Gastro 4

Universitatea Titu Maiorescu
Student Objectives
Explain the main functions of the
gastrointestinal system.
Identify the main organs and accessory
organs.
Explain the role of the liver and gallbladder
in digestion.
Explain the main digestive disease
BASIS IN
GASTROENTERELOGY
Digestive System
Organization
Gastrointestinal (Gl) tract
Tube within a tube
Direct link/path between organs
Structures
Mouth
Pharynx
Esophagus
Stomach
Small intestine
Large Intestine
Rectum
4
Mouth
Teeth mechanically Epiglottis is a flap-like
break down food into structure at the back
small pieces. Tongue of the throat that
mixes food with saliva closes over the
(contains amylase, trachea preventing
which helps break food from entering it.
down starch). It is located in the
Pharynx.
Getting & Using Food
Ingest
taking in food
Digest
mechanical digestion
breaking up food into smaller pieces
intracellular
chemical digestion digestion
breaking down food into molecules small
enough to be absorbed into cells
enzymes
Absorb
absorb nutrients across cell membranes
diffusion
active transport
Eliminate
undigested material passes out of body
extracellular
digestion
Digestive System
Two groups of organs
1-Alimentary canal (gastrointestinal or GI tract)
Digests and absorbs food
Mouth, pharynx, esophagus, stomach, small
intestine, and large intestine
2-Accessory digestive organs
Teeth, tongue, gallbladder
Digestive glands
Salivary glands
Liver
Pancreas
Human digestive
system
Ingestion
Food
Mechanical
digestion Pharynx
Chewing (mouth) Esophagus
Churning (stomach) Propulsion
Segmentation Swallowing
(small intestine) (oropharynx)
Chemical Peristalsis
digestion Stomach (esophagus,
stomach,
small intestine,
large intestine)
Absorption
Lymph
vessel
Small
intestine
Large Blood
intestine vessel
Mainly H2O
Feces
Defecation Anus
Figure 23.2
Digestion
Phases
Ingestion
Movement
Digestion
Absorption
Further digestion
10
Esophagus
ESOPHAGUS
Receives food from pharynx and propels it

to stomach
Cardia sphincter (lower esophageal
sphincter) controls passage of food from
esophagus into the stomach
Relaxes = food enters stomach
Contracts = stomach contents prevented
from reentering the esophagus
ESOPHAGUS ANATOMY .
Drawing illustrates the AJCC divisions (left) and clinical
divisions (right) of the esophagus.
Kim T J et al. Radiographics 2009;29:403-421
2009 by Radiological Society of North America

Peristalsis and
Segmentation
14
Stomach
Anatomy of the Stomach
16
Stomach
3 muscle layers
Oblique
Circular
Longitudinal
Regions
Cardiac sphincter
Fundus
Antrum (pylorus)
Pyloric sphincter
Vascular
Inner surface thrown
into folds Rugae
Contains enzymes that work
best at pH 1-2
17
Stomach
Functions
disinfect food
hydrochloric acid = pH 2
kills bacteria
food storage
can stretch to fit
~2L food
digests protein
pepsin enzyme
But the stomach is made out of protein!
What stops the stomach from digesting itself?
mucus secreted by stomach cells protects stomach
lining
Stomach
Absorbs
Functions
Alcohol
Mix food
Reservoir Water
Start digestion of Lipophilic acid
Protein
B 12
Nucleic acids
Fats
Activates some enzymes
Destroy some bacteria
Makes intrinsic factor B12
absorption
19
The Duodenum and
Related Organs
The Duodenum and
Related Organs
21
Duodenum
The bile duct and main pancreatic duct
Join at the hepatopancreatic ampulla
Enter the duodenum at the major duodenal
papilla
Are controlled by the hepatopancreatic
sphincter
Right and left
hepatic ducts
of liver
Cystic duct
Common hepatic duct
Bile duct and sphincter
Accessory pancreatic duct
Mucosa
with folds Tail of pancreas
Gallbladder Pancreas
Major duodenal Jejunum
papilla Main pancreatic duct
Hepatopancreatic and sphincter
ampulla and sphincter Duodenum Head of pancreas
Figure 23.21
Small Intestine
Small Intestine: Gross
Anatomy
Major organ of digestion and absorption
24 m long; from pyloric sphincter to
ileocecal valve
Subdivisions
1. Duodenum (retroperitoneal)
2. Jejunum (attached posteriorly by
mesentery)
3. Ileum (attached posteriorly by mesentery)
Small intestine
Functions
digestion
digest carbohydrates
amylase from pancreas
digest proteins This is
where all the
trypsin & chymotrypsin from pancreas work is done!
digest lipids (fats)
bile from liver & lipase from pancreas
absorption
nutrients move into body cells by:
diffusion
active transport
Absorption in Small
Intestines
Absorption through villi & microvilli
finger-like projections
increases surface area for absorption
SMALL INTESTINES
6 meters long,
but can stretch
to cover a
tennis court
Small Intestine
Absorbs Lipids
80% ingested water Monoglycerides
Electrolytes Fatty acids
Vitamins
Micelles
Minerals
Chylomicrons
Carbonates
Active/facilitated
transport
Monosaccharides
Proteins
Di-/tripeptides
Amino acids
28
Small Intestine
Secretes digestive
enzymes
Peptidases
Amino-
Di-
Tri-
Sucrases
Maltase
Lactase
Saccharidases
Di-
Tri-
Lipase
Nucleases
29
Large Intestine
Intestine
Right colic Left colic
(hepatic) (splenic) flexure
flexure Transverse
Transverse mesocolon
colon Epiploic
Superior appendages
mesenteric
artery Descending
Haustrum colon
Ascending
Cut edge of
colon
mesentery
IIeum
Teniae coli
IIeocecal
valve
Sigmoid
Cecum colon
Vermiform appendix Rectum
Anal canal External anal sphincter
(a)
Figure 23.29a
Large intestines (colon)
Function
re-absorbs water
use ~9 liters of water every day in
digestive juices
if dont reabsorb water
would die of dehydration
> 90% of water re-absorbed
not enough water re-absorbed
diarrhea
can be fatal!
too much water re-absorbed
constipation
reabsorb by diffusion
Large Intestine
Functions
Mechanical digestion Absorbs
Haustral churning
More water
Peristalsis Vitamins
Reflexes B
Gastroileal K

Gastrocolic
Chemical digestion
Bacterial Concentrate/eli
digestion minate wastes
Ferment
carbohydrates
Protein/amino acid
33
breakdown
Feces Formation and
Defecation
Chyme dehydrated to Control
form feces
Parasympathetic
Feces composition
Water Voluntary
Inorganic salts
Epithelial cells
Bacteria
Byproducts of digestion
Defecation
Peristalsis pushes feces
into rectum
Rectal walls stretch
34
Liver
Right and left
hepatic ducts
of liver
Cystic duct
Common hepatic duct
Bile duct and sphincter
Accessory pancreatic duct
Mucosa
with folds Tail of pancreas
Gallbladder Pancreas
Major duodenal Jejunum
papilla Main pancreatic duct
Hepatopancreatic and sphincter
ampulla and sphincter Duodenum Head of pancreas
Figure 23.21
Interlobular veins
(to hepatic vein) Central vein
Sinusoids
Plates of Bile canaliculi
hepatocytes
Bile duct (receives

bile from bile
canaliculi)
Fenestrated
lining (endothelial
cells) of sinusoids
Bile duct
Hepatic Portal venule Portal triad
macrophages Portal arteriole
in sinusoid walls
Portal vein
(c)
Figure 23.25c
Liver
Location
R. Hypochondrium
Epigastric region
4 Lobes
Left
Quadrate
Caudate
Right
Each lobe has lobules Contains
hepatocytes Surround sinusoids Feed
into central vein
38
Liver
Functions
Makes bile
Detergent emulsifies
fats
Release promoted by:
Vagus n.
CCK
Secretin
Contains
Water
Bile salts
Bile pigments
Electrolytes
Cholesterol
Lecithin
39
Liver
Detoxifies/removes
Drugs
Alcohol
Stores
Gycolgen
Vitamins (A, D, E, K)
Fe and other minerals
Cholesterol
Activates vitamin D
Fetal RBC production
Phagocytosis
Metabolizes absorbed
food molecules
Carbohydrates
Proteins
40
Lipids
Liver
Dual blood supply
Hepatic portal vein
Direct input from
small intestine
Hepatic artery/vein
Direct links to heart
41
Biliary Tract
.
The Gallbladder
The gallbladder concentrates and stores bile.
Bile:
Secreted by the liver
Contains cholesterol, bile pigments and
phospholipids
Flows from the liver, through the hepatic
ducts, into the gallbladder
Exits the gallbladder via the cystic duct
Flows from the cystic duct into the
common bile duct, into the small intestine
In the small intestine, aids digestion
by breaking down fatty foods and
fat-soluble vitamins
Pancreas
Pancreas
Pancreas
Produces digestive enzymes
digest proteins
trypsin, chymotrypsin
digest starch
amylase
digest lipids
lipase
Buffers
neutralizes
acid from small pancreas
stomach intestine
Pancreatic Duct
Main duct (Wirsung) runs the entire length of
pancreas
Joins CBD at the ampulla of Vater
2 4 mm in diameter, 20 secondary branches
Ductal pressure is 15 30 mm Hg (vs. 7 17
in CBD) thus preventing damage to panc.
duct
Lesser duct (Santorini) drains superior
portion of head and empties separately into
2nd portion of duodenum
Pancreatic Arterial Supply
Venous Drainage of the Pancreas
Pancreas
Endocrine function
Pancreatic islets secrete insulin and
glucagon
Exocrine function
Acini (clusters of secretory cells) secrete
pancreatic juice
Zymogen granules of secretory cells
contain digestive enzymes
Small
duct
Acinar cells
Basement
membrane
Zymogen
granules
Rough
endoplasmic
reticulum
(a)p
Figure 23.26a
Pancreatic Juice
Watery alkaline solution (pH 8)
neutralizes chyme
Electrolytes (primarily HCO3)
Enzymes
Amylase, lipases, nucleases are secreted
in active form but require ions or bile for
optimal activity
Proteases secreted in inactive form
Pancreatic Juice
Protease activation in duodenum
Trypsinogen is activated to trypsin by brush
border enzyme enteropeptidase
Procarboxypeptidase and chymotrypsinogen
are activated by trypsin
Regulation of Bile
Secretion
Bile secretion is stimulated by
Bile salts in enterohepatic circulation
Secretin from intestinal cells exposed to HCl
and fatty chyme
Regulation of Bile
Secretion
Gallbladder contraction is stimulated by
Cholecystokinin (CCK) from intestinal cells
exposed to proteins and fat in chyme
Vagal stimulation (minor stimulus)
Cholecystokinin also causes the

hepatopancreatic sphincter to relax
mouth stomach
break up food kills germs
digest starch break up food
kill germs digest proteins
moisten food store food
liver
produces bile
- stored in gall bladder
break up fats small intestines
breakdown food
pancreas - proteins
produces enzymes to - starch
digest proteins & carbs - fats
absorb nutrients
large intestines
absorb water
COMMON SIGNS and
SYMPTOMS
Common Signs and
Symptoms
Abdominal pain
Common Signs and
Symptoms
Achlorhydria
Abnormal condition characterized by the
absence of hydrochloric acid in the gastric
juice
Anorexia
Lack or loss of appetite, resulting in the
inability to eat
Common Signs and
Symptoms
Anorexia
Condition characterized by the loss of the
ability to swallow as a result of organic or
psychologic causes
Ascites
Abnormal accumulation of fluid within the
peritoneal cavity
Fluid contains large amounts of protein and
electrolytes
Common Signs and
Symptoms
Borborygmus
An audible abdominal sound
produced by hyperactive
intestinal peristalsis
Borborygmi are rumbling,
gurgling, and tinkling noises
heard when listening with a
stethoscope
Common Signs and
Symptoms
Constipation
Difficulty in passing stools, or an
incomplete or infrequent passage of
hard stools
Diarrhea
Frequent passage of loose, watery
stools
Common Signs and
Symptoms
Dyspepsia
Vague feeling of epigastric discomfort after
eating
Involves an uncomfortable feeling of fullness,
heartburn, bloating, and nausea
Dysphagia
Difficulty in swallowing, commonly associated
with obstructive or motor disorders of the
esophagus
Common Signs and
Symptoms
Emaciation
Excessive leanness caused by disease or
lack of nutrition
Emesis
Material expelled from the stomach during
vomiting
Vomitus
Common Signs and
Symptoms
Eructation
Act of bringing up air from the stomach with a
characteristic sound through the mouth
Belching
Flatus; Flatulence
Air or gas in the intestine that is passed
through the rectum
Common Signs and
Symptoms
Gastroesophageal Reflux
Backflow of contents of stomach into esophagus
Often result of incompetence of the lower esophageal
sphincter
Icterus
A yellowish discoloration of the skin, mucous
membranes, and sclera of the eyes, caused by
greater than normal amounts of bilirubin in the blood
Also called jaundice
Common Signs and
Symptoms
Melena
An abnormal, black, tarry stool containing
digested blood
Nausea
Unpleasant sensation often leading to the
urge to vomit
Pruritus ani
A common chronic condition of itching of the
skin around the anus
COMMON DIAGNOSTIC
METHODS
Laboratory investigations
ESR: increased: inflammation, tumors
(but can be normal)
Blood count
leukocytes: : inflammation
eosinophilia: helminthiasis, allergy
anemia (Hb, HCT): GI bleeding (manifest or

occult)
Se Iron : bleeding, malabsorption,
chr.infection
Laboratory investigations
Liver tests:
AST(GOT), ALT(GPT): cell damage
ALP, GGT, bilirubin: cholestasis
prothrombin time , se albumin : liver failure
Pancreas: amylase, lipase, functional tests
Fecal occult blood test (FOBT)
Stool cultures for bacteria and
parazites
Urine: jaundice, uroinfection, kidney stone
Duodenal aspiration
Abdominal ultrasound
Specific US methods
Doppler-ultrasound - for vascular lesions
US-guided biopsy
EUS- endoscopic ultrasound -
endosonography
Abdominal ultrasound
Liver
echogenity, masses, cysts, bile ducts, veins
Biliary tract
gallstones (hyperechoic lesion with acoustic
shadow), sludge, CBD stones, cholecystitis
Pancreas
acute pancreatitis, chr.pancreatitis,
pseudocysts, tumors
Others
ascites, organomegalies, lymph nodes,
appendicitis, intraabdominal masses (tumor,
abscess, cyst, inflammatory mass), kidneys
Radiology
Plain abdominal X-ray
free air (upright position)
gas/fluid levels within dilated loops
calcifications
Upper GI barium radiography

