Med3C Cham – Prelim Topics Gastro 3a

Course: Gastroenterology
Week: 1-5
Lect urer: Dra. Cham
Topic: Esophagus & Stomach
Source: L ecture

Stomach ..................................................... 6
Table of Contents
Esophagus ...................................................1
2 Major functions ...................................................... 1
2 esophageal sphincters .............................................. 1
Esophageal Diseases .......................................... 1
Symptoms ................................................................. 1
Diagnostic Tests ........................................................ 1
Esophageal Motor Disorders ...................................... 2
GERD ...................................................................... 3
Barrett’s Esophagus ................................................... 3
Esophageal Carcinoma .............................................. 4
Diverticula ................................................................ 4
Webs and Rings ......................................................... 5
Hiatal Hernia ............................................................ 5
Mallory-Weiss Syndrome........................................... 5
Foreign Body in Esophagus ....................................... 5
Caustic Ingestion ....................................................... 5
Esop hagus
2 Major functions 2 esophageal sphincters
• Transport of food from mouth to 1) Upper sphincter
stomach -­‐ Elastic wall
• Prevent backflow of GI contents -­‐ Tonic contraction
o Cricopharyngeus m.
o Inf pharyngeal m.
Gastritis .........................................................6
Acute Gastritis .......................................................... 6
Chronic Gastritis ....................................................... 6
Upper GI Bleeding .............................................7
Peptic Ulcer Disease ................................................. 7
Zollinger-Ellison Syndrome ....................................... 9
Gastric Adenocarcinoma .....................................9
Stomach Cancer Types .............................................. 9
GAC Major Environmental Risk Factors ................... 9
High Risk Factors for GAC ....................................... 9
GAC Precursors ........................................................ 9
GAC Clinical Features .............................................. 9
GAC Dx ................................................................... 9
GAC Management.................................................... 9
2) Lower sphincter
-­‐ Intrinsic myogenic tone
o Pre-ganglionic vagus n.
o Post-ganglionic nerve

ESOPHAGEAL DISEASES

Symptoms Diagnostic Tests

1. Dysphagia – difficulty swallowing 1. Radiologic studies
a. Determine if motility problem or obstruction -­‐ Most widely used
b. Can liquid or solid pass through? -­‐ Evaluates structural and motor disorder
2. Heartburn or pyrosis o Ba swallow with fluoroscopy
a. Most common sx for reflux esophagitis o Esophagogram
(Bernstein test)
3. Odynophagia
2. Esophagoscopy (upper endoscopy)
a. Barrett’s ulcer, esophageal Ca, perforation -­‐ Direct visualization method of diagnosis
4. Atypical chest pain -­‐ Biopsy and brush biopsy
a. Influx esophagitis, DES, Ca, PUD 3. Esophageal motility
5. Regurgitation -­‐ Record esophageal pressure
a. Achalasia, large diverticula, severe GE reflux -­‐ Catheter connected to Pressure transducer – records
pressure to dx achalasia, spasms, etc.
-­‐ Dx of achalasia, DES, scleroderma

Lecture 1 mra
Med3C Cham – Prelim Topics Gastro 3a

Esophageal Motor Disorders

3 parts – upper (striated), middle (mixed), lower (smooth)

A. Striated Muscles – Proximal 3rd

1)  Pharyngeal  paralysis   2)  Cricopharyngeal  achalasia   3)  Globus  pharyngeus  
-­‐ Dysphagia – solids and -­‐ Failure of CP Muscle to relax -­‐ Constant bump on throat
liquids -­‐ Causes Hypertensive -­‐ Usually females, middle age
-­‐ Nasal regurgitation pressure (40s)
-­‐ Tracheobronchial aspiration -­‐ Swallowing -­‐ No difficulty in swallowing
complication -­‐ Prominent BAR on post -­‐ Hypertensive upper
-­‐ Seen in CVA/Stroke pharyngeal wall on Ba sphincter
swallow (see image) -­‐ Have probably already
consulted
-­‐ Tx: none, reassurance,
endoscopy to show to pt,
muscle relaxants and maybe
anxiolytics

