feeding and eating disorder

1. FEEDING AND EATING
DISORDER
DR.SHUCHI PANDE

2. DSM 5
• PICA
• RUMINATION DISORDER
• AVOIDANT /RESTRICTIVE FOOD INTAKE DISORDER
• ANOREXIA NERVOSA
• BULIMIA NERVOSA
• BINGE EATING DISORDER
• OTHER SPECIFIED FEEDING OR EATING DISORDER
• UNSPECIFIED FEEDING OR EATING DISORDER

3. Dsm-5 and eating disorders
• Additionally, the category that was known as Eating Disorder Not
Otherwise Specified (EDNOS), has been removed. There are two new
categories; Other Specified Feeding or Eating Disorder (OSFED) and
Unspecified Feeding or Eating Disorder (UFED).
• These new categories are intended to more appropriately recognize
and categorize conditions that do not more accurately fit into Anorexia
Nervosa, Bulimia Nervosa, BED, or the other eating and feeding
disorders. It is important to note that these new categories are not an
indication of a less severe eating disorder, simply a different
constellation of symptoms.
• Another significant change is the inclusion of some types of ‘Feeding
Disorders’ that were previously listed in other chapters of the DSM,
and now listed together with eating disorders.

4. Feeding and Eating Disorders
are Characterized by a persistent disturbance of eating and eating-
related behavior that results in the altered consumption or absorption
of food and that significantly impairs physical health or psychosocial
functioning.

5. Pica
Diagnostic Criteria:
1.Persistent eating of nonnutritive, nonfood substances over a period of at least 1
month.
2.The eating of nonnutritive, nonfood substances is inappropriate to the
developmental level of the individual.
3.The eating behavior is not part of a culturally supported or socially normative
practice.
4.If the eating behavior occurs in the context of another mental disorder (e.g.,
intellectual disability [intellectual developmental disorder], autism spectrum
disorder, schizophrenia) or medical condition (including pregnancy), it is
sufficiently severe to warrant additional clinical attention.

6. Pica
• The term nonfood is included because the diagnosis of pica does not
apply to ingestion of diet products that have minimal nutritional
content.
• Onset of pica can occur in childhood, adolescence, or adulthood,
although childhood onset is most commonly reported. Pica can occur
in otherwise normally developing children,whereas in adults, it
appears more likely to occur in the context of intellectual disability or
other mental disorders.
• The eating of nonnutritive, nonfood substances may also manifest in
pregnancy, when specific cravings (e.g., chalk or ice) might occur.

7. Rumination Disorder
Diagnostic Criteria:
1. Repeated regurgitation of food over a period of at least 1 month. Regurgitated
food may be re-chewed, re-swallowed, or spit out.
2. The repeated regurgitation is not attributable to an associated gastrointestinal or
other medical condition (e.g., gastroesophageal reflux, pyloric stenosis).
3. The eating disturbance does not occur exclusively during the course of anorexia
nervosa, bulimia nervosa, binge-eating disorder, or avoidant/restrictive food
intake disorder.
4. If the symptoms occur in the context of another mental disorder (e.g.,
intellectual disability [Intellectual developmental disorder] or another
neurodevelopmental disorder), they are sufficiently severe to warrant additional
clinical attention.

8. Avoidant/Restrictive Food Intake Disorder
Diagnostic Criteria:
A. An eating or feeding disturbance (e.g., apparent lack of interest in eating
or food; avoidance based on the sensory characteristics of food; concern
about aversive consequences of eating) as manifested by persistent
failure to meet appropriate nutritional and/or energy needs associated
with one (or more) of the following:
1. Significant weight loss (or failure to achieve expected weight gain or
altering growth in children).
2. Significant nutritional deficiency.
3. Dependence on enteral feeding or oral nutritional supplements.
4. Marked interference with psychosocial functioning.

9. B. The disturbance is not better explained by lack of available food or
by an associated culturally sanctioned practice.
C. The eating disturbance does not occur exclusively during the course
of anorexia nervosa or bulimia nervosa, and there is no evidence of
a disturbance in the way in which one’s body weight or shape is
experienced.
D. The eating disturbance is not attributable to a concurrent medical
condition or not better explained by another mental disorder. When
the eating disturbance occurs in the context of another condition or
disorder, the severity of the eating disturbance exceeds that
routinely associated with the condition or disorder and warrants
additional clinical attention.

10. Anorexia Nervosa
Diagnostic Criteria:
A. Restriction of energy intake relative to requirements, leading to a
significantly low body weight in the context of age, sex, developmental
trajectory, and physical health. Significantly low weight is defined as a
weight that is less than minimally normal or, for children and
adolescents, less than that minimally expected.
B. Intense fear of gaining weight or of becoming fat, or persistent
behavior that interferes with weight gain, even though at a significantly
low weight.
C. Disturbance in the way in which one’s body weight or shape is
experienced, undue influence of body weight or shape on self-
evaluation, or persistent lack of recognition of the seriousness of the
current low body weight.

11. Subtypes AN (DSM-5):
Restricting Type: during last 3months, the person has not engaged in
recurrent episodes of binge eating or purging behavior
Binge-Eating/Purging Type: during last 3 months, the person engaged
in recurrent episodes of binge eating or purging behavior

12. HISTORY
• Cases of anorexia nervosa like illness (severely reduced appetite and
weight loss without any medical cause)were first reported by the English
physician Edward Morton in 1689
• The French physician ernest-Charles lasegue called it anorexie histerique in
18 73.
• In the same year the term anorexia nervosa was first used by sir William
gull a personal physician of queen Victoria.
• The concept of bulimia nervosa was introduced by professor gerald russel
in the uk in 1979
• a subset of Binge Eating Disorder called night eating syndrome was first
described by the American psychiatrist albert stunkard in 1959.

