Pathology of the Stomach Flashcards by Matthew Miller

What cells line the entire surface of the stomach? What do they contain?

Simple columnar, mucous-secreting foveolar cells which contain bicarbonate critical for gastric mucosal protection

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What special cells are found primarily in the fundus and body of the stomach vs primarily the antrum?

Fundus / body:
Parietal cells - Pink cells, secrete acid and IF

Chief cells - secrete pepsinogen - basophilic due to RER

Antrum: enteroendocrine cells at base of glands:

D cells - somatostatin

G cells - gastrin

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How does spread of cancer from the stomach differ from colon and why?

Spreads much easier from stomach than colon because the lamina propria of the stomach DOES contain lymphatic tissue -> can metastasize with this little invasion of mucosa

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What is the difference between an erosion and an ulcer?

Erosion - loss of mucosa of the stomach, not into the submucosa (last layer of mucosa is muscularis mucosa)

Ulcer - Penetration into the submucosa or deeper

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What is contained in the muscularis propria of the stomach?

Three layers of smooth muscle:
Innermost oblique
Inner circular
Outer longitudinal

Auerbach (myenteric) plexus sits between inner circular and outer longitudinal

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What stimulates gastrin release and what is its action?

Stimulated by: Antral distension, alkalinization of the stomach, amino acids

Action: Increased HCl secretion and increased gastric motility

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What stimulates histamine release in the stomach, what releases it, and what is its action?

Gastrin stimulates histamine production via enterochromaffin-like-cells (ECL cells)

Histamine acts on parietal cells to increase HCl secretion

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What stimulates CCK, what releases it, and what are its actions?

Increased fatty acids in duodenum stimulates secretion by I cells in the duodenum / jejunum

Actions: Increased pancreatic secretions, gallbladder contractions, decreased gastric emptying, and relaxation of sphincter of Oddi

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What stimulates secretin, what releases it, and what are its actions?

Acidic chyme in duodenum stimulates release by S cells

Actions - increase pancreatic and brunner’s glands bicarbonate secretions, decrease gastric acid secretion

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What stimulates somatostatin, what releases it, and what are its actions?

Stimulated by increased acid or loss of vagal stimulation

Released by D cells of pancreas and stomach / duodenum, as well as hypothalamus -> widespread inhibitory action on release of hormones, including gastrin and histamine

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What are the three broad etiologies of acute gastritis?

Increased mucosal injury
Decreased mucosal protection
Decreased mucosal regenerative ability - i.e. chemotherapy

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What things cause increased mucosal injury to cause acute gastritis?

Ingestion of toxic chemicals or excessive alcohol
Radiation / chemotherapy
Bile reflux - biliary contents, post-surgery

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What things cause decreased mucosal protection to cause acute gastritis?

Advanced age - decreased mucus production
NSAIDS - loss of PGE2, which is needed to maintain blood flow to mucosa, and maintain production of HCO3- / mucin
Uremia - acidosis will allow less bicarbonate to be excreted
Low O2 -> shock, high altitudes, severe burns

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What is mild vs severe acute gastritis characterized by?

Mild = Nonerosive gastritis - neutrophils and slight edema

Severe = Erosive hemorrhagic gastritis - extensive inflammation, superficial ulcerations limited to mucosa (erosions)

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What are the clinical manifestations of acute gastritis?

Range from asymptomatic to nausea/vomiting/epigastric pain and upper GI bleed (causing hematemesis or melena)

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What things tend to induce acute gastric ulcers?

NSAIDs
Intracranial trauma - stimulation of vagal nerve increases gastric acid secretion
Major physiologic stress - shock, sepsis, burns leads to decreased perfusion of mucosa (decrease nutrients) and systemic acidosis (Decrease bicarbonate excretion)

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What is it called when you have an ulcer due to intracranial injury vs significant burns?

Intracranial injury = vagal stimulation -> Cushing ulcer (think of Cushing’s triad)

Burns = hypovolemia -> Curling ulcer (think of Curling irons are hot)

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What are the potential complications of acute gastric ulceration and do these tend to occur alone?

Potential for significant blood loss and perforation

-> often happen in groups due to major inciting events, may be groups of ulcers and erosions

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What is the most common cause of chronic gastritis? Where does it start and how do you get it?

H. pylori - 90% of cases

Typically starts in the antrum of the stomach

More a disease of lower SES in the US, thought to spread via oral-oral or fecal-oral

What is the pathogenesis of H. pylori-induced gastritis?

CAGA-encoded proteins (toxins) -> mediate inflammatory infiltrate which induces increased secretion of gastrin by G cells -> increased gastric acid production and ulcerations

How does H.pylori-induced gastritis appear grossly and microscopically?

Grossly - Erythematous, rough-appearing gastric mucosa with active inflammation. Mucosal atrophy and intestinal G-cell metaplasia and hyperplasia is also present

Microscopically - acute on chronic inflammation (neutrophils + chronic inflammatory infiltrate) + presence of spiral-shaped bacteria in superficial mucus

What tests can be used to detect H. pylori infection?

Fecal antigen test
Carbon-labelled urea test
H. pylori serology - just says if you had past infection
Gastric biopsy with direct test - best test

What causes autoimmune gastritis and what part of the stomach does it affect?

Loss of self-tolerance of CD4+ T cells to gastric parietal cells

> stimulation of autoantibodies to parietal cells or intrinsic factor
> chronic inflammation and destruction of gastric body and fundus by CD8 activation

What are the consequences of autoimmune destruction in autoimmune gastritis?

