Stomach Pathology

STOMACH

Fundus

Specialized glands containing chief and parietal cells

Pit/gland = 3:1

Antrum, cardia

Mucous glands

Pit/gland = 1:1

Cardia up to 1.5cm from esophagus

Parietal (acid-producing): pale eosinophilic, fried eggs, located more proximal in neck

Chief (enzyme-producing): amphophilic, basal nuclei, more towards base of pits

 

Mucus neck cells

Foveolar cells

APUD cells

Endocrine: clear cytoplasm, apical nuclei, in neck

Antrum: Gà gastrin, ECà serotonin, Dà somatostatin

Fundus: ECLà histamine, Xà unknown

 

Histochemistry and Immunohistochemistry of the Stomach

Stomach: MUC1, MUC5AC, MUC6, PAS

Intestine: MUC2, Alcian blue pH=2.5

 

METAPLASIA

Pyloric – replacement of fundic glands by mucous glands

Intestinal – Paneth, brush border cells, goblet cells

Intestinal: neutral mucinà acid mucin

Small bowel: sialomucin

Large bowel: sialomucin and sulfomucin

Complete: columnar – goblets and enterocytes

Incomplete: differs by mucin type

Pyloric: specialized cells replaced by mucus-secreting

Ciliated

Subnuclear vacuolated

Pancreatic acinar: no islets

APPROCH TO GASTRIC BIOPSY

Surface: ulcer, organism

Epithelium: intestinal metaplasia, surface lymphocytes

Glands: injury by PMN or lymphocytes

LP: expanded by inflammation (type), infiltration by tumor

Granuloma

Lymphoid follicles

CONGENITAL ANOMALIES

Pancreatic heterotopia

Duplication: cystic mass, not always attached to stomach

Diverticula: rare

Cysts: Menetrier, gastritis cystica profunda, intramural congenital cysts…

Pyloric stenosis

GASTRITIS

• Reactive gastropathy / chemical gastritis
  • Bile and/or duodenal contents (alkaline) reflux
    • +/- Post-surgical
  • Alcohol
  • NSAIDS
  • Steroids
• Chronic gastritis / chronic active gastritis
  • Non-atrophic, predominantly antral
    • Helicobacter
      • Multi-focal atrophy in later stages
  • Atrophic, fundic
    • Autoimmune
• Other drugs
  • Iron
    • Stainable iron crystalline material present
  • Aluminum based antacids (gastric mucosal calcinosis)
    • Small, pink, partially calcified. refractile crystals
  • Kayexalate
    • Rhomboid or triangular, non-polarizable basophilic crystals
  • Chemotherapy
• Hypertrophic/hyperplastic gastritis
  • Menetrier disease
  • Zollinger Ellison syndrome
• Special types
  • Collagenous
  • Lymphocytic
  • Eosinophilic gastroenteritis
  • Granulomatous
• Vascular
  • Gastric vascular antral ectasia (GAVE)
  • Portal hypertensive gastropathy
  • Ischemic
• Infectious
  • Helicobacter
  • Viral
  • Fungal
  • Parasitic

	H. pylori	Autoimmune
Location	Antrum	Body
Infiltrate	Neutrophils, subepithelial plasma cells	Lymphocytes, macrophages
Acid production	Increased to slightly decreased	Decreased
Gastrin	Normal to decreased	Increased
Other lesions	Hyperplastic/inflammatory polyps	Neuroendocrine hyperplasia
Serology	Antibodies to H. pylori	Antibodies to parietal cells (H+-K+-ATPase, IF)
Sequelae	Peptic ulcer, adenocarcinoma	Atrophy, pernicious anemia, adenocarcinoma, carcinoid tumor
Association	Low SES, poverty, rural residence	Autoimmune diseases: thyroiditis, DM, Graves