13. Clinical features
• Reduced body weight due to self –induced weight loss resulting in:
- icd 10: body weight less than 85% for age /height/gender,or bmi less than
17.5[BMI= wt.in kg/(ht.in meters)2]
-DSM 5 : ‘SIGNIFICANTLY LOW BODY WEIGHT’
• Self perception that one is too fat (even though clearly under weight )
• Intense fear of gaining weight and becoming fat.
• Self induced weight loss by:
 restriction of food intake /starvation
Vomiting
Excessive exercise
Misuse of laxatives,diuretics,appetite suppressants ,etc
• Denial of seriousness of low body weight
• Females- amenorrhoea

14. Some behaviours seen in Anorexia
nervosa
• WEARING MULTIPLE LAYERS OF CLOTHING
• WHILE EATIG :
 CUTTING FOOD INTO SMALL PIECES
EATING VERY SLOWLY/PICKING AT FOOD
INFLEXIBILITY REGARDING FOOD THAT ONE EATS
• COUNTING CALORIES IN FOOD ITEMS BEFORE EATING
• PREPARING ELABORATE MEAL FOR OTHERS

15. PURGE IN EATING DISORDER
TERMINOLOGY
• THE DICTIONARY MEANING OF PURGE IS : TO GET RID OF
SOMETHING (UNWANTED)
• IN GENERAL MEDICAL USAGE .THE WORD PURAGATIVE IS USED
SYNONYMOUSLY WITH LAXATIVE,AND THE WORD EMETIC IS USED
FOR A DRUG THAT INDUCES VOMITING
• IN EATING DISORDERS, THE WORD PURGING REFERS TO BOTH SELF
IINDUCED VOMITING AND ABUSE OF LAXATIVES.
• INFACT THE MOST COMMON MODE OF PURGING IN BOTH ANOREXIA
NERVOSA AND BULIMIA NERVOSA IS SELF INDUCED VOMITING.

16. • TYPES OF ANOREXIA NERVOSA
1.RESTRICTING TYPE:STARVATION OR HIGHLY RESTRICTED INTAKE ARE
THE PREDOMINANT MEANS OF ACHIEVING WEIGHT LOSS.
2.BINGE-PURGE TYPE SELF: –INDUCED VOMITING AND ABUSE OF
LAXATIVES/DIURETICS ARE THE MAIN METHODS OF ACHIEVING
WEIGHT LOSS.

17. SELF –EVALUATION OF BODY WEIGHT IN AN

18. Bulimia Nervosa
Diagnostic Criteria:
A. Recurrent episodes of binge eating. An episode of binge eating is characterized
by both of the following:
1. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount
of food that is definitely larger than what most individuals would eat in a similar
period of time under similar circumstances.
2. A sense of lack of control over eating during the episode (e.g., a feeling that
one cannot stop eating or control what or how much one is eating).

19. Bulimia Nervosa
B. Recurrent inappropriate compensatory behaviors in order to prevent
weight gain, such as self-induced vomiting; misuse of laxatives, diuretics, or
other medications; fasting; or excessive exercise.
C. The binge eating and inappropriate compensatory behaviors both occur,
on average, at least once a week for 3 months.
D. Self-evaluation is unduly influenced by body shape and weight.
E. The disturbance does not occur exclusively during episodes of anorexia
nervosa.

20. Bulimia Nervosa
Specify if:
In partial remission: After full criteria for bulimia nervosa were previously met, some, but
not all, of the criteria have been met for a sustained period of time.
In full remission: After full criteria for bulimia nervosa were previously met, none of the
criteria have been met for a sustained period of time.
Specify current severity:
The minimum level of severity is based on the frequency of inappropriate
compensatory behaviors (see below). The level of severity may be increased to reflect
other symptoms and the degree of functional disability.
Mild: An average of 1-3 episodes of inappropriate compensatory behaviors per week.
Moderate: An average of 4-7 episodes of inappropriate compensatory behaviors per
week.
Severe: An average of 8-13 episodes of inappropriate compensatory behaviors per
week.
Extreme: An average of 14 or more episodes of inappropriate compensatory behaviors
per week.

21. Clinical features
RECURRENT EPISODE OF BINGE EATING:
• STRONG DESIRE OR COMPULSION TO EAT
• LARGE AMOUNT OF FOOD CONSUMED WITH IN A SHORT PERIOD
(UNDER2 HRS)
• LACK OF CONTROL OVER EATING
• ATLEAST ONE EPISODE A WEEK FOR ATLEAST 3MONTHS
EPISODE FOLLOWED BY ATTEMPTS TO COUNTERACT “FATTENING”AFFECTS OF FOOD
CONSUMED BY:
• SELF INDUCED VOMITING /ABUSE OF LAXATIVES ETC
• PERIODS OF STARVATION
• SELF PERCEPTION OF BEING TOO FAT(EVEN IF NORMAL BODY WT)
• MAY BE COMORBID WITH ANOREXIA NERVOSA

23. Binge-Eating Disorder
Diagnostic Criteria:
A. Recurrent episodes of binge eating. An episode of binge eating is characterized
by both of the following:
1. Eating, in a discrete period of time (e.g., within any 2-hour period), an
amount of food that is definitely larger than what most people would eat in a
similar period of time under similar circumstances.
2. A sense of lack of control over eating during the episode (e.g., a feeling
that one cannot stop eating or control what or how much one is eating).

24. Binge-Eating Disorder
B. The binge-eating episodes are associated with three (or more) of the
following:
1. Eating much more rapidly than normal.
2. Eating until feeling uncomfortably full.
3. Eating large amounts of food when not feeling physically hungry.
4. Eating alone because of feeling embarrassed by how much one is
eating.
5. Feeling disgusted with oneself, depressed, or very guilty afterward.
C. Marked distress regarding binge eating is present.
D. The binge eating occurs, on average, at least once a week for 3 months.
E. The binge eating is not associated with the recurrent use of
inappropriate compensatory behavior as in bulimia nervosa and does not
occur exclusively during the course of bulimia nervosa or anorexia
nervosa.

25. Binge-Eating Disorder
Specify if:
In partial remission: After full criteria for binge-eating disorder were
previously met, binge eating occurs at an average frequency of less than
one episode per week for a sustained period of time.
In full remission: After full criteria for binge-eating disorder were previously
met, none of the criteria have been met for a sustained period of time.
Specify current severity:
The minimum level of severity is based on the frequency of episodes of
binge eating (see below). The level of severity may be increased to reflect
other symptoms and the degree of functional disability.
Mild: 1-3 binge-eating episodes per week.
Moderate: 4-7 binge-eating episodes per week.
Severe: 8-13 binge-eating episodes per week.
Extreme: 14 or more binge-eating episodes per week.

