Stomach pathology


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Stomach pathology

  3. 3. GASTRITISInflammation of gastric mucosa Acute Gastritis Chronic Gastritis
  4. 4. Acute GastritisTransient mucosal acute inflammationFrequently associated with: Heavy use of NSAIDs Excessive Alcohol consumption Heavy smoking Chemotherapeutic drugs Uremia Systemic infections (Salmonella, CMV) Severe stress –trauma, burns, surgery Ischemia & shock Suicidal ingestion of corrosive Gastric irradiation
  5. 5. Pathogenesis of Acute GastritisPathogenesis poorly understoodFollowing influences thought to be operative Increased acid secretion with back diffusion Decreased production of HCO3 buffer Reduced blood flow Disruption of adherent Mucus layer Direct damage to epithelium Regurgitation of bile acids fron duodenum Inadequate synthesis of PG’s Idiopathic gastritis
  6. 6. MorphologyMild – Mucosal hyperemia Lamina propria edema & congestion Surface epithelium intact, Scattered intraepithelial & intraluminal neutrophils (activity)Severe –Mucosal erosion & hemorrhage Erosion denotes loss of surface epithelium generating defect in mucosa that does not cross muscularis mucosae Rich inflammatory infiltrate Fibrinous purulent exudate into lumen Hemorrhage –punctate dark spots in hyperemic mucosa Concurrent erosion & hemorrhage called acute erosive hemorrhagic gastritis large areas of mucosa may be denuded seen in alcoholics and NASIDs ingestion
  11. 11. C/F Of Acute Gastritis May be asymptomatic Epigastric pain Nausea & vomiting Overt hemorrhage Massive hematemesis & malena
  12. 12. Chronic GastritisDefined as chronic mucosal inflammatorychanges leading to eventually mucosal atrophyand intestinal metaplasia usually in the absenceof erosionsEpithelial changes may become dysplasticprovide background for development ofcarcinoma
  13. 13. CHRONIC GASTRITISHISTOLOGICAL CLASSIFICATION: Chronic superficial gastritis Chronic atrophic gastritis Gastric atrophyCLASSIFICATION BASED ON PATHOGENESIS: Type A or immune gastritis Type B or non immune gastritis
  14. 14. Pathogenesis of Chronic GastritisMajor etiologic associations are: H.Pylori chronic infection Autoimmune (P. Anemia) Toxic as with alcohol & cigarette smoking Post surgical- antrectomy with gastroenterostomy with reflux of bile Motor & mechanical including obstruction, bezoars & gastric atony Radiation Granulomatous (crohns disease) Uremia GVHD
  15. 15. Trichobezoars
  16. 16. CHRONIC GASTRITISCHRONIC SUPERFICIAL GASTRITIS: Inflammatory infiltrate limited to foveolar region, no glandular atrophy ↓ cytoplasmic mucin, ↑ nuclear and nucleolar size and some ↑ in foveolar mitosis—may be seenCHRONIC ATROPHIC GASTRITIS: Extensive inflammation, glandular atrophy Grade: mild, moderate, severe—estimated by thickness of glands to whole mucosal thickness ↑ in distance between glandsGASTRIC ATROPHY: Thinning of mucosa in absence of inflammation End stage of chronic atrophic gastritis
  17. 17. CHRONIC GASTRITISTYPE A/ IMMUNE GASTRITIS: Site: fundus, spares antrum Antibodies against parietal cells, Intrinsic Factor, acid producing enzymes- hypo or achlorhydria, ↑ serum gastrin and pernicious anemia Also seen Hashimoto thyroiditis, Addisons disease & type 1 diabetes Patient are at risk of developing carcinoma / carcinoid tumoursTYPE B/ NON IMMUNE GASTRITIS: Site: begins in antrum and progress proximally to fundus Associated with H.pylori, alcohol, Cigarette smoke Types:  Hypersecretory gastritis: restricted to antrum and
  18. 18. CHRONIC GASTRITISEndoscopically: Thin, smooth mucosa with prominent submucosal vessels— atrophic gastritis and gastric atrophy
