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PCM1 Exam 4 > DERS 04 - GIT Pathology 2 - Stomach > Flashcards

DERS 04 - GIT Pathology 2 - Stomach Flashcards

1
Q

Identify where the following stomach structures are located:

  • Body
  • Pyloric antrum
  • Cardia
  • Fundus
  • Pyloric canal
  • Cardiac notch
  • Pylorus
  • Lesser and Greater Curvatures
A
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2
Q

List the names, functions, and locations of the different stomach glands we need to know about for stomach pathology

A
  • Glands in the cardia (antrum) secrete mucus
  • The glands in the corpus (body) and fundus contain:
    • Chief cells, which secrete pepsinogen
    • Parietal cells, which secrete acid and intrinsic factor
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3
Q

What are the etiologies and typical pathogenesis of pyloric stenoses?

A
  • Congenital
    • Turner Syndrome
    • Trisomy 18
    • Esophageal Atresia
  • Acquired
    • Chronic antral gastritis
    • Peptic Ulcers
    • Malignancy

Pathogenesis is usually concentric hypertrophy of circular muscle in pylorus

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4
Q

What are the clinical features of pyloric stenosis? How is it usually treated?

A
  • Regurgitation
  • Projectile Vomiting
  • Palpable epigastric mass
  • Visible peristalsis

Treatment is usually surgery (myotomy - cutting of muscle)

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5
Q

List the primary types of gastritis and their major causes

A
  • Erosive - mucosa (superficial epithelium) is eroded away
    • Acute Gastritis
      • NSAID, EtOH, Oral Iron, KCL, and/or tobacco overuse
      • Ischemia and shock
      • Severe stress (burns, surgery)
      • Chemotherapy
      • Systemic infections
      • Uremia
  • Chronic - typically not erosive
    • Helicobacter pylori infection
    • Autoimmune (pernicious anemia)
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6
Q

What are the clinical features of gastritis?

A
  • Could be asymptomatic
  • Epigastric Pain
  • Nausea
  • Vomiting
  • Hematemesis and melena
  • If not resolved, bleeding can lead to anemias and could be fatal
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7
Q

What is seen upon endoscopy and histology of acute gastritis?

A
  • Endoscopy
    • Erosions and hemorrhage
    • Hyperemia punctuating areas of hemorrhage
  • Histology
    • Superficial mucosal injury
    • Ulcers (full thickness mucosal injury)
    • Edema and congestion of lamina propria
    • Neutrophils in the surface epithelium and glands
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8
Q

What is seen upon endoscopy and histology of chronic gastritis?

A
  • Endoscopy - patch/diffuse erythema with possible hemorrhage and thick mucosal folds
  • Histology
    • Lymphocytes and plasma cells in the lamina propria
    • Neutrophils in surface epithelium
    • In extreme cases you’ll see metaplasia, dysplasia, and glandular atrophy

See image

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9
Q

How do you distinguish chronic gastritis caused by H. pylori from chronic gastritis caused by pernicous anemia with endoscopy and histology?

A
  • Endoscopy
    • H. Pylori - you’ll really only see the erythema/hemorrhage in the cardia/antrum of the stomach
    • Autoimmune - you’ll really only see the erythema/hemorrhage in the fundus and body of the stomach
  • H. pylori infections will cause reactive lymphoid aggregates to appear on the luminal surface of the micrograph. See image
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10
Q

Aside from chronic gastritis, what disorders do H. pylori infections cause? Why?

A
  • Peptic ulcers from the mucosal damage
  • Lymphoma - the infection attracts PMNs and other inflammatory cells eventually leading to uncontrolled B cell proliferation
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11
Q

What is the pathogenesis of autoimmune gastritis?

A
  1. The body produces autoantibodies against parietal cells and intrinsic factor
  2. Oxyntic glands (acid producing glands) are destroyed leading to achlorhydria (loss of acid production), which causes an increase in gastrin levels. IF production is also lost (pernicous anemia)
  3. Gastric mucosa undergoes intestinal metaplasia (change to an epithelium resembling the intestines), producing goblet cells, which can become dysplasia and eventually carcinoma
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12
Q

Describe the histological findings of autoimmune gastritis.

A
  • Chronic inflammation
  • Glandular atrophy
  • Appearance of goblet cells

See image

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13
Q

What is the difference between a gastric, peptic, and duodenal ulcer?

A

An ulcer is a loss of mucosa that extends through to the muscularis mucosae or deeper

  • A peptic ulcer is an ulcer that is exposed to acidic peptic juices. There are two primary types
    • Gastric ulcers in the stomach
    • Duodenal ulcers in the first part of the duodenum
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14
Q

Describe the most common etiologies and pathogeneses of acute gastric ulcers

A
  • Curling Ulcers are caused by extensive burns, severe trauma, or major surgery. These can cause decreased plasma volume leading to hypoxia and necrosis of gastric mucosal cells
  • Cushing Ulcers are caused by head traumas leading to intracranial lesions that increase vagal stimulation of the parietal cells, resulting in increased gastric acid secretion.
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15
Q

What are the most common sites of a peptic ulcer?