26. Clinical features-
RECURRENT EPISODE OF BINGE EATING (AS FOR BN):
• STRONG DESIRE OR COMMPULSION (CRAVING) TO EAT.
• LARGE AMOUNT OF FOOD CONSUMED WITH IN A SHORT PERIOD(2 HOURS)
• LACK OF CONTROL OVER EATING(WHAT OR HOW MUCH ONE EAT)
BINGE EATING EPISODES CHARACTERISED BY:
• EATING MORE RAPIDLY THAN USUAL
• EATING ALONE(DUE TO EMBARASSMENT)
• EATINNG EVEN WHEN NOT HUNGRY
• FEELING DISGUSTED WITH SELF OR GUILTY AFTERWARDS
• NO ASSOCIATED COMPULSATORY BEHAVIOR LIKE VOMITING/LAXATIVE
/STARVATION

27. USUAL BODY WEIGHT IN EATING DISORDER
• An-underweight
• BN-normal body weight
• Bed –over weight

28. EATING DISORDER IN ICD 10 F50
• F50.0 ANOREXIA NERVOSA
• F50.1 ATYPICAL ANOREXIA NERVOSA
• F.50.2 BULIMIA NERVOSA
• F.50.3 ATYPICAL BULIMIA NERVOSA
• F50.4 OVEREATING ASSOCIATED WIT OTHER PSYCHOLOGICAL
DISTURBANCES
• F.50.5 VOMITING ASSOCIATED WITH OTHER PSYCHOLOGICAL
DISTURBANCES
• F.50.8 OTHER EATING DISORDERS
• F.50.9 EATING DISORDER,UNSPECIFIED

29. • THE CATEGORY OSFED (OTHER SPECIFIED FEEDING OR EATING
DISORDER0IN DSM 5 INCLUDES-
• ATYPICAL AN:SOME CRITERIA NOT MET(E.G. PT HAS NORMAL WT)
• SUBTHRESHOLD BN/SUBTHRESHOLD BED:BINGE EATING EPISODES
NOT AS SEVERE IN TERMS OF FREQUENCY OR DURATION
• PURGING DISORDER:RECURRENT SELF –VOMITING MISUSE OF
LAXATIVES,DIURETICS,ETC. WITHOUT ANY BINGE EATING
• NIGHT EATING SYNDROME:RECURRENT EPISODES OF EATING AT
NIGHT WHEN WAKING UP FROM SLEEP,INDEPENDENT OF ANY
MENTAL ILLNESS OR SLEEP DISORDER.

30. EPIDEMIOLOGY-ANOREXIA NERVOSA
• LIFETIME PREVALENCE IS ABOUT 1% IN THE COMMUNITY(IN
FEMALES)
• MORE COMMON IN FEMALES:
 A 10:1 F:M RATIO IS WIDELY QUOTED
SOME STUDIES SUGGEST THAT THIS GAP MAY BE NARROWING
• INCIDENCE IS ABOUT 8 PER 100,000 POPULATION
• HIGHEST INCIDENCE(MORE THAN 100 PER 100,000) IS IN THE 15 TO
19 AGE GROUP

31. EPIDEMIOLOGY –BULIMIA NERVOSA
• LIFE TIME PREVALENCE IS ABOUT 2%(IN FEMALES)
• INCIDENCE IS ABOUT 12 PER 100,000 POPULATION
• MUCH MORE COMMON IN FEMALES ,WITH A F:M RATIO OF ABOUT
5:1
• AGE OF ONSET IS DECREASING :HIGHEST INCIDENCE USED TO BE IN
THE 25 TO 29 AGE GROUP,BUT NOW IT IS THE 15 TO 19 AGE
GROUP(MAY BE DUE TO EARLIER DETECTION)

32. EPIDEMIOLOGY-BINGE EATING DISORDER
• LIFETIME PREVALENCE IS ABOUT 4% IN FEMALES,AND 2%IN MALES
• SO F:M RATIO IS ABOUT 2:1
• PEAK AGE OF INCIDENCE :BETWEEN 25 AND 34 YEARS

33. AETIOLOGY OF EATING DISORDER
• EXACT AEITIOLOGY NOT KNOWN
• BEST TO CONSIDER EATING DISORDERS AS HAVING A COMPLEX
MULTIFACTORIAL AETIOLOGY INVOLVING CULTURAL,FAMILY,GENETIC
AND OTHER BIOLOGICAL FACTORS.
• FOR MANY YEARS,ANOREXIA NERVOSA WAS THOUGHT TO BE A
PRIMARILY CULTURALLY INFLUENCED DISORDER DUE TO
PREOCCUPATION OF WESTERN SOCIETIES WITH THINNESS
• INCREASE IN PREVALENCE IN NON –WESTERN SOCIETIES COINCIDED
WITH INCREASING WESTERN INFLUENCE THERE.

34. AETIOLOGY OF EATING DISORDERS
• FAMILY AND TWIN STUDIES SUGGEST A GENETIC COMPONENT
• FAMILY DYSFUNCTION HAS BEEN SHOWN TO BE RELEVANT
• HIGH CO-MORBIDITY WITH DEPRESSION AND ANXIETY DISORDERS
SUGGESTS POSSIBLE SHARED AETIOLOGY WITH THOSE DISORDERS
• OTHER POTENTIAL RISK FACTORS INCLUDE:
-EARLY CHILDHOOD EATING /GESTROINTESTINAL PROBLEMS
-CHILDHOOD SEXUAL ABUSE

35. AETIOLOGY OF EATING DISORDERS
• ROLE OF PERSONALITY:
POOOR SELF ESTEEM/EXCESSIVE SELF CRITICISM SEEN IN BOTH AN AND BN
PERFECTIONISM /OBSESSIVE COMPULSIVE PERSONALITY DISORDER
ASSOCIATED WITH AN
IMPULSIVITY /BORDERLINE PERSONALITY DISORDER ASSOCIATED WITH BN
• A CRITICAL COMMENT (‘YOU ARE FAT’)MADE BY A PARENT OR OTHERS(E.G
SPORTS COACH) MAY TRIGGER ANOREXIA NERVOSA IN VULNERABLE
CHILDREN/ADOLESCENTS.
• IN SOME PATIENTS ,THE INITIAL WEIGHT LOSS MAY GENERATE ‘POSITIVE “
COMMENTS FROM OTHERS(‘YOU HAVE LOST WEIGHT ,WELL DONE’).THIS
BECOMES PSYCHOLOGICALLY REWARDING TO PTS ,AND REINFORCES THE
SELF-STARVATION AND OTHER MALADAPTIVE BEHAVIOURS,SO AS TO LOSE
MORE WEIGHT.