AUTOIMMUNE ATROPHIC GASTRITIS

• Atrophic gastritis accompanied by anti-parietal cell and anti-intrinsic factor antibodies
• AKA autoimmune metaplastic atrophic gastritis, type A gastritis
• Clinicopathological diagnosis
• Frequently results in
  • Achlorhydria
  • Hypergastrinemia
  • Vitamin B12 deficiency
  • Iron deficiency
  • Loss of pepsin
• Associated with development of intestinal type gastric adenocarcinoma
• Dutch women
• Requires biopsies from body and antrum
• Atrophic gastritis restricted to gastric body
• Antrum normal but shows focal inflammation and atrophy
• Active phase
  • Lymphocytic and plasma cell infiltrate
  • Centered in deep lamina propria of body
  • Sparse in cases with advanced atrophy
• Chronic phase
  • Markedly thinned mucosa composed largely of foveolae
  • Atrophy of oxyntic glands
  • Destruction and loss of both parietal and chief cells
    • Extensive but not complete
    • Results in pseudopyloric metaplasia
  • Intestinal metaplasia is usually extensive
  • Endocrine cell proliferation
    • No G cells in body
    • G cell hyperplasia restricted to antrum
• Anti-parietal cell and anti-intrinsic factor antibodies
• Pernicious anemia may develop in long-standing cases
• Takes years for body vitamin B12 stores to be depleted
• Low prevalence of Helicobacter
• DDx
  • Helicobacter associated chronic gastritis can result in antral atrophy with or without intestinal metaplasia indistinguishable from atrophic body mucosa of autoimmune gastritis
  • Endocrine cell hyperplasia not seen as G-cells destroyed in early phases of H. pylori gastritis
  • Clinicopathologic correlation and of biopsy location necessary for distinction

HELICOBACTER GASTRITIS

• Most common cause of chronic active gastritis
• H pylori
  • Most common species to infect humans
  • Small curved rods
  • Frequently in chain of two, resembling a seagull
  • May become coccoid after treatment
• H heilmanni
  • Domestic cats, dogs
  • Occasionally infects humans
  • Larger than H pylori
  • Spirochete structure visible on light microscopy
• Gastric antrum
• May extend to body and cardia
• May wash into duodenum or involve gastric surface metaplasia in duodenum
• Present in mucus or attached to epithelial cell surface
• Localized to surface foveolar epithelium and gland necks
• Less frequently attached to parietal and chief cells
• Intraepithelial PMNS in surface and gland necks
• Moderate to marked lympho-plasmacytoid infiltrate in superficial LP
• Basal lymphoid hyperplasia
• Long-standing cases produce multifocal atrophic gastritis
  • Patchy process
  • Destruction of glands
  • Lamina propria fibrosis
  • Intestinal metaplasia
  • May involve all regions of stomach
  • Active inflammation may resolve
  • Helicobacter may become difficult to identify
  • Non-atrophic areas may revert to normal
• Untreated cases
  • 70-80% organisms easily found on H&E
  • 10-25% require careful search on H&E
  • 10-20% require special stain
    • Alcian Yellow
    • Giemsa
    • Dif-Quik
    • Steiner and Steiner
    • Warthin Starry
    • Genta
• Special stains +/- IHC
  • Pediatric cases with clinical suspicion
  • Pediatric and adult cases with chronic active gastritis
  • Cases refractory to treatment
  • GEJ with gastric type mucosa and acute inflammation, unless biopsies of stomach available for examination
• DDx
  • Mixed bacterial flora in bed of an ulcer or as contaminants washed into stomach from oral cavity
    • Lack uniform appearance of Helicobacter
    • Lack intimate association with epithelial cell surface
  • Occasionally after treatment Helicobacter may appear almost spherical
• Associated disorders
  • Duodenal ulcer
  • Gastric ulcer
  • Gastric adenocarcinoma
  • Gastric extranodal marginal zone B cell lymphoma

