(01:17:22) (01) 1b Pathology of The Stomach by DR FSK

Pathology of the
Gastrointestinal Tract
Farrah Kristine Q. Fontilla-Santiago, MD FPSP
OUTLINE
Congenital Abnormalities
Esophagus
Stomach
Small Intestine
Colon
Peritoneal Cavity
Stomach
Gastric
Disorders
Gastropathy and Acute Gastritis

Gastric Ulceration
Gastric Tumors
Gastric
Disorders
GASTRITIS
Inflammatory Disorders
Gastric Ulceration
Gastric Tumors
✤ mucosal inflammatory process
✤ ACUTE GASTRITIS :
GASTRITIS ✤ when neutrophils are present
✤ GASTROPATHY:
✤ when inflammatory cells are

Chronic Gastritis rare or absent
Acute Gastritis
✤ includes gastric injury or
dysfunction
✤ Irritants: NSAIDs, alcohol, bile

Inflammatory Gastric Diseases
Gastritis
Gastritis
Disruption of Protective Mechanisms in
Gastropathy and Gastritis
✤ Inhibition of cyclooxygenase (COX) by NSAIDs
✤ Inhibition of gastric bicarbonate transporters
✤ Reduced mucin and bicarbonate secretion
✤ Decreased oxygen delivery

Gastritis
Gastropathy & Mild Acute Gastritis

Gastropathy & Gastritis
✤ As injury progresses, erosions, i.e. superficial mucosal defects are

accompanied by neutrophilic infiltrates and fibrin-containing
exudate within the lumen.
✤ ACUTE EROSIVE HEMORRHAGIC GASTRITIS
✤ concurrent erosion & hemorrhage
✤ erosion is accompanied by pronounced neutrophilic infiltrate

within the mucosa
Acute Gastritis
✤ sloughing of the superficial mucosa (EROSION) - impt cause of bleeding
Acute Gastritis
✤ infiltration of neutrophils, plasma cells in the lamina propria
Stress-Related Mucosal Disease
✤ Occurs with severe trauma, excessive burns, intracranial disease,

major surgery, serious medical disease & other forms of severe
physiologic stress.
✤ specific names based on location & clinical associations:
✤ STRESS ULCERS - shock, sepsis or severe trauma
✤ CURLING ULCERS - severe burns and trauma
✤ CUSHING ULCERS - intracranial disease

Stress-Related Mucosal Injury
✤ PATHOGENESIS:
✤ often related to local ischemia
✤ systemic hypotension>> reduced blood flow due to stress-

induced splanchnic vasoconstriction
✤ also due to upregulation of inducible NO synthase and

increased release of endothelin-1 (vasoconstrictor)
✤ from shallow erosions to deeper

lesions (mucosa)
✤ acute ulcers: rounded , <1cm in

diameter
✤ Base is stained brown-black;

found anywhere in the stomach,
multiple
✤ margins and base of ulcers are

not indurated

✤ (-) scarring and thickening of blood vessels

Non-Stress-Related causes of
Gastric Bleeding
✤ DIEULAFOY LESION
✤ GAVE (Gastric Antral Vascular

Ectasia)
Gastritis
Gastritis
Chronic Gastritis
Acute Gastritis
Chronic Gastritis
✤ most common cause : infection with H.pylori
✤ Other causes: autoimmune gastritis, radiation injury, chronic bile

reflux, mechanical injury, Crohn disease, amyloidosis, GVHD
✤ Symptoms are less severe but more persistent
✤ Nausea, upper abdominal pain
✤ Vomiting, hematemesis
Gastritis
Chronic Gastritis
Acute Gastritis
Helicobacter pylori gastritis
Autoimmune Gastritis
H.pylori Gastritis seen in almost all patients

with duodenal ulcers
Helicobacter pylori Gastritis
✤ acute infection: no symptoms
✤ chronic gastritis : causes the

patient to seek treatment
✤ present in 90% of pxs with

chronic gastritis affecting the
antrum
Chronic Gastritis - H.pylori

✤ US: poverty, household crowding, limited education, African
American or Mexican American ethnicity, residence in rural areas,
birth outside the US
✤ acquired in childhood and persists for life without treatment
✤ transmission: fecal oral route

