine;
- mirtazapine and zofran can limit sx of insomnia, agitation, GI px
- venlafaxine: reduces number and improves anticipatory anxiety, fear and avoidance;
- should be kept on for at least 6 months to prevent relapse
- valproate: moderately effective for panic disorders; used if comorbid with bipolar
- CBT 12-15 weks
OCD definition
chronic illness characterized by thoughts, images, or impulses that are expereinced as anxiety producing intrusive obsessions
themes of OCD
most relate to issues of security, safety and survival
spectrum d/o of OCD
- relate to body:bodyt dysmorphic d/o, depersonalization, anorexia, hypochondriasis
- neurological: tourette’s, sydenhgam’s chorea, torticollis, autism
- impulse d/o: sexual compulsions, trichotillomania, pathological gambling, kelptomania, self injurious behavior
OCD epidemiology and etiology
fourth most common psych d/o 10th leading cause of death men tend to have earlier onset onset may be as young as 2-4 high heritability; genetic predisposition; infection with sydneham chorea (neuro px that causes rheumatic fever); strep infecti9ons; PANDAS (pedieatric autoimmune neuro disorders associated with strept)
theories of OCD
- cognitive theory: obsessions are misinterpretations of intrusive thoughts or impulses. these unwanted intrusive thoughts and impulsions become more intense and persistent and distressing; the person veiws them as being more important; develop thinking that if they dont fulfill the thought or compulsion then something bad will happen; they veiw themselves as evil, dangerous or worry that others will see them as weird
- dimensional model of OCD: sets of symptoms (1. aggressive, sexual, religious, somatic, checking) (2. symetry, ordering, counting, repeating)(3. contamination, cleaning)(4. hoarding and collecting)
- Biological basis: abnomalities in structures within CSTC tract
Basal ganglia and OCD
- may be the primary site for OCD
- it facilitates some movements and suppresses others
- it is involved in thinking about movement and planning it and executing that movement
CSTC path
begins in the PFC, then cingulated cortex, then caudate nucleus, then thalamus, then back to PFC
it is involved in sensorimotor fx, emotional and motivational fx, inhibition of responses, working memory, and executive fx
Striatum and OCD
signals to the CNS; recieves input from cerebral cortex, processes info, filters out unneeded info; then transmits info to thalamus;
controls what goes to and from thalamus
it is involved in motor and cognitive fx
striatum includes the nucleus accumbens: reward fx
neurotrasmitters in OCD
serotonin: inhibits bnehavior such as impulsivity, SI, aggression, and anxiety
dopamine: in OCD it is over active resulting in obsessions and compulsions/repeatative behaviors; overactivity may be from issue with serotonin system
gluatmate: hyperglutamatergic coditions in the PFC (orbito-frontal-cingulate-caudate-pallido-thalamic neural circuitry)
abnormal brain structures in OCD
enlargement of ventricles
reduction of white matter volume (myelin)
corpus callosum
CSTC px
OCD presentation sx
they tend to be pesimistic, pay more attention to negative aspects than to positive, may over generalize negative things, difficulty ignoring intrusive thoughts, feel certain thougths can be harmful, sense of responsiblity for things happening over estimation of threat, perfectionism, intolerance to uncertaninty,
safety seeking behaviors: rituals, neutralizing acts, avoidance, suppression of negative thoughts, reistance to change, need to be certain of things,
OCD 4 common obsessions
contaminiation
pathological doubt
symmetry
somatic
obsession of pathological doubt
believe that they will cause a dire event by their carelessness, worry about leaving stove on, doubt their own perceptions, often use checking rituals
obsession for symmetry
arrage things perfectly, have magical thinking often, feel they must arrang something or their family will get sick,
pts with extreme perfectionism or obsessional slowness may not respond to CBT
somatic obsessions
develop serious illness; often chekcing rituals like checking the body, hypochondriasis,
hoarding obsessions
patients with hoarding have more severe OCD sx and greater disability than with other obsessions
OCD tx
SSRIs (hoarding may have no response or little response, in that case may use atypical antipsychotic for adjunctive and SNRIs may be used) CBT Hoarding (multicomponent CBT model) sessions start later in therapy: 3-6 hour sessions at their lead