(single or double contrast studies)
esophagus (first examination in
dysphagia)
contour, peristalsis, folds
motility disorders, stenoses

Radiology
Upper GI barium radiography
stomach and duodenum
peristalsis, emptying, shape, folds, retrogastric

space
perforation: with water-soluble contrast agent
in case of GI hemorrhage: endoscopy
Barium study of the small bowel

small bowel follow through study
enteroclysis
stenoses, polyps, mucosal alterations, ileitis

terminalis
Radiology - angiography
diagnosis of vascular diseases,
obscure GI bleedings
therapeutic angiography is evolving
(chemoembolisation of tumors,
occluding bleeding vessels, dilation of
vessels)
Computer tomography
features
specific CT methods
spiral/helical CT
contrast agents (orally administered, iv.)
CT-guided biopsy
virtual colonoscopy
Computer tomography
Liver
masses (benign, malignant [primary or
metastatic neoplasms], hemangiomas,
cysts, abscesses) , cirrhosis, ascites and
other signs of portal hypertension, lymph
nodes
Biliary tract
dilated bile ducts, imaging of CBD, distal
bile duct stones, CBD neoplasms
Computer tomography
Pancreas - (the most useful method)
neoplasms: diagnosis, staging
acute pancreatitis: extent of necrosis,
peripancreatic fluid collections, guided
biopsies
chr. pancreatitis: pseudocysts,
calcifications
Miscellaneous
staging of gastrointestinal
malignancies, intra-abdominal masses
(abscess, inflammatory, tumors),
invasion of adjacent structures
Magnetic resonance
imaging
generally not superior to CT in
abdominal diseases
sensitive
very expensive
special methods
MR angiography
MRCP - magnetic resonance cholangio-
pancreatography
Endoscopy
features
diagnostic endoscopy
provides histological sampling (biopsy,
brush cytology)
therapeutic endoscopy
Upper GI endoscopy
Esophagogastroduodenoscopy
(EGD)
Diagnostic
GI bleeding
refractory vomiting
dysphagia, odynophagia
gastroesophageal reflux
ulcers
suspicion of neoplasm (weight loss, etc.)
surveillance of healing lesions
surveillance of polyps, tumors

Upper GI endoscopy
Therapeutic
treatmentof variceal and nonvariceal
GI bleeding
injection technics, hemoclip, ligation,
thermal technics (elelctrocoagulation, heat
probe, laser, argon plasma)
removal of polyps, early neoplasms
dilation of strictures
placement of feeding gastrostomy tube
removal of foreign bodies
Capsule endoscopy
Lower GI endoscopy
Colonoscopy, rectosigmoidoscopy,
rectoscopy
Diagnostic
Bleedings (occult or hematochezia, iron
deficiency)
Chronic diarrhea
Suspicion of cancer
Suspicion of inflammatory bowel disease
Screening for cancer (altered bowel habits,

risk groups for colon cancer)
Lower GI endoscopy
Colonoscopy, rectosigmoidoscopy,
rectoscopy
Therapeutic
Removal of polyps, early cancers
Dilation of stenoses
Decompression
Endoscopic retrograde cholangio-
pancreatography - ERCP
Diagnostic
suspicion of choledocholithiasis
unexplained jaundice and cholestasis
acute gallstone pancreatitis
some cases of chr. pancreatitis
Therapeutic
endoscopic sphincterotomy - EST
endoscopic biliary/pancreatic drainage
endoscopic biliary/pancreatic stenting
dilation of strictures
endoscopic lithotripsy
Miscellaneous diagnostic
methods
Biopsies (US/CT-guided)- liver, pancreas,
masses
Punctions - ascites, cysts
Percutaneous transhepatic cholangiography (PTC)
or drainage (PTD)
Laparoscopy
Helicobacter pylori diagnostics
stains, rapid urease-test, urease breath test (UBT)
24h pH monitoring
Manometry (esophageal, rectal, Oddi-sphincter,
bowel)
ENDOSCOPY
ENDOSCOPY
Endoscopy, is the
examination of internal
body cavities using a
specialized medical
instrument called an
endoscope.
Physicians use
endoscopy to diagnose,
monitor, and surgically
treat various medical
problems.
ENDOSCOPY
The endoscope also has a channel

through which surgeons can
manipulate tiny instruments, such
as forceps, surgical scissors, and
suction devices.
A variety of instruments can be
fitted to the endoscope for
different purposes.
A surgeon introduces the

endoscope into the body either
through a body opening, such as
the mouth or the anus, or through
a small incision in the skin.
Endoscopic TREATMENT
ENDOSCOPY The endoscope
gives visual
evidence of the
problem, such as
ulceration or
inflammation
It can be used to
collect a sample
of tissue; remove
problematic
tissue, such as
polyps
It is used to take
photograph of the
hollow internal
organs
EUS ESOPHAGIAL US
EUS - Characteristics
Layer of origin
Size
Echogenicity
Vascularity
PET/CT
PET /CT
ADVANTAGES functional information
DISADVANTAGES lack of anatomic precise localisation
ESOPHAGIAL
PATHOLOGY
ESOPHAGIAL PATHOLOGY
GERD Achalasia
Esophagitis Esophageal
Esophageal Diverticulum
Dysmotility Paraesophageal
Gastroparesis Hernia
Esophageal Cancer Gastric outlet
obstruction
Esophageal Motility
Disorders
Motility
.
Disorders
upper esophageal primary disorders
UES disorders achalasia
neuromuscular disorders diffuse esophageal spasm
esophageal body nutcracker esophagus
achalasia nonspecific esophageal dysmotility
diffuse esophageal spasm secondary disorders

nutcracker esophagus severe esophagitis
nonspecific esophageal dysmotility scleroderma
LES diabetes
achalasia Parkinsons
hypertensive LES stroke

Achalasia
,
failure to relax which is said of any sphincter that

remains in a constant state of tone with periods of
relaxation
Your own footer

clinical presentation
dysphagia
regurgitation
weight loss
heartburn
postprandial choking
nocturnal coughing
diagnosis
esophagram
motility study
1. hypertensive LES (> 35 mm Hg)
2. fail to relax
3. a pressure above baseline
4. simultaneous mirrored contractions with no evidence of
progressive peristalsis
5. low-amplitude waveforms
treatment
surgical
1. Esophagomyotomy (Heller myotomy)
2. Esophagectomy
3. resection
nonsurgical
1. medications : sublingual nitroglycerin, nitrates, or calcium channel blockers,
Injections of botulinum toxin
2. endoscopic : Dilation with a Gruntzig-type (volume-limited, pressure-control)
balloon
Diffuse Esophageal Spasm
,
Hypermotility disorder of the esophagus

esophageal contractions are repetitive, simultaneous, and
of high amplitude
Symptoms and Diagnosis
chest pain
Dysphagia
Regurgitation
Esophagram
manometric studies :
simultaneous, multipeaked contractions of high amplitude (>120 mm Hg) or
long duration (>2.5 sec)
erratic contractions occur after more than 10% of wet swallows
Treatment
Nonsurgical
Pharmacologic
endoscopic intervention
Surgical : long esophagomyotomy

treatment
Medical:
Calcium channel blockers, nitrates, and antispasmodics
Bougie dilation
avoid caffeine, cold, and hot foods
Hiatal Hernia
Rolling or
Para-
esophageal
hernia
Hiatal Hernia
The esophageal hiatus is formed by the
right crus and little or no left crus.
The phrenoesophageal ligament, which
holds the distal esophagus in place is
formed by fusion by endothoracic and
endoabdominal fascia at the esophageal
hiatus.
113
Type I Hiatal Hernia the
most common.
The E-C junction moves through the hiatus
to the visceral mediastinum.
Increased abdominal pressure(

pregnancy, obesity, or vomiting ) and
vigorous esophageal contraction may
contribute the development of the hernia
.
G-E reflux and esophagitis may occur due
to loss of tone of the LES.
114
Type II Hiatal Hernia
It is uncommon.
The phrenoesophageal membrane is not
weakened diffusely but focally.
The gastric fundus protrudes through the

hiatus.
115
Type III Hiatal Hernia
It is combined with type I and type II.
It is frequently present when a type II
hiatal hernia have been present for many
years.
116
Type IV Hiatal Hernia
It refers hernia of organs other than the
stomach.
The T-colon and the omentum are the
most common involved.
The spleen and the small intestine may be
involved.
117
SYMPTOMS
Many type I and type II hernia have few or
no symptoms.
Bleeding results from gastritis and ulcer
can induce IDA, resulting in fatigue and
exertional dyspnea.
Postprandial discomfort may occur. The
substernal fullness is often mistaken MI.
118
SYMPTOMS
In type II hernia, G-E reflux and true
dysphagia is uncommon.
If vovulus occurs, severe pain and
pressure in the chest or epigastic region.
Fever, hypovolemic shock will be present
if volvulus progresses and strangulation
occurs. In this situation, mortality rate is
50%.
119
DIAGNOSIS
The diagnosis is suspected first on the
CXR.
The most common finding is retrocardiac
bubble with or without air-fluid level.
In a giant hiatal hernia, the herniated
organ may be found in the right thoracic
cavity.
D.D: mediastinal cyst or abscess, dilated
obstructed esophagus, as end stage of
achalasia.
120
DIAGNOSIS
The barium study of the UGI confirms the
diagnosis.
Endoscopy and esophageal function test
can detect the function of LES.
121
Surgery
or
Medical treatment?
Presentation objectives
Review current treatment options
Medical treatment
Surgical treatment
Endoscopic treatment
Identify existing controversies

Evidence-based
Keep you awake!
Medical Therapy
Acid suppression is the mainstay of GERD
treatment today
70-90% of patients will experience relapse
within12 months of healing of acute disease
without prophylactic medical treatment
Agents used
Proton Pump Inhibitors
Histamine blockers
Prokinetic agents
(PPI)
Most effective available pharmacologic
agent for GERD
Acid suppression by 99%
Esophagitis healing rates 80-100%
Inhibit H+/K+ ATPase enzyme system on
parietal cells
Omeprazole, lansoprazole, rabeprazole,
pantoprazole, esomeprazole
Histamine blockers
Reversible competitive blockade of H2
receptors of the parietal cell
Acid suppression by 70%
Esophagitis healing rates up to 70%
Healing rates dependent on dosage,
treatment duration and severity of disease
Ranitidine, cimetidine, famotidine,
nizatidine
Surgery
Works by restoring the barrier function of the
LES
Careful selection of patients with well
documented GERD is imperative
Laparoscopic fundoplication is considered the
gold standard in antireflux surgery
Nissen and Toupet the most common
Number of cases risen exponentially
THERAPY
There is no accepted medical treatment
for hiatal hernia.
Surgery is indicated to prevent
complications.
In type II hernia, if gastric volvulus or
obstruction is present without toxic signs,
NG decompression must be performed.
The surgery is scheduled.
128
Goals of surgery
Prevent significant reflux
Improve quality of life
Minimize complications (dysphagia)
Principles of operation
Adequate mobilization of distal esophagus
and gastric cardia
Restoration of 2-3 cm of intraabdominal
esophageal length
Crural reapproximation
Creation of a wrap
Indications for surgery
Patients with incomplete symptom control or
disease progression on PPI therapy
Patients with well-controlled disease who do
not want to be on life-long antisecretory
treatment
Patients with proven extra-esophageal
manifestations of GERD like cough, wheezing,
aspiration, hoarseness, sore throat, otitis
media, or enamel erosion.
The presence of Barrett esophagus is a
controversial indication for surgery
Operative Approaches
The operation or operative approach is
controversial.
The principles of operation is
- reduction of the hernia,
- resection of the hernia sac and
closure of the defect.
It is easy to do intrathoracic dissection via
thoracotomy.
However, transthoracic reduction may lead
to volvulus of the gastric body.
131
Operative Approaches
Abdominal approach is also suggested.
Additional procedures can be done, such
as gastrotomy, which obviates the NG
tube and decreases the risk of recurrent
volvulus.
Abdomional approach is difficult to do in
type III hiatal hernia with G-E reflux and a
foreshortened esophagus.
Laparoscopic repair is also advocated.
132
Operative Technique:
Conventional Abdominal
Approach
The author prefers abdominal approach via
upper midline incision.
In type II hernia, the E-C junction is still in the
abdomen, bounded posteriorly with a fibrous
band. It is careful not to take down the
attachment.
Dissection is done on the lower 4 to 8 cm of the
esophagus.
The repair is done with nonabsorbable O
sutures.
133
Operative Technique:
Conventional Abdominal
Approach
Antireflux procedure is done when
significant reflux esophagitis is present.
A loose Nissen fundoplication is
suggested by authors.
If no fundoplication is performed then the
stomach can be fixed by two methods
- Hill suture plication and
- gastrostomy.
134
Open Procedure
versus Laparoscopic
Open Procedure:
Incision of roughly 20-25
cm in the abdomen
Hospital stay: Several
days
Recovery time: 4-6 weeks
Indicated in patients who
have had multiple
abdominal surgery
Laparoscopic:
Minimally invasive
technique producing five
0.5-1cm incisions
Hospital stay: 1-2 days
Recovery time: 2-3 weeks
Trocar Placement
Midline2/3 from xiphoid to
umbilicus, 10mm
Laparascope
Immediately below Xiphoid Process,
5mm
Grasping forceps
Anterior Axillary Line just below
Costal Margin
Right, 10mm
Liver retractor around middle
of left lobe to retract ventrally
Exposes anterior surface of the
proximal stomach near the
gastroesophageal junction
Left, 5mm
Grasping forceps, suction,
scissors
Midclavicular Line, Left Upper
Quandrant, 5mm
Dissecting and Suturing Devices
Procedure Steps
1. Crural Dissection
2. Circumferential
Dissection of the
Esophagus
3. Fundic Mobilization
4. Preparation of Crural
Closure
5. Crural Closure
6. Fundoplication
around the Lower
Esophagus
Fundoplication
Three sutures are placed with
bites taking full thickness gastric
fundus and partial thickness
anterior esophageal wall
1 cm bite of stomach, I muscular
bite around 10-o-clock position
of esophagus, 1 cm bite on other
side of stomach
Take Penrose Drain out after the 1st
stitch
Bottom stitch with no esophagus,
just stomach bites
When completed, wrap should be
no greater than 2cm in length
Advance French Bougie and check
the tightness of the wrap
Be able to fit forceps in between
the wrap while the French Bougie
is still in
Possible Complications
Main Complications:
Bleeding
Perforation of esophagus
Perforation of stomach
Splenic injury.
Approximately 5% of patients require conversion
to open surgery because of bleeding, perforation
or other complications.
About 95% of all cases can be performed
laparoscopically, while 5% of laparoscopic cases
can result in a conversion to the open procedure.
Current Treatment
Options and
Controversies in Hiatal
Hernia
EGD images
Normal GE junction Mr. Burns EGD showing erosive

esophagitis
with regular Z-line (erosions indicated by arrows)
(arrows)
Operative findings -
Hiatal Hernia
On the right a small hiatal hernia is demonstrated.

