Stomach Flashcards
What is the right gastric artery?
A branch of the proper hepatic artery that comes off after the gastroduodenal artery (GDA) take off.
What does the gastroduodenal artery supply?
It comes off the common hepatic artery and gives blood to the pylorus.
What are the characteristics of atrophic gastritis?
Low HCl, achlorhydria, high gastrin, low pepsin, and low intrinsic factor.
What hormones are released from the duodenum with duodenal acidification?
Somatostatin, CCK, and secretin.
What is the #1 cause of rapid gastric emptying?
2 ulcers
Previous surgery.
What is a trichobezoar?
A hairball that cannot be removed with EGD and requires gastrostomy.
What is a phytobezoar?
A type of bezoar made of fiber or vegetable matter. Cellulase is the best treatment. Can try papaine. Coca-cola also works really well, or EGD
What is Dieulafoy’s lesion?
A congenital submucosal arterial malformation, usually located on the lesser curvature, treated with EGD and clipping.
What is gastric antral vascular ectasia?
“Watermelon stomach” characterized by dilated mucosal blood vessels containing thrombus, leading to acute/chronic blood loss. Associated with collagen disorders.
What is Menetrier’s disease?
Massive gastric folds (also seen in gastrinoma), excessive mucous= results in protein loss and ZERO acid production (achlorhydria)
- Foveolar hyperplasia, lots of mucus secreting cells and loss of parietal cells
- RF: CMV infection in children, H pylori in adults
- 24-hour pH reveals achlorhydria no acid
- NEED biopsy to rule out CA
- Related to excessive TGF alpha.
- Treatment is high protein diet, test for H.pylori. cetuximab (new treatment)
What is hypergastrinemia?
Caused by retrained gastric antrum, G cell hyperplasia, PPI use, pernicious anemia, renal insufficiency, and gastrinoma.
What is a Mallory-Weiss tear?
Mallory-Weiss tear – Tear is in STOMACH
Linear mucosal/submucosal tear usually below GEJ, MC lesser curve of cardia
RF: hiatal hernia
Usually self-limited
1st line: EGD, 2nd line: angiography and left gastric embolization. 3rd line: surgery
During EGD: if it is not actively bleeding, don’t do anything to it. Most resolve on its own
What is gastric volvulus?
Associated with paraesophageal hernia
Nausea without vomiting
Associated with wandering spleen – lacks peritoneal attachments
Borchardt’s triad – epigastric pain, retching without vomiting, unable to pass NGT
Organoaxial – MC: twisting between GEJ and pylorus
Mesenteroaxial – twisting between lesser and greater curvature
Dx: BEST IS BARIUM SWALLOW
Treatment:
- Untwist and Diaphragmatic hernia repair with Nissen fundoplication if there is a hernia
- If no hernia at all needs gastropexy
What is the most common complication of duodenal ulcers?
worsens with eating
90% associated with H. pylori
MC peptic ulcer
MC in 1st portion and anterior
MC complication is bleeding
Anterior ulcers: perforate
Posterior ulcers bleed from GDA
Curling ulcer – Burn and duodenal ulcer
Tx: PPI, H. pylori- amoxicillin, metronidazole, tetracycline
Gastric ulcers
Older men, slow healing
RF: male, tobacco, ETOH, NSAID, H. pylori, uremia, stress, steroids, chemo
Relieved with eating but recurs in 30 minutes
H. pylori found in 90% duodenal ulcers and 70% gastric ulcers increased acid
Hemorrhage in gastric ulcers associated with higher mortality than duodenal ulcer
Perforation is the MC complication of gastric ulcers
MC 80% on lesser curvature
Cushing’s ulcer – head trauma and gastric ulcer
Gastric ulcer types
Type I – MC TYPE Lesser curvature, proximal to incisura. Decreased mucosal protection
- Refractory disease (failed PPI X 3 months) tx: Antrectomy, vagotomy, with Billroth I
Type II – 2 ulcers. Lesser curvature (distal to incisura angularis) and duodenal. High acid secretion
- Refractory disease (failed PPI X 3 months) tx: Antrectomy, vagotomy, with Billroth I
Type III – Pre-pyloric; high acid secretion
- Antrectomy, vagotomy, with Billroth I (preferred, but if can’t reach) Billroth II or Roux-en-Y gastroJ
Type IV - lesser curve high along the cardia. Decreased mucosal protection
Type V - Diffuse ulcers; NSAID use
-Types of ulcer associated with increased acid output: Type II and III
-Types of ulcer associated with decreased mucosal protection: Type I and IV
Type A blood – associated with type I ulcers
Type O blood –associated with II-IV ulcers
What is the follow-up protocol for peptic ulcers?
