Weight Management: Common Tropical Infection - Tropical Medicine System
Weight Management: Common Tropical Infection - Tropical Medicine System
Weight Management: Common Tropical Infection - Tropical Medicine System
Case
03
WEIGHT MANAGEMENT
2014 - 2015.
Block title : Family Medicine
Case description:
The data collected in the past few years shows that not only developed countries’ people, but
so is the rest of the world having problem with nutrition. Men as a group, are more overweight
than women in every age group. Women however tend to be more obese than men.
Scientific knowledge and advice vary about the health implications of increasing weight. Some
studies indicate weight gain for a woman over her life time significantly increases her risk of
cancer.
Physical activity
Diet
Behavioural modification
CASE SYNOPSIS
Susan, a 15-year-old girl who visited your practice. Her mother noted that Susan
has always been heavier than other children in her class and this is becoming a
concern socially for Susan. She becomes introvert and has low self confidence.
She is not complaining others diseases. She never goes for sport, only activity in
school.
Food intake: she eat three times a day and many times for snack especially when
she feels stressed, angry, anxious, or any other uncomfortable emotions. She
rarely eats vegetables and fruits. She prefers fast food, soft drinks, crackers and
noodles. She had menarche at 9 year-old and her periods is reguler. Susan has a
10-year-old brother who is a few Kg overweight, but is very active playing
football. Her mother appears to be of normal weight and sated that Susan’s father
is quite thin.
On physical examination, Susan is 145 cm tall and weights 52 kg.Other
examination are within normal limit.
Your diagnosis was overweight and the management are counsel her and her
mother about control meal pattern (food intake) and physical activity.
2
Reference for the student:
1. Shils ME, Olson JA, Shike M, Ross AC, editors. Modern Nutrition in Health and
Disease. Maryland: Lippincott Williams & Wilkins, 2006
2. Thompson ME. Noel MB. Weight management and nutrition. In Sloane PD. Slatt LM.
Ebell MH. Jacques LB. Essentials of family medicine. Fourth edition. Lippincott
Williams & Wilkins. Baltimore. 2002. pp 783-801.
3. Bray GA, Bouchard G, Handbook of Obesity, Clinical Application, 3rd Ed, 2008,
Informa Healthcare.
4. Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 9th Edition, 2009.
Tutorial 1 page 1
TUTOR GUIDE
Problem:
1. 15-year-old girl (teenager)
2. Malnutrition
Hypotheses:
1. Overweight
2. Obese
3
Tutorial 1 page 2
Her mother noted that Susan has always been heavier than other children in her class
and this is becoming a concern socially for Susan. She becomes introvert and has low
self confidence.
She is not complaining others diseases. She never goes for sport, only activity in school.
Food intake: she eat three times a day and many times for snack especially when she
feels stressed, angry, anxious, or any other uncomfortable emotions. She rarely eats
vegetables and fruits. She prefers fast food, soft drinks, crackers and noodles.
She had menarche at 9 year-old and her periods is reguler.
TUTOR GUIDE
Nutritional Status:
Assessment of the nutritional status can be done based on:
1. Dietary history:
a. Quantitative: 24-h food recall/record.
b. Qualitative: food frequency questionaire.
2. Laboratory test.
3. Anthropometric measurement.
4. Physical examination.
Disadvantages:
- 24-hour recall does not always show typical eating patterns, since day-to-day
dietary intake may vary considerably
- The clients may report information they feel the clinician wants to hear (over
or underreport their intake)
- May be inaccurate, requires dependence on the client’s memory
- Food models, cups, and spoon to improve recall of portion sizes
5
2. PHYSICAL ACTIVITY PATERN:
1. Kind of daily activity living, duration and frequency.
2. Kind of physical activity: intensity, duration and frequency.
3. ANTHROPOMETRIC MEASUREMENT:
Measure body composition and fat distribution.
BW (kg)
BMI
Height (m) 2
Based on CDC Growth chart cut off point for normoweight, overweight and obese.
Physical examination focus on nutrition status: pseudoacanthosis nigrans.
Tutorial 1 page 3
Susan has a 10-year-old brother who is a few Kg overweight, but is very active playing
football. Her mother appears to be of normal weight and sated that Susan’s father is
quite thin.
