Curs-Gastroenterologie Final - 1 Martie 2017

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
 2–4 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 don’t 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
 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
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 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  Parkinson’s
 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
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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.
111
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.
112
Type II Hiatal Hernia
 It is uncommon.
 The phrenoesophageal membrane is not
weakened diffusely but focally.
 The gastric fundus protrudes through the

hiatus.
113
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.
114
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.
115
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.
116
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%.
117
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.
118
DIAGNOSIS
 The barium study of the UGI confirms the
diagnosis.
 Endoscopy and esophageal function test
can detect the function of LES.
119
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
Proton Pump Inhibitors
(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.
126
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.
129
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.
130
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.
131
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.
132
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
 Midline—2/3 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. Burn’s 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 Barrett’s esophagus or even lead to its
regression?
…and does that lead to decreased

incidence of adenocarcinoma?
Barrett
Esophagus
(epithelial methaplasia)
Barrett Esophagus
• In patients with multiple risk

factors, we suggest screening
for Barrett’s esophagus.
Norman Barrett
Sequelae Of Prolonged G-E
Reflux
Barrett’s Esophagus:
Development And Anatomic
Relationships
Endoscopic Landmarks In The
GEJ Region: Normal Versus
Barrett’s (Columnar-lined)
Esophagus With Location Of
Lower Esophageal Sphincter
(LES)
By Biopsy When The Squamo-
columnar Junction Is Displaced
Or Highly Irregular
Barrett’s Esophagus: Gross
Appearance
• Endoscopy reveals Barrett’s
esophagus.
• Biopsy specimens
show high-grade
dysplasia.
Barrett’s
Esophagus
Metaplastic
Epithelium
Columnar
Stratified
Squamous
Epithelium
.
Barrett’s 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) (Barrett’s Esophagus)
GEJ
(Gastro-Esophageal
Junction)
Z-Line
(Squamo-Columnar
Junction)
X
Columnar
Lined
Esophagus
Specialized
Intestinal
Metaplasia
Adapted from Spechler. Gastroenterology 1999;117:218
Estimates of Cancer Risk for Individual
Patients with Non-Dysplastic Barrett’s Have
Been Getting Lower
• 2014 Estimate: 0.25% per year

1 in 400 patients per year
Do Proton Pump Inhibitors (PPIs) Prevent Cancer in
Barrett’s 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 Barrett’s esophagus is indirect and not
proven in controlled trials.
The Cancer Risk for High-Grade Dysplasia in Barrett’s is
Sufficient to Warrant Intervention
~6%
per
year
High Grade Dysplasia Cancer
4.
Management Options for High-Grade
Dysplasia in Barrett’s Esophagus
Intensive endoscopic surveillance

(every 3 months)
Endoscopic ablation
Endoscopic mucosal resection
Esophagectomy
Radiofrequency Ablation of
Barrett’s Esophagus
Ablated
Barrett’s
Metaplasia
Endoscopic Therapy for Mucosal Neoplasia
In Barrett’s Esophagus 2014
• EMR of mucosal irregularities for

staging and therapy
• Ablate the remaining Barrett’s metaplasia to minimize

metachronous neoplasia
Barett esophagus
 Procedures
Radiofrequency ablation of Barrett’s
Esophagus (BARRX®)
 Endoscopic mucosal resection (EMR)
 High-definition endoscopy with narrow
band imaging (NBI)
 Endoscopic ultrasound (EUS)
 Bravo pH Probe
 Stretta Anti-Reflux Therapy
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)
Squamous
cell carcinoma
Adenocarcinoma of the
distal esophagus
Cancer of the cardia

Subcardial cancer Non-cardia
cancer
Adenocarcinoma of the GE Junction
Adenocarcinoma of
the I
distal esophagus
Cancer of the cardia II
Subcardial cancer
II
I
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.
T Staging of Esophageal Cancer
Muscularis
T1 mucosae
T2
T3 T4
T2-T4 None considered curable by endoscopic therapy.

Surgical Approaches for Esophageal Cancer
Ivor-Lewis
Esophagectomy
3 Field
Esophagectomy
Transhiatal
Esophagectomy
Esophagectomy –
Types of operations
 Incision strategies:
 Ivor-Lewis
 Laparotomy, thoracotomy
 Transhiatal
 Conduit strategies:
 Gastric pull-up
 Colonic interposition
 Jejunal interposition
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
 Mortality 3 - 5%, Morbidity 15-18%
 Anastomotic leaks -- 1 - 5%
 Cervical
 leak rate 0-12%, post-op day 5-10
 fever, crepitance, drainage, erythema, leukocytosis
 requires wide incision and drainage, not repair
 1/3 develop stricture --> I&D (not repair)

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
 20 to 40 Gy over 2 - 4 weeks (1.75 to 3.75 Gy/fx)

 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
Esophageal CA --
chemoradiation
 Pre-op chemoradiation (cisplatin/5-FU)
 40% (histologic) response rate (average)
 Similar response rates for SCC and AdenoCA
 Response rate dependent on time to surgery
following chemoradiation
 What is ideal delay to surgery?

