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PHAR358 > Eating Disorders > Flashcards

Eating Disorders Flashcards

1
Q

What is the diagnostic criteria for anorexia nervosa?

A

intense fear of gaining weight or becoming fat
significantly low body weight (less than what is ideally expected) in relation to age, sex, development, and physical health
disturbance in the way one’s body weight or shape is experienced and denial of the seriousness of the current low body weight

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2
Q

How is the severity of anorexia classified?

A

based on BMI
-mild: BMI > 17 kg/m2
-moderate: BMI 16-16.99 kg/m2
-severe: BMI 15-15.99 kg/m2
-extreme: BMI < 15 kg/m2

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3
Q

What is the diagnostic criteria for bulimia nervosa?

A

recurrent episodes of binge eating
-large amounts of food consumed in short time period
-lack of control of eating during the episode
recurrent compensatory behavior to prevent weight gain
-laxatives, vomiting, diuretics, diet, drugs, exercise
binge eating and compensation 1x /week x 3 months
self-evaluation is disproportionately influenced by body shape & weight

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4
Q

How is the severity of bulimia classified?

A

based on the numbers of inappropriate compensatory behaviors per week
-mild: 1-3
-moderate: 4-7
-severe: 8-13
-extreme: 14
BN severity/diagnostic criteria does not include a specific BMI. Patients with BN are commonly normal to slightly overweight

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5
Q

What is the etiology of AN and BN?

A

genetic predisposition
-AN 22-76% heritability
-BN 30% heritability
physiologic state
-imbalance of neurotransmitters and neuropeptides
environment - complex biopsychosocial
-trauma and stress
-family dynamics
-participation in athletics with high focus on weight
-societal pressures

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6
Q

Describe the pathophysiology of AN and BN.

A

neurobiological dysfunction
-starvation, chronic stress, excessive exercise to lead to an increased release of cortisol from adrenals causing HPA, HPT, HPG suppression
neurotransmitter dysfunction

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7
Q

What is the impact of HPG suppression in AN and BN?

A

decrease in estradiol, progesterone, LH production = amenorrhea and decreased libido

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8
Q

What is the impact of HPT suppression in AN and BN?

A

TSH inhibition reduces T4 –> T3 = reduced resting metabolic state

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9
Q

Describe the impact of neurotransmitter dysfunction in AN and BN.

A

5HT is synthesized from tryptophan (from diet) and regulates postprandial satiety, mood, sleep, anxiety, impulse control, and OCD
DA deficiencies lead to decreased energy, anhedonia, decreased feelings of reward
NE deficiencies from starvation lead to hypotension, bradycardia

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10
Q

Compare the death rates of AN and BN.

A

AN: 10%
BN: 1-2%

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11
Q

Which psychiatric illness has the highest mortality rate?

A

AN
-eating disorders have high morbidity and mortality

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12
Q

What kind of disease is bulimia associated with an increased risk of?

A

CVD

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13
Q

What is the onset of an eating disorder usually related to?

A

stressful events

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14
Q

Describe the common course of AN.

A

course and outcome are highly variable
-no recovery after 1st episode
-fluctuating pattern of weight gain and loss
-chronic deteriorating course

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15
Q

Describe the common course of BN.

A

waxes and wanes
-chronic or intermittent, with periods of remission and reoccurrence

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16
Q

Describe the psychiatric comorbidity often seen with AN.

A

anxiety (OCD 30%, social phobia)
mood disorders (MDD, dysthymia, bipolar)
personality disorders
SUD
70% have other psychiatric conditions

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17
Q

Describe the psychiatric comorbidity often seen with BN.

A

personality disorders (30-50%)
substance use (30%)
anxiety (OCD, panic, social phobia)
mood disorders (MDD, dysthymia, bipolar)
impulse control disorder

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18
Q

Describe the general principles of treatment for eating disorders.

A

approaches emphasize both normalization of eating behavior and attention to underlying psychological and social issues
consider the eating abnormality to be a coping mechanism, therefore, need to develop other coping mechanisms
form a treatment alliance by offering help with sx or behaviors which are distressing to the patient
identify stressors that predispose to eating disorder

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19
Q

What are the risks associated with amenorrhea due to an eating disorder?

A

without estrogen and normal menstrual cycle increases risk of:
-osteoporosis/osteopenia
-decreased growth velocity
-lack of sexual desire/sexual dysfunction
-unexpected pregnancies

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20
Q

When do periods return if an eating disorder caused amenorrhea?