All patients with peptic ulcer need follow up EGD 8-12 weeks after dx/treatment
- Can DC PPI if ulcer completely healed
- If still present after 3 months, will require surgery (refractory to treatment)
What are the criteria for surgery following EGD for bleeding peptic ulcer disease?
Criteria for surgery following EGD attempt to control bleeding peptic ulcer dz.
- > 4 units and still bleeding
- In shock despite transfusion
- Recurrent bleed after maximal EGD tx
Vagotomy in perforation
The use of highly selective vagotomy in perforation is not recommended, too soiled and too delicate of procedure
Billroth 1/2
Roux en y gastroj has higher risk of marginal ulcers than Billroth II
Billroth I – is preferred over Billroth II in benign gastric ulcer surgery to avoid, duodenal stump leak, afferent loop obstruction etc
Bilroth II – is preferred over RNY GJ when vagotomy is also performed due to risk of gastric atony (roux stasis syndrome)
Antrectomy = Billroth I or Billroth II
- Afferent limb should be 20 cm and performed retrocolic to avoid afferent loop obstruction
Roux en y GJ – Roux limb should be 40 cm to prevent bile reflux
Indications to perform definitive acid reducing surgery:
Never perform definitive ulcer surgery (vagotomy OR antrectomy) if patient has any below, instead just do graham patch
- Shock
- Perforation
Indications to perform definitive acid reducing surgery:
- Intractable dz X 3 months and treated for H. Pylori
- Continued smoking
- Continued NSAID use
Perforated gastric ulcer/ bleeding gastric ulcer
Perforated gastric ulcer – Going to OR
- Always start work up with upright x-ray straight to OR if free air
- Always need biopsy and send for frozen section
- If not on PPI or H. pylori has not been treated or UNSTABLEWedge resection (send for frozen) preferred over patch
- If on PPI and treated for H. Pylori AND STABLE Distal antrectomy (include ulcer) or vagotomy with drainage procedure
- Pauchet’s procedure – Antrectomy with a tongue proximally to get Type IV (cardia ulcers)
- Csend’s procedure – Subtotal gastrectomy with RNY GJ to get proximal cardia ulcer
- Giant gastric ulcer = 3 cm. 30% of these are cancer needs antrectomy
Bleeding gastric ulcer- Going to OR
- Vagotomy is never needed
- Avoid any definitive ulcer surgery if in shock/unstable
- Gold standard: gastrostomy and overdew, especially if unstable
Gastric ulcer hemorrhage has higher mortality vs duodenal
Perforated duodenal ulcer/ bleeding duodenal ulcer / duodenal ulcer obstruction
Perforated duodenal ulcer – Going to OR
- Always start work up with upright x-ray straight to OR if free air
- If operating on duodenal ulcer, Routine biopsy is not recommended
- Gold standard tx: Omental patch
- Patients treated for H. Pylori, on PPI, Stable, minimal contamination HSV, truncal vagotomy with drainage or Truncal vagotomy and antrectomy (best for giant ulcer)
- Giant duodenal ulcer = > 2 cm – consider ANTRECTOMY (risk of CA) in stable patient
- If not going to perform antrectomy for giant ulcer you must do graham patch with pyloric exclusion and gastroJ (this will leak with just graham
Bleeding duodenal ulcer-Going to OR
- Tx: Oversew alone
- If patient stable, can oversew, truncal vagotomy and pyloroplasty
- Antrectomy and truncal vagotomy can be done for giant ulcers
Duodenal ulcer obstruction GOO
- Fluid resuscitation 1st, PPI, serial dilation with biopsy 1st
- Gold standard surgery: truncal vagotomy and antrectomy, B1
Perforated/ bleeding marginal ulcer
Marginal ulcer after bariatric surgery
Perforated marginal ulcer and already going to OR: resect anastomosis
Bleeding marginal ulcer, and already going to OR: resect anastomosis
NSAID Use
NSAID use is the highest risk factor for causing peptic ulcer bleeding. Higher than H. Pylori
Predictors of rebleeding after endoscopic therapy
Newest studies show the following ulcer size larger than 2 cm, hypotension, initial hemoglobin less than 10 mg/dL, fresh blood in the stomach, visible vessel, active bleeding.