 In rectal CA, 6-8 week gap allows more restorative
surgery than does a 2 week gap
 Allow healing ability to recover
 Allow clinical tumor shrinkage
Esophageal CA --
chemoradiation
 Increases surgical M/M by 5-15%
 With high does rad’n (high dose (3.5 Gy)
/fraction (TE fistula)
 Anastomotic leaks, strictures
 Toxicities
 myelotoxicity if Mitomycin C, etoposide, vinblastine
added
 Average results, not controlled by delay to
surgery
Esophageal CA --
chemoradiation

 Survival differences may be lost by 5 years
 Benefits not yet substantiated by long-term
studies (2002 review)
Esophageal CA --
chemoradiation alone
 Chemoradiation instead of surgery
 Studies show pathologic and clinical response
rates comparable to historical esophagectomy
survivals in Stage 2 and 3 carcinomas
 EORTC trial in progress -- 30 Gy with 5
FU/Cisplatin
 Comparisons are not against “en bloc”
resections
Esophageal CA --
 Chemoradiation (CRT) instead of surgery
 40-60% of CRT alone die with local recurrence/failure
 Compare 9% with CRT plus surgery
 Surgical salvage following CRT alone

 no difference in salvage versus CRT alone
Esophageal CA --
 Chemoradiation instead of surgery
 Current methods to determine complete
(clinical) response are inadequate to predict
which patients might not require surgery in
addition to chemoradiation
 Endoscopic U/S or MRI -- accuracy inadequate in
determining local and regional tumor
 PET, CT -- can’t detect regional nodes well
 Histologic response -- not avail. without resection
 Future: biologic serum markers ?

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/Barrett’s, 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
S-aterminat ?
Rectum
 Last section of large intestines
 eliminate feces
 what’s left over?
 undigested materials
 mainly cellulose from plants
 called roughage or fiber
 keeps everything moving & cleans out
intestines
 masses of bacteria
So don’t forget
to wash
your hands!
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 Ab’s
- 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, intractability, cancer, obstruction,
inability to follow medical regimen
MNT:
 Oral intake suspended until GI function returns.
 Initiation of liquids
 Ice or frequent sips of water
 Progress to larger amounts and variety of fluids, preferably isotonic
 Progression to solids as tolerated
 Small amounts of soft, starchy, low-fat protein foods
 Small frequent meals
 Enteral tube feeding if healing period extended
 TPN if postoperative complications that delay enteral feeding
Gastric Surgical Procedures
Zeman, M. et al., Speciální 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
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
 Proton Pump Inhibitors
 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
 2 histamine receptors?
 If histamine stimulates acid secretion why do
antihistamines fail to inhibit other actions of
histamine? The possibility of a second
histamine receptor …
H2 Receptor Antagonist
 Must bind but not activate H2 receptor site
 Addition of a functional group to bind
with another binding region and prevent
the conformational change
 Addition of aromatic ring: unsuccessful
 Addition of non-polar, hydrophobic

substituents, none antagonists, but …
4-methylhistamine
 Not an antagonist, but highly H2 selective
 Conformational isomers show preferential
binding
4-methylhistamine 4-methylhistamine
Conformation I Conformation II
Na -Guanylhistamine
 First partial agonist
 First signs of antagonistic activity
 Still allows partial conformational change
 Guanidine present in A.A. residue arginine
Na –Guanylhistamine
Carbon chain lengthened
 Two-carbon chain, speculation of a carboxylate
binding region
 Three-carbon chain, speculation of different binding

region
Burimamide
 Enhanced antagonist activity
 Longer chain allows for proximity to binding
region
 Terminal methyl group increases
hydrophobicity
Burimamide
Imidazole Ring
Development
 Two tautomers possible, protonation on alternating
nitrogens through inductive effects
 Enhance basicity: addition of electron donating group
 Decrease basicity: addition of electron withdrawing group
Metiamide
Cimetidine (Tagmet®)
 Metiamide is toxic
 Nitroguanidine and Cyanoguanidine
showed similar antagonistic activity
 NO2>CN>OMe>CONH2>Ac>Ph>H
Cimetidine
 (anTAGonist ciMETidine)
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
Proton Pump Inhibitors
 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
 Prevalenţa variază mult în funcţie de zona

geografică, în funcţie de obiceiurile
alimentare
 Foarte mare în Japonia
 În Europa mai frecvent în nord
 Raportul bărbaţi : femei = 2-3:1
 Frecvenţa creşte cu vârsta (vârsta medie de
diagnostic peste 60 de ani
 Rar sub 45 de ani
CANCERUL GASTRIC -
Etiopatogenie
 Helicobacter Pylori
 Oncogen de ordinul I (OMS)
 Determină gastrită atrofică cu
metaplazie intestinală, cu potenţial
evolutiv spre displazie şi neoplazie
 Eradicarea sa în ţările avansate
a determinat  incidenţei CG
 Factori de risc
 Alimentaţia
 conţinut crescut în nitrozamine  incidenţa CG
 bogată în vitamina C şi A (fructe şi legume proaspete)  incidenţa
 Factorul genetic – există o predispoziţie familială
 Standardul economico-social scăzut (prin alimentaţie, HP)
CANCERUL GASTRIC -

Etiopatogenie
Afecţiuni gastrice predispozante:
 Gastrita cronică atrofică
 Frecvent determinată de HP
 Apar leziuni displazice, de la uşoare
la severe (cancer intra-epitelial)