36. AETIOLOGY –BIOLOGICAL HYPOTHESIS
• ABNORMALITIES IN:
DOPAMINE/SEROTONIN NEUROTRANSMISSION
BDNF (BRAIN –DERIVED NEUROTROPHIC FACTOR) LEVELS
• OBSTETRIC COMPLICATIONS
• ABNORMAL LEVELS OF THE HORMONES LEPTIN AND GHRELIN:
LEPTIN ,PRODUCED IN ADIPOSE TISSUE ,HAS ANOREXIGENIC
(APPETITE-INHIBITING)EFFECT
GHRELIN,PRODUCED BY STOMACH AND SMALL INTESTINE ,HAS
OREXIGENIC(APPETITE –STIMULATING) EFFECT

37. • STRUCTURAL NEUROIMAGING STUDIES HAVE SHOWN :
REDUCED GRAY MATTER IN ANOREXIA NERVOSA IN MANY BRAIN REGIONS
INCLUDING ANTERIOR CINGULATE CORTEX AND CEREBELLUM
REDUCED VOLUME OF THE CAUDATE NUCLEUS
• FUNCTIONAL NEUROIMAGING HAS SHOWN REDUCED CEREBRAL BLOOD
FLOW IN TEMPORAL LOBES
• NUMEROUS POTENTIAL GENETIC POLYMORPHISMS HAVE BEEN NOTED
• ROLE OF AUTOANTIBODIES THAT ACT AGAINST APPETITE REGULATING
NEUROPEPTIDES
• DISTURBED GUSTATORY (TASTE)PROCESSING-
IMPAIRED PROCESSING IN ANOREXIA NERVOSA LEADS TO RESTRICTED
INTAKE
EXAGGERATED PERCEPTION IN BN/BED LEADS TO OVEREATING

38. OCCUPATIONS WITH HIGHER RISK OF EATING
DISORDERS
• MODELS
• ACTORS
• TV PERSONALITIES
• DANCERS(E.G BALLET)
• SPORTS:
GYMNASTS
JOCKEY
SWIMMERS
ATHLETES(E.G LONG DISTANCE RUNNERS)

39. COMORBIDITY OF EATING DISORDERS
• A CONSIDERABLE PROPORTION OF PATIENTS WITH EATING
DISORDERS HAVE OTHER PSYCHIATRIC DISORDERS
• MOST COMMON CO-MORBID ILLNESS IS DEPRESSION ,FOLLOWED BY
ANXIETY DISORDERS AND PERSONALITY DISORDERS
• PSYCHOSIS ,OCD AND PTSD ARE MORE COMMON IN AN THAN IN
OTHER EATING DISORDERS
• ALCOHOL AND SUBSTANCE MISUSE ARE MORE COMMON IN BN
THAN IN OTHER EATING DISORDERS

40. COMPLICATION OF ANOREXIA NERVOSA
GENERAL-
• ANAEMIA
• CYANOSIS
• HYPOTENSION
• HYPOTHERMIA
• HYPOGLYCAEMIA
-SKIN/HAIR/NAIL
• DRY/SCALY SKIN
• YELLOW SKIN
• PRURITIS
• PURPURA
• BRITTLE HAIR
• HAIR LOSS
• LANUGO HAIR
• BRITTLE NAILS
ENDOCRINE-
• DELAYED MENARCHE(IF ONSET IS
PREPUBERTAL)
• AMENORRHOEA
• INFERTILITY
• MISCARRIAGE
• HYPOTHYROIDISM
• HYPERCORTISOLEMIA
• INCREASED RISK OF DIABETIC
COMPLICATIONS(E.G. RETINOPATHY)
• NEUROGENIC DIABETES INSIPIDUS

41. CARDIAC-
• BRADYCARDIA
• OTHER ARRHYTHMIAS(WHICH
MAY LEAD TO SUDDEN DEATH)
• CARDIAC ATROPHY
• LOW CARDIAC OUTPUT
BONE-
• OSTEOPENIA(EVEN MANY YEARS
AFTER RECOVERY)
• OSTEOPOROSIS
• HIGHER RISK OF FRACTURES
(DISPROPORTIONATE TO ANY
REDUCTION IN BONE MINERAL
DENSITY)
• JOINT SWELLING
• SHORT STATURE (BOTH IN BOYS
AND GIRLS,ESPECIALLY FOR PRE
PUBERTAL ONSET)
GI-
• CONSTIPATION
• DELAYED GASTRIC EMPTYING
• DYSPHAGIA
• GASTRIC DILATATION
• LIVER DYSFUNCTION

42. METABOLIC/RENAL-
• REDUCED:
1.SODIUM
2.POTASSIUM
3.PHOSPHATE
4.MAGNESIUM
• RENAL STONES
• RENAL IMPAIRMENT
PULMONARY-
SPONTANEOUS PNEUMOTHORAX
ASPIRATION PNEUMONIA
EMPHYSEMA
RESPIRATORY FAILURE

43. COMPLICATION OF BN
• COMPICATION CAN BE SUBDIVIDED INTO THOSE:
1.DUE TO SELF INDUCED VOMITING
2.DUE TO LAXATIVE ABUSE

44. DUE TO SELF INDUCED VOMITING
1.DUE TO FREQUENT EXPOSER OF ORAL CAVITY TO GASTRIC ACID:
• HYPERSENSITIVE TEETH
• DENTAL CARIES( WORSENED BY EATING HIGH SUGAR FOOD /DRINKS)
• DENTAL EROSION
• PERIODONTAL DISEASE
• GINGIVITIS
• XEROSTOMIA(DRY MOUTH)
• 2.RUSSELLS SIGN:CALLUSES ON THE BACK OF THE HAND DUE TO
REPEATED CONTACT WITH ACIDIC CONTENTS

45. ORAL COMPLICATION OF SELF INDUCED
VOMITING

46. RUSSELL’S SIGN

47. OTHER COMPLICATIONS OF SELF INDUCED VOMITING-
• PAROTID GLAND ENLARGEMENT(PUFFY CHEEKS)
• SUB CONJUNCTIVAL HAEMORRHAGE
• EPISTAXIS
• DYSPHAGIA,ODYNOPHAGIA,GERD,BARRETTS OESOPHAGUS,OESOPHAGEAL
RUPTURE(BOERHAAVE’S SYNDROME)
• VOCAL CORD OEDEMA LEADING TO CHANGE IN VOICE
• PULMONARY ASPIRATION LEADING TO CHANGE IN VOICE
• PULMONARY ASPIRATION LEADING TO RESPIRATORY SYMPTOMS
• RARELY ,SWALLOWING A FOREIGN OBJECT(E.G. TOOTHBRUSH) USED TO
INDUCE VOMITING

