Midterm 2 Flashcards

1
Q

Panic Disorder

A

Discrete periods of intense fear
Peaks within minutes

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2
Q

Panic disorder diagnostic criteria

A

Recurrent unexpected panic attacks - no valid reason to feel panic
Panic attacks followed by over 1 month of persistent concern or worry about additional attacks or consequences
Significant change in behaviour

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3
Q

Prevalence and course of panic disorder

A

Lifetime prevalence of 28%
Affects 1.5-3% of Canadians
Two to three time more common in women

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4
Q

Agoraphobia

A

“Fear of the marketplace”
Anxiety about being in places where escape might be difficult - particularly a fear of having panic symptoms
Often co occurs with PD
need marked fear of two or more places:
Public transit, open space, closed space, standing in line/crowds, being outside home alone
Fear of not being able to escape
Situations almost always provoke fear
Fear is out of proportion
Persistent over 6 months

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5
Q

Cognitive mod of Panic Disorder

A

People with PD pay close attention to bodily sensations
They misinterpret sensation
And engage is spiralling / catastrophic interpretations

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6
Q

GAD symptoms

A

Worry and anxiety occurring more days then not about a number of different events or activities for at least 6 months
Worry is difficult to control
Associated with 3+ of the following for 6 months:
Restlessness or feeling on edge
Easily fatigued
Difficulty concentrating or mind going blank
Irritability
Muscle tension
Sleep disturbance
Impairment or distress
Not due to substance use or other medical problems

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7
Q

Prevalence and course of GAD

A

highly comorbid with other anxiety disorder, depression, and substance use
9% of Canadian population is effected

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8
Q

Biological theories of GAD

A

GABA theory: neurotransmitter preventing neurotransmitter from firing, individuals with GAD may have deficits in GABA receptors leading to excessive firing in limbic or emotional systems
Genetic theory: GAD is inherited, general trait anxiety may increase risk

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9
Q

Cognitive theories of GAD

A

Beck: people with GAD think about threat constantly
Overpredict likelihood and cost of aversive outcomes
Under-predict their ability to cope with outcomes
Believe that worry prevents bad things from happening
Worry is negatively reinforced - allows individual to avoid negative aspect of arousal

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10
Q

Specific phobias

A

There is a phobia for everything
Criteria:
Marked fear about specific object or situation
Out of proportion to the threat
Always provokes fear
object/ situation is almost always avoided or endured with intense distress
Persistent > 6 months
impairment/ distress

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11
Q

5 main types of phobias

A

Animal type
Natural environment type - earthquakes, ocean, thunderstorms
Situational type - airplanes, cars, elevators, escalator
Blood injection-injury type - needles, seeing blood, injection
Other - literally anything else, emetophobia
Specific phobias are most prevalent psych disorder - 11%

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12
Q

Biological theories of phobias

A

Evolutionary
Biological preparedness
Disgust sensitivity -individual differences in levels of disgust to things

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13
Q

Behavioural theories of phobias

A

John B. Watson - Little Albert experiment
Avoidance – decreased anxiety – operant conditioning
Old behavioural theories thought that you had to have experience/ trauma to develop phobia

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14
Q

Social anxiety disorder

A

Specific phobia to social situations
Severely disrupts daily life
Fear of negative evaluation from others
Specify if:
Performance only: fear is related to public speaking or performing

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15
Q

Cognitive theories of Social anxiety

A

Exaggerated likelihood of negative evaluation
Exaggerated cost of negative evaluation

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16
Q

Therapies for social anxiety

A

Social skills training
CBT
Exposure
Modelling
Cognitive restructuring
CBT group therapy - can be super effective because you see modelling of behaviour, treatment is itself an exposure

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17
Q

Pharmacological treatments of anxiety

A

SSRIs - prozac, paxil, zoloft, celexa etc.
Tricyclic Antidepressants
Paxil, Tofranil
SNRIs - Effexor
Benzodiazepines - Xanax, valium
Short term anxiety relief
Physically addictive
Interfere with cognitive and motor functioning
Bupropion - NDRI norepinephrine dopamine reuptake inhibitor