REACTIVE GASTROPATHY

• Full thickness specimens and clinical and endoscopic correlation required to demonstrate extent of foveolar hyperplasia and atrophy of oxyntic glands
• Most common causes
  • Ingested agents
    • Alcohol
    • Drugs
    • Aspirin / NSAIDs
    • Iron and potassium
    • Corrosive agents
  • Physical injury
    • Radiation
    • Instrumentation
    • Hepatic artery chemotherapy
  • GI motility problems
    • Prolapse gastropathy
    • Post-gastrectomy bile reflux
      • Occasionally seen with intact stomach
  • Ischemia
  • Stress
  • Idiopathic
• Microscopy
  • Usually involves antrum
  • May involve body if post-antrectomy
  • Foveolar hyperplasia
    • Corkscrew/serrated elongated crypts
  • Muscularis mucosae hyperplasia
    • Muscle fibers in lamina propria
    • Extending to surface
    • Similar to solitary rectal syndrome
  • Minimal to absent PMNs and chronic inflammation
    • Acute without chronic inflammation occasionally
    • Eosinophils may be present
  • Regenerative changes in foveolar cells
    • Enlarged and hyperchromatic nuclei
    • Prominent nucleoli
    • Decreased cytoplasmic mucin
  • Lamin Propria edema and congestion
  • Changes similar to ischemic injury
    • Hemorrhage and necrosis of superficial mucosa
    • Erosions and ulcers
    • Inflammation restricted to ulcer
    • Little or no inflammation in surrounding mucosa
  • Difficult to sort out if complicated by Helicobacter
• DDx
  • Foveolar hyperplasia
  • Localized hyperplasia adjacent to other lesions
  • Hyperplastic polyps
  • Menetrier disease
  • Cronkhite-Canada polyps

COLLAGENOUS GASTRITIS

-   Children and young adults

• Age 1-22
• Iron deficiency anemia
• Endoscopy shows gastric nodularity
• No associated colitis or autoimmune disorders

-   Adults

• Age 34-80
• Frequently present with diarrhea
• Endoscopy shows erythema
• Frequent associations
  • Collagenous colitis
  • Celiac disease
  • Collagenous sprue

-   Autoimmune diseases

-   Microscopy

• Involves antrum and/or body
• Patchy or diffuse
• Irregular, thickened subepithelial collagen layer
  • > 10 microns
  • Average 30-40 microns
  • Ragged interface with LP
  • Envelops capillaries
  • Glandular atrophy
  • Luminal surface epithelium flattened, may detach
  • LP inflammatory infiltrate
    • Predominantly lymphocytes and plasma cells
    • Variable intraepithelial lymphocytes
    • From normal to 61/100 enterocytes
    • Fewer neutrophils and eosinophils
  • Trichrome stain

-   Associated lymphocytic gastritis in 33% of cases

-   DDx

• RT: diffuse fibrosis rather than just below BM
• Scleroderma: fibrosis around crypts, +/- diffuse

LYMPHOCYTIC GASTRITIS

-   Severe cases have nodular targetoid and eroded lesions along proximal rugae

• Termed “varioliform gastritis”

-   May result in atrophy

-   May be associated with:

• Collagenous gastritis
• Celiac disease
  • Predominantly antral
  • Helicobacter
    • Predominantly in body mucosa or diffuse
  • Crohn disease
  • HIV infection
  • Lymphoma

-   Endoscopic appearance ranges from normal to nodular targetoid erosions (varioliform) to giant mucosal folds resembling hypertrophic gastritis

-   Microscopy

• Prominent intraepithelial lymphocytes (IELs)
  • T cell phenotype
  • Usually CD8+
  • > 25 lymphocytes per 100 epithelial cells
  • Lymphoepithelial lesions, if present, are small, < 3 lymphocytes
  • Lymphocytes fill lamina propria
  • Neutrophils can be seen
  • Mild foveolar hyperplasia
  • Variable degeneration of surface and foveolar epithelium

-   DDx

• Extranodal marginal zone B cell lymphoma
  • Monomorphic infiltrate in LP
  • B cell lineage
  • Plasma cell differentiation with Dutcher bodies
  • Lymphoepithelial lesions
    • > 3 lymphocytes in epithelium

GRANULOMATOUS GASTRITIS

-   Granulomas usually superficial

-   May be transmural on resection specimens

-   Usually non-necrotic

-   Variable acute and chronic inflammation

-   May be focal or diffuse

-   Most common in antrum

-   DDX

• Crohn disease (most common cause)
• Sarcoidosis
• Helicobacter (controversial)
  • Most common cause after above excluded
  • Syphilis
    • 2nd: plasma cells
    • 3rd: gumma (granuloma), endarteritis
  • Foreign body reaction (polarize)
  • Drugs, including antacids
  • Infection
    • Mycobacteria
    • Fungi
    • Parasites
  • Common variable immunodeficiency
    • Rare granulomas in stomach
  • Adjacent to gastric neoplasms
  • Isolated granulomatous gastritis (IGG)
    • Isolated, idiopathic
    • Very rare, if it exists at all
    • Primarily reported in adults
    • Endoscopic appearance ranges from non-specific minor changes to thickened mucosal folds with outlet obstruction

