Gastric Pathologies Flashcards

1
Q

Gastritis

Acute vs. Chronic

Result of acid damage

Patient population

A

Acute = Inc. acid/dec. mucosal protection

  • NSAIDS –> dec. PGE2 –> dec. gastric mucosa protection
  • Burns (Curling ulcer) –> hypovolemia –> mucosal ischemia
  • Brain injury (Cushing ulcer) –> inc. intracranial P –> inc. vagal stimulation –> inc. ACh –> inc. H+ production

Acid damage –> superficial inflammation, erosion (loss of superficial epithelium), or ulcer (loss of mucosal layer)

Patient population:

  • Alcoholics
  • Patients taking daily NSAIDs (e.g., patients with rheumatoid arthritis)
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2
Q

Gastritis

Acute vs. Chronic

A

Chronic = mucosal inflammation, often leading to atrophy (hypochlorhydria (low HCl production) –> hypergastrinemia) and intestinal metaplasia (inc. risk of gastric adenocarcinoma - intestinal type)

  • H. pylori
    • Most common
    • Inc. risk of peptic ulcer disease, MALT lymphoma
    • Affects antrum first –> spread to body
  • Autoimmune
    • Autoantibodies to parietal cells and IF
      • Pathogenesis mediated by T cells (type IV hypersensitivity)
      • Consequence, not cause
    • Inc. risk of megaloblastic (pernicious) anemia due to lack of IF
    • Affects body/fundus
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3
Q

Menetrier disease

A

Gastric hyperplasia of mucosa –> hypertrophied rugae (looks like brain gyri), excess mucus production + resultant protein loss and parietal cell atrophy –> dec. acid production

Precancerous

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4
Q

Gastric cancer

Spread/presentation

A
  • Most common: gastric adenocarcinoma
  • Early aggressive local spread with node/liver metastases
  • Often presents late, w weight loss, early satiety
    • Sometimes: acanthosis nigricans (discoloration) or Leser-Trelat sign (pigmentation)
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5
Q

Gastric cancer

Two types

A
  1. Intestinal:
    1. Associated w H. pylori, dietary nitrosamines (smoked foods), tobacco smoking, achlorhydia, chronic gastritis
    2. Presentation: ulcer with raised margins
  2. Diffuse:
    1. NOT associated with H. pylori
    2. Signet ring cells (mucin-filled cells w peripheral nuclei)
    3. Stomach wall thickened and leathery (linitis plastica)
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6
Q

Gastric cancer

Virchow node

Krukenberg tumor

Sister Mary Joseph nodule

A

Virchow node:

  • involvement of L supraclavicular node by metastasis from stomach

Krukenberg tumor:

  • bilateral metastases to ovaries
  • Abundant mucin-secreting, signet ring cells
  • Seen with diffuse type

Sister Mary Joseph nodule:

  • Subcutaneous periumbilical metastasis
  • Seen with intestinal type
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7
Q

Peptic Ulcer Disease: Gastric Ulcer (10%) vs. Duodenal Ulcer (90%)

Pain

H. pylori infection

Mechanism

Other causes

Risk of carcinoma

Other

A

Pain: can be Greater with meals –> weight loss

H. pylori infection –> ~70%

Mechanism –> dec. mucosal protection against gastric acid

Other causes –> NSAIDs

Risk of carcinoma –> Inc

Other –> biopsy margins to rule out malignancy

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8
Q

Peptic Ulcer Disease: Gastric Ulcer (10%) vs. Duodenal Ulcer (90%)

Pain

H. pylori infection

Mechanism

Other causes

Risk of carcinoma

Other

A

Pain: Decreases with meals –> weight gain

H. pylori infection –> ~90%

Mechanism –> dec. mucosal protection or inc. gastric acid secretion

Other causes –> Zollinger-Ellison syndrome

Risk of carcinoma –> Generally benign

Other –> Hypertrophy of Brunner glands

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9
Q

Ulcer complications:

Hemorrhage

Obstruction

Perforation

A
  • Gastric, duodenal (posterior > anterior)
  • Ruptured gastric ulcer on lesser curvature of stomach –> bleeding from left gastric a.
  • Ulcer on posterior wall of duodenum –> bleeding from gastroduodenal a.
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10
Q

Ulcer complications:

Hemorrhage

Obstruction

Perforation

A

Pyloric channel, duodenal

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11
Q

Ulcer complications:

Hemorrhage

Obstruction

Perforation

A

Duodenal (anterior > posterior)

May see free air under diaphragm w referred pain to shoulder via phrenic n.

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