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PSYT 500 > Eating Disorders > Flashcards

Eating Disorders Flashcards

1
Q

there are ___ out of 40 million Canadians with a diagnostic of ED which represents > ___%, and ___% of them are women

A

1.7 million; 4%; 80%

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2
Q

Some researchers consider a total of ___% of girls before the age of 20 yo suffer from diagnostic of ED

A

13%

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3
Q

what is the average age of onset of AN?

A

16-17 yo

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4
Q

young Canadians are increasingly engaging in ____ which put them at risk of developing ED

A

dieting behavior

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5
Q

the global ED prevalence in 2018 is __%, with ___ million people internationally living with ED

A

7.8; 70

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6
Q

ED have the highest overall mortality rate: ___%. Why?

A

10-15%; due to multi-organ failure and suicide

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7
Q

without treatment, ___% of ED results in premature death

A

20

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8
Q

which type of ED has the highest mortality rate?

A

AN

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9
Q

what is anorexia nervosa?

A

Persistent restriction of energy intake leading to significantly low body weight and intense fear to gain weigh.

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10
Q

what are the two subtypes of AN?

A
  • Restricting type (AN-R): Weight loss accomplished by dieting, fasting and excessive
    exercise.
  • Binge eating Purging type (AN-BP): Recurrent eating large amount of food and
    feeling a ‘loss of control’. Followed by self-induced vomiting, or deliberately misusing laxatives, diuretics or enemas (lavement) to compensate for eating food
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11
Q

what is bulimia nervosa (BN)?

A

Binge eating followed by purging.

Binge : eating a large amount of food in a short amount of time.

Purging: attempts to get rid of the food consumed (vomiting or laxatives).

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12
Q

(T/F): in BN, patients have normal weight or even above

A

true

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13
Q

what is binge eating disorder (BED)?

A

Compulsive overeating or consuming abnormal amounts of food while feeling unable to stop and a loss of control. No action is taken to eliminate the
calories

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14
Q

AN and BN affect mostly ___ while BED affects ___

A

women; both genders equally

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15
Q

(T/F) in several diseases like cancer or depression, patients can have feeding difficulties. This is considered AN.

A

false; considered ANOREXIA

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16
Q

what is the definition of eating disorders?

A

A persistent disturbance of eating or eating related behavior that results in the
altered consumption or absorption of food and that significantly impairs physical health or psychosocial functioning

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17
Q

in the DSM-IV, ED includes 3 other disorders. what are they?

A
  • Pica: persistent eating of substances such as dirt or paint that have no nutritional value (at
    least one month)
  • Rumination disorder: condition in which people repeatedly and unintentionally spit up
    (regurgitate) undigested or partially digested food from the stomach, rechew it, and then either reswallow it or spit it out. Infants and very young children (between 3 and 12 months).
    (at least one month)
  • Avoidant Restrictive food intake disorder (ARFID): Restrictive food intake disorder. Unlike anorexia ARFID lacks the drive for thinness. No distress about body shape or fears of fatness
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18
Q

(T/F): obesity is a mental disorder.

A

false

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19
Q

AN is less than ___% in the general population, but ___% of patients with AN are 12-15yo and are women, with __% of teens/YA having full blown form. AN is the ___ most common psychiatric condition affecting teen girls

A

1; 90; 5; third

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20
Q

what comorbid disorders are associated with AN? (4)

A

mood and anxiety disorders, PTSD and substance use

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21
Q

where does the term “anorexia nervosa” come from?

A

Ancient Greek origin: an-(negation)-orexis (appetite)
nervosa (nerve) = “absence of appetite from nervous origin”

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22
Q

who coined the term AN and at when?

A

1873 by , Sir William Gull, Queen Victoria’s personal physician

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23
Q

when and who first medically described AN?

A

Richard Morton in 1689

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24
Q

which famous 16th century historical figure most likely suffered from AN?

A

Mary Stewart, Queen of Scots

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25
Q

what 6 characteristics are unique to AN?

