Professional Documents
Culture Documents
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
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!
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
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)
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
calcifications
enteroclysis
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 cancer
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
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
LES diabetes
achalasia Parkinson’s
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
,
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
111
Type I Hiatal Hernia the
most common.
The E-C junction moves through the hiatus
to the visceral mediastinum.
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
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
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?
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
GERD
Reflux
Esophagitis
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
~6%
per
year
High Grade Dysplasia Cancer
4.
Management Options for High-Grade
Dysplasia in Barrett’s Esophagus
Endoscopic ablation
Esophagectomy
Radiofrequency Ablation of
Barrett’s Esophagus
Ablated
Barrett’s
Metaplasia
Endoscopic Therapy for Mucosal Neoplasia
In Barrett’s Esophagus 2014
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
Adenocarcinoma of
the I
distal esophagus
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
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
Toxicities
myelotoxicity if Mitomycin C, etoposide, vinblastine
added
Average results, not controlled by delay to
surgery
Esophageal CA --
chemoradiation
Surgery:
16.5 months
Radiotherapy and Chemotherapy
14.5 months
Surgery, Radiotherapy,
Chemotherapy
16-18.6 months
Gastrostomy/ Jejunostomy (GJ)
Percutaneous Endoscopic
1
Lymphangioma
Hemangioma
Fibrovascular Polyps
Granular Cell Tumors
Adenomas
Papillomas
Esophageal Duplication Cysts
Lipomas, Leiomyomas, Desmoid Tumors,
Schwannomas
Lymphangioma
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
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
multifactorial
reduced nutrition
loss of weight
Complications:
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:
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
Zeman, M. et al., Speciální chirurgie, ISBN 80-7262-260-9, 2004
Billroth II
Zeman, M. et al., Speciální chirurgie, ISBN 80-7262-260-9, 2004
Gastro-enteroanastomosis on
Roux Y crankle
Zeman, M. et al., Speciální chirurgie, ISBN 80-7262-260-9, 2004
Vagotomy
Complications after stomach resection:
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
4-methylhistamine 4-methylhistamine
Conformation I Conformation II
Na -Guanylhistamine
First partial agonist
First signs of antagonistic activity
Still allows partial conformational change
Na –Guanylhistamine
Carbon chain lengthened
Two-carbon chain, speculation of a carboxylate
binding region
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
often asymptomatic
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
CANCERUL GASTRIC –
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
CANCERUL GASTRIC –
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
CANCERUL GASTRIC –
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
C. Diagnostic laparoscopy
Laboratory tests
Endoscopic diagnosis
--- biopsy needed for definitive
diagnosis
Radiologic diagnosis
Gastric Cancer
Gastric Ulcer
CANCERUL GASTRIC –
Diagnostic paraclinic:
Endoscopia
CG avansat:
1 – CG tip protruziv
2 – CG tip ulcerat
3 – CG tip infiltrativ
3
CANCERUL GASTRIC –
Diagnostic paraclinic:
Endoscopia
CG incipient (superficial - care prinde doar
mucoasa 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%
CANCERUL GASTRIC –
Diagnostic paraclinic
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
CANCERUL GASTRIC –
Diagnostic paraclinic
Ecografia transabdominală :
Metastaze hepatice
Adenopatii perigastrice
Therapy:
EMR
Adjuvant therapy
Palliative
therapy
Endoscopic mucosal
resection
Gastric cancer
lesion confined
to mucosa layer
peptic ulcer
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
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.
Gallstones – Types
Pigment stones (15%) occur in 2 subtypes—
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
Jaundice
Pruritus:
Fatigue
Weight loss
Miscellaneous:
Gas
Bloating
Dyspepsia
Complications of
Gallstones
In the gallbladder
Biliary colic
Acute and chronic cholecystitis
Empyema
Mucocoele
Carcinoma
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
Ultrasound of abdomen
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
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
Ultrasound of abdomen
Thickened gallbladder wall, distended gallbladder, pericholecystic fluid, stones
Treatment
Nil by mouth
Analgesia
Intravenous antibiotics
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
Ultrasound of abdomen
Treatment
Intravenous antibiotics
Endoscopic Retrograde CholangioPancreatogram
Acute Pancreatitis
Acute inflammation of pancreas and other retroperitoneal tissues.
Symptoms
Severe central abdominal pain radiating to back, vomiting
Signs
Variable – None to Sepsis (Fever, tachycardia, low BP), Jaundice, acute
abdomen
Investigations
Bloods – U&E, FBC, LFT, Amylase, CRP
Ultrasound of abdomen
MRCP
CT Pancreas
Treatment
Supportive
Endoscopic Retrograde CholangioPancreatogram
Cholecystectomy
Laparoscopic
cholecystectomy standard of
care
Timing
Early vs interval operation
Patient consent
Conversion to open
procedure 10%
Bleeding
2. Pathophysiology
a.Gallstones form due to
2.Biliary stasis
3.Inflammation of gallbladder
.