On the left a moderate size paraesophageal hernia is
seen.
Hiatal Closure
Esophagus
Esophagus
Left Crus
Right Crus Crural Closure
On the right the crura have been dissected out and on the left
they are approximated with permanent sutures over a
Bougie
Nissen fundoplication
Esophagus
Fundoplication
Endoscopic Images
Preoperative
retroflexed view of Retroflexed view
GE junction with of GE junction
patulous hiatus after Nissen
(arrow) fundoplication
Does fundoplication halt the progression
of Barretts esophagus or even lead to its
regression?
and does that lead to decreased

incidence of adenocarcinoma?
Barrett
Esophagus
(epithelial methaplasia)
Sequelae Of Prolonged G-E
Reflux
Barretts Esophagus:
Development And Anatomic
Relationships
Endoscopic Landmarks In The
GEJ Region: Normal Versus
Barretts (Columnar-lined)
Esophagus With Location Of
Lower Esophageal Sphincter
(LES)
By Biopsy When The Squamo-
columnar Junction Is Displaced
Or Highly Irregular
Barretts Esophagus: Gross
Appearance
Endoscopy reveals Barretts
esophagus.
Biopsy specimens
show high-grade
dysplasia.
Barretts
Esophagus
Metaplastic
Epithelium
Columnar
Stratified
Squamous
Epithelium
.
Barretts Metaplasia
Esophageal
Adenocarcinoma
Metaplasia
One adult cell type replaces another type
Response to Chronic Tissue Injury
GERD
Reflux
Esophagitis
Stratified Squamous Specialized Intestinal

Epithelium Metaplasia
(Normal Esophagus) (Barretts Esophagus)
GEJ
(Gastro-Esophageal
Junction)
Z-Line
(Squamo-Columnar
Junction)
X
Columnar
Lined
Esophagus
Specialized
Intestinal
Metaplasia
Adapted from Spechler. Gastroenterology 1999;117:218
Do Proton Pump Inhibitors (PPIs) Prevent Cancer in
Barretts Esophagus?
PPIs are the most effective medical

treatment for reflux esophagitis
Decrease gastric acid production
Decrease acid reflux
Heal reflux esophagitis
PPI use associated with 75%
reduction in risk of neoplastic
progression
Evidence that PPIs prevent carcinogenesis
in Barretts esophagus is indirect and not
proven in controlled trials.
The Cancer Risk for High-Grade Dysplasia in Barretts is
Sufficient to Warrant Intervention
~6%
per
year
High Grade Dysplasia Cancer
4.
Management Options for High-Grade
Dysplasia in Barretts Esophagus
Intensive endoscopic surveillance

(every 3 months)
Endoscopic ablation
Endoscopic mucosal resection
Esophagectomy
Radiofrequency Ablation of
Barretts Esophagus
Ablated
Barretts
Metaplasia
Endoscopic Therapy for Mucosal Neoplasia
In Barretts Esophagus
EMR of mucosal irregularities for

staging and therapy
Ablate the remaining Barretts metaplasia to minimize

metachronous neoplasia
CANCER OF THE
ESOPHAGUS
Predisposing Factors
for SCCA Esophagus
Tobacco Age
Alcohol Race
Diet Gender
Chronic
esophagitis
Esophageal
diverticula
Barrett's
Esophagus
Presenting Symptoms
Retrosternal discomfort or indigestion.
Friction or burning when swallowing food.
Dysphagia,
Weight loss.
Hoarseness, cough
Regurgitation, vomiting
Hematemesis or melena (uncommon)
Adenocarcinoma
of the GE
Junction
Adenocarcinoma of the
distal esophagus
Cancer of the cardia

Non-cardia
Subcardial cancer cancer
T Staging of Esophageal Cancer
Muscularis
T1 mucosae
T2
T3 T4
T2-T4 None considered curable by endoscopic therapy.

Diagnosis of Esophageal
Cancer.
Staging
Endoscopy
Endoscopic ultrasound
CT scans
Mediastinoscopy or Laparoscopy
(PET Scan)
Therapy: Cancer
of the Esophagus
Complete resection is the goal.
If complete resection not possible, no role
for palliative resection.
No survival benefit.
Palliation of dysphagia with stents or
combined chemoradiotherapy.
Preoperative Surgical
Staging
Mediastinoscopy: difficulty in
sampling AP window, left paraaortic
nodes.
Thoracoscopy: accurate in detecting
node metastases in 93%.
Laparoscopy: accurate in detecting
node metastases in 94%.
Can identify small volume lymph node or
visceral disease.
Esophagectomy
Types of operations
Incision strategies:
Ivor-Lewis
Laparotomy, thoracotomy
Transhiatal
Conduit strategies:
Gastric pull-up
Colonic interposition
Jejunal interposition
Surgical Approaches for Esophageal Cancer
Ivor-Lewis
Esophagectomy
Gastric pull-up
Colonic interposition
Esophagectomy
Jejunal interposition
Esophagectomy
Esophagectomy
Intra-operative complications
Bleeding
average < 800 cc for Ivor-Lewis
transhiatal esophagectomy bleeding
left thoracoabdominal extension vs. left thoractomy
Aortic a., bronchial a., azygous v. bleeding -->
pack, then upper sternal split
Tracheobronchial injury
secure airway by advancing ETT, then repair
primarily vs. pedicled flap buttress
Esophagectomy --
Complications
Anastomotic strictures -- 5 - 42%
More often if lye, leak, small EEA staplers, suture
technique, irradiation
Requires dilatation (80% dilatation success)
Early after leak
Combined with endoscopy
Use 46 Fr or larger Maloney dilators, balloons when
necessary
Repeat until 6 months of stability
use extra care if colon, small bowel conduit
Chronic (> 12 mo) cervical anastomotic strictures
Stricturoplasty / SCM flap (50% failure) / Lat. Dorsi flap /
free radial arm flap / pectoralis myocutaneous flap (like
Esophageal CA -- radiation
Squamous cell carcinoma -- more radiosensitive

Preoperative radiation versus surgery alone
no improved survival in long-term
randomized trials
Post-op radiation versus surgery alone
no improved survival, but higher stricture rate
improved local recurrence rates in node

negative mid- to upper-third SCCs
Esophageal CA -- chemo
Pre-operative chemo (Cisplatin, 5-FU)

Only 19% response
No change in survival
No change in local recurrence rates or

patterns
Benefits not yet substantiated by long-
term studies
Comparison of Treatment
Modalities: Median Survivals
Surgery:
16.5 months
Radiotherapy and Chemotherapy
14.5 months
Surgery, Radiotherapy,
Chemotherapy
16-18.6 months
Gastrostomy/ Jejunostomy (GJ)
Percutaneous Endoscopic
1
Video Journal and Encyclopedia of GI Endoscopy 2014 2, 40-45DOI: (10.1016/j.vjgien.2013.10.004)

Copyright 2014 The Authors Terms and Conditions
2

4

ESOPHAGIAL
BENIGN LESIONS
Benign Lesions
Lymphangioma
Hemangioma
Fibrovascular Polyps
Granular Cell Tumors
Adenomas
Papillomas
Esophageal Duplication Cysts
Lipomas, Leiomyomas, Desmoid Tumors,
Schwannomas
Lymphangioma
Malformation of sequestered lymphatic tissue

<15 reported cases, children <2 years old
Translucent, yellowish, compressible mass,
<5mm
Dilated endothelial spaces with cavities lined
by flat endothelial cells containing
eosinophilic material
Solid on EUS, in submucosa, confirmed with
tunneled biopsies
Resection for 4-5cm by band-assisted
mucosectomy and endoscopic submucosal
Hemangioma
Prevalence 0.04%
Mostly cavernous, come capillary
Nodular, soft, bluish-red, and typically
blanch when pressed with biopsy forceps
(ddx - Kaposi's sarcoma)
Usually asymptomatic but can p/w bleeding
and/or dysphagia
Surgical or endoscopic resection
Fibrovascular Polyps
Fibromas, fibrolipomas, myomas, and lipomas
Mix of fibrous, vascular, and adipose tissue covered by
squamous epithelium
Upper third of the esophagus, attach directly to the
inferior aspect of the cricopharyngeus
75% M, 50-60s y/o
Arise from a nodular thickening of redundant mucosal
fold that elongate as the result of propulsive forces
during repeated swallowing
Asx but large lesions can prolapse into the larynx
asphyxiation, dysphagia, cough, n/v, ulceration/bleeding
Endoscopic or surgical rsxn if large feeding vessel
present or base inaccessible
Adenomas
Associated with GERD/Barretts, distal
esophagus and GE-junction
Up to 1.5cm, sometimes multiple
Inflammatory fibroid polyps include
hamartomas, inflammatory pseudopolyps,
and eosinophilic granulomas
More common in stomach, small bowel, and
colon than the esophagus
Benign, reactive inflammatory lesions with
connective tissue stroma and diffuse
eosinophilic infiltrate
Usually asx but can cause hemorrhage or
dysphagia
Resect only when symptomatic
Papillomas
Fingerlike projections, lined by squamous cells,
connective tissue core
Incidence 0.01-0.45%
50s, M>F, mostly solitary
Chronic inflammation/GERD (70% in distal 1/3) vs
HPV (5-46% in study)
HPV detected in esophageal SCC with papillomas
Small, whitish-pink, wart-like exophytic
projections (ddx - verrucous squamous cell
carcinoma, granulation tissue, papillary
leukoplakia)
Association with tylosis, acanthosis nigricans,
Goltz syndrome
Usually asymptomatic, if large may cause
Diverticulosis
Diverticulitis
obstipation
diverticulectomy
Nu s-a
terminat ?
GASTRIC DISEASES
GASTRIC
INFLAMATION
Stomach
Acute Gastritis
inflammation of gastric mucosa

acute presence of neutrophils
Chronic lymphocytes and plasma cells
Caused by ingestion of strong acids or alkalies, NSAIDs,

cancer chemotherapy, irradiation, alcohol, uremia, severe
stress & shock states
Proposed mechanisms: acid production with surface
bicarbonate buffer
Morphology: Mucosal edema, hyperemia, PML infiltration,
erosions (not deeper than muscularis mucosa) &
hemorrhages
Acute Gastritis
Gastric mucosa
demonstrates
infiltration by
Neutrophils
Acute Gastritis
diffusely hyperemic
gastric mucosa
causes for acute
gastritis
alcoholism
drugs
infections, etc.
Stomach
Chronic Gastritis
= Chronic mucosal inflammation
Leading to mucosal atrophy, intestinal metaplasia & dysplasia.
Pathogenesis:
Chronic infection by Helicobacter pylori
(90%): MCC of chronic gastritis, Elaboration of urease
produces ammonia that buffers gastric acid, protecting
organism from acid
Other diseases associated with H. pylori
Infection
Peptic ulcer disease
Gastric carcinoma
Gastric lymphoma
Autoimmunity (>10%): Antibodies to parietal cells cause
parietal cell destruction (HCl & intrinsic factor)
Stomach
Chronic Gastritis
Morphology:
Autoimmune diffuse mucosal damage of the body-fundic
mucosa
H. pylori affect antral mucosa
Histology: Lymphocytic & plasma cell infiltrate of the lamina

propria
atrophy, regeneration, metaplasia (to intestinal type mucosa)
& dysplasia.
H. pylori detected on the mucosal surface
Clinically:
Mild abdominal discomfort, nausea, vomiting;
hypochlorhydria, hypergastrinemia & rarely
Overt pernicious anemia (in autoimmune) gastritis).
Autoimmune gastritis
Autoimmune gastritis -
pernicious anemia
Chronic atrophic
gastritis is associated
with Abs
- intrinsic factor
- patietal cell
bright green IF- in the
parietal cells of the
gastric mucosa.
Gastric and duodenal
ulcer
Ulcer disease
ulcer is a defect of gastric or duodenal mucosa

which interfere over lamina muscularis mucosae,
submucosa or penetrates across whole gastric or
duodenal wall
rise of ulcer is conditioned by presence of acid

gastric content
frequent disease, men are afected 3-4x more than

women
A.Stomach and
Duodenum with
Eroded Lesions
B.Gastric Ulcer
C.Duodenal Ulcer
Pathogenesis:
multifactorial
dysbalance between protective and

aggressive factors
- Protective f.: saliva, food, alcalic duodenal fluid,

mucus - mucine, fast regeneration of gastric
epithelial cells, well perfused gastric mucosa
- Aggressive f.: HCl, pepsin, bile acids (reflux),

helicobacter pylori, drugs (analgetics, aspirin,
korticoids), nicotine, alcohol
Classification:
Acute ulcer (ulcus acutum)

smooth non-elevated borders and smooth base
major bleeding into upper GIT
Chronic ulcer (ulcus chronicum)

rushed and elevated boders, inflammation with
hypertrophic and fibrotic proliferation is
present
the most frequent form of ulcer disease
Ulcus chronicum mediogastricum

Ulcus chronicum ventriculi et duodeni
Ulcus chronicum praepyloricum
Ulcus chronicum duodeni
Symptoms of gastric ulcer disease:
epigastric pain 2 hours after meal or on a empty

stomach or during night
-upper dyspeptic syndrome loss of appetite,
nauzea, vomiting, flatulence
Pyrosis
Seasonal dependence (spring, autumn)
-vomiting brings relief
reduced nutrition
loss of weight
Complications:
Bleeding - chronic (minor, cause anaemia)

- acute (major, form affected vessel)
Perforation - mostly bulbus duodeni, anterior gastric wall

- acute violent pain
- bleeding can be present
Penetration - of the ulcer deeply through whole wall into

neighbor organ (pancreas, liver)
Stenosis - narrow of the lumen caused by scar, oedema or

inflammatory infiltration after healing of the ulcer
- rise only at pyloric localization
- vomiting of huge volume of gastric content
A penetration B perforation
C bleeding D - stenosis
Therapy:
Conservative
regular lifestyle
prohibition of the smoking and alcohol
diet (proteins, milk and milky products)
pharmacology (antagonists of H2 receptors,
antacids, anticholinergics
Surgical
BI, BII resection
proximal selective vagotomy
vagotomy with pyloroplastic
suture of perforated or haemorrhagic ulcer
Stomach resections:
Billroth I (BI) gastro-duodenoanastomosis end-to-end
Billroth II (BII) gastro-jejunoanastomosis end-to-side

with blind closure of duodenum
Proximal selective vagotomy denervation of parietal

gastric cells
Gastric Surgery
Indications:
hemorrhage,
perforation,
cancer,
obstruction,
inability to follow medical regimen
Gastric Surgical Procedures
Zeman, M. et al., Speciln chirurgie, ISBN 80-7262-260-9, 2004
Billroth I
Billroth II
Gastro-enteroanastomosis on
Roux Y crankle
Vagotomy
Complications after stomach resection:
Early dehiscence, stenosis of anastomosis,

bleeding, pancreatitis, obstructive icterus,
affection of neighbour tissues
Late - days, weeks