  19. 19. H. Pylori Colonizes gastric mucosa esp antrum and cardia by:1. Surface adhesion2. Free in mucus3. Intercellularly Intracellular colonization4. → ↑↑ epithelial damage Disintegration and loss of apical mucin, epithelial pits, erosions and ulceration Lymphoid follicles Special stains: Giemsa, Warthin-Starry stain or IHC Found in 90% chronic gastritis, 95% duodenal ucler,
  20. 20. Giemsa stain H. Pylori
  21. 21. Diagnostic tests for H. pylori Serological tests for H.pylori antibodies Fecal bacterial detection Urea breath test (production of NH3 by bacterial urease) Gastric biopsy demonstration of bacteria, bacterial culture, rapid urease test Bacterial DNA detection by PCR
  22. 22. Diseases Associated with Helicobacter pylori Infection Chronic gastritis Strong causal association Peptic ulcer disease Strong causal association Gastric carcinoma Strong causal association Gastric MALT lymphoma * Definitive etiologic role* MALT, mucosa-associated lymphoid tissue
  23. 23. Gastric pathology Part-II
  24. 24. Morphology of Chronic GastritisRegenerative Change. Proliferative response to epithelial injury Neck region of gastric glands mitotic figures increased Enlarged epithelial cell with hyperchromatic nuclei and higher N/C ratio & prominent nucleoli Regenerative changes if severe with active inflammation resemble dysplasiaMetaplasia. Antral, body, and fundic mucosa may become partially replaced by metaplastic columnar absorptive cells and goblet cells of intestinal morphology (intestinal metaplasia). Occasionally, villus-like projections or features of colonic epithelium may be present. H.pylori absent from areas of intestinal metaplasia
  25. 25. Morphology of Chronic GastritisAtrophy. Marked loss in glandular structures associated with autoimmune gastritis and pangastritis caused by H. pylori. Persisting glands frequently undergo cystic dilatation. Atrophic autoimmune gastritis or chronic gastritis treated by inhibitors of acid secretion- hyperplasia of gastrin-producing G-cells in antral mucosa, attributed to hypochlorhydria or achlorhydria arising from severe parietal cell loss. Increased gastrinemia stimulates hyperplasia of enterochromaffin-like cells in gastric body, provides background for gastric carcinoid tumorDysplasia. Long-standing chronic gastritis, epithelium develops cytologic atypia-dysplasia. Intestinal metaplasia may precede dysplasia. Dysplastic alterations if severe constitute in situ carcinoma. Dysplasia thought to be precursor lesion of gastric cancer in atrophic autoimmune gastritis and H. pylori- associated chronic gastritis.
  26. 26. Sydney System of Grading Chronic Gastritis1. Site: Antral, Corporal mucosa2. Grading of: (Mild, Moderate, Marked)  H-Pylori  Chronic inflammation  Activity  Atrophy  Intestinal metaplasia *Normal lymphocytes & plasma cells in lamina propria = up to 5/HPF *No Neutrophils in lamina propria
  27. 27. H. pylori H. pylori is a nonsporing, curvilinear gram-negative rod measuring approximately 3.5 × 0.5 μm. Gastric mucus, which is lethal to most bacteria. The specialized traits that allow it to flourish include: • Motility (via flagella), allowing it to swim through viscous mucus • Elaboration of a urease, which produces ammonia and carbon dioxide from endogenous urea, thereby buffering gastric acid in the immediate vicinity of the organism • Expression of bacterial adhesins, such as BabA, which binds to the fucosylated Lewis B blood-group antigens, enhances binding to blood group O antigen bearing cells • Expression of bacterial toxins, such as cytotoxin association gene A (CagA) and vacuolating cytotoxin gene A (VacA).
