L8 - Anxiety Disorders Flashcards

1
Q

What is the general adaptation syndrome (GAS)?

A

we have a bit of reserve (resistance phase) which becomes eroded after time with stres.. then comes exhaustion.

aka coping to a point..

alarm –> resistence –> exhaustion

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2
Q

There are two pathways in the brain that handle our stress/anxiety response. Describe this.

A

• COGNITIVE -> Parts of the brain involved in fear response = thalamus, amygdala, hypothalamus, which then instruct the endocrine glands and autonomic nerv.sys.

sensory input > thalamus > cortex > thalamus > SC and endocrine system

• Evolved fear module (pink) versus considered response (green) = “fight or flight” versus “feel the fear and do it anyway (or do it differently)”!

sensory input > thalamus > sc to create fight/fight response.

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3
Q

What are the three dsm chapters of anxiety and related disorders?

A

Anxiety Disorders, Obsessive-Compulsive and Related Disorders, and Trauma- and Stressor-Related Disorders. This move emphasizes the distinctiveness of each category while signalling their interconnectedness.

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4
Q

What are some general considerations for anxiety disorders?

A

 Often have an early onset- teens or early twenties
 Show 2:1 female predominance
 Have a waxing and waning course over
lifetime
 Similar to MDD and chronic diseases such as diabetes in functional impairment and decreased quality of life

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5
Q

How does normal and pathologic anxiety differ?

A

Normal anxiety is adaptive. It is an inborn response to threat or to the absence of people or objects that signify safety can result in cognitive (worry) and somatic (racing heart, sweating, shaking, freezing, etc.) symptoms.

Pathologic anxiety is anxiety that is excessive, impairs function.

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6
Q

What does medial prefrontal cortex do?

A

(includes the anterior cingulate cortex, the subcallosal cortex and the medial frontal gyrus)- involved in modulation of affect

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7
Q

What does amygdala do

A

processing of emotionally salient stimuli

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8
Q

primary vs secondary anxiety?

A

Anxiety may be due to one of the primary anxiety disorders OR secondary to substance abuse (Substance-Induced Anxiety Disorder), a medical condition (Anxiety Disorder Due to a General Medical Condition), another psychiatric condition, or psychosocial stressors (Adjustment Disorder with Anxiety)

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9
Q

What are the anxiety disorders?

A
 Specific phobia
 Social anxiety disorder
(SAD)
 Panic disorder (PD)
 Agoraphobia
 Generalized anxiety disorder (GAD)
 Anxiety Disorder due to another Medical Condition
 Substance-Induced Anxiety Disorder
 Anxiety Disorder NOS
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10
Q

Whats the comorbidity between depression and anxiety?

A

50-60%!!! high

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11
Q

heritability of anxiety?

A

0.43 for PD and 0.32 for GAD in twins.

sig familial aggregation.

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12
Q

in SAD.. what do we see in their brains?

A
  • increased medial PFC in response to intentional relative to unintentional social transgression in NORMAL and SAD
  • SAD had significant response to unintentional transgression, though
  • SAD also had significant increase in amygdala and insula actvity, bilaterally.
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13
Q

What have functional imaginign studies in SAD found

A

 Several studies have found hyperactivity of the amygdala even with a weak form of symptom provocation namely presentation of human faces.
 Successful treatment with either CBT or citalopram showed reduction in activation of amygdala and hippocampus

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14
Q

Treatment for SAD?

A

 Social skills training, behaviour therapy, cognitive therapy

 Medication – SSRIs, SNRIs, MAOIs, benzodiazepines,
gabapentin

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15
Q

OCD onset?

A

male earlier than female

mean onst 19.5 age

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16
Q

OCD etiology?

A
  • genetics
  • serotinergic dysfunc
  • cortico-striato-thalamo-cortical (CSTC) loop
  • paediatric autoimmune neuropsychiatric disorder associated with streptococcal (PANDAS)
17
Q

What do people with OCD supposedly have deficit in?

A

visual memory consistently reduced - makes sense because they cant recall whether they’ve completed their compulsive act.

visuospatial function ??

confounding factors of those studies though

  • psychomotor slowing in OCD probably slowed them down
  • checking and ritualisation mst have also slowed them down.

need to be careful bc people with OCD clients bc they complete tasks in an obsessive way

18
Q

visuospatial function in OCD?

A

thought to be impaired, but.

confounding factors of those studies though

  • psychomotor slowing in OCD probably slowed them down
  • checking and ritualisation mst have also slowed them down.

need to be careful bc people with OCD clients bc they complete tasks in an obsessive way

19
Q

Treatment for OCD?

A

 40-60% treatment response
 Serotonergic antidepressants
 behaviour therapy
 Adjunctive antipsychotics, psychosurgery
 PANDAS – penicillin, plasmapharesis, IV immunoglobulin

20
Q

What should you never treat bipolar with?

A

serotinergic drug!!! can make them manic.

also shouldnt use atyptical antipsychotics, D2 blockers with some 5-ht effect

21
Q

what have fMRI studies found in OCD.

A
  • increased activity in right caudate
    this is decreased with CBT
    similar results obtained with pharmacotherapy
22
Q

PTSD aetiology?

A
 Conditioned fear
 Genetic/familial vulnerability
 Stress-induced release
 Norepinephrine, CRF, Cortisol
 Autonomic arousal immediately after trauma predicts PTSD
23
Q

What is usually found in the pTSD brain

A

reduced hippocampal volume

 More recent reviews including the meta-analysis of Smith (2005) indicate that on average PTSD sufferers had a 6.9% smaller left hippocampal volume and a 6.6% smaller right hippocampal volume in comparison to controls.

24
Q

memory in PTSD?

A

Verbal > visual

small to moderate effect

HYPER remebering the trauma event
HYPO remembering everything else.

25
Q

neuropsych performance in pTSD

A
  • ef
  • PROCESSING SPEED
  • VERBAL MEMORY and learning
  • atttention, working memory
26
Q

What can also affect cog deficits in PTSD

A

 Medical illness
 Somatization including non epileptic seizures  Psychiatric and psychological problems
 Substance abuse
 Dissociative symptoms

27
Q

PTSD treatment?

A
Pharmacotherapy 
Antidepresssants 
Anxiolytics 
Antipsychotics 
Mood stabilizers

Psychotherapy- Cognitive behaviour Therapy

28
Q

What is the cornerstone for pharmacological treatment for anxiety?

A

CRANK UP THE SEROTONIN!!!!!

SSRI or SNRIs

29
Q

who for sure cant use a benzo?

A

people with ETOH or substance dependence!! NOOOO

30
Q

first and second line treatment?

A

see tables in lecture!!!

31
Q

How to start using medication for anxiety?

A

 Start at 1⁄2 the usual dose used for antidepressant benefit i.e citalopram at 10mg rather than the usual 20mg
 WARN THEM THEIR ANXIETY MAY GET WORSE BEFORE IT GETS BETTER!!
 May need to use an anxiolytic while initiating and titrating the antidepressant