✤ PATHOGENESIS
✤ presents as predominantly antral gastritis with normal or

increased acid production
✤ if limited in the antrum, increased acid production results in

greater risk of duodenal peptic ulcer
✤ MULTIFOCAL ATROPHIC GASTRITIS - if involving the

gastric body & fundus
✤ In contrast to autoimmune gastritis, atrophy is typically patchy

H.pylori Gastritis
✤ 4 FEATURES
LINKED TO H.
PYLORI
VIRULENCE
✤ 1. Flagella
✤ 2. Urease
✤ 3. Adhesins
✤ 4. Toxins
Chronic Gastritis
✤ H. pylori are found nestled within the mucus layer overlying mucosa
H.pylori Gastritis
✤ Distribution can be irregular,

with heavy colonization
adjacent to those with few
organisms
✤ Organisms most easily

demonstrated with
immunostains or
histochemical stains
H.pylori Gastritis
✤ Antrum: preferred biopsy
site
✤ Antral mucosa is usually

erythematous, coarse or
nodular appearance
✤ Plasma cells in clusters or

sheets + lymphocytes,
macrophages, neutrophils
within lamina propria
H. pylori gastritis
✤ tropism for gastric epithelial cells, not found in intestinal metaplasia
or duodenal epithelium
special stain for

H.pylori
H. pylori gastritis
✤ pit abscesses, intraepithelial neutrophils, subepithelial plasma cells

H. pylori gastritis
✤ organisms abundant in the surface mucus
✤ intraepithelial lamina propria cells are prominent

H. pylori gastritis
✤ lymphoid aggregates with

germinal centers, abundant
subepithelial plasma cells
within the lamina propria
✤ Represent induced MALT
✤ potential to develop into

lymphoma

✤ diagnostic tests: serologic tests for antibodies, fecal bacterial

detection, urea breath test
✤ generation of ammonia by the bacterial urease
✤ gastric biopsy specimens : rapid urease test, bacterial culture,

bacterial DNA detection by PCR
✤ treatment: combination of antibiotics and PPIs

Gastritis
Chronic Gastritis
Acute Gastritis
Helicobacter pylori gastritis
Chronic Gastritis -
Autoimmune Atrophic Gastritis
✤ typically spares the antrum
✤ associated with hypergastrinemia
✤ <10% of cases of chronic gastritis
✤ Estimated prevalence or 2% in those >60y/o

Chronic Gastritis -
✤ antibodies to parietal cells and intrinsic factor that can be detected

in serum & gastric secretions
✤ reduced pepsinogen I concentration
✤ antral endocrine cell hyperplasia
✤ vitamin B12 deficiency
✤ defective gastric secretion (achlorhydria)

Chronic Gastritis -
Autoimmune Atrophic Gastritis
✤ loss of parietal cells >> stimulates gastrin release >> hypergastrinemia >>
hyperplasia of G cells
✤ no parietal cells >> no intrinsic factor >> Vitamin B12 absorption disabled >>
Vitamin B 12 deficiency
✤ PERNICIOUS ANEMIA
✤ High frequency of associated intestinal metaplasia has led to the term autoimmune
metaplastic atrophic gastritis
✤ chief cell destruction >> reduced pepsinogen I concentration
✤ principal agents of injury : CD4+ T cells directed against parietal cell components
(including H+ K+ ATPase)
Chronic Gastritis -
✤ diffuse mucosal damage of acid-producing mucosa within the body and

fundus
✤ Antrum & cardia spared
✤ diffuse atrophy >> rugal folds are lost
✤ inflammatory infiltrates: lymphocytes, macrophages, plasma cells with

lymphoid aggregates & follicles
✤ Inflammation is deeper & centered around glands

Chronic Gastritis
✤ lymphocytic & plasma cell infiltrate in the lamina propria
Chronic Gastritis -
✤ endocrine cell hyperplasia

demonstrated by
chromogranin A staining
✤ Rarely: may progress

into small, multicentric
low grade
neuroendocrine
(carcinoid) tumors
Chronic Gastritis
✤ occasional neutrophilic infiltration of the mucosal pits
Chronic Gastritis
✤ variable gland loss and mucosal atrophy
Chronic Gastritis
✤ progression to gastric atrophy over 2 to 3 decades
✤ slow and variable progression
✤ associated with other autoimmune diseases
✤ Hashimoto thyroiditis, Type I DM, Addison disease, primary

ovarian failure, primary hypoparathyroidism, Graves disease,
vitiligo, myasthenia gravis, Lambert-Eaton syndrome
✤ s/sx linked to sx of anemia : atrophic glossitis
✤ neuropathic findings : paresthesias & numbness