A

usually within 6 months of achieving a body weight of about 90% of the average for age and height (BMI ~19-20)
return of menstrual cycle is not related to amount of body fat but with amount of serum estrogen levels

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21
Q

List the electrolyte disturbances seen with AN.

A

dehydration
hyponatremia
hypokalemia
hypomagnesemia
hypocalcemia
hypozincemia (taste disturbances and appetite changes)
hypochloremia (if vomiting)
hypophosphatemia
hypoglycemia

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22
Q

List the HEENT complications seen with AN.

A

loss of tooth enamel
perioral dermatitis
enlarged parotid glands

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23
Q

List the neuro complications seen with AN.

A

seizures (related to large fluid shifts and electrolyte disturbances)
brain atrophy on CT
lethargy

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24
Q

What are examples of eating behaviors that may be seen with AN?

A

cutting food into small pieces
water loading
avoiding meals
vegan/vegetarian diet
calorie counting

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25
Q

List the cardio complications of AN.

A

ECG changes
bradycardia
tachycardia
orthostatic hypotension (dehydration)
dizziness and light headedness (from dehydration)
peripheral edema (cessation of laxative and diuretic abuse)
cardiac muscle atrophy
arrhythmia

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26
Q

What is a common ECG change seen in AN patients?

A

QT prolongation
-predicts cardiac arrhythmia and sudden death
-controversial (ED or electrolyte disturbances?)
requires monitoring with serial ECGs

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27
Q

What is the QT interval that increases the risk of torsades de pointes and cardiac death?

A

> 470 ms

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28
Q

How does cardiac muscle atrophy occur in AN?

A

prolonged starvation leads to wasted cardiac muscle
myofibrillar atrophy and destruction secondary to malnutrition +/- due to decreased preload

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29
Q

What are the consequences of cardiac muscle atrophy in AN?

A

decreased myocardial mass
decreased ventricular cavity size
MV prolapse
decreased contractile forces and CO
alters conduction and ventricular repolarization

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30
Q

What causes sinus bradycardia in AN?

A

due to vagal hyperactivity to decrease energy utilization
decreased T3 level may contribute

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31
Q

What causes cardiac arrythmias in AN?

A

hypokalemia due to malnutrition and diuretic abuse

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32
Q

What causes decreased heart rate variability in AN?

A

due to abnormal autonomic NS function
-predictor of sudden cardiac death

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33
Q

What causes hypotension in AN?

A

chronic volume depletion
decreased cardiac output

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34
Q

What is a pulmonary complication of AN?

A

atrophied vasculature

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35
Q

What are the outcomes of cardio complications in AN?

A

most CV abnormalities normalize with weight restoration
QTc returns to baseline
persistent MV prolapse
-little clinical significance
irreversible myocarditis with emetine toxicity
-seen with chronic ipecac ingestion

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36
Q

What is the pharmacists role in caring for cardiac complications of AN?

A

ECG monitoring for arrhythmias, HR variability, and prolonged QTc
avoid QT prolonging meds
monitor for electrolyte abnormalities
monitor for orthostatic hypotension
to avoid refeeding induced CV complications:
-refeed slowly, phosphorus supp, clinical surveillance

37
Q

List the GI complications of AN.

A

hypomotility
hypoactive bowel sounds
hypertrophy of salivary glands
gastritis
abdominal pain
abdominal distention
bloating
constipation

38
Q

List the GU complications of AN.

A

amenorrhea
infertility
low estrogen levels (low testosterone in males)
low FSH/LH

39
Q

List the hepatic complications of AN.

A

hypoalbuminemia
increase in INR and other LFTs
increase in GGT if alcohol abuse

40
Q

List the renal complications of AN.

A

elevations in BUN (dehydrated)
decreased GFR

41
Q

List the endocrine complications of AN.

A

reduction in T3 and T4
increase in cortisol
metabolic alkalosis (if vomiting)
metabolic acidosis (if laxative abuse)

42
Q

List the MS complications of AN.

A

osteoporosis, osteopenia
muscle weakness and leg cramps
delayed linear growth

43
Q

List the skin complications of AN.

A

dry, scaling skin
calluses on back of hand (from hand-induced vomiting)
hair loss
Lanugo hair (fine hair growing on skin)

44
Q

What is the medical treatment for gastroparesis?

A

domperidone

45
Q

What is the MOA of domperidone?

