module 9 Flashcards
1
Q
defining characteristics of eating disorder
A
- self-worth is highly influenced by body shape
- criteria needs to be present for 3 months
2
Q
eating disorder
A
- binge-eating disorder
- bulimia nervosa
- anorexia nervosa
3
Q
binge-eating disorder
A
- recurrent episodes of binge eating which must include:
1. eating an amount of food that is far larger than most people would consume in that situation
2. sense of lack of control over eating - must occur once a week for 3 months
- twice as likely in women
4
Q
binge eating symptoms
A
- 3/5 for a diagnosis:
1. eating much more rapidly than normal
2. eating till we are uncomfortably full
3. eating alone due to embarrassment
4. feeling disgusted with oneself, depressed or very guilty afterwards
5. bingeing when not hungry
5
Q
bulimia nervosa
A
- binging and compensatory behaviours must occur once a week for 3 months
- recurrent episodes of binge eating
- recurrent compensatory behaviours to prevent weight gain; binging follows by purging through vomiting, laxatives, or diuretics
- excessive influence of weight and shape on self-evaluation
- characterized by a strong desire to be thin
- 10x more common in women
6
Q
anorexia nervosa
A
- meet 3 criteria:
1. food intake restriction leading to significantly low body weight
2. intense fear of gaining weight or becoming fat, or persistent engagement in behaviour that interferes with weight gain
3. distorted body image, self-worth influenced by body weight or shape, or persistent lack of recognition of seriousness of low bodyweight - 10% will die within 10 years because of starvation and suicide is also very common
- experience long-term weight suppression
- 10x for likely in females over men
7
Q
2 subtypes of anorexia nervosa
A
- restricting: Severe restrictions on amount and type of food eaten, which can be done through counting calories, skipping meals or eliminating certain food; can also be combined with excessive exercises
- binge-eating and/or purging: restrict food intake and engaging in binge eating and/or purging behaviours (i.e., vomiting, laxatives or diuretics)
8
Q
onset of eating disorders
A
- tends to onset in adolescence or young adulthood
- 90% of cases are diagnosed before 20yrs
- onset associated with stressful life event
- e.g. exposure to violence, family conflict, a significant loss etc
- chronic unless treated
- relapse is common
9
Q
gender differences of eating disorders
A
- vast majority are women
- men diagnosed with eating disorders tend to be gay or bi
- young athletes are vulnerable
- more competitive and also involve managing body weight to an extent
- can go undetected in athletes for a long time
10
Q
biological etiology of eating disorders
A
- genetic contribution
- low level of serotonergic activity: lack of a proper diet affects serotonin systems in the brain; low serotonin specifically
- the runners high/exercise may reinforce disordered behaviour
11
Q
genetic contribution of eating disorders
A
- family members of individuals with eating disorders are 5x more likely to develop one themselves
- genetics may contribute directly to poor impulse control and emotional instability and in some cases may even directly contribute to the symptoms themselves
12
Q
biological treatment of eating disorders
A
- SSRIs: short-term effectiveness and best used in combo with CBT
- atypical antipsychotics: poor evidence in support for helping eating disorders but does help gain weight
13
Q
psychological etiology of eating disorders
A
- culture
- views on weight
- other cognitive factors
- family influences
14
Q
culture - psychological etiology of eating disorders
A
- significant increase in rates since the 1950s
- significantly less common in developing and non-Western countries
- exposure to media is a direct connection/increase to body dissatisfaction
- African-Americans women experience less eating disorders compared to caucasian women due to direct targeting by media
15
Q
views on weight - psychological etiology of eating disorders
A
- 60% of females and only 28% of males report dieting as teenagers; risk factor for later development of an eating disorder
- view and perceptions about what they believe the other sex wants; men assume women want a more muscular man; women tend to think men want a thin woman
