This document summarizes the pathology of obesity. It defines obesity and classifications based on BMI. It discusses the accumulation of adipose tissue and measurements used. It describes the role of the hypothalamus in regulating appetite and energy expenditure. Key hormones involved include leptin, adiponectin, ghrelin, PYY, and others. Obesity is associated with increased risk of cardiovascular diseases like hypertension, stroke, coronary artery disease, and obesity cardiomyopathy.

1. PATHOLOGY OF OBESITY
MODERATOR:
Dr. M.L. YADAVProfessor
pathology
PRESENTED BY:
Dr. REEMAAGRAWAL
secondyr. resident
pathology

2. • Obesity is defined as an
accumulation of adipose tissue that
is of sufficient magnitude to impair
health.
• As with weight loss, excess weight
is best assessed by the body mass
index or BMI.
• Normal BMI range is 18.5 to 25
kg/m2.
• Individuals with BMI above
30kg/m2 are classified as obese;
those with BMI between 25 to 30
kg/m2 are considered overweight.
• The term obesity will be applied to
both the truly obese and the
overweight.

3. Weight Classifications
• Body mass index (BMI) is a
mathematical ratio which is
calculated as weight (kg)/ height
squared meter (m2). It is used to
describe an individuals relative
weight for height, and is
significantly correlated with total
body fat content. BMI is intended
for those 20 years of age and older.
With a BMI
of:
You are considered:
Below 18.5 Underweight
18.5 - 24.9 Healthy Weight
25.0 - 29.9 Overweight
30 or higher Obese

4. Measurements of
accumulation of body fat
• Triceps skin thickness measurement
• Various body circumferences, particularly the
ratio of waist to hip circumference.
• Mid arm circumference.

5. Central or visceral obesity, in
which fat accumulates in the
trunk and in the abdominal
cavity (in the mesentery and
around viscera), is associated
with a much higher risk for
several diseases than is
excess accumulation of fat
diffusely in subcutaneous
tissue.

6. Prevalance
• The prevalence of obesity increased from 13% to
32% between 1960 and 2004
• If the current trend continue, it is projected that by the
year 2015, 41% of adults will be obese.

7. • Simply put, obesity is a
disorder of energy balance.
When food derived energy
chronically exceeds energy
expenditure, the excess
calories are stored as
triglycerides in adipose
tissue.

8. environmental
Neurohumoral
mechanisms
genetics
nutritional Psychological stimulus

9. There are three components of this system:
1. The afferent system, which generates humoral
signals from the adipose tissue (leptin and
adiponectin), pancreas(insulin), and stomach
(ghrelin), ileum and colon(PYY).
2. The central processing unit, located primarily in
the hypothalamus, which integrates the afferent
signals
3. The efferent system, which carries out "orders"
from the hypothalamic nuclei in the form of
feeding behavior and energy expenditure.
Neurohumoral mechanisms:

10. The central processing unit
• The arcuate nucleus in hypothalamus processes and
integrates neurohumeral peripheral signals and
generates the efferent signal. It contain two subsets of
first order neurons:
1. POMC (pro-opiomelanocortin)/CART (cocaine and
amphetamine regulated transcripts)
2. NPY (neuropeptide Y) and AgRP (agouti-related
peptide).

11. • POMC/CART neurons enhance energy
expenditure and weight loss through the
production of anorexigenic α-melanocyte
stimulating hormone(MSH) and the activation of
melanocortin receptors 3 and 4(MC3/4R)in
second order neurons.
• NPY/AgRP neurons promote food intake
(orexigenic effect) and weight gain, through the
activation of Y1/5 receptors in the secondary
neurons.

13. Leptin
• Leptin, a 16 kd hormone synthesized by fat cells, is
the product of ob gene.
• The leptin receptor(OB-R), a single transmembrane
protein that belongs to the gp130 family of type I
cytokine receptor superfamily ,is expressed in a
variety of peripheral tissues, suggesting that leptin
works as a pro-inflammatory cytokine in the
periphery.
• Mutation in genetic obesities leads to decrease in
sensitivity to leptin.

14. Regulation of leptin levels
• Leptin secretion is stimulated when fat
stores are abundant.
• Insulin stimulated glucose metabolism is
an important factor.
• In the hypothalamus, leptin stimulates
POMC/CART neurons that produce
anorexigenic neuropeptides( primarily
melanocyte-stimulating hormone) and
inhibits NPY/AgRP neurons that produce
feeding-inducing (orexigenic)
neuropeptides.