 Polipi adenomatoşi gastrici
 Stare precanceroasă, mai ales cei mari
 Polipectomie la cei peste 1 cm
 Rezecţia gastrică
 La peste 15 ani de la intervenţie
 Stomită inflamatorie
 Gastrită a bontului gastric
 Gastrita cu pliuri gigante (Menetriere) – 15% risc
 Ulcerul gastric – risc mic
 Frecvent confuzie endoscopică, obligatorii biopsii multiple ale
ulcerelor gastrice şi verificarea endoscopică a vindecării
 Posibilă existenţa unor cancere ulcerate care se pot cicatriza sub
tratament
CANCERUL GASTRIC –
Tablou clinic
 Polimorf
 Cel mai frecvent:
 Epigastralgie care poate mima ulcerul, cedând la antiacide
 Apetit capricios  inapetenţă totală (refuzul complet de a
consuma carne)
 Pierdere ponderală progresivă  caşexie neoplazică
 Mai rar:
 HDS (hematemeză şi/sau melenă)
 Masă palpabilă epigastrică – în formele avansate
 Sindroame paraneoplazice (flebite migratorii, acantosis nigricans)
 Cancerul precoce
 De obicei asimptomatic sau cu uşoare simptome dispeptice –
descoperire întâmplătoare
 Întotdeauna trebuie investigată o anemie, chiar şi uşoară, mai
ales la vârstnici
Morfopatologie
 Macroscopic
 Aspect protruziv, burjonat
sângerând, tipic pentru CG
 Aspect ulcerat, margini neregulate,

infiltrate, dure
 Aspect infiltrativ, difuz, întins

al peretelui gastric  rigiditate
(linita plastică)
CANCERUL GASTRIC – Extindere
 Extensia CG se face:
 Transparietal, precoce,
cu invadarea organelor vecine
 Colon transvers
 Corp pancreatic
 Pe cale limfatică
 Teritoriile de drenaj limfatic gastric
 La distanţă
 Metastazare
 Cel mai frecvent: - ficat 
- plămân
 Uneori peritonită carcinomatoasă
Stadializare TNM
Permite stabilirea prognosticului şi a atitudinii terapeutice
 T – tumora cuprinde:
 T1 – mucoasa şi submucoasa
 T2 – musculara
 T3 – seroasa
 T4 – organele din jur
 N – adenopatia:
 N0 – fără invazie ganglionară
 N1 – invadaţi ganglionii
de vecinătate (până la 3 cm de tumoră)
 N2 – invazia ganglionilor la distanţă
(gg. supraclavicular – semnul Virchow)
 M – metastaze:
 M0 – fără metastaze
 M1 – cu metastaze la distanţă
Diagnostic clinic
 Subiectiv, cel mai frecvent apar:
 Sindrom dispeptic
 Epigastralgie
 Pierdere ponderală progresivă
 Anemie neelucidată
 Eventual agregarea familială de CG
 Prezenţa unor leziuni precanceroase
 Examenul obiectiv:
 De obicei sărac
 Posibilă paloare datorită anemiei
 În formele avansate, masă palpabilă epigastică,
adenopatie supraclaviculară
Diagnostic paraclinic
 Biologic:
 Cel mai frecvent anemie feriprivă moderată sau
severă
 Există CG care nu determină anemie (linita
plastică)
 Gastroscopia – metoda diagnostică de elecţie,
permite:
 Vizualizarea leziunii
 Aprecierea caracterelor ei:
 Friabilitate
 Sângerare
 Preluarea de biopsii multiple, obligatorii pentru
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
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 markers (CEA, Ca19-
9)
Diagnosis
Endoscopic diagnosis
--- biopsy needed for definitive
diagnosis
Radiologic diagnosis
Detection of early gastric cancer

•In patients with signs and symptoms suggestive of

GC, and/or with compatible risk factors or
paraneoplastic
conditions, the diagnostic procedure of choice could
be
an endoscopic examination
•The diagnostic criteria for early or advanced gastric

cancer under endoscopy are based on the JRSGC
and
Endoscopic features of gastric
cancer
• Classi For reasons of cost and availability,

radiography may sometimes be the first diagnostic
procedure performed
•c radiography signs of malignant gastric ulcer
asymmetric/distorted ulcer crater

ulcer on the irregular mass
irregular/distorted mucosal folds
adjacent mucosa with obliterated /distorted area gastricae
nodularity, mass effect, or loss of distensibility
Distal GC Proximal GC Linitis plastica

Differential diagnosis
Gastric Cancer
Gastric Ulcer
Diagnostic paraclinic:
Endoscopia
 CG avansat:
1 – CG tip protruziv
2 – CG tip ulcerat
3 – CG tip infiltrativ
3
Diagnostic paraclinic:
Endoscopia
 CG incipient (superficial - care prinde doar
mucoasa şi submucoasa)
 Clasificarea japoneză:
 Tip I – protruziv
 Tip II – superficial:
 IIa – supradenivelat
 IIb – plan
 IIc – deprimat
 Tip III – excavat
 În Europa diagnosticarea CG incipient este rară
 În Japonia, ţară cu endemie mare de CG, se face screening în
populaţia generală peste 40 de ani  depistare frecventă
 Supravieţuirea la 5 ani postoperator în CG incipient este de
peste 95%
 Ecoendoscopia: permite stadializarea T şi N
 Bariu pasaj:
Metodă depăşită pentru diagnostic
Eficace în cancerele avansate
În linita plastică superior endoscopiei
Nu diagnostichează formele incipiente
 Ecografia transabdominală :
 Metastaze hepatice
 Adenopatii perigastrice
 Masă epigastrică “în cocardă”
sugestivă pentru CG, obligatorie

