You are on page 1of 16

OBESITY

By Group 3

1. Agil Wira Kesuma 17310010


2. Mohamad Imam Istawa 17310167
3. Virllyya Andiny S 17310300
4. Fadhilan Nur R 17310092

LANGUAGE CENTRE OF MALAHAYATI


UNIVERSITY
2019
Case

Group 3

A 47-year-old man presents to your office for a follow-up visit. He


was seen 3 weeks ago for an upper respiratory infection and noted
incidentally to have a blood pressure of 164/98 mm Hg. He vaguely
remembered being told in the past that his blood pressure was
“borderline.” He feels fine, has no complaints, and his review of systems is
entirely negative. He does not smoke cigarettes, drinks “a couple of beers
on the weekends,” and does not exercise regularly. He has a sedentary
job. His father died of a stroke at the age of 69 years. His mother is alive
and in good health at the age of 72 years. He has two siblings and is not
aware of any chronic medical issues that they have. In the office today, his
blood pressure is 156/96 mm Hg in his left arm and 152/98 mm Hg in the
right arm. He is afebrile, his pulse is 78 bpm, respiratory rate 14 breaths
per minute, he is 70 in tall, and weighs 210 lb. A general physical
examination is normal.

KEY WORDS
 A 47-year-old man
 seen 3 weeks ago for an upper respiratory infection
 noted incidentally to have a blood pressure of 164/98 mm Hg.He
does not smoke cigarettes.
 drinks a couple of beers on the weekends.
 does not exercise regularly
 His father died of a stroke at the age of 69 years
 his blood pressure is 156/96 mm/Hg in his left arm and 152/98
mm/Hg in the right arm.
 He is afebrile, his pulse is 78 bpm
 respiratory rate 14 breaths per minute
 he is 70 in tall (177 cm) , and weighs 210 lb (95 kg)

Problems
A 47-year-old man presents to your office for a follow-up visit. was
seen 3 weeks ago for an upper respiratory infection and noted incidentally
to have a blood pressure of 164/98 mm Hg.

Diagnosa Differential
 Obesity
 Tension Iskemik Attack

Hipotesa
A 47-year-old man presents to your office for a follow-up visit. was
seen 3 weeks ago for an upper respiratory infection and noted incidentally
to have a blood pressure of 164/98 mm Hg, because he get obesity.

1. Theory / Definition
Obesity is a complex, multifactorial, and largely preventable disease
, affecting, along with overweight, over a third of the world’s population
today. If secular trends continue, by 2030 an estimated 38% of the world’s
adult population will be overweight and another 20% will be obese. While
growth trends in overall obesity in most developed countries seem to have
leveled off, morbid obesity in many of these countries continues to climb,
including among children. In addition, obesity prevalence in developing
countries continues to trend upwards toward US levels.
Obesity is typically defined quite simply as excess body weight for
height, but this simple definition belies an etiologically complex phenotype
primarily associated w

ith excess adiposity, or body fatness, that can manifest


metabolically and not just in terms of body size. Obesity greatly increases
risk of chronic disease morbidity—namely disability, depression, type 2
diabetes, cardiovascular disease, certain cancers — and mortality.
Childhood obesity results in the same conditions, with premature onset, or
with greater likelihood in adulthood. Thus, the economic and psychosocial
costs of obesity alone, as well as when coupled with these comorbidities
and sequealae, are striking.

In this article, we outline the prevalence and trends of obesity, then


review the myriad risk factors to which a preventive eye must be turned,
and finally present the costs of obesity in terms of its morbidity, mortality,
and economic burden.

2. Classification of Body Weight

The current most widely used criteria for classifying obesity is the
body mass index (BMI; body weight in kilograms, divided by height in
meters squared), which ranges from underweight or wasting (<18.5 kg/m 2)
to severe or morbid obesity (≥40 kg/m 2). In both clinical and research
settings, waist circumference, a measure of abdominal adiposity, has
become an increasingly important and discriminating measure of
overweight/obesity. Abdominal adiposity is thought to be primarily visceral,
metabolically active fat surrounding the organs, and is associated with
metabolic dysregulation, predisposing individuals to cardiovascular
disease and related conditions. Per internationally used guidelines of
metabolic syndrome—a cluster of dysmetabolic conditions that predispose
individuals to cardiovascular disease of which abdominal adiposity is one
component—a waist circumference resulting in increased cardiovascular
risk is defined as ≥94 cm in European men, and ≥80 cm in European
women, with different cut points recommended in other races and
ethnicities (e.g., ≥90 and ≥80 cm in men and women, respectively, in
South Asians, Chinese, and Japanese).