Greatest risk factor = visible vessel.
Vagotomy
Indicated if on PPI/treated for H. Pylori and going to the OR, AND for any Billroth procedures
Type II or III ulcers only, located distal to incisura angularis
All type of Vagotomy increase liquid emptying vagally mediated receptive relaxation is removed (results in increased gastric pressure that accelerates liquid emptying)
All forms of vagotomy result in an increase in gastrin and gastrin cell hyperplasia
Truncal vagotomy
- Ant and post vagus above GE junction divided 4-5 cm above EGJ
- Causes delayed gastric emptying gastroparesis
- MC problem is diarrhea 2/2 to sustained MMC forcing bile acids to colon
- Dumping syndrome
- Causes gallstones
- Decreases emptying of solids from pyloric constriction
- Requires pyloroplasty or antrectomy to increase emptying of solids
Selective vagotomy
- Divides the nerves of laterjet (innervates antrum)
- Spares the branches to liver and small intestine by dividing distal to these branches, this decreases risk of dumping syndrome, diarrhea and gallstone formation
- Need to make sure to divide posterior criminal nerve of grassi (Off of right (posterior) vagus), unlike truncal
- Decreases Emptying of solids
- Requires pyloroplasty or antrectomy to increase emptying of solids
Highly selective vagotomy (proximal vagotomy)
- Divides the nerves of Letarjet but preserves Crow’s foot (supplies pylorus) Preserves the celiac, hepatic branches
- Does not require drainage procedure
- Normal emptying of solids, increased emptying of liquids
- Decreased risk of dumping syndrome
Other alterations caused by truncal vagotomy
- Gastric effects – decrease acid output by 90%, increase gastrin, gastrin cell hyperplasia
- Nongastric effects – decreases exocrine pancreas function, decrease postprandial bile flow, increase gallbladder volume, decrease release of vagally mediated hormones
- Post vagotomy Diarrhea 40% - The most common problem following truncal vagotomy. Caused by sustained migrating motor complex forcing bile acids to the colon. Tx: Initial treatment = Cholestyramine treatment of choice. or very rarely interposition of reversed jejunal segment
What is H. pylori?
H. pylori
- Helix shaped, gram negative rod
- Reduces number of antrum D cell Decrease somatoastatin release increases gastrin increases acid level
- Produces urease splits urea into ammonia and bicarb allows H. pylori bacteria to survive in acidic environment
Tx:
(Triple therapy) PPI + Clarithyromycin + amoxicillin/flagyl (7-10 days)
Refractory ulcers – (USE DIFFERENT ABX THAN BEFORE) (Quadruple therapy) PPI, Flagyl, tetracycline/doxycycline, bismuth salt
Allergic to PCN – flagyl, PPI, and clarithromycin
4-6 weeks After treatment, all patients need confirmatory tests with urease breath test (Best)
What is the treatment for H. pylori infection?
Triple therapy: PPI + Clarithromycin + Amoxicillin/Flagyl for 7-10 days.
What is the risk associated with fundic gland polyps?
Negligible risk of cancer, but associated with PPI use.
Stress gastritis
-3-10 days after event (multiple trauma, burns, complicated post)
-Lesions appear in fundus first -> can progress to ulcers
Tx: PPI
PPI Prophylaxis indicated
UGIB but can’t find source (too much blood or food) angiography
Lower rates of GI Bleeding with PPI vs H2 blocker
Prophylaxis only for high risk:
- Coagulopathy INR > 1.5, platelets < 50k
- Mechanical vent > 48 hours
- History of GIB or GI ulcer in the last year
- Traumatic brain injury or spinal cord injury
- Severe Burn > 35%
Fundic gland polyp
Fundic gland polyp – MC gastric polyp
Associated with PPI (biggest association)
Can be associated with FAP
Risk of cancer is negligible
Not associated with H. Pylori
Often regress after stopping PPI
If polyps > 1 cm or > 20 in number then stop PPI. If not, don’t need to do anything
Don’t need to remove all polyps
If >20 polyps should think of FAP if it is from FAP resect all polyps perform colonoscopy
Hyperplastic polyp in stomach
caused by H. Pylori infection !!!!!
