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06. Gastrointestinal Pathology > 4. Stomach > Flashcards

4. Stomach Flashcards

1
Q

Diseases of the stomach

A
  1. Congenital anomalities
    - Diaphragmatic Hernia
    - Pyloric Stenosis
  2. Acute gastritis
  3. Chronic gastritis
    - Helicobacter pylori gastritis
    - Autoimmune gastritis
    - Eosinophilic gastritis
    - Lymphocytic gastritis (Varioliform gastritis)
    - Tuberculous gastritis
  4. Peptic ulcer disease
  5. Hypertrophic gastropathies
    - Ménétrier Disease
    - Zollinger-Ellison Syndrome
  6. Neoplasms
    - Gastric adenocarcinoma
    - Gastric neuroendocrine tumours (Carcinoids)
    - Gastric lymphoma
    - Gastrointestinal Stromal Tumours (GIST)
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2
Q

Diaphragmatic Hernia

A
  1. Due to incomplete closure of pleuroperitoneal canals
  2. Leads to herniation of abdominal viscera into thoracic cavity
    - May lead to pulmonary hypoplasia due to space-filling effect of the displaced viscera
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3
Q

Pyloric stenosis

A
  1. Congenital pyloric stenosis
    - More common in males
    - Genetic associations: trisomy 18, Turner syndrome
    - Presents in 2nd-3rd week of life as persistent projectile vomiting
    - Can be corrected surgically with myotomy
  2. Acquired pyloric stenosis
    - Due to antral gastritis or peptic ulcers near pylorus
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4
Q

Definition of acute gastritis

A

Acute, transient gastric mucosal inflammatory process

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5
Q

Causes of acute gastritis

A
  1. Drugs
    - Non-steroidal anti-inflammatory drugs
    - Corticosteroids
    - Cigarette smoking
  2. Direct-acting luminal chemicals
    - Alcohol
    - Bile salts (in bile reflux, e.g. post-gastrectomy)
    - Corrosives
  3. Stress
    - Severe burn or trauma (gives rise to Curling’s ulcers)
    - Intracranial lesions (gives rise to Cushing’s ulcers)
    - Post-myocardial infarction
  4. Ischemia
    - Shock
    - Portal hypertension
    - High altitudes
  5. Chemotherapy
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6
Q

Pathogenesis of acute gastritis

A
  1. Increased acid secretion with back-diffusion
  2. Decreased bicarbonate buffer production
    - By NH4+ produced due to action of Helicobacter pylori urease activity on urea
  3. Reduced blood flow
    - Decreased gastric perfusion (e.g. in shock)
    - Decreased production of cytoprotective prostaglandins (by NSAIDs & corticosteroids)
  4. Disruption of adherent mucus layer
  5. Direct damage to gastric epithelium
    - By direct-acting luminal agents (alcohol, bile salts)
    - Chemotherapy reduces epithelial regeneration
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7
Q

Pathological Effects & Complications of acute gastritis

A
  1. Erosions (loss of superficial epithelium, generating a defect limited to the lamina propria)
  2. Ulcers (extension of erosion beyond lamina propria)
  3. Epigastric pain, indigestion
  4. Bleeding, which may present as:
    - Hematemesis, with coffee grounds (gastric-digested blood seen in the esophagus during endoscopy)
    - Melena (tarry foul-smelling stools)
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8
Q

Definition of chronic gastritis

A

Chronic gastric mucosal inflammation leading to mucosal atrophy & intestinal metaplasia of gastric epithelium; has several types but by far, the most important & common type is Helicobacter pylori gastritis

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9
Q

Most common form of chronic gastritis

A

Helicobacter pylori gastritis

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10
Q

Cause of Helicobacter pylori Gastritis

A

Due to H. pylori colonization of the gastric mucosa

  1. H. pylori found within mucous layer on surface
  2. H. pylori has tropism for gastric-type mucosa
  3. Colonization increases with age
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11
Q

Helicobacter pylori gastritis typically affects

A

The antrum (antral gastritis)

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12
Q

Histology of Helicobacter pylori gastritis

A
  1. Active inflammation (intraepithelial neutrophils which may accumulate in gastric pits to form crypt abscesses, subepithelial macrophages, plasma cells & lymphocytes which in severe cases may form lymphoid follicles with germinal centres)
  2. Regenerative changes (mitoses in epithelium, loss of mucous vacuoles)
  3. Intestinal metaplasia (appearance of goblet cells)
  4. Mucosal atrophy (loss in glandular structures &
    specialized cells)
  5. Potentially: hyperplasia → dysplasia → carcinoma-
    in-situ → carcinoma
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13
Q