Uncommon Forms of Gastritis
✤ EOSINOPHILIC GASTRITIS - commonly in allergic

reactions
✤ LYMPHOCYTIC GASTRITIS – 40% associated with

Celiac disease
✤ GRANULOMATOUS GASTRITIS - gastric

involvement of Crohn disease
Complications of
Chronic Gastritis
✤ PEPTIC ULCER DISEASE

✤ MUCOSAL ATROPHY AND INTESTINAL
METAPLASIA
✤ GASTRITIS CYSTICA
Peptic Ulcer Disease
✤ chronic mucosal
ulceration affecting the
duodenum or stomach
✤ Almost always
associated with H.
pylori infection,
NSAIDs or cigarette
smoking
✤ most common form of PUD:
✤ gastric antrum or duodenum due to chronic, H.pylori-

induced antral gastritis
✤ associated with increased gastric acid secretion and

decreased duodenal bicarbonate secretion
✤ PUD in the fundus or body: lesser acid secretion d/t

mucosal atrophy
✤ ileal Meckel diverticulum can also cause PUD (ectopic
gastric mucosa)
Peptic Ulcers -
H.pylori & NSAIDs
✤ H.pylori and NSAID use : primary underlying causes

of PUD in patients >60 years
✤ especially if combined with low-dose aspirin
✤ associated with cigarette use & cardiovascular diseases
✤ due to reduced blood flow, oxygenation, & healing

Risk factors for PUD
Peptic Ulcer Disease -
Pathogenesis
✤ imbalance between defense mechanisms & damaging

factors that cause chronic gastritis
✤ usually in a background of chronic gastritis
✤ in H. pylori gastritis:
✤ pathogenesis linked to host factors & variation in

bacterial strains
Peptic Ulcers
✤ common in the proximal duodenum
✤ within a few cms from the pyloric valve; anterior duodenal wall
Peptic Ulcers
Peptic Ulcers
✤ usually solitary
✤ classic: oval, sharply punched-

out defect
✤ Mucosal margin is usally level

with the surrounding mucosa but
may overhang the base
✤ CA: heaped-up margins
✤ complication: perforation
Ulcer vs Cancer
Peptic Ulcer ✤ round, sharply punched-out craters 0.2-
0.4cm in diameter; clean base
Peptic Ulcer
✤ 4 ZONES
✤ 1. necrosis - thin layer of fibrinoid

debris
✤ 2. active nonspecific
inflammatory infiltration
(neutrophils predominating)
✤ 3. granulation tissue
✤ 4. fibrous collagenous scar

Peptic Ulcer
✤ scarring may involve the

entire thickness of the wall
and pucker the surrounding
mucosa into folds that radiate
outward
✤ malignant transformation
occurs rarely
✤ unlike ulcerated cancers there is no
Peptic Ulcer significant elevation or beading of the
edges
Peptic Ulcer ✤ surrounding mucosal folds may radiate
like wheel spokes
Peptic ulcer
Complications of Chronic Gastritis
Peptic Ulcers
✤ chronic, recurring lesions
✤ s/sx: epigastric burning or aching pain; IDA, hemorrhage,

perforation
✤ pain: 1-3hours after meals during the day, worse at night,

relieved by alkali or food
✤ nausea, vomiting, bloating, belching, significant weight

loss
✤ pain: left upper quadrant, or chest (misinterpreted as

cardiac)
Peptic Ulcer - Treatment
✤ current therapies: H.pylori

eradication + neutralization
of gastric acid
✤ withdraw NSAIDs, COX-2

inhibitors
✤ surgical approaches only for

bleeding and perforated
peptic ulcers
Peptic Ulcer - Acute Gastric Ulceration
PUD:
Complications
Complications of
Chronic Gastritis
✤ MUCOSAL ATROPHY
AND INTESTINAL
METAPLASIA
✤ DYSPLASIA
✤ GASTRITIS CYSTICA
Complications of
Chronic Gastritis ✤ DYSPLASIA
Complications of
Chronic Gastritis ✤ GASTRITIS CYSTICA
Gastric
Disorders
MENETRIER DISEASE
ZOLLINGER-ELLISON
SYNDROME
Hypertrophic Gastropathies
Menetrier
Disease
✤ excessive secretion of TGF-

alpha
✤ diffuse hyperplasia of foveolar

epithelium of body & fundus
due to protein-losing
enteropathy
✤ irregular enlargement of rugae