DIEULAFOY LESION

-   Abnormally large artery in mucosa or higher

-   50 year old

-   Primarily gastric but been reported in other sites

-   Artery of size expected in submucosa

-   Artery normal in structure

-   Accompanied by vein

-   Risk of ulceration + bleeding

-   Small ulcer (2-10 mm)

-   Localized to area where artery and vein reach mucosa

-   Perforated artery and vein show inflammation and necrosis

 

GASTRIC ANTRAL VASCULAR ECTASIA

-   Involves antrum

-   Women

-   > 40 years old

-   Present with iron deficiency anemia

-   Associated with cirrhosis, autoimmune disorders, connective tissue disorders (CTDs)

• Autoimmune atrophic gastritis
• Hypothyroidism
• Primary biliary cirrhosis
• Reynaud phenomenon, sclerodactyly, CREST

-   Endoscopic appearance

• “Watermelon stomach”
• Parallel longitudinal red stripes in antrum converging on pylorus

-   Microscopy

• Mucosal vascular capillary ectasia
• No vascular malformations
• Submucosa may have tortuous vessels
• Fibrin thrombi in capillaries
• CD61 highlights thrombi
• Edema and hemorrhage
• Fibromuscular hyperplasia of lamina propria
• LP hyalinization
• Mild chronic inflammation in lamina propria
• Atrophic gastritis with intestinal metaplasia frequent
• Endocrine cell hyperplasia

-   Microscopic changes less spectacular than endoscopic findings

-   Does not respond to lowering of portal pressure, even if associated with cirrhosis

-   Ablation of vessels may help

-   DDx

• Portal HTN

 

Portal Hypertensive Gastropathy

-   Involves fundus and  corpus

-   Gastric vascular changes associated with portal hypertension

-   Dilated, tortuous vessels in submucosa of gastric body

-   May not be visible on shallow biopsy specimens

-   Mucosal vascular distension

-   Nearly always associated with HTN due to cirrhosis

-   Endoscopic appearance

• Diffuse changes
• Cherry red spots
• White reticular pattern
  • § May resemble snakeskin
  • Mosaic appearance in proximal stomach

-   Responds to lowering of portal pressure

 

ACUTE EROSIVE GASTRITIS

-   Called acute hemorrhagic gastritis when severe with bleed

-   Risk factors

• NSAIDs, ASA, CTSD, Fe (polarizable), crack
• Shock
• Sepsis
• Cushing ulcer (head injury)
• Curling ulcer (severe burn)
• Chemoradiation

-   Microscopy

• Sloughing of surface epithelium
• Base with necrotic debris
• Hemorrhage in LP
• Reactive epithelium

 

CHEMOTHERAPY AND RADIATION GASTRITIS

-   Patchy distribution

-   Early

• Erosion
• Dilated bleeding capillaries
• Regenerative atypia

-   Late

• Flat mucosa
• Deep nonhealing ulcers
• Profound atrophic gastritis
• Surface maturation of foveola and glands
• Submucosal obliterative enarteritis

-   Preserved nuclear polarity

-   Vesicular nuclei, prominent nucleoli

-   Mitoses permitted but no atypical

-   Eosinophilic vacuolated cytoplasm

-   Normal N/C ratio

-   Atypical FB and endothelial cells

-   No intestinal metaplasia

STOMACH POLYPS

HAMARTOMATOUS POLYPS

-   Fundic gland polyp

• FAP-associated
  • 50% dysplasia
  • APC mutations
  • 90% multiple
  • Sporadic
    • Beta-catenin mutations
    • Rare dysplasia
    • 40% multiple

-   Peutz-Jeghers polyp

• Other GI polyps
• Mucocutaneous pigmentation

-   Juvenile polyp

• Other GI polyps
• Smooth-surfaced
• Short narrow stalk causing repeated torsion

-   Cronkhite-Canada syndrome-associated polyp

INFLAMMATORY POLYPS

-   Inflammatory retention polyp

-   Polypoid gastritis

 