3. Risk Factors for Obesity

Currently, our greatest gap in knowledge is not regarding the


numbers of risk factors, nor in their independent impact on risk, but rather
in how they interact with one another—their confluence—to produce
today’s aptly if unfortunately named “globesity” epidemic. Obesity arises
as the result of an energy imbalance between calories consumed and the
calories expended, creating an energy surplus and a state of positive
energy balance resulting in excess body weight. This energy imbalance is
partially a result of profound social and economic changes at levels well
beyond the control of any single individual. These “obesogenic” changes—
economic growth, growing availability of abundant, inexpensive, and often
nutrient-poor food, industrialization, mechanized transportation,
urbanization—have been occurring in high-income countries since the
early 20th century, and today these forces are accelerating in low- and
middle-income countries. And yet, not all of us living in obesogenic
environments experience the same growth in our waistlines. Hereditary
factors—genetics, family history, racial/ethnic differences—and our
particular socioeconomic and sociocultural milieus have been shown to
affect risk of obesity

Risk Factors (non-exhaustive)

 Individual
 Energy intake in excess of energy needs
 Calorie-dense, nutrient-poor food choices (e.g., sugar-
sweetened beverages)
 Low physical activity
 Sedentariness
 Little or excess sleep
 Genetics
 Pre- and perinatal exposures
 Certain diseases (e.g., Cushing's disease)
 Psychological conditions (e.g., depression, stress)
 Specific drugs (e.g., steroids)
 Socioeconomic
 Low education
 Poverty
 Environmental
 Lack of access to physical activity resources / low walkability
neighborhoods
 Food deserts (i.e., geographic areas with little to no ready
access to healthy food, such as fresh produce/grocery)
 Viruses
 Microbiota
 “Obesogens” (e.g., endocrine-disrupting chemicals)
Comorbidities and Sequelae (non-exhaustive)

 Type 2 diabetes
 Hypertension
 Dyslipidemia
 Heart and vascular diseases
 Osteoarthritis
 Infertility
 Certain cancers (e.g., esophageal, colon, postmenopausal
breast)
 Respiratory conditions/diseases (e.g., sleep apnea, asthma)
 Liver diseases (e.g., nonalcoholic fatty liver disease,
nonalcoholic steatohepatitis)
 Gallstones
 Trauma treatment/survival
 Infection
 Psychological conditions (e.g., depression, psychosocial
function)
 Physical disability
 Years of life lost/early mortality
 Absenteeism/loss of productivity
 Higher medical costs

4. Pathophysiology of Obesity

Dyslipidemia, hypertension, and atherogenesis are comorbid conditions, in


addition to insulin resistance, that are associated with obesity and
adversely influenced by the secretion of diverse inflammatory adipokines,
particularly from white adipose tissues (WAT) in visceral fat depots.
Specific adipokines enhance endothelial vasomotor tone by secreting
renin, angiotensinogen, and angiotensin II, which are similar to those
within the renal renin-angiotensin system (RAS), but when secreted from
adipocytes, enhance hypertension in obese patients. TNF-α secretion
increases in proportion to increased total body-fat mass and enhances
inflammation in fatty livers and fat depots elsewhere, particularly in
pancreas, mesentery, and gut visceral sites. Inflammatory markers that
are increased in obesity commonly contribute to inflammatory conditions
such as NASH and in the bronchial tree of patients with obstructive sleep
apnea. These markers include not only TNF-α and IL-6, but also acute-
phase reactants such as C-reactive protein, α1 acid glycoprotein, and the
specific amyloid antigen, particularly in the fatty liver.23 The acute-phase
reactants are important inflammatory markers that are also upregulated in
the insulin-resistant state associated with diabetes mellitus type 2 and
NASH.
5. Symptoms
Symptoms and complications of obesity as well as health risks
include, breathing disorder such as sleep apnea and chronic obstructive
pulmonary disease, and certain types of cancer such as prostate, bowel in
men, breast and uterine cancer in women, coronary heart disease,
diabetes (type 2 in children), depression, liver and gall bladder problems,
gastro-esophageal reflux disease, high blood pressure, high cholesterol,
stroke, and diseases of joints such as osteoarthritis, pain in knees and
lower back. Obese individuals are likely to have more medical and health
problems. Additionally, they are likely to have an accumulation of
abdominal fat.