verificarea endoscopică
Prognostic
 Depinde de:
 extensia TNM
 tipul histologic – slab sau bine diferenţiat
 vârsta pacientului
 Supravieţuire foarte bună doar în cancerele
superficiale – 95% la 5 ani
 Intervenţia chirurgicală cu intenţie de
radicalitate oncologică – posibilă doar în 1/3
din cazuri
 Supravieţuirea la 5 ani – 25%
Tratament
 Chirurgical – de elecţie
 Gastrectomie cu limfadenectomie
 Frecvent gastrectomie subtotală sau totală (cu eso-
jejuno-stomie), în funcţie de localizarea şi extensia
tumorii
 Endoscopic:
 Mucosectomia în CG incipient
piesa rezecată va fi examinată histologic în totalitate pentru a
verifica dacă excizia a fost radicală
 Paliativ – hemostază cu Argon beamer
 Chimioterapia – postchirurgical, în formele
avansate
 Mai multe cure cu Adriamicină + 5 Fluorouracil
Profilaxie
 Protocoale de diagnostic precoce al CG (în

Japonia)
 Polipectomia endoscopică a polipilor gastrici
 Urmărirea endoscopică a stomacului operat
(la 15 ani de la rezecţie)
 Eradicarea Helicobacter Pylori (oncogen de
ordinul I, conform OMS) la anumite categorii
de pacienţi, inclusiv la descendenţii
pacienţilor cu CG
 În perspectivă, dezvoltarea unui vaccin anti
HP
Genetic factors
• The majority of gastric tumor are sporadic in nature
• There are rare inherited gastric cancer predisposition

traits
such as germline p53 (Li-Fraumeni syndrome)
E-cadherin (CDH1) alterations
in diffuse gastric cancers
Stomach cancer
 Therapy:
 Currative – total gastrectomy, sub-total

gastrectomy
 Paliative – gastrostomy, jejunostomy
Gastric cancer
Gastric stub cancer after B
II resection
Schwanoma fundi
vetriculi
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
Endoscopic mucosal
resection
Gata 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
.
Summary
 Gallstones
 In the gallbladder • In the bile ducts
 Biliary colic • Obstructive jaundice
 Acute and chronic cholecystitis • Pancreatitis
 Empyema
 Mucocoele • Cholangitis
 Biliarytract tumours
 Other conditions
 Acute acalculous cholecystitis
 Mirizzi’s syndrome
 Primary Biliary Cirrhosis
 Primary Sclerosing Cholangitis
 Biliary tract cysts
 Biliary strictures
Biliary Tract
Part of the digestive
system.
Made up of:
 Intra hepatic ducts
 Exta hepatic ducts
 Gallbladder
 Common Bile Duct

The Gallbladder
Bile:
phospholipids
 Flows from the liver, through the hepatic
ducts, into the gallbladder
 Flows from the cystic duct into the
common bile duct, into the small intestine
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 subtypes—pure (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.
brown and black.
 Brown stones are made up of calcium bilirubinate
and calcium-soaps. Bacteria involved in formation
via secretion of beta glucuronidase and
phospholipase
 Black stones result when excess bilirubin enters
the bile and polymerizes into calcium bilirubinate
(patients with chronic hemolysis)
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
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
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.
 Murphy’s 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.
Empyema / Mucocoele
 Symptoms
 Signs
 Murphy’s sign
 2 fingers on RUQ, ask patient to breathe in. Positive if pain and arrest of inspiration
 Investigations
 Thickened gallbladder wall, distended gallbladder, pericholecystic fluid, stones
 Treatment
 Nil by mouth
 Analgesia
 Cholecystectomy
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
 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
 MRCP
 CT Pancreas
 Treatment
 Supportive
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

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
.
Gall Stones
 b. Most gallstones are composed primarily of bile
(80%); remainder are composed of a mixture of bile
components
 c. Excess cholesterol in bile is associated with
obesity, high-cholesterol diet and drugs that lower
cholesterol levels
 d. If stones from gallbladder lodge in the cystic duct
 1. There can be reflux of bile into the gallbladder and
liver
 2. Gallbladder has increased pressure leading to
ischemia and inflammation
 3. Severe ischemia can lead to necrosis of the gall
bladder
 4. If the common bile duct is obstructed, pancreatitis
can develop
Common locations of gallstones
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 cholelithiasis
 a. Many persons are asymptomatic
 b. Early symptoms are epigastic fullness
after meals or mild distress after eating a
fatty meal
 c. Biliary colic (if stone is blocking cystic or
common bile duct): steady pain in epigastric
or RUQ of abdomen lasting up to 5 hours
with nausea and vomiting
 d. Jaundice may occur if there is
obstruction of common bile duct
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
Collaborative Care
 a. Treatment depends on the acuity of symptoms and
client’s health status
 b. Clients experiencing symptoms are usually treated
with surgical removal of the stones and gallbladder
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
Treatment
 a. Treatment of choice is laparoscopic
cholecystectomy
 b. If surgery is inappropriate due to client condition
 1. May attempt to dissolve the gallstones with
medications
 2. Medications are costly, long duration
 3. Stones reoccur when treatment is stopped
Laparoscopic cholecystectomy
 a. Minimally invasive procedure with low risk of
complications; required hospital stay< 24 hours.
 b. Learning needs of client and family/caregiver
include pain control, deep breathing, mobilization,
incisional care and nutritional/fluids needs
 c. Client is given phone contact for problems
Some clients require a surgical laparotomy (incision inside
the abdomen) to remove gall bladder
 a. client will have nasogastric tube in place post-
operatively and require several days of hospitalization
 b. If exploration of the common bile duct is done with
the cholecystectomy, the client may have a T-tube
inserted which promotes bile passage to the outside as
area heals
Clients with cholelithiasis and cholecystitis prior to surgery