A
  1. weight loss (below 15% of ideal body weight)
  2. alteration of body image
  3. fear to gain weight, aversion for caloric food
  4. minimization and denial of seriousness of low weight
  5. physical/intellectual hyperactivity
  6. lack of cognitive flexibility
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26
Q

what are the BMI markers for AN?

A

Normal BMI: 18-25

Below 17.5 in adults : common physical characteristics used to diagnose anorexia.

Severity index of anorexia based on BMI:
mild (<17.5), moderate (16-16.99), severe (15-15.99), extreme (<15).

BMI 15 - 18.5 => increased risk of death of ≈ 50%

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27
Q

what are the physical symptoms of AN? (5)

A

Heightened sensitivity to cold.

Gastrointestinal symptoms (constipation, fullness after eating, bloatedness (feeling swollen).

Dizziness and syncope.

Amenorrhoea, low sexual appetite, infertility.

Poor sleep with early morning wakening

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28
Q

what are the physical signs of AN? (7)

A

Emaciation; stunted growth and failure of breast development

Dry skin; fine downy hair

Swelling of parotid and submandibular glands

Erosion of inner surface of front teeth

Cold hands and feet; hypothermia.

Bradycardia; orthostatic hypotension; cardiac
arrhythmias

Weak proximal muscles

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29
Q

what anomalies are seen in the endocrine system of AN? (5)

A

Low concentrations of leutenising hormone, follicle stimulating hormone, and oestradiol.

Low T3, T4 in low normal
range, normal TSH (low T3 syndrome)

Mild increase in plasma cortisol.

Raised growth hormone concentration.

Low leptin

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30
Q

what are cardiovascular anomalies seen in AN?

A

ECG abnormalities (especially in those with electrolyte disturbance): conduction defects, especially prolongation of the Q-T interval

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31
Q

what are gastrointestinal anomalies in AN?

A

Delayed gastric emptying. Decreased colonic motility (secondary to chronic laxative misuse). Acute gastric dilatation (rare, secondary to binge eating or excessive re-feeding)

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32
Q

what are haematological anomalies in AN?

A

Moderate normocytic normochromic anaemia Mild leucopenia with relative lymphocytosis Thrombocytopenia

33
Q

what anomaly is in the brain of AN?

A

Enlarged cerebral ventricles and external cerebrospinal fluid spaces (pseudoatrophy)

34
Q

what are the brain consequences of AN? (4)

A

Enlarged cerebral ventricles and external cerebrospinal fluid spaces (pseudoatrophy)

Reductions in brain size (loss of brain cells & connections between them ?)

Reduction of cortical thickness, subcortical volumes and cortical surface area

Widespread white matter abnormalities

35
Q

what re the main mental heath features of AN?

A

depression (2x in ED); anxiety; OCD; social phobia; substance use; suicide

36
Q

(T/F): Early onset AN can lead to stunted growth.

A

true

37
Q

at the evolution of AN (slide 14)

A

slide 14

38
Q

after 18-20yo:
- ___% of patients have complete remission
- ___% retain abnormalities in ED
- ___% chronic patients

A

30; 30; 30

39
Q

what is the spontaneous recovery rate in ED?

A

60%

40
Q

what are the long-term starvation consequences?

A

changes in thinking, emotions, and behaviors that are difficult to reverse.

Severe starvation causes negative, obsessive, and manipulative behaviors.

41
Q

what are the current treatments of AN? (3)

A
  1. Antidepressant (SSRI help alleviate alleviate depression, anxiety, or obsessive thinking, prevent relapse)
  2. Psychological counseling, Psychotherapy, Group therapy, psychanalysis, Cognitive behavioral
    therapy; family-based therapy for teens
  3. Nutritional support
42
Q

are the psychological interventions for AN effective?

A

effective in 50% of cases

43
Q

whats the main issue in AN treatment?

A

no current specific biological therapy –> needed for chronic patients

44
Q

what are the causes of AN?