On physical examination, Susan is 145 cm tall and weights 52 kg.Other examination are
within normal limit
Research over the past 2 decades has provided an unprecedented expansion in our knowledge
about the physiological and molecular mechanisms regulating body fat. Perhaps the greatest
impact has resulted from the cloning of genes corresponding to the 5 mouse monogenic obesity
syndromes and the subsequent characterization of pathways identified by these genetic entry
points. The description of 3 of these genes (ob, db, and Ay) has already led to potential drugs
or drug targets currently in pharmaceutical development: leptin, leptin receptor, and
melanocortin-4 (MC4) receptor. In addition, extensive molecular and reverse genetic studies
(mouse knockouts) have helped identify other critical players in energy balance, as well as
validate or refute the importance of previously identified pathways.
As a framework for this discussion we will use a feedback model. In such a system, afferent
signals tell central controls in the brain about the state of the external and internal environment
as they relate to food. In turn, this central controller transduces these messages into efferent
control signals governing the search for and acquisition of food, as well as modulates the
subsequent disposal of food once inside the body. Finally, there is a control system that
ingests, digests, absorbs, transports, stores, metabolizes, and excretes waste from the ingested
food. Begin with the controlled system (Figure 2)t
6
Figure 2. Feedback model. The elements of the system that controls obesity are presented as a
feedback model with a controlled system that ingests, metabolizes, and stores food; afferent
signals that tell the brain about the internal and external environment; the central controller in
the brain that transduces messages from the periphery into action; and the efferent or action
system. From Bray GA. Am J Clin Nutr. 1998;67:1-4.[6] (Courtesy of George A. Bray, MD)
Resting energy expenditure. Energy expenditure is most strongly associated with fat free
body mass. A low rate of basal energy expenditure has predicted future weight gain in some
studies.[] The metabolic mixture oxidized by the body is related to the types of foods eaten, to
the adaptive capacity of the body, and rate of energy expenditure. To maintain energy balance
requires that the mix of fuels eaten be oxidized.
The capacity for storing carbohydrates as glycogen is very limited and the capacity to store
protein is also restricted. Only the fat stores can readily expand to accommodate increasing
levels of energy intake above those required for daily energy needs. Several studies show that a
high rate of carbohydrate oxidation predicts future weight gain. One explanation for this
phenomenon is that when carbohydrate oxidation exceeds carbohydrate intake, the body needs
carbohydrate to replace the limited stores. Since fatty acids cannot be converted to
carbohydrate, amino acids are converted to carbohydrate equivalents that mobilize fat stores.
Obese individuals who have lost weight are less effective in increasing fat oxidation in the
presence of a high-fat diet than are individuals of normal weight.
7
Physical activity. The amount of energy expended in physical activity is directly related to
body weight. Physical activity gradually declines with age, and maintaining a regular exercise
program is difficult for many people, particularly as they get older. Adapting to a change from
a lower- to a higher-fat diet takes time and can be accelerated by increasing exercise.
Thermic effect of food. The thermic effect of food is the third component of energy
expenditure. After food ingestion, there is a rise in energy expenditure equivalent to
approximately 10% of the day's total energy expenditure. The sympathetic nervous system
controls part of this process. The control of sympathetic activity and its noradrenergic output
offers a possible strategy for treating obesity. The thermic effect of food is blunted when
insulin resistance is high.
Stimulation of thermogenesis has been an approach to obesity treatment for more than 100
years when thyroid extract was first used. Although thyroid hormones increase energy
expenditure and reduce body fat, they also increase the loss of lean body mass and bone
calcium. If these effects could be eliminated, the thermogenic effect and loss of fat might be
beneficial. The use of dinitrophenol, a thermogenic drug that uncouples oxidative
phosphorylation, produced weight loss but had the highly undesirable side effect of producing
cataracts and neuropathy.
Beta3-adrenergic receptor agonists have the potential to increase energy expenditure and are
currently being widely investigated. Previous versions of beta3-agonists did not meet with
success in clinical trials, largely due to lack of specificity and potency for the human beta3-
receptor. Within the next few years, data on the improved beta3-agonists currently in
development will likely demonstrate whether this is a viable strategy.
Uncoupling proteins
The original brown fat uncoupling protein (UCP1) has a well-established role in rodent
temperature and body weight regulation. Increased expression and/or activation of this protein
uncouples oxidative phosphorylation, resulting in the conversion of energy to heat
(thermogenesis). There has always been skepticism about the importance of this molecule in
humans due to the very low levels of brown fat, and hence UCP1 expression, in adult humans.