- early dumping syndrome
- late dumping syndrome
- incoming crankle syndrome
- outcoming crankle syndrome
- ulcer in anastomosis or in outcoming
crankle
Haemorrhagic mediogastric ulcer
Chronic gastric ulcer
Pylorostenosis and
gastrectasia
Duodenal ulcer
Stress ulcers
Peptic Ulcer
What is Peptic Ulcer?
An Ulcer is
Localized erosion in stomach or duodenum
Symptoms and Causes
What are the symptoms of a peptic ulcer?
Burning pain in the gut
Starts 2/3 hours after meals, or in the middle of

the night
What causes peptic ulcers?
Non-Steriodal Anti-Inflammatory Drugs (NSAIDS)
Helicobacter pylori
ANTI-ULCER AGENTS
Rational Approach to Drug
Design
Histamine 2 Receptors
Tagamet, Zantac, Pepcid, Axid
Protonix, Prilosec, Prevacid, Aciphex, Nexium
Antibiotics
Clarithromycin, Amoxycillan, Tetracyclin
H2 Receptor
Histamine receptor on parietal cells
Autonomic system: food stimulates gastrin
release, gastrin stimulates ECL cells,
stimulates histamine release, histamine
stimulates parietal cells secretion of HCl
Rantidine (Zantaz)
Replace imidazole ring with furan ring
10x more active than Cimetidine
Rantidine
Famotidine (Pepcid)
30x more active than cimetidine
Famotidine
Proton Pump
H+/K+ ATPase
F-ATPase: in mitocondria and chloroplasts;
make ATP with proton gradient
V-ATPase: (vacuolar) hydrolyze ATP to
generate electrochemical gradient Proton-
Pump
ATPase Animations
Exist in inactive form - prodrugs
Readily converted into active form under low
pH
Become thiol-reactive: sulfenic acid or
cyclosulfenamide
Intramolecular rearrangment
PPIs in clinical use
Rabeprazole
Esomeprazole Mg
Lansoprazole
Pantoprazole Omeprazole
Current Treatment
Treatment
H2 anatagonist / PPI
Antibiotic against Helicobacter Pylori
Future
Increase activity, long-lasting effects
HELICOBACTER
PYLORI
Helicobacter pylori
Naturally found in stomach of many people
Can cause inflammation; leading to membrane
erosion
Treated with variety of antibiotics

Clarithromycin, Amoxycillan, Tetracyclin
Inca nu s-a
terminat !!
Questions?
Benign stomach tumors
rise from all layers of stomach wall
often asymptomatic
Polypus, Leiomyoma, Lipoma,

Fibroma, Neurofibroma, Neurinoma,
Hemangioma, Karcinoids, Lymfoma
Diagnostic: endoscopy, X ray
Therapy: local excision, stomach resection

GASTRIC CANCER
CANCERUL GASTRIC
CANCERUL GASTRIC -
Epidemiologie
Prevalena variaz mult n funcie de zona

geografic, n funcie de obiceiurile
alimentare
Foarte mare n Japonia
n Europa mai frecvent n nord
Raportul brbai : femei = 2-3:1
Frecvena crete cu vrsta (vrsta medie de
diagnostic peste 60 de ani
Rar sub 45 de ani
CANCERUL GASTRIC -
Etiopatogenie
Helicobacter Pylori
Oncogen de ordinul I (OMS)
Determin gastrit atrofic cu
metaplazie intestinal, cu potenial
evolutiv spre displazie i neoplazie
Eradicarea sa n rile avansate
a determinat incidenei CG
Factori de risc
Alimentaia
coninut crescut n nitrozamine incidena CG
bogat n vitamina C i A (fructe i legume proaspete) incidena
Factorul genetic exist o predispoziie familial
Standardul economico-social sczut (prin alimentaie, HP)
CANCERUL GASTRIC -
Etiopatogenie
Afeciuni gastrice predispozante:
Gastrita cronic atrofic
Frecvent determinat de HP
Apar leziuni displazice, de la uoare
la severe (cancer intra-epitelial)

Polipi adenomatoi gastrici
Stare precanceroas, mai ales cei mari
Polipectomie la cei peste 1 cm
Rezecia gastric
La peste 15 ani de la intervenie
Stomit inflamatorie
Gastrit a bontului gastric
Gastrita cu pliuri gigante (Menetriere) 15% risc
Ulcerul gastric risc mic
Frecvent confuzie endoscopic, obligatorii biopsii multiple ale
ulcerelor gastrice i verificarea endoscopic a vindecrii
Posibil existena unor cancere ulcerate care se pot cicatriza sub
tratament
CANCERUL GASTRIC
Tablou clinic
Polimorf
Cel mai frecvent:
Epigastralgie care poate mima ulcerul, cednd la antiacide
Apetit capricios inapeten total (refuzul complet de a
consuma carne)
Pierdere ponderal progresiv caexie neoplazic
Mai rar:
HDS (hematemez i/sau melen)
Mas palpabil epigastric n formele avansate
Sindroame paraneoplazice (flebite migratorii, acantosis nigricans)
Cancerul precoce
De obicei asimptomatic sau cu uoare simptome dispeptice
descoperire ntmpltoare
ntotdeauna trebuie investigat o anemie, chiar i uoar, mai
ales la vrstnici
CANCERUL GASTRIC
Morfopatologie
Macroscopic
Aspect protruziv, burjonat
sngernd, tipic pentru CG
Aspect ulcerat, margini neregulate,

infiltrate, dure
Aspect infiltrativ, difuz, ntins

al peretelui gastric rigiditate
(linita plastic)
CANCERUL GASTRIC Extindere
Extensia CG se face:
Transparietal, precoce,
cu invadarea organelor vecine
Colon transvers
Corp pancreatic
Pe cale limfatic
Teritoriile de drenaj limfatic gastric
La distan
Metastazare
Cel mai frecvent: - ficat
- plmn
Uneori peritonit carcinomatoas
CANCERUL GASTRIC
Stadializare TNM
Permite stabilirea prognosticului i a atitudinii terapeutice
T tumora cuprinde:
T1 mucoasa i submucoasa
T2 musculara
T3 seroasa
T4 organele din jur
N adenopatia:
N0 fr invazie ganglionar
N1 invadai ganglionii
de vecintate (pn la 3 cm de tumor)
N2 invazia ganglionilor la distan
(gg. supraclavicular semnul Virchow)
M metastaze:
M0 fr metastaze
M1 cu metastaze la distan
CANCERUL GASTRIC
Diagnostic clinic
Subiectiv, cel mai frecvent apar:
Sindrom dispeptic
Epigastralgie
Pierdere ponderal progresiv
Anemie neelucidat
Eventual agregarea familial de CG
Prezena unor leziuni precanceroase
Examenul obiectiv:
De obicei srac
Posibil paloare datorit anemiei
n formele avansate, mas palpabil epigastic,
adenopatie supraclavicular
Presentation
Early cancer Advanced cancer

Asymptomatic Abdominal pain
Anaemia Weight loss
Dyspepsia 50% Epigastric mass
May respond to PPI Ascites
Acanthosis nigricans
Supraclavicular mass
Dysphagia
Jaundice
CANCERUL GASTRIC
Diagnostic paraclinic
Biologic:
Cel mai frecvent anemie feripriv moderat sau
sever
Exist CG care nu determin anemie (linita
plastic)
Gastroscopia metoda diagnostic de elecie,
permite:
Vizualizarea leziunii
Aprecierea caracterelor ei:
Friabilitate
Sngerare
Preluarea de biopsii multiple, obligatorii pentru
confirmarea histologic a diagnosticului
INVESTIGATIONS:
A. Upper gastero intestinal endoscopy
with multiple biopsy and brush
cytology
B. Radiology:
CT Scan of the chest and abdomen
USS upper abdomen
Barium meal
C. Diagnostic laparoscopy
Laboratory tests
Iron deficiency anemia
Fecal occult blood test

(FOBT)
Tumor marker (CEA, Ca19-9)
Endoscopic features of gastric
cancer
Radiologic diagnosis
Distal GC Proximal GC Linitis plastica

Differential diagnosis
Gastric Cancer
Gastric Ulcer
CANCERUL GASTRIC Diagnostic
paraclinic: Endoscopia
CG avansat:
1 CG tip protruziv
2 CG tip ulcerat
3 CG tip infiltrativ
3
CANCERUL GASTRIC Diagnostic
paraclinic: Endoscopia
CG incipient (superficial - care prinde doar
mucoasa i submucoasa)
Clasificarea japonez:
Tip I protruziv
Tip II superficial:

IIa supradenivelat
IIb plan
IIc deprimat
Tip III excavat

n Europa diagnosticarea CG incipient este rar
n Japonia, ar cu endemie mare de CG, se face screening n
populaia general peste 40 de ani depistare frecvent
Supravieuirea la 5 ani postoperator n CG incipient este de
CANCERUL GASTRIC
Ecoendoscopia: permite stadializarea T i N
Bariu pasaj:
Metod depit pentru diagnostic
Eficace n cancerele avansate
n linita plastic superior endoscopiei
Nu diagnosticheaz formele incipiente
CANCERUL GASTRIC
Ecografia transabdominal :
Metastaze hepatice
Adenopatii perigastrice
Mas epigastric n cocard
sugestiv pentru CG, obligatorie

verificarea endoscopic
Stomach cancer
Therapy:
Currative total gastrectomy, sub-total

gastrectomy
Paliative gastrostomy, jejunostomy
CANCERUL GASTRIC
Tratament
Chirurgical de elecie
Gastrectomie cu limfadenectomie
Frecvent gastrectomie subtotal sau total (cu eso-
jejuno-stomie), n funcie de localizarea i extensia
tumorii
Endoscopic:
Mucosectomia n CG incipient
piesa rezecat va fi examinat histologic n totalitate pentru a
verifica dac excizia a fost radical
Paliativ hemostaz cu Argon beamer
Chimioterapia postchirurgical, n formele
avansate
Mai multe cure cu Adriamicin + 5 Fluorouracil
Treatment
Surgical resection
EMR
Adjuvant therapy
Palliative
therapy
Endoscopic mucosal
resection
Gastric cancer
lesion confined
to mucosa layer
Endoscopic ultrasound (EUS) is

helpful in stageing GC
Endoscopic mucosal resection
CANCERUL GASTRIC
Prognostic
Depinde de:
extensia TNM
tipul histologic slab sau bine difereniat
vrsta pacientului
Supravieuire foarte bun doar n cancerele
superficiale 95% la 5 ani
Intervenia chirurgical cu intenie de
radicalitate oncologic posibil doar n 1/3
din cazuri
Supravieuirea la 5 ani 25%
CANCERUL GASTRIC
Profilaxie
Protocoale de diagnostic precoce al CG (n

Japonia)
Polipectomia endoscopic a polipilor gastrici
Urmrirea endoscopic a stomacului operat
(la 15 ani de la rezecie)
Eradicarea Helicobacter Pylori (oncogen de
ordinul I, conform OMS) la anumite categorii
de pacieni, inclusiv la descendenii
pacienilor cu CG
n perspectiv, dezvoltarea unui vaccin anti
HP
Gastric cancer
Gastric stub cancer after B
II resection
Schwanoma fundi
vetriculi
Nu s-a
terminat !!
Helicobacter pylori
Spiral shaped, flagellated

microaerophilic Gram
negative bacteria
Colonizes the gastric
mucosa in more than 50% of
the human population
Transmitted within the family
in childhood, likely by fecal-
oral transmission
H. pylori
Present in oral cavity ->
reinfection of gastric
mucosa?
Majority of infected
population remains
asymptomatic
In some cases development of

chronic gastritis
peptic ulcer
gastric mucosa associated

lymphoid tissue (MALT)
lymphoma
associated with increased
risk of cancer
H. Pylori is a risk factor for gastric
cancer
H. pylori is recognized as a class I
carcinogen since 1994
Helicobacter and gastric
cancer
High risk profile for gastric cancer
active corpus gastritis (34 x risk)
gastric atrophy und IM (5-6 x risk)
gastric hypochlorhydria
lack of ascorbic acid (scavenges
carcinogenic N-nitrosamines and
ROS)
gastric ulcer
Uemura, NEJM 2001; Sobala, Carcinogenesis 1991 Ekstrom, Gastroenterology 2001

Helicobacter pylori and gastric
cancer - conclusion
H. pylori is an essential factor in 71%-95% of all
gastric cancers
Eradication makes sense in high risk patients
corpus-dominant gastritis
first degree relatives of patients with gastric cancer
serum pepsinogen I as marker of atrophy
serological testing for H. pylori
Prospective trials: Eradication can only prevent gastric cancer if

there are no major histological abnormalities such as atrophy,
metaplasia or dysplasia
Eradication should therefore take place in early stages of

infection to prevent carcinogenesis
Bucuresti
Biliary Tract
.
Biliary Tract
Part of the digestive
system.
Made up of:
Intra hepatic ducts
Exta hepatic ducts
Gallbladder
Common Bile Duct