  29. 29. Moderate Gastritis
  30. 30. Chronic Gastritis
  31. 31. Intestinal Metaplasia
  32. 32. Anti-parietal cell antibody- bright green immunofluorescence
  33. 33. OTHER TYPES OF GASTRITISLYMPHOCYTIC ALLERGIC GASTRITIS: GASTRITIS:  Seen in children associated with 45-60% associated with diarrhea vomiting & growth failure celiac disease  Eosinophilic infiltration Lymphocytosis of foveolar EOSINOPHILIC GASTRITIS: ad surface epithelium mostly  Site: distal part of stomach and T CD8+ lymphocytes proximal duodenum  Typically affects middle-aged womenGRANULOMATOUS GASTRITIS:  Allergic phenomenon, peripheral Cause: TB, mycosis, eosinophilia  L/M: edema, prominent diffuse sarcoidosis, Crohn’s disease or idiopathic eosinophilic infiltration, eosiniphilic microabscesses Narrowing & rigidity of  Gastric outlet obstruction antrum due to transmural  Related to eosinophlic enteritis granulomas  D/D: inflammatory fibroid polyp
  34. 34. TYPES OF GASTRITISMELAKOPLAKIA: GRAFT VS HOST Histiocytic infiltrate conatining Michaelis- DISEASE: Gutmann bodies  Bone marrow transplantedREACTIVE GASTROPATHY patient Group of disorder characterized by foveolar  Apoptosis, gland hyperpasia, loss of mucin , glandular destruction, sparse regenerative changes, edema ,dilatation of lymphocytic infiltrate in mucosal capillaries, smooth muscle lamina propria and granular extending into lamina propria key to eosinophilic debris in defination is absence of neutrophils dilated glands Fairly common with Aspirin NSAID’s or bile reflux MELAKOPLAKIA: Endoscopic longitudinal stripes of Histiocytic infiltrate conatining erythematous mucosa alternating with less severely mucosa (Water Melon Stomach) Michaelis-Gutmann bodies
  35. 35. Clinical Features - Chronic Gastritis Nausea Vomiting Upper abdominal Discomfort- burning pain Hypochlorhydia due to parietal cell loss Pernicious Anemia in autoimmune gastritis
  36. 36. ACUTE GASTRIC ULCERATION Acutely developing mucosal defects Well known complication of NSAID’s therapy Causes: any debilitating illness, sepsis, shock, extensive burns, severe trauma, intracranial injury , long term steroid and aspirin ingestion, radio or chemotherapy Erosion- shedding of superficial epithelium Ulceration of mucosa deep lesion involving full mucosal thickeness If muscle involved→ fibrosis and pit formation Deep ulcer may perforate, especially seen in radiotherapy ulcers
  37. 37. TYPES-ACUTE GASTRIC ULCERS1. STRESS ULCERS• Due to severe physiologic stress of any nature• Multiple lesions located mainly in stomach• Range in depth from erosions to ulcers• NSAID-induced ulcers related to decrease production of PG’s which favors production of mucus ,HCO37 inhibit acid secretion2. CURLING ULCERS• Associated with severe burns or trauma• Occurs in proximal duodenum3. CUSHING ULCERS• Gastric ,duodenal ,esophageal ulcers associated with Intracranial injury, operations or tumours• Direct stimulation of vagal nuclei by increase intracranial pressure leading to hypersecretion of gastric acid- epithelial damage• Carry high incidence of perforation
  38. 38. MORPHOLOGY Of ACUTE ULCERGROSS: Acute stress ulcers usually less than 1 cm in diameter Circular and small. Ulcer base frequently stained a dark brown by the acid digestion of extruded blood Unlike chronic peptic ulcers, acute stress ulcers found anywhere in stomach, Margins and base of ulcers not indurated. May occur singly, more often multiple stress ulcers throughout stomach & duodenum.MICROSCOPICALLY: Stress ulcers abrupt lesions, with essentially unremarkable adjacent mucosa. Depending on duration of ulceration, may be a suffusion of blood into mucosa, submucosa and some inflammatory reaction. Conspicuously absent are scarring & thickening of blood vessels, as seen in chronic peptic ulcers. Healing with complete reepithelialization, after causative factors removed. Time required for complete healing varies from days to several weeks.