Menetrier
Disease
✤ Hyperplasia of
foveolar
mucous cells
✤ elongated
glands,
corkscrew-like
appearance
Zollinger-Ellison
Syndrome
✤ caused by gastrin-secreting
neuroendocrine tumors (small
intestine or pancreas)
✤ duodenal ulcers & chronic diarrhea
✤ Marked increase in number of

parietal cells >> doubling of oxyntic
mucosal thickness
✤ gastrinomas 60-90% malignant
✤ part of MEN1 (25% of gastrinomas)

Gastric MESENCHYME
Disorders
MUCOSA
POLYPS
CARCINOMA
Congenital Anomalies
Gastric Ulceration
Gastric Polyps & Tumors
Gastric Tumors
Gastric Polyps
✤ POLYP- any nodule or

mass that projects
above the level of the
surrounding mucosa
✤ d/t epithelial or
stromal hyperplasia,
inflammation, ectopia
or neoplasia
Gastric Tumors
Gastric Polyps
✤ INFLAMMATORY & HYPERPLASTIC POLYPS - 75% of all

gastric polyps
✤ develop in association with chronic gastritis
✤ gastritis >> reactive hyperplasia >> polyp growth
✤ common in 50-60 y/o
✤ polyps greater than 1.0cm should be resected and examined

histologically: risk of dysplasia is greater
Gastric Tumors
Gastric Polyps ✤ usually smaller than 1cm,

frequently multiple
Gastric Tumors
Gastric Polyps ✤ irregular, cystically dilated,

elongated foveolar glands
✤ edematous lamina propria with variable degrees of inflammation

Gastric Tumors > Gastric Polyps
Fundic Gland Polyps
✤ sporadic
✤ occur in individuals with familial adenomatous polyposis (FAP)
✤ common in women, average age : 50 y/o
✤ increased prevalence in recent years as a result of proton pump

inhibitor therapy
✤ PPIs inhibit acid production >> gastrin secretion >> oxyntic

gland growth
✤ may be asymptomatic, or with nausea, vomiting or epigastric pain

Fundic Gland Polyps
✤ occur in the gastric body & fundus
✤ well-circumscribed lesions with a smooth

surface
✤ may be single or multiple
✤ cystically dilated, irregular glands lined by

flattened parietal & chief cells
✤ inflammation typically absent or minimal
✤ Sporadic fundic gland polyps do not carry

a significant risk of neoplasia.
Fundic Gland Polyps

Gastric Adenoma
Most develop on a background of chronic gastritis with atrophy and
intestinal metaplasia
• except those associated with germline mutations in APC or MUTYH
✤ 10% of all gastric polyps
✤ increases progressively with age (50-60 years old)
✤ males > females
✤ incidence is increased in individuals with FAP
✤ risk of adenocarcinomas: lesions greater than 2cm in diameter

Gastric Adenoma ✤ usually <2cm, frequently

multiple, located in the
antrum
✤ endoscopically similar to hyperplastic polyps

Gastric Adenoma
✤ solitary antral lesions
✤ all GI adenomas have varying

degrees of epithelial dysplasia
(low grade or high grade)
Dysplasia in Gastric
Adenoma
✤ low grade or high grade

dysplasia
✤ both grades: nuclear

enlargement, elongation,
hyperchromasia; epithelial
crowding,
pseudostratification
✤ high grade: more severe

cytologic atypia
BREAK!
Gastric MESENCHYME
Disorders MUCOSA
POLYPS
CARCINOMA
Congenital Anomalies
Gastric Ulceration
Gastric Tumors
Gastric MESENCHYME
MUCOSA
Disorders POLYPS
ADENOCARCINOMA
INTESTINAL TYPE
Congenital Anomalies DIFFUSE TYPE
Gastric Ulceration
Gastric Tumors
OTHER TUMORS:
LYMPHOMA
GASTROINTESTINAL STROMAL TUMOR
Gastric Tumors
Gastric Adenocarcinoma
✤ most common
malignancy of the
stomach (>90%)
✤ dyspepsia, dysphagia,
nausea (early symptoms)
✤ weight loss, anorexia,

altered bowel habits,
anemia & hemorrhage
Gastric Tumors
✤ Japan, Chile, Costa Rica, Eastern Europe higher incidence than

in North America, Northern Europe, Africa & Southeast Asia
✤ Japan: 35% are early gastric cancers

