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Pathophysiology - Gastrointestinal > Pathology of the Stomach > Flashcards

Pathology of the Stomach Flashcards

1
Q

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

A

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

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2
Q

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

A

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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3
Q

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

A

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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4
Q

What is the difference between an erosion and an ulcer?

A

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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5
Q

What is contained in the muscularis propria of the stomach?

A

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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6
Q

What stimulates gastrin release and what is its action?

A

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

Action: Increased HCl secretion and increased gastric motility

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7
Q

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

A

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

Histamine acts on parietal cells to increase HCl secretion

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8
Q

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

A

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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9
Q

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

A

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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10
Q

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

A

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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11
Q

What are the three broad etiologies of acute gastritis?

A
  1. Increased mucosal injury
  2. Decreased mucosal protection
  3. Decreased mucosal regenerative ability - i.e. chemotherapy
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12
Q

What things cause increased mucosal injury to cause acute gastritis?

A
  1. Ingestion of toxic chemicals or excessive alcohol
  2. Radiation / chemotherapy
  3. Bile reflux - biliary contents, post-surgery
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13
Q

What things cause decreased mucosal protection to cause acute gastritis?

A
  1. Advanced age - decreased mucus production
  2. NSAIDS - loss of PGE2, which is needed to maintain blood flow to mucosa, and maintain production of HCO3- / mucin
  3. Uremia - acidosis will allow less bicarbonate to be excreted
  4. Low O2 -> shock, high altitudes, severe burns
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14
Q

What is mild vs severe acute gastritis characterized by?

A

Mild = Nonerosive gastritis - neutrophils and slight edema

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

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15
Q

What are the clinical manifestations of acute gastritis?

A

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

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16
Q

What things tend to induce acute gastric ulcers?

A
  1. NSAIDs
  2. Intracranial trauma - stimulation of vagal nerve increases gastric acid secretion
  3. Major physiologic stress - shock, sepsis, burns leads to decreased perfusion of mucosa (decrease nutrients) and systemic acidosis (Decrease bicarbonate excretion)
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17
Q

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

A

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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18
Q

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

A

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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19
Q

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

A

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

20
Q

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

A

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

21
Q

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

A

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

22
Q

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

A
  1. Fecal antigen test
  2. Carbon-labelled urea test
  3. H. pylori serology - just says if you had past infection
  4. Gastric biopsy with direct test - best test
23
Q

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

A

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
24
Q

What are the consequences of autoimmune destruction in autoimmune gastritis?

A

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

25
Q

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

A

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

26
Q

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

A

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

27
Q

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

A

Duodenal (90%), but very common in both

28
Q

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

A

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

29
Q

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

A

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

30
Q

What are the complications of peptic ulcers?

A

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

Perforation - especially anterior duodenal ulcers

31
Q

What happens to Brunner’s glands in duodenal ulcer?

A

They hypertrophy -> produce mucin-like substance for defense

These are duodenal submucosal glands

32
Q

What is a hypertrophic gastropathy? Give two examples.

A

Uncommon conditions of gastric mucosal hyperPLASIA leading to rugal fold thickening

  1. Menetrier disease
  2. Zollinger-Ellison syndrome
33
Q

What causes Menetrier disease and how does it appear?

A

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

34
Q

What are the complications of Menetrier disease?

A

Protein-losing enteropathy -> increased mucin secretion leads to diarrhea, weight loss, and hypoproteinemia which can lead to peripheral edema

Increased risk for adenocarcinoma (premalignant)

35
Q

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

A

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)

36
Q

What is the most common type of gastric polyp?

A

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

37
Q

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

A

Fundic Gland Polyp - associated with proton pump inhibitor use

38
Q

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

A

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
39
Q

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

A

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)

40
Q

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

A

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

41
Q

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

A

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)

42
Q

How does signet-ring cell adenocarcinoma appear grossly?

A

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

43
Q

What are common presenting symptoms for gastric adenocarcinoma?

A

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

44
Q

What are some more uncommon presenting symptoms for gastric cancer?

A

Acanthosis nigricans - axillary browning

Leser-Trelat sign - multiple keratoses appearing all over body

45
Q

What defines early vs late gastric carcinoma?

A

Early - invasion is limited to mucosa or submucosa

Advanced - invasion is in muscularis propria

Presence of lymph node involvement is NOT diagnostic of progression

46
Q

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

A

Virchow node - left supraclavicular node

47
Q

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

A
  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)

Pathophysiology - Gastrointestinal (24 decks)

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