  39. 39. Clinical Presentation of Acute Ulcer Bleeding from erosion or ulcers Associated history of critical illness
  40. 40. Multiple Stress Ulcers
  41. 41. PEPTIC ULCERUlcer defined as breach in mucosa of alimentarytract that extends through out the muscularismucosa into submucosa or deeperPeptic ulcers are chronic most often solitary occur inany portion of GIT exposed to aggressive action ofacid/peptic juices(Usually less than 4cm in diameter)
  42. 42. Peptic UlcerSITE (In order of decreasing frequency) Duodenum first portion Stomach usually antrum (95% lesser curvature) G-E junction in setting of GERD/Barrett esophagus Margins of gastrojejunostomy Zollinger-Ellison syndrome Ileal Meckel diverticulum with ectopic gastric mucosa
  43. 43. Epidemiology In USA 4 million people have peptic ulcer 5000die each year as a result of peptic acid disease Middle age to older adults, may first become evident in young adult life Lifetime likelihood of developing peptic ulcer about 10% for Americam males & 4% for females Male to female ratio is for duodenal ulcer is 3:1 & for gastric ulcer is 1.5-2:1
  44. 44. Pathogenesis Peptic ulcers produced by imbalance between gastroduodenal mucosal defence mechanisms & damaging forces particularly gastric acid & pepsin H.pylori infection major factor in pathogenesis of peptic ulcer Hyperacidity as in Zollinger-Ellison syndrome Chronic use of NSAID suppress PG synthesis Cigarette smoking impair mucosal blood flow & impair healing Alcoholic cirrhosis, increase incidence of peptic ulcer Corticosteroid in high dose or repeated use Chronic renal failure-uremia Hyperparathyroidism –hypercalcemia stimulate gastrin production and acid secretion Personality and psychological stress (10-20% of individuals worldwide infected by H. pylori actually develops peptic ulcer)
  45. 45. H. Pylori –Pathogenesis of P. ulcer H. pylori does not invade tissues it induces an intense inflammatory and immune response by increase production of pro-inflammatory cytokines IL 1,6, & TNF and IL8 by mucosal epithelial cells which recruits neutrophils Bacterial gene products involved in epithelial injury & induction of inflammation, secrete urease which breakdown urea to form toxic ammonium chloride & monochloramine, also elobrate phospholipases that damage surface epithelial cells H.pylori enhances gastric acid secretion and impair duodenal HCO3 production thus lowering luminal pH in duodenum which favors gastric metaplasia in 1st part of duodenum, provide environment for H. pylori colonization H.pylori protiens evoke immune response in mucosa with activation of T & B lymphocytes. T cell dirven activation of B cell may be involved in pathogenesis of gastric lymphomas Thrombotic occlusion of surface capillaries is promoted by bacterial platelet activating factor
  46. 46. H. PyloriInfection with CagA positive strain is associated with More organism in tissue More severe epithelial damage Greater acute and chronic inflammation Higher likelihood of peptic ulceration Increase risk of gastric cancer * CagA gene is essential for expression of VacA (Vacuolating toxin) which causes cell injury * Over 80% patient with duodenal ulcers are infected by CagA positive strain
  47. 47. MORPHOLOGY PEPTIC ULCER 98% of peptic ulcers located in 1st part of duodenum or in stomach in ratio of 4:1 Most duodenal ulcers occur within a few cm of pyloric ring Anterior wall of duodenum is affected more than posterior wall Gastric ulcer predominantly located along lesser curvature, less commonly anterior or posterior wall or greater curvature Great majority are single ulcer 10 to 20% of patient with gastric ulcers may have coexistent duodenal ulcers
  48. 48. PEPTIC ULCER MORPHOLOGYGross: Small lesion less than 0.3cm are shallow erosions over 0.6cm are ulcers Over 50% of peptic ulcer are less than 2cm about 10% are greater than 4cm in diameter Classic peptic ulcer oval to round sharply punched out defect with relatively straight wall, converging mucosal folds extending to its margin Proximal ulcer margin-overhanging edges, distal-sloping borders Ulcer margins are level with surrounding mucosaCut Section: Undermining of edges, complete replacement of muscle by grayish white fibrous tissue Base of ulcer is smooth & clean owing to peptic digestion of any exudate Subserosal fibrosis and inflammatory enlargement of regional lymph nodes Deep ulcers base formed by adherent pancreas ,omental fat Free perforation into peritoneal cavity(Multiple biopsies recommended for standard size ulcer)
