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GI- Week 2 > Nelson: Gastric Pathology > Flashcards

Nelson: Gastric Pathology Flashcards

1
Q

What are the normal damaging forces of the gastric mucosa?

A

Gastric acidity

Peptic enzymes

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2
Q

What are the main mechanisms of gastric mucosal injury?

A
  1. H. pylori infection
  2. NSAIDS
  3. Aspirin
  4. Alcohol
  5. Cigarettes
  6. Gastric hyperacidity
  7. Duodenal gastric reflux
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3
Q

What are the main defenses of the gastric mucosa?

A
  1. surface mucus secretion
  2. bicarbonate secretion into the mucus
  3. mucus blood flow
  4. apical surface membrane transport
  5. epithelial regenerative capacity
  6. increased PGs
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4
Q

What is the difference between a mucosal erosion and a mucosal ulcer?

A

A mucosal erosion is the loss and necrosis of surface epithelium that is CONFINED to the LP.

An acute ulceration is a necrotizing process that often extends beyond the mucosa into the submucosa and maybe even the muscle wall.

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5
Q

What are the main causes of acute gastric ulceration?

A
  1. Acute infection w/ H. Pylori
  2. First time use of large dose of NSAIDS or ASPIRIN (COX inhibitor)
  3. ingestion of large doses of alcohol
  4. Shock, trauma, sepsis, uremia, burns and intracranial disease
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6
Q

What is the MC pathological finding in H. pylori gastritis?

A

Active chronic gastritis beginning in the antrum and progressing to the body.

Histologically you would see lymphocytes in the active germinal center and a bunch of neutrophils indicating acute inflammation.

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7
Q

What complications are associated w/ an h. pylori infection?

A

MALT lymphoma

Gastric adenocarcinoima

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8
Q

What are hallmarks of chronic gastritis?

A

Evidence of CHRONIC inflammation= lymphocytes + plasma cells + reactive gastropaty

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9
Q

How do you acquire H. helmannji gastritis?

A

It’s reservoir is cats, dogs, pigs and nonhuman primates

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10
Q

Which H. pylori diagnostic tests are indicative of an active infection?

A

H & E, blue stain and immunohistochemical stain of biopsy specimen.

H. pylori stool antigen, urea breath test or rapid urease test on tissue biopsy

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11
Q

Describe the pathogenesis of autoimmune gastritis.

A

An autoimmune response causes CD4 T cells to target and destroy parietal cells (chief cells are also lost–collateral damage).

Abs to parietal cells and IF are also produced as part of the immune response. They ARENT pathogenic but can be used as a diagnostic test.

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12
Q

What are the key findings of autoimmune gastritis?

A
  1. Fewer parieatl cells> Decreased acid secretion (achlorhydria
  2. Hypergastrinemia and hyperplasia of G cells> compensatory endocrine hyperplasia in the body of the stomach
  3. B12 def d/t loss of IF
  4. Inflammatory damage in teh body and fundus sparing the antrum and cardia.
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13
Q

What are signs of B12 def?

A

Pernicious anemia w/ increased MCV

Megaloblastic anemia

Atrophic glossitis

malabsorptive diarrhea

Peripheral neuropathy

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14
Q

What are common causes of chronic reactie gastropathy?

A

Chemical mucosal injury associated w/ NSAIDS, aspirin, bile reflux and alcohol

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15
Q

What are two common causes of peptic ulcer disease?

A

H. Pylori

Chronic use of NSAIDs

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16
Q

What are the three complications of peptic ulcer disease?

A
  1. Bleeding (clinical hemorrhage and iron def)
  2. Perforation
  3. Obstruction (ulcer located in pyloric channel secondary to edema and fibrosis)
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17
Q

What are the key pathologic and clinical features of eosinophilic gastritis?

A

Eosinophilic rich inflammation–> peripheral (blood) eosinophilia and elevated IgE.

Absence of known cause but thought to be secondary to food allergy.

Often involves MULTIPLE GI sites.

Pt presents w/ mass, ulcer or pyloric obstruction.

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18
Q

What are the key pathologic and clinical features of granulomatous gastritis?

A

Gastritis w/ granulomatous inflammation.

Usually d/t an underlying disorder:

Crohn’s- most common cause in US
Sarcoidosis
Mycobacterial, fungal and parasitic infections (rare)
Foreign body rxn
Association with gastric adenocarcinoma and non-MALT lymphomas

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19
Q

What are the key pathologic and clinical features of lymphocytic gastritis?

A

Intraepithelial lymphocytic inflammation (CD8 T cells)

40% of cases are seen in pt/s w celiac so it suggests an immune pathogenesis.

Also seen w/ menetrier’s, h. pylori and lymphocytic/collagenous colitis.

20
Q

What is Menetrier’s disease? What does this mean clinically? What is Menetrier’s disease associated with? Which cancer can it predispose you to?

A

Excess secretion of TGF-α leads to diffuse hyperplasia of the body and fundus of stomach.

Pt’s lose protein with diarrhea (enteropathy), hypoprotenemia weight loss and peripheral edema.

