Week 4 - Eating Disorders Flashcards

1
Q

disordered eating occurs in __% of women

A
80%
Low calorie intake
Excessive exercise
Vegetarianism*
Fat restriction
Carbohydrate restriction
Candida diets, wheat free, dairy free*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Men comprise what percentage of individuals with ED in clinical settings?

A

5-10%
with significantly more gay and bisexual men suffering from these disorders compared with heterosexual men .

However, there is evidence that more men in the general population have ED and that ED in men are under-diagnosed and under-treated. Men may not seek treatment due to experiencing fewer severe symptoms or because they may not consider themselves at risk for eating disorders (Woodside).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the spectrum of eating disorders

A
  1. anorexia nervosa; restrictive; binge-eating, purging
  2. bulimia nervosa
  3. binge eating disorder
  4. eating disorders not otherwise specified; female athlete triad; anything else (e.g. orthorexia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Diagnostic criteria for anorexia nervosa

A

Body weight <85% expected weight
Intense fear (pathological) of becoming fat
Inaccurate perception of own body size, weight or shape
Excessive dieting leading to severe weight loss

Criterion removed:
Amenorrhea of at least 3 consecutive mos.
(in girls or women after menarche)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Mortality rates for AN: __% at 10 years; __% at 20 years

A

Mortality rates: 10% at 10 years; 20% at 20 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

More than __% of patients with AN become chronically ill over 10 years

A

More than 30% of patients with AN become chronically ill over 10 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the profile of high risk for death that causes AN to have the highest mortality rate of any psychiatric disorder?

A

Profile of high risk for death:
Chronic illness (> 2yr)
Very low weight (BMI <19) – irrespective of dx.
History of suicidal behaviour or self harm
Presence of affective disorders
Alcohol misuse
History of hospitalization for mental health problems
Daily vomiting; Daily bingeing
Laxative misuse &/or Diuretic misuse
Ipecac use; Stimulant use (cocaine, ephedrine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

14 signs of AN

A
Emaciation
Hyperactivity
Bradycardia
Tachycardia
Hypotension
Dry skin
Brittle hair
Hair loss on scalp
"Yellow” skin especially on palms
Lanugo - very fine, soft, and usually unpigmented, downy hair as can be found on the body of a fetus or newborn baby; d/t malnutrition
Peripheral cyanosis
Raynaud’s phenomenon
Edema: ankle, periorbital
Sialadenosis - Enlargement of the salivary glands, usually the parotids, often seen in conditions such as alcoholism and malnutrition.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

16 symptoms of AN

A
Weight loss	
Amenorrhea
Irritability
Sleep disturbances
Fatigue
Headache
Dizziness
Food sensitivities/allergies
Faintness
Constipation
Nonfocal abdominal pain or bloating
Feeling of “fullness”
Polyuria
Cold intolerance
Leg pains
Infertility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Temperament of person with AN

A
Cautious
Inhibited
Controlled thinking
Restricted 
Rigid
Fearful of intimacy
< New experience 
Extremely persistent
Fear
Decreased self directedness
Perfectionist
Anxious (even as child)
Struggle with identity 
Low self esteem
Hyperactivity (cycle)
(zinc defic, malnutrition)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

8 physiological sequelae of AN

A
Electrolyte imbalance (K+, Cl-, Na+)
Cardiac insufficiency
Reproductive stunting/imbalance
Gastrointestinal dysfunction
Osteoporosis
Immune stress - infections
Organ failure (heart, liver, kidney)
Death – due to physiological shut down or suicide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Symptoms of electrolyte imbalance

A
Weakness			Muscle twitches
Constipation			Hypotension
Dizziness			Polyuria
Depression			Polydipsia
Fatigue
Paraesthesia
Leg (muscle) pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cardiac complications found in eating disorders

A
Fatigue		bradycardia small HT,  EKG changes					(AN)
Syncope		orthostatic/systolic hypotension
					(AN, BN, EDNOS)
Acrocyanosis	poor peripheral circulation
					(AN)
Palpitations		abnormal EKG
					(AN, BN, EDNOS)
Chest pain		mid-systolic click	MVP & TVP
			(AN)	
Calf pain		hypokalemia * (AN, BN)

Dyspnea rapid respiratory rate (AN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Factors For Increased Cardiac Risk In Person With AN