HYPERPLASTIC POLYPS

-   Hyperplastic polyp

• 75% of all gastric polyps
• Antrum > body

-   Polypoid foveolar hyperplasia

-   Foveolar polyp

-   Gastritis cystica polyposa/profunda

• Post-surgical
• Associated with severe atrophic gastritis

-   Menetrier’s disease

• Fundus only
• Diffuse rugal hypertrophy
• Hyperproteinemia

 

EPITHELIAL POLYPS

-   Adenoma

-   Polypoid carcinoma

-   Carcinoid tumour

 

MESENCHYMAL POLYPS

-   Inflammatory fibroid polyp

-   Inflammatory myofibroblastic tumour

-   Gastrointestinal stromal tumour

-   Vascular tumour

 

LYMPHOID POLYPS

-   Lymphoid hyperplasia

-   Lymphoma

 

HETEROTOPIC POLYPS

-   Heterotopic pancreatic polyp

-   Pancreatic acinar metaplasia

-   Brunner’s gland hyperplasia

 

POLYPOID LESIONS

-   Oxyntic gland hyperplasia/adenoma

-   Xanthoma

-   Langerhans histiocytosis

-   Granuloma

-   Amyloidosis

-   Hemosiderosis

-   Calcium deposits

HYPERTROPHIC GASTROPATHIES AND POLYPS

-   Hamartomatous

• Fundic gland polyp (beta-catenin, APC)
• Peutz-Jeghers (STK11)
• Juevenile polyp (PTEN, DPC/SMAD4, BMPR1A)
• Cowden’s syndrome polyp (PTEN)
• Cronkhite-Canada

-   Inflammatory/hyperplastic

• Hyperplastic polyp
• Prolapse
• Lymphoid hyperplasia
• Mentrier (TGF-alpha)

-   Neoplastic

• Adenoma
• Carcinoma
• Carcinoid
• Mesenchymal
  • Schwannoma (Schwannomin/Merlin)
  • GIST (CD117, PDGFR-alph)
  • Inflammatory fibroid polyp (PDGFR-alpha)
  • Lymphoma

-   Mucosal folds

• Menetrier
• ZES
• Hypertrophic hypersecretory gastropathy
• Malignant or inflammatory infiltration

Fundic gland polyp

Juevenile polyp

Peutz-Jeghers polyp

-   AD

-   11 yo

-   Phenotype

• Multiple GI hamartomatous polyps
  • Most common in small intestine
  • Also occur in stomach, colon
  • Lower frequency in bladder and lungs
  • Can initiate intussusception, occasionally fatal
  • Mucocutaneous hyperpigmentation
    • Dark blue to brown macules around mouth, eyes, nostrils, buccal mucosa, palmar surfaces of hands, genitalia, perianal region

-   Increased risk of malignancies

• Colon
  • Arise independently of hamartomatous polyps
  • Hamartomtous polyps are not precursor lesions
  • Pancreas
  • Breast
  • Lung
  • Ovaries: SCTATs
  • Uterus
  • Cervix: minimal deviation adenocarcinoma
  • Testicles: LGCSCT

-   LKB1/STK1

• Kinase
• Regulates cell polarization, growth, metabolism

-   Gross

• Large, pedunculated with lobulated contour

-   Micro

• Arborizing network of connective tissue, smooth muscle, lamina propria, glands lined by normal-appearing intestinal epithelium

 

Cowden Syndrome

Bannayan-Ruvalcaba-Riley Syndrome

-   AD

-   Hamartomatous polyp syndrome

-   PTEN

• Loss-of-function mutations
• Lipid phosphatase
• Inhibits signaling through PI3K/AKT pathway
• Also mutated in some patients with juvenile polyposis

-   Phenotype

• Macrocephaly
• Intestinal hamartomatous polyps
• Benign skin tumors
  • Trichilemmomas
  • Papillomatous papules
  • Acral keratoses
  • Bening soft tissue tumors
    • Subcutaneous lipomas
    • Leiomyomas
    • Hemangiomas
  • Pigmented macules on glans penis

-   No have increased risk of GI malignancy

-   Increased risk

• Breast carcinoma
• Follicular carcinoma of thyroid
• Endometrial carcinoma

-   Bannayan-Ruvalcaba-Riley syndrome distinguished from Cowden syndrome on clinical grounds