can avoid future attacks by limiting fat intake
Nursing Diagnoses
 a. Pain
 b. Imbalanced Nutrition: Less than body requirements
 c. Risk for Infection
Gallstone Pathogenesis
 Bile contains:
 Cholesterol
 Bile salts
 Phospholipids
 Bilirubin
 Gallstones are formed when cholesterol

or bilirubinate are supersaturated in bile
and phospholipids are decreased
Gallstone Pathogenesis
 Stone formation is:
1. Initiated by cholesterol or bilirubinate super
saturation in bile
2. Continued to crystal nucleation (microlithiais
or sludge formation)
3. And gradually stone growth occur
 Gallstone types
1. Cholesterol
2. Pigment
 Brown
 Black
.
Porcelain gallbladder
.
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
.
Sclerosing cholangitis in a patient with

ulcerative colitis
T-tube placement in the common
bile duct
Placement of a T-tube
Cholendoscopic removal of gallstones
Biliary lithotripsy
.
Operative procedure of laparoscopic Cholecystectomy

Risk Factors for
Gallstones
 Obesity
 Rapid weight loss
 Childbearing
 Multiparity
 Female sex
 First-degree relatives
 Drugs: ceftriaxone, postmenopausal estrogens,
 Total parenteral nutrition
 Ethnicity: Native American (Pima Indian),
Scandinavian
 Ileal disease, resection or bypass
 Increasing age
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
 Biliary colic
 Wax/waning postprandial epigastric/RUQ
pain due to transient cystic duct obstruction
by stone
 No fever, No leukocytosis, Normal LFT

Definitions
 Chronic cholecystitis
 Recurrent bouts of biliary colic leading to
chronic GB wall inflammation/fibrosis.
 No fever, No leukocytosis, Normal LFT

.
 Recurrent inflammatory process due to
recurrent cystic duct obstruction, 90% of
the time due to gallstones
 Overtime, leads to scarring/wall thickening
 Attacks of biliary colic may occur overtime
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
…
Definitions
 Acute cholecystitis
 Acute GB distension, wall inflammation &
edema due to cystic duct obstruction.
 RUQ pain (>24hrs) +/- fever, ↑WBC,

Normal LFT,
 Murphy’s sign = inspiratory arrest
.
 Ultrasound is the first choice for imaging
 Distended gallbladder
 Increased wall thickness (> 4 mm)
 Pericholecystic fluid
 Positive sonographic Murphy’s sign (very specific)
 Nuclear HIDA scan shows no filling of GB

 If U/S non-diagnostic, order HIDA
CT scan
 → denotes the GB
→ wall thickening
►
 ► denotes the
fluid around the
GB
 GB also appears
distended
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

Emphysematous cholecystitis
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
Gallstone
Ileus
Acute acalculous
cholecystitis
 5-10% of cases of acute cholecystitis
 Seen in critically ill pts or prolonged TPN
 More likely to progress to gangrene, empyema

& perforation due to ischemia
 Caused by gallbladder stasis from lack of

enteral stimulation by cholecystokinin
 Emergent operation is needed

 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,
(Charcot’s triad) ↑WBC, ↑LFT,
 Suppurative:
 Persistent RUQ pain + fever + jaundice,

↑WBC, ↑LFT,
 Hepatic encephalopathy or hypotension
may ensue (Reynold’s pentad)
MRCP & ERCP
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
Spectrum of Gallstone Disease
 Symptomatic Cholelithiasis
cholelithiasis
can be a herald
to:
an attack of
Asymptomatic Symptomatic
acute
cholelithiasis cholelithiasis
cholecystitis
 ongoing chronic
cholecystitis
 May also Chronic Acute
resolve calculous calculous
cholecystitis cholecystitis
Porcelain
Gallbladde
 A precancerous
condition
 Needs
cholecystectomy
Treatment
Medical Treatment
 Medical treatment for

 Acute biliary colic attack
 Acute cholecystitis with comorbid diseases
Including:
 GI rest
 NG tube if vomiting
 IV Fluids
 Analgesics (not morphine)
 Antibiotics for cholecystitis (against GNR &
enterococcus)
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
T-tube placement in the common
bile duct
Placement of a T-tube
Cholendoscopic removal of gallstones
Biliary lithotripsy
.
Operative procedure of laparoscopic Cholecystectomy

Pigment stone
Choledocholithiasis
Treatment
 Endoscopic retrograde cholangiopancreatography

