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Patho - GIT > Stomach > Flashcards

Stomach Flashcards

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1
Q

Conditions of the stomach

A
  1. Congenital
    - Diaphragmatic hernia - herniation of abdo viscera into thoracic cavity
    - Congenital pyloric stenosis - persistent projectile vomiting
  2. Acquired
    - Gastropathy & acute gastritis
    - Chronic gastritis
    - Peptic Ulcer Disease
    - Neoplasms
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2
Q

Gastropathy vs acute gastritis

A
  • Gastritis is a mucosal inflammatory process
  • Neutrophils present: Acute Gastritis
  • Neutrophils absent: Gastropathy
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3
Q

Causes of acute gastritis (5)

A
  1. Reactive (chemical)
    - alcohol, bile, corrosives, NSAIDs, corticosteroids, cigarette smoking
  2. Chemotherapy/radiation-induced
  3. Vascular - portal HTN
  4. Stress-induced mucosal injury (local ischemia)
    - shock, sepsis, severe trauma, post-MI (stress ulcers)
    - severe burns (Curling ulcers)
    - intracranial disease (Cushing ulcers)
  5. Uremia
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4
Q

Pathogenesis of acute gastritis (5)

A
  1. Increased acid secretion with back diffusion
  2. Decreased bicarb buffer production
  3. Reduced blood flow (decreased gastric perfusion & decreased prod of cytoprotective prostaglandins)
  4. Disruption of adherent mucus layer
  5. Direct damage to epithelium
    - direct acting luminal agents - alcohol, bile salts
    - chemo - reduces epithelial regeneration
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5
Q

Effects & complications of acute gastritis (4)

A
  1. Asymptomatic, epigatric pain, indigestion, n/v
  2. Bleeding - hematemesis, melena)
  3. Erosions - loss of superficial epithelium
  4. Ulcers
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6
Q

Features of chronic gastritis

A
  • chronic inflammation leading to mucosal atrophy & intestinal metaplasia
  • most commonly H. pylori-associated chronic gastritis
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7
Q

Pathology associated with H. pylori (4)

A
  1. Chronic gastritis
  2. Peptic ulcer
  3. Gastric carcinoma
  4. Gastric lymphoma
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8
Q

Histology of chronic gastritis (4)

A
  1. Active inflammation - neutrophils, lymphocytes, plasma cells, lymphoid aggregates
  2. Regenerative changes - mitoses in epithelium, loss of mucus vacuoles
  3. Intestinal metaplasia, goblet cells
  4. Atrophy - loss in glandular structures & specialised cells
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9
Q

Effects & complications of chronic gastritis

A
  • mostly asymptomatic
    1. Peptic ulcer disease
    2. Chronic atrophic gastritis
    3. Malignancies - carcinoma, lymphoma
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10
Q

Features of autoimmune gastritis (<10%)

A
  • due to autoantibodies produced against gastric parietal cells & intrinsic factor (detected in serum & gastric secretions)
  • associated with other autoimmune disorders - Hashimoto, DM, Graves
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11
Q

Effects & complications of autoimmune gastritis (5)

A
  1. Defective gastric acid secretion - hypo/achlorhydria
  2. Endocrine cell hyperplasia - hypergastrinemia
  3. Disabled ileal vit B12 absorption - megaloblastic (pernicious) anemia
  4. Chief cell destruction - reduced serum pepsinogen conc
  5. Increased risk of adenocarcinomas, carcinoid tumour
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12
Q

Other uncommon forms of gastritis

A
  1. Eosinophilic gastritis
    - due to allergies, parasitic infections, immune disorders
  2. Lymphocytic gastritis
    - assoc w women, celiac disease
  3. Granulomatous gastritis
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13
Q

Definition of peptic ulcer disease

A
  • chronic mucosal ulceration affecting duodenum, stomach

- penetrates muscularis mucosae & beyond

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14
Q

Sites of peptic ulcers

A
  • duodenum, 1st part (75%)
  • stomach, lesser curve, antrum 20%
  • lower esophagus in GERD, stomal ulcer, Merkel diverticulum, distal duodenum/jejunum
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15
Q

Risk factors for peptic ulcers

A
  1. H. pylori infection
  2. Drugs - illicit eg cocaine, NSAIDs
  3. Smoking, alcohol
  4. Physiological stress - increases acid secretion
  5. Endocrine hyperplasia - stim parietal cell growth
  6. Zollinger-Ellison syndrome
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16
Q