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18
Q

Exposure works by

A

Stops reinforcing effects of avoidance
Allows practice of skills
Provides evidence against irrational thoughts
Habituating to a feared stimulus

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19
Q

Relaxation techniques for anxiety

A

Can’t be both relaxed and scared at the same time
PMR
Relaxation alone doesn’t work but in combination with cognitive techniques can be helpful

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20
Q

Major depressive episode

A

need at least 5 of symptoms:
1. Required: Depressed mood or anhedonia (diminished p;easure in things you used to enjoy)
2. Appetite or weight changes
3. Sleep problems
4. Psychomotor changes - agitation, fidgety, or moving/ talking slower then usual
5. Loss of energy
6. Feelings of worthlessness or inappropriate guilt
7. Concentration problems
8. Suicidality
Must cause distress and last for 2 weeks

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21
Q

Major Depression

A

Episode needs to be present
Causes distress, lasts 2 weeks
Can’t have history of mania or hypomania
Can occur in presence of loss but has to be considered carefully
Mood symptoms: Anhedonia/ sadness
Physical symptoms: weight, appetite, sleep, psychomotor
Cognitive symptoms: worthlessness, indecisiveness, suicidality

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22
Q

MDD vs Grief

A

MDD:
Persistent depressed mood
Decreased ability for pleasure
worthlessness/ self loathing
Not deserving of life, unable to cope
Grief:
Comes in waves
Moments of pleasure between waves
Thoughts are tied to loss
Self-esteem generally maintained
Thoughts of death are more joining the loss then harming oneself

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23
Q

Prevalence and course of MDD

A

1.3 million canadians in any given year will experience MDD
Lifetime prevalence is 8-12% in women, men 4-6%
One of leading causes of disability worldwide
Why 2:1 ratio for women to men:
Genetics
hormones(estrogen,progesterone)

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24
Q

PDD

A

Depressed mood lasts 2 years
At least 2 of following:
Appetite
Sleep
Low energy
Low self-esteem
Poor concentration
Feeling hopeless
Lifetime prevalence 3%
Onset typically before 21
Tends to be chronic

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25
Q

Bipolar 1&2

A

Manic or hypomanic
Elevated mood periods

Both require three of following symptoms:
Grandiosity or inflated self esteem
Decreased need for sleep
More talkative
Flight of ideas
Distractibility
Increase in goal directed activities
Excessive involvement in high risk activities

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26
Q

Difference between mania and hypo mania

A

Manic: 1 week at least OR hospitalization at any point
Hypomanic: at least 4 consecutive days
Hypomania does not have psychotic features, impairment in functioning or necessary hospitalization, mania could have these symptoms
Duration and severity differentiate between hypomania and mania

27
Q

Bipolar 1

A

1 or more lifetime manic episodes
History of MDE not required but usually depression
Many also have hypomanic episodes
Equally common in men and women

28
Q

Bipolar 2

A

One or more MDE
One or more hypomanic episodes
No history of manic episodes
Equally common in men and women
1-year prevalence
0.3% of people

29
Q

Cyclothymia

A

Numerous periods of hypomanic symptoms and subclinical depression for more then 2 years
Can’t be symptom free for more than two months
No MDE or Manic episodes
Can develop in adolescence or early adulthood
Increases risk for developing full blow MDE or manic episodes

30
Q

Heritability estimates of mood disorders

A

MDD: 0.36
Bipolar: 0.75

31
Q

Neurotransmitter theories of mood disorders

A

Serotonin: mood, anxiety, aggression, eating, sleeping, pain, sexual behaviour, memory
Norepinephrine: regulates arousal, energy, activity, appetite - more in BP
Dopamine: pleasure, reward, mood, attention, activity - low levels associated with depression

32
Q

Bio psychosocial theories of depression

A

Environmental events can modify gene expression, affect brain functioning
Early life stress - altered gene expression in hippocampus - greater HPA stress response in adulthood - increased vulnerability for depression