Summary
Gallstones
In the bile ducts
In the gallbladder
Biliary colic Obstructive jaundice
Acute and chronic cholecystitis Pancreatitis
Empyema Cholangitis
Mucocoele
Biliarytract tumours
Other conditions
Acute acalculous cholecystitis
Primary Biliary Cirrhosis
Primary Sclerosing Cholangitis
Biliary tract cysts
Biliary strictures
Gallbladder Disorders
A. Cholelithiasis and Cholecystitis
1. Definitions
a. Cholelithiasis: formation of stones (calculi) within
the gallbladder or biliary duct system
b. Cholecystitis: inflammation of gall bladder
c. Cholangitis: inflammation of the biliary ducts
2. Pathophysiology
a.Gallstones form due to
1.Abnormal bile composition
2.Biliary stasis
3.Inflammation of gallbladder
The Gallbladder
The gallbladder concentrates and stores bile.
Bile:
Secreted by the liver
Contains cholesterol, bile pigments and

phospholipids
Flows from the liver, through the hepatic

ducts, into the gallbladder
Exits the gallbladder via the cystic duct
Flows from the cystic duct into the

common bile duct, into the small intestine
In the small intestine, aids digestion

by breaking down fatty foods and
fat-soluble vitamins
Common locations of gallstones
Gallstones
Pathophysiology
Cholesterol, ordinarily insoluble in water, comes into
solution by forming vesicles with phospholipids
If ratio of cholesterol, phospholipids, and bile salts
altered, cholesterol crystals may form
Gallstone formation involves a variety of factors:
Cholesterol supersaturation
Mucin hypersecretion by the gallbladder mucosa

creates a viscoelastic gel that fosters nucleation.
Bile stasis
Occurs in diabetes, pregnancy, oral contraceptive

use, and prolonged fasting in critically ill patients
on total parenteral nutrition.
Gallstones
Sex
Higher among females than males (lifetime
risk of 35% vs 20%, respectively)
Due to endogenous sex hormones (enhance
cholesterol secretion and increase bile
cholesterol saturation)
Progesterone may contribute by relaxing smooth
muscle and impairing gallbladder emptying.
Age
Increased age is associated with lithogenic
bile and increased rate of gallstones
Gallstones Types
Two main types:
Cholesterol stones (85%):
2 subtypespure (90-100% cholesterol) or
mixed (50-90% cholesterol).
Pure stones often are solitary, whitish, and larger
than 2.5 cm in diameter.
Mixed stones usually are smaller, multiple in
number, and occur in various shapes and colors.
Pigment stones (15%) occur in 2 subtypes
brown and black.
Gallstones Natural
History
80% of patients, gallstones are clinically
silent
20% of patients develop symptoms over
15-20 years
About 1% per year
Almost all become symptomatic before
complications develop
Biliary-type pain due to obstruction of the
bile duct lumen
Predictive value of other complaints (eg,
intolerance to fatty food, indigestion) too
low to be clinically helpful
Gallstones Diverse
Abdominal pain
symptoms
Aching or tightness, typically severe and located in the
epigastrium
May develop suddenly, last for 15 minutes to several hours, and
then resolve suddenly
Referred pain posterior scapula or right shoulder area
Nausea and vomiting
Jaundice
Pruritus:
Itching, typically worse at night.
Fatigue
Weight loss
Miscellaneous:
Fatty food intolerance
Gas
Bloating
Dyspepsia
Complications of
Gallstones
In the gallbladder
Biliary colic
Acute and chronic cholecystitis
Empyema
Mucocoele
Carcinoma
In the bile ducts

Obstructive jaundice
Pancreatitis
Cholangitis
Biliary Colic
Symptoms
Right upper quadrant pain
Signs
Usually none
Investigations
Bloods U&E, FBC, LFT, Amylase,
CRP
Ultrasound of abdomen
OGD
(Oesophagogastroduodenoscopy)
Treatment
Analgesia
Cholecystectomy
Definitions
Biliary colic
Wax/waning postprandial epigastric/RUQ
pain due to transient cystic duct obstruction
by stone
No fever, No leukocytosis, Normal LFT

Asymptomatic Gallstone
Incidentally found gallstone in ultrasound exam
for other problems
Many individuals are concerned about the problem
Sometimes pt. has vague upper abdominal
discomfort and dyspepsia which cannot be
explained by a specific disease
If other work up are negative may be
Routine cholecystectomy is not indicated
Definitions
Acute cholecystitis
Acute GB distension, wall inflammation
& edema due to cystic duct obstruction.
RUQ pain (>24hrs) +/- fever, WBC,

Normal LFT,
Murphys sign = inspiratory arrest
Definitions
Chronic cholecystitis
Recurrent bouts of biliary colic leading to
chronic GB wall inflammation/fibrosis.
No fever, No leukocytosis, Normal LFT

Differential diagnosis of RUQ
pain
Biliary disease
Acute or chronic cholecystitis
CBD stone
cholangitis
Inflamed or perforated peptic ulcer
Pancreatitis
Hepatitis
Rule out:
Appendicitis, renal colic, pneumonia, pleurisy and

Acute Calculous Cholecystitis
Inflammation of the gallbladder that develops in the
setting of an obstructed cystic or bile duct
Most patients have complete remission within 1-4 days.
25-30% of patients either require surgery or develop
some complication
Perforation occurs in 10-15% of cases.
Acute Calculous
Cholecystitis
Symptoms
Right upper quadrant pain continuous, longer duration
Signs
Fever, Local peritonism.
Murphys sign
2 fingers on RUQ, ask patient to breathe in. Positive if pain and arrest of
inspiration
Investigations
Bloods U&E, FBC, LFT, Amylase, CRP
Thickened gallbladder wall, pericholecystic fluid and stones
OGD (Oesophagogastroduodenoscopy)
Treatment
Nil by mouth
Analgesia
Intravenous antibiotics
Cholecystectomy
Empyema / Mucocoele
Empyema refers to a
gallbladder filled with pus due
to acute cholecystitis
Mucocele refers to an
overdistended gallbladder
filled with mucoid or clear and
watery content.
Ascending Cholangitis
Obstruction of biliary tree with bile duct infection
Symptoms
Unwell, pain, jaundice, dark urine, pale stools
Charcot triad (ie, fever, right upper quadrant pain, jaundice) occurs
in only 20-70% of cases
Signs
Sepsis (Fever, tachycardia, low BP), Jaundice.
Investigations
Bloods U&E, FBC, LFT, Amylase, CRP, Coagulation screen
Treatment
Intravenous antibiotics
Endoscopic Retrograde CholangioPancreatogram
Acute Pancreatitis
Acute inflammation of pancreas and other retroperitoneal tissues.
Symptoms
Severe central abdominal pain radiating to back, vomiting
Signs
Variable None to Sepsis (Fever, tachycardia, low BP), Jaundice, acute
abdomen
Investigations
Bloods U&E, FBC, LFT, Amylase, CRP
MRCP
CT Pancreas
Treatment
Supportive
Endoscopic Retrograde CholangioPancreatogram
Gall Stones
Pigment stone
.
Risk factors for cholelithiasis
a. Age
b. Family history, also Native Americans
and persons of northern European heritage
c. Obesity, hyperlipidemia
d. Females, use of oral contraceptives
e. Conditions which lead to biliary stasis:
pregnancy, fasting, prolonged parenteral
nutrition
f. Diseases including cirrhosis, ileal disease
or resection, sickle-cell anemia, glucose
intolerance
.
Manifestations of acute cholecystitis
a. Episode of biliary colic involving RUQ

pain radiating to back, right scapula, or
shoulder; the pain may be aggravated by
movement, or deep breathing and may
last 12 18 hours
b. Anorexia, nausea, and vomiting
c. Fever with chills
Complications of cholecystitis
a. Chronic cholecystitis occurs after

repeated attacks of acute cholecystitis; often
asymptomatic
b. Empyema: collection of infected fluid
within gallbladder
c. Gangrene of gall bladder with perforation
leading to peritonitis, abscess formation
d. Pancreatitis, liver damage, intestinal
obstruction
Diagnostic Tests
a. Serum bilirubin: conjugated bilirubin is elevated with

bile duct obstruction
b. CBC reveals elevation in the WBC as with infection

and inflammation
c. Serum amylase and lipase are elevated, if obstruction

of the common bile duct has caused pancreatitis
d. Ultrasound of gallbladder: identifies presence of

gallstones
e. Other tests may include flat plate of the abdomen, oral

cholecytogram, gall bladder scan
.
Porcelain gallbladder
Porcelain
Gallbladde
A precancerous
condition
Needs
cholecystectomy
.
Plain radiograph showing radio-opaque

stones in the gall bladder.
Ultrasound
Curved arrow
Two small stones
at GB neck
Straight arrow
Thickened GB wall

Pericholecystic
fluid = dark lining
outside the wall
Ultrasound examination. Single large gallstone casting an
acoustic shadow
Gall bladder ultrasound
Shows
gallstones
the acoustic
shadow due to

absence of
reflected sound
waves behind
the gallstone
CT scan
denotes the GB
wall thickening
denotes the
fluid around the
GB
GB also appears
distended
Emphysematous cholecystitis
.
Gallstone
Ileus
Differential diagnosis of RUQ
pain
Biliary disease
Acute or chronic cholecystitis
CBD stone
cholangitis
Inflamed or perforated peptic ulcer
Pancreatitis
Hepatitis
Rule out:
Appendicitis, renal colic, pneumonia, pleurisy and

Complications of acute
cholecystitis
Hydrops
Obstruction of cystic duct followed by
absorption of pigments and secretion of
mucus to the gallbladder (white bile)
There may be a round tender mass in RUQ
Urgent Cholecystectomy is indicated

cholecystitis
Empyema of gallbladder
Pus-filled GB due to bacterial proliferation
in obstructed GB. Usually more toxic with
high fever
Emergent operation is needed

cholecystitis
Emphysematous cholecystitis
More commonly in men and diabetics.
Severe RUQ pain, generalized sepsis.
Imaging shows air in GB wall or lumen
Emergent cholecystectomy is needed

cholecystitis
Perforated gallbladder
Pericholecystic abscess (up to 10% of
acute cholecystitis)
Percutaneous drainage in acute phase
Biliary peritonitis due to free perforation
Emergent Laparotomy
cholecystitis
Chronic perforation into adjacent viscus
(cholecystoenteric fistula)
Air is seen in the biliary tree
The stone can cause small bowel obstruction if large enough
(gallstone ileus)
Laparotomy is needed for extraction of stone,

cholecystectomy and closure of fistula
Cholangitis
Infection within bile ducts due to
obstruction of CBD.
Infection of the bile ducts due to CBD obstruction
secondary to stones, strictures
May lead to life-threatening sepsis and septic

shock
It may present as two forms:

Suppurative
Non-suppurative
Non suppurative:
Persistent RUQ pain + fever + jaundice,
(Charcots triad) WBC, LFT,
Suppurative:
Persistent RUQ pain + fever + jaundice,

WBC, LFT,
Hepatic encephalopathy or hypotension
may ensue (Reynolds pentad)
Gallstone pancreatitis
35% of acute pancreatitis secondary to stones
Pathophysiology
Reflux of bile into pancreatic duct and/or obstruction
of ampulla by stone
ALT > 150 (3-fold elevation) has 95% PPV for
diagnosing gallstone pancreatitis
Tx: ABC, resuscitate, NPO/IVF, pain meds
Once pancreatitis resolving, ERCP & stone
extraction/sphincterotomy
Cholecystectomy before hospital discharge in
mild case
Gallbladder treatment
.
Medical Treatment
Medical treatment for

Acute biliary colic attack
Acute cholecystitis with comorbid diseases
Including:
GI rest
NG tube if vomiting, T-tube
IV Fluids
Analgesics (not morphine)
Antibiotics for cholecystitis (against GNR &
enterococcus)
Choledocholithiasis
Treatment
Endoscopic sphincterotomy and stone extraction
Interval cholecystectomy after recovery from ERCP
Surgical CBD exploration if dilated (1.5-2 cm) or stone

larger than 1.5 cm
Open
Laparoscopic
Surgical Treatment
Early cholecystectomy for acute cholecystitis
(usually within 48hrs)
Laparoscopic
Open
Elective cholecystectomy for biliary colic, chronic
cholecystitis and some asymptomatic stones
Laparoscopic
Open
Endoluminal?
Cholecystostomy is the best choice If patient is too
sick or anatomy is deranged
Percutaneous
Open
Cholecystectomy
Laparoscopic
cholecystectomy standard
of care
Timing
Early vs interval operation
Patient consent
Conversion to open
procedure 10%
Bleeding
Bile duct injury
Damage to other organs

.
Operative procedure of laparoscopic Cholecystectomy

Acute Calculous Cholecystitis
Inflammation of the gallbladder that develops in the
setting of an obstructed cystic or bile duct
Most patients have complete remission within 1-4 days.
25-30% of patients either require surgery or develop
some complication
Perforation occurs in 10-15% of cases.
ERCP
endoscopic .
sphincteroto
my
T-tube placement in the common
bile duct
Placement of a T-tube
Cholendoscopic removal of gallstones
Biliary lithotripsy
Cholangitis
Medical management (successful in 85% of
cases):
NPO
IV Fluids
IV AB.
Emergent decompression if medical
treatment fails
1. ERCP
2. Percutaneous transhepatic drainage (PTC)
3. Emergent laparotomy
.
Choledocholithiasis
Treatment
Endoscopic sphincterotomy and stone extraction
Interval cholecystectomy after recovery from ERCP
Surgical CBD exploration if dilated (1.5-2 cm) or stone

larger than 1.5 cm
Open
Laparoscopic
Biliary Tract Tumours
Cholangio-carcinoma
. Cancer of the Gall Bladder

Biliary Tree Neoplasms
Clinical symptoms:
Weight loss (77%)
Fever (21%)
Nausea (60%)
Malaise (19%)
Anorexia (56%) Diarrheoa (19%)
Abdominal pain (56%) Constipation (16%)
Fatigue (63%) Abdominal fullness (16%).
Pruritus (51%) Associated with a poor

prognosis.
Symptomatic patients usually have advanced

disease, with spread to hilar lymph nodes before
obstructive jaundice occurs
Cholangiocarcinoma
Associated with chronic cholestatic liver
disease such as:
Primary Sclerosing Cholangitis
Choledochal cysts
Asbestos.
Accounts for 25% of biliary tract cancers

Presentation:
Jaundice
Vague upper or right upper quadrant
abdominal pain
Anorexia, weight loss ,Pruritus.
Cholangiocarcinoma
Slow growing malignancy of biliary tract
which tend to infiltrate locally and
metastasize late.
Gall Bladder cancer
Bile duct cancer
Hepatocellular
Cholangiocarcinoma
Diagnosis and Initial Workup
Jaundice
Weight loss, anorexia, abdominal pain,
fever
US bile duct dilatation

Quadruple phase CT
MRCP/MRI
ERCP with Stent and Brush Biopsy
Percutaneous Cholangiogram with Internal Stent
and Brush Biopsy
MRCP: Cholangiocarcinoma at the Bifurcation
Klatskin tumour = Cholangiocarcinoma of junction of right & left

hepatic ducts
ERCP: Distal CBD Cancer
Surgical Removal
Node Dissection in Bile Duct
Roux-en-Y
Excision Hepaticojejunostomy
Cholangiocarcinoma
If positive Margins or Unresectable:

Stent
Chemotherapy +/- Radiation Therapy
Survival with surgery and

chemo/radiation is 24 to 36 months
With chemotherapy / radiation alone
survival is 12 to 18 months
Gallbladder Cancer
6th decade
1:3, Male:Female
Highest prevalence in Israel,
Mexico, Chile, Japan, and Native
American women.
Risk Factors: Gallstones, porcelain
gallbladder, polyps, chronic typhoid
and some drugs
Gall Bladder Cancer
Presentation (1)
Discovered on pathology after a routine

cholecystectomy. (T-1a/b - invades
muscularis)
CT/Chest and Abdomen, 4 phase CT of liver
If negative for metastasis:
Radical cholecystectomy with nodal dissection,
central hepatectomy, w or w/o bile duct
excision
Excise port sites
Followed by Chemo/Radiation
5 year survival = 60%
Indications For Biliary Stenting
Ampullary Stenosis
Management of patients with bile duct injury
Management of benign or malignant biliary

obstruction
Prevention of obstruction where stone

extraction is not possible at that time
Management of selected pancreatic duct

strictures, stones and sphincter of Oddi
dysfunction
Stent Placement - Endoscopic
Approach
The Endoscope is
positioned in the
duodenum at the
opening of the bile duct.
Stent Placement -Endoscopic Approach
A catheter is inserted
through the endoscope
into the ostium of the
common bile duct.
While maintaining the
endoscope position in the
duodenum, a wire is
inserted through the
catheter into the bile duct.
The stent delivery system is
then inserted over the wire
to the site of obstruction,
where the stent is deployed.
Stent Placement Endoscopic
Approach
Success rate of ERCP 90-95%
Complication rate of approximately 3-5%.
Complications:
Pancreatitis
Bleeding
Perforation
Infection
Cardiopulmonary depression from conscious sedation.
Biliary Stent - Percutaneous Approach
Transhepatic Approach
For biliary stent placement

using a percutaneous
approach:
A fine needle is inserted
between the 4th and 5th rib
on the patients right side
The puncture is through the
liver
The needle is inserted into
an intrahepatic duct under
Photo on file at Medtronic
LIVER DISEASES
Physical Characteristics
Largest solid organ of the body, weighing about 150 g at birth.
male: 1.4 to 1.8 kg; female: 1.2 to 1.4 kg.
Transverse diameter: 20 to 23 cm
Anteroposterior diameter: 10 to 12.5 cm
Anatomic and nonanatomic factors responsible for the fixation of
the liver at the right upper quadrant of the abdomen:
Anatomic
Inferior vena cava
Suprahepatic veins
Several ligaments such as the round ligament and coronary ligament
Peritoneal folds
Nonanatomic
Positive intraabdominal pressure
Motion and Activity
The position of the liver in the body is not
static.
moves up and down with the diaphragm and
rotates during respiration.
rotates backward when an individual lies down in
the supine position.
The upper surface of the liver can move
upward from 1 cm to 10 cm when full
expiration follows deep inspiration.
Lobes and Segments of the
Liver
Appears to be
divided into a large
right portion and a
much smaller left
portion.
The apparent plane
of division (left
fissure) passes
through the falciform
ligament, the round
ligament, and the
ligamentum venosum.
This apparent
division does not
correspond to the
internal distribution of
Lobes and Segments of the
The true right and Liver
left lobes of the liver
are about the same
size.
The lobes are
separated by a plane
called the median
fissure that passes
through the bed of the
gallbladder below and
the fossa of the
inferior vena cava
above.
True Left Lobe and Right
Lobe
The left lobe consists
of a left medial segment
and a left lateral
segment.
Each of these two segments

can be further divided into
superior and inferior
subsegments on the basis of the
distribution of the bile ducts,
hepatic arteries, and portal
veins.
The true right lobe is

divided by the right
fissure into anterior and
posterior segments.
Each segment of the

right lobe can be
subdivided into superior
and inferior subsegments.
Caudate Lobe
The caudate (spigelian) lobe is the "third

liver" of Bismuth.
Independent vascularization that receives
branches from the right and left sides of
the portal vein and hepatic artery, and its
veins drain directly into the IVC.
It is located between the IVC posteriorly,
the left and right hepatic lobes anteriorly
and superiorly, and the main portal vein
Soyers segmental
anatomy of the liver: utility of
a nomenclature accepted worldwide
Soyer urged that the Bismuth system be accepted worldwide to put an end to ongoing
confusion
3 vertical fissures (the
homes of the three
hepatic veins) and a
single transverse fissure
to divide the liver into
seven subsegments.
Adding the caudate lobe
to the seven
subsegments produces
eight hepatic.
Two functional lobes
separated by the middle
hepatic vein.
The right has an
anterior and a posterior
segment separated by
the right hepatic vein.
The left has a medial
and a lateral segment
separated by the left
hepatic vein.
The transverse fissure
is an imaginary line through the right
and left portal branches.
Note: there are no definite landmarks by
which to place it, and because it is a
morphologic rather than functional division.
The transverse fissure
subdivides the segments into:
Left
Left lateral superior subsegment (segment II)
Left lateral inferior subsegment (segment III)
Left medial subsegment (segment IV)
Right
Right anterior inferior subsegment (segment V)
Right anterior superior subsegment (segment VIII)
Right posterior inferior subsegment (segment VI)
Right posterior superior subsegment (segment VII)
Adding the caudate lobe (segment 1), to the

seven subsegments embraces all eight
subsegments.
By definition, the vertical fissures are planes that divide
the liver along the pathways of the three hepatic veins.
Right Fissure
Oblique 40 imaginary
line at the anterior
surface of the right
functional lobe of the
liver.
It starts in the middle of

the anterior border
between the right
angle and the right
side of the gallbladder
and extends to the
confluence between
the right hepatic vein
and the inferior vena
cava posteriorly.
The right hepatic vein

is located within the
vicinity of this
imaginary fissure.
Middle Fissure
An oblique, 75
imaginary line at the
anterior surface of
the liver which
connects the left side
of the fossa for the
gallbladder and the
IVC.
The middle hepatic

vein is located in the
vicinity of this line
and, therefore,
between the right and
left functional hepatic
lobes.
Left Fissure
The left fissure is located
within the left functional lobe
of the liver, in the superior
aspect of the umbilical
fissure, just to the left of the
line of attachment of the
falciform ligament.
It separates the lobe into
lateral and medial
segments.
The left hepatic vein is
located along this line.
In most cases, the middle
hepatic vein drains into the
left hepatic vein.
Occasionally it is very close
to the upper part of the vein
near the inferior vena cava
(IVC).
Arterial Blood Supply
The hepatic artery
supplies the liver with
arterial blood within the
investment of the hepatic
pedicle and via branches
that run close to the portal
vein branch and the bile
ducts.
Variations- most common
arrangement arises from
the celiac axis and
branches to form the GDA
inferiorly and the main
hepatic artery branch
superiorly.
Hepatic Veins
The central lobar veins of the acini drain into larger segmental and
sectorial veins before forming the main hepatic veins.
The hepatic veins are not accompanied by other structures, have no

capsular investment, and are in direct contact with the hepatic
parenchyma.
Bile Ducts
The biliary confluence is in the
hilum, outside the hepatic
parenchyma, and leads to the
common hepatic duct.
This classic junction is found in

The right anterior sector is drained
approximately 56% of patients,
by segments 5 and 8, the right
with several anatomic variants. posterior by segments 6 and 7,
the left anterior by segments 3
Segment 1 is drained by two or and 4, the left posterior by
three ducts that enter the right segment 2 only, and small
branches mostly from the left
or left hepatic duct close to the
hepatic duct drain segment 1.
confluence.
The Extrahepatic Duct
The extrahepatic bile ducts are
composed of the segments
originating from the right and
left hepatic ducts that join to
form the biliary confluence and
the main biliary channel, which
drains into the duodenum.
Note that the most common
arrangement consists of a
single main right branch, which
divides into right anterior and
posterior sectorial branches.
The left main branch is usually
a single trunk before entering
the main hepatic duct.
Gallbladder and
Cystic Duct

The cystic duct lengthens the
infundibulum of the gallbladder
and joins the common hepatic
duct to form the choledochus.
The insertion can be angular (75%
The veins of the gallbladder of patients), parallel (20% of
drain into the right portal patients), or spiral (5% of
branches and, intrahepatically, patients)and is found at the
into the middle hepatic vein. In supraduodenal part of the
gallbladder carcinoma, it is common hepatic duct in 80% of
therefore necessary to remove patients.
segments 4 and 5 with the However, it can extend downward
origin of the middle hepatic to the retroduodenal or even
vein. retropancreatic area.
Hepatic Resections
Microscopic Liver
Anatomy
Acinar unit
afferent portal venule
hepatic arteriole
bile ductule.
Portal venous blood flows along sinusoids

and comes in contact with hepatocytes
through a perisinusoidal space of Disse.
The liver is also the largest repository of

the reticuloendothelial system.
Kupffer cells, tissue-based macrophages,

line the sinusoidal spaces and are
exposed to portal venous blood as a
result.
The hepatic acinus. BC = bile cannaliculus; BD = bile

duct; CV = central vein; E = endothelial cell; HA =
hepatic artery; H = hepatocyte; K = Kupffer cell; PV =
portal vein.
THE HEPATOCYTE
metabolically highly active
covered with microvilli and are in close

approximation with each other, allowing their
common membranes to generate vital canaliculi.
close proximity through the perisinusoidal space to

sinusoidal endothelial cells and blood.
sinusoidal endothelial cells are highly permeable,

and there is generally free flow of both large- and
small-molecular-weight substances to the
hepatocyte.
SYNTHETIC FUNCTIONS
production and release of circulating factors critical to the
coagulation cascade
the single most sensitive tests of liver function are measures of

coagulation functionInternational Normalized Ratio (INR) and
factor VII and factor V levels.
synthesizes a wide variety of plasma proteins, the most

important of which is albumin.
variety of acute-phase proteins and cytokines that have

important interactions with a variety of inflammatory, infectious,
and regulatory processes.
Metabolism
Carbohydrate Metabolism
critical storage site of glycogen and is essential to the maintenance of systemic
glucose homeostasis through a complex process involving broad interactions
with lipid metabolism.
The liver also metabolizes lactate, and the Cori cycle is important in maintaining
peripheral glucose availability in the setting of anaerobic metabolism.
Lipid Metabolism
modulator of lipid metabolism, critical role in the synthesis of lipoproteins,
triglycerides, gluconeogenesis from fatty acids, and cholesterol metabolism.
cholesterol is synthesized in the liver and is used most importantly for bile salt
synthesis.
Bilirubin Metabolism
Bilirubin circulates bound to albumin in the blood.
It is actively taken up by hepatocytes, where it is glucuronidated and actively
secreted into bile.
Benign disorders of bilirubin metabolism include:
Dubin-Johnson and Rotor's syndrome, which produce conjugated (direct)
hyperbilirubinemia.
Unconjugated hyperbilirubinemia is seen in Crigler-Najjar type II and Gilbert's
Bile and the Enterohepatic
Circulation
Bile is a mixed micelle composed of bile acids and pigments,
phospholipids and cholesterol, proteins, and electrolytes.
The volume of bile secreted in an adult ranges from 500 to 1000 mL/24 h.
Since the electrolyte composition of bile is similar to plasma, intravenous

volume replacement of a high-volume biliary fistula output can be made
milliliter for milliliter with lactated Ringer's solution.
Role of the distal ileum in the reabsorption of bile salts became clear
when patients undergoing resection of the ileum for Crohn's ileitis
developed malabsorption and steatorrhea.
It was also noted that such patients had lower serum cholesterol levels,
ultimately found to be a result of increased hepatic metabolism of
cholesterol to bile acids to replace the bile acids not absorbed and
recirculated.
Benign hepatic tumors
Hemangiomas
Cysts
Hepatic Adenoma
Focal Nodular Hyperplasia
Hemangiomas
most common benign hepatic tumor
up to 75% of patients are female
The only reasons to resect hemangiomata are

for symptoms, most commonly pain, or
diagnostic uncertainty.
Cysts
Simple hepatic cysts, the most common, are
unilocular fluid-filled lesions that generally produce
no symptoms.
The possibility of echinococcosis should be

considered.
Solitary cysts lined with cuboidal epithelium are

classified as cystadenomas and should be resected,
since they are premalignant.
There are few indications for aspirating hepatic

cysts.
Cysts
Large symptomatic cysts are difficult to
eradicate with alcohol injections, and
serious superinfection of the cyst cavity
may occur.
The simplest method consists of
laparoscopic cyst fenestration (wide
excision of the cyst wall).
A tongue of omentum is fixed so it lies in
the residual cyst cavity as an ancillary
measure to prevent the edges from
coapting.
Hepatic Adenoma
oral contraceptives - Small adenomas may regress when
agents are discontinued
Two-thirds are solitary
Transition from benign to HCC may occur
association of acute bleeding episodes with pregnancy.
The general consensus is that adenomas should be resected
because of the risks of malignant change and spontaneous
hemorrhage.
Symptomatic and large asymptomatic should be resected.
Emergent resection or hepatic artery embolization for
hemorrhage.
Focal Nodular
Hyperplasia
young women
oral contraceptive agents does not appear to predispose

to the development of FNH
Symptomatic lesions should be removed, while

asymptomatic tumors (the majority) should be left
undisturbed
Inability to distinguish FNH from adenoma or malignant

disease is an indication for resection in some patients.
Discontinuation of oral contraceptives probably has no

impact.
HEPATIC ABSCESS
bacterial, parasitic, or fungal in origin
USA, pyogenic abscesses are the most common,

followed by amebic abscesses
90% of right lobe abscesses are solitary, while only 10%

of left lobe abscesses are solitary.
40% of patients have an underlying malignancy
25% of cases, no antecedent infection can be

documented ("cryptogenic" abscesses).
most cases, the organism is of enteric origin

HEPATIC ABSCESSTreatment
drainage catheters inserted percutaneously
The catheters can be removed in 12 weeks after output

becomes nonpurulent and scant.
40% of patients, the catheters do not drain well following

initial placement and must be repositioned.
when difficulties are encountered with percutaneous

drainage, laparotomy should be performed promptly.
Surgical intervention is more often necessary in cases of

multiple, loculated collections or when the abscess cavity
contains a large amount of necrotic debris.
Biliary obstruction or other causes of sepsis must also be

corrected.
LIVER FAILURE
Acute liver failure, uncommon, approx. 5000 new cases annually in
the US.
In chronic liver failure - progressive hepatocyte necrosis produces a

fibrotic response and liver cell regeneration that leads to cirrhosis.
Twenty-five thousand people die each year from cirrhosis, making it

the eighth leading cause of death from disease in the United States.
Liver stellate cells (Ito cells) are the principal mediators of fibrosis in
the liver, and are stimulated by hepatocyte necrosis and cytokines
(tumor necrosis factor- , interleukin-1, interleukin-6), growth factors
(epidermal growth factor, platelet-derived growth factor, transforming
growth factor 1) released by platelets, and Kupffer and endothelial
cells.
CIRRHOSIS
The incidence of the cirrhosis is increasing, due in large
measure to hepatitis C, and at present is the third most
common cause of death in men in the fifth decade of life.
Alcohol abuse remains the leading cause of cirrhosis in most

Western countries.
Up to 30% of patients die within a year from hepatic failure or

complications of portal hypertension
Bleeding episodes occur in up to 40% of all patients with

cirrhosis, and the initial episode of variceal hemorrhage is fatal
in 50% or more.
At least two-thirds of those who survive their initial hemorrhage

will bleed again
Portal Hypertension
Normal pressure ranges from 7 to 10 mm Hg.
In portal hypertension, pressure exceeds 10 mm Hg, averaging

around 20 mm Hg and occasionally rising as high as 5060 mm
Hg.
In extrahepatic portal vein thrombosis (without liver disease),

collaterals in the diaphragm and in the hepatocolic,
hepatoduodenal, and gastrohepatic ligaments transport blood
into the liver around the occluded vein (hepatopetal).
In cirrhosis, collateral vessels circumvent the liver and deliver

portal blood directly into the systemic circulation (hepatofugal);
these collaterals give rise to esophageal and gastric varices.
Portal Hypertension
Isolated thrombosis of the splenic vein causes localized splenic
venous hypertension and gives rise to large collaterals from
spleen to gastric fundus.
From there, the blood returns to the main portal system through
the coronary vein.
In this condition, gastric varices are often present without
esophageal varices.
spontaneous bleeding is relatively uncommon except from
those at the gastroesophageal junction; spontaneous bleeding
from gastric varices can sometimes occur.
Compared with adjacent areas of the esophagus and stomach,
the gastroesophageal junction is especially rich in submucosal
veins, which expand disproportionately in patients with portal
hypertension.
The cause of variceal bleeding is most probably rupture due to
sudden increases in hydrostatic pressure.
Primary Liver Cancer
Liver malignancy may arise from
Hepatocytes
Biliary epithelial cells

uncommon in the USA, but its incidence is
increasing.
In Asia and Africa > primary liver cancer is

extremely common
over age 50, but a few are found in

children, mainly under 2 years of age.
Risk Factors - HCC
Chronic HBV and HCV
Cirrhosis
Chronic underlying liver disease.