fluvoxamine, fluoxetine, sertraline and paroxetine first line (se: n/v, sleepiness, insomnia, tremor, sexual dysfunction) may take 3 months for response: increases SA in PFC
ECT for somatic may be useful; exposure and ritual prevention is more effective than SSRIs
cluster d/o of OCD
cluster 1: peroccupations with bodily sensations/appearance (body dysmorphia, anorexia, hypochondriasis)
cluster 2: impulsive d/o (gambling, trichotillomania, self injury behavior, kleptomania, compulsive shopping)
cluster 3: neurological d/o (effect basal ganglia: autism, sydenhams chorea, torticollis, tourettes)
cluster 4: schizo-obsesive: schizophrenia pts some have comorbid OCD; category can include tics, eating, dissociative disorder, hoarding
hypochondriasis and treatment
- SSRIs paroxetine, fluoxetine, fluvoxamine
- CBT
- onset is usuall 19-23; first line tx is CBT;
Body dysmorphic d/o and treatment
- image flaw
- risk factor: perfectionist personality traits; hx of childhood abuse or neglect; genetic influence; px with SA system and frontal-striatal and temporo-parietal-occipital system;
- misinterpretation of neutral facial expressions as angry and deficits in memory and executive fx
trichotillomania etiology and tx
recurrent pulling out one’s hair; distressful and chronic; tend to be in those with sedentary or contemplative activities like watching tv; onset is in middle childhood or early adolescents; risk factors include having family member with OCD and possible early exposure to trauma; genetic influence and abnormalities in cortico-striatal-thalamic circuitry; involvment of SA system
they may have rituals like eating the hair
tx: habit reversal therapy (HRT) and sertraline together are very effective; other SSRIs
TCA clomipramine (Anafranil) has been effective in this
Skin picking
- or dermatotillomania: form of self injurous behavior
- unknown cause
- thought to be a repetitive behaivor to regulate negative emotions/thoughts;
- tx: fluoxetine (Prozac); clomipramine (a TCA);
pathological gambling
- brings about a sense of release or gratification; very rare; ment tend to start in adolescence and women start later;
- tx: fluvoxamine, mood stabilizers and naltrexoin have been found effective
comorbidities and tx in compuslive buying and kleptomania and sexual obsessions, paraphilias
- compulsive buying: depression, anxiety d/o, substance abuse, d/o with impulsivity
- kleptomania: bipolar d/o, substance, eating, anxiety, compulsive behaviors
- paraphilias are repetitive sexual fantaises and acts that involve arousal from inappropriate objects or individual; usually ppl dont act on sexual compulsions they are just images an thoughts;
- non-paraphilic sexual compulsions re socially acceptable but are more intense for the person; associated with sexual gratificaiton
Tourette’s syndrome
vocal or motor tics that persist for greater than one year
(to meet criteria for dx there must be multiple motor tics and at least one vocal tic)
onset must be before 18 years old
-complex vocal tics include words or phrases
-simple vocal tics can include grunting or sounds
risk fx: stressers; genetic vulnerabgility; prenatal exposure to nicotine, caffiene, alcohol; neonatal anoxia; maternal stress during pregnancy; delivery with forceps; it is associated with maternal complications and childhood streptococcal infections;
-biological changes: caudate nucleus and basal ganglia; DA activity; changes in amygdala, hippocampus, cerebellum
-may have nail biting, hair pulling, skin scratching occuring w/ anxiety
comorbidities: sleep disturbances, nightmares, oppositional behavior, panic disorder, agoraphobia, separation anxiety, aggressive behaviors, explosive tantrums; learning difficulties like ADHD; deficit in memorization, visuospatial
- may feel a sensation like a tingle or pressure prior to tic; feel urge or something “not right”
tx: beta blockers, antipsychotics; HRT is effective in reducing tics;
usually onset is 7; simple ones start then complex, usually decrease by adolescence or have non present
higher in males
PANDAS
thought to be caused by GAS infection and genetic link and an autoimmune reaction with damage to the basal ganglia
one of the etiolgies to OCD spectrum d/os
Theory: molecular mimicry: response to GAS infection the body creates antibodies and proteins of cell wall from bacteria are similar to proteins of basal ganglia and therefor the antibodies damage the basal ganglia and can result in sx of OCD