A

dopamine antagonist (peripheral)
-does not cross BBB

46
Q

What are the outcomes of using domperidone for gastroparesis?

A

to reduce abdominal distention, pain, and bloating
increases esophageal peristalsis and motility
for delayed gastric emptying

47
Q

What is the risk with domperidone?

A

QT prolongation
-limit use to short term

48
Q

What is the use of metoclopramide for gastroparesis?

A

avoid as can cause EPS (crosses BBB)

49
Q

What is the treatment for constipation in AN?

A

bowel retraining
-Peg Lyte 250 ml TID-QID
-Peg 17 g po daily
-Milk of Magnesia 15-30 ml hs
bowel taper
-sennosides or cascara prn
individualize regimen based on individual patient

50
Q

What is osteoporosis?

A

loss of BMD/bone mass
breakdown of bone tissue

51
Q

What are the symptoms of osteoporosis?

A

early on: usually no sx
later on osteoporosis can lead to:
-increased risk of fracture
-Kyphosis (curving of upper spine)
-pain
-reduced height

52
Q

How does an eating disorder contribute to osteoporosis?

A

decreased nutrition –> decreased peak bone mass
decreased weight –> amenorrhea –> low estrogen levels
decreased serum androgen levels
decreased levels of IGF-1
increased cortisol levels

53
Q

When is most bone built?

A

during adolescent years
-problems with bone formation during these years can result in permanent deficits

54
Q

Which eating disorder is highest risk for osteoporosis?

A

anorexia
-40 to 66% of those with anorexia have osteoporosis

55
Q

What is the role of estrogen replacement for osteoporosis in eating disorders?

A

has NOT been found to be helpful for increasing BMD in eating disorders
-overall: we dont use estrogen replacement

56
Q

How does the body handle calcium differently in eating disorders?

A

less calcium is absorbed from food and supps
calcium is cleared from the body faster

57
Q

What is the role of calcium and vitamin D for osteoporosis in eating disorders?

A

there are no studies of calcium + vitamin D increasing BMD in ED’s but it is believed it may be helpful as it has been shown to decrease fractures in post menopausal women
-overall, they are benign and we tend to recommend them

58
Q

What is the daily recommended intake of calcium and vitamin D in eating disorders?

A

calcium 1200-1500 mg
vitamin D 1000 IU

59
Q

What is the MOA of bisphosphonates?

A

suppress bone breakdown and turnover

60
Q

What is the role of bisphosphonates for osteoporosis in eating disorders?

A

may use in women > 30 BUT not great evidence
-studies of teens: not shown benefit in improving BMD
-adult women w AN: no good quality studies, mixed results
-adult women w/o AN: prevent fractures, maybe extrapolate to adult women with EDs, case by case basis

61
Q

What is the role of weight recovery for osteoporosis in eating disorders?

A

BEST way to prevent more bone breakdown and recover BMD
-may relate more to increased fat mass vs increased BMI
can take as long as 1-2 yrs with sustained wt to see increased BMD
although wt recovery improves BMD, some ppl have permanent deficits
-act now to prevent worsening!

62
Q

Which AN patients will be treated as inpatients?

A

not medically stable from a physical health standpoint
-continued wt loss despite outpatient tx
-SBP < 80 mmHg
-arrhythmia on ECG
-Na < 125, K < 3
-suicidal ideation, active self-harm

63
Q

What are the goals of therapy for AN?

A

stabilize medical and nutritional status
restore and maintain a healthy body weight
re-establish healthy eating patterns
reduce distorted body image concerns
identify and treat underlying psychiatric conditions
prevent relapse

64
Q

What is the non-pharm treatment for AN?

A

nutritional rehabilitation: to restore wt gradually and prevent re-feeding syndrome
-caloric intake lvls usually start around 30-40 kcal/kg/day (1000-1600 kcal/day) may advance to 70-100 kcal/kg/day
-NG > IV when life-preserving nutrition must be provided to a patient who refuses to eat
psychotherapy
-CBT (improve problem solving and coping skills)

65
Q

What occurs when malnourished patients are fed high CHO loads?

A

refeeding syndrome

66
Q

What are the symptoms of refeeding syndrome?

A

gastric bloating, nausea, edema
intolerance in gut may cause nausea and diarrhea

67
Q

What is all occurring during refeeding syndrome?