Gall Stones
Gallbladder Disorders
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
Gallbladder Disorders
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
Gallbladder Disorders
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
Gallbladder Disorders
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
Nursing Diagnoses
a. Pain
b. Imbalanced Nutrition: Less than body requirements
c. Risk for Infection
Gallstone Pathogenesis
Bile contains:
Cholesterol
Bile salts
Phospholipids
Bilirubin
Porcelain gallbladder
.
◄
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
.
Biliary colic
by stone
Chronic cholecystitis
Recurrent bouts of biliary colic leading to
chronic GB wall inflammation/fibrosis.
Acute cholecystitis
Acute GB distension, wall inflammation &
edema due to cystic duct obstruction.
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
Perforated gallbladder
Pericholecystic abscess (up to 10% of
acute cholecystitis)
Percutaneous drainage in acute phase
Emergent Laparotomy
Complications of acute
cholecystitis
Chronic perforation into adjacent viscus
(cholecystoenteric fistula)
Air is seen in the biliary tree
(gallstone ileus)
Non-suppurative
Non suppurative:
Persistent RUQ pain + fever + jaundice,
(Charcot’s triad) ↑WBC, ↑LFT,
Suppurative:
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
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
Perforation occurs in 10-15% of cases.
Cholecystectomy
Laparoscopic
cholecystectomy standard of
care
Timing
Early vs interval operation
Patient consent
Conversion to open
procedure 10%
Bleeding
Asbestos.
Jaundice
Weight loss, anorexia, abdominal pain,
fever
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)
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
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)
The central lobar veins of the acini drain into larger segmental and
sectorial veins before forming the main hepatic veins.
The volume of bile secreted in an adult ranges from 500 to 1000 mL/24 h.
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.
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.
Hepatocytes
Cirrhosis
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
Fine-needle aspiration
minimal criteria
disease confined to the liver
disease amenable to a complete resection.
For small and peripherally placed lesions, sublobar,
segmental resections are preferred
Direct invasion
Blood spread
Intraperitoneal colonization
Sister Mary Joseph’s
node
Laboratory tests
Endoscopic diagnosis
--- biopsy needed for definitive
diagnosis
Radiologic diagnosis
• Careful observation
Complications
• GI bleeding 5%
• Pylorus/cardia obstruction
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
Alopecia
Mucositis
Pulmonary fibrosis
Nausea/vomiting
Cardiotoxicity
Diarrhea
Cystitis Local reaction
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
Performance status
Physiological assessment
Cardio-pulmonary function
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%
A. Benign Tumours
B. Malignant Tumours
THE BENIGN TUMORS:
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:
C. Diagnostic laparoscopy
TREATMENTS OF GASTRIC CANCER:
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.
peptic ulcer
Lundgren Infect Immun 2005; Freire de Melo, Microbes Infect 2012; Kido, BBRC 2011
H. pylori and mutagenesis
Touati, Gastroenterology 2003; Helicobacter 2006; Sheh, PNAS 2010; Machade, BBA 2010; CCR 2009
Pathological outcome of H pylori
host response
susceptibility
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
• 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
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
lactoferrin
Goturk, Am J Med Sci 2011; Bekar J Med Food 2011; Niv, WJG 2008
What to do in case of high risk
(after eradication)?
LECTURE IV
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
Total Bilirubin
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
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 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
Cholangitis
Biliary Colic
Symptoms
Right upper quadrant pain
Signs
Usually none
Investigations
Bloods – U&E, FBC, LFT,
Amylase, CRP
Ultrasound of abdomen
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
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
Ultrasound of abdomen
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
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
Ultrasound of abdomen
Thickened gallbladder wall, distended gallbladder, pericholecystic fluid, stones
Treatment
Nil by mouth
Analgesia
Intravenous antibiotics
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
Ultrasound of abdomen
Treatment
Intravenous antibiotics
Endoscopic Retrograde CholangioPancreatogram
Acute Pancreatitis
Acute inflammation of pancreas and other retroperitoneal tissues.
Symptoms
Severe central abdominal pain radiating to back, vomiting
Signs
Variable – None to Sepsis (Fever, tachycardia, low BP), Jaundice, acute
abdomen
Investigations
Bloods – U&E, FBC, LFT, Amylase, CRP
Ultrasound of abdomen
MRCP
CT Pancreas
Treatment
Supportive
Endoscopic Retrograde CholangioPancreatogram
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
Conversion to open
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
Choledochal 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%)
Asbestos.
Jaundice
Weight loss, anorexia, abdominal pain,
fever
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)
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