A
Severe and/or rapid weight loss
Purge frequency
Ipecac use
Co-morbid physiological disorder
Underlying cardiac disease
Older age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Red Flags (physical aspect) of AN

A

Very low weight
High frequency of binge/vomiting
Low vitals – HR & BP
Arrhythmia
Appearance – weak, peripheral edema
Abnormal lab- electrolytes, liver enzymes
Patient complains of chest pain, leg cramps
History – alcohol misuse; self harm/suicide, hospitalization, chronic illness, etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Effects on Reproductive System 
in Anorexia Nervosa

A

Normally, pulsatile GnRH release induces LH-FSH
In AN, LH-FSH pulses diminish with reversion to prepubertal pattern
60% women with oligomenorrhea or amenorrhea seen at infertility clinics have eating disorders
Amenorrhea not likely due to starvation alone
Study: Nutrition (fats) and reproductive hormones:
non-dieters, intense dieters, risk group
–> women who ovulated consumed more energy from fat vs. non-ovulating women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Factors Contributing to the Development of Osteoporosis in Anorexia Nervosa

A

Estrogen deficiency state –> high turnover bone resorption state –> osteoporosis
Osteoclast-stimulating cytokines:
- IL-1, IL-6, IL-11, TNF
High cortisol implicated also.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Mechanisms of estrogen regulation of bone resorption

A
  • Bone cells contain E receptors
  • L-1, IL-6, TNF-α, granulocyte macrophage colony-stimulating factor, macrophage colony-stimulating factor (M-CSF), and prostaglandin-E2 (PGE2). These factors increase bone resorption, mainly by increasing the pool size of pre-OCs in bone marrow (2, 3), and are downregulated by E.
  • E upregulates TGF-β, an inhibitor of bone resorption that acts directly on OC to decrease activity and increase apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Effects of ED on GI system

A
  • gastroparesis
  • GERD
  • gall stones
  • constipation - reflex hypo functioning of colon; cathartic colon syndrome
  • abdominal pain
  • dysphagia, hoarseness
  • stomach rupture via gastric dilation (binges) BN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

cathartic colon syndrome

A

Cathartic colon is the anatomic and physiologic change in the colon that occurs with chronic use of stimulant laxatives (> 3 times per week for at least 1 year). Signs and symptoms of cathartic colon include bloating, a feeling of fullness, abdominal pain, and incomplete fecal evacuation. Radiologic studies show an atonic and redundant colon. Chronic use of stimulant laxatives can lead to serious medical consequences such as fluid and electrolyte imbalance, steatorrhea, protein-losing gastroenteropathy, osteomalacia, and vitamin and mineral deficiencies. When the drug is discontinued, radiographic and functional changes in the colon may only partially return to normal because of drug-induced neuromuscular damage to the colon.

Anthranoid laxatives (aloe, cascara sagrada, and senna) are derived from naturally occurring plants and are considered to be stimulant laxatives. Short-term use of stimulant laxatives is safe, but abuse of these drugs can cause melanosis coli and possibly increases the risk of colonic cancer. Melanosis coli, a benign condition, is characterized by dark pigmentation of the colonic mucosa that usually develops 9 months after initiating the use of these drugs and disappears just as quickly after the drug is discontinued.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Bulimia Nervosa diagnostic criteria

A

Recurrent binge eating
Recurrent purging, excessive exercise or fasting
Excessive concern about body weight or shape
Absence of anorexia nervosa
Usually normal weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

12 Symptoms Found in Patients with Bulimia Nervosa

A
Irregular menses
Esophageal burning
Nonfocal abdominal pain
Abdominal bloating
Lethargy
Fatigue
Constipation
Diarrhea/Irritable Bowel Syndrome
Frequent sore throats
Depression
Water retention
Swollen cheeks
23
Q

12 Signs of Bulimia Nervosa

A

Can be seen in AN also if vomiting

Russell’s sign (calluses on the knuckles or back of the hand due to repeated self-induced vomiting over long periods of time)
Sialadenosis
Perimolysis (Decalcification of the teeth from exposure to gastric acid in people with chronic vomiting)
Periodontal disease
Gingivitis
Dental caries
Perioral irritation
Mouth ulcers
Hematemesis
Edema (ankle, periorbital)
Periorbital petechiea
Arrhythmia
Injected sclera (red eye)
24
Q