48. 2.COMPLICATIONS OF LAXATIVE ABUSE
• THERE ARE DIFFERENT TYPES OF LAXATIVES :EG STIMULANT,OSMOTIC,BULK –FORMING
ETC
• THE MOST COMMON TYPE ABUSED IN BN IS THE STIMULANT VARIETY(E.G. SENNA
,BISACODYL)
• THESE DIRECTLY STIMULATE COLONIC MOTILITY,AND HAVE A RELATIVELY RAPID EFFECT
IN PRODUCING A WATERY DIARRHOEA
COMPLICATION:
• LOSS OF NORMAL COLONIC PERISTALSIS
• ATONIC ,DILATED COLON
• MELANOSIS COLI:DISCOLORATION OF THE COLONIC MUCOSA
VOMITING,LAXATIVES (AND DIURETIIC ABUSE) CONTRIBUTE TOWARDS:
• DEHYDRATION
• HYPOCHLOREMIC ,HYPOKALAEMIC METABOLIC ALKALOSIS
• PERIPHERAL OEDEMA

49. COMPLICATION OF BED
PSYCHOLOGICAL DISTRESS (GUILT ,FEELING WORTHLESS,ETC) DUE TO INABILITY
TO CONTROL BINGEING URGES (PSYCHOLOGICAL DISTRESS BOTH PRECEDES AND
FOLLOWS EPISODES)
IN SEVERE CASES ,BINGING TAKES PRECEDENCE OVER OTHER ASPECTS OF LIFE
SUCH AS WORK,FAMILY,SOCIAL ACTIVITIES ETC(SIMILAR TO ALCOHOL
DEPENDENCE
OBESITY RELATED PROBLEMS:
• TYPE II DIABETES
• HTN
• DYSLIPIDAEMIA
• GERD
• ARTHRITIS
• GALL STONES
• SLEEP APNOEA

50. ASSESMENTS –GENERAL POINTS
• MAJORITY OF PATIENTS WITH EATING DISORDERS (ESPECIALLY BN AND
BED) DO NOT RECEIVE PROPER TREATMENT (EITHER PATIENT DOES NOT
SEEK T/T OR THE DIAGNOSIS IS OVERLOOKED)
• PERFORM THOROUGH PSYCHIATRIC ASSESS MENT:
ASSESS FOR CO MORBID PSYCHIATRIC DISORDERS LIKE DEPRESSION
CO MORBID AN AND BN IS NOT AN UNCOMMON PRESENTATION
• TAKE A COMPREHENSIVE MEDICAL HISTORY
• MEASURE BMI
• DO A GENERAL PHYSICAL EXAMINATION,LOOKING FOR SIGNS OF AN /BN
• THE EXTENT OF PHYSICAL EXAMINATION AND INVESTIGATIONS DEPENDS
ON THE SETTING (OUTPATIENT OR INPATIENT),LIKELY DIAGNOSIS(AN OR
BN) AND SEVERITY(HIGHER RISK OF PHYSICAL COMPLICTAIONS)

51. • DO ROUTINE BLOOD TESTS BEFORE INITIATING T/T (CBC ,LFT,U&E
,TFT,GLUCOSE,ETC)
• BASELINE ECG
• UNLESS SPECIFICALLY INDICATED (E.G. HIGHLY ATYPICAL SYMPTOMS )
NO NEED FOR:
• NEUROIMAGING LIKE CT OR MRI
• EEG
• PSYCHOMETRIC TESTING/NEUROPSYCHOLOGICAL
TETSING/STRUCTURED PERSONALITY QUESTIONNAIRES

52. SOME RATING SCALES USED FOR ASSESMENT OF
EATING DISORDERS
• EATING DISORDERS INVENTORY(EDI)
• EATING ATTITUDE TEST(EAT)
• BINGE EATING SCALE(BES)
• YALE BROWN CORNELL EATING DISORDER SCALE
• ANORECTIC BEHAVIOR OBSERVATION SCALE
• SCOFF QUESTIONNAIRE:
A SCREENING TOOL SIMILAR TO THE CAGE QUESTIONNAIRE USED IN
ALCOHOL MISUSE DISORDERS’ HAS 5 QUESTIONS ;A SCORE OF 2 OR
MORE WARRANTS A MORE THOROUGH ASSESMENT

53. SCOFF QUESTIONNAIRE
• DO YOU MAKE YOURSELF SICK BECAUSE YOU FEEL UNCOMFORTABLY
FULL?
• DO YOU WORRY THAT YOU HAVE LOST CONTROL OVER HOW MUCH
YOU EAT?
• HAVE YOU RECENTLY LOST MORE THAN ONE STONE (14lb) IN A 3
MONTH PERIOD?
• DO YO BELIEVE YOURSELF TO BE FAT WHEN OTHERS SAY YOU ARE
TOO THIN?
• WOULD YOU SAY THAT FOOD DOMINATES YOUR LIFE??

54. MANAGEMENNT OF EATING DISORDERS
• THERE ARE A WIDE VARIETY OF TREATMENTS USED FOR ED
• FOR MOST PT,A COMBINATION OF APPROACHES IS NEEDED
• NORMALIZATION OF NUTRITION AND EATINNG HABITS IS A CENTRAL
GOAL IN THE TREATMENT OF PTS
• AS EATING DISORDERS TEND TO RUN A CHRONIC COURSE ,IT IS
IMPORTANT TO MONITOR AND ADDRESS ,ON AN ONGOING BASIS:
PSYCHIATRIC COMORBIDITIES
PHYSICAL HEALTH COMPLICATIONS
CHANGES IN SOCIAL CIRCUMSTANCES

55. MANAGEMENT OF ANOREXIA NERVOSA
• DEPENDING ON AVAILABILITY/NEED,PT CAN BE TREATED IN A;
• ROUTINE PSYCHIATRY OUTPATIENT (ADULT CHILD AND ADOLESCENT
SERVICES)CLINIC
• GENERAL PSYCHIATRY INPATIENT UNIT
• GENERAL MEDICAL INPATIENT UNIT
• SPECIALIST EATING DISORDRS OUTPATIENTS CLINIC
• SPECIALIST EATING DISORDERS INPATIENTS UNIT
• HOWEVER STUDIES HAVE SHOWN THAT ADHERENCE TO TREATMENT
IS POOR WITH HIGH DROP OUT RATES

56. PSYCHOLOGICAL INTERVENTIONS FOR EATING
DISORDERS
• FAMILY THERAPY:MANY SMALL AND RELATIVELY SHORT TERM
STUDIES HAVE SUGGESTED POSITIVE BENEFIT IN ANOREXIA NERVOSA
• COGNITIVE BEHAVIOURAL THERAPY (CBT) :T/T OF CHOICE FOR BN
• INTERPERSONAL THERAPY(IPT)
• PSYCHODYNAMIC THERAPY
• A FEW MOTIVATIONAL INTERVIEWING SESSIONS EARLY IN T/T MAY
IMPROVE READINESS TO CHANGE