Endoscopy of Helicobacter pylori gastritis

A

Erythematous antral mucosa with coarse/nodular appearance

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14
Q

Diagnosis of H. pylori infection for Helicobacter pylori gastritis

A
  1. Urea breath test (drink radioactively labeled urea, if
    H. pylori present, urease activity on urea will released
    radioactive CO2 that can be detected in the breath)
  2. Serology (H. pylori antibodies in serum)
  3. Histology (detection of spiral organisms within
    surface mucous with special stains – e.g. Warthin-
    Starry silver stain)
  4. Culture (microaerophilic conditions)
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15
Q

Pathological effects & complications of Helicobacter pylori gastritis

A
  1. Mostly asymptomatic
  2. Peptic ulcer disease
  3. Chronic atrophic gastritis
  4. Malignancies (gastric carcinoma, gastric lymphoma)
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16
Q

Autoimmune Gastritis

A

Due to autoantibodies produced against gastric
components:
1. Gastric parietal cells (90%)
2. Intrinsic factor (60%)

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17
Q

Association of autoimmune gastritis

A

Associated with other autoimmune disorders:

  1. Graves disease
  2. Diabetes mellitus
  3. Hashimoto’s thyroiditis
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18
Q

Autoimmune gastritis typically affects

A

The body of the stomach

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19
Q

Pathological effects & complications of autoimmune gastritis

A
  1. Hypochlorhydria & secondary hypergastrinemia
  2. Vitamin B12 deficiency (due to decrease in intrinsic factor production by parietal cells) with resultant megaloblastic (pernicious) anemia
  3. Increased risk of adenocarcinoma
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20
Q

Causes of reactive gastritis

A
  1. Chemical injury
  2. NSAID use
  3. Bile reflux
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21
Q

Histology of reactive gastritis

A
  1. Foveolar hyperplasia
  2. Glandular regenerative changes
  3. Mucosal edema
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22
Q

Endoscopy of reactive gastritis

A

Endoscopically: Watermelon stomach

- Longitudinal stripes of edematous erythematous mucosa alternating with less severely injured mucosa

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23
Q

Eosinophilic gastritis

A

Due to allergies & parasites

- May co-exist with eosinophilic (gastro)enteritis

24
Q

Lymphocytic gastritis (Varioliform Gastritis)

A
  1. Idiopathic
    - Associated with celiac disease
  2. Histologically:
    - Marked increase in intraepithelial CD8+ T cells
  3. Endoscopy:
    - Thickened folds covered by small nodules with central aphthous ulcerations
25
Q

Tuberculous Gastritis

A

Due to chronic granulomatous inflammatory conditions

  • Idiopathic
  • Tuberculosis
  • Crohn disease
  • Sarcoidosis
26
Q

Definition of peptic ulcer disease

A

Breach in mucosa of alimentary tract which penetrates the muscularis mucosae & beyond, typically associated with chronic H. pylori gastritis

27
Q

Causes of peptic ulcer disease

A
  1. Helicobacter pylori infection
  2. Drugs
    - Analgesics
    - Anti-inflammatory drugs (NSAIDs, corticosteroids)
  3. Smoking & alcohol
  4. Psychological stress
28
Q

Site of peptic ulcers

A
  1. Duodenum – 1st part (75%)
  2. Stomach – lesser curve, antrum (20%)
  3. Lower esophagus
    - In the setting of gastroesophageal reflux disease
  4. Stomal ulcer
    - At the stoma of a gastroenterostomy
  5. Meckel diverticulum – specifically when it possess ectopic gastric mucosa
  6. Distal duodenum + jejunum
    - In addition to stomach & 1st part of duodenum in Zollinger-Ellison syndrome
29
Q

Pathogenesis of peptic ulcer disease

A
  1. Peptic ulcers form as a result of imbalances between mucosal defences & damaging forces
  2. Mechanisms of peptic ulceration in H. pylori infection
    - H. pylori urease: generates free NH3 from endogenous urea, elevating gastric pH
    - H. pylori proteases: breaks down glycoproteins in gastric mucous
    - H. pylori phospholipases: damages epithelial cells to allow leakage of nutrients into surface microenvironment for bacterial sustenance; may release bioactive leukotrienes
    - H. pylori platelet activating factor: promotes thrombotic occlusion of mucosal capillaries
    - Neutrophil myeloperoxidase: involved in neutrophil respiratory burst to release cytotoxic free radicals
    - Chronically inflamed mucosa (with perpetually recruitment of inflammatory cells by bacterial antigens) more susceptible to acid injury
  3. Main mechanisms involved in gastric ulcers
    - Motility defects
    - Mucosal ischemia
    - Mucosal inflammation
  4. Main mechanisms involved in duodenal ulcers
    - Excessive acid-pepsin secretion that overwhelms (impaired) mucosal defences (hence epigastric pain experienced when hungry, which is relieved by food)
30
Q

