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MS2 GI > 10/7- Stomach Pathology > Flashcards

10/7- Stomach Pathology Flashcards

1
Q

In the US, ___ disease causes 1/3 of all health care spending on GI disease

A

In the US, gastric acid related disease causes 1/3 of all health care spending on GI disease

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2
Q

What are the 4 regions of the stomach?

A
  • Cardia
  • Fundus
  • Body (corpus)
  • Antrum
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3
Q

What are the tissue layers int he stomach?

A
  • Mucosa (rugae)
  • Muscularis
  • Oblique layer (innermost)
  • Circular layer
  • Longitudinal layer (outermost)
  • Serosa
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4
Q

Stomach anatomy (picture)

A
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5
Q

How are pyloric glands different from gastric/fundic glands?

A

…

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6
Q

What is seen here?

A

Antral (cardiac) mucosa

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7
Q

What cells are these?

Color and function?

A
  • Parietal cells are pink and secrete acid
  • Chief cells are purple and secrete pepsinogen
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8
Q

Describe the gastric environment

  • pH
  • Mucosa protection
  • Vascular supply
A

Acidic pH of 1

Protective mechanism of mucosa

  • Mucin secreted by foveolar cells
  • Layer of mucus: prevents large food particles from direct contact with epithelium
  • Layer of fluid over the epithelium that protects the mucosa with a neutral pH

Rich vascular supply: delivers oxygen, bicarbonate, and nutrients and washing away acid that back-diffused

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9
Q

Disruption of the protective mechanisms of the gastric environment will result in what?

A

Gastritis

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10
Q

What is the pathogenesis of gatritis?

A
  • Reduced mucin synthesis in the elderly: increased susceptibility to gastritis
  • NSAIDs interfere with cytoprotection of prostaglandins or reduce bicarbonate secretion
  • Ingestion of harsh chemicals: severe gastric injury, direct mucosal and stromal injury
  • Direct cellular injury
  • Excessive alcohol consumption and NSAIDs
  • Radiation therapy and chemo
  • Gastric mucosa is replaced every 2-6 d, so mitotic inhibitors cause generalized mcusoal damage due to insufficient epithelial regeneration
  • Decreased oxygen delivery: increased incidence of acute gastritis at high altitudes
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11
Q

What can cause drug gastritis?

A

Mucosal injury caused by prolonged direct mucosal contact

  • NSAIDs, antibiotics, potassium, gold, corticosteroids and caffeine: damage to gastric mucosa
  • Iron tablets widely used for treatment of anemia (Can happen in the esophagus too)
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12
Q

What is iron pill gastritis histologically?

A
  • Characteristic brown pigment (fragments of iron tablets) in granular debris on mucosal surface in the ulcer or inflamed tissue
  • Coarse granular brown material in the lamina propria, foveolar and glandular epithelial cells
  • Stainable iron in cases of ferrous sulfate–induced
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13
Q

What is seen here?

A

Iron pill gastritis

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14
Q

What is seen here?

A

Iron pill gastritis

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15
Q

What is seen here?

A

Iron pill gastritis with iron staining blue

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16
Q

What is the initial phase of H pylori infection?

  • Symptoms?
A

Acute gastritis

  • Acute inflammatory response
  • Asymptomatic or short-lived clinical manifestations like nausea and vomiting
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17
Q

What are endoscopic findings in H pylori gastritis?

A

Findings in antrum with hemorrhage and multiple erosions and ulcers

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18
Q

What is this? Characteristics?

A

H. pylori

  • Gm (-)
  • Urease-producing; essential for colonization and survival
  • Seagull-shaped, curved organism
  • Its shape and flagella allow penetration of and movement through the gastric mucus layer
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19
Q

Epidemiology of H. pylori

  • Prevalence
  • Geography
  • Developed vs. Undeveloped
A
  • Infects >50% of the world’s adult population
  • Geographic distribution closely correlates with socioeconomic development
  • Developing countries: up to 80% - 90% by 20 yo
  • Developed countries: under 20% in people under 25 years and increases about 1% per year to 50% to 60% by 70
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20
Q

What is the method of H pylori transmission?

  • Reservoir?
A
  • Transmission route unknown; most likely fecal-oral or oral-oral
  • Humans are the major reservoir (isolated from domestic pets and primates)
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21
Q

T/F: H. pylori causes damage by directly invading epithelial cells

A

False

  • Indirectly makes the gastric mucosa more vulnerable to acid peptic damage by disrupting the mucous layer, liberating a variety of enzymes and toxins, and adhering to and altering the gastric epithelium
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22
Q

How does H pylori cause damage?