B. Smooth muscles – Distal 3rd

  1)  Achalasia   2)  Diffuse  esophageal  spasm  (DES)   3)  Scleroderma  involving  the  
esophagus  
Pathophys Hypertensive LES (↑pressure) Not known Weak lower esophagus 2/3
S/Sx • Dysphagia, chest pains, • Multiple, spontaneous continuation • Thin and atrophic esoph wall
regurgitation • Swallow induced continuation w/ patchy fibrosis
• Classic achalasia – • Large amplitude • Hypotensive LES will be wide
simultaneous continuation open
of small amplitude
• Vigorous achalasia –
simultaneous continuation
of large amplitude
Dx • (-) Peristalsis in distal 2/3 • Corkscrew esophagus (Ba swallow), • Patulous LES
• Beak-like narrowing of curlings, multiple ripples, sacculations, • Ba swallow: dilated and (-)
terminal part pseudodiverticulum continuation of middle and
distal esoph

Bird’s Beak
Cork Screw

Tx • Balloon dilatation of LES

• Surgery: Heller’s
extramucosal myotomy
• SMRs: Ca channel blockers
and Nitrates

Lecture 2 mra
Med3C Cham – Prelim Topics Gastro 3a

GERD 1) Strictures – from fibrosis d/t recurrent esophagitis

• Esophageal mucosal damage d/t reflux of gastric and 2) Esophageal ulcers and bleeding
intestinal contents 3) Pulmonary manifestations
a. Chronic cough
b. Laryngitis
GERD Pathophysiology (need to know character of reflux) c. Aspiration pneumonia
1. Esophagus reflux episode d. Hoarseness
a. GI contents ready to reflux 4) Barrett’s esophagus – squamous to columnar epithelium
b. Compromised anti-reflux mechanism of LES (metaplasia)
2. Cumulative or net esophageal reflux
a. Amount of refluxed material / episode
b. Frequency of refluxed episode
GERD Treatment
c. Rate of esophageal clearing 1.  Dietary  and  lifestyle  changes  
d. Neutralization of gastric acid • Weight reduction
• Elevation of head (4-6”) while sleeping
GERD Etiology • Avoid smoking, fatty foods, alcohol, caffeine containing
drinks and foods
• Weak or defective sphincter
• No food 3-4h prior to sleep – allows complete digestion
• Transient LES relaxation
• Avoid overeating or drinking
• Hiatal hernia
• Avoid tight belts and girdles which increases abdominal
• Poor acid clearance from esophagus
pressure
• ↓Salivary flow
• Lie of the left lateral position
• ↑Acid production
• Delayed gastric emptying of solids 2.  Pharmacologic  therapy  
• Obstructive sleep apnea • Antacids
• H2 blockers – ↓gastric acid output
st
Factors affecting LESP • Proton pump inhibitors - 1 line of therapy
o Inhibit acid secretion for 19-24h
↑LESP ↓LESP o ↑Gastric pH >4 or 5
Gastrin Secretin • Drugs that ↑LES pressure and esophageal clearance
Pitressin Cholecystokinin o Metoclopromide, Demperidone, Cisapride
Angiotensin II Glucagon, VIP • Enhance mucosal resistance
Cholinergics Fatty meals o Sucralfate, PG Analog (Misoprostol)
Gastric alkalization PG (Birth control pills)
Metoclopromide Theophylline Barrett’s Esophagus
Anticholinesterase Caffeine content • Assoc w/adenocarcinoma
Smoking • Requires endoscopic and patho criteria for dx
• Endoscopy: Salmon-colored mucosa
Gastric distention
• Bx: Intestinal metaplasia with goblet cells
Belching reflex
• Make sure not to biopsy at Z line – go above
where you see salmon colored mucosa
GERD Clinical manifestations: • Can lead to strictures peptic ulcerations and
• Heartburn (pyrosis) – most common, sometimes adenocarcinoma
mistaken for heart attack
• Dysphagia - ~d/t peptic stricture Types of BE
• Regurgitation – d/t delay in gastric emptying
1. Long segment BE - > 3cm from GE junction
• Odynophagia
2. Short segment BE - < 3cm from GE junction
• Chest pains
• LSBM >> SSBM malignant component gastric cardia
• Water brash – hyper-salivation; clear slightly salty fluid
intestinal metaplasia
due to response of salivary gland to GER
o Metaplasia w/GCs at Z line = NOT Barrett’s
• Weight loss
• Hemorrhage
Risk Factors for BE
GERD Diagnosis: • Advancing age – mean age: 63 yo
1) Prescription acid suppression trial – 2 weeks o LSBE rare in children
a. If pt improves it is likely GERD • M: F = 2:1
2) Ba swallow and esophagogram • Reflux sx – seen among GERD
3) Endoscopy with mucosal biopsy • White race – LSBE
a. Rule out - Barrett’s, Ca, reflux esoph • Rare in Japan
4) Manometry
5) Bernstein tests - provoke s/sx with acid Complications of Barrett’s Esophagus
6) 24g pH monitoring of esophagus • Structures
7) GE scintiscan - rarely used • Peptic ulceration
• Adenocarcinoma
GERD Complications:
Lecture 3 mra
Med3C Cham – Prelim Topics Gastro 3a

