Stomach and Duodenum

Gastric wall 7-10mm, duodenal wall <3mm when fully distended. Pseudotumour when inadequately distended, esp near GOJ. Folds thickened if >10mm in fundus or >5mm in antrum. Valvulae conniventes (circular/Kerckring folds) begin in D2, thickened if >2-3mm.

The stomach is lined by surface mucous cells (simple columnar epithelium). Gastric pits (foveolae) contain glands. Cardiac and pyloric glands contain almost entirely mucous secreting cells with the occasional enteroendocrine cell. Fundic/gastric glands (most of the stomach) contain the following cell types:

  • Mucous neck cell – Secrete mucous under vagal stimulation.
  • Parietal (onxynctic) cell – Secrete HCl (in response to gastrin) and intrinsic factor (binds to B12).
  • Chief cell – Secrete pepsinogen (converts to proteolytic pepsin after contact with acid) and a weak lipase.
  • Enteroendocrine cell – Secretes gastrin, glucagon, serotonin, substance P and VIP.

Narrowed stomach:

  • Neoplasm (linitis plastica) – Adenocarcinoma, lymphoma, metastases (breast carcinoma), KS (AIDS).
  • Inflammatory
    • H.pylori gastritis (usually antral)
    • Corrosives
    • Radiotherapy
    • AIDS (cryptosporidium, antrum and SB)
    • Eosinophilic gastroenteritis
    • Infection (rare, TB, syphilis)
    • Crohn (rare)
    • Sarcoid (usually asymptomatic)
  • Extrinsic compression – Pancreatitis, pancreastic carcinoma, omental caking.

Multiple filling defects:

  • Hyperplastic polyps
  • Adenomatous polyps (esp polyposis syndromes)
  • Metastases
  • Lymphoma
  • Varices

Upper GI haemorrhage is proximal to ligament of Treitz. Causes (in order) include duodenal ulcer, oesophageal varices, gastric ulcer, acute haemorrhagic gastritis, oesophagitis, Mallory-Weiss tear, neoplasm, vascular malformation, vascular enteric fistula.

Hiatal Hernia (HH)

GOJ >10mm above oesophageal hiatus which is widened >15mm. Sliding/axial HH (99%, GOJ and cardia) or paraoesophageal/rolling type (1%, fundus ± other parts). Rolling types have high risk of strangulation.

  • Type I (sliding HH) – Limited clinical significance in most (GOR more important).
  • Type II – Paraoesophageal with GOJ in normal position under diaphragm.
  • Type III (mixed/compound) – Paraoesophageal with GOJ in chest.
  • Type IV – Intrathoracic stomach, at risk of volvulus, obstruction, ischaemia.

Cameron ulcers and erosions within herniated stomach in 5%. Riding ulcers at hiatal orifice.

DDx phrenic ampulla/vestibule (high presure zone at lower oesophageal sphincter, between A and B rings).

Gastric volvulus – 2 air-fluid levels within the stomach. Organoaxial rotated around the longitudinal plane (between GOJ and pylorus); mesenteroaxial around the transverse plane of stomach. OEJ may be abnormally positioned.

Gastritis

Normal gastric lumen has pH close to 1. Mucin secreted by surface foveolar cells which is mixed with secreted bicarbonate (protecting epithelium from acid). Rich blood supply helps wash away acid that has back-diffused into lamina propria. Entire gastric mucosal surface is replaced every 2-6 days. Acute or chronic gastritis from disruption to one of these protective mechanisms. Signs include:

  • Wall thickening – Nonspecific.
  • Thickened folds – Oedema, inflammatory infiltrate. Nodular in duodenum (enlarged Brunner glands).
  • Erosions – Superficial mucosal ulcerations with loss of the superficial epithelium that don’t penetrate muscularis mucosae, heal without scarring. Associated with neutrophil infiltration. Acute erosive haemorrhagic gastritis – concurrent erosion and haemorrhage.
    • Incomplete erosions – Linear streaks and dots of barium.
    • Aphthous ulcers – Complete erosions. Tiny central flecks of Ba surounded by halo of oedema (cf no halo with Ba precipitates).
  • Deformity of duodenal bulb.

Acute gastritis causes haemorrhage, erosions, ulcers. Causes include:

  • Drugs – NSAIDs, alcohol, cocaine.
  • Bile reflux
  • Infection – Bacteria (including H.pylori in antrum which is usually asymptomatic), viruses (CMV esp immunocompromise), fungi.
    • Phlegmonous gastritis – Acute bacterial infection (esp streptococci). Cx of septicaemia, gastric surgery or ulcers. Multiple abscess in wall with marked thickening, swollen rugae. Barium may penetrate abscess crypts. Peritonitis in 70%. Healing -> severely contracted stomach.
    • Emphysematous gastritis – Gas forming organisms including E.coli, Clostridium perfringens. Most from caustic ingestion, surgery, trauma or ischaemia. Multiple intramural gas bubbles.
  • Ischaemia
  • Severe physiologic stress – Shock
  • Radiation
  • Eosinophilic – Including food and drug allergies.
  • Trauma

Chronic gastritis causes:

  • Helicobacter pylori chronic gastritis (most common) – Associated with chronic gastritis, duodenitis, ulcers (80% of gastric, 95% of duodenal), adenocarcinoma (in 50%) or MALT lyphoma. G-neg spiral/curved bacillus, variable colonisiation between 10-80% worldwide. Infects only gastric-like epithelium, concentrated in the superficial mucous, usually antrum, increasd risk with age, low SES, developing countries. Starts in antrum (acute gastritis) before extending elsewhere. Uses urease to break urea into ammonia and bicarbonate to make local environment more alkaline. Increased acid production, with disruption of normal protective mechanisms. Normal or reduced gastrin (hypogastrinemia). Intra-epithelial neutrophils and subepithelial plasma cells. Most have chronic superficial antral gastritis, usually asymptomatic. <5mm fold thickening, nodular folds, erosions, antral narrowing, inflammatory polyps, enlarged