Associated with atrophic gastritis
Has malignant potential
2% cancer risk
Tx: remove ALL polyps > 0.5 cm and H. Pylori treatment
Adenomatous polyp
Adenomatous polyp in stomach
Occur in the setting of Chronic atrophic gastritis
Can be related to H. pylori infection
Can be sporadic or associated with FAP
Has the highest risk of cancer
Definite CA risk for polyps > 2 cm (50%)
Tx: endoscopic resection of ALL polyps and H. Pylori treatment
Gastric Cancer
Gastric CA
MC site: antrum
90% are adenocarcinoma
RF: #1 H. Pylori, HNPCC, EBV, adenomatous polyps, atrophic gastritis, pernicious anemia, achlorhydria, blood type A. BRCA2,
Staging for gastric cancer
Stage with:
- Endoscopy WITH EUS + FNA (Best for T and N),
- CT chest/abd/pelv (best for resectability and mets).
- PET-CT is optional but very useful for mets
-Staging laparoscopy: NCCN recommends laparoscopic staging with peritoneal washing for clinical stage > T1b tumors if chemoradiation or surgery being considered (not needed if known metastasis and undergoing definitive chemoradiation or palliative options)
Hereditary diffuse gastric CA
Have CDH1 mutation. Need Prophylactic total gastrectomy for CDH1 carriers between 18-41. Need 5 cm margins
Women with CDH1= inc risk of breast cancer
Adenocarcinoma
Adenocarcinoma: Intestinal type gastric CA – MC type. 5 YS 25%
- Path shows glands and goblet cells
- Most often seen in the setting of atrophic gastritis (H. Pylori, autoimmune gastritis) – MC related to environment
Adenocarcinoma: Diffuse Gastric CA (linitis plastica). 5YS 10%
- Diffuse connective tissue invasion. Early lymphatic spread
- NO GLANDS
- Less favorable prognosis. Usually beyond resection at time of Dx
Siewart classification of EGJ adenocarcinoma
All GE junction tumors need esophagectomy
Siewart classification of EGJ adenocarcinoma that is 5 cm proximal and distal to EGJ
* Type I - 1-5 cm proximal to EGJ: Ivor Lewis (preferred b/c need to take mediastinal LN) and PROXIMAL gastrectomy with gastric pullup with thoracic esophagogastrostomy
- Type II - 1 cm proximal to 2 cm distal to EGJ: Transhiatal proximal gastrectomy and esophagectomy
- Type III – 2 -5 cm distal to EGJ: Treated like gastric cancer: Transhiatal TOTAL gastrectomy and esophagectomy
Gastric Cancer Treatment
Splenic invasion: resect stomach + splenectomy
Chemo
- 5FU, leucovorin and oxaliplatin = MC used = FOLFOX
- cisplatin + capecitabine + epiribucin used in trials
- Trustuzumab used for Her-2 expression only
-Neoadjuvant therapy: cT2 or higher and any N
Early gastric cancer = Tis or T1a (lamina propria or muscularis mucosa): You have two options:
- 1. Straight to Gastrectomy with D1. No adjuvant chemo/radiation unless node positive
- 2. Endoscopic mucosal resection only IF T1a < 2 cm, no lymphovascular invasion, mod-well differentiated, no ulceration
Locoregional advanced gastric cancer (resectable) = T1b (submucosa) or greater
- All patients with locally advanced cancer need a diagnostic laparoscopy with peritoneal washing PRIOR to neoadjuvant chemo to rule out mets
- T1b (submucosa) N0: straight to surgery (Need D2 lymphadenectomy), no neoadjuvant therapy
- T2 (muscularis propia) or greater or any N: Neoadjuvant chemo then surgery is preferred then post op chemo-radiation
Locoregional advanced gastric cancer but unresectable: chemotherapy or chemoradiotherapy
Metastatic: non-op unless palliative
D1 LN 1-6 – perigastric
D1+ - resect all D1 and as many D2 that seem likely to harbor CA, without need for splenectomy or pancreatectomy
D2 LN 7-11 – nodes near common hepatic, left gastric, celiac, and splenic hilum
D3 LN 12-16– Portahepatis and aortic nodes
Treatment: For tumors > T1b or any N
- Total gastrectomy with RNY esophagojejunostomy for proximal 1/3 tumors
- Distal gastrectomy with RnY gastroJ or Bilroth II for distal 2/3
- Never do Bilroth I for distal gastric CA b/c duodenal recurrence can obstruct
- D2 Resection is current guideline without routine splenectomy or pancreatectomy unless they are grossly affected then must take en bloc
