Pathology of the Stomach and Small Bowel Flashcards Preview

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Flashcards in Pathology of the Stomach and Small Bowel Deck (23)
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Hypertrophic pyloric stenosis


Hyperplasia of pyloric muscularis propria, obstructs gastric outflow

M:F = 4:1
Presents in 2-3rd week of life with regurgitation and persistent projectile non-bilious vomiting
Firm ovoid abdominal mass

Treatment: Surgical splitting of muscularis propria (“myotomy”)


Gastritis vs gastropathy

gastritis: inflammation + injury
Gastropathy: non-inflammatory injury

Drugs (NSAIDs)
H. pylori
alcohol, tobacco
chemical injury (bile, strong acids/bases)


Stress related mucosal disease

-resembles acute gastritis:
injury mediated by vasoconstriction/ischemia
erosion and ulceration may be widespread

Occur in 75% of critically ill pts
-trauma, shock, or sepsis (stress ulcers)
-Burns (Curling ulcers)
-Intracranial disease (Cushing ulcers)


Chronic gastritis

-H. pylori infection
-Autoimmune gastritis

-Eosinophilic gastropathy
Allergic disease [e.g. cow’s milk] and parasitic infection
-Lymphocytic gastropathy
associated with celiac disease
-Granulomatous gastropathy
Crohn’s disease, sarcoidosis, infection


H. pylori gastritis

Gram-negative bacillus adapted to gastric environment:
Flagella to maneuver through gastric mucus
Adhesion molecules bind to gastric foveolar cells
Acid resistance through abundant urease
Elaboration of toxins cause tissue damage
Minimization and evasion of immune response

Oral-oral, fecal-oral, and environmental spread
Associated with poverty, household crowding, and rural areas


Histology of h. pylori gastritis

-Lymphocyte and plasma cell infiltrate
-neutrophilic infiltrate
-can see H. pylori on high mag


Diseases assoc w/ H. pylori

Gastric and duodenal ulcers (15% lifetime risk)
Gastric adenocarcinoma (1% lifetime risk)
Gastric lymphoma


Autoimmune Gastritis

Corpus restricted chronic atrophic gastritis
Anti-parietal cell and anti-intrinsic factor antibodies
+/- pernicious anemia

Scandinavian and northern
European descent

On histology:
intestinal metaplasia
lymphocyte and plasma cell infiltrate in body of stomach and glandular atrophy


Peptic ulcer disease

acid mediated ulceration of stomach and duodenum

Bleeding 15%, perforation 5%, obstruction 2%

H pylori
Cigarette use
illicit drugs
psych stress
endocrine cell hyperplasia
Zollinger Ellison syndrome (PUD of stomach, duod, jejunum)
Viral infection (CMV, HSV)

Gross: mucosa hangs over the edge and ulcer has a "clean base"

Necrotic debris in ulcer bed


Mass-like inflammatory lesions

gastritis cystica
gastritis polyposa


Hypertrophic gastropathies

Menetrier disease (leads to markedly enlarged RUGAE of stomach)
Zollinger-Ellison Syndrome


Benign neoplastic diseases

inflammatory/hyperplastic polyp (rare progression to cancer, assoc with helicobacter and other chronic gastritidies)
Histology: inflamm, edema, cystically dilated foveolae

fundic gland polyp (very rare progression to cancer-- in FAP pts; FAP assoc and sporadic, usally PPI assoc)
Histology: cystically dilated oxyntic gland

adenomatous polyp (adenoma) (common progression to cancer, increased incidence in FAP, Helicobacter gastritis, and other chronic gastritides)


Potentially Malignant neoplastic diseases

carcinoid tumor
GI stromal tumor



Epithelial tumor derived from malignant transformation of gastric epithelium; malignant behavior; associated with chronic gastritis (especially Helicobacter) and diet

90% of all malignant gastric tumors
second most common fatal malignancy in world (in US 2.5% of cancer deaths)
High incidence: Japan, Chile, E. Europe

early: dyspepsia, dysphagia, and nausea
Late: weight loss, anorexia, early satiety, anemia

High mortality unless detected early
5 yr: 3-% survival (90% for early gastric cancer)
-Less than 20% of gastric cancers in USA detected early

can see signet ring cell (diffuse type)
or intestinal type

Ulcerating pattern (heaped edges, no clean base) or linitis plastica (thickened wall)(see pics!!)



Lymphoid tumor usually derived from malignant transformation of resident B-cells; malignant behavior but varies from low-grade to high-grade; associated with Helicobacter gastritis


Carcinoid tumor

Epithelial tumor derived from neuroendocrine cells; variable behavior from indolent to malignant; some tumors are sporadic and others are associated with gastric atrophy (e.g. autoimmune gastritis)


GI stromal tumor

Stromal tumor derived from interstitial cells of Cajal; variable behavior from indolent to malignant; tumors harbor activating mutations in the tyrosine kinase CKIT or PDGFRA


Adenocarcinoma mutation

Wnt signalling pathway activation
Common in intestinal type cancers
Can occur with loss of APC (as in FAP)

Loss of CDH1 (mutation or methylation)
Common in diffuse type cancers
Germline loss of CDH1 in familial gastric cancer

Amplification of Her2/neu
Occurs in a minority of tumors (intestinal > diffuse)
Susceptible to tyrosine kinase inhibitor trastuzumab


TNM staging

T: tumor characteristics (depth of invasion into gastric wall)

N: regional lymph node mets

M: distant metastatic disease



Most extranodal lymphomas arise in GI tract and, in particular, the stomach
5% of gastric cancers are lymphomas

Most are MALT lymphomas (low-grade B-cell)
Given time, will transform to high-grade DLBCL

Associated with chronic gastritis. often driven by Helicobacter infection
(eradication cures MALT lymphomas)

Histology of MALT lymphoma:
diffuse infiltrate of B cells
-B cells disrupt gastric glands (lymphoepithelial lesions)


Carcinoid (Neuroendocrine) Tumor

-“well-differentiated endocrine neoplasm”

Neoplastic proliferation of ECC in body/fundus

Variable behavior
Sporadic: higher rate of malignant behavior
Atrophy associated: typically indolent

Associated with gastric atrophy and MEN-I


GI stromal tumor (GIST)

-mesenchymal neoplasm of interstitial cell of Cajal
-mutation in CKIT oncogene
-targeted therapy with TKI imatinib

Variable clinical course: indolent to malignant

risk: location, mitotic rate, size


Key Points

Inflammatory gastric diseases occur when there is a mismatch between protective and damaging “forces”

Stress-related gastritis very common in sick patients

Helicobacter infection is a huge “player” in gastric disease

Adenocarcinoma is the most common cancer in the stomach, is decreasing in incidence in the USA, and typically presents at an advanced stage

Many gastric lymphomas can be cured with antibiotics

Gastrointestinal stromal tumors have a variable behavior and many are driven by CKIT mutations