Gastric Tumors
✤ environmental & dietary

factors also are responsible
✤ metastatic sites most

commonly involved:
supraclavicular node,
periumbilical node, left
axillary lymph node,
ovary, pouch of Douglas
Gastric Tumors
✤ Virchow node - supraclavicular
sentinel lymph node
Gastric Tumors
Gastric Carcinomas
✤ SISTER MARY JOSEPH NODULE
✤ metastasis to periumbilical region to form a nodule

Gastric Tumors
✤ Irish node - left axillary lymph node
Gastric Tumors
✤ Krukenberg tumor - metastasis to the ovary
Gastric Tumors
✤ Blumer shelf - pouch of Douglas
Gastric Tumors
✤ common in lower socioeconomic groups
✤ gastric dysplasia with adenomas : precursor lesions
✤ decline of incidence in the US and other Western countries,

suggesting environmental and dietary factors contributing to
development of gastric cancers
✤ migrants from high-risk to low-risk regions : gastric cancer rates in

second-generation immigrants are similar to those in their new
country of residence
✤ decrease is linked to decrease in H.pylori incidence

Gastric Tumors
✤ increasing incidence
of cancer of the
gastric cardia
✤ related to Barrett
esophagus
✤ reflecting incidence
of chronic GERD
and obesity
Gastric Tumors
PATHOGENESIS
✤ germline mutations in CDH1 are associated with familial gastric cancers

(diffuse type)
✤ CDH1 encodes E-cadherin, which is decreased in gastric CA
✤ loss in E-cadherin function seems to be a key step in the development of

diffuse gastric cancer
✤ intestinal type gastric cancers : mutations that result in increased

signaling via Wnt pathway (APC gene & beta catenin pathway)
✤ FAP patients who carry germline APC mutations : increased risk of

intestinal type gastric cancers (e.g.Japan)
Gastric Tumors
PATHOGENESIS
✤ chronic inflammation promotes gastric neoplasia
✤ H.pylori + genetic variants of proinflammatory & immune

response genes (encoding for IL-1beta, TNF, IL-10, IL-8,
TLR4)
Gastric Tumors
PATHOGENESIS
Gastric Tumors
Gastric Carcinomas
✤ classified according to
location in the
stomach & according
to gross & histologic
morphology
✤ antrum: most often

involved
✤ lesser curvature
involved more than
the greater curvature
Gastric Tumors : Gastric Carcinomas
Intestinal-Type CA
✤ tend to form
bulky tumors
Gastric adenocarcinoma showing an irregular ulcer crater with piling up of the mucosa around the ulcer.
Intestinal-Type CA
✤ grow along broad cohesive fronts to form either an exophytic mass or an ulcerated tumor
Intestinal-Type CA
Loss of rugal folds

Intestinal-Type CA
✤ glandular w/ apical mucin vacuoles, abundant mucin in gland lumens
Intestinal-Type Carcinoma
Intestinal-Type Carcinoma
Intestinal-Type CA
✤ glandular w/ apical mucin vacuoles, abundant mucin in gland lumens
Diffuse Type CA
✤ mass may be difficult to appreciate: rigid, thickened wall
LINITIS PLASTICA
Diffuse Type Gastric Cancer

✤ signet ring cells: discohesive cells with large mucin vacuoles that
expand the cytoplasm & push the nucleus to the periphery
Diffuse Type CA
Diffuse Type CA Gastric Tumors : Gastric Carcinomas
Gastric Tumors
Gastric Carcinomas
✤ intestinal type predominates in high-risk areas
✤ diffuse CA- uniform across countries
✤ mean age of presentation: 55 years
✤ M:F ratio- 2:1
✤ remarkable decrease in gastric CA: intestinal-type (closely associated

with atrophic gastritis & intestinal metaplasia)
✤ incidence similar for intestinal & diffuse