33
Q

Cognitive theories for mood disorders

A

Beck’s model: depressive self schema - faulty information processing - negative thoughts about self, world , future
Hopelessness model: if you attribute negative events internally, these views are stable and you think it will never improve, global thinking - implied to things beyond just negative event
Interpersonal theories:
How social relationships impact depression
Marital dissatisfaction is strongly related to depression
Lack of social and family support is related to depression
Stress generation hypothesis; individuals with depression are more likely to experience negative stressful life events
Excessive reassurance seeking

34
Q

Psychosocial theories of bipolar

A

Stressful life events - may trigger new episodes
Sensitivity to reward
Changes in bodily rhythms or usual routines

35
Q

Bio treatments for depression

A

SSRI’s - relief within a couple weeks, less severe side effects
SSNRI’s - wellbutrin
ECT - given when patient doesn’t respond to treatment after 2 types of medication
Relieves depression in 50-60% but 85% relapse
rTMS - patient stays awake, few side effects, magnetic fields stimulating brain

36
Q

Bio treatments for bipolar

A

Mood stabilizers - Lithium - ED and LD are very close so regular blood work must be done
Anticonvulsants
Atypical Antipsychotics
Treated as chronic conditions - remain on medication through lifetime

37
Q

Psychological treatments for bipolar

A

Interpersonal and social rhythms therapy - help build support and maintain routine
Family-focused therapy - educating family members, learning communication
CBT

38
Q

Interpersonal theory of suicide

A

cognitive states that make you susceptible to suicidal ideation - thwarted belongingness and perceived burdensomeness
Both cognitive states plus capability for suicide required as risk for suicide

39
Q

Capability for suicide:

A

fearlessness (about death) and pain tolerance - these things are acquired over time through environment (ex. war)
Plus thwarted belongingness and perceived burdensomeness

40
Q

Treatment and prevention of suicide

A

Decrease burdensomeness and increase belongingness
Interpersonal coping skills
Challenging untrue beliefs
Activities that foster connectedness
Crisis intervention:
Hospitalization
Suicide hotlines
Medication
DBT:

41
Q

Signs of suicidality

A

Ideation
Substance use
Purposelessness
Anxiety
Trapped
Hopeless
Withdrawal
Anger
Recklessness
Mood changes

42
Q

AN

A

Restriction of intake leading to low body weight
Intense fear of weight gain
Disturbance in body image

43
Q

Subtypes of Anorexia

A

Atypical
Restricting
Binge eating/ Purging

44
Q

Features of people with AN

A

Perfectionism
High intellectual functioning
fidgety/ restless
Food rituals and strict rules around eating
Cold
High comorbidity with depression and anxiety

45
Q

Minnesota Semi-Starvation study (1944):

A

Took group of men and restricted their calorie intake and required to walk a lot for several weeks and then were refed, tracking their metabolism and relating it to refeeding people after the war
These men ended up exhibiting AN symptoms - effects of disorder are due to starvation and did not come before disorder

46
Q

Medical complications of AN

A

constipation , cold intolerance
Major organ failure
cardiovascular complication
Kidney and liver damage
Osteoporosis
Impaired immune functioning

47
Q

Prevalence and course of AN

A

1–2% prevalence
Least prevalent disorder
90% diagnosed are women - men often don’t seek treatment
Usually begins in adolescence 15-19
Often chronic course - long standing if left untreated
Early intervention important
Standardized mortality rate - 5.86

48
Q

Bulimia

A

Recurrent episodes of binge eating
Recurrent episodes of compensatory behaviour: excessive exercising, self induced vomiting, fasting, taking laxatives
Must occur once per week for three month period
Self evaluation heavily influenced by shape or weight
These behaviors with low weight - receive diagnosis of ANBP
Average or above weight - Bulimia
Binge: eating an amount of food that is definitely larger than what most people would eat in a similar context - loss of control over eating during episode