- All need 5 cm margins unless its diffuse CA then it is 8 cm
- Need at least 15 LN for staging
- Post op chemo-radiation for all T2, T3, T4 or node positive
- Stage IV: with bleeding/obstruction -> palliative total gastrectomy provides good palliation
- Mets to outside area of resection: unresectable, palliation
- For patients with (small volume, limited peritoneal disease (unresectable really) you can increase survival with cytoreductive surgery and HIPIC
-Lymph node dissection:
-NCCN recommendation is for R0 resection with at least D1 or modified D2 lymph node dissection
-D1 dissection = removal of N1 nodes (perigastric nodes along greater/lesser curve, stations 1-6)
-D2 dissection = removal of N1 and N2 nodes (nodes along left gastric, common hepatic, celiac and splenic arteries, stations 7-11)
-R0 = negative microscopic margin
-R1 = negative gross margin, positive microscopic margin
-R2 = positive gross margin
-Adjuvant therapy: Adjuvant 5-fluorouracil for T3, T4, or node positive disease following R0 resection
Palliation
- Obstruction – proximal lesions can be stented, distal lesions bypassed with gastreojejunostomy
- Bleeding or pain: XRT
GIST (Gastrointestinal stromal tumor).
– MC benign gastric tumor
Mesenchymal tumor!! = SARCOMA Does not spread to lymph nodesNO lymphadenopathy
Comes from interstitial Cells of Cajal
MC found in stomach. Non-gastric GIST = poor prognostic factor
MC mets to liver.
Sx: MC present with GI bleed!!
On Imaging: Hypervascular, exophytic, heterogeneous mass, often with central necrosis.
C-KIT+, CD117, DOG-1 and CD34
Work up: CT scan is the image of choice to diagnose!!!
- Don’t need biopsy, imaging is enough. Even if biopsy is negative, and imaging concerning for GIST, they need surgical resection
Submucosal mass on EGD – most EGD biopsy is negative
US – hypoechoic, smooth edges
Path – spindle cells and connective tissue
Malignant > 5 cm or > 5 mitosis/50HPF or IF GIST LOCATION IS OUTSIDE THE STOMACH
GIST treatment
- If in stomach and < 2 cm and asymptomatic and confirmed with US f/u EUS every 6-12 months
- > 2 cm or symptomatic, need wedge (Not formal) resection with negative margin only. No Nodes taken
- Imatinib for recurrence
If metastatic disease or borderline resectable, present start with imatinib, then reassess for surgery
R0 vs R1 no difference in mortality. Do not need to go back to surgery for R1 margin give imatinib
Imatinib after resection for 3 years S/E = CHF
Imatinib (Gleevec) also recommended for unresectable, metastatic, or recurrence
MALT lymphoma
MALTOMA – low grade B cell NHL
Patients present with nausea, epigastric pain/burn, weight loss
Do not present with B symptoms: fevers, chills, night sweats
MC location Is stomach
Depth of invasion through stomach wall correlates with decreasing responsiveness to H. Pylori treatment
- Stage I: IE = lesions restricted to stomach = Will respond to H. Pylori treatment
- Stage II: IIE = lesions spread to lymph nodes = IIE or above; likely won’t respond to H. Pylori treatment
- IIIE = Lesion in GI, + lymph nodes on both sides of diaphragm
- IVE = Extension to extra GI tissue
Related to H. Pylori
Dx: Need EUS with Bx
Tx: Treat H. pylori for all 1st regardless of stage. If it does not regress on repeat EGD; Tx: XRT is curative
- If H. Pylori negativE: go straight to XRT
- Success of H. Pylori treatment should be done with urea breath test 6 weeks after
- Need serial endoscopy to assess response for treatment too. If minimal histologic disease: continue to do serial EGD
No real role for surgery here unless bleeding or perf
Advanced disease nodes outside of perigastric: stage III or IV: H. pylori Tx and chem-XRT (CHOP-R)
Gastric lymphoma
Gastric lymphoma – have ulcer symptoms. MC location for extra-nodal lymphoma. MC NHL diffuse large B cell 60%
Dx: EGD and biopsy. Tx: chemo-XRT. Surgery very rare, only for stage I (Confined to mucosa) disease and palliative treatment
What are elevated gastrin levels associated with?