LA Classification of Esophagitis
Grade Mucosal Breaks Description
A 1+ <5mm
B 1+ >5mm but not continuous btwn tops of 2 mucosal folds
C Continuous btwn tops of 2+ mucosal folds <75% of circumference
D Mucosal breaks involving >75% of circumference

Barrett's esophagus. A. Pink tongues

of Barrett's mucosa extending
proximally from GEJ. B. Barrett's
esophagus with a suspicious nodule
(arrow) identified during endoscopic
surveillance. C. Histologic finding of
intramucosal adenocarcinoma in
resected nodule.

Esophageal Carcinoma Esoph Ca Diagnosis:

• 90% is squamous cell carcinoma 1. Barium swallow – irregular luminal narrowing
o Due to smoking a. Difficult to differentiate from benign peptic
o ↑Alcohol intake stricture
o Plummer-Vinson syndrome 2. Endoscopy: Retro-flexion biopsy and brushing
o Achalasia 3. CT Scan: Extent and spread
o Tylosis 4. EUS: Most accurate method for extent and depth
o Lye stricture 5. MRI: Better than CT to see infiltrating growth
• 10% is adenocarcinoma 6. Exfoliative cytology
o Extension from gastric cardia Ca
o Barrett’s esophagus Esoph Ca Treatment:
• M: F Ratio = 2:1 1. Surgery – mainstay
a. Procedure of Choice: Total
esophagectomy
2. Radiation therapy
a. Sq. Cell Ca – unsatisfactory
b. Pre-surgical radiation tx = ↑cure rate
c. AdenoCa: resistant
3. Other palliative measures
a. Mechanical dilatation
Esophageal Adenocarcinoma with Barrett’s esophagus b. Tube placement
c. Yag-laser treatment
Esoph Ca Predisposing factors:
• Chronic alcohol and smoking Esoph Ca Prevention and Surveillance
• Lye structure • Stop smoking, alcohol in moderation
• Achalasia Recurrent GERD à EGD with biopsy for Barrett’s
• Previous exposure to ionizing radiation esophagus
• Head and neck Ca Low grade à Annual EGD
• Plummer Vinson syndrome dysplasia
• Tylosis (+) Barrett’s à Biannual EGD
• Barrett’s esophagus esoph
High grade à Esophagectomy
Esoph Ca Clinical manifestations: dysplasia
• Progressive dysphagia 90%
• Anorexia and weight loss 75% Diverticula
• Odynophagia 50% • Outpouching of the pharyngeal wall
• Substernal pains Zenker’s weak posterior hypopharyngeal wall
• Hoarseness – recurrent laryngeal involvement = halitosis and regurgitation
• Iron deficiency anemia Epiphrenic assoc with achalasia; usually asx
• Aspiration
diverticula
Midesophageal c/b traction from old adhesions or
by propulsion
diverticula
Lecture 4 mra
Med3C Cham – Prelim Topics Gastro 3a

Webs and Rings Foreign Body in Esophagus

1) Plummer-Vinson Syndrome • Above the upper esoph sphincter – airway obstruction
-­‐ Hypopharyngeal web • Most above benign or Ca stricture
-­‐ Iron deficiency anemia • Sharp objects (fish or chx bones, pins, toothpicks) =
-­‐ Middle aged women perforation, sepsis and hemorrhage
• >15mm impacted = necrosis, perforation & hemorrhage
2) Schatzki ring
-­‐ LE ring
-­‐ Thin-web like const’n at sq-co junction near LES
FB Clinical Manifestations
• Sub-sternal pains – may mimic MI
3) Lower esophageal mucosal ring • Profuse salivation
-­‐ Contractile ring • Regurgitation
-­‐ Proximal to the site of mucosal ring • Odynophagia
• Sensation of object lodge in esophagus
Hiatal Hernia • Crepitus of neck and upper thorax – subQ air
• Herniation of part of stomach through hiatus in diaphragm
o Sliding HH – GE junction and fundus of stomach FB Diagnosis
slide upward 1. Plain X-Ray – radio-opaque objects
o Paraesophageal HH – Pouch of stomach 2. X-ray with contrasts – water-soluble dye (wood, Al, glass)
herniated beside GEJ thru esoph hiatus 3. Endoscopy – direct (under sedation)