(ERCP)
 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
ERCP
endoscopic  .
sphincteroto
my
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
.
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
Cholecystectomy
 Laparoscopic
cholecystectomy standard of
care
 Timing
 Early vs interval operation
 Patient consent
procedure 10%
 Bleeding
 Bile duct injury
 Damage to other organs

Biliary Tract Tumours
Cholangiocarcinoma
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:
 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 = 6,900/yr
 Bile duct cancer = 3,000/yr
 Hepatocellular Ca = 15,000/yr
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
Indications for stent insertion include:
 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 patient’s right side
The puncture is through the
liver
The needle is inserted into
an intrahepatic duct under
Photo on file at Medtronic
LIVER DISEASE
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
Soyer’s 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 function—International 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.
Enterohepatic
circulation
 As a result of enterohepatic circulation,
approximately 95% of bile acids are
actively transported and returned back
to the liver via the portal circulation.
 Bile acids are critical to the

solubilization of intestinal lipids (fatty
acids, monoglycerides, and the fat
soluble vitamins A, D, E, and K).
 After ingestion of food, bile acid

concentration in the portal blood
decreases and inhibition of cholesterol
7-hydroxylase decreases, leading to
increased bile acid synthesis.
 During fasting, high portal bile acid

concentrations inhibit the activity of
this enzyme, thereby downregulating
bile acid synthesis
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


TX
drainage catheters inserted percutaneously
 The catheters can be removed in 1–2 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 50–60 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
MODEL FOR END –STAGE LIVER
DISEASE: THE MELD SCORE
 calculate a patient’s likelihood of dying within three months from

their liver disease.
 In other words under the MELD scoring system - the sickest
patient gets the liver transplant.
 3.8 x log (e) (bilirubin mg/dL) + 11.2 x log (e) (INR) + 9.6 log (e)
(creatinine mg/dL)
 The four MELD levels are:

 greater than or equal to 25
 24-19
 18-11
 less than or equal to 10
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 Joseph’s
node
Laboratory tests
Iron deficiency anemia
Fecal occult blood test

(FOBT)
Tumor markers (CEA, Ca19-9)
Diagnosis
--- biopsy needed for definitive
diagnosis
Detection of early gastric cancer

•In patients with signs and symptoms suggestive of

GC, and/or with compatible risk factors or
paraneoplastic
conditions, the diagnostic procedure of choice could
be
an endoscopic examination
•The diagnostic criteria for early or advanced gastric

cancer under endoscopy are based on the JRSGC
and
Endoscopic features of gastric
cancer
•For reasons of cost and availability, radiography may

sometimes be the first diagnostic procedure
performed
• Classic radiography signs of malignant gastric ulcer

asymmetric/distorted ulcer crater
ulcer on the irregular mass
irregular/distorted mucosal folds
adjacent mucosa with obliterated /distorted area gastricae
nodularity, mass effect, or loss of distensibility
Proximal GC Linitis plastica

Distal GC
Detection of early
gastric cancer
• Endoscopic screening
general population or high risk persons
• Careful observation
Complications
• GI bleeding 5%
• Pylorus/cardia obstruction
• Perforation ulcer type

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
Endoscopic mucosal
resection
AIM OF COMBINATION THERAPY
INCREASED EFFICACY
ACTIVITY SAFETY
Different mechanisms of action Compatible side effects

Different mechanisms of resistance
Side effects of chemotherapy
Alopecia
Mucositis
Pulmonary fibrosis
Nausea/vomiting
Cardiotoxicity
Diarrhea
Cystitis Local reaction
Sterility Renal failure

Myalgia
Myelosuppression
Neuropathy
Phlebitis
Metal stent
Prognosis
•The TNM classification/staging of gastric cancer is
the best prognostic indicator
•The 5 years survival rate depends on the depth of

gastric cancer invasion
•Patients in whom tumors are resectable for cure

also have good prognosis
Prevention
• Eradication of H. Pylori infection in those high risk
population
family history of gastric cancer chronic gastritis with
apparent abnormality (atrophy, IM)
post early gastric cancer resection
gastric ulcer
• Management of dietary risk factor

intake adequate amount of fruits, vegetables
minimize their intake of salty/smoked foods
Prevention
• Tightly follow up those with precancerous condition
• Endoscopic or radiologic screening

Pathology
 Gastric cancer
 Adenocarcinoma
 GIST (gastro-intestinal stromal tumour)
 Carcinoid
 Lymphoma
 other
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, Barrett’s 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 (Troisier’s 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
½ (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 Hodgkin’s 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. Țintoiu
GASTROENTEROLOGY
576
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 LFT’s (but they’re 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
Biliary Tract Disease
.
Overview
 Gallstones
 Biliary tract tumours
Biliary Tract
Part of the digestive
system.
Made up of:
 Intra hepatic ducts
 Exta hepatic ducts
 Gallbladder
 Common Bile Duct