49
Q

Medical complications of BN

A

Not die to starvation but binging and purging
Electrolyte imbalance - affects potassium and cardiac
Erosion of enamel on teeth
Enlarged salivary glands
Ruptured esophagus
Ruptured stomach

50
Q

Binge Eating Disorder

A

Recurrent episodes of binge eating in the absence of compensatory behaviours
Need three symptoms:
Eating faster
Eating until uncomfortable
Eating when not hungry
Eat alone due to embarrassment
Feeling depressed, disgusted or guilty about overeating

51
Q

OS feeding or eating disorders

A

Atypical AN: meets all criteria for AN but is not low weight
Subthreshold BN
Subthreshold BED
Purging Disorder - no binge, just self induced vomiting to influence shape or weight
Night Eating Syndrome
Represents MOST cases of eating disorders

52
Q

General prevalence of ED’s

A

Canadian adolescents between 11 and 20- 2.2% of boys, 4.5% of girls had current symptoms of full blown eat disorder
And additional 1.1% of boys and 5.1% of girls had subthreshold eating disorder symptoms
By midlife 15% of women have had an eating disorder
OFSED was most common lifetime eating disorder affecting 7.6% of surveyed women
Prevalence has been increasing - unsure if this is due to more cases or better detection
Large proportion of individuals with ED do not seek help

53
Q

Obsessions

A

recurrent and uncontrollable thoughts, impulses, or ideas that individual finds anxiety provoking r distressing

54
Q

Compulsions

A

repetitive behaviours or cognitive acts that are intended to reduce anxiety

55
Q

DSM criteria for OCD

A

Presence of either obsessions or compulsions
Obsessions tend to be more bizarre and involve more vivid imagery then just uncontrollable worrying thoughts
Thoughts that are unwanted are ignored or suppressed through efforts of neutralizing
In order to be considered compulsions acts must serve purpose of alleviating anxiety
Must be considered excessive or have little connection with thought or event they are trying to avoid
Spending more than 1 hour a day engaged in OC acts

56
Q

Basal ganglia and frontal cortex theory for OCD

A

Basal ganglia controls motor behaviour, frontal cortex responsible for higher cognitive functioning like abstract reasoning and decision making
these areas are connected with loop system allowing info to travel back and forth
Structural and or functional abnormalities in this brain system may be responsible for OC
One study shows patients with OCD have less brain volume in frontal cortex and more brain volume in basal ganglia

57
Q

Serotonin hypothesis of OCD

A

Serotonin deficiency thought to be involved cuz SSRI’s effective in treating OCD - evidence inconclusive

58
Q

Cognitive behavioural theory of OCD

A

obsessions are caused by reaction to intrusive thoughts because these individuals have high personal responsibility
Compulsions are reinforced when negative event doesn’t occur

59
Q

General Fear vs Anxiety Diagnosis

A

Distress and impairment
Severe enough to lower quality of life
Chronic and frequent enough to interfere with functioning

60
Q

PTSD diagnostic criteria

A

Exposure to traumatic event by direct experience or learning they occurred to close person
Presence of one or more of following intrusions:
Recurrent memories of event
Distressing dreams
Disassociative reactions
Physiological cues that resemble event

Negative alterations in cognitions
Depression symptoms

61
Q

Pre event risk factors to PTSD

A

Low socioeconomic status, education, and intelligence testing
Previous psychiatric history
Childhood adversity

62
Q

Dual representation theory

A

ways traumatic memories are stored and retrieved differently than non traumatic memories
Traumatic memories may be stored and retrieved in non-verbal-sensory-based instead of verbal form like non traumatic memories
These sensory memories need to be transferred into verbal memories in order to process event which can be achieved through writing and talking about event in therapy

63
Q

Biological theories of PTSD

A

Dysfunction in brain areas associated with processing and responding quickly to threat
Brainstem, amygdala, frontotemporal cortex
HPA axis functioning
Decreased cortisol and enhanced negative feedback of adrenal functioning
Less volume in hippocampus - unsure if these reductions represent cause or effect