Elevated gastrin levels found in:
- Gastrinoma
- Retained gastric antrum
- GOO
- Vagotomy
- Pernicious anemia
- PPI use
- Chronic gastritis
What deficiencies are common after gastric resection?
- MC #1 iron deficiency! (iron needs acidity to be absorbed in duodenum)
- B12/Folate
- Calcium (osteoporosis)
What is the Psoas sign indicative of?
Psoas sign (pain on extension of the thigh) - retrocecal appendicitis
What is the Obturator sign indicative of?
Obturator sign (pain on passive internal rotation of a flexed hip) - pelvic appendicitis
Total gastrectomy for gastric CA:
Preserve short gastric for subtotal
Start with diagnostic laparascopy
1. Divide falciform
2. Divide gastrocolic ligament, left gastroepiploic, and short gastric, omentectomy (station 4)
3. Infrapyloric mobilization, divide right gastroepiploic and GDA
4. Suprapyloric mobilization, divide gastrohepatic lig, Divide hepatoduodenal lig to find and divide right gastric
5. Transect duodenum 1 cm distal to pylorus
6. D2 lymphadenectomy
7. Gastric transection
8. Roux En Y EJ/GJ
Hereditary syndromes with inc risk of gastric cancer
-Lynch syndrome (DNA mismatch genes)
-Juvenile polyposis syndrome (SMAD4)
-Peutz-Jehgers Syndrome
-Familial adenomatous polyposis (APC gene on 5q21)
Retained antrum syndrome
Retained antral tissue within duodenal stump after gastric resection
-G cells bathed in alkaline fluid= continuous gastrin release= acid production in proximal stomach remnant and ulceration
-Check gastrin to r/o gastrin-secreting tumor
-With Billroth II or Roux-en-Y
-Tx: PPI; vagotomy, resection of retained antrum
Dumping syndrome:
-Tachycardia, diaphoresis, dizzy, flushing
-Tx= small meals, no sugary drinks; refractory= octreotide
-Early dumping syndrome (20-30 min after meal): abrupt hyperosmolar load to small intestine
-Late dumping syndrome (1-4 hours after meal): rapid carbohydrate load to small intestine resulting in large insulin surge and rebound hypoglycemia
-After gastrectomy or vagotomy and pyloroplasty
Alkaline reflux gastritis:
-post-prandial epigastric pain, N/V; not relieved with vomiting
-After Bilroth I and Bilroth II reconstructions
-Dx: impedance studies
-Tx: pro kinetic agents, bile acid binding resins; conversion to RNY
-At least 50 cm for Roux limb will avoid recurrent bile reflux
-Braun enterostomy: anastomosis between afferent and efferent limb
Afferent limb syndrome:
-acute or chronic obstruction of afferent jejunal limb following Bilroth II reconstruction
-Increased luminal pressure of afferent limb
-Obstructive jaundice, cholangitis, pancreatitis from back pressure up biliopancreatic system
-Duodenal stump blow out
-Bacterial overgrowth in afferent limb -> bacteria deconjugate bile acids= steatorrhea, malnutrition, avitamin B-12 deficiency leading to megaloblastic anemia.
-Tx: conversion to Roux-en-Y or Bilroth I; bacterial overgrowth can be managed first with antibiotics (high relapse rate though)
-If B2 patient presents with bowel obstruction, no NGT and decompression; emergent surgery. Similar to bypass patients with internal hernia.
-Patient with history of antrectomy and Bilroth II reconstruction in distant past presents with intermittent abdominal pain and distention which is relieved after bilious emesis, megaloblastic anemia on laboratory work up. What is this?
-Afferent limb syndrome
Stamm gastrostomy
-Open gastrostomy tube placement
-Chosen when anatomy is hostile, multiple operations, adhesions present -> PEG not safe
-3 cm below costal margin, 3 cm to left of midline in anterior wall of stomach; purse string
EBV associated gastric cancers
-EBV associated with nasopharyngeal cancer, Hodgkin disease, Burkitt lymphoma, subset of gastric cancer, lymphoproliferative disease in AIDS
EBV associated gastric cancers: male predominance, located more commonlyh in gastric cardia or post-surgical gastric stump, finding of lymphocytic infiltration, decreased occurence of lymph node metastasis, better prognosis