A

Indirectly makes the gastric mucosa more vulnerable to acid peptic damage by disrupting the mucous layer, liberating a variety of enzymes and toxins, and adhering to and altering the gastric epithelium

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23
Q

Process of H pylori causing gastritis?

A
  • The host immune response to H. pylori incites an inflammatory reaction: tissue injury
  • Chronic inflammation upsets gastric acid secretory physiology … chronic gastritis (mostly asymptomatic, but lead to ulcers and even gastric cancer in some)
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24
Q

What is seen here?

A

Chronic active gastritis

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25
Q

What is seen here?

A

Higher power chronic active gastritis

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26
Q

What is seen here?

A

H pylori associated Chronic active gastritis

  • Neutrophils infiltrating epithelial cells
27
Q

What is seen here?

A

H pylori associated Chronic active gastritis

28
Q

What is seen here?

A

IHC stain for H pylori

29
Q

What are other tests that can be done to detect H. pylori as cause of gastritis?

A
  • Serologic test: antibodies to H. pylori
  • Fecal bacterial detection
  • Urea breath test based ammonia production by bacterial urease
  • Gastric biopsy can be analyzed rapid urease test, bacterial culture, or bacterial DNA detection by PCR
30
Q

What is treatment for H. pylori infection?

A

Current preferred initial treatment = triple therapy twice daily for 10-14 d

  • Proton pump inhibitor (PPI)
  • Amoxicillin 1000 mg
  • Clarithromycin 500 mg

Success rate > 75%

Once treatment is complete: confirm eradication (noninvasively) in 4 -8 wks after completion

  • Urea breath testing
  • Stool antigen testing
31
Q

What would 2nd treatment regimen be in H pylori?

  • Persistent infections?
A

Second-treatment regimen:

  • 2-week course of quadruple therapy
  • PPI BID
  • Bismuth subsalicylate [Pepto-Bismol] 2 tablets
  • Tetracycline 500 mg
  • Metronidazole 500 mg QID
  • Combination capsule treatment

In persistent infections

  • Third and even fourth course of antibiotics
  • Quinolone-, rifabutin-, or furazolidone-based therapies
32
Q

What is intestinal metaplasia?

A

Replacement of gastric mucosa with small intestinal cells (goblet cells, enterocytes..)

33
Q

What does intestinal metaplasia typically indicate?

A

Usually indicates an underlying chronic atrophic gastritis

  • More in patients with H. pylori infection
  • Intestinal metaplasia in chronic H. pylori gastritis: may regress after eradication of organism

Strongly associated with increased risk of gastric adenocarcinoma

34
Q

What is seen here?

A
35
Q

What is dysplasia (morphological hallmarks)?

What causes it?

A
  • Chronic gastritis: exposes epithelium to inflammation-related free radical damage… proliferative stimuli… accumulation of genetic alterations result in carcinoma
  • Dysplasia: in situ lesion

Morphologic hallmarks of dysplasia:

  • Variations in epithelial size, shape, and orientation
  • Coarse chromatin texture
  • Hyperchromasia
  • Nuclear enlargement
36
Q

What is seen here?

A

Examples of dysplasia

37
Q

What is the most common malignancy of the stomach?

A

Gastric adenocarcinoma

  • > 90% of all gastric cancers
38
Q

What are symptoms of gastric adenocarcinoma?

A

Early (similar to symptoms of chronic gastritis)

  • Dyspepsia
  • Dysphagia
  • Nausea

Often discovered at advanced stages (triggers for further diagnostic evaluation):

  • Weight loss
  • Anorexia
  • Altered bowel habits
  • Anemia
  • Hemorrhage
39
Q

Where are there especially high rates of gastric adenocarcinoma?

A
  • Japan
  • Eastern Europe

(incidence up to 20x that in N America)

40
Q

T/F: The incidence of gastric adenocarcinoma is dropping in the US

A

True

  • Was most common cancer death in 1930, but rates dropped by >85% in 1900s
  • Currently less than 2.5% of US cancer deaths (due to reduced use of dietary carcinogens, salt/smoking food, widespread food refrigeration and improved food transportation
41
Q

Epidemiology of gastric adenocarcinoma

  • Gender
  • Populations
A
  • Men > women (2x)

More common in:

  • Lower SE group
  • Individuals with multifocal mucosal atrophy and intestinal metalpasia
42
Q

The increased incidence of cardiac cancer and Barrett esophagus may reflect what?