Mallory-Weiss Syndrome FB Management

• Mucosal tear precipitated by vomiting and retching prior
IV Glucagon Relaxes esoph
to hematemesis
• Dx via endoscopy Upright To avoid aspiration
• Bleeding – stops simultaneously; bipolar electrocautery or position, NGT
epi inj (continue bleeding) Papain Enzymatic digestion of meat bolus; may
digest esoph wall à perforation & aspiration
Endoscopy Snares, forceps and baskets
Surgery If sharp object imbedded

Caustic Ingestion
Alkali – Lye, KOH CI Management:
• Liquefaction necrosis • Maintain on NPO
• Deep penetration – full thickness burn • TPN
• Critical ph • IV H2 Blocker or PPI
o 12.5 à ulceration • Antibiotics for serious infection
o 14 à stricture (Lye) • Surgery in extensive tissue necrosis, perforation,
Acid – HCl, Sulfuric, Sodium Bisulfate peritonitis and severe hemorrhage
• Coagulation necrosis
• Eschar – protective (limit deep tissue injury) CI Complications:
• Shallow burn esoph; worse if in antrum • Severe hemorrhage
• Esoph and gastric Va dev in scarred mucosa 10-15y after • Perforation
• Peritonitis
CI Diagnosis • Inferior Mediastinitis
1. Barium or soluble contrast studies - not accurate • Stricture – noted in 2-8 weeks after
a. After 1-2months extent of fibrosis and stricture o Tx: dilatation – after acute injury heals
2. Endoscopy o Surgery: for severe strictures
a. w/in 24h of digestion
b. Remove by suction remaining substance
3. Serial plain abdomen and chest XR = perforation

Classification of Tissue Injury and Management

Description Management
Grade 0 Normal Heals w/ no specific therapy
Grade I Edema and hyperemia of mucosa
Grade IIA Friable, hemorrhage, erosions, blisters, whitish membrane or exudates, Some recovers and discharge in 5-12 days
superficial ulcers Healing in 3-4 weeks
Grade II B Grade II A plus deep discrete ulcers Some with scarring
Grade III A Grade II + multiple ulcers, necrosis (areas of blown black or grayish Most w/complications - bleeding and
discolor) perforation
Grade III B Grade II + Extensive necrosis Requires surgery

Lecture 5 mra
Med3C Cham – Prelim Topics Gastro 3a

Sto mach
GASTRITIS
• Inflammation of gastric mucosa o CMV, herpes, MTb, candida – in
• Diffuse or localized immunocompromised
• 2 types of gastritis
o Acute – usually self limited AG Clinical features
o Chronic – superficial lymphocytic infiltrates • “Dyspepsia” – any discomfort in the epigastrium
in the lamina propria o GI upset
§ Chronic type A o May feel nausea or Indigestion even leading
§ Chronic type B to vomiting
o Dysphagia
Acute Gastritis • Epigastric pain – burning; most common
Etiology of Acute Gastritis • GI bleeding – may be severe; hematemesis or melena
• Drugs – aspirin, NSAIDs
o Especially seen in the elderly AG Diagnosis
• Caustic substances ingestion • Endoscopy (EGD) w/ or w/o biopsy
o Strong alkali and acid o Test for H. pylori
o Suicide attempt
• Stress AG Treatment
o Related to severe illness 1) Medical: Antacids, PPI, H2A – neutralize the acidity
o ICU patients – Sepsis, CVA, elderly pts 2) Surgery
• Infections a. Rarely necessary
o H. pylori – most significant b. Unless there is severe bleeding
o Phlegmonous gastritis – bacterial invasion
of stomach wall esp Grp B strep; rare but
fatal
Images: Terms to describe types of injury, more than one term can be applied
Erosive gastritis Pan gastritis Radial gastritis