• Mental deficiencies
• Developmental delays
• Lower incidence of neoplasia

 

Cronkhite-Canada Syndrome

-   Nonhereditary

-   50 years old

-   Diarrhea, weight loss, abdominal pain, weakness

-   Polyps (stomach, small intestine, colorectum) histologically indistinguishable from juvenile polyps

• However, nonpolypoid intervening mucosa shows cystic crypt dilatation, LP edema, and inflammation

-   Associated abnormalities

• Nail atrophy and splitting
• Hair loss
• Areas of cutaneous hyperpigmentation and hypopigmentation

-   Cause unknown and no specific therapies available

-   Supportive nutritional therapy alleviates cachexia and anemia, occasionally induces remission

MENETRIER DISEASE

-   3M:F

-   Excessive TGF-alpha secretion

-   Risk of developing adenocarcinoma

-   No associated extra-GI lesions

-   No associated colorectal polyps

-   Massive gastric foveolar hyperplasia involving full thickness of mucosa

-   Decreased acid production

-   Hypoproteinemia, hypoabuminemia, peripheral edema, weight loss

-   GI bleeding

-   Adults

• Chronic, insidious onset
• Fundus only

-   Pediatric

• Sudden onset
• Antrum and fundus
• Associated with CMV (blood, urine, stomach)
• Often self-limited

-   Microscopy

• Foveolar hyperplasia of gastric body/fundus
  • Corkscrew shaped and cystically dilated
  • May extend into submucosa
  • Produces giant gastric folds
  • Atrophy of oxyntic glands
    • Mucous cells extend to base of glands
    • Decreased acid secretion
  • Variable edema
  • Mixed inflammatory infiltrate, usually mild
  • Hypertrophic muscularis mucosae may extend into lamina propria
  • Intestinal metaplasia late in disease
  • Granulomas late in disease

-   Differential Diagnosis on Biopsy

• Hyperplastic polyps
• Reflux gastropathy
• Localized hyperplasia adjacent to other lesions
• Cronkhite-Canada polyp
  • Hair, nail, skin pigmentation changes present
  • Colorectal polyps very common

-   Full thickness specimens, clinical + endoscopic correlation required to demonstrate extent of foveolar hyperplasia and atrophy of oxyntic glands or presence of a discrete polyp

GASTRITIS CYSTICA POLYPOSA

mucosal prolapse

Clin: ­ colorectal and gastric carcinomas?, near stoma site

Gross: large polyp

Micro

Resembles HP, may get glands into the muscularis

Reactive gastropathy changes (due to prolapse)

Ddx: invasive adenocarcinoma

 

PANCREATIC HETEROTOPIA

Stomach (antrum), deuodenum, jejunum, Meckel, GB, umbilicus, mediastinum

Gross

Central mucosal dimple

Micro

Submucosal

Acini, ducts, islets, SM.

Called adenomyoma if no acini and islets.

 

XANTHOMA

Related to bile reflux, not with hyperlipidemia

Gross: small yellow nodules

Micro: lipid-laden histiocytes cells, not discrete, upper LP, small bland nuclei

IHC/SS: CD68, Sudan black, oil red O. PAS- (because it’s fat)

DDx

Xanthoma	PAS-
Malakoplakia	PAS-, MGB
Signet ring carcinoma	PAS+
Whipple	PAS+
MAI	PAS+, AFB+

 

THICK RUGAE

Inflammatory infiltration: H pylori, lymphocytic gastritis

Neoplastic infiltration: lymphoma, signet-ring

Hypertrophic hypersecretory gastropathy

ZES

Menetrier

Sarcoidosis

 

ZOLLINGER-ELLISON SYNDROME

20% MEN-1, 80% sporadic

Gastrinomas in pancreas, duodenum, Meckel, gastric antrumà hypergastrinemiaà parietal cells hypertrophy/HPà ulcers

Alsoà ECL HPà carcinoids

Fundus/body (where parietal cells are) but antrum normal (don’t know why G-cell HP does not affect)

Large rugal folds

Micro

Parietal cells HP/hypertrophy (fundus/body)

ECL cell linear HP (body)