A

unknown but combo of:
1. genes: 50-80% heritable
2. environmental factors
3. personality traits
4. comorbid disorders

45
Q

how can we understand and treat AN?

A

To specifically treat anorexia nervosa we need to understand underlying
neurobiological mechanisms

To understand anorexia nervosa we need to combine pre-clinical and clinical
investigation

2 step process:
1) Develop animal model (rodents) of endophenotypes of anorexia
2) Test new hypothesis in patients

46
Q

AN is characterized by what habits/compulsion?

A
  1. Aberrant reward processing (delay discounting)
  2. Lack of cognitive flexibility
  3. Loss of behavioral control and compulsive self starvation
47
Q

what is the most recent hypothesis for habits/compulsion of AN?

A

excessive habit formation or difficulty to re-gain control over habits

48
Q

what 3 functions does the striatum regulate?

A
  1. reward guided behavior
  2. goals directed behaviors
  3. habit formation
49
Q

how does the striatum differ in humans vs in mice?

A

Humans:
- Nucleus accumbens
- Caudate nucleus
- Putamen

Mice:
- Nucleus accumbens
- Dorsomedial striatum
(caudate in human)
- Dorsolateral striatum
(putamen in human)

50
Q

the striatum is involved in:
1) elaboration and repetition of ____ movement
2) reward is piloted by ____
3) goal directed behavior which is piloted by the ___ and is highly sensitive to ___ and ___
4) habit which is piloted by the ___ and is considered ___ behavior that is insensitive to ___ and ____

A

voluntary; NAcc; caudate; outcome reward value; contingency; reward devaluation; contingency degradation

51
Q

whats the difference btw goal-directed behavior and habits?

A

Goal-directed behaviors are based on the expectation that they will be reinforced with desirable outcomes. (Conscious behavior)

Habits are stimulus-response associations that are insensitive to reward (consequences). (Automatic behavior)

52
Q

put the following terms in the right order:
1. goal directed behavior
2. compulsion
3. habits
4. transition from reward

A
  1. transition from reward
  2. goal directed behavior
  3. habits
  4. compulsion
53
Q

what is the normal vs. pathological transitions btw striatal compartments?

A
  1. NAcc (reward)
    1.a gets info from/sends info to….
  2. caudate (goal directed behavior)
    2.a through repetition, sends info to putamen
    2.b also receives info from putamen
  3. putamen (habits)
    3.a leads to automatization (learning)

BECOMES MALADAPTIVE WHEN AUTOMATISATION LEADS TO COMPULSION (EXCESSIVE HABITS VS DIFFICULTY CONTROLLING)

54
Q

which psychiatric disorders have a compulsive dimension?

A
  • Gilles de la Tourette syndrome (tic)
  • addiction
  • OCD
  • ED
55
Q

which 3 psychiatric disorders maybe have a compulsive dimension?

A

autism, depression, PTSD

56
Q

place the following terms where they belong: (VGLUT1,2,3)

__ and __ are expressed in classic Glu neurons while ___ is expressed in small pops of neurons using other NT

A

VGLUT1 and 2; VGLUT 3

57
Q

where is VGLUT3 in the rodent and human brain?

A
  • Cholinergic interneurons striatum (ChIs)
  • GABA interneurons (hippocampus cortex)
  • Serotonin neurons (raphe nuclei)

NB: strong expression of VGLUT3 in the striatum

58
Q

the striatum is constituted by a large population of ___ neurons named ____. It also contains ___ and ___ interneurons. It receives a massive ___ projection from the ___ and ___ and well as a massive ___ projection from the ____.

A

GABA; medium spiny neurons; GABAergic; Cholinergic; glutamatergic; cortex and thalamus; dopaminergic; SNC/VTA

59
Q

what is the cortico-striato-cortical loop?