Pathogenesis of peptic ulcer disease

A

Imbalance between mucosal defences & damaging forces

  1. ureases generate free ammonia from endogenous urea - increases gastric pH
  2. proteases break down glycoprotein in gastric mucus
  3. phospholipase damage epithelial cells, release bioactive leukotrienes, damaged mucosa allows leakage of nutrients in
  4. neutrophils affected by H. pylori release myeloperoxidase
  5. H. pylori damages epithelial/endothelial cells, bacterial platelet activating factor promotes thrombotic occlusion of mucosal capillaries
  6. other antigens recruit inflam cells to the mucosa
  7. chronically inflamed mucosa is more susceptible to acid injury
17
Q

Features of gastric ulcers

A
  • gastric body/fundus
  • impaired mucosal defence - motility defects, mucosal ischemia, mucosal inflammation
  • mucosal atrophy
18
Q

Features of duodenal ulcers

A
  • most common
  • excessive acid-pepsin secretion that overwhelms impaired mucosal defences
  • epigastric pain relieved by food
  • increased gastric acid secretion, decreased duodenal bicarbonate secretion
19
Q

Morphology of peptic ulcer

A

G:

  • round to oval, sharply demarcated, punched out defect
  • mucosal margin may overhang base slightly, variable depth, smooth & clean base
  • scarring & puckering of wall - stellate appearance

M:

  • surface zone of fibrinopurulent exudate
  • acidophilic layer of necrotic tissue
  • zone of granulation tissue
  • zone of dense scar tissue
  • interruption of muscularis propria & mucosae
20
Q

Effects & complications of peptic ulcer (5)

A
  1. Epigastric burning pain, relived by food (DU), alkali (antacids), worse when hungry & at night
  2. Bleeding (15-20%) - mild & chronic - iron def anemia, severe & acute - hematemesis
  3. Perforation (5%) - with consequent acute peritonitis
  4. Obstruction (2%) - due to edema, scarring & strictures
  5. Gastric adenocarcinoma
21
Q

Neoplasms & precancerous lesions of the stomach

A
  1. Polyps
  2. Adenocarcinoma
  3. Neuroendocrine cell tumours - carcinoid tumours
  4. Gastrointestinal stromal tumours (GIST)
  5. Gastric lymphomas
22
Q

Polyps of the stomach

A
  1. Hyperplastic polyps
    - benign, common, reaction to chronic inflammation, precedes chronic gastritis
    - surface erosions may cause bleeding
  2. Fundic gland polyps
    - causes: sporadic or familial
    - associated w reduced acidity or hypergastrinemia leading to oxyntic glandular hyperplasia
23
Q

Definition of gastric adenocarcinoma

A

malignant neoplasm showing GI epithlial glandular differentiation

24
Q

Risk factors of gastric adenocarcinoma (5)

A
  1. General
    - age >55, M, Japan, Korea, E Europe, Latin America
  2. Body - obesity
  3. Lifestyle
    - smoking, diet (preserved food), working in coal, metal, rubber industries
  4. Genetics eg Lynch syndrome, HNPCC
  5. Others - H. pylori infection
25
Q

Types of gastric adenocarcinoma

A

G: patterns of growth

  1. Exophytic
  2. Flat/depressed
  3. Excavated

M:

  1. Intestinal type - papillary, tubular, mucinous
  2. Diffuse type - signet ring cell, undifferentiated
26
Q

Clinical features of gastric adenocarcinoma

A
  • often asymptomatic, non specific symptoms, late detection, poor prognosis
  • early gastric cancer - invasive, invades no deeper than submucosa
  • prognosis depends on depth of invasion, extent of nodal & distant mets
  • treatment - surgical resection +/- adjuvant chemo & radiation
27
Q

Growth & spread of gastric adenocarcinoma

A
  • pylorus & antrum > cardia, lesser curvature > greater curvature, distal > proximal
  • invades esophagus, duodenum, omentum, colon, pancreas, spleen
  • death due to widespread seeding of peritoneum & liver/lung mets
  • also mets to adrenals, peritoneum, ovary spleen, supraclavicular nodes (Virchow’s node, Trousseau’s sign)
  • extensively infiltrated gastric wall - rigid, thickened - linitis plastica
28
Q

Gastric neuroendocrine tumours (Carcinoids)

A
  • derived from enterochromaffin-like cells (ECL) in gastric mucosa
  • assoc w chronic atrophic gastritis, MEN type I, Zollinger-Ellison syndrome
  • results in a hypergastrinemic state - ECL cell hyperplasia - presumed precursor lesion
29
Q

Gastrointestinal stromal tumours (GIST)

A
  • can occur as polypoidal intramural tumour masses
  • ulcerate overlying GI mucosa
  • most frequent sarcoma of GIT

Patho - GIT (5 decks)

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