- choosing friends who reinforce body-image ideas can have a negative impact on disordered eating
16
Q
other cognitive factors - psychological etiology of eating disorders
A
- low sense of control: diminished sense of control is always present in bulimia; in anorexia you will see a low sense of control at onset but as the disorder progresses they are often proud of their level of self control
- high perfectionism is linked with low self-esteem
- perceptions of body shape: a single meal can lead them to view their body as significantly heavier
- inaccurate beliefs about what is a healthy weight
17
Q
family influences - psychological etiology of eating disorders
A
- perfectionistic mothers: reinforce cultural beliefs on weight and prioritize self-control
- family preoccupation with appearance
18
Q
psychological treatment of eating disorders
A
- CBT and IPT
- best used in combo with medications
19
Q
CBT - treatment for eating disorders
A
- psychoeducation around the health effects, damage to the body and their beliefs around weight
- meals controlled by therapist and family
- challenge dysfunctional thoughts regarding body shape, weight, and eating
- 40-60% have success
20
Q
IPT - treatment for eating disorders
A
- targets dysfunctional relationships in hopes to improve them
- family therapy tends to be a big component, especially in anorexia and can increase success rates
- may work as well as CBT over the long term
21
Q
issues of treatment for eating disorders
A
- very unlikely to seek treatment, often needs to be forced by loved ones
- people with anorexia deny they have a disorder
- people with bulimia will avoid treatment due to shame
- often fake agreement with treatment; go along with it and then stop once they get out
- if too thin, weight must be restored first
22
Q
2 states of sleep-wake disorders
A
- slow-wave sleep: restorative sleep
- rapid eye movement (REM): when we dream and seems to be connected to things like memory and mood
23
Q
sleep in other disorders
A
- anxiety, mood, and psychotic disorders have sleep issues
- sleep issues may be caused by, and/or precipitate/cause, these disorders
24
Q
insomnia disorder
A
- a predominant complaint of dissatisfaction with sleep quantity or quality, with at least 1 of the following:
- difficulty initiating/falling sleep
- difficulty maintaining sleep
- early-morning awakening with inability to return to sleep
- 3x a week for 3 months
- 1.5-2 women are diagnosed for every 1 man
- onset typically in young adulthood
25
Q
episodic insomnia disorder
A
- meet at least one of the insomnia criteria; and experience distress
- meet symptoms for more the a month but less then 3 months
- diagnosed with “other-specified” insomnia disorder
26
Q
persistent insomnia
A
criteria for more than 3 months
27
Q
recurrent insomnia
A
2 or more 3 month episodes a year
28
Q
biological etiology of insomnia
A
- delayed body temperature rhythm: our bodies naturally cool down at night which increases drowsiness, a delayed body temperature rhythm could explain difficulty
- substance use
- hyperthyroidism: rare
29
Q
biological treatment of insomnia
A
- sleeping pills: work in the short-term and may cause rebound insomnia when coming off of them
- melatonin
- antithyroid medications
30
Q
psychological etiology of insomnia
A
- environmental issues such as living near an airport, busy intersection, not having a dark enough room, etc
- association between bed and wakefulness cues: brain isn’t learning to associate your bed with just sleep
- dysfunctional beliefs regarding sleep: how much they need etc
- napping impacts insomnia
31
Q
psychological treatment for insomnia
A
- elimination of environmental issues/naps
- behavioural therapy for extinction of wakefulness cues: e.g. doom scroll in your couch & stop studying or watching T.V. in bed
- cognitive therapy for beliefs
- exercise
- relaxation training
32
Q
hyper somnolence/hypersomnia disorder
A
- excessive sleepiness despite sleeping for at least 7 hours, with at least 1 of the following:
- recurrent periods of sleep or lapses into sleep in the same day
- prolonged sleep of more than 9 hours that is unrefreshing/still feel tired
- naps are also not restorative
- difficulty being fully awake after abrupt awakening
- sleep inertia: trouble shifting from sleep to wake