Morphology of peptic ulcer

A
  1. [Grossly]
    - Round to oval, sharply demarcated, punched-out defect (in contrast to tumours with central cavitating necrosis which will appear as an ulcer with raised, heaped-up edges)
    - Mucosal margin may overhang base slightly
    - Variable depth
    - Base is smooth & clean
    - Stellate appearance due to scarring & puckering of wall
  2. [Histologically]
    - Surface zone of fibrinopurulent exudate
    - Acidophilic layer of necrotic tissue
    - Zone of granulation tissue
    - Zone of dense scar tissue
    - Interruption of muscularis propria
    - Proximation of muscularis propria & mucosae
    - Endarteritis obliterans
    (eroded thickened artery which is stiff, unable to undergo vasospasm, hence can cause massive bleeding)
31
Q

Pathological effects & complications of peptic ulcer disease

A
  1. Epigastric burning pain
    - Occurs when hungry (for duodenal ulcers) & at night (nocturnal acid secretion)
    - Relieved by food & ingestion of alkali (e.g. antacids)
  2. Bleeding
    - If mild & chronic: iron deficiency anemia
    - If severe & acute: hematemesis
  3. Perforation
    - With consequent acute peritonitis
  4. Scarring & strictures
    - Can result in obstruction (e.g. in stomach where ulcers are mostly found in the antrum, may lead to acquired pyloric stenosis)
  5. Gastric adenocarcinoma
32
Q

Definition of hypertrophic gastropathies

A

Uncommon diseases characterized by giant cerebriform enlargement of gastric rugal folds due to epithelial hyperplasia without inflammation, linked to excessive release of growth factors

33
Q

Types of hypertrophic gastropathies

A
  1. Ménétrier Disease

2. Zollinger-Ellison Syndrome

34
Q

Ménétrier Disease

A
  1. Rare disorder due to excessive secretion of TGF-alpha

2. Diffuse hyperplasia of foveolar epithelium of gastric body & fundus

35
Q

Morphology of Ménétrier Disease

A
  1. Grossly: irregular enlargement of rugae in body & fundus with antral sparing
  2. Histologically: foveolar mucous cell hyperplasia, parietal & chief cell hypoplasia
36
Q

Pathological effects & complications of Ménétrier Disease

A
  1. Hypoproteinemia due to resultant protein-losing enteropathy
  2. Increased risk of gastric adenocarcinoma
37
Q

Zollinger-Ellison Syndrome

A

Gastrin-secreting tumour (gastrinoma) of pancreas or duodenum

38
Q

Histology of Zollinger-Ellison Syndrome

A
  1. Proliferation of parietal cells, mucous neck cells & endocrine cells
  2. Hence increasing oxyntic mucosal thickness
39
Q

Pathological effects & complications of Zollinger-Ellison Syndrome

A
  1. Peptic ulcers (gastric, duodenal, jejunal)

2. Chronic diarrhoea

40
Q

Neoplasms of the stomach

A
  1. Gastric adenocarcinoma
  2. Gastric Neuroendocrine Tumours (Carcinoids)
  3. Gastric Lymphoma
  4. Gastrointestinal Stromal Tumours (GIST)
41
Q

Gastric adenocarcinoma

A

Derived from columnar epithelial cell in gastric mucosa

42
Q

Etiologies & associations of gastric adenocarcinoma

A
  1. Helicobacter pylori chronic gastritis (intestinal metaplasia as a precursor lesion)
  2. Diet (nitrites, smoked food, lack of vegetables)
  3. Cigarette smoking
  4. Partial gastrectomy (allows reflux of bile, induces chronic gastritis)
  5. Barrett esophagus (increased risk of gastroesophageal junction tumours)
43
Q

Location of gastric adenocarcinoma

A

Typically at gastric antrum & lesser curvature

44
Q

Histological types of gastric adenocarcinoma

A
  1. Intestinal types (papillary, tubular, mucinous)
    - Intestinal histological morphology
    - Typically arise from precursor lesion of
    intestinal metaplasia (as in chronic gastritis)
  2. Diffuse types (signet-ring cell, undifferentiated)
    - Signet-ring cells have large cytoplasmic mucin vacuoles & peripherally displaced crescent- shaped nuclei
    - Involves CDH1 mutation (encodes E-cadherin), which is also seen in lobular carcinomas of the breast (some of which have signet-ring cells too)
45
Q