Some cases associated with infection (CMV in children).

Increased risk for gastric adenocarcinoma.

21
Q

What causes ZE syndorme?

A

Gastrin secreting tumors in the pancreas and small bowel leads to elevated levels of gastrin that increase the number of parietal cells and in turn acid production.

It also leads to hyperplasia of mucus neck cells w/ increased mucin production.

22
Q

Who does ZE syndrome predispose you to cancer?

A

Stomach endocrine cell proliferation can lead to gastric CARCINOID tumors.

23
Q

How do pt’s with ZE syndrome present?

A

PUD or chronic diarrhea

24
Q

How do you treat ZE syndrome?

A

Remove tumor and give PPI

25
Q

What are the key features of a hyperplastic polyp?

A

Most hyperplastic polyps are an exaggerated response to injury that are associated w/ CHRONIC GASTRITIS in the ANTRUM.

The polyps themselves are susually covered in normal appearing mucosa but may have a elongated tortuous foveolar epithelium.

26
Q

What complications can occur w/ a hyperplatic polyp?

A

Dysplasia and adenocarcinoma

27
Q

What are the key features of a cystic fundic gland polyp?

A

Associated with use of PPI’s secondary to increased gastrin in response to decreased acid.

Also on familial adenomatous polyposis.

Note DILATED GLANDS on histology

28
Q

What is a gastric adenoma? What cancer is commonly observed w/ this adenoma?

A

A neoplastic polyp similar to other adenomas in GI that is often associated w/ chronic gastritis leading to polyploid areas of dysplasia.

Incidence increases w/:
Age
familial adenomatous polyposis

Endoscopically similar to hyperplastic polyps.

Adenocarcinoma in up to 30%.

29
Q

What is an inflammatory fibroid polyp?

A

Mesenchymal polyploid proliferation of stromal spindle cells, small blood vessels and inflammatory cells (eosinophils) that are often see in the STOMACH and SI.

30
Q

Inflammatory fibroid polyps are usually observed in what population?

A

Middle aged females

31
Q

What is seen histologically in an inflammatory fibroid polyp?

A

Loose bland mesenchyme fills submucosa and musclaris mucosae.

Also lymphoctes eosinophils and blood vessels.

32
Q

A 2-3 week old male w/ new onset regurgitation and persistent projectile non-bilious vomiting. What do you see on exam? How do you treat them?

A

Congenital hypertorphic pyloric stenosis caused by proliferation of the pyloric muscularis propria.

Exam reveals abdominal OVOID MASS.

Myotomy is curative.

33
Q

What are the risk factors for gastric adenocarcinoma?

A
  1. chronic gastritis (h. pylori, autoimmune)
  2. Dietary carciniogens (smoked foods)
  3. Mesetrier’s disease
  4. Lack of fruits and veggies
  5. Familial adenomatosis polyposis
34
Q

What are the two types of gastric adenocarcinomas?

A
  1. Intestinal type

2. Diffuse type

35
Q

Intestinal type gastric adenocarcinoma

A

Polpyploid invasive mass of ulcer

Glandular differentiation is seen microscopically

36
Q

Diffuse type gastric adenocarcinoma?

A

Inolvement/thickening of gastric wall and loss of rugae folds (mucosa, submucosa, and muscularis propria)–> rigidity/leather bottle appearance

Microscopically: singlet ring cells

Younger adult

37
Q

What is the MC location for a GIST tumor?

A

Stomach

38
Q

What type of cells do GIST tumors differentiate to?

A

Differentiate towards interstitial cells of Cajal (peristalsis).

39
Q

What is the key genetic defect related to GIST tumors?

A

85% of GIST tumors have gain of function mutation for genes encoding receptor tyrosine kinase KIT

8% mutation activating related receptor tyrosine kinease platelet derived growth factor receptor- α.

40
Q

What is the rationale for using Gleevec to treat GIST tumors?

A

Gleevec is a tyrosine kinase inhibitor.

41
Q

What does a GIST tumor look like? What can you stain it for?

A

Tumor is composed of bundles of spindle shaped tumor cells.

Tumor can be stained for c-KIT with CD117 immunochemistry

42
Q

What is the MC RF for gastric MALT lymphoma?

A

H. pylori> chronic inflammation

43
Q

What first line therapy is used for primary treatment of MALT?

A

Antibiotics to eradicate H. pylori cause regression in up to 90% of cases.

*MALT due to translocations do not respond

44
Q

A pt presents w/ cutaneous flushing and sweating, bronchospasms, colicky abdominal pain, diarrhea, and right sided valvular fibrosis.

A

Carcinoid syndrome

Symptoms caused by bioactive substance secreted from tumor (5-HT, histamine, bradykinin) because these are metabolized by the liver presence of carcinoid syndrome suggests there has been metastasis.

45
Q

Where do carcinoid tumors arise form?

A

endocrine cells in the GI tract

46
Q

How do you diagnose carcinoid tumors?

A

24 hr urinary 5-HIAA (serotonin metabolite)

GI- Week 2 (11 decks)

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