Recently the identification of 2 additional uncoupling proteins (UCP2 and UCP3) highly
expressed in adult human thermogenic tissues has attracted considerable interest.]It is possible
that drugs activating or increasing the expression of UCP2 and UCP3 may have important
effects on energy expenditure.
Fat cells
Obesity is a reflection of increased fat stores, in both subcutaneous and visceral fat deposits.
Obese individuals have enlarged, or hypertrophic, fat cells that be can viewed as the pathology
of obesity. The many products made and secreted from fat cells play an important role in the
pathogenic consequences of obesity. Controlling the processes of fat synthesis, deposition, and
mobilization are important components of the controlled system. Insulin plays an important
role in the activation of lipogenesis in fat cells. It also inhibits lipolysis and is involved in fat
cell differentiation.
Fat cell differentiation is a multistep process that requires a number of factors in addition to
insulin. One of the early steps involves fatty acids interacting with the peroxisome proliferator-
activated receptor (PPAR-gamma). This PPAR-gamma forms a heterodimer with the retinoid
X receptor (RXR) to initiate the process of fat cell differentiation.
8
Activation of the process increases fat cell differentiation, and inhibition of RXR inhibits this
process. One clinical report suggests that defects in the gene for PPAR-gamma may be related
to obesity.[
Enzymes
The enzyme protein tyrosine phosphatase-IB (PTP-1B) has been implicated in insulin
resistance. Recently it has been demonstrated that in PTP-1B knockout mice, insulin resistance
is reduced, yet the mice appear otherwise healthy. Of particular interest, is that PTP-1B
knockout mice do not become obese when eating a high-fat diet. A mechanism to explain this
protection from diet-induced obesity is not yet clear.
Enzymes involved in fat metabolism are also important in obesity. Because the enzyme acyl
CoA:diacylglycerol transferase (Dgat), catalyses the final step in the glycerol phosphate
pathway, it has been considered necessary for adipose tissue formation. Recently Smith and
colleagues[ demonstrated that Dgat-deficient mice are lean and resistant to diet-induced obesity
and can still synthesize triglycerides. This finding suggests that inhibition of Dgat-mediated
triglyceride synthesis may be useful for treating obesity.
The controlled system and the external environment both provide signals that play a role in the
control of feeding. The external signals from sight, sound, and smell are all distance signals for
identifying food.
Peptides
Gastrointestinal peptides have long been studied as potential regulators of satiety.
Cholecystokinin (CCK) was one of the first peptides shown to reduce food intake in animal
models and humans. Gastrin-releasing peptide, neuromedin B, and bombesin, have also been
shown to reduce food intake in animals and humans.
Pancreatic peptides also modulate feeding. Both glucagon and its 6-29 amino acid derivative,
glucagon-like peptide-1 (GLP-1), reduce food intake after peripheral administration in animals
and humans. Analogs or small molecules that might influence GLP-1 receptors, GLP-1 release,
or duration of action are interesting candidates for drugs to treat obesity. Enterostatin, the
pentapeptide signal portion of pancreatic co-lipase, selectively reduces fat intake in
experimental animals. This peptide increases satiety in humans and reduces food intake in
baboons.
The successful introduction of orlistat (Xenical) to the market has also demonstrated that
inhibiting the absorption of dietary fat can be an important component of antiobesity therapy.
However, the side effects of orlistat resulting from fecal fat loss can be troublesome for some
patients.
9
The weight loss associated with the use of orlistat with meals indicates that short-acting
medications taken with meals can successfully reduce food intake and body weight. This
observation suggests that short-term modification of satiety signals might lead to weight loss
when used on a meal to meal basis.
Nutrients
Nutrients may also alter food intake peripherally by decreasing food intake. These afferent
signals act primarily by producing satiety. Pyruvate, lactate, and 3-hydroxybutyrate all reduce
food intake when injected into experimental animals.
Furthermore, hydroxycitric acid found in the herb Garcinia cambogia interacts with
citrate:ATP lyase and has been shown to reduce food intake in animals, but not in humans.
Leptin
Leptin is the best known of the afferent fat signals and the best candidate for primary signal
communication of body fat information to the central controller. Identification of this peptide
through positional cloning in 1994 provided major new insights into the regulation of food
intake, energy expenditure, and body fat. It is now clear that this cytokine -- derived primarily
from fat cells, but also from the placenta and possibly the stomach -- reduces food intake and
increases the activity of the thermogenic components of the sympathetic nervous system.