Temperament of a person with BN

A
Distracted easily
Aware of others’ opinion of them
Impulsive; but can be fearful
Chemical dependency
High risk behaviours
Dependent on praise
Give up easily
25
Q

Relationship of CCK with Bulimia

A

Studies have shown that CCK is decreased in individuals with BN when compared with healthy controls. Decreased CCK functioning may contribute to impaired satiety and thus binge eating in this patient population. Depending on the macronutrient composition of food choices, CCK release can be differentially influenced. For instance, protein is a potent stimulator of a CCK response. Eating more protein-rich meals increases the release of CCK, increasing satiety and ending a meal.
Knowledge of CCK functioning and the utility of manipulating the macronutrient composition of meals may inform standard behavioral treatment strategies for those who suffer from BN.

26
Q

6 Physical Sequelae to 
Bulimia Nervosa

A
  • Electrolyte imbalance
  • Cardiac arrest
  • Gastric dysfunction
  • Endocrine abnormalities – reproductive,
    thyroid, adrenal etc
  • Immune insufficiency
  • Blood sugar dysregulation
27
Q

Binge Eating Disorder description

A

Distinct group among the obese
Less severely disturbed compared to individuals with BN
Uncontrollable episodes of binge eating without the inappropriate physical compensatory behaviours ie no purging or over exercise
Individuals feel extremely upset after bingeing
Often feel calm when bingeing
Affects 4-5% of all adults in US
Approximately 40% of people who are mildly obese and who try to lose weight

28
Q

Binges & willpower

A

“Binges are purposeful acts, not demented journeys. They do not signify a lack of willpower or the inability to care for yourself. On the contrary, a binge can actually be an urgent attempt to care for yourself when you feel uncared for. Bingeing is the only way many of us know how to give to ourselves without holding back.” Geneen Roth

29
Q

6 comorbidities with bulimia & binge eating disorder

A
ADHD
Bipolar disorder
Depression
OCD
Substance Abuse
Personality Disorder
30
Q

General Temperament of Person with Binge Eating Disorder

A
Responsible
Sensitive
Rebellious
Perfectionist in work
Critical (internally or externally of others)
Mixed messages
Impatient
Assertive – not afraid to voice opinion
31
Q

Sequelae to Binge Eating Disorder

A
Diabetes mellitus
Hypothyroidism; adrenal exhaustion
High blood pressure
High cholesterol
Gall stones
Inflammatory state – arthritis, skin infections (fungal)
Metabolic syndrome (HBP, HChol, DM)
32
Q

Eating Disorders Not Otherwise Specified;

What is the Female Athlete Triad?

A

Syndrome found in athletic women, consisting of three inter-related components:

4a1. Disordered eating
4a2. Amenorrhea (in women)
4a3. Osteoporosis

33
Q

Eating Disorders Not Otherwise Specified;

Orthorexia

A

Excessive focus on righteous eating (ultra puritan, vitamin obsession)

34
Q

7 Potential Risk Factors for Developing an Eating Disorder

A
  • Perinatal stress and low birth weight
  • Genetics
  • Temperament – often seen at 18mos
  • Early puberty
  • Dieting
  • Standard North American diet
  • Comorbid mental health ailments: Anxiety, OCD, Depression etc
35
Q

Explain the Correlation of Perinatal Stress 
and Anorexia Nervosa

A

Swedish study (Cnattingius, 1999)
All live born girls in Sweden from 1973-1984
Relative to controls – individuals with AN
Were 3x more likely to have been born pre-term
More likely low birth weight and multiple birth; 2x more likely to have experienced birth trauma; more likely to have instrumental delivery

36
Q

Inner beliefs/perceptions of Anorexia Nervosa

A

Anorexia nervosa: (gases, muriaticum, oxidatum)
“I need nothing/no one, but I am afraid”
“I don’t deserve to take much”

37
Q

Inner beliefs/perceptions of Bulimia Nervosa

A

Bulimia nervosa: (father, carbonicum, snake family)
“I am not worthy of holding/taking this in.”
i.e. struggle with praise, success etc

38
Q

Inner beliefs/perceptions of Binge Eating

A

AN + BN?
“I need nothing/no one, but I am afraid”
“I don’t deserve to take much”
“I am not worthy of holding/taking this in.”
i.e. struggle with praise, success etc.