57. FAMILY THERAPY FOR ANOREXIA NERVOSA
• PSYCHOTHERAPY IS DELIVERED TO PT AND FAMILY ,USUALY PARENTS
• THEY ARE GENERALLY SEEN TOGETHER(JOINT THERAPY),BUT
SOMETIMES SEPRATELY (SEPRATED THERAPY)
• SOME TYPE OF FAMILY THERAPY USED IN ANOREXIA NERVOSA:
1. STRUCTURAL FAMILY THERAPY
2. SYSTEMIC FAMILY THERAY
3. STRATEGIC FAMILY THERAPY
4. FAMILY BASED THERAPY(MAUDSLEY MODEL)
5. BEHAVIOURAL FAMILY THERAPY

58. FAMILY THERAPY FOR AN
DEPENDING ON THE TYPE ,THE THERAPY MAY ADDRESS:
• INDIVIDUAL VULNERABILITY
• DYSFUNCTIONAL FAMILY DYNAMICS
• CONFLICTS WITH IN FAMILY(PARENTAL DISCORD)
• HIGH EXPRESSED EMOTIONS SUCH AS UNFAIR PARENTAL CRITICISM OF PATIENT
• SYMPTOMS SYMBOLISM
• TRANSFERENCE
• PERSONALITY DIFFICULTIES IN PATIENT/PARENTS
• IMPACT OF AN ON FAMILY MEMBERS/IMPACT OF THE BEHAVIOUR OF FAMILY MEMEBERS ON AN
• For young patients,parents may be asked to take active role in treatment at home:
Ensuring patient has regular meals
Ensuring that patient does not indulge in compensatory behaviours after meals(e.g. vomiting,exercise
etc)

59. PHARMACOTHERAPY FOR AN
• LIMITED NUMBER OF RCTS IN EDS COMPARED TO OTHER MAJOR
MENTAL DISORDERS.SO ,MORE RESEARCH NEEDED
• AN:
ATYPICAL ANTIPSYCHOTICS(PARTICULARLY OLANZAPINE)
ZINC SUPPLEMENTATION
TREAT CO-MORBID DEPRESSION AND ANXIETY ACCORDINGLY,WITH
ANTIDEPRESSANTS

60. RATIONALE FOR USING ATYPICAL
ANTIPSYCHOTICS IN ANOREXIA NERVOSA
• TO PROMOTE WEIGHT GAIN (PARTICULARLY OLANZAPINE)
• TO REDUCE HYPERACTIVITY(USED BY PATIENTS AS A WEIGHT LOSING
TACTIC)
• IF BODY IMAGE DISTURBANCES IS ALMOST DELUSIONAL IN NATURE
• SOME EVIDENCE FROM NEUROENDOCRINE STUDIES THAT DOPAMINE
NEUROTRANSMISSION IS INCREASED IN ANOREXIA NERVOSA

61. RATIONALE FOR USING ZINC IN ANOREXIA
NERVOSA
• IN ANOREXIA NERVOSA,THERE IS ZINC DEFECIENCY
• ZINC PLAYS A ROLE IN NEUROTRANSMITTER FUNCTION
• ZINC HAS APPETITE STIMULANT EFFECT
• ZINC IS CHEAP AND WELL TOLERATED
• DOSE SUGGESTED IN 1 STUDY WAS 14 MG OF ELEMENTAL ZINC DAILY
FOR 2 MONTHS

62. TREATMENT OF BULIMIA NERVOSA
• GENERALLY TREATED AS OUTPATIENTS
• CBT THE TREATMENT OF CHOICE-EITHER INDIVIDUAL CBT OR GROUP
CBT
• OTHER CBT OPTIONS:WEB BASES /TELEMEDICINE CBT,GUIDED SELF –
HELP,BIBLIOTHERAPY(SELF HELP BOOKS)
• IPT MAY BE ANOTHER OPTION
• FAMILY THERAPY MAY BE USEFUL FOR ADOLESCENTS WITH BN
• EDUCATION ABOUT HEALTHY DIETING

63. PHARMACOTHERAPY OF BULIMIA NERVOSA
• SSRI(PARTICULARLY HIGH DOSE FLUOXETINE)CAN HELP REDUCE
BINGEING USAGE AND OBSESSIONAL PREOCCUPATION WITH WEIGHT
• TRICYCLIC ANTIDEPRESSANTS
• ANTIEPILEPTIC TOPIRAMATES(MAY HAVE APPETITE REDUCING
EFFECT)
• SIBUTRAMINE:WAS USED FOR BINGE EATING DISORDER,BUT NO
LONGER APPROVED DUE TO INCREASED RISK OF MI AND STROKE.

64. CBT FOR BULIMIA NERVOSA (AND BED)-
PRACTICAL POINTS
 COGNITIVE:
• TO IDENTIFY DYSFUNCTIONAL THOUGHT PATTERN AND BELIEFS(E.G.
LOW SELF –ESTEEM ,PERFECTIONISM,ETC)THAT PREDISPOSE TO AND
MAINTAIN THE EATING DISORDER
 BEHAVIOURAL:
• THE AIM IS TO BREAK THE BINGEING-PURGING VICIOUS CYCLE
• EXPOSURE AND RESPONSE PREVENTION;HELPING PATIENT TO DEAL
WITH PRE BINGE CUES AND PRE PURGE CUES IN WAYS OTHER THAN
BINGEING OR PURGING RESPECTIVELY

65. MANAGEMENT OF BINGE EATINNG DISORDER
• RESEARCH STUDIES SHOW HIGH PLACEBO RESPONSE
• SIMILAR TREATMENT APPROACHES AS FOR BULIMIA NERVOSA
• PSYCHOTHERAPY OPTIONS:
CBT : INDIVIDUAL/GROUP/ONLINE/GUIDED SELF HELP/BIBLIOTHERAPY
OTER PSYCHOTHERAPIES:IPT,PSYCHODYNAMIC-BASED
MEDICATION:
SSRI(ESP.SERTRALINE/ESCITALOPRAM/CITALOPRAM)IMIPRAMINE ,TOPIRAMATE
(SIBUTRAMINE NO LONGER APPROVED DUE TO RISK OF MI AND STROKE)
WEIGHT LOSS TREATMENT PROGRAMMES /INDIVIDUAL COACHING ETC CAN HELP
WITH OBESITY
BARIATRIC SURGERY FOR BINGE EATING DISORDER ASSOCIATED WITH MORBID
OBESITY