Chronic Gastritis
Etiology of chronic gastritis Helicobacter  pylori  
• Gram (-), microacrophilic curved bacillus
• Prolongation use of alcohol, aspirin and NSAIDS
• Motile, flagella
• Radiation or thermal injury
• Predisposition to human gastric mucosa
• Immunologic factors
• 92% in active chronic gastritis (type B)
• Infections (H. pylori)
o 88 – 100% in DU
o 58 – 100% in GU
o 46 – 94% among gastric Ca
• Live beneath the mucus layer
• Ability to pro urease (normally found in stomach)
• (+) Bx for Hp – main choice for dx
o Usually in antrum – site for biopsy
o Best at the margins but if you suspect
diffuse chronic gastritis get additional
samples from greater and lesser curvature
• (+) Urea breath test (C13 and C14)
o If endoscopy is not available

Lecture 6 mra
Med3C Cham – Prelim Topics Gastro 3a

Types of chronic gastritis

Chronic  type  A   Chronic  type  B  
• Fundus and body • Antrum – major site
• Antrum is spared • Body and fundus relatively spared
• Pernicious anemia • Reflux of duodenal and biliary secretions
• Assoc parietal cell Ab • (+) Gastrin Ab
• ↑Serum gastrin • Normal acid level
• Associated hypochlorydia, achlorydia • Most associated with
• More associated with chronic problems - DM, vitiligo o infection - (+) H. pylori
and hypothyroidism o malignancies - GU, atrophy and gastric Ca

Other  types  of  gastritis  

Eosinophilic gastritis
• Infiltration of antrum and SI
(duodenum) with eosinophils
• Immune-mediated
• If long-standing à thickening of
intestinal wall and antral
obstruction
• Tx: steroids, PPIs
Granulomatous gastritis Hypertrophic gastritis
• Infiltrative disease with non- • Uncommon
caseating granuloma • Massive enlargement of gastric
• Gastric outlet obstruction is folds
common • Menetrier’s disease is severe
• Tx: steroids and surgery form
• Dx: EGD with biopsy
• Tx: PPI, steroids, surgery

UPPER GI BLEEDING

Keep NGT
for (-) Active Remove
Clear several bleeding NGT Endoscopy
hours

Melena or Angiogram
Hematemesis NGT
Non-
Saline diagnostic
irrigiation
– Surgery
Bleeding
(+) bleeding stops EGD
rapidly,
clears
stomach Specific
Diagnostic Rx ?

• Hematemesis
• Melena Peptic Ulcer Disease
• Do NGT • Disorders/ulcers/problems of upper GIT
o Distinguish upper and lower GI bleeding o Upper GIT: Stomach, duodenum
o See if active bleeding or not o Duodenum most commonly involved
• Irrigation • Caused by acid and pepsin
o Cold saline solution but do not aspirate à • M>F; DU 3x > GU
adds pressure which can damage already o Males are more prone
injured mucosa à ~bleed to death • Relapse: DU is 80%, GU is 33% after 1yr
• Bleeding stops in 24h • Spectrum of illness, chronology
o Endoscopy and therapeutics 1. Undetectable mucosal injury
• Variceal bleeding 2. Erythema
o From varices in esophagus and stomach; 3. Erosions
discussed with liver 4. Frank ulcers
• Non-variceal bleeding – Peptic Ulcer disease
o Do injection therapy with 1:100000
epinephrine à vasoconstriction to stop
bleeding

Lecture 7 mra
Med3C Cham – Prelim Topics Gastro 3a

Types of PUD
Gastric  Ulcer   Duodenal  Ulcer  
• Pain aggravated by food • Relieved by food and antacid
• Weight loss is common • Usually 3h after eating
• Awakens patient at night
st
• Peak in > 60 y/o • 3x common in 1 degree relatives
• Increased in bld grp O non-secretors
• Increased in HLA-B5 aging white males
• ↑Serum gastrin • N fasting gastrin level
• More commonly leads to malignancy • Higher incidence of severe bleeding (related to higher
• Giant ulcers may lead to Ca recurrence)
o Important to rule these out

A. Benign gastric ulcer – B. Malignant gastric ulcer

borders are still regular involving greater curvature of A.Ulcer with a clean base. B. Ulcer w/visible vessel
stomach (arrow) in a patient with
recent hemorrhage

PUD Pathogenesis
Aggressive  factors  (injurious  agents)   Protective  factors  (mucosal  defense)  
• Endogenous – acid, pepsin, bile acids • Normal mucosa resist corrosive effect of acid and
• Exogenous – ethanol, aspirin, HP, NSAIDS, smoking, pepsin
steroids • Gastric mucosal barrier = gastric mucosa resist back
• Gastrin – most potent gastric acid stimulant diffusion of H++
o Normal in fasting; increased in post-prandial • Cytoproduction = endo PG is protective
(DU) • Mediators of mucosal protection
o Increased in fasting and PP state (GU) o Mucus
o ACID + PEPSIN à Tissue injury à PUD o Bicarbonate
o Hydrophobic layer of phospholipid

