Wk2 Gastric Pathology Flashcards

1
Q

Two normal damaging forces of gastric mucosa:

A
  1. Gastric acid

2. peptic enzymes

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2
Q

Six normal defensive forces of gastric mucosa:

A
  1. surface mucous secretion
  2. bicarb secretion into mucous
  3. mucosal blood flow
  4. apical surface transport
  5. epithelial regeneration
  6. elaboration of prostaglandins
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3
Q

Seven main mechanisms of gastric mucosal injury:

A
  1. H. pylori
  2. cigarette smoke
  3. alcohol
  4. NSAIDs
  5. Aspirin
  6. gastric hyperacidity
  7. duodenal gastric reflux
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4
Q

loss and necrosis of surface epithelium, confined to the lamina propria, i.e. mucosa

A

mucosal erosion

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5
Q

necrotizing process extends beyond the mucosa into the submucosa and even into and through the muscle wall

A

mucosal ulcer

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6
Q

Most common finding in H. pylori gastritis:

A

active chronic gastritis

antrum —> fundus

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7
Q

Two complications of H. pylori infection:

A
  1. MALT lymphoma

2. gastric adenocarcinoma

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8
Q

How do humans acquire H. helmannii gastritis?

A

letting dogs lick your face

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9
Q

Stain to help visualize H. pylori?

A

diff quick blue

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10
Q

Dx test for active H. pylori:

A

H. pylori stool antigen

urea breath test

rapid urease test on fresh tissue biopsy

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11
Q

Pathogenesis of autoimmune gastritis:

A

CD4+ T-cell mediated destruction of parietal cells

chief cells also lost during destruction of the gastric glands (“bystander damage”).

Antibodies to parietal cells and intrinsic factor are also produced as part of the autoimmune response, but are not pathogenic (can be used as a diagnostic test).

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12
Q

Findings in autoimmune gastritis:

A

Decreased gastric acid secretion (achlorhydria).

Compensatory hypergastrinemia and hyperplasia of antral gastrin-producing G cells

endocrine cell hyperplasia in the fundus and body of the stomach.

Vitamin B12 deficiency due to loss of secreted intrinsic factor (pernicous anemia with increased RBC MCV).

Reduced serum pepsinogen I concentration.

Inflammatory mucosal damage

atrophy of the gastric mucosa in the body and fundus with sparing of the antrum and cardia

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13
Q

Causes of chronic reactive gastropathy:

A

chemical mucosal injury

NSAIDs

aspirin

bile reflux

alcohol ingestion

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14
Q

Two common causes of peptic ulcer disease:

A
  1. H. pylori

2. NSAIDs

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15
Q

Three complications of PUD:

A

Bleeding

perforation

obstruction

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16
Q

eosinophilic inflammation

usually multiple GI sites

maybe food or other allergy

A

eosinophilic gastritis

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17
Q

characterized by marked intraepithelial inflammation (CD8+ T cells).

Can be seen as an isolated finding, or in patient’s with either co-existing celiac disease or in patients with co-existing ________/collagenous colitis

A

lymphocitic gastritis

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18
Q

granulomatous inflammation.

Most cases are secondary to an underlying disorder, such as Crohn’s disease, sarcoidosis, mycobacterial or fungal infections.

A

granulomatous gastritis

19
Q

excessive secretion of transforming growth factor alpha (TGF-α).

marked diffuse hyperplasia of the foveolar epithelium of the body and fundus of the stomach

protein losing enteropathy and hypoproteinemia, with diarrhea, weight loss, and peripheral edema

Some cases of are associated with an infection (e.g. CMV in children).

Patients are also at risk for gastric adenocarcinoma.

A

Menetrier’s disease

20
Q

Caused by gastrin secreting tumors:

A

Zollinger-Ellison syndrome

21
Q

exaggerated mucosal response to chronic gastritis:

A

hyperplastic polyp

22
Q

associated with PPI

increased gastrin in response to decrease acid

A

cystic fundic gland polyp

23
Q

Neoplasm morphologically similar to other GI adenomas:

A

gastric adenoma

24
Q

Mesenchymal polypoid proliferation

stromal spindle cells

small blood vessels,

inflammatory cells, particularly eosinophils.

middle aged females

A

inflammatory fibroid polyp

25
Q

Risk factors for gastric adenocarcinoma:

A
  • Chronic gastritis, H. pylori gastritis and autoimmune gastritis (intestinal metaplasia-dysplasia-carcinoma sequence).
  • Dietary carcinogens (nitrosamines, smoked foods).
  • Menetrier’s disease.
  • Diets lacking in fruits/vegetables (antioxidants).
  • familial adenomatosis polyposis (FAP).
26
Q

can present as a polypoid invasive mass or invasive ulcer. Microscopically, tumor shows glandular differentiation.

A

Intestinal type gastric adenocarcinoma

27
Q

involvement and thickening of the gastric wall (mucosa, submucosa, and muscularis propria).

signet-ring cells

involvement of the gastric wall

rigidity and a leather bottle appearance (linitis plastica).

A

Diffuse type gastric adenocarcinoma

28
Q

Tumor that differentiates towards interstitial cells of Cajal:

A

GIST

29
Q

Key genetic mutation of GIST tumors:

A

KIT tyrosine kinase

30
Q

Tx for GIST:

Why?

A

imatinib (Gleevec)

tyrosine kinase inhibitor

31
Q

Most common RF for MALT lymphoma?

A

H. pylori

32
Q

Tx for MALT lymphoma:

A

antibiotics

33
Q

Tumors from endocrine cells of GI tract:

A

carcinoid

**now called neuroendocrine

34
Q

Test for neuroendocrine tumors:

A

24 hour urinary 5-hydroxyindoleacetic acid (5-HIAA), a metabolite of seratonin

35
Q

inflammation of the thin, mesothelial covered layer of tissue that lines the abdominal cavity

A

peritonitis

36
Q

Causes of peritonitis:

A

bacteria

bile

acute hemmorrhagic pancreatitis

foreign material

endometriosis

37
Q

accumulation fo fluid in peritoneal cavity

A

ascites

38
Q

By far most common cause of ascites:

A

cirrhosis –> portal hypertension

39
Q

Common complication of ascites:

A

spontaneous bacterial peritonitis

40
Q

Two types of ascites:

A

transudative (hypoalbuminemia, cirrhosis)

exudative (infection, malignancy)

41
Q

Two most common causes of malignant ascites:

A

ovarian carcinoma

pancreatic carcinoma

42
Q

a dense fibrosing process that can result in renal failure due to ureteral obstruction

A

idiopathic retroperitoneal fibrosis

43
Q

foveolar hyperplasia

mucin depletion

vascular congestion

edema

lamina propria fibrosis

A

Chronic reactive gastropathy