Glucose dip
A brief dip in the circulating level of glucose precedes the onset of eating in more than 50% of
meals consumed by animals and humans. When this dip is blocked, food intake is delayed.
This established pattern is independent of the level from which the drop in glucose begins. In
addition, a small decrease in glucose continues even when food is not available. The dip
follows a small increase in insulin, suggesting an interdependent relationship between these 2
signals.
Efferent Signals
The motor system for food acquisition, the endocrine system, and the autonomic nervous
system are the major efferent control systems involved in acquiring food and regulating body
fat stores. (Figure 2). Among the endocrine controls are growth hormone, thyroid hormone,
gonadal steroids (testosterone and estrogens), glucocorticoids, and insulin.
Growth hormone
During development, growth hormone and thyroid hormone work together to increase body
growth. At puberty, gonadal steroids enter the picture causing shifts in the relationship of the
proportion of fat to lean body mass in boys and girls. Testosterone increases lean mass relative
to fat, and estrogen has the opposite effect. Testosterone levels fall when human males grow
older, with a corresponding increase in visceral and total body fat and a decrease in lean body
mass. This may be compounded by the decline in growth hormone associated with an increase
in fat relative to lean mass.
Both testosterone and growth hormone have been used to treat obesity. Growth hormone
increases energy expenditure and increases the loss of fat. Growth hormone also reduces
visceral fat more than total fat. Testosterone and anabolic steroids in males can lower visceral
fat relative to total body fat, suggesting selective effects on different fat deposits. However,
testosterone and growth hormone have undesirable side effects.
10
Testosterone is associated with the development of prostatic hypertrophy and prostatic cancer.
Excess growth hormone, on the other hand, has been associated with enhanced risk of
cardiovascular disease. Likewise, local injection or topical application of lipolytic drugs has
also been reported to have a modest effect on reducing local fat deposits.] This cosmetic effect
could be particularly appealing to some individuals.
Glucocorticoids
Adrenal glucocorticoids play an important role in the neuroendocrine control of food intake
and energy expenditure. Furthermore, experimental evidence demonstrates that glucocorticoids
are critical for the development and maintenance of obesity. Conversely, adrenalectomy in
animals with a lesion to the ventromedial hypothalamus will reverse obesity. In genetically
obese animals, adrenalectomy stops the progression, but does not reverse the syndrome. In
humans, excess production of glucocorticoids produces modest obesity, and destruction of the
adrenal glands is associated with loss of body fat.
Insulin
Insulin is also essential for the development of obesity. It plays a key role in lipogenesis and
inhibition of lipolysis. Using insulin or drugs that increase insulin secretion to treat diabetes
leads to greater increases in body fat compared with other forms of diabetes treatment.
Conversely, in experimental forms of obesity, destruction of beta cells slows or arrests the
development of obesity. Similarly, the absence of insulin, as seen in patients with type 1
diabetes, is associated with normal body weight.
The immense importance of the control of energy expenditure and some of its underlying
mechanisms to the understanding of obesity and its treatment is clear.
11
Patients with less impulse control and less self-discipline tended to struggle more with
maintaining weight loss. Patients with very strict diets and rigid unrealistic goals or those with
“habits” surrounding food (e.g., emotional eating) tended to “yo-yo” diet or weight cycle.
Although the consensus of opinion is that no specific personality is associated with obesity,
traits of poor impulse control, lower compliance, and self-discipline are associated with poor
self-esteem, depressive traits, and emotional eating, leading to obesity.
12
Psychiatric Comorbidities
Obese patients have a heavy burden of low self-esteem, poor functionality, reduced
employment, and stigma, all of which predispose to depression. Obese patients often respond
to depression with comfort eating and perpetuating a vicious cycle that entraps the patient in its
net. Several studies have reported that psychiatric symptoms in obese patients are similar to
those of other depressed patients. However, among treatment-seeking obese patients there is a
higher prevalence of comorbid psychiatric illness by 40 to 60 percent. A recent study by
Melissa A. Kalarchian and colleagues reported that patients presenting for bariatric surgery
with greater obesity and lower functional health status are more likely to have current and past
DSM-IV psychiatric illness. Almost 66 percent had a lifetime history of at least one Axis I
disorder, while 29 percent met the criteria for one or more Axis II disorders. Axis I disorders,
but not Axis II disorders, were positively correlated with BMI, and both were associated with
lower functional health status. The prevalence of binge eating disorder in obese patients has
been reported to be about 40 percent. However, among patients presenting for bariatric surgery
the prevalence is about 70 percent. Obesity is comorbid with depression anxiety and binge
eating disorders.