  49. 49. PEPTIC ULCER MORPHOLOGYMicroscopically: In active ulcers Four Layers:1. Surface coat purulent exudate, bacteria & necrotic fibrinoid debris2. Inflammatory infiltrate includes neutrophils3. Granulation tissue infiltrated by mononuclear inflammatory cells4. Fibroous or collagenous scar replacing muscle wall & extending into subserosa Muscularis mucosae fusion with muscularis externa at edges Hypertrophied nerve bundles Superimposed Candida infection on necrotic surface Chronic inflammation virtually universal in peptic ulcer and persist after ulcer has healed but in healed erosion or stress ulcers no chronic inflammation seen
  51. 51. ULCER
  52. 52. CHRONIC PEPTIC ULCERHealing phase: Regenerating epithelium grows over surface Epithelium may show intestinal metaplasia Malignant transformation does not occur with duodenal ulcer and is extremely rarely with gastric ulcers
  53. 53. Clinical Presentation Epigastric gnawing , burning or aching pain Bleeding, iron deficiency anemia Nausea, vomitin ,bloating, belching Weight loss Gastric ulcer pain immediately after taking meal Doudenal ulcer pain empty stomach reduced by taking meal Milk reduces pain in gastric ulcer not in duodenal ulcer
  54. 54. Complications of Peptic Ulcer Disease Bleeding• Occurs in 15% to 20% of patients• Most frequent may be life-threatening• Accounts for 25% of ulcer deaths Perforation• Occurs in about 5% of patients• Accounts for two thirds of ulcer deaths Obstruction from edema or scarring• Occurs in about 2% of patients• Most often due to pyloric channel ulcers• May also occur with duodenal ulcers• Causes incapacitating, crampy abdominal pain• Rarely, may lead to total obstruction with intractable vomiting
  55. 55. Hypertrophic Gastropathy Menetrier Disease Zollinger- Ellison Syndrome
  56. 56. MENETRIER’S DISEASE Associated with hypochlorhydria or achlorhydria, hypoproteinemia Site: greater curvature of stomach, diffuse involvement of fundus and sparing antrum Gross: marked hypertrophic rugae L/M: foveolar hyperplasia, tortuous cystically dilated glands and extension into base of glands and beyond muscularis mucosae Glandular componenet ↓ed Edematous and inflammed stroma Carcinoma may develop but incidence is same as that Ca originating in atrophic gastritis D/D: carcinoma
  57. 57. ZOLLINGER-ELLISON SYNDROME Accompanied by gastric changes radiographically and grossly similar to Menetrier’s disease L/M: hyperplasia affecting secretory rather than foveolar part of fundic gland Hyperplasia of mainly parietal cells, but ECL cells also ↑ed Fundic gland polyps and intramucosal cysts maybe seen May be associated with MEN
  58. 58. Gastric Pathology Part III
  60. 60. WHO Histologic Classification of Gastric TumorsEPITHELIAL TUMORSIntraepithelial neoplasia: adenomaAdenocarcinoma * ••• Papillary adenocarcinoma ••• Tubular adenocarcinoma ••• Mucinous adenocarcinoma ••• Signet-ring cell carcinoma ••• Undifferentiated carcinoma ••• Adenosquamous carcinomaSmall-cell carcinomaCarcinoid tumorNON-EPITHELIAL TUMORSLeiomyomaSchwannomaGranular cell tumorLeiomyosarcomaGastrointestinal stromal tumor (GIST) (gradation from benign to malignant)Kaposi sarcomaMALIGNANT LYMPHOMA* The Laurén classification subdivides adenocarcinomas into intestinal and diffusetypes
  61. 61. Gastric Polyps-Classification1. Hyperplastic2. Adenomas Intestinal adenomatous villoglandular3. Mixed villous4. Fundic gland Gastric5. Inflammatory fibroid polyp Familial polyposis6. Polyposis syndrome Gardner syn.7. others PJ syn. Cowden syn. Cronkhite-canada syn. Focal hyperplasia Antral gland hyperplasia
  62. 62. Hyperplastic polypsAssociated with  Hypochlorhydria  Dec. pepsinogen  Hypergastrinemia  Ch. Gastritis  Gastric atrophy 95% of gastric polypsGross: Small, sessile, may be multiple up to 20 Located in antrum Several cm in diameterMicroscopically: Hyperplastic (regenerative) surface epithelium Cystically dilated glands Inflammatory cells and smooth muscle in lamina propria No Malignant transformation