Sydenhams Chorea
associated with rheumatic fever; causes involuntary and incordinated movemenst/muscular weakness/px with concentration/mood swings/obsessions;
Treatment of neurological cluster of OCD
SSRIs like fluvoxamine
venlafaxine is thought to improve repetitive behaviors in children and adolescents and young adults with autism
Emotional responses to trauma
fear, anger and sadness
cogntive reactions to trauma
denial, depersonalization, derealization
depersonalization
feeling of unreality, detachment from one’s self or one’s body
derealization
other people or the world seems strange
clinical presentation from children experiencing traumatic event
somatic: GI, respiratory sx, cardiovascular sx, musclular like numbness or tingling
may fear their safety, fear being separated from family, fear of abandonment
may have nightmares; difficulty concentrating and remembering details; often depressed and lonely; their view of themselfs in relation to others is altered
acute stress disorder: dissociation
requires the presence of dissociative sx
dissociation during a traumatic event causes disorganization of memories assoicated with event and this causes processing px results in PTSD
dissociation is a defense mechanism “compartmentalization”; can be adaptive at the time of event
1. primary dissociation: sensory and emotional info may not be integrated in memory and sense of personal idendity: doesn’t become part of person’s life sotry and results in nightmares, flashbacks and intrusive thoughts
feelings of detachment, numbing
decreased awareness of surroundings and can be derealization
dissociative amnesia
2. secondary: furthur disociative; sense of detachment; altered passage of time
3. tertiary: ppl develop distinct egos/alters: dissociative identity disorder
what do alters represent
fear, pain, anger
man contain other aspects of traumatic event like shame, humiliation, and powerlessness
ASD dx criteria
- occur within one month after exposure
- last at least 2 days
- marked interference with soical or occupational fx or prevent individual from pursuing some necessary task
- may last from minimum of 2 days to a max of 4 weeks
- may be disoriented, confused, intense agitation, dazed detachment, sometimes amnesia
- children may have sleep disturbances, fear, anxiety, regressive sx, hallucinations, delusions
interpersonal sx of trauma
irritability with others and difficulty with trust and intimacy
behavioral sx of trauma
avoidance of places and people that are reminders; motor restlessness, changes in sleep patterns;
ASD and PTSD tx
psychological first aid (PFA): empathy compassion, stabilizing pt, resources, safety, information, food, shelter
-SSRIs and other antidepressants; imipramine (Tofranil) found to reude intrusive and hyperarousal sx; fluoxetine
beta blockers prevent physiological reactions (increased adrenergic acitivty results in sx so want to decrease NE at presynapses and postsynapses and both beta blockers and opiods do that)
CBT
self activities to reduce distressful feelings like distraction techniques;
what ASD sx leave pt at increased risk for PTSD
hypervigalience/arousal
fear
dissociative features
depression
increased risk for developing PTSD
female
hx of other exposures
other added stressors
NE in PTSD and ASD
NE is associated with persistent memories so we want to reduce NE
Opiates and PTSD
the belief that the opiod system is involved in modulating memories and the release of NE following exposure to severe stressors
morphine in children post burns decreased rate of PTSD
military personnel injured and morphine early assoicated with reduced PTSD rates
antidepressants and PTSD and ASD
antidepressants are not only being used to treat but prevent for those that are at increased risk;
PTSD dx criteria
usually sx will dissipate in one month, but if they extend one month you meet the criteria for PTSD
primary feature is distrubance of memory; the memory was not processed and integrated with others so there for it repeats
if you cannot stop the fear then you cannot recover
PTSD protective factors
affiliation (sense of emotional attachment with family, friends and others) secure pattern of attachment basic needs met mastery of prior traumatic events financial support social support religion preparation for traumatic events
Biological basis of PTSD
-biological basis: response to trauma causes changes and they should go back to normal but in PTSD they do not go back to normal