A

Dopamine (DA) binds to:
- D1 receptors and activate the GO pathway
- D2 receptors and inhibit the NOGO pathway

Overall: each striatal compartment is built on the
same model

  • Too much DA will favor reward/GDB/habits
  • Not enough DA will do the reverse (Parkinson disease)

slide 32-33

60
Q

how are cholinergic interneurons involved in the regulation of the striatal network ?

A

ChIs regulation of the striatum is more complex and less well understood since ChIs express 2 vesicular transporters:
* VAChT (acetylcholine)
* VGLUT3 (glutamate)

ChIs can release 2 neurotransmitters ACh and glutamate

61
Q

what are the molecular consequences of VGLUT3 expression in Chls?

A

1) ChIs co-release acetylcholine and glutamate

2) Increases vesicular accumulation of acetylcholine (vesicular synergy) and increase cholinergic transmission

62
Q

what rare gene variant is found in humans with severe addiction (5%)?

A

VGLUT3 - pT8l allele

63
Q

a point mutation of VGLUT3 can…? (4)

A
  • Be silent
  • Alter 3D structure
  • Alter expression or distribution
  • Alter transport capacity
64
Q

what does VGLUT3-p.T8l alter?

A
  1. blunts vesicular synergy
  2. reduces ACh in synaptic vesicles
65
Q

what is vesicular synergy?

A

Vesicular synergy : Acetylcholine vesicular uptake in striatal synaptic vesicles in the presence or absence of glutamate

66
Q

whats the relation btw EACh efflux in VGLUT3-p.T8l mice?

A

Basal ACh release is reduced in the striatum

67
Q

how is DA efflux related to VGLUT3-T8l in mice?

A
  1. Reduces dopamine release in the caudate (DMS)
  2. No change in the putamen (DLS)
  3. uneven DA signalling in the striatum: less DA released in NAc/caudate vs putamen OR relatively more DA in the putamen
68
Q

what does the uneven DA signaling in the striatum of VGLUT-p.T8l have to do with addiction?

A

favor excessive habitudes, loss of control and compulsion

69
Q

(T/F): VGLUT-p.T8l mice have strange behaviors and obvious phenotypes

A

false: in normal environment mice behave normally (no phenotypes)

70
Q

how is VGLUT-pT8l mice behavior altered in non-normal conditions?

A

Not sensitive to reward devaluation

More prone to excessive habits

71
Q

what happens to VGLUT pT8l mice after the splash test?

A

compulsive grooming (mouse model of OCD)

72
Q

what happens to VGLUT pT8l mice after cocaine self-administration?

A

cue-induced relapse (to cocaine)!

73
Q

how do we model AN in mice?

A

The Activity-Based Anorexia (ABA) model:
- Rodent (like humans) love to run
- Add a running-wheel in cage will create a conflict between eating and running
- Then progressively reduce time with access to food
- A running wheel in the cage will create a conflict between eating and running
- Measurement of the number of mice below 75% of “normal” body weight

74
Q

is there maladaptive eating in VGLUT pT8l mice?

A

Self-starvation in the Activity-based anorexia (“Anorexia”)

Binge-like sucrose overconsumption (“bulimia”)

75
Q

what is Donepezil and how does it work?

A

acetylcholinesterase inhibitor

Administration of donepezil prevent acetylcholine degradation and hence increases acetylcholine tone

76
Q

what happens when you give donepezil to VGLUT-pT8l mice?

A

compulsive grooming and anorexia-like phenotypes are reversed!

77
Q

what does the efficacy of donepezil confirm?

A

existence of decreased EACh signalling in VGLUT pT8l mice

78
Q

what did we learn from the clinical case series ?

A

treatment of anorexic patients with donepezil lead to:
- improvement in all items of eating disorder examination Q
- reductions in comorbid symptoms (anxiety, OCD, depression, skin picking, self-harm)

79
Q

what are issues with treatment by donepezil in humans?

A
  • no RCT study yet
  • problems of side effects -> need low dose
  • slow recovery

PSYT 500 (11 decks)

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