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Gastrointestinal 1 > Pathology of the Stomach > Flashcards

Pathology of the Stomach Flashcards

1
Q

What is Gastroschisis? (gastro= stomach, schisis= to split)

A

congenital malformation of the abdominal wall leading to exposure of abdominal contents.

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2
Q

What is omphalocele?

A

persistent herniation of bowel into umbilical cord due to failure of herniated intestines to return to the body cavity during development.
*contents covered by peritoneum and amnion of the umbilical cord.

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3
Q

What is pyloric stenosis?

A

congenital hypertrophy of pyloric smooth muscle; more common in males.

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4
Q

Does pyloric stenosis present at birth?

A

NO. Classically presents 2 WEEKS after birth as projectile nonbilious vomiting, visible peristalsis, and olive-like mass in the abdomen.

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5
Q

How do you treat pyloric stenosis?

A

myotomy

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6
Q

What is acute gastritis?

A

acidic damage to the stomach mucosa due to imbalance between mucosal defenses and acidic environment (aka burning of the stomach due to too much acid or not enough protection).

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7
Q

What mucosal defenses exist in the stomach?

A
  • mucin layer produced by foveolar cells
  • bicarbonate secretion by surface epithelium
  • normal blood supply (provides nutrients and picks up leaked acid).
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8
Q

What are the risk factors of acute gastritis?

A
  • severe burn (CurLing ulcer) causing hypovolemia, which leads to decreased blood supply.
  • NSAIDS (decreased PGE2)
  • heavy alcohol consumption
  • chemotherapy (knock out cells that turn over)
  • increased intracranial pressure (CuSHing ulcer causing increased stimulation of vagus nerve= increased Ach= increased acid production.
  • Shock= decreased blood flow. Multiple stress ulcers may be seen in ICU patients
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9
Q

What 3 receptors exist on the parietal cell that stimulate acid production?

A
  1. Acetylcholine receptors
  2. Gastrin receptors
  3. Histamine receptors
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10
Q

In what does acid damage result?

A
  • superficial inflammation
  • erosion (loss of superficial epithelium)
  • ulcer (loss of mucosal layer)
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11
Q

What is chronic gastritis?

A

chronic inflammation of stomach mucus due to either:

  1. chronic autoimmune gastritis= autoimmune destruction of gastric parietal cells (BODY and FUNDUS).
  2. chronic H. pylori gastritis= H. pylori-induced acute and chronic inflammation; most common form (90%) .
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12
Q

What causes the autoimmune destruction in chronic gastritis?

A

T cell (type IV hypersensitivity) mediated damage and as a result of this damage you will see antibodies against parietal cells and/or intrinsic factor in the blood.

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13
Q

What are some clinical features of chronic autoimmune gastritis?

A
  • atrophy of mucosa with intestinal metaplasia
  • achlorhydria (low acid production) and thus increased gastrin levels (to try to increase this acid production) and antral G-cell hyperplasia.
  • megaloblastic (pernicious) anemia due to lack of intrinsic factor (normally produced by the parietal cells which are being destroyed).
  • increased risk for gastric adenocarcinoma (intestinal type).
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14
Q

** What is the most common cause of vitamin B 12 deficiency?

A

chronic autoimmune gastritis

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15
Q

How does H. pylori induce chronic H. pylori gastritis?

A

it produces ureases and proteases along with inflammation that weaken mucosal defenses (ANTRUM is most common site).
*they just sit on the surface and do not invade the stomach mucosa.

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16
Q

How does chronic H. pylori present?

A

epigastric abdominal pain; incresed risk for ulceration (peptic ulcer disease), gastric adenocarcinoma (intestinal type), and MALT (mucosa associated lymphoid tissue) lymphoma (B-cell lymphoma remember; markers are CD19 and CD20)

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17
Q

What is the therapy for chronic H. pylori gastritis?

A

triple therapy, which resolves gastritis/ulcer and reverses intestinal metaplasia! :)
*use negative urea breath test to confirm eradication of H. pylori

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18
Q

What is peptic ulcer disease?

A

solitary mucosal ulcer involving proximal duodenum (90%) or distal stomach (10%).

19
Q

What is almost always the culprit for duodenal peptic ulcers?

A

H. pylori
*rarely due to Zollinger-Ellison syndrome (gastronoma= tumor that produces excess gastrin= excess acid production. Also hyperchlorhydria).

20
Q

How do duodenal peptic ulcers present?

A

epigastric pain that IMPROVES with meals (due to pancreatic neutralizing enzymes).
*diagnostic endoscopic biopsy shows ulcer with hypertrophy of Brunner’s glands.

21
Q

What is a complication of duodenal peptic ulcers?

A
  • may rupture and lead to bleeding from the gastroduodenal artery or acute pancreatitis (posterior wall of duodenum; rare).
22
Q

What is another type of peptic ulcer disease?

A

gastric ulcer, which is usually due to H. pylori and sometimes NSAIDS or bile reflux.

23
Q

How do gastric peptic ulcers present?

A
  • epigastirc pain that WORSENS with meals (acid production increases in the stomach with meals).
  • usually located on LESSER curvature of the antrum and rupture carries risk of bleeding from left gastric artery.
24
Q

What is an important DDX of ulcers?