Gastric Tumors
Gastric Carcinomas
✤ most powerful prognostic

indicator:
✤ depth of invasion and

extent of nodal and distal
metastasis at the time of
diagnosis
remember TNM?
Gastric Tumors
Gastric Carcinomas
✤ local invasion into

duodenum,
pancreas &
retroperitoneum
✤ surgical resection
still preferred
treatment
✤ survival rate
>90% even with
nodal metastasis
Intestinal or Diffuse Type?
Gastric MESENCHYME
MUCOSA
Disorders POLYPS
ADENOCARCINOMA
INTESTINAL TYPE
Gastric Ulceration
Gastric Tumors OTHER TUMORS:
LYMPHOMA
CARCINOID TUMOR
Gastric MESENCHYME
MUCOSA
Disorders POLYPS
ADENOCARCINOMA
INTESTINAL TYPE
Gastric Ulceration
LYMPHOMA
CARCINOID TUMOR
Gastric Tumors
Gastric Lymphoma
✤ extranodal lymphomas are common in the GIT (esp stomach)
✤ 5% of all gastric malignancies are primary lymphomas
✤ most are extramarginal zone B-cell lymphomas
✤ in the GIT, often referred to as lymphomas of mucosa-associated

lymphoid tissue (MALT) >> MALTomas
✤ arise in the setting of chronic inflammation (H.pylori)

Gastric Tumors
Gastric
Lymphoma
Gastric Tumors
Gastric Lymphoma
✤ usually arise at sites of chronic inflammation
✤ commonly arise in sites devoid of organized lymphoid tissue
✤ MALT is induced due to chronic chronic gastritis
✤ H.pylori seen in association with most cases of gastric MALToma
✤ H.pylori eradication >> remissions with low recurrence rates in

most MALToma patients
Gastric Tumors
Gastric Lymphoma
MALToma
✤ dense lymphocytic infiltrate in

the lamina propria
✤ lymphocytes infiltrate the gastric

glands to create
LYMPHOEPITHELIAL LESIONS
✤ express B-cell markers (CD19

and CD20)
✤ restricted expression of kappa or

lambda immunoglobulin light
chains
Gastric Tumors
Gastric Lymphoma MALToma

Gastric Tumors MALToma
Gastric Tumors
Gastric Lymphoma
MALToma
Gastric MESENCHYME
MUCOSA
Disorders POLYPS
ADENOCARCINOMA
INTESTINAL TYPE
Gastric Ulceration
LYMPHOMA
NEUROENDOCRINE NEOPLASMS
Gastric Tumors
Neuroendocrine Neoplasms
✤ arise from diffuse components of the endocrine system
✤ majority are found in the GIT (>40% in the small intestine)
✤ gastric carcinoids: associated with endocrine cell hyperplasia, chronic

atrophic gastritis, and Zollinger-Ellison syndrome
✤ carcinoid or “carcinoma-like” - tend to have a more indolent course

than GI carcinomas
✤ release peptide & non-peptide hormones to coordinate gut function

Gastric Tumors
Carcinoid Tumor
✤ intramural or submucosal masses - polypoid lesions
✤ coarse chromatin texture - “salt and pepper” pattern
✤ EM: dense core neurosecretory granules

Gastric Tumors
Carcinoid Tumor
✤ peak incidence: 60y/o
✤ symptoms determined by the hormones produced
✤ if gastrin-producing : Zollinger-Ellison syndrome

Carcinoid
Syndrome
Gastric Tumors
Carcinoid Tumor
✤ most important prognostic
factor: location
✤ FOREGUT CARCINOID
TUMORS
✤ within stomach,
duodenum, proximal to
the ligament of Treitz &
esophagus
✤ rarely metastasize & are

cured by resection
Gastric Tumors
Carcinoid Tumor
✤ MIDGUT CARCINOID
TUMORS
✤ jejunum & ileum
✤ multiple, tend to be
aggressive
Gastric Tumors
Carcinoid Tumor
✤ HINDGUT CARCINOID
TUMORS
✤ appendix & colorectum
✤ appendix : generally located