A
  1. Duodenum (lacks the defenses of the stomach)
  2. Stomach
  3. Gastroesophageal junction
  4. Margins of gastrojejunostomy
  5. Meckel’s diverticulum (if gastric mucosa develops)
  6. Stomach, duodenum, and jejunum in Zollinger Ellison Syndrome
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16
Q

How does a peptic ulcer typically appear upon endoscopy and histology?

A
  • Endoscopy - usually a <2cm round to oval punched out hole with relatively straight walls and slightly raised margins (>2cm or highly raised margins suggests gastric adenocarcinoma). Typically the surrounding mucosa is normal or shows signs of gastritis.
  • Histology - the bottom of the ulcer will be necrotic and granulation tissue will be present in the base, with possible fibrosis.

See images

17
Q

List the most common etiopathogeneses of peptic ulcers

A
  1. H. pylori infection - 70% of gastric and 90% of duodenal ulcers
  2. NSAIDS - inhibit prostaglandin synthesis
  3. Smoking - impairs mucosal blood flow
  4. Alcohol
  5. Psychological stress
  6. Zollinger Ellison Syndrome - tumors cause the stomach to produce too much acid, resulting in multiple tumors in the stomach, duodenum, and jejunum
18
Q

List the typical clinical features and associated complications for peptic ulcers.

A
  • Clinical Features
    • Burning epigastric pain 1-3 hours postprandial
      • Relieved by food and alkali
      • Worse at night
    • Associated weight loss
  • Complications - bleeding, perforation, gastric outlet obstruction.
19
Q

Describe how a peptic ulcer can lead to malignant transformation.

A

It almost never does

20
Q

How do NSAIDs damage the gastric mucosa?

A

They inhibit prostaglandin synthesis. Prostaglandins are important for:

  • Maintaining blood flow to the gastric mucosa
  • Maintaining mucus and bicarb secretion

The NSAID itself also directly irritates the surface epithelium by increasing mucosal permeability to ions

21
Q

What is the most common type of malignant tumor found in the stomach? Where does it occur most often and why?

A

Gastric adenocarcinoma

Highest occurence is in Japan and South Korea because this disease is heavily associated with H. pylori infections and these regions experience the highest rates of untreated infections.

22
Q

Describe the subtypes of gastric adenocarcinoma and their primary causes.

A
  • Intestinal - the development of neoplastic cells in GIT glands. Typically caused by an H. pylori infection that leads to chronic gastritis and intestinal metaplasia (change to a cell type resembling intestinal epithelium)
  • Diffuse - the development of neoplastic cells in the walls of the GIT. Typically caused by a mutation in E-cadherin that people are born with
23
Q

How does diffuse gastric adenocarcinoma typically appear upon endoscopy and histology?

A
  • Endoscopy - most often seen in the stomach. The neoplasm in the wall causes the rugae to flatten and also causes desmoplastic changes (fibrosis of tissue adjacent to the neoplasm) leading to the typical linitis plastica appearance (aka - leather bottle stomach).
  • Histology - the appearance of signet ring cells (a cell with a large vacuole) in the mucosa

See image

24
Q

How does intestinal gastric adenocarcinoma typically appear upon endoscopy and histology?

A
  • Endoscopy - the neoplasm in the gland cuts off blood supply leading to an ulcer with highly raised margins surrounded by intact rugae
  • Histology - the formation of glandular structures by neoplastic cells

See image

25
Q

Where is gastric adenocarcinoma usually seen?

A

50-60% in pylorus/antrum

25% in cardia

26
Q

What are the clinical features and associated complications of gastric adenocarcinoma? What is its prognosis?

A
  • Clinical Features
    • Usually asymptomatic in early stages
    • Weight loss/anorexia
    • Abdominal pain
  • Associated Complications
    • Pyloric outlet obstruction
    • Krukenberg tumor (spread to ovaries)
    • Spread to Virchow Node (left supraclavicular)

Prognosis is usually unfavorable but depends upon depth of invasion and nodal status

27
Q

What is a GI Stromal Tumor (GIST)? Where does it usually occur? What usually causes it? Is it usually benign or malignant?

A
  • GISTs are mesenchymal tumors derived from the cells of Cajal (peristaltic pacemaker cells)
  • Can be found anywhere in the GIT
  • Usually caused by Kit mutations (the Kit gene codes for a TKR)
  • Can be benign or malignant
28
Q

Describe the gross and histological appearance of GIST

A
  • Gross - when cut, the tumor will have holes in it. Also, usually the overlying gastric mucosa appears normal
  • Histology - like all mesenchymal tumors, whorls and/or bundles of spindle fibers will be seen

See image

PCM1 Exam 4 (19 decks)

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