66. OTHER TREATMENT OPTIONS FOR EATING
DISORDERS
• EXERCISE PROGRAMMES(E.G. LIGHT RESISTANCE TRAINING):
• MAY CHANGE PATIENT ATTITUDE TOWARDS EXERCISE
• MAY INCREASE BONE /JOINT STRENGTH
• MINDFULLNESS TRAINING
• DBT
• EMDR
• YOGA
• RTMS
• BODY AWARENESS THERAPY
• BISPHOPHONATES
• PARENTING SKILLS TRAINING FOR YOUNG MOTHERS WITH ED TO REDUCE RISK OF THEIR
CHILDREN LEARNING MALADAPTIVE EATING –RELATED BEHAVIOURS FROM AN EARLY AGE

67. SOME INDICATION FOR INPATIENT
TREATMENT IN AN• SEVERITY OF PRESENTATION:MEASURED BY BMI
• CONTINUING WEIGHT LOSS
• PATIENT UNMOTIVATED /UNABLE TO EAT
• METABOLIC ABNORMALITIES THAT NEED CLOSE MONITORING
• VITAL SIGN ;FALLING BP,RISING PR,HYPOTHERMIA
• PROMINENT SUICIDAL IDEAS
• IF RISK TO LIFE AND THE PATIENT IS UNABLE/UNWILLING TO CONSENT TO ADMISSION ,SHE/HE
MAY NEED TO BE ADMITTED AGAINST THEIR WISHES
• DEPENDING ON AVAILABILITY ,ADMISSION MAY BE TO A :
SPECIALIST EATING DISORDER UNIT
GENERAL PSYCHIATRIC WARD
GENERAL MEDICAL WARD OR ICU
• AFTER ADMISSION ,MOST OF THE PATIENT WHO REFUSE TO EAT,NASOGASTRIC FEEDING IS
RECOMMENDED

68. REFEEDING SYNDROME
• REFERS TO THE COMPLICATIONS THAT OCCUR AS
A RESULT OF FLUID AND ELECTOLYTE CHANGES
DURING NUTRITIONAL REINSTITUTION OF
SEVERELY MALNOURISHED PATIENTS-EG-
HOMELESS,POWS)
• RISK FACTORS FOR REFEEDING SYNDROME:
VERY LOW BMI
LONGER DURATION OF STARVATION
CO MORBID ILLNESSES (EG DIABETES )OR
INFECTIONS
INTRODUCING FEEDING SUDDENLY
MOST COMMON CAUSE OF DEATH:CARDIAC
ARRHYTHMIAS
OTHER RISKS:DELIRIUM,SEIZURE
,COMA,CARDIAC FAILURE
• METABOLIC ABNORMALITIES INCLUDE;
HYPOKALAEMIA
HYPOPHOSPHATAEMIA
HYPOCALCAEMIA
• GASTRIC DILATATION(RARELY RUPTURE)
• REFEEDING OEDEMA
• REFEEDING PANCREATITIS
• PREVENTION /MANAGEMENT:
MONITOR ELECTROLYTE ,ECG,BODY
WEIGHT,ETCREGULARLY
START LOW GO SLOW’ IN TERMS OF REFEEDING
:
EXAMPLE;START AT 30 KCAL/KG/DAY
GRADUALLLY INCRASING UPTO 100 KCAL/KG/DAY
• AIM FOR WEIGHT GAIN OF 1 TO 1.5 KG PER
WEEK

69. PROGNOSIS
• IN RESEARCH STUDIES IN EATING DISORDERS ,CLINICAL RECOVERY IS
USUALLY DEFINED AS:
• RESTORATION OF WEIGHT AND MENSTRUATION FOR A PERIOD OF
TIME(EG 1 YR)FOR ANOREXIA NERVOSA
• THE ABSENCE OF BINGEING AND PURGING FOR A PERIOD OF TIME (EG 3
MONTHS)FOR BULIMIA NERVOSA
• OVER 50% ACHIEVE CLINICAL (BUT NOT FULL) RECOVERY WITH IN 5 YRS IN
ANOREXIA NERVOSA,WITH HIGHER RATES OF RECOVERY FOR BULIMIA
NERVOSA AND BINGE EATING DISORDER ( SUBSEQUENT RELAPSE IS ALSO
POSSIBLE)
• IN AN AN ,RECOVERY RATES ARE HIGHER FOR ADOLESCENTS(ABOUT
70%)THAN FOR ADULTS (ABOUT 30%)

70. POOR PRGNOSTIC FACTORS FOR AN
• CHRONICITY
• SEVERITY
• CO MORBIDITY
• POOR MOTIVATION TO CHANGE /POOR
ADHERENCE TO TREATMENT
• POOR SOCIAL ADJUSTMENT
• OBSESSIE COMPULSIVE PERSONALITY
TRAITS
• A DIET THAT IS VERY LIMITED IN
VARIETY
GOOD PROGNOSTIC FACTORS
• CONVERSE OF ABOVE POOR
PROGNOSTIC FACTORS
• GOOD INITIAL RESPONSE(E.G.
SIGNIFICANT REDUCTION IN
FREQUENCY OF PURGING EARLY IN
TREATMENT)
• GOOD SOCIAL SUPPORT(EG
PARENTS,FRIENDS,ONLINE
GROUPS,ETC)
• IN SOME ,THERE MAY BE IMMEDIATE
TRIGGERS FOR CHANGE:
WANTING TO BECOME PREGNANT
NOT WANTING TO DIE
BECOMING AWARE OF SIMILAR EATING
BEHAVIOURS IN THEIR YOUNG CHILD

71. MORTALITY IN AN
• AMONG ALL PSYCHIATRIC DISORDERS,AN HAS THE HIGHEST MORTALITY
• 5 TO 10% DIE WITH IN 10 YEARS OF DISEASE ONSET,AND ABOUT 20% DIE WITH IN 20
YEARS OF DISEASE ONSET
• MORTALITY RATE IN AN PATIENTS AGED 15 TO 24 YEARS IS MORE THAN 10 TIMES THAT
EXPECTED IN MATCHED NON AN CONTROLS
• THE STNDARDIZED MORTALITY RATE (SMR) FOR A LIFETIME DIAGNOSIS OF AN IS MORE
THAN 4
• SUICIDE IS AN IMPORTANT CAUSE OF THE HIGHER MORTALITY IN AN
• OTHER CAUSES OF/CONTRIBUTIORS TO DEATH INCLUDE:
COMPLICATION OF STARVATION /MANUTRITION
ONGOING ALCOHOL/SUBSTANCE MISUSE
ORGAN FAILURE:RENAL ,CARDIAC,ETC
CARDIAC ARRHYTHMIAS DUE TO METABOLIC COMPLICATIONS(E.G. HYPOKALAEMIA)

