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MS2 GI > 10/7- Stomach Pathology > Flashcards

10/7- Stomach Pathology Flashcards

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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
What is seen here?
Higher power chronic active gastritis
26
What is seen here?
H pylori associated Chronic active gastritis - Neutrophils infiltrating epithelial cells
27
What is seen here?
H pylori associated Chronic active gastritis
28
What is seen here?
IHC stain for H pylori
29
What are other tests that can be done to detect H. pylori as cause of gastritis?
- 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
What is treatment for H. pylori infection?
**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
What would 2nd treatment regimen be in H pylori? - Persistent infections?
**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
What is intestinal metaplasia?
Replacement of gastric mucosa with small intestinal cells (goblet cells, enterocytes..)
33
What does intestinal metaplasia typically indicate?
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
What is seen here?
35
What is dysplasia (morphological hallmarks)? What causes it?
- 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
What is seen here?
Examples of dysplasia
37
What is the most common malignancy of the stomach?
Gastric adenocarcinoma - \> 90% of all gastric cancers
38
What are symptoms of gastric adenocarcinoma?
_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
Where are there especially high rates of gastric adenocarcinoma?
- Japan - Eastern Europe (incidence up to 20x that in N America)
40
**T/F**: The incidence of gastric adenocarcinoma is dropping in the US
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
Epidemiology of gastric adenocarcinoma - Gender - Populations
- Men \> women (2x) _More common in:_ - Lower SE group - Individuals with multifocal mucosal atrophy and intestinal metalpasia
42
The increased incidence of cardiac cancer and Barrett esophagus may reflect what?
Increasing incidence of chronic GERD and obesity
43
What is the pathogenesis of gastric adenocarcinoma?
- 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
What is seen grossly in adenocarcinoma?
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
What is seen here?
?
46
What is seen here?
Gastric adenocarcinoma, diffuse type (thick wall)
47
What is the morphology of gastric adenocarcinoma? - Intestinal type - Diffuse type
**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
What is the clinical presentation of the intestinal type of gastric cancer? Diffuse type?
**_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
The decrease in gastric cancer incidence is related to which type?
Intestinal type
50
What is seen here?
Adenocarcinoma- intestinal type
51
What is seen here?
Adenocarcinoma- intestinal type
52
What is seen here?
Adenocarcinoma- poorly differentiated or signet ring cell type
53
What is the treatment for gastric cancer?
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
Case) - 80 yo woman - Mass arising from stomach for at least 5 yrs - Noticed to have omental implants intraoperatively
---
55
What are these layers?
- Submucosal tumor with spindle cells - Muscularis mucosa - Oxyntic mucosa
56
What is seen here?
Monomorphic spindle cells with perinuclear halos
57
What is seen here?
Monomorphic spindle cells with perinuclear halos
58
What is seen here?
Spindle cell staining diffusely and strongly with c-Kit
59
What is GIST? - Stats - Presentation
**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
What is the cell of origin of GIST?
Interstitial cells of Cajal
61
What are the underlying genetics of GIST?
- 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
What is the morphology of GIST? - Metastases/spread - Best marker
- 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
Describe the disease progression in gastric GIST?

MS2 GI (26 decks)

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