Our society still stigmatizes obese patients; Albert J. Stunkard and colleagues described it as
the “last remaining socially acceptable prejudice.” The patients are under the spell of a vicious
cycle of obesity-stigma-depression-comfort eating-obesity. The habit of eating in response to
stress is learned early and continues throughout adult life. It is difficult to break and becomes
an impulse control problem. It is very much akin to addiction to substances. Many patients are
unable to recognize hunger or satiety. In bariatric surgery patients, those who have never been
able to discern hunger and satiety seem to lose the weight in the initial postoperative period,
but have a difficult time 2 to 3 years after surgery when the usually fall back into old patterns
of behavior, “grazing,” resulting in weight regain.
Tutorial 1 page 4
Your diagnosis was overweight and the management are counsel her and her mother
about control meal pattern (food intake) and physical activity
TUTOR GUIDE
Scientific knowledge and advice vary about the health implications of increasing weight. Some
studies indicate weight gain for a woman over her life time significantly increases her risk of
cancer.
Stage 1: behavioral counseling with a focus on dietary habits and physical activity. This
early intervention focuses on reduction of intake of sugar-sweetened beverages and
between meal snack except fruit or low calorie snack, consuming five servings of fruit
and vegetables daily, limiting meals outside the home, eating breakfast daily. Nutrient
composition in every main course menu consist of balance diet from high fiber
content/complex carbohydrate, high quality protein sources from animal and plant food
sources) with low fat content, and vegetable. Reducing screen time to less than two hours
per day, and encouraging one hour or more of physical activity daily. This intervention
should be implemented over a three- to six-month period. If there is little or no
improvement based on this approach, then stage 2 intervention is warranted.
Stage 2 recommendations can also be performed in a primary care office setting but may
be improved by involvement of allied health professionals in behavioral pediatric weight
management. This stage includes a more structured approach to diet and activity
14
behaviors. This intervention should be carried out over a three- to six-month period with
a goal of weight maintenance. If stage 2 is unsuccessful, stage 3 intervention may be
considered. Stages 3 to 4 include a comprehensive multidisciplinary approach to weight
management.
Stage 3 may occur in a primary care setting with appropriate referrals. Stage 3
intervention includes even more regimented and aggressive behavioral therapy, often
directed by a psychiatrist in behavior modification approaches. Often the approach,
which is more labor intensive, involves setting one behavior goal at a time and then
moving on to additional goals once the initial favorable behavior has been established.
For adolescents, this stage should involve individual approaches to behavior changes and
skill building around decision making. For younger children, the focus is often on the
parents and may involve teaching parenting skills, which can be applied to diet and
activity behaviors in the child. The behavioral approach in stage 3 should also include
self-monitoring (or family monitoring) of behaviors and stronger behavioral support,
which includes setting specific behavioral goals and rewarding accomplishment of those
goals. Rewards should be structured in a way to be positive reinforcement but should not
be overly expensive. This can include opportunities for time spent with a parent or with
friends and should not include
food. If there is no improvement in weight or BMI after three to six months and or has
comorbidities related to obesity, then stage 4 should be implemented.