A

carcinoma.

* duodenal ulcers are almost never malignant, but gastric ulcers can be caused by gastric carcinoma.

25
Q

What are the features that distinguish benign from malignant peptic ulcers?

A
  • benign= small, sharply demarcated and surrounded by radiating folds of mucosa.
  • malignant= large and irregular with heaped up margins.
  • biopsy is required for definitive diagnosis.
26
Q

What is gastric carcinoma?

A
  • malignant proliferation of surface epithelial cells (adenocarcinoma).
27
Q

What are the 2 subtypes of gastric carcinoma?

A
  1. intestinal type (more common)= large, irregular ULCER with heaped up margins (usually on lesser curvature of antrum).
  2. diffuse type= SIGNET RING CELLS (nucleus pushed to side by significant mucus production within the cell) that diffusely infiltrate the gastric wall, resulting in desmoplasia (thickening of stomach wall from fibrous tissue and blood vessels; linitis plastica).
28
Q

What are the risk factors for INTESTINAL TYPE gastric carcinoma?

A

intestinal metaplasia (due to H. pylori and autoimmune gastritis), nitrosamines in smoke foods, and blood type A.

29
Q

Is DIFFUSE TYPE gastric carcinoma associated with H. pylori?

A

NO, nor intestinal metaplasia, nor nitrosamines.

30
Q

Does gastric carcinoma (whether intestinal or diffuse type), present early or late?

A

LATE with weight loss, abdominal pain, anemia, and early satiety.
*may present with acanthosis nigricans (darkening of skin under the arm-pits) or Leser-Trelat sign (dozens of seborrheic keratoses).

31
Q

** Where does gastric carcinoma often metastasize?

A
  • left supraclavicular node (Virchow node)
  • liver or periumbilical region (Sister Mary Joseph nodule; INTESTINAL TYPE).
  • bilateral overares (Krukenberg tumor; DIFFUSE TYPE).
32
Q

What are some toxins produced by H. pylori?

A
  • cytotoxin-associated gene A (cagA) and Cag pathogenicity island, which promotes inflammation and tissue damage.
  • Vacuolating toxin (VacA) causes direct cell injury
33
Q

What are some uncommon gastritis forms?

A
  • reactive gastropathy= foveolar hyperplasia, mucosal edema, glandular regenerative changes, and GAVE (gastric antral vascular ectasia) .
  • eosinophilic gastritis= allergic reactions
  • lymphocytic gastritis= increased intracellular T lymphocytes, more common in women.
  • granulomatous gastritis= contains granulomas or aggregates of tissue macrophages, sarcoid…
34
Q

What is Menetrier disease?

A
  • rare excessive secretion of transforming growth factor alpha (TGF-a) causing diffuse hyperplasia of foveolar epithelium of the body and fundus due to protein losing enteropathy.
  • glands have corkscrew appearance with cystic dilation.
  • has association with H. pylori
35
Q

What are hyperplastic polyps?

A
  • common gastric polyps where the surface epithelium may be eroded leading to blood loss and iron deficiency anemia.
  • may be seen in autoimmune atrophic gastritis and H. pylori.
36
Q

What are Adenomatous polyps?

A

neoplasms found mostly in the antrum and may occur sporadically and in association with FAP.

37
Q

In Neuroendocrine tumors (aka carcinods or well differentiated carcinomas), what immunohistochemical marker stains positive?

A

synaptophysin and chromogranin A

38
Q

Side step to small intestine…What do carcinoid tumors produce?

A

carcinoid syndrome= cutaneous flushing, sweating, bronchospasm, abdominal pain, diarrhea and right sided cardiac valvular fibrosis.

39
Q

What are the 3 types of gastric smooth muscle tumors?

A
  1. leiomyoma= small often multiple, but benign.
  2. leiomyosarcoma= more mitoses, necrosis, hemorrhage, and metastasizes to liver and lungs.
  3. leiomyoblastoma= round cells with a central nucleus, most are benign, but malignant type is seen in the posterior wall.
40
Q

What are gastrointestinal stromal tumors (GIST)?

A
  • usually arise from interstitial cells of Cajal in the muscularis propria.
  • most common mesenchymal tumor of the abdomen
  • may be palpable
  • may be benign or malignant
  • Carney’s triad in youth (RARE)= young females with gastric GIST, paraganglioma, and pulmonary chondroma.
41
Q

What are gastric xanthomas?

A

yellow nodules or plaques that barely protrude form the surrounding mucosa. Consist of lipid laden macrophages containing cholesterol and fat.
*NOT associated with hypercholesterolemia.

42
Q

What is pancreatic heterotopia?

A

polyp consisting of small submucosal nodules of pancreatic tissue at the lower esophageal sphincter, antral, or prepyloric regions.

43
Q

What is phytobezoars?

A
  • accumulation of vegetable products in the stomach.
  • can be associated with swallowing gum.
  • causes delayed gastric emptying
  • treat with cellulase
44
Q

What is trichobezoar?

A

hairball with gelatinous matrix from people with long hair who nervously eat their hair.

Gastrointestinal 1 (21 decks)

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