72. Obesity: Definition
• A condition in which excessive body fat may put a person at health
risk.
• A metabolic disorder that is primarily induced and sustained by an
over consumption or underutilization of caloric substrate
Storage of fat :Fat is stored as triglycrides in adipose tissues and the
distributed mainly under skin in
Abdomen
Breast
Buttocks
Thighs

73. Obesity Classification
Standards
(BMI)
Research
Under
weight
< 20 < 18.5
Normal 20 – 25 18.5 – 27.5
Over weight 25 – 30 27.5 – 30
Obese 30 – 40 > 30
Severely
obese
> 40

74. Obesity measureament tools
• Ideal body wt. (IBW)
• Body mass index (BMI)
• weight in Kg / height (m) 2
• Moderate obesity
• Associated with increase in cell size
• Sever obesity
• Associated with increase in no. of fat cells

75. Causes of Obesity
• Complex and multifactorial
• Genetic predisposition
• Endocrine disorders
• Socialization
• Age
• Sex
• Race
• Economic status
• Psychological
• Cultural
• Emotional
• Environmental factors
• Cessation of smoking

76. Leptin
• Released from fat tissues
• Interact with
• Hypothalamus
• Adipose tissue
• Inhibits neuropeptide Y and Aguoti-related peptide (AGRP) in CNS
• Binds to central melanocortin receptors
• Decreases food intake
• Increases energy expenditure

77. How leptin causes obesity
• Primary decrease of leptin (low leptin)
• Leptin receptor resistance (high leptin)
• So increase neuropeptide Y and AGRP increase in food intake and low energy
expenditure  severe obesity
Insulin
↑ Insulin  inhibit Hormone Sensitive lipase (HSL)
Dec. break down of fat  ↑ body fat
↑ insulin  stimulation of lipoprotien lipase  ↑ storage of
triglycrides in fat cells  ↑ total body fat

78. Diseases Linked to Obesity
• Diabetes
• Coronary Heart Disease
• High Blood Pressure
• Stroke
• Arthritis
• Gastroesophageal reflux
• Cancer
• High cholesterol
• Endocrine disease
• Hypertrophic
Cardiomyopathy
• Infertility
• Depression
• Obstructive sleep apnea
• Gallstones
• Fatty liver
• Stress incontinence
• Venous ulcers
• Sudden death

79. What About the Role of Serotonin?
• Theory that low serotonin levels leads to “carbohydrate craving” and plays a major role in the
development of obesity.

80. Psychological Complications
of Obesity
• Emotional distress
• Discrimination
• Social stigmatization

81. Volume Replacement
• Adult total body water percentage is 60% to 65%.
• Severely obese total body water is 40%.
• Estimated blood volume in obese patient is 45 to 55 mL/kg
• 70 mL/kg for the non-obese

82. Selected Medications That Can Cause
Weight Gain
• Psychotropic medications
• Tricyclic antidepressants
• Monoamine oxidase
inhibitors
• Specific SSRIs
• Atypical antipsychotics
• Lithium
• Specific anticonvulsants
• -adrenergic receptor blockers
SSRI=selective serotonin reuptake inhibitor
 Diabetes medications
– Insulin
– Sulfonylureas (glipizide /
glucotrol)
– Thiazolidinediones
(pioglitazone )
 Tamoxifen (anti-estrogen)
 Steroid hormones
– Glucocorticoids

83. Aim of treatment
To achieve a modest weight loss that is also maintained long term
Diet Physical Activity
Lifestyle Modification
Pharmacotherapy
Surgery
Obesity Treatment Pyramid

84. Treatment of Obesity
• Goal of treatment: 10% weight loss
• Caloric restriction: -500 kcal/day
• Moderate physical activity
• 30 minutes daily
• Behavioral modification
• Drug therapy
National Institutes of Health. Obes Res. 1998; 6 (suppl 2): 51S–209S.

85. Diet
• Reduce fatty diets
• Increase fiber diet
• Take calories according to requirements
(1000 to 1500 Kcal)
• Stop bing eating
Exercise
Take 30 min. daily for physical activity

86. Behavior Therapy
Eating and physical activity patterns are learned behaviors and can be modified.
• Behavior Modification Techniques
• Self Monitoring
• Stimulus Control
• Behavioral Contracting
• Cognitive Restructuring
• Stress Management
• Relapse Prevention
• Social Support
• Hyder et al Behavior Modification in the treatment of Obesity: Practical Approaches for Family Physicians Clinics in Family Practice June 2002;2

87. Drug treatment in
adults
• Record initial weight
• Discuss decision to start drug treatment, choice potential benefit and limitations,
adverse effect and monitoring requirement with patient
• Review regularly to monitor compliance, effectiveness, adverse effect
• Reinforce lifestyle advice

88. Drugs Approved by FDA for Treating
Obesity
Generic Name
Trade
Names
Approved
Use
Year
Approved
Orlistat Xenical Long-term 1999
Sibutramine
Reductil /
Meridia
Long-term 1997
Diethylpropion Tenulate Short-term 1973
Phentermine
Adipex,
lonamin
Short-term 1973
Phendimetrazine
Bontril,
Prelu-2
Short-term 1961
Benzphetamine Didrex Short-term 1960

89. Anti-obesity drugs
Drug name Orlistat Sibutramine
Brand name Xenical Reductil / trim fast
Primary indication Obesity Obesity
Use Long-term Long-term
Mechanism of action GI lipase inhibitor CNS monoamine reuptake
inhibitor
Dosing 120 mg TID 5-15 mg OD
Side Effects Steatorrhea Insomnia
Oily spotting
Incontinence
Dry mouth
Increased BP

90. SURGICAL THERAPY
Only Recommended in Selected Adult Patients
BMI > 40 or with Co-morbid Condition
• Liposuction
• Abdomeno plasty
• Restrictive bariatric procedures
 Banding
 Stapling

91. Conclusion
• Lifestyle changes such as diet and exercise are still the mainstay of obesity
management.
• Aim of treatment should be modest weight loss maintained in the long term
• Add anti-obesity drugs only if above fails
• Consider the risk vs. benefit of prescribing these drugs.

92. THANK YOU