  63. 63. Gastric Hyperplastic Polyps
  64. 64. Fundic gland Fundic gland hyperplasia, hamartomatous cystic polyp, Site: multiple polyps in fundus Microscopy:  Microcysts with fundic epithelium (oxyphil cells)  Crypts are short  Increase smooth muscles in pericystic area Associated With  Zollinger ellison syndrome  Proton pump use (prolonged)
  65. 65. Peutz-Jeghers polyps Gastric P-J polyps seen as a part of P-J syndrome Juvenile polyps seen as part of juvenile polyposis syndrome
  66. 66. Inflammatory Fibroid polyp Eosinophilic granuloma, inflammatory pseudotumor Associated with hypochlorhydria Site: antrum Gross: elevated, sessile Microscopy:  Submucosal  Vascular+fibroblatic proliferation, whorling around blood vessels  Polymorphic infiltrate, numerous eosinophils  Many fibers are myofibroblastic  Immunohistochemictry: CD34, bcl-2 +ve
  67. 67. Inflammatory Fibroid Polyp
  68. 68. Adenomatous Polyps/Adenomaso Proliferative dysplastic epithelium with malignant potentialo Back ground chronic gastritis /intestinal metaplasia or autoimmune gastritiso Site: antrumo 5-10% of polypoid lesion in stomacho Increase with age, seventh decadeGross: Single, large, sessile/ pedunculated, grow up to 3-4cm Some time adenomatous change cover large area of gastric mucosa without forming mass lesionMicroscopy:  Dysplatic glands  Pseudostratified epithelium, abnormal nuclei  Increase mitoses  Type: Gastric or intestinal (Tubular/Villous)  40% contain carcinoma at time of diagnosis  Risk of malignancy in adjacent mucosa is 30%
  69. 69. Gastric Adenomatous polyp
  71. 71. Epidemiology of Gastric cancer Second most common tumor in the world High in Japan, Chile, Costa Rica, China, Colombia, Portugal, Russia and Bulgaria Four to six fold less common in USA, UK, Canada, Australia, New Zealand, France & Sweden Male to female ratio 2:1 Intestinal type develops in high risk areas from precursor lesion with mean age of incidence 55yrs, male to female ratio of 2:1, drop in incidence occurred in this type Diffuse type no precursor lesion with mean age of incidence 48yrs, equal male to female ratio
  72. 72. Factors Associated with Increased Incidence of Gastric CarcinomaEnvironmental FactorsInfection by H. pyloriDiet • Nitrites derived from nitrates (water, preserved food) • Smoked and salted foods, pickled vegetables, chili peppers • Lack of fresh fruit and vegetablesLow socioeconomic statusCigarette smokingHost FactorsChronic gastritis • Hypochlorhydria: favors colonization with H. pylori • Intestinal metaplasia is a precursor lesionPartial gastrectomy • Favors reflux of bilious, alkaline intestinal fluidGastric adenomas • 40% harbor cancer at time of diagnosis • 30% have adjacent cancer at time of diagnosisBarrett esophagusGenetic FactorsSlightly increased risk with blood group AFamily history of gastric cancerHereditary non-polyposis colon cancer syndromeFamilial gastric carcinoma syndrome (E-cadherin mutation)
  73. 73. MOLECULAR GENETIC FEATURES Aneuploidy—intestinal > diffuse Germline mutations of E-cadherin gene in families with hereditary Ca of diffuse type Microsatellite instability —20% of gastric Ca, Accumulation of p53 mutation—50% Somatic mutation of APC gene—4% Overexpression of ras p21 product Membrane immunostaining for c-erbB-2—few cases Loss of p16—1/4th gastric Ca Bcl-2 and Bax expression—intestinal>diffuse Loss of Fhit expression—diffuse type and Krukenberg tumor Overexpression of cyclin D1
  74. 74. Morphology Gross Microscopic Special stains Immunohistochemistry Metastases- Virchow node Krukenberg Tumour- Bilateral ovarian Sister Mary Joseph nodule- paraumbilical
  75. 75. MorphologyGROSS:Location; Pylorus and Antrum 50-60% Body and Fundus 25% Lesser curvature 40% Greater curvature 12%Gastric carcinoma is classified on the basis of1. Depth of invasion2. Macroscopic growth pattern3. Histologic subtype Morphologic feature having the greatest impact on clinical out come is the depth of invasion