6. Physical Examination

According to the National Heart, Lung, and Blood Institute “Clinical


Guidelines on the Identification, Evaluation, and Treatment of Overweight
and Obesity in Adults,” the Practical Guide on the Identification,
Evaluation, and Treatment of Overweight and Obesity in Adults, and the
World Health Organization, assessment of risk status resulting from
overweight or obesity is based on the patient's BMI, waist circumference,
and existence of comorbid conditions. A desirable or healthy BMI is 18.5
to 24.9 kg/m2; overweight is 25 to 29.9 kg/m2; and obesity is ≥30 kg/m2.
Obesity is further subdefined into class I (30.0–34.9 kg/m2), class II (35.0–
39.9 kg/m2), and class III (≥40 kg/m2), although lower cut points have been
suggested for the Asian population. Although BMI does not directly
measure body fat, its utility as a risk estimate has been demonstrated in
multiple population studies.Nonetheless, in some instances, the use of
height and weight alone for calculation of BMI as a surrogate measure of
body fat may lead to an incorrect estimation of risk. Patients with an
unusual body habitus, body builders with increased muscularity, or the
elderly with reduced lean body mass may be misclassified. Although
accurate methods to assess body fat such as dual-energy x-ray
absorptiometry or air displacement plethysmography exist, they are
impractical and too expensive for routine clinical application. The inherent
problems with using BMI alone to estimate risk is exemplified by the
obesity paradox, the observed inverse correlation between BMI and
mortality in patients with existing chronic heart failure, coronary heart
disease, and chronic kidney disease. Although reasons for the obesity
paradox remain uncertain, proposed confounding factors include the poor
sensitivity of BMI to detect excess adiposity versus lean muscle mass,
body fat distribution, and the independent contribution of fitness.

In addition to BMI, the risk of overweight and obesity is independently


associated with excess abdominal fat and fitness level. Population studies
have shown that people with large waist circumferences have elevated
obesity-related health risk compared with those with normal waist
circumferences and within similar BMI categories.The threshold for
excessive abdominal fat appears to vary between racial and ethnic
groups. Proposed cut points have been suggested by the International
Diabetes Federation. Determination of fitness level is another modifier of
assessing risk associated with BMI. Longitudinal studies have shown that
cardiorespiratory fitness (as measured by a maximal treadmill exercise
test) is an important predictor of all-cause mortality independently of BMI
and body composition. More specifically, fit obese men had a lower risk of
all-cause and CVD mortality that did unfit lean men.Similarly, among
women, cardiorespiratory fitness was a more important predictor of all-
cause mortality than was baseline BMI.
7. Treating obesity

The best way to treat obesity is to eat a healthy reduced-calorie diet and
exercise regularly.

To do this, you should:

 eat a balanced calorie-controlled diet as recommended by a GP or


weight loss management health professional (such as a dietitian)
 join a local weight loss group
 take up activities such as fast walking, jogging, swimming or tennis
for 150 to 300 minutes (2.5 to 5 hours) a week
 eat slowly and avoid situations where you know you could be
tempted to overeat

You may also benefit from receiving psychological support from a trained
healthcare professional to help change the way you think about food and
eating. If lifestyle changes alone do not help you lose weight, a medicine
called orlistat may be recommended. If taken correctly, this medicine
works by reducing the amount of fat you absorb during digestion. Your GP
will know whether orlistat is suitable for you. In some cases, weight loss
surgery may be recommended.

8. Medical Treatment
According to current Food and Drug Administration guidance,
pharmacotherapy is approved for patients with a BMI ≥30 kg/m 2 or ≥27
kg/m2 when complicated by an obesity comorbidity. Although sound in
principle, few agents are currently approved for treatment of obesity. They
fall into 2 major categories: appetite suppressants or anorexiants and
gastrointestinal fat blockers. The 2 most commonly used sympathomimetic
amines are phentermine and diethylpropion, both labeled schedule IV
drugs by the Drug Enforcement Agency. A full discussion of
pharmacological treatment for obesity was previously provided by Bray
and Ryan. Three medications were submitted to the Food and Drug
Administration for a new drug application.However, at the
time of this writing, none of the medications has been approved. A
concern about two of these medications, phentermine/topiramate
extended release (Qnexa; Vivus, Inc, Mountain View, CA) and

naltrexone/buproprion (Contrave; Orexigen, La Jolla, CA), is the potential


cardiovascular risk from the slight increase in pulse rate. Regardless of
whether new antiobesity agents are available, it is important to avoid or
minimize weight-gaining medications when possible.
Non-pharmacological approaches