3 macroscopic growth patterns of gastric adenocarcinoma

A
  1. Exophytic growth (typical of intestinal types)
  2. Excavated growth (typical of intestinal types)
  3. Flat/depressed growth (typical of diffuse types)

***Note: extensive infiltration of a broad region of the stomach in advanced flat growth patterns creates a rigid, thickened leather bottle appearance of the stomach termed linitis plastica (metastatic lung & breast cancers to the stomach can also give a similar appearance)

46
Q

Clinical features of gastric adenocarcinoma

A
  1. Insidious clinical course, remains asymptomatic until late in its course
  2. Non-specific symptoms: weight loss, abdominal pain, anorexia, vomiting, altered bowel habits,
    dysphagia, anemia, hematemesis
  3. Prognostic factors: depth of invasion, nodal & distant metastases, HER-2/neu (allows treatment with trastuzumab)
  4. Treatment: surgical resection with or without adjuvant chemotherapy & radiotherapy
  5. Prognosis: 5-year survival rate for surgically treated early gastric cancer = 90-95%; that for advanced gastric cancer < 15%
47
Q

Gastric neuroendocrine tumours (carcinoids)

A

Derived from enterochromaffin-like (ECL) cells in gastric
mucosa
- Carcinoids can also be derived from the scattered
endocrine cells found elsewhere in the GIT

48
Q

Etiologies & associations of gastric neuroendocrine tumours (carcinoids)

A
  1. Setting of chronic atrophic gastritis with secondary hypergastrinemia
  2. Multiple endocrine neoplasia type I
  3. Zollinger-Ellison syndrome

***Note: all of them essentially result in a hypergastrinemic state which causes ECL cell hyperplasia, a presumed precursor lesion

49
Q

Morphology of gastric neuroendocrine tumours (carcinoids)

A
  1. Grossly: intramural or submucosal masses that create small polypoid lesions; may ulcerate through epithelial or serosal surfaces
  2. Histologically: islands or uniform cells with scant, pink granular cytoplasm & a round stippled nucleus; positive immunohistochemical staining for endocrine granule markers (chromogranin A, synaptophysin)
50
Q

Clinical features of gastric neuroendocrine tumours (carcinoids)

A
  1. Carcinoid syndrome: due to release of vasoactive
    substances into systemic circulation; characterized by cutaneous flushing, sweating, bronchospasm, colicky abdominal pain, diarrhea, right-sided cardiac valvular fibrosis

(note: carcinoids confined to the GIT typically do not cause carcinoid syndrome as vasoactive substances produce undergo ‘first-pass’ effect in liver, hence carcinoid syndrome is strongly associated with metastatic disease)

  1. Prognostic factors: location (gastric carcinoids –
    good prognosis; midgut carcinoids – very aggressive)
51
Q

Gastric lymphoma

A

Derived from lymphocytes in gastric mucosa
1. Almost all gastric lymphomas are B-cell lymphomas of the extranodal mucosa-associated lymphoid tissue (MALT) type

  1. Gastric lymphomas constitute 5% of all gastric tumours & 20% of all extranodal lymphomas
52
Q

Etiologies & associations of gastric lymphoma

A
  1. Helicobacter pylori chronic gastritis

2. Trisomy 3 & t(11;18) translocation

53
Q

Morphology of gastric lymphoma

A
  1. [Grossly]
    - May grow as discrete nodules or infiltrate gastric wall diffusely
  2. [Histologically]
    - Dense lymphocytic infiltrate in lamina propria
    - Inset shows lymphoepithelial lesions (neoplastic lymphocytes surrounding & infiltrating gastric glands)
    - Reactive-appearing B-cell follicles may be present
54
Q

Gastrointestinal stromal tumours (GIST)

A

Derived from the interstitial cells of Cajal

- GIST can also be found elsewhere in the GIT

55
Q

Etiologies & associations of gastrointestinal stromal tumours (GIST)

A
  1. c-KIT (a receptor tyrosine kinase, receptor for stem cell factor) gain-of-function mutation (75-80%)
  2. PDGFRA (platelet-derived growth factor receptor alpha) gene mutation (8%)
  3. May rarely be part of a tumour syndrome: Carney’s triad (gastric GIST, paraganglioma, pulmonary chondroma), neurofibromatosis type I
56
Q

Morphology of gastrointestinal stromal tumours (GIST)

A
  1. Grossly: can grow up to 30cm in diameter, usually
    forms a solitary, fleshy, well-circumscribed mass
  2. Histologically: spindle cells &/or epithelioid cells
  3. Positive immunohistochemical staining for c-KIT
57
Q

Clinical features of gastrointestinal stromal tumours (GIST)

A

c-KIT positive tumours can be treated with imatinib

06. Gastrointestinal Pathology (5 decks)

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