IHC: chrA, syn, gastrin+

STOMACH TUMORS

GASTRIC ADENOMA

-Not major precursor for adenoma. Intestinal metaplasia is a higher risk

Types

-Intestinal: goblets, Paneth

-Gastric: columnar with neutral mucin

Microscopy

-LG to HG dysplasia

-Villous,…

-Can be flat or depressed

 

GASTRIC DYSPLASIA

Classes

-LG: crowding, nuclear elongation

-Indeterminate: next to ulcer

-HG: rounded, prominent nucleoli,

 

GASTRIC CARCINOMA

Risks: SNL (smoking, nitrates/nitrites, low socioeconomic status), Japan, H.pylori, autoimmune chronic gastritis, genetics, prior partial gastrectomy, adenoma, intestinal metaplasia

Gross: flat, ulcerated, exophytic

 

Peptic ulcer	Ulcerated cancer
	Larger
	More irregular
	Head-up or rolled edge
	Radial???
	Immobile mucosa

 

 

WHO classification

Adenocarcinoma (intestinal, diffuse)

Papillary

Tubular

Mucinous: >50%

Signet-ring: >50%

Medullary: >50% undifferentiated areas without fibrous stroma

Adenosquamous

Squamous

Small cell

Undifferentiated

 

Lauren classification

Intestinal

Diffuse

Mixed

 

Grading: 5%-50%-95%

 

Location

Esophageal: >50% in esophageus

Junctional: 50-50%

Gastric: >50% in stomach

 

Microscopy

intestinal

-resembling colonic carcinoma, forming glands with solid or papillary areas

diffuse/signet ring

-Desmoplasia

-Thickened, rigid, leather bottle-like stomach

Mets (3)

-LN: supraclavicular (Virchow’s nodes)

-Blood: liver

-Intraperitoneal: Krukenberg

IHC: CDX2 (not sure), CK7, CEA, CK20+/-

Prognosis

-Staging: no1

-Age >70

-Proximal

-CEA>10ng/mL

-CA19-9 high

-Diffuse type

Differential Diagnosis

Histiocytes	Signet ring
Negative	Alcian blue+, PAS+
Nuclei similar to adjacent normal histiocytes	Larger nuclei, different from adjacent histiocytes
	CK+

 

GLOMUS TUMOR

Clin: seen in distal extremities and stomach

-subungual (painful here)

-women

Gross: small with mucosal ulceration

Micro: small round epithelioid cells that surround dilated bv

Positive stains: actin, h-caldesmon, collagen type 4

EM: cytoplasm packed with myofilaments with focal condensations

 

GASTROINTESTINAL STROMAL TUMOR (GIST)

-PAS+ skenoid fibres

-CD34, c-kit +

-c-kit or PDGFR-α mutations

 

HISTIOCYTOID CELLS

-Xanthoma/malakoplakia: CD68+

-Signet-ring cell carcinoma: CK+, mitoses, infiltration

-MAI: AFB+

-Whipple: PCR, EM, Giemsa?

-Granular cell tumor

 

SPINDLE CELLS

Benign

-Inflammatory fibroid polyp: eosinophils, CD34+

-SFT: CD34, BCL2, CD99

-GIST

-Glomus tumor

-Schwannoma

-Lipoma

-Leiomyoma

Malignant

-Malignant GIST

-Malignant SFT

-LMS

-Melanoma

 

STAGING

T1   up to submucosa

T2   into MP

T3   visceral peritoneum

T4   adjacent structures

 

N0

N1   6 LN

N2   15 LN

 

References:

1. Robbins & Cotran Pathologic Basis of Disease, 8th edition. Vinay Kumar, MBBS, MD, FRCPath; Abul K. Abbas, MBBS; Nelson Fausto, MD; Jon Aster, MD. Saunders. Published June 2009.

2. Sternberg’s Diagnostic Surgical Pathology, 5th edition. Darryl Carter, Joel K. Greenson, Victor E. Reuter , Mark H. Stoler. Lippincott Williams & Wilkins. Published Aug 26 2009.

3. College of American Pathologists Cancer Protocols and Checklists:

http://www.cap.org/apps/cap.portal?_nfpb=true&cntvwrPtlt_actionOverride=/portlets/contentViewer/show&_windowLabel=cntvwrPtlt&cntvwrPtlt{actionForm.contentReference}=committees/cancer/cancer_protocols/protocols_index.html&_pageLabel=cntvwr