15. • The net effect of leptin is to reduce food intake and
promote energy expenditure.
• Mutation of melanocortin receptor 4(MC4R) leads to
loss of sensing satiety which in turn leads to obesity.

16. Effects of leptin
• Stimulates physical activity,
heat production and energy
expenditure.
• As a pro inflammatory
cytokine and participates in
the regulation of hematopoesis
and lymphopoiesis.

18. Adipocytes
• The adipose tissue is not merely an energy storage
organ but an important endocrine organ that secretes
many biologically active substances such as leptin,
free fatty acids (FFAs), tumor necrosis factor-α
(TNF-α),IL-6, IL-1,and IL-18, chemokines, steroid
hormones and adiponectin, which are collectively
termed adipocytokines.
Fat cells

19. • The metabolic syndrome is a constellation of
abdominal obesity, insulin resistance,
hyperlipidemia, and hypertension, all of which
increase independently a risk of atherosclerotic
diseases. It is a multi-factorial pathologic
condition that arises from complex interactions
between genetic and environmental factors.
However, the molecular basis for the clustering
of such independent risks for atherosclerosis
has not been fully elucidated, with visceral fat
obesity considered most important.

20. • The total number of adipocytes is established
during chidhood and adolescence.
• They are higher in obese than in lean
individuals.
• In adults the number of adipocytes remain
constant, however, there is continuous turn
over of the cell population.
• Approx. 10% of adipocytes are renewed
annually.

21. Adiponectin
• Adiponectin stimulates fatty acid oxidation in
muscle, causing a decrease in fat mass.
• Also called as “fat-burning molecule” and
“guardian angel against obesity”
• This hormone is produced mainly by
adipocytes.

22. Effects of Adiponectin
Decreases the influx of fatty acids to the liver
Decrease in the total hepatic triglyceride
content
Decreases the glucose production in the liver
Leading to increase in insulin sensitivity.

24. Gut hormones
• These include:
1. Ghrelin
2. PYY
3. Pancreatic polypeptide
4. Insulin
5. Amylin

25. Ghrelin
• It is produced in the stomach and in the
arcuate nucleus of the hypothalamus.
• It is the only known gut hormone that
increases food intake leading to weight gain.
• It acts by binding the growth hormone
secretagogue receptor, which is abundant in
the hypohalamus and the pituitary.
• It stimultes NPY/AgRP neurons to increase
food intake.

26. PYY and Amylin
• PYY is secreted from the endocrine cells in the
ileum and colon.
• Plasma levels of PYY are low during fasting and
increase shortly after food intake.
• It reduces energy intake and its levels generally
increase after gastric bypass surgery.
• Amylin is a peptide secreted with insulin from
pancreatic β cells. It reduces food intake and weight
gain.
• Both PYY and Amylin act by stimulating the
POMC/CART neurons in the hypothalamus,
causing a decrease in food intake.
• Both of these are being evaluated for the treatment
of obesity.

28. Cardiovascular Disorders
Associated with Obesity
Hypertension
Stroke
Coronary Artery Disease
Obesity cardiomyopathy
Sudden death in obese
Obese individuals are at a greater risk of developing these cardiovascular disorders:

29. Hypertension
• Hypertension (HTN) is the term
for high blood pressure.
• Hypertension is identified when
a blood pressure is sustained at
≥140/90 mmHg.
• High blood pressure is referred
to as the “silent killer,” since
there are usually no symptoms
with HTN.

31. Hypertension
The Dangers
– The heart become larger, which may lead to heart failure.
– Small bulges (aneurysms) form in blood vessels.
– Blood vessels in the kidney become narrow, which may lead to kidney
failure.
– Arteries in the body harden faster, especially those in the
heart, brain, kidneys, and legs. This can cause a heart attack, stroke,
kidney failure, or can lead to amputation of part of the extremities.
– Blood vessels in the eye may burst or bleed. This may cause
vision changes and can result in blindness.
Failure to find and treat HTN is serious, as untreated HTN can cause:

32. Stroke
• Normally, blood containing
oxygen and nutrients is delivered
to the brain, and carbon dioxide
and cellular wastes are removed.
• A stroke occurs when the blood
supply to part of the brain is
suddenly interrupted by a blocked
vessel or when a blood vessel in
the brain bursts.
• Once their supply of oxygen and
nutrients from the blood is cut
off to the brain cells, they die.

33. Stroke
• There are two forms of stroke: ischemic and hemorrhagic.
• Ischemic stroke occurs when an artery to the brain is blocked.
• Overweight and obesity increase the risk for ischemic stroke in
men and women.
• With increasing BMI, the risk of ischemic stroke increases
progressively and is doubled in those with a BMI greater than 30
kg/m2 when compared to those having a BMI of less than 25
kg/m2.
• Hemorrhagic strokes occur when a blood vessel in the brain
erupts.
• Overweight and obesity do not increase the risk for hemorrhagic
strokes.

34. Coronary Artery Disease
• Coronary artery disease (CAD) is a type of atherosclerosis that
occurs when the arteries supplying blood to the heart muscle
(coronary arteries) become hardened and narrowed.
• This hardening and narrowing is caused by plaque buildup.
• As the plaque increases in size, the insides of the coronary
arteries get narrower, and eventually, blood flow to the heart
muscle is reduced.
• Obesity is known to be an independent risk factor
for the development of coronary heart disease.

35. Obesity cardiomyopathy
• It typically occurs in those who have severe and
long standing obesity.
• Multifactorial causes are:
1. Metabolic disturbances (insulin resistance,
increased free fatty acid levels and increased
levels of adipokines).
2. Activation of RAAS and sympathetic nervous
systems
3. Myocardial remodelling and small vessel
disease.

36. Increased metabolic activity of adipose tissue
Increase in total blood volume and cardiac output
Ventricular dilatation
Left and right ventricular hypertrophy
Systolic dysfunction
Congestive cardiac failure
Obesity cardiomyopathy

37. • Hypertensive heart
disease can be
differentiated from
obesity
cardiomyopathy by
LVH being
concentric in
hypertension
versus eccentric in
obesity.
Concentric cardiomyopathy
Normal heart
Eccenteric cardiomyopathy

38. Dilated
cardiomyopathy
Obesity
cardiomyopathy
Cause genetical multifactorial
LVH Ventricular dilatation with
an inadequate degree of
LVH
LVH and ventricular
dilatation is marked
Wall thickness of left
ventricle
<10mm >10mm
Microscopy
Myocardial fibrosis is
present
Myocardial fibrosis is absent
Fat not present in right
ventricle
Fat present in right ventricle

39. Right ventricular endomyocardial biopsy
showing a severe fibrofatty infiltration of
the myocardium ( hematoxylin eosin
100×)

40. • Criteria for issuing a cause of death
due to obesity cardiomyopathy:
1. Heart weight increased over value
predicted for normal body weight
2. Left ventricular or biventricular
hypertrophy and dilatation of atria and
ventricles. Small foci of interstitial fibrosis
may be present but not etensive ischaemic
fibrosis.
3. There may be marked fat in the right
ventricle usually in the epicardial surface
and extending in with blood vessels.
4. Exclusion of significant CAD,
myocarditis, myocardial infarction or other
clear alternative cause of death.

41. Sudden death in obese
• Obese subjects have an increased risk of arrythmias
and sudden death, even in the absence of obvious
cardiac disease.
• The sudden cardiac mortality rate is 40X higher than
unexplained cardiac arrest in non-obese population.

42. Gastrointestinal Disorders
Associated with Obesity
Obese individuals are at greater risk of developing these
gastrointestinal disorders:
Colon Cancer
Gall stones

43. Colon Cancer
Findings Relating to Obesity
• Colon cancer has been shown to occur more frequently in
people who are obese than in people who are of a healthy
weight.
• An increased risk of colon cancer has been consistently
reported for men with high BMIs.
• Women with high BMI are not at increased risk of colon
cancer.
There is evidence that abdominal obesity may be
important in colon cancer risk.

44. Gall bladder disease
• Cholelithiasis is the primary hepatobiliary
pathology associated with overweight.
• Cholelithiasis is a condition characterized
by the presence or formation of gallstones
in the gallbladder or bile ducts.
• Normally, a balance of bile salts, lecithin,
and cholesterol keep gallstones from
forming. However, if there are abnormally
high levels of bile salts or, more
commonly, cholesterol, then stones can
form.

45. Gallstones
Findings Related to Obesity
• Ironically, weight loss leads to an increased
risk of gallstones-- because of the increased
flux of cholesterol through the biliary
system.
• Diets with moderate levels of fat that trigger
gallbladder contraction and subsequent
emptying of the cholesterol content may
reduce the risk of gallstone formation.
• Bile acid supplementation can be used to
lower ones risk for gallstone formation.

46. Metabolic Disorders
Associated with Obesity
Obese individuals are at greater risk of developing these
metabolic disorders:
Diabetes Mellitus
Dyslipidemia
Liver Disease

47. Diabetes Mellitus
• Type 2 diabetes mellitus (DM) is
strongly associated with overweight
and obesity in both genders and in all
ethnic groups.
• The risk for Type 2 DM increases with
the degree and duration of overweight
in individuals.
• The risk also increases in individuals
with a more central distribution of body
fat (abdominal).

49. Dyslipidemia
• Dyslipidemia is defined
as abnormal
concentration of lipids or
lipoproteins in the blood.
• As BMI increases, there
is an increased risk for
heart disease.
• This is because a positive
correlation between BMI
and triglyceride (TG)
levels has been
demonstrated.

50. Dyslipidemia
Findings Related to Obesity
• An inverse relationship between HDL cholesterol and
BMI has been noted.
• This relationship may be more important than the
relationship between BMI & TG levels.
• Low level of HDL carries more relative risk for
developing heart disease than do elevated triglyceride
levels.
• Central fat distribution also plays an important role in
lipid abnormalities.
HDL

52. Liver Disease
• Nonalcoholic fatty liver disease
(NAFLD) is the term given to
describe a collection of liver
abnormalities that are associated
with obesity.
• In a cross-sectional analysis of liver
biopsies of obese patients, it was
found that the prevalence of
steatosis, steatohepatitis, and
cirrhosis were approximately 75%,
20%, and 2% respectively.

53. Liver Disease
Fatty Liver
• Steatosis is the term for “fatty liver” and it
is not actually a disease, but rather a
pathological finding.
• Most cases of fatty liver are due to obesity.
• Other causes of fatty liver include:
– Diabetes
– Certain drugs
– Intestinal bypass operations
– Starvation
– Protein malnutrition
– Alcoholism

54. • Histological features
of NASH (non
alcoholic
steatohepatitis) are
1. Steatosis
2. Balloning of hepatocytes
3. Lobular inflammation
4. Mallory bodies
5. Pericellular pattern of
fibrosis

55. • Histological assessment cannot distinguish
between alcoholic steatohepatitis and NASH.
• Features favouring alcoholic over nonalcoholic
causes are neutrophils, prominent mallory
bodies and extensive zone 3 fibrosis.
• Features favouring NASH over alcoholic
causes are less severe steatohepatitis with
nuclear vacuolation.

57. Obesity and kidney disease
1. Obesity is associated with renal
hemodynamic changes known to cause
CKD
2. Adipose tissue possesses inflammatory
and hormonal mediators of kidney injury
3. Population studies have shown an
association of obesity with CKD
4. CKD patients who are obese progress to
ESRD more rapidly.
5. Obesity is associated with known risk
factors for CKD – metabolic syndrome,
DM, HTN, and sleep apnea.

58. Obesity is associated with renal hemodynamic
changes known to cause CKD
Pathophysiology
• Obesity is associated with an increased GFR
(hyperfiltration), increased renal plasma flow,
and increased filtration fraction, vasodilatation
of efferent arteriole, vasoconstriction leading to
glomerular hypertension.

59. Obesity Related Glomerulopathy
• Renal biopsies in obese patients reveal
glomerulomegaly and focal sclerosis
• Hyperfiltration and glomerular hypertension leads
to damage as evidenced by decrease in GFR and
proteinuria
• Hyperfiltration and diabetic nephropathy

60. • Histologically, this
manifests as increase
in mesangial matrix
and secondary focal
segmental
glomerulosclerosis
(FSGS) with sclerosis
and hyalinosis
adjacent to the
vascular pole of the
glomerulus.
Light micrograph showing the characteristic
features of focal segmental
glomerulosclerosis, with collapse of
capillaries, hyalinosis, and adhesion (area
highlighted by arrows).

61. Oxalate nephropathy
Gastric bypass surgery is associated
with risk of enteric hyperoxaluria and
oxalate nephropathy
Diabetic nephropathy
With nodular glomerulosclerosis
Oxalate stones

62. Obstructive Sleep Apnea
• Obstructive sleep apnea is a
condition of recurrent episodes
of apnoea due to obstruction of
the upper airway during sleep,
followed by transient
awakening to restore airway
patency.
• The condition occurs in obese
because of accumulation of fat
in the neck region.
• The diagnosis is confirmed by
polysomnography and it is
usually treated by continous
positive airway
pressure(CPAP).
American Academy of Family Physicians

64. • A post mortem where OSA is being considered
as the cause of death requires full histological
and toxicological assessment.
• The suggested criteria for issuing a cause of
death at post mortem due to OSA are
1. A diagnosis during life of OSA, even in the
absence of respiratory failure. Without an
established diagnosis, an appropriate history,
e.g. snoring.
2. The circumstances of death, in particular death
always in bed, during sleep in the supine
position, often whilst not using CPAP
3. Absence of specific autopsy findings such as an
acute cardiac or cerebral event.
4. Evidence of intoxication with alcohol or other
sedatives.

65. Obesity hypoventilation syndrome
• Also known as ‘Pickwickian
syndrome’.
• It is a condition comprising of
hypoventilation, daytime
hypercapnia and hypoxaemia
(PaCO2>45mmHg and
PaO2<70mmHg) in an obese
patient with sleep-disodered
breathing (usually OSA) in the
absence of any other causes of
hypoventilation such as COPD.

66. • Chronic daytime hypercapnia distinguishes it
from OSA.
• These patient are more prone to develop cor
pulmonale than those with sleep apnoea.
• The diagnostic test for OHS is a daytime
arterial blood gas.

68. • A post mortem where OHS is being
considered as the cause of death requires full
histological and toxicological assessment
• The suggested criteria for issuing a cause of
death at post mortem due to OHS are
1. A history during life of OHS. In the absence
of this, a history of OSA or snoring during
life. There may be no prior history.
2. Sudden death in the absence of a clear
alternative cause of death such as an acute
cardiac or cerebral event.
3. Features of pulmonary hypertension and cor
pulmonale such as right ventricular
hypertrophy and dilatation.

69. Osteoarthritis
• Osteoarthritis (OA) is the most
common type of arthritis
• It is a degenerative disease which
frequently leads to chronic pain and
disability.
• For individuals over the age of 65, it
is the most disabling disease.
• Currently, only the symptoms of OA
can be treated; there is no cure.

70. Osteoarthritis
Findings Relating to Obesity
• The incidence of OA is significantly increased in
overweight individuals.
• OA that develops in the knees and ankles is probably
directly related to the trauma associated with the
degree of excess body weight.
• Osteoarthritis in other non-weight bearing joints
suggests that there must be some component of the
overweight syndrome responsible for altering
cartilage and bone metabolism, independent of the
actual stresses of body weight on joints.
Areas of the body
most commonly
affected by OA

72. Cancer
Findings Relating to Obesity
• Overweight and obesity are
associated with an increased
risk of: esophageal, gallbladder,
pancreatic, cervical, breast,
uterine, renal, and prostate
cancers.
• Obesity and physical inactivity
may account for 25 to 30
percent of several major
cancers, including--- colon,
breast (postmenopausal),
endometrial, kidney, and cancer
of the esophagus.

73. • Approx. 4% of cancers in men and
7% in women are associated with
obesity.
• Million women study examined the
relationship between BMI and
cancer in women aged 50 to 64 years
in the united kingdom and analysis
of published data sets involving
more than 280000 cases of cancer in
men and women.

74. 1. In men, a BMI >25kg/m2 correlated
strongly with an increased incidence
of adenocarcinoma of the
esophagus, and cancers of thyroid,
colon, and kidney.
2. In women, a BMI >25kg/m2
correlated strongly with an
increased incidence of
adenocarcinoma of the esophagus,
and of endometrium, gall bladder,
and kidney cancers.

76. Psychological Disorders
Associations with Obesity
• Obesity is associated with an impaired
quality of life.
• Higher BMI values are associated with
greater adverse effects.
• When compared to obese men, obese
women appear to be at a greater risk for
psychological dysfunction.
• This may be due to the societal pressure
on women to be thin.

77. Metabolic syndrome
• The WHO definition of the metabolic syndrome is of
insulin resistance, impaired glucose tolerance or
diabetes mellitus together with at least two of the
following:
a) Hypertension
b) Obesity
c) High triglycerides and/or low HDL and
d) Microalbuminaemia.

78. Idiopathic Intracranial
Hypertension:
• Idiopathic intracranial hypertension (IIH) is a
condition characterised by elevated intracranial
pressure (ICP) and papilloedema, typically occurring
in obese young women
• The role of obesity in IIH
Of particular interest in IIH, is that over 93% of
patients are obese. The prevalence of IIH is likely to
rise in conjunction with the global epidemic of
obesity contributing to significant morbidity in young
obese women over the next decade.

79. Obesity and pregnancy
Being obese during pregnancy increases the risk of
various pregnancy complications, including:
• Gestational diabetes
• Preeclampsia
• Infection
• Thrombosis
• Obstructive sleep apnea
• Overdue pregnancy
• Labor problems
• C-section
• Pregnancy loss
•

80. Genetic mutations
• Melanocortin 4 receptor deficiency, is one of the
most common Mendelian disorders in humans. It
is present in 5- 6% of severely obese children and
0.5- 1% of obese adults.
• Genes that have been studied and contribute to
obesity include: Fat Mass and Obesity Associated
(FTO), Leptin (LEP), Leptin Receptor (LEPR),
Melanocortin 4 Receptor (MC4R), Adiponectin
C1Q and Collagen Domain Containing (ADIPOQ),
Proprotein Convertase Subtilisin/Kexin Type 1
(PCSK1), and Peroxisome Proliferator-Activated
Receptor Gamma (PPARG) (Centers for Disease
Control and Prevention

81. Congenital syndromes associated
with obesity
• Constitutional obesity and mental
retardation co-occur in several
multiple congenital anomaly
syndromes:
o Prader-Willi syndrome,
o Bardet-Biedl syndrome,
o Cohen syndrome,
o Albright hereditary osteodystrophy,
and
o Borjeson-Forssman-Lehmann
syndrome

82. Treatment of Obesity

83. Anti obesity drugs
• Orlistat (also known as Xenical and Allī)- reversal inhibitor
of lipases.
• Metformin:is an oral antidiabetic drug in the biguanide class.
It is the first-line drug of choice for the treatment of type 2
diabetes, in particular, in overweight and obese people.
• Phentramine and amphetamine: appetite suppressant
• Lorcaserine (belviq): serotonin, dopamine, nor epinephrine
reuptake inhibitors.
• Bupropion : inhibits the neuronal uptake of serotonin,
dopamine and nor epinephrine .
• Topiramate : enhancing the GABA signals to promote the
anorexigenic signalling.
• Rimonabant It is a selective inhibitor of the canabinoid
CB1-receptors. ADRs: Depression. Rimonabant is out of date
and not use.
• Pramlyntide (amylin analogue)
• OTC fiber supplements glucomannan and guar gum have
been used for the purpose of inhibiting digestion and
lowering caloric absorption.
.

84. • Statins (or HMG-CoA reductase inhibitors) are a class
of drugs used to lower cholesterol levels by inhibiting the
enzyme HMG-CoA reductase, which plays a central role in the
production of cholesterol in the liver, which produces about 70
percent of total cholesterol in the body
• However, this drug is given as specific indication as not all obese
persons have high cholesterol levels.
• Clofibrate is a fibric acid derivative- interacts with the peroxisome
proliferator activated receptor alpha (PPARα), which regulates gene
expression of enzymes involved in fatty acid oxidation. Clofibrate
increases lipoprotein lipase levels which enhances clearance of
triglyceride rich lipoproteins.
• It was withdrawn from use in 2002.

85. Bariatric surgery
• Bariatric surgery should be offered to those with
a BMI of 40 kg/m2 or over, and also to those with
a BMI of 35-40kg/m2 who also have obesity
related complications, such as DM.(current
National Institute guidelines)
• This reduces the overall mortality by approx. 40%
with reduction in deaths from heart disease, DM
and cancer, together with improvement in cardiac
function and reversal of obesity cardiomyopathy.

86. • All are performed laproscopically
• Divided into
a) Restrictive procedures- laproscopic gastric
banding and vertical sleeve gastrectomy
b) Combined restrictive and malabsorptive- Roux-
en-Y gastric bypass

88. Conclusion

89. Obesity complications

90. Thank you