The Gallbladder
Bile:
phospholipids
 Flows from the liver, through the hepatic ducts,
into the gallbladder
 Flows from the cystic duct into the common
bile duct, into the small intestine
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
Gallstones – Frequency
 Gallstone disease is one of the most
common and costly of all digestive
diseases
 9% of those > 60 years
 In USA, 6.3 million men and 14.2 million
women aged 20-74 years have gallbladder
disease
 Incidence of gallstones is 1 million new
cases per year
 Prevalence is 20 million cases in USA
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
 Two main types:
 Cholesterol stones (85%):
 2 subtypes—pure (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.
brown and black.
 Brown stones are made up of calcium bilirubinate
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
Gallstones – Diverse
symptoms
 Abdominal pain
 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
 OGD
(Oesophagogastroduodeno
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
Acute Calculous
Cholecystitis
 Symptoms
 Signs
 Murphy’s sign
 Investigations
 Thickened gallbladder wall, pericholecystic fluid and stones
 OGD (Oesophagogastroduodenoscopy)
 Treatment
 Nil by mouth
 Analgesia
 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.
Empyema / Mucocoele
 Symptoms
 Signs
 Murphy’s sign
 Investigations
 Thickened gallbladder wall, distended gallbladder, pericholecystic fluid, stones
 Treatment
 Nil by mouth
 Analgesia
 Cholecystectomy
Obstructive Jaundice
 Blockage of the biliary tree by gallstones
 Symptoms
 Pain, Jaundice, dark urine, pale stools
 Signs
 Jaundice.
 Investigations
 Bloods – U&E, FBC, LFT, Amylase, CRP,
Hepatitis screen, Coagulation screen
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
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
 MRCP
 CT Pancreas
 Treatment
 Supportive
Gallstone ileus
 Obstruction of the small bowel by a large gallstone
 A stone ulcerates through the gallbladder into the duodenum and
causes obstruction at the terminal ileum
 Symptoms
 Small bowel obstruction (vomiting, abdominal pain, distension, nil pr)
 Signs
 Abdominal distension, obstructive bowel sounds.
 Investigations
 Bloods – U&E, FBC, LFT, Amylase, CRP, Hepatitis screen, Coagulation
screen
 Plain film of abdomen – Air in CBD, small bowel fluid levels and stone
 Treatment
 Laparotomy and removal of stone from small bowel.
Cholecystectomy
 Laparoscopic
cholecystectomy
standard of care
 Timing
 Early vs interval
operation
 Patient consent
procedure 10%
 Bleeding
Mirizzi Syndrome
 Refers to common hepatic duct
obstruction caused by an extrinsic
compression from an impacted stone in
the cystic duct
 Estimated to occur in 0.7-1.4% of all
cholecystectomies
 Often not recognized preoperatively, which
can lead to significant morbidity and biliary
injury, particularly with laparoscopic
surgery.
Acute Acalculous
Cholecystitis
 Presence of an inflamed gallbladder in the absence of an
obstructed cystic or common bile duct
 Typically occurs in the setting of a critically ill patient (eg,
severe burns, multiple traumas, lengthy postoperative care,
prolonged intensive care)
 Accounts for 5% of cholecystectomies
 Aetiology is thought to have ischemic basis, and gangrenous
gallbladder may result
 Increased rate of complications and mortality
 An uncommon subtype known as acute emphysematous
cholecystitis generally is caused by infection with clostridial
organisms and occlusion of the cystic artery associated with
atherosclerotic vascular disease and, often, diabetes.
Primary Sclerosing
Cholangitis
 Chronic cholestatic biliary disease characterized by non-
suppurative inflammation and fibrosis of the biliary ductal
system
 Cause is unknown but is associated with autoimmune
inflammatory diseases, such as chronic ulcerative colitis and
Crohn colitis, and rare conditions, such as Riedel thyroiditis
and retroperitoneal fibrosis
 Most patients present with fatigue and pruritus and,
occasionally, jaundice
 Natural history is variable but involves progressive destruction
of the bile ducts, leading to cirrhosis and liver failure
 Clinical features of cholangitis (ie, fever, right upper quadrant
pain, jaundice) are uncommon unless the biliary system has
been instrumented.
Primary Sclerosing
Cholangitis
Medical Care
 Chronic progressive disease with no curative medical therapy
 Goals of medical management are to treat the symptoms and
to prevent or treat the known complications
 Liver transplantation is the only effective therapy and is
indicated in end-stage liver disease.
Surgical Care
 Indications for liver transplantation include variceal bleed or
portal gastropathy, intractable ascites, recurrent cholangitis,
progressive muscle wasting, and hepatic encephalopathy.
 Recurs in 15-20% of patients after transplantation.
Primary Biliary Cirrhosis
 Progressive cholestatic biliary disease that presents with
fatigue and itching or asymptomatic elevation of the alkaline
phosphatase.
 Jaundice develops with progressive destruction of bile ductules
that eventually leads to liver cirrhosis and hepatic failure.
 Autoimmune illness has a familial predisposition
 Antimitochondrial antibodies (AMA) are present in 95% of
patients
 Goals of treatment are to slow the progression rate of the
disease and to alleviate the symptoms (eg, pruritus,
osteoporosis, sicca syndrome)
 Liver transplantation appears to be the only life-saving
procedure.
Biliary Tract Cysts
 Consist of cystic dilatations of
the extra-hepatic biliary tree
 Uncommon abnormality
 50% present with combination
of jaundice, abdominal pain,
and an abdominal mass.
 ? Due to anomalous union of
the pancreatic and biliary ductal
system.
Biliary Tract Tumours
Cholangiocarcinoma
Cancer of the Gall Bladder
Biliary Tree Neoplasms
 Clinical symptoms:
• Fever (21%)
 Weight loss (77%) • Malaise (19%)
 Nausea (60%) • Diarrheoa (19%)
• Constipation (16%)
 Anorexia (56%)
• Abdominal fullness (16%).
 Abdominal pain (56%)
 Fatigue (63%)
 Pruritus (51%)
 Symptomatic patients usually have

advanced disease, with spread to hilar
lymph nodes before obstructive jaundice
Cholangiocarcinoma
 Adenocarcinoma of the bile ducts
 May occur without associated risk factors
 Associated with chronic cholestatic liver
disease such as:
 Asbestos.
 Accounts for 25% of biliary tract cancers