PUD Diagnosis PUD Treatment

• History and PE • Diet
• EGD – allows direct visualization • Lifestyle modification
• UGIS – not helpful, cannot see bleeding and uclers • Stop smoking
• Serum gastrin • Drug therapy
• Amylase – only request to r/o DU perforation o Antacids
o H2 antagonist
X-­‐ray  criteria  for  Benign  GU   o PPI
• Ulcer crater extend beyond gastric wall o PGs – misoprostol (cytotec)
• Gastric folds radiate to the base of ulcer o Colloidal bismuth citrate (denol)
• Thick, radiolucent collar of edema (Humpton’s line) • Surgery
• Smooth, reg, round or ovoid ulcer crater
• Pliable and normally distensible gastric wall

PUD Complications
• Hemorrhage – most common
• Perforation – more common in DU
o X-ray: air under diaphragm; pneumo-
peritoneum
• Gastric outlet obstruction
• Penetration – posteriorly to the pancreas; ↑amylase,
↑lipase

Lecture 8 mra
Med3C Cham – Prelim Topics Gastro 3a

Zollinger-Ellison Syndrome
• Non-islet beta cell tumopr à Gastrin ZES Dx
• Assoc w/ ↑gastric acid secretion + PUD • X-RAY – Large mucosal folds
• Malignant in 60% - slow-growing Ca • Angio + CT – Tumors highly vascular
• 1/3-2/3 - - pancreas (head) • RIA – increased serum gastrin level
• Other sites: stomach, duodenum, spleen and LN
• Assoc w/MEN-1 (Pancreas, pituitary, PTh tumors) ZES Tx
• Mistaken as carcinoid tumor • Surgery
• Medical – PPI, H2A
ZES S/Sx
• Ulcer/s
• LBM, Steatorrhea
• Vit B12 malabsoption

GASTRIC ADENOCARCINOMA
• M 2x > F High Risk Factors for GAC
• Usually bet 50-70 y/o • Family hx
• Unknown cause • Prior hx of Gastric carcinoma
• Most common type of gastric CA and GI • Chronic active gastritis
(except esophagus( (90%) • Intestinal metaplasia
• Seen in blood group A • Post-antrectomy (10-20 yrs post-Billroth II)
• Polyps (only adenomatous >2cm)
Stomach Cancer Types • Gastric dysplasia
85% adenocarcinomas, 15% lymphoma, GIST and leiomyoma • Menetrier’s dse
1. Diffuse Type GAC • GU (+) H. pylori – 10% à Ca
• No cellular cohesion • Males, elderly
• Infiltrates and
thickens abdominal GAC Precursors
wall • Pernicious anemia
o Linitis plastic • Atrophic gastritis – especially in elderly
– leather-like • Adenomatous polyps (<2cm)
thickening of • Achlorhydria
mucosa • Giant hypertrophic gastritis (Menetrier’s)
o Seen in • Post – gastrectomy (10-20 yrs post Billroth II)
severe • H. pylori infection
adenoca
o Poor prognisis
GAC Clinical Features
• Epigastric pains – 70%
2. Intestinal Type GAC • Early satiety – common with linitis plastic
• Characterized by • (+/-) N/V
glandular-like • Weight loss
tubular structures • Anemia
• Ulcerative, seen • Upper GI bleeding
in lesser
curvature GAC Dx
• UGIS X-ray - Mass, ulcer or thickened and non-
distensible “leather-bottle” stomach (linitis plastic)
3. Lymphoma • DoC: Endoscopy – with biopsy or brush
4. Gastrointestinal Stromal Tumors cytology
• Pink looking, smooth mucosa with pus • EUS – best to determine depth of invasion
5. Leiomyoma o There are 5 layers of gastric mucosa
• CEA – tumor marker
CT Scan
GAC Major Environmental Risk Factors •
• Hgb/Hct
• H. pylori
• Alk Phos
• Diet
o Salted & preserved foods (nitrates– tocino,
tapa) GAC Management
• Cigarette smoking • Surgery – procedure of choice
o 5 yr SR (EGC = 90%; AGC = 10%)
• Chemotherapy
o 5 FU, Mitomycin, Doxo,,,
Lecture 9 mra