39
Q

5 possible aetiologies of eating disorders

A
  • Nutritional Deficiencies: Zn, EFA, B12
  • Genetics: AN – family hx – 1st degree relatives of indiv with AN have 10x incr.; 12x BN
  • Family dynamics:
    Boundary violation (emotional & physical)
    Family Hx: depression, alcoholism, death
    History of sexual, physical or emotional abuse
    Expectations
  • Society and Culture: media, dieting, over exercise
  • Self and sensitivity: CNC theory [confirmed negativity condition]
40
Q

Explain the Confirmed Negativity Condition

A

Although a person can have C.N.C. without an eating disorder, all eating disorder sufferers must have C.N.C. According to Claude-Pierre, there are many self-negating manifestations of C.N.C. and these can include depression, agoraphobia, panic attacks, obsessive compulsive disorder, or somatic disorders. An eating disorder is one such manifestation, albeit one of greater concern because of high mortality rates associated with eating disorders.
Sufferers of C.N.C. feel a sense of self-loathing and unworthiness. They have a negative “voice” inside their head who’s sole purpose is to destroy them. With a person who has an eating disorder, the “voice” will often concentrate on their main weakness of food. For example, it might say “You’re fat, you don’t deserve to eat”, “You’ll never get better, you’ll only get worse”, or “You deserve to die, therefore you don’t deserve to eat.”

Claude-Pierre describes this constant battle as being like a civil war in the person’s mind. The “voice” or Negative Mind is totally powerful when the eating disorder symptoms are present. However, the “voice” is louder for some than it is for others. For some people, it is loud and constant, whereas for others it may be like a whisper or a number of whispers that are hard to distinguish.

Sufferers of C.N.C. feel guilty about not being perfect, that they are not worthy of anybody’s attention and that they are to blame for things that are clearly beyond their control. Inevitably, this leads to a sense of failure and reinforces the Negative Mind’s opinion that they are useless and unworthy. Many sufferers feel they are so unworthy to the point that they refuse to eat in front of other people for fear of being in the way.

C.N.C. sufferers will often punish themselves for going back on a bargain with their Negative Mind or for things that they perceive as being their fault, even if in reality they are not. Punishments usually take the form of denying themselves pleasure and happiness. Food is the obvious example (after all, we all need food to survive) but the Negative Mind is also often telling the sufferer that they deserve to die.

Punishment may also include self-injury. The sufferer will cut, scratch, pinch, hit, burn or slap themselves in order to repent for “breaking the rules” in some way. Even if the individual is not self-injuring in that regard, it is likely they are using starvation, binging and/or purging as indirect methods of punishment.

41
Q

What are the 6 general treatment goals for an ED?

A

Build trust and rapport
Stabilize weight (loss or gain)**
Strengthen coping skills
Empower the individual – connection to self
Assist them to decrease fear of food/living
Develop regular eating patterns

42
Q

5 requirements of recovery

A
  1. Willingness or desire to think differently
  2. Physical: sleep, diet, exercise, supps etc
  3. Emotional: support (friends, family)
  4. Therapy: CBT, Non specific supportive psychotherapy, NLP, Homeopathy etc
  5. Spiritual: Yoga, meditation, breath work, creativity, art work; nature, etc.
43
Q

Process of recovery

A
Mourning, shame and guilt
Regaining hope
Taking responsibility for the healing process
Regaining a purpose in life *
Developing choices
Helping others
Disappearance of symptoms
44
Q

How to calculate BMI?

A

weight (kg) / height (m2)

45
Q

What constitutes a PE for a suspected or known ED?

A
State of hydration
Vitals
Weight and height*
Teeth and gums
CDV (EKG)
BP: lying, seated and standing
Abdominal
Neurologic
Gynecologic
46
Q

Recommended lab tests

A
CBC*
Serum electrolytes*
EKG*
Serum glucose*
Dual energy x-ray absorptometry (DEXA)
Liver function*
KI function
Serum; salivary amylase levels
Serum BUN, creatine levels
T3, T4 and TSH
Urinalysis*
Stool (GI bleeding, abdominal, anemia)
Serum zinc levels
Zinc tally
47
Q

AN is a symptom or complication of which 4 conditions?