 Presentation:
Cholangiocarcinoma
 Slow growing malignancy of biliary tract
which tend to infiltrate locally and
metastasize late.
 Gall Bladder cancer = 6,900/yr
 Bile duct cancer = 3,000/yr
 Hepatocellular Ca = 15,000/yr
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
MRCP: Cholangiocarcinoma at the Bifurcation
Klatskin tumour = Cholangiocarcinoma of junction of right & left

hepatic ducts
ERCP: Distal CBD Cancer
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
Gallbladder Cancer
 Uncommon malignancy
 2.5 per 100,000 population
 Represents 54% of biliary tract cancers.
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%
Gall Bladder Cancer
Presentation 2
 RUQ pain, jaundice, weight loss: CT

 Biopsy yields adenocarcinoma consistent
with GB primary
 Biliary Decompression
 Chemo/Radiation
 Median survival with chemoradiotherapy is
9 months.
Biliary Stricture
Biliary stricture is an abnormal

narrowing of the bile duct.
Among biliary strictures:
90% are malignant
Pancreatic cancer is the most
common malignant cause, followed
by cancers of the gallbladder, bile
duct, liver, and large intestine.
Biliary Stricture – Non Cancerous
Causes
Noncancerous causes of bile duct stricture include:
 Injury to the bile ducts during surgery for
gallbladder removal (accounting for 80% of
nonmalignant strictures)
 Pancreatitis (inflammation of the pancreas)
 Primary sclerosing cholangitis (an inflammation
of the bile ducts that may cause pain, jaundice,
itching, or other symptoms)
 Gallstones
 Radiation therapy
 Blunt trauma to the abdomen
Biliary Stricture – Patient
Symptoms
Patients with biliary strictures may present

with:
Jaundice (yellow skin color)
Abdominal pain
Fever
Vomiting
Biliary Stricture – Diagnostic
Tests
Common diagnostics for biliary stricture are:
 Ultrasound
 CT
 MRI
 Biopsy
 Cholangiography
A cholangiogram is an X-ray of the bile
ducts
 Can be performed:
 Endoscopically
 Percutaneously
Cholangiogram- Endoscopic
Approach
Endoscopic retrograde
cholangiopancreatography
(ERCP)
 Endoscopic tube is placed into
the patient’s mouth, through the
stomach, and into the duodenal
portion of the small intestine.
 Contrast is introduced into the
biliary tract through the
endoscope, in a retrograde
manner.
 X-rays taken.
Indications For Biliary Stenting
Indications for stent insertion include:
 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 patient’s right side
The puncture is through the
liver
The needle is inserted into
an intrahepatic duct under
Photo on file at Medtronic
Biliary Stent - Percutaneous
Approach
Success rate of percutaneous transhepatic cholangiography approaches
95% when ducts are dilated.
Percutaneous approach associated with a 5-10% rate of major

complications which include:
Sepsis
Bile leak
Intraperitoneal haemorrhage
Haemobilia
Hepatic and perihepatic abscess
Pneumothorax
Skin infection and granuloma at the catheter entry site.
Percutaneous transhepatic cholangiography is contraindicated in patients
with bleeding diatheses and significant ascites.
Summary
 Gallstones
 In the gallbladder • In the bile ducts
 Biliary colic • Obstructive jaundice
 Acute and chronic cholecystitis • Pancreatitis
 Empyema
 Mucocoele • Cholangitis
• In the Gut
 Biliary
tract tumours • Gallstone ileus
Definition

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Curs-Gastroenterologie Final - 1 Martie 2017

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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. Burn’s EGD showing erosive

On the right a small hiatal hernia is demonstrated.

…and does that lead to decreased

• In patients with multiple risk

Response to Chronic Tissue Injury

Stratified Squamous Specialized Intestinal

• 2014 Estimate: 0.25% per year

• PPIs are the most effective medical

Intensive endoscopic surveillance

Endoscopic mucosal resection

• EMR of mucosal irregularities for

• Ablate the remaining Barrett’s metaplasia to minimize

Cancer of the cardia

Cancer of the cardia II

T2-T4 None considered curable by endoscopic therapy.

 requires wide incision and drainage, not repair

 1/3 develop stricture --> I&D (not repair)

 20 to 40 Gy over 2 - 4 weeks (1.75 to 3.75 Gy/fx)

 improved local recurrence rates in node

 Pre-operative chemo (Cisplatin, 5-FU)

 No change in local recurrence rates or

 What is ideal delay to surgery?

 Pre-op chemoradiation (cisplatin/5-FU)

 Surgical salvage following CRT alone

 Histologic response -- not avail. without resection

 Future: biologic serum markers ?

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)