Destruction of parietal cells:
-> decreased gastric acid secretion, leading to hyperplasia of antral G cells

-> decreased intrinsic factor predisposes to pernicious anemia and subacute combined degeneration

Destruction of chief cells:
->decreased pepsinogen

How can the inflammation in autoimmune gastritis be told apart from H. pylori gastritis?

Autoimmune - chronic inflammatory infiltrate will be deep within the mucosa near the parietal and chief cells, and will also be in the body / fundus rather than antrum

What type of metaplasia does chronic gastritis (both types) cause and why does it predispose to cancer?

Intestinal metaplasia -> recognized by presence of goblet or Paneth cells Predisposes to cancer because it causes dysplasia -> chronic inflammation with repeated cellular injury, eventual dysplastic cell populations arise

Is H. pylori more common in gastric or duodenal peptic ulcer disease?

Duodenal (90%), but very common in both

Other than H. pylori, what are some other causes of Peptic ulcer disease?

NSAIDs - especially gastric Corticosteroid use and psychological stress - inhibit repair by immune system Hypercalcemia -> increases gastrin (abdominal pain in hypercalcemia) Zollinger-Ellison syndrome -> Gastrinoma

Where due ulcers typically appear and how do they appear grossly (vs adenocarcinoma)

Typically proximal duodenum, but sometimes gastric antrum or elsewhere Grossly - Well-delineated defect with edges not raised, and a clean base. Mucosal folds may radiate around it with chronicity

What are the complications of peptic ulcers?

Hemorrhage - especially posterior ulcer in duodenum, bleeding of gastroduodenal artery. Also left gastric artery in lesser curvature of stomach Perforation - especially anterior duodenal ulcers

What happens to Brunner's glands in duodenal ulcer?

They hypertrophy -> produce mucin-like substance for defense These are duodenal submucosal glands

What is a hypertrophic gastropathy? Give two examples.

Uncommon conditions of gastric mucosal hyperPLASIA leading to rugal fold thickening 1. Menetrier disease 2. Zollinger-Ellison syndrome

What causes Menetrier disease and how does it appear?

Increased production of TGF-alpha leads to diffuse hyperplasia of mucous glandular epithelium in body and fundus, with atrophy of parietal and chief cells -> thick rugae

What are the complications of Menetrier disease?

Protein-losing enteropathy -> increased mucin secretion leads to diarrhea, weight loss, and hypoproteinemia which can lead to peripheral edema Increased risk for adenocarcinoma (premalignant)

What is Zollinger-Ellison syndrome and how is it usually detected?

Gastrinoma (low-grade malignancy) which leads to gastric mucosal hyperplasia, especially parietal cells -> increased gastric acid secretion leads to intractable peptic ulcers arising in unusual locations (i.e. jejunum)

What is the most common type of gastric polyp?

Inflammatory or hyperplastic polyp - sessile / superficial polyp associated with acute and chronic inflammation due to enlarged foveolar glands during repair

What type of polyp is characterized by irregularly dilated gastric glands without inflammation and what prediposes to it?

Fundic Gland Polyp - associated with proton pump inhibitor use

What is gastric adenoma? When does it typically arise? Where?

A premalignant gastric polyp typically arising in the gastric antrum in chronic atrophic gastritis - > epithelial dysplasia which will progress to adenocarcinoma - > picked up in Japan where they actually screen for it

What are the two types of gastric adenocarcinoma and the risk factors for each?

Intestinal-type - Chronic atrophic gastritis of both types (causes intestinal metaplasia), dietary nitrosamines, gastric adenoma, smoking Diffuse-type - risk factors unknown (thus increasing in prevalence)

Where does intestinal-type gastric adenocarcinoma occur? What does it look like grossly and microscopically?

In the antrum / pyloric region, where intestinal metaplasia is occuring Appears as heaped up, ulcerating, necrotic or exophytic mass Microscopically - resembles colon adenocarcinoma with invasive glands / some desmoplasia

What is Diffuse-Type Gastric Adenocarcinoma also called? What mutation is associated with it? What does it look like microscopically?

Signet-Ring Cell Adenocarcinoma Associated with loss of E-cadherin Microscopically - mucin-filled cells with peripheral nuclei, widespread over stomach. Infiltrating singly or in small nests (glandular differentiation with intracellular mucin)

How does signet-ring cell adenocarcinoma appear grossly?

Linitis plastica - "leather bottle" - stomach wall is grossly thickened and leathery due to diffuse invasion by cells with prominent desmoplasia

What are common presenting symptoms for gastric adenocarcinoma?

Frequently presents very late, nonspecific symptoms such as weight loss, abdominal pain, anemia, and early satiety

What are some more uncommon presenting symptoms for gastric cancer?

Acanthosis nigricans - axillary browning Leser-Trelat sign - multiple keratoses appearing all over body

What defines early vs late gastric carcinoma?

Early - invasion is limited to mucosa or submucosa Advanced - invasion is in muscularis propria Presence of lymph node involvement is NOT diagnostic of progression

What lymph node is commonly involved in metastasis from the stomach (local)?

Virchow node - left supraclavicular node

What are other important sites of distant metastasis for gastric carcinoma? Which one of these is only seen with one of the two types?

1. Sister Mary Joseph nodule - periumbilical nodular metastasis 2. Krukenberg tumor - bilateral metastases to ovaries, with abundant mucus secretion. Only signet-ring cell type. 3. Liver / lungs (duh)