Subjects were offered and were required to be followed up for three


non-medical modalities:

a. Behavioral therapy. A psychologist provided cognitive behavioral


therapy (CBT) that could be done outside the clinic. The adherence
criteria were regular follow-up for at least 1 year with 45 min of
therapy sessions per week.
b. Exercises. A certified personal trainer, either from the clinical staff
or outside, provided monthly follow-up and prescribed exercise
regimens that were to be followed at least three times a week. The
exercise training consisted of 40 min of moderate-to-intense
resistive and cardiovascular exercises (>3 METs, World Health
Organization). Subjects were required to adhere to the training
program for at least 10 months in a year (2 months of absence were
allowed due to vacations). Subjects had to fulfill the criteria for
exercise frequency, regularity and intensity in order to be
considered adherents. Additionally, the personal trainers had to
provide feedback about the performance and adherence to
exercises for each subject, whenever the subjects practiced outside
the clinic.
c. Diet prescription. A 500–1500-kcal deficit was aimed for via a
hypocaloric diet consisting of 50–55% carbohydrates, 20–25%
lipids and 20–30% protein. Additionally, 0.2–0.4 g/kg/day of whey
protein was prescribed (whey protein was not taken into account in
the calculation of the calorie balance). Subjects were required to
attend follow-up appointments with a registered dietician once in
every 2 months. A 500-kcal deficit diet was offered in patients with
BMI < 40 kg/m2, whereas a 1000-kcal deficit diet was prescribed for
subjects with a BMI of 40–45 kg/m2. A 1500-kcal deficit was
prescribed in those with BMI > 45 kg/m2. Personalization of diets
was performed according to two aspects. First, subjects were
actively required to provide individual food preferences as well as
most visited restaurants and places to eat. From this, menus and
nutritional facts were assessed in order to provide the best options
for each place, whenever the chosen meal or place could be
included in the diet plan. Second, a general list of foods and
ingredients was provided, and subjects had to point out their
preferences. With this information, a specific weekly menu was sent
to each subject by the dietician. To be considered as adherents,
subjects were required to stick to their prescribed diets, in terms of
meal sizes and quality, at least 80% of the time and regularly make
follow-up visits to a registered dietician (at least six visits yearly)

Bariatric Surgery

According to the 1991 NIH Consensus Development Conference


Panel on bariatric surgery, patients with a BMI ≥40 kg/m2 or those with a
BMI ≥35 kg/m2 who have associated high-risk comorbid conditions such
as cardiopulmonary disease or type 2 diabetes mellitus could be
considered surgical candidates. Consequently, Medicare and other third-
party insurance payers have followed these criteria for reimbursement
qualifications. The bariatric laparoscopic adjustable gastric banding
surgical procedures were previously reviewed by Dixon et al. Compared
with standard care, differences in BMI levels from baseline to year 1 are
−2.4 kg.m2 for laparoscopic adjustable gastric band, −10.1 kg/m2 for
laparoscopic gastric sleeve, −9.0 kg.m2 for Roux-en-Y gastric bypass, and
−11.3 kg.m2 for biliopancreatic diversion. Significant improvement in
multiple obesity-related comorbid conditions, including type 2 diabetes
mellitus, hypertension, dyslipidemia, obstructive sleep apnea, and quality
of life, has been reported. A recent meta-analysis of controlled clinical
trials comparing bariatric surgery and no surgery showed that surgery was
associated with a reduced odds ratio risk of global mortality (odds ratio,
0.55), cardiovascular mortality (odds ratio, 0.58), and all-cause mortality
(odds ratio, 0.70).

The decision to recommend bariatric surgery is dependent primarily on the


patient's BMI and the presence of comorbid conditions that are likely to be
responsive to weight loss. Other patient-related factors such as
psychosocial health, adherence, expectations, and past weight loss
attempts are taken into consideration. There is not enough predictive
information available to differentially select 1 procedure over another for
an individual patient. However, restrictive-malabsorptive procedures
appear to result in greater weight loss and improvement in comorbid
conditions than restrictive procedures. Furthermore, the surgeon's
experience and risk-to-benefit ratio are considered. Contraindications
include an extremely high operative risk, active substance abuse, or a
major unstable or uncontrolled psychopathological condition such as major
depressive disorder, schizophrenia, or bulimia.

All patients who are considering weight loss surgery should undergo a
comprehensive assessment by a multidisciplinary team of healthcare
providers that includes a physician, registered dietitian, and mental health
professional. During the preoperative process, patients are typically
instructed on healthy eating and physical activity patterns, behavioral
strategies to implement the lifestyle changes, and the importance of stress
reduction and social support for long-term success. Evidence-based
recommendations for best practice patient care have recently been
published.
9. Conclusions

Obesity is a serious and highly prevalent disease associated with


increased morbidity and mortality. Healthcare providers must take an
active role in the identification, evaluation, and treatment of high-risk
individuals. Broaching the topic of weight and conducting an obesity-
focused history need to be incorporated by all physicians. All patients
should be provided lifestyle therapy with consideration for
pharmacotherapy and bariatric surgery when indicated. Primary treatment
should be directed at preventing further weight gain for overweight
patients and achieving a modest 10% weight loss for obese patients.

You might also like