A

rapid uptake of phosphates, Mg, and K into cells
body retains fluid and extracellular space expands
reduction in serum elytes and fluid retention increases cardiac workload
insulin causes shift of extracellular phosphate to intracellular space
may precipitate cardiac changes and heart failure

68
Q

How is refeeding syndrome prevented?

A

initiate refeeding slowly
supplemental phosphorus

69
Q

What is the role of adjunctive pharmacotherapy in AN?

A

adjunctive pharmacotherapy NOT effective in malnourished and underweight patients

70
Q

What is often suggested for nutritional deficiency?

A

zinc

71
Q

Which mineral has been studied for weight/BMI restoration in AN?

A

zinc
-three RCTs: children and adolescents

72
Q

What is the role of zinc for AN?

A

mixed results for weight/BMI restoration
-1/3 trials = benefit
may benefit mood/anxiety
remains controversial
because it is benign, we consider it

73
Q

What is the role of antipsychotics for AN?

A

atypical 2nd gen AP’s currently used
-OLZ, QUE, RIS, ARP studied but no difference in BMI/psychopathology/depressive sx in recent meta-analysis
-only olanzapine has modest wt increase (no benefit for ED cognitions or obsessionality)
overall very limited evidence of effect with SGA, if OLZ used then combine with behavioral interventions

74
Q

Which side effects of AP’s do patients with AN tend to be more sensitive to?

A

cardiac and movement related ADEs

75
Q

What is the role of TCAs for AN?

A

limited evidence for benefit
lethal risk with overdose and the potential for arrhythmia at low body weight
not recommended

76
Q

What is the role of SSRIs for AN?

A

citalopram and fluoxetine studied in RCTs but not found to be beneficial for wt
may help with comorbid depression and OCD after wt restoration has occurred
-limited and mixed efficacy data
-dont introduce prior to wt restoration

77
Q

What is the role of bupropion in AN?

A

not recommended as can precipitate seizures in ED patients

78
Q

What are the complications of BN?

A

symptoms of “purging”
-parotid gland enlargement, callus on hands, dental caries, esophageal rupture, gastric rupture
commonly upper end of normal weight or slightly overweight
consequences of abused subs (ipecac, diuretics, laxatives)
-elyte imbalance
-cardiac/skeletal myopathies (ipecac)
-irreversible submucosal nerve fiber damage (phenothalein)
amenorrhea
orthostasis, bradycardia, ECG changes
osteoporosis/osteopenia
guilt & depression after binge

79
Q

What are the goals of therapy for BN?

A

stabilize medical and nutritional status
restore and maintain a healthy body weight
decrease and eventually eliminate binging & purging behaviors
re-establish healthy eating patterns
reduce distorted body image concerns
identify and treat underlying psychiatric conditions
prevent relapse

80
Q

What is the treatment plan for BN?

A

psychotherapy
-CBT
nutritional rehabilitation
pharmacotherapy
-moderately effective for treating Bn

81
Q

Describe the role of CBT for BN.

A

most effective psychotherapy
superior in efficacy to drug therapy (50-60% sx remission)
focuses on change of thought pattern and specific behaviors
20 hour long sessions over 6 months

82
Q

Describe proper weight gain in BN.

A

initially 1000-1600 kcal/day
slowly titrating upward to 2000-3000 kcal/day
goal weight: 90% of ideal or when menses start

83
Q

What is the drug of choice for BN?

A

SSRIs
-fluoxetine, citalopram, sertraline well studied
-fluoxetine is only FDA approved med for BN
pts need not to be depressed to benefit

84
Q

What is the benefit of SSRIs for BN?

A

at high doses SSRIs decrease binge-purge episodes regardless of co-occurring depression

85
Q

What is the onset of effect for fluoxetine in BN?

A

2-4 weeks

86
Q

What is the duration of treatment for fluoxetine in BN?

A

6-12 months (longer for some)

87
Q

What is the benefit of topiramate for BN?

A

at mean doses of 100 mg/day has demonstrated short term efficacy (10 wks) in decreasing binge/purge episodes (3 RCTs)

88
Q

What limits the use of topiramate?

A

ADEs (brain fog)

89
Q

What are some monitoring parameters for BN?

A

frequency and severity of binge/purge episodes
exercise patterns
use of laxatives, enemas, diuretics, ipecac
eating habits
daily caloric intake
mood and anxiety sx
weight and BMI (weekly, no more than 2-3 lbs/wk)
labs

PHAR358 (20 decks)

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