  76. 76. MorphologyEarly gastric carcinoma Lesion confined to mucosa and submucosa regardless of presence or absence of perigastric lymph node metastasesAdvanced gastric carcinoma A neoplasm extended below submucosa into muscular wallThree Macroscopic Pattern Exophytic Flat /Depressed Excavated (Ulcerated)
  77. 77. Malignant Gastric Ulcer Heaped-up, beaded margins Shaggy necrotic bases Overt neoplastic tissue extending into surrounding mucosa and wallLinitis plasticaRigid thickened leather bottle wall infiltrated byMalignancy
  78. 78. MorphologyHistologic Types Intestinal- Glandular Diffuse- Signet Ring Cell (more than 50% signet ring cell)- PAS positive, CK +, EMA+, CEA+Histologic Grade Well-differentiated Moderately-differentiated Poorly-differentiated Undifferentiated
  79. 79. Clinical Presentation Generally asymptomatic Anorexia ,vomiting Abdominal pain Weight loss Dysphagia Anemia HemorrhageDiagnosis Radiographic techniques for exophytic lesions Endoscopy Biopsy
  80. 80. Virchow node: Mets from Carcinoma of stomach to supraclavicular lymph node (Sentinel)Metastatic Cancers of stomach Includes Mets from Systemic lymphoma, Malignant melanoma, Ca breast , Ca lung
  81. 81. Gastric Malignant Ulcer(with depth of invasion) 
  83. 83. Gastric Adenocarcinoma
  84. 84. Intestinal & Diffuse type of Adenocarcinoma
  86. 86. PAS Positive Signet Ring Cell
  87. 87. Prognosis of Gastric Carcinoma Depends on Depth of invasion Extent of Lymph Node involvement Distant metastases Histologic type Resection margins DNA Ploidy , P53 mutation Five year S.R of surgically treated early carcinoma is 90- 95% in advanced cases it is 15%
  88. 88. Gastrointestinal Stromal Tumors Non- epithelial neoplasms of gut Site: stomach, small bowel, other portions of gut, omentum, mesentry, retroperitonium 60% submucosal, 30% subserosal, 10% intramural Origin interstitial cell of CajalPROGNOSIS: Tumor size, mitoses, necrosis, Stomach GIST has better prognosis than intestinal
  89. 89. New Concept-GISTSmooth muscle Neuronal (GANT) Both UndifferentiatedSm. Muscle Actin NeuronSp.Enolase Morpholigically & Unable to classifyDesmin Leu 7 immunohistoche- mically exhibitMyosin S-100 both sm. muscle Usually CD34+ve and neuronal differentiation C-Kit positive (CD117)
  90. 90. GIST c-KIT Positive
  91. 91. Stomach Lymphoma Classification:  Low grade: Small lymphoid cells  High/ intermediate: large lymphoid cells Rare…1-4% of GI malignancies Primary GI lymphoma exhibit no evidence of liver, spleen, mediastinal lymph node or bone marrow involvement at time of diagnosis Regional lymph node involvement may be present Collision tumors:  Lymphoma+adenocarcinoma Carcinoma can develop after treatment of lymphoma
  92. 92. Grading system indicating degree of certainty of diagnosis of MALT LymphomaGrade 0 (Normal) Scattered plasma cells in lamina propria. NO lymphoid folliclesGrade 1 (Active chronic Small clustes of lymphocytes in laminagastritis) propria. NO follicles/ LELsGrade 2 (Active chronic gastritis Prominent follicles with surroundingwith florid follicles) mantle zone+plasma cells. NO LELsGrade 3 (suspicious lymphoid Follicles surrounded by small lymphocytesinfiltrate in lamina propria, infiltrate diffusely in lamina propria andreactive probably) Occasionally into epitheliumGrade 4 (suspicious lymphoid Folicles surrounded by MZ cells diffuseinfiltrate in lamina propria, infiltrate in lamina propria and intolymphoma probably) epithelium in small gps.Grade 5 (low grade B-Cell Dense diffuse infiltrate of MZ cells inlymphoma of MALT) lamina propria with prominent LELs
  93. 93. MALT
  94. 94. MALT Lynphoma
  95. 95. NEUROENDOCRINE DIFFERENTIATION1. Well differentiated neuroendocrine tumors (carcinoid): Slow growing Neuroendocrine cells of gastric mucosa2. Atypical carcinoid/ neuroendocrine carcinoma/ large cell neuroendocrine ca Tumors with obvious morphological features of neuroendocrine differentiation but obvious atypia: Trabaculae, rosettes, insulae; dense core secretory granules, NSE+ Atypia—invasiveness, necrosis, mitosis3. Small cell carcinoma: Analogous to pulmonary counterpart Aggressive behavior4. Otherwise typical adenocarcinoma of diffuse or intestinal type having cells with argyrophilia or neuroendocrine differentiation
  96. 96. Carcinoid