Stage 4 should usually occur in a referral setting and should be delivered by a
multidisciplinary team. The team should include pediatric physicians with training and
experience in weight management, exercise physiologists, psychiaytrist, and may include
a pediatric bariatric surgeon. Other disciplines that may be included are social workers,
physical therapists, and occupational therapists. This team must also have ready access to
pediatric subspecialists who can evaluate and treat comorbid conditions related to
obesity. This would include endocrinologists (diabetes), pulmonary medicine specialists
(sleep apnea), cardiologists (hypertension, dyslipidemia), gastroenterologists
(nonalcoholic fatty liver disease), orthopedic surgeons, and neurologists. Pediatric
psychiatrists may also be needed for patients with established psychopathology. Stage 4
is the most intensive therapeutic approach used and is reserved for the most severely
affected patients. This stage may include implementation of special diets, including very
low-calorie diets, which require more intensive medical monitoring. Stage 4 may also
include the use of pharmacologic agents and bariatric surgery. However, even with more
aggressive treatment, behavior therapy should remain as an important component of the
treatment plan. In stage 4, standard clinical protocols for patient selection, evaluation,
and treatment should be in place. Mechanisms for evaluation of the treatment protocol
and quality improvement should also be included. It should be recognized that the
development of pediatric obesity has a variety of important components, including the
overall environment, the home environment, family behavioral dynamics, peer
behavioral influences, and individual behavioral issues. Treatment paradigms at all four
stages should address all of these to some extent. Perhaps the most important focus,
especially for younger patients, is the home environment and family dynamics. This
requires a family-based approach to therapy. If treatment is focused only on an individual
child and his or her behaviors, then success is much less likely. Parents must understand
the environmental factors that influence diet and physical activity behaviors. Intervention
in a family context may be difficult because changing behaviors related to diet and
physical activity often requires that everyone in the family make substantial changes. It
may also be important for treatment team members to identify saboteurs who are not
helping or who are actively working against the treatment plan. This staged approach
15
should be applicable to almost all general practitioner patients. However, patients with
physical or mental disabilities may require additional support.
The National Health and Examination Survey (NHANES I) showed that people who engage in
limited recreational activity were more likely to gain weight than more active people. Other
studies have shown that people who engage in regular strenuous activity gain less weight than
sedentary people.
Physical activity and exercise help burn calories. The amount of calories burned depends on
the type, duration, and intensity of the activity. It also depends on the weight of the person. A
200-pound person will burn more calories running 1 mile than a 120-pound person, because
the work of carrying those extra 80 pounds must be factored in. But exercise as a treatment for
obesity is most effective when combined with a diet and weight-loss program. Exercise alone
without dietary changes will have a limited effect on weight because one has to exercise a lot
to simply lose one pound. However regular exercise is an important part of a healthy lifestyle
to maintain a healthy weight for the long term. Another advantage of regular exercise as part of
a weight-loss program is a greater loss of body fat versus lean muscle compared to those who
diet alone.
Improved blood sugar control and increased insulin sensitivity (decreased insulin
resistance)
Remember, these health benefits can occur independently (with or without) achieving weight
loss. Before starting an exercise program, you should talk to your doctor about the type and
intensity of the exercise program.
Start slowly and progress gradually to avoid injury, excessive soreness, or fatigue. Over
time, build up to 30 to 60 minutes of moderate to vigorous exercise every day.
16
People are never too old to start exercising. Even frail, elderly individuals (ages 70-90
years) can improve their strength and balance.
Exercise precautions:
The following people should consult a doctor before vigorous exercise:
Men over age 40 or women over age 50.
Individuals with heart or lung disease, asthma, arthritis, or osteoporosis.
Individuals who experience chest pressure or pain with exertion, or who develop
fatigue or shortness of breath easily.
Individuals with conditions or lifestyle factors that increase their risk of developing
coronary heart disease, such as high blood pressure, diabetes, cigarette smoking, high
blood cholesterol, or having family members with early onset heart attacks and
coronary heart disease.
A patient who is obese
Four major strategies have been used in the rapidly growing field of preventive medicine.
These include health screening, lifestyle change, risk factor control and vaccination programs.
17
Epilogue
A month later you meet her at the Sabuga while she is jogging with her family.
-case ended-
Tutorial 1 page 1
Tutorial 1 page 2
Her mother noted that Susan has always been heavier than other children in her class
and this is becoming a concern socially for Susan. She becomes introvert and has low
self confidence.
She is not complaining others diseases. She never goes for sport, only activity in school.
Food intake: she eat three times a day and many times for snack especially when she
feels stressed, angry, anxious, or any other uncomfortable emotions. She rarely eats
vegetables and fruits. She prefers fast food, soft drinks, crackers and noodles.
She had menarche at 9 year-old and her periods is reguler.
Susan has a 10-year-old brother who is a few Kg overweight, but is very active playing
football. Her mother appears to be of normal weight and sated that Susan’s father is
quite thin.
On physical examination, Susan is 145 cm tall and weights 52 kg.Other examination are
within normal limit
Your diagnosis was overweight and the management are counsel her and her mother
about control meal pattern (food intake) and physical activity
Epilogue
A month later you meet her at the Sabuga while she is jogging with her family.
-case ended-
19