A

Clinical marker of Beriberi (Thiamine Def)
AN also an early symptom of Pellagra (Niacin B3 deficiency)
AN – complication of Scurvy (Vit C Def)
AN is a symptom of zinc deficiency

48
Q

Symptoms of zinc deficiency?

A
Depression
Attention difficulties
Decreased appetite
Meat avoidance*
Amenorrhea
Inhibition of EFA metabolism
Decreased taste &  
Hypercarotenemia (chrnc)
Poor wound healing
Poor sleep
Decreased melatonin
Nausea
Bloating/GI discomfort
Distorted body image
Vulnerability to stress
Change in opiate receptors
Rough, dry skin
49
Q

10 supplements/modalities for a nutritional approach to EDs

A
  • zinc - (liquid) 15-60mg daily divided doses
  • 5HTP - 50-1200mg/day (Bulimia & BEDs)
  • homeopathy - individualize
  • St. John’s Wort: 3% hypericin: 300mg tid ; caution w antidepressants (serotonin syndrome)
  • GABA - for anxiety
  • EFAs - Low levels of EFA’s lead to weight gain
    without omega 3 intake during periods of weight loss, patients regain weight more readily because omega 3 deficiency results in poor insulin regulation and slow metabolism
    ** Long term effect of omega 3 deficiency is sluggish metabolism
  • Theanine - 200mg 1-2x/d as needed
  • rhodiola - 50-500mg/d (high % rosin = use lower dose)
  • thiamine (B1) - anorexia is a beriberi symptom
  • acupuncture: HT7, PC6, CV16
50
Q

What is serotonin syndrome

A

Serotonin syndrome occurs when you take medications that cause high levels of the chemical serotonin to accumulate in your body.

Serotonin syndrome can occur when you increase the dose of such a drug or add a new drug to your regimen. Certain illegal drugs and dietary supplements also are associated with serotonin syndrome.

Serotonin is a chemical your body produces that’s needed for your nerve cells and brain to function. But too much serotonin causes symptoms that can range from mild (shivering and diarrhea) to severe (muscle rigidity, fever and seizures). Severe serotonin syndrome can be fatal if not treated.

Milder forms of serotonin syndrome may go away within a day of stopping the medications that cause symptoms and, sometimes, taking drugs that block serotonin.

Serotonin syndrome is not an idiopathic drug reaction; it is a predictable consequence of excess serotonin on the CNS and/or peripheral nervous system. For this reason, some experts strongly prefer the terms serotonin toxicity or serotonin toxidrome which more accurately reflect that it is a form of poisoning.

No laboratory tests can currently confirm the diagnosis. Hence it is diagnosed based on symptoms, disease course (that is, the progression of the disease) and the exclusion of other possible causes of the presenting symptoms.

Sxs: increased heart rate, shivering, sweating, dilated pupils, myoclonus (intermittent tremor or twitching), as well as overresponsive reflexes

51
Q

Factors contributing to zinc deficiency

A

Phytates impair zinc absorption
Easiest sources of zinc are animal products
High number of individuals with AN avoid meat &/or have been vegetarian for years *
Puberty – zinc demands increased (B12, EFAs)
High stress (glucocorticoids)
BCP’s (reduce albumin decr. Zn)
Strenuous physical activity
Poor diet

52
Q

What is the relationship between zinc deficiency and appetite control?

A
  • Majority of digestive enzymes are Zn-dependent
  • Aminopeptidase A is a Zn-dependent enzyme which metabolizes CCK
  • CCK secreted in duodenum to decr gastric emptying and enhance satiety
  • After a meal, AN patients show peak levels of CCK that is 2x normal levels
  • Zinc also controls appetite by stimulating
    Norepinephrine, Dopamine, Serotonin, GABA
    & Opiate receptors of CNS
53
Q

Why is zinc awesome for EDs?

A
  • Zinc increases serotonin uptake
  • Study of children with ADHD showed improved attention levels with Zn supplementation
  • AN patients supplemented with Zn gained more weight that AN patients without Zn supplementation
54
Q

Dosage & form of zinc for teens/adults?

A
  • elemental zinc
  • 30-60mg/d
  • max 90mg/d in divided doses

add 1-2mg of copper after approx 2-3 months of higher doses of zinc