- sleep an average of 9.5 hours a night
- 3x a week for 3 months
- equal between men and women
- onset typically between 17-24 years old but diagnosis is normally 15 years later
33
Q
narcolepsy
A
- recurrent periods of irrepressible need to sleep, lapsing into sleep, or napping occurring in the same day, with at least 1 of the following:
- episodes of cataplexy
- hypocretin/orexin deficiency
- nocturnal REM sleep latency less than 15 minutes, or a mean sleep latency test of less than 8 minutes and two or more sleep onset REM periods
- 3x a week for 3 months
- slightly more common in men
- the earlier it is diagnosed the worse the outcomes are
- onset has 2 age ranges: 15-25 or 30-35
34
Q
cataplexy episodes
A
- individuals will loose complete muscle tone; fainting without loss of consciousness; can last seconds to minutes and is often triggered by a strong emotion
- decrease with age
35
Q
hypocretin/orexin deficiency
A
- hormone in the brain that regulates wakefulness and is measured in cerebrospinal fluid
- often hand in hand with cataplexy
36
Q
other features of narcolepsy
A
- sleep paralysis (the old hag): sensation of being awake but you can’t move and you often times feel like there is something or someone sitting on your chest
- hypnagogic hallucinations: very intense dreams
- naps are restorative
37
Q
biological etiology of hypersomnia & narcolepsy
A
- genetics
- orexin deficiency: possible autoimmune disorders as a contributing factors and occasionally brain damage
- histamine system: wake promoting neurotransmitters that individuals may lack
- hypothyroidism
38
Q
biological treatment for hypersomnia & narcolepsy
A
- modafinil (Provigil) and amphetamines: amphetamines can be very unpredictable in terms of the consistency in them working
- antidepressants for cataplexy can suppress the strong emotions that can trigger cataplexy
- thyroid medications
39
Q
psychological etiology of hypersomnia
A
are individuals with hypersomnia using sleep as a coping mechanism?
40
Q
psychological treatment for hypersomnia & narcolepsy
A
- psychoeducation regarding disorder
- development of coping strategies: if sleep is being used to cope you can introduce newer more beneficial strategies
- adjustment to life circumstances: e.g. losing your license or missing out on school
41
Q
circadian rhythm disorders
A
- sleep disruption due to alteration of the circadian system, or misalignment between endogenous circadian system and the individual’s required sleep-wake schedule
- leads to excessive sleepiness, insomnia, or both
- short in duration
- 5 subtypes
42
Q
5 subtypes of circadian rhythm disorders
A
- delayed sleep type
- advanced sleep type
- non-24 hour type
- shift work type
- jet lag type
43
Q
delayed sleep type
A
- consistently going to bed later than desired
- seen in 7% of adolescence and less than 1% of adults
44
Q
advanced sleep type
A
- going to bed earlier than desired
- effect older adults more
45
Q
non-24 hour type
A
keep going to bed later and later because your body is on a 25 or 26 hour circadian rhythm clock
46
Q
shift work type
A
your awake and sleepy at the wrong times due to changing work schedules
47
Q
jet lag type
A
sleep schedule being off from traveling
48
Q
biological etiology of circadian rhythm
A
- Suprachiasmatic nucleus (SCN)
- melatonin
49
Q
Suprachiasmatic nucleus (SCN) - etiology of circadian rhythm
A
- found in the hypothalamus and is what tells our body to change our sleep-wake schedule in response to changes in light entering our eyeballs
- ideally tries to keep us on a schedule of awake during the day and sleeping at night
50
Q
melatonin - etiology of circadian rhythm
A
- endogenous melatonin promotes sleep
- increases based on circadian rhythm when it’s time to go to sleep
51
Q
biological treatment for circadian rhythm
A
melatonin
52
Q
psychological etiology of circadian rhythm
A
changing work schedules
53
Q
psychological treatment for circadian rhythm
A
- phase delaying: easier to get someone to sleep later then get them to sleep earlier; attempt to get them on the appropriate sleep schedule
- exposure to sunlight/bright light therapy: good for jet lag and keeping yourself awake
- changing expectations regarding employment: change jobs or adjust your current one based on the circumstances