A

Increasing incidence of chronic GERD and obesity

43
Q

What is the pathogenesis of gastric adenocarcinoma?

A
  • Multifocal: environmental and host-related
  • Increased risk of intestinal-type gastric cancer in patients with FAP (25-62% of FAP patients)
  • Sporadic intestinal-type gastric carcinoma
  • Mutations in β-catenin, a protein that binds to both E-cadherin and adenomatous polyposis coli (APC)
  • Microsatellite instability
  • Hypermethylation TGFβRII, BAX, IGFRII, and p16/INK4a
44
Q

What is seen grossly in adenocarcinoma?

A

Most common site: antrum

  • Lesser curvature > greater curvature

Intestinal type: Bulky tumor

Diffuse type: no discrete mass

  • Neoplastic cells evoke a desmoplastic reaction that stiffens the gastric wall
  • Rugal flattening and a rigid, thickened wall: linitis plastica
  • Metastatic breast and lung cancers can cause linitis plastica-like appearance
45
Q

What is seen here?

A

?

46
Q

What is seen here?

A

Gastric adenocarcinoma, diffuse type (thick wall)

47
Q

What is the morphology of gastric adenocarcinoma?

  • Intestinal type
  • Diffuse type
A

Intestinal type

  • Glands
  • Neoplastic cells have apical mucin vacuoles

Diffuse type:

  • Signet-ring cells: discohesive cells with large mucin vacuoles that expand the cytopasm and push the nucleus to the priphery
48
Q

What is the clinical presentation of the intestinal type of gastric cancer? Diffuse type?

A

Intestinal type

  • More in high-risk areas
  • Develops from precursor lesions like dysplasia and adenomas
  • Mean age of presentation: 55 years
  • Males 2x females

Diffuse type:

  • Incidence uniform across countries
  • No identified precursor lesions
  • Males = females
49
Q

The decrease in gastric cancer incidence is related to which type?

A

Intestinal type

50
Q

What is seen here?

A

Adenocarcinoma- intestinal type

51
Q

What is seen here?

A

Adenocarcinoma- intestinal type

52
Q

What is seen here?

A

Adenocarcinoma- poorly differentiated or signet ring cell type

53
Q

What is the treatment for gastric cancer?

A

Treatment of metastatic disease: chemotherapy or radiation therapy and palliative care

Surgical resection: preferred treatment

  • 5-year survival rate of early gastric cancer after surgery > 90%, even if lymph node metastases are present
  • 5-year survival rate for advanced gastric cancer under 20%
54
Q

Case)

  • 80 yo woman
  • Mass arising from stomach for at least 5 yrs
  • Noticed to have omental implants intraoperatively
A
55
Q

What are these layers?

A
  • Submucosal tumor with spindle cells
  • Muscularis mucosa
  • Oxyntic mucosa
56
Q

What is seen here?

A

Monomorphic spindle cells with perinuclear halos

57
Q

What is seen here?

A

Monomorphic spindle cells with perinuclear halos

58
Q

What is seen here?

A

Spindle cell staining diffusely and strongly with c-Kit

59
Q

What is GIST?

  • Stats
  • Presentation
A

Gastrointestinal stromal tumor (GIST)

  • The most common mesenchymal tumor of abdomen
  • Most common in stomach (60%),
  • Males > females
  • Peak age of diagnosis: 60 yo
  • Presentation depends on site and size
  • Asymptomatic to GI bleeding and pain
  • Incidental finding
60
Q

What is the cell of origin of GIST?

A

Interstitial cells of Cajal

61
Q

What are the underlying genetics of GIST?

A
  • 75%-80% oncogenic, gain-of-function mutations of the gene encoding the tyrosine kinase c-KIT gene (4q12) most common at exon 11.. 9, 13, or 7
  • 8% mutations that activate a related tyrosine kinase, platelet-derived growth factor receptor α (PDGFRA)

EXON 11 mutation is RESPONSIVE to GLEEVEC

62
Q

What is the morphology of GIST?

  • Metastases/spread
  • Best marker
A
  • Spindle cell and epithelioid type
  • Metastases: multiple serosal nodules in peritoneal cavity or liver nodules
  • Spread outside abdomen: uncommon
  • The most useful diagnostic marker: c-KIT with 95% positivity
  • Treatment: Excision and …
63
Q

Describe the disease progression in gastric GIST?

A

MS2 GI (26 decks)

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