-thalamus transmits fear, memories, sights, sounds to amygdala and PFC
-amygdala evaluates the threats, fear conditioning, and memory of stressful events
in PTSD the amygdala is overactive, sending more fear response
-hippocampus forms conscious memories and facts and detaisl and connects them with other autobiographical informatoin
-anterior cingulated cortex integrates emotional and cogntive aspects of expereinces and it inhibits amygdala activity to extinguish fear so in PTSD is is not working correctly
-PFC compares previous with present experiences, plan acitons and makes decisions; in PTSD it can be smaller
-in PTSD increased blood flow to orbitofrontal cortex, insula, amygdala, (fear, agitation, hypervigalance); decreased blood flow to the Borcas area that is supposed to but your thoughts into words “speechless terror”
brain hemispheres in PTSD
right hemispheric acitvity is increased in ares that are associated with emotional appraisal
left is decreased in areas involved with speech, cognitive analysis and interpretation of meaning of expereinces
neurotransmitters and making memories
gamma-amino-butyric acid (GABA) registers factual memories
NE and SA register emotional memories
in trauma: NE is released to brain cortex: hypervigilance, flashbacks, nightmares, dissociation, over-consolidation of memories
in trauma: SA is low and results in anxiety, ruminations, irritability, impulsiveness, aggression, suicidal thoughts
Automatic Activation System and Impairment
it is a response to stress
with PTSD: SOB, racing heart, sweaty palms or cold sweats, feeling dizzy, faint, nausea, numbness, tingling, chills or hot flashes, dry mouth, difficulty controlling bowel or bladder
Self regulatory system impairment
if you dont have secure attachment patterns in childhood you are at risk for px later; self regulatory systme fx later in life to manage responses to stress and trauma;
regulate anger, anxiety, sexual impulses, focusing attention and impulse control
subjective feelings of PTSD
shame, being unable to protect self, didn’t meet expectations to protect self
anger: was not deserved
revenge
timelessness: tendency to see similarities between present situations and previous trauma; no beginning and no end; can’t get over the past therefore cannot more into the future
PTSD in children
more likely to experience disorganized or agitated behavior versus fear and horror
- put events in incorrect sequence
- dissociate can be adaptive but will dissociate in new situations
- may believe there was an omen or warning sign before trauma and therefore they should be more alert to warning signs to preven another; avoid talking about trauma, have px with school and less integrated in former activities; and feel estranged from others
PTSD in adolescents
adolescents are likely to engage in reenactment, exhibit impulsive behaviors, and aggressive behaviors
- comorbid MDD, panic disorder GAD, substance abuse
- feel like they will live a short life; do not make plans for future
comorbid medical with PTSD
angina, heart failure, bronchitis, asthma liver, PAD, alcohol, DM, thyroid, lupus, joint conditions like arthritis
comorbid neurological d/o with PTSD
epilepsy, MS, stroke, HA, migraine,
comorbid psychiatric d/o with PTSD
panic disorder, social phobia, simple phobia, GAD, dysthymia, MDD, substance abuse
what therapy is not effective in PTSD
debriefing is not good in preventing or tx PTSD
drugs approved for PTSD
sertraline (zoloft)
paroxetine (paxil)
avoidance and regulation of sleep in PTSD is regulated by what pathways?
SA
mood stabilizers in PTSD
good for those not responding to SSRIs and that have aggressive behavior px with regulation
they are believed to decrease limbic system sensitization
N-methyl-d-aspartate (NMDA) and D-cycloserine
NMDA is receptor involved in learning and memory
D-cycloserine is antibiotic given to enhance cognition with exposure therapy; facilitates the NMDA receptor fx in amygdala, promotes fear extinction, and new learning
Propranolol in PTSD
reduce consolidation of emotional memories; given within hours of event can decrease PTSD sx and have less physiological sx
Prazosin
alpha1 adrenergic receptor blocker; minipress and vasoflex
it inhibits adrenergic activity
can be effective in reducing nightmares among veterans with PTSD
improve overall clinical status, improve avoidance and hypervigilance
Morphine and PTSD
an opiate that may inhibit NE in areas of brain associated with consolidation of traumatic memories