Risk Factors -
cholangioCA
Infrequently associated with cirrhosis.
Primary sclerosing cholangitis
Widespread infection with liver flukes

(Clonorchis sinensis
A large proportion of patients will have intra- or extra-hepatic

metastases at presentation.
infiltration of the portal venous system with subsequent

dissemination of tumor cells.
Vascular invasion is more common with larger tumors (> 5 cm).
Most common mets include the hilar and celiac lymph nodes
and the lungs; metastases to bone and brain are less common
and peritoneal disease (ie, carcinomatosis)
DX
percutaneous core biopsy or aspiration biopsy.
Fine-needle aspiration
A negative result therefore does not rule out malignant

disease
In patients with cirrhosis, the presence of a hypervascular

mass > 2 cm on two different imaging studies or a
hypervascular mass > 2 cm on one imaging study
combined with a serum alpha-fetoprotein level > 400
ng/mL is dx of HCC
Tumor Marker - AFP
hepatomas and testicular tumors.
upper limit of normal is 20 ng/mL;
values above 200 ng/mL are suggestive of

hepatoma
>400 ng/mL in a cirrhotic patients with a

hypervascular liver mass > 2 cm in diameter
are dx.
METASTATIC
NEOPLASMS
20 times more common than primary tumors in the liver
via the systemic or portal venous circulation
colon, pancreas, esophagus, stomach, neuroendocrine, breast,

lung, kidney, adrenal, ovary and uterus, melanoma, and
sarcomas
Tx: most > chemotherapy is the only treatment option

TX-Partial Hepatectomy
most effective therapy
minimal criteria
disease confined to the liver
disease amenable to a complete resection.
For small and peripherally placed lesions, sublobar,
segmental resections are preferred
Anatomical segmentectomies are preferred to non-

anatomical resections.
TX-Partial Hepatectomy
cirrhosis constitutes the major obstacle to resection in

patients with HCC.
Careful patient selection
cirrhotic patients have a late risk of death
highly selected patients may be better treated with liver

transplantation rather than resection.
Child-Pugh Classification of
Severity of Liver Disease
Precancerous lesions
Defined as those pathological changes predisposed to
gastric cancer
dysplasia
10% of patients may progress in severity

majority of patients either regress or remain stable
High-grade dysplasia may be only a transient phase in
the
progression to gastric cancer
occurs in atrophic gastritis or intestinal metaplasia
Metastasis
Direct invasion
Lymph node dissemination
Blood spread
Intraperitoneal colonization
Sister Mary Josephs
node
Hepatic Physiology
Liver:
Largest solid organ in the body
Performs over 500 chemical processes
Produces over 160 different proteins
Makes clotting factors for the blood
Stores & releases sugar as glycogen
Metabolizes, detoxifies, synthesizes
Aetiology
HP
5 fold increase in incidence, 100% vs 0% infection
Reflux disease
Cardia cancer, Barretts cancer
Risk factors
Previous gastric surgery
Bile gastritis
Pernicious anaemia
Chronic atrophic gastritis type A
3 5x risk of adenocarcinoma
Family history
Hereditary diffuse gastric cancer
CDH1 mutation (inactivates e-cadherin)
Junctional
cancer
Increase in proximal
gastric and GOJ cancer
GOJ cancer (<5cm)
classified by origin
Siewert I
Lower oesophageal
Siewert II
True GOJ
Siewert III
Proximal gastric
Adenocarcinoma
Lauren classification
Diffuse
Linitis plastica type
Poorer prognosis
Intestinal
Localised
Better prognosis
Distal stomach
T stage (UICC TNM
2002)
T3
T2b
T2a T4
Adjacent
T1 structure
N & M stage (UICC TNM
2002)
N stage M stage
N0 - no nodes M0 no distant
N1 - 1-6 nodes metastases
N2 - 7-15 nodes M1 distant
N3 > 15 nodes metastases (includes
distant nodes)
Early (T1) gastric cancer
1970 1990
Incidence of EGC increased from 1% to 15%
Open access endoscopy
46 cases
Age 69 (38 86)
98% 5 yr survival
Sue Ling et al (1992) Gut

Current incidence of early
gastric cancer
Leeds ~ 2%
Tokyo > 50%

Presentation
Early cancer Advanced cancer

Asymptomatic Abdominal pain
Anaemia Weight loss
Dyspepsia 50% Epigastric mass
May respond to PPI Ascites
Acanthosis nigricans
Supraclavicular mass
Dysphagia
Jaundice
Guidelines for referral
2 week suspected cancer referral
5% positive endoscopy
NICE guidance, August 2004

Management of dyspepsia in adults in primary
care
Referral for endoscopy
(NICE 2004)
Review medications
Urgent (<2 weeks) specialist referral for
endoscopic investigation when dyspepsia with
Chronic GI bleeding
Progressive unintentional wt loss
Progressive dysphagia
Persistent vomiting
Iron deficiency anaemia
Epigastric mass
Suspicious barium meal
Referral for endoscopy
(NICE 2004)
Routine endoscopy not necessary without alarm
signs !!!
Consider endoscopy when symptoms persist despite
HP eradication or if patients have
Prior gastric ulcer
Prior gastric surgery
Need for NSAID usage
Raised gastric cancer risk
Anxiety about cancer
Empirical PPI therapy for other patients
NICE dyspepsia guidance
Not adequately researched
No representation from upper GI surgeons
Updated NICE guidance
(August 2005)
New onset dyspepsia age >55 requires
endoscopy
Investigations for patients with
gastric cancer
Endoscopy & biopsy
Performance status
Physiological assessment
Cardio-pulmonary function
CT chest & abdomen

EUS (endoscopic ultrasound)
Laparoscopy
CT scanning
Technique
Spiral CT of chest and
abdomen
Treatment of gastric
cancer
Endoscopic treatment
EMR (endoscopic mucosal resection)
ablation
Surgery
Multimodal treatment
Neo-adjuvant
Adjuvant
Palliative treatment
Endsocopic mucosal
resection
T1 mucosal disease
Minimal risk of LN
metastases
Various techniques
Specimen obtained
Surgery
Total gastrectomy
Subtotal gastrectomy
Gastric vascular
anatomy
Lymph node metastasis
Radial spread
D1 nodes
Perigastric nodes
D2 nodes
Hepatic, splenic, coeliac
D3 nodes
Para-aortic nodes
Stomach resection
Total gastrectomy
Subtotal
gastrectomy
Lymphadenectom
y
D1, D2, D3 etc
Total
gastrectomy
Whole stomach
resected
Duodenum
oversewn
Small bowel
reconstruction
Results of therapy stomach
cancer
Surgery with curative intent
42% of patients
5 year survival 60%
Node positive - 35%
Node negative - 88%
Sue Ling et al (1993) BMJ

Multimodal therapy
Adjuvant chemotherapy Neo-adjuvant
Possible small advantage chemotherapy (ECF)
OR 0.84 (0.74 0.96) MAGIC trial
Western 0.96 Surgery +/- chemo
Asian 0.58 503 patients
Janunger 2001 Higher curative resection
rate
79% vs 69%
Better survival at 2 years
48% vs 40%
Palliative chemotherapy
Median survival benefit 3 6 months
Combination therapy superior
50% gain improvement in QOL
Consequences of surgery
Weight loss
Food restriction
B12, calcium, iron deficiency
Dumping
Early
Late hypoglycaemic
Diarrhoea
Gallstones
Stomal ulceration
Stromal tumours
GIST (Gastro-Intestinal Stromal Tumour)
Presentation
Incidental
Bleeding
Pathology
Blend sheets of spindle cells
Previously mistaken for leiomyomata
Origin cell interstitial cell of Cahal
C-kit +ve
Actin -ve
GASTRIC TUMOURS
Anatomy of the stomach

Aetiology of Gastric cancer
Types of Gastric cancer
Pathology of Gastric Cancer
Evaluation of Gastric Cancer
Treatment of Gastric Cancer
ANATOMY:
The stomach J-shaped. The stomach

has two surfaces (the anterior &
posterior), two curvatures (the greater &
lesser), two orifices (the cardia &
pylorus). It has fundus, body and pyloric
antrum.
BLOOD SUPPLY:
a. The left gastric artery
b. Right gastric artery
c. Right gastro-epiploic artery
d. Left gastro-epiploic artery
e. Short gastric arteries
The corresponding veins drain into
portal system. The lymphatic drainage
of the stomach corresponding its blood
supply.
AETIOLOGY:
Gastric cancer is the second most

common fatal cancer in the world with
high frequency in Japan.
The disease presents most commonly in

the 5th and 6th decades of life and affect
males twice as often as females.
Contn
The cause of the disease multistep process
but several predisposing factors attributed
to cause the disease :
a. Environment e. Atrophic gastritis

b. Diet f. Chronic gastric ulcer
c. Heredity g. Adenomatous polyps
d. Achlorhydria h. Blood group A
i. H. Pyloric colonisation
TYPES OF GASTRIC CANCER:
A. Benign Tumours
B. Malignant Tumours
THE BENIGN TUMORS:
Although benign tumors can

occur in the stomach most
gastric tumours are malignant.
The benign groups includes:-
1. Non-neoplastic gastric polyps
2. Adenomas
3. Neoplastic gastric polyps
4. Smooth muscles tumours benign
(Leiomyomas)
5. Polyposis Syndrome (eg:- Polyposis coli,
Juvenile polyps and P.J. Syndrome)
6. Other benign tumours are fibromas,
neurofibromas, aberrat pancreas and
angiomas.
PATHOLOGY OF GASTRIC (MALIGNANT)
TUMOURS:
The gastric cancer may arise in

the antrum (50%), the gastric
body (30%), the fundus or
oesophago-gastric juntion (20%).
Types of Malignant Tumours:
a. Adenocarcinoma
b. Leiomyosarcoma
c. Lymphomas
d. Carcinoid Tumours
The macroscopic forms of gastric cancers are
classified by (Bormann classification) into:-
1. Polypoid or Proliferative
2. Ulcerating
3. Ulcerating/Infiltrating
4. Diffuse Infiltrating (Linnitus-
Plastica)
Microscopically the tumours commonly
adenocarcinoma with range of differentiation.
The most useful to clinician and
epidemiologist is Lauren Histological
Classification:
a. Intestinal gastric cancer

b. Diffuse gastric cancer
Early Gastric Cancer: Defined as
cancer which is confined to the
mucosa and submucosa regard-
less of lymph nodes status.
Advanced Gastric Cancer:

Defined as tumor that has involved
the muscularis propria of the
stomach wall.
STAGING OF GASTRIC CANCER:
a. TNM System
b. CT Staging
c. PHNS Staging System (Japanese)
P-factor (Peritoneal dissemination)
H-factor (The presence of hepatic metastases)
N-factor (Lymphnodes involvement)
S-factor (Serosal invasion)

SPREAD OF GASTRIC CANCER:
The diffuse type spreads rapidly
through the submucosal and serosal
lymphatic and penetrates the gastric
wall at early stage, the intestinal variety
remains localized for a while and has less
tendency to disseminate.
The spread by:
1. Direct (loco regional)
2. Lymphatic
3. Blood (Haematogenous)
4. Transcoelomic
EVALUATION OF GASTRIC CANCER:
History
Clinical Examination
Investigations
The clinical features of gastric cancer

may arise from local disease, its
complications or its metastases.
SUMMARY:
Often asymptomatic until late stage.
Marked weight loss
Anorexia
Feeling of abdominal fullness or discomfort
Epigastric mass
Iron Deficiency Anaemia
Left supraclavicular mass (Troisiers Sign)
Obstructive Jaundice (Secondary in porta
hepatitis)
Pelvic mass (Krukenberg)
INVESTIGATIONS:
A. Upper gastero intestinal endoscopy
with multiple biopsy and brush
cytology
B. Radiology:
CT Scan of the chest and abdomen
USS upper abdomen
Barium meal
C. Diagnostic laparoscopy
TREATMENTS OF GASTRIC CANCER:
Surgery (Early or Advanced Cancer)