at the tip, >2cm in diameter
✤ rectal : produce polypeptide

hormones, (+) abdominal
pain & weight loss
Gastric MESENCHYME
MUCOSA
Disorders POLYPS
ADENOCARCINOMA
INTESTINAL TYPE
Gastric Ulceration
OTHER TUMORS:
Gastric Tumors
LYMPHOMA
NEUROENDOCRINE TUMORS
GASTROINTESTINAL STROMAL
TUMOR
Gastric Tumors
Gastrointestinal Stromal Tumor
✤ most common mesenchymal tumor of the abdomen
✤ more than half of GISTs occur in the stomach
✤ peak age of diagnosis: 60y/o
✤ some are related to Carney Triad:
✤ gastric GIST, paraganglioma & pulmonary chondroma

Gastric Tumors
✤ appear to arise from, or

share a common stem cell
with, interstitial cells of
Cajal
✤ located in the
muscularis propria &
serve as pacemaker cells
for gut peristalsis
Gastric Tumors
✤ peak age: 60y/o
✤ mutations of the cKit gene

(75%)
✤ mutations in KIT or
PDGFRA detectable in
small lesions (3mm)
GIST
Gastric Tumors
GIST
✤ large (>30cm in diameter)
✤ solitary, well-circumscribed fleshy

mass
✤ spindle-cell type & epithelioid

type
✤ spindle cell type: bundles, fascicles

of spindle-shaped tumor cells
Gastric Tumors
GIST
Gastric Tumors
GIST KIT: most useful diagnostic marker

(95%) of gastric GISTS

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(01:17:22) (01) 1b Pathology of The Stomach by DR FSK

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Pathology of the

Gastropathy and Acute Gastritis

GASTRITIS ✤ when neutrophils are present

✤ when inflammatory cells are

✤ Irritants: NSAIDs, alcohol, bile

✤ Inhibition of cyclooxygenase (COX) by NSAIDs

✤ Inhibition of gastric bicarbonate transporters

✤ Reduced mucin and bicarbonate secretion

✤ Decreased oxygen delivery

Gastropathy & Mild Acute Gastritis

Gastropathy & Gastritis

✤ As injury progresses, erosions, i.e. superficial mucosal defects are

✤ ACUTE EROSIVE HEMORRHAGIC GASTRITIS

✤ concurrent erosion & hemorrhage

✤ erosion is accompanied by pronounced neutrophilic infiltrate

Stress-Related Mucosal Disease

✤ Occurs with severe trauma, excessive burns, intracranial disease,

✤ specific names based on location & clinical associations:

✤ STRESS ULCERS - shock, sepsis or severe trauma

✤ CURLING ULCERS - severe burns and trauma

✤ CUSHING ULCERS - intracranial disease

Stress-Related Mucosal Injury

✤ often related to local ischemia

✤ systemic hypotension>> reduced blood flow due to stress-

✤ also due to upregulation of inducible NO synthase and

Stress-Related Mucosal Injury

✤ from shallow erosions to deeper

✤ acute ulcers: rounded , <1cm in

✤ Base is stained brown-black;

✤ margins and base of ulcers are

Stress-Related Mucosal Injury

Stress-Related Mucosal Injury

✤ GAVE (Gastric Antral Vascular

✤ most common cause : infection with H.pylori

✤ Other causes: autoimmune gastritis, radiation injury, chronic bile

✤ Symptoms are less severe but more persistent

✤ Nausea, upper abdominal pain

H.pylori Gastritis seen in almost all patients

Helicobacter pylori Gastritis

✤ acute infection: no symptoms

✤ chronic gastritis : causes the

✤ present in 90% of pxs with

Chronic Gastritis - H.pylori

✤ acquired in childhood and persists for life without treatment

✤ transmission: fecal oral route

Chronic Gastritis - H.pylori

✤ presents as predominantly antral gastritis with normal or

✤ if limited in the antrum, increased acid production results in

✤ MULTIFOCAL ATROPHIC GASTRITIS - if involving the

✤ In contrast to autoimmune gastritis, atrophy is typically patchy

✤ Distribution can be irregular,

✤ Organisms most easily

✤ Antral mucosa is usually

✤ Plasma cells in clusters or

special stain for

✤ pit abscesses, intraepithelial neutrophils, subepithelial plasma cells

✤ organisms abundant in the surface mucus