Distal tumours which involve the lower
(sub-total or partial gasterectomy).
Proximal tumours which involve the

fundus, cardia or body (total
gasterectomy).
Inoperable tumours: Whenever
possible it is advisable to do even
a limited gastric resection. If
resection is impossible an anterior
gastrojejunostomy.
Chemotherapy for gastric cancer
(Pre-operatve & post-operative)
Radiotherapy
(Pre-intra & post-operatively)
OTHER GASTRIC TUMOURS:
Gastric Lymphomas:
Primary lymphomas of the stomach of the
non Hodgkins type (NHL).
The symptoms are similar to those of
gastric cancer (adenocarcinoma).
The diagnosis is made principally from
endoscopic examination with biopsy and
cytology.
CT Scanning is important in staging the
disease.
Treatment:
- Well-localized disease should be treated
with resection (surgery) followed by
radiotherapy or chemotherapy.
- Extensive disease by adjuvant chemo-

therapy & radiotherapy than surgery.
Leiomyosarcoma:
Arise in the stomach representing 1% of
gastric tumors.
They may be sessile or pedanculated
projecting into the gastric lumen or
extragastrical or both (dumb-bell
tumour).
Presentation due to blood loss anaemia or
epigastric mass or vague dyspepsia.
Malignancy is suggested by the size more
than 5cm and confirmed by noting
increased mitosis on histology.
Gastric Carcinoid Tumour:
Are very rare. There is established
association between atrophic gastritis &
carcinoid & pernicious anemia.
Gastric carcinoids are best treated by

local resection. If very small by
endoscopic resection.
Helicobacter pylori
and
gastricAcancer
Helicobacter pylori
Spiral shaped, flagellated

microaerophilic Gram
negative bacteria
Colonizes the gastric
mucosa in more than 50% of
the human population
Transmitted within the family
in childhood, likely by fecal-
oral transmission
H. pylori
Present in oral cavity ->
reinfection of gastric
mucosa?
Majority of infected
population remains
asymptomatic
In some cases development of

chronic gastritis
peptic ulcer
gastric mucosa associated

lymphoid tissue (MALT)
lymphoma
associated with increased
risk of cancer
H. Pylori is a risk factor for gastric
cancer
H. pylori is recognized as a class I
carcinogen since 1994
Pathological outcome of H pylori:
H. pylori and the mucosal immune
system
H pylori specific Treg in gastric
mucosa
suppress mucosal immune responses
contribute to infection persistence
modulate H pylori-induced gastritis
immune response to H pylori infection
and pathological oucome might be
different according to the age of
infection (children adult)
role of CagA: CagA-positive, but not
Szczepanik, JPP 2008
CagA-negative bacteria promote
CagA dependent T-cell priming
Lundgren Infect Immun 2005; Freire de Melo, Microbes Infect 2012; Kido, BBRC 2011
H. pylori and mutagenesis
H. pylori has direct mutagenic

effects in mice
F (duration of infection, gender)
Causes genetic instability of
chromosmal and mitochondrial
DNA
Causes preneoplastic lesions
and cancer in experimental
models
Touati, Gastroenterology 2003; Helicobacter 2006; Sheh, PNAS 2010; Machade, BBA 2010; CCR 2009
Pathological outcome of H pylori
Pathological outcome of H pylori infection depends on

bacterial action
host response
susceptibility
gastric cancer susceptibility <->

inflammation-related gene polymorphisms
Allele 2 of IL1R antagonist <-> gastric cancer
> causes high circulating IL-1Ra and IL-1b levels
> severe and prolonged inflammatory response
Persson, Am J Epidemiol 2011

H. pylori
pathophysiology
Types of pathogen-host interaction
Type 1:
H pylori escapes immune system and gets
nutrients from the host tissue
Asymptomatic gastritis
Type 2:
Proinflammatory genetic backgound plus H pylori
strains with dangerous factors ->
Immune response initiates
chronic inflammation
hypochlorhydria
malignancy
Bacterial action: H- pylori strains
Type I:
Cag PAI complex
in their genome Type II:
Express CagA protein Cag negative
More toxic s1 allele of less toxic s2m2 allele
VacA of VacA
Most severe Mainly asymptomatic
infections gastritis
H pylori bacterial action
cagPAI complex: encodes
T4SS type IV secretion
system
Molecular syringe that
translocates CagA into
eukaryotic cells
Phosphorylation and nuclear
translocation of CagA
IL-8 production
NF-kB production
remodeling of cytoskeleton
by epithelial cells
Onishi PNAS 2008

CagA pathogenetic
mechanisms
CagA induces p53

degradation via
binding to and
inactivation of
ASPP2 (activates
p53) -> inhibition
of apoptosis
Buti, PNAS 2011; Ruggiero, Co infectious diseases 2012;

CagA is a bacterial oncogene
CagA attaches H. pylori

near the intracellular
junctional complex and
alters the differentiation
and behaviour of polarized
cells
Intracellular Cag
contributes to EMT
CagA-expressing
transgenic mice:
gastric epithelial hyperplasia
gastric adenocarcinomas in
the absence of gastritis Ohnishi, PNAS 2008
Helicobacter and gastric
cancer
High risk profile for gastric cancer
active corpus gastritis (34 x risk)
gastric atrophy und IM (5-6 x risk)
gastric hypochlorhydria
lack of ascorbic acid (scavenges
carcinogenic N-nitrosamines and
ROS)
gastric ulcer
Uemura, NEJM 2001; Sobala, Carcinogenesis 1991 Ekstrom, Gastroenterology 2001

What can be achieved by H pylori
eradication?
H pylori eradication
abolishes the inflammatory response
slows or may arrest the progression of atrophy
may even reverse atrophy to some degree
Abolishing the active inflammatory process with

infiltration of polymorphonuclear cells takes 4
weeks
Chronic inflammation with lymphocyte infiltration

persists up to 1 year.
Metaanalysis:
corpus atrophy potentially reversible
antral atrophy most likely irreversible
IM is irreversible
Tulassy, Scand J Gastroenterol 2010; Rokkas, Helicobacter, 2007
Eradication of H pylori and
prevention of gastric cancer
Cohort studies show Multicenter prospective cohort

positive effect of H pylori Yamagata/Japan (high incidence region)
eradication on prevention 2000-2007, mean f-u 5.6 y; n = 4133
of gastric cancer Mean age: 53 years
Patients choice to receive eradication
RCTs show benefit of H therapy (3090) or only antacid therapy
pylori eradication (rest)
on preneoplastic Annual endoscopy
conditions Eradication rate: 80%
in primary and
Incidence of gastric cancer decreased by
secondary gastric 40% in the eradication group
cancer prevention
Correa, JNCI 2000; Leung, GUT 2004; Mera, GUT 2005, Fukase Lancet 2008; Wong, JAMA 204
Take, AJG 2005; Yanaoka, Int J Cancer 2009; Uemra, NEJM 2001; Kosunen, Int J Cancer 2011, Ogura, J Cli
Gastroenterol 2008; Fuccio, Annals Internal Medicine 2009; Mabe, WJG 2009
Since 2004 mass eradication of H pylori for Taiwanese
population with prevalent H pylori infection and age > 30
years
Endpoint prevalence of:
HP
Premalignant gastric lesions
Comparison between premalignant lesions and
gastric cancer before (1995-2003) and after (2004-
2008) mass eradication
Lee, GUT 2012

Results:
Reduction
H pylori infection:
78.7%
Peptic ulcer:
67.4%
gastric atrophy
77.2%
intestinal
metaplasia: n. s.
H pylori eradication treatment
open issues
Eradication more efficacious in long term aspirin
users?
Can probiotics increase the efficacy of H pylori
tretament?
saccharomyces boulardii
lactoferrin
Kefir - fermented milk containing probiotics:
50% -> 78%
Goturk, Am J Med Sci 2011; Bekar J Med Food 2011; Niv, WJG 2008
What to do in case of high risk
(after eradication)?
Endoscopic follow up in case of

pernicious anemia with histologically confirmed
diagnosis of type A autoimmune atrophic
gastritis
histological or serological signs of subtotal or
total atrophic gastritis with hypo- or achlorhydria
intervals:
Dysplasia: 3-6 months
Moderate Reinfection
to severeoratrophy:
reoccurence after2-3 years
eradication
About 1% in developed countries
Malfertheiner GUT 2012 Around 13% in developing countries
Niv, Helicobacter 2008 -> retesting/rescreening
Helicobacter pylori and gastric
cancer - conclusion
H. pylori is an essential factor in 71%-95% of all
gastric cancers
Eradication makes sense in high risk patients
corpus-dominant gastritis
first degree relatives of patients with gastric cancer
serum pepsinogen I as marker of atrophy
serological testing for H. pylori
Prospective trials: Eradication can only prevent gastric cancer if

there are no major histological abnormalities such as atrophy,
metaplasia or dysplasia
Eradication should therefore take place in early stages of

infection to prevent carcinogenesis
Gastric Carcinoid Tumours
Type 1 : Hypergastrinaemia with
Autoimmune chronic atrophic gastritis
(Type A)
Pernicious anaemia
Type 2 : Hypergastrinaemia with
hypertrophic gastropathy
Zollinger-Ellison syndrome
Type 3 : Sporadic, no relation to
hypergastrinaemia
Gastric Carcinoid Tumours
: Rindi et al
n = 45 Type 1 Type 2 Type 3
Mc+/-SMc 26 (92%) 6 (86%) 3 (30%)
Musc Prop 1 (4%) 1 (14%) 3 (30%)
Serosa 1 (4%) 0 4 (40%)
Multiple 18 (64%) 6 (86%) 0
Solitary 10 (36%) 1 (14%) 10 (100%)
Metastases 0 2 (29%) 6 (60%)
Type 1 Gastric Carcinoid
Type 1 Gastric carcinoid tumours :
associated with Type A Autoimmune
Chronic Active Gastritis
Autoimmune process leads to destruction
and gradual atrophy of chief and parietal
cells of body/fundus - sparing of
body/fundic neuroendocrine cells
Hypochlorhydria or achlorhydria
Gastric Carcinoid
Tumours
Hyperplastic precursor sequence
Hypergastrinaemia -- Neuroendocrine
hyperplasia -- Dysplasia -- Neoplasia
Pernicious anaemia only present in 20-
46% of patients (latent effect)
Natural history : most probably remain
stationary; some regress and some
metastasize
Gastric lymphoma
MALT lymphoma
Usually associated with HP infection
Responds to HP eradication
Non MALT lymphoma

Variable pathology
Prognosis dependent on stage and cell type
Surgery reserved for salvage

Esophagus: Normal Lower
Esophageal and Squamo-
columnar Junction Mucosae
Esophagus: Normal Squamous
Epithelium
Esophagus: Normal Squamo-
columnar Junction
Esophagitis (Inflammation and
Reactive Epithelial Changes of
the Esophageal Mucosa) Has
Many Causes
Bucuresti
LECTURE IV
Prof Univ Dr Ion C. intoiu
GASTROENTEROLOGY
517
LIVER DISEASE
Hepatic Physiology
Liver:
Largest solid organ in the body
Performs over 500 chemical processes
Produces over 160 different proteins
Makes clotting factors for the blood
Stores & releases sugar as glycogen
Metabolizes, detoxifies, synthesizes
The Anatomy of the Liver
CT
Liver Histology
Defining Terms
Hepatitis: refers to any swelling,
inflammation, or irritation of the liver
Over 100 causes including:

Viruses, alcohol, enzyme deficiencies
Iron or copper overload, microvesicular fat
Genetic disorders, licit & illicit drugs, toxins
Hypotension (shock liver / reperfusion)

Defining Terms
Inflammation that lasts long enough will
create fibrosis
Extreme fibrosis is called cirrhosis
Cirrhosis can be either compensated or
decompensated
Compensated cirrhosis can be subtle
Decompensated cirrhosis is more obvious
Normal Liver
Cirrhotic Liver
Defining Terms
Normal Lab Values: 95% of normal,
asymptomatic patients have numbers in
this range on a bell shaped curve
Abnormal Labs: By definition, 2.5% of

normal patients have lab values either
above or below the normal range
Liver Function Tests
ALT: alanine aminotransferase (SGPT)
AST: aspartate aminotransferase (SGOT)
Alkaline Phosphatase & Bilirubin
Known as LFTs (but theyre really not)

Liver Synthetic Function
Total Protein and serum albumin
Total Bilirubin
Prothrombin Time (PT / INR)
These are true tests of liver function

Spider Angiomata
Spider Nevi
Nail Clubbing
Dupuytren's Contracture
Ascites
Jaundice or Scleral
Icterus
Segmental anatomy of the Liver
liver
Caudate lobe
seg 1
Left H.V and hep. Margin
seg 2
Left H.V and falciform lig.
seg 3
Quadrate lobe seg 4
G.B and right hep. V seg 5,8
Rt hep. V. and margin of the liver seg 6,7
Definition

Gastro 4

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Universitatea Titu Maiorescu

Receives food from pharynx and propels it

Kim T J et al. Radiographics 2009;29:403-421

2009 by Radiological Society of North America

too much water re-absorbed

Bile duct (receives

Cholecystokinin also causes the

anemia (Hb, HCT): GI bleeding (manifest or

gas/fluid levels within dilated loops

Upper GI barium radiography

motility disorders, stenoses

peristalsis, emptying, shape, folds, retrogastric

in case of GI hemorrhage: endoscopy

Barium study of the small bowel

stenoses, polyps, mucosal alterations, ileitis

suspicion of neoplasm (weight loss, etc.)

surveillance of healing lesions

surveillance of polyps, tumors

Suspicion of inflammatory bowel disease

Screening for cancer (altered bowel habits,

The endoscope also has a channel

A surgeon introduces the

neuromuscular disorders diffuse esophageal spasm

esophageal body nutcracker esophagus

achalasia nonspecific esophageal dysmotility

diffuse esophageal spasm secondary disorders

nonspecific esophageal dysmotility scleroderma

hypertensive LES stroke

failure to relax which is said of any sphincter that

Your own footer

Hypermotility disorder of the esophagus

Surgical : long esophagomyotomy

Increased abdominal pressure(

The gastric fundus protrudes through the

Identify existing controversies

Normal GE junction Mr. Burns EGD showing erosive

On the right a small hiatal hernia is demonstrated.

and does that lead to decreased

Response to Chronic Tissue Injury

Stratified Squamous Specialized Intestinal

PPIs are the most effective medical

Intensive endoscopic surveillance

Endoscopic mucosal resection

EMR of mucosal irregularities for

Ablate the remaining Barretts metaplasia to minimize

Cancer of the cardia

T2-T4 None considered curable by endoscopic therapy.

Squamous cell carcinoma -- more radiosensitive

improved local recurrence rates in node

Pre-operative chemo (Cisplatin, 5-FU)

No change in local recurrence rates or

Video Journal and Encyclopedia of GI Endoscopy 2014 2, 40-45DOI: (10.1016/j.vjgien.2013.10.004)

Video Journal and Encyclopedia of GI Endoscopy 2014 2, 40-45DOI: (10.1016/j.vjgien.2013.10.004)

Video Journal and Encyclopedia of GI Endoscopy 2014 2, 40-45DOI: (10.1016/j.vjgien.2013.10.004)

Malformation of sequestered lymphatic tissue

inflammation of gastric mucosa

Chronic lymphocytes and plasma cells

Caused by ingestion of strong acids or alkalies, NSAIDs,

Histology: Lymphocytic & plasma cell infiltrate of the lamina

ulcer is a defect of gastric or duodenal mucosa

rise of ulcer is conditioned by presence of acid

frequent disease, men are afected 3-4x more than

dysbalance between protective and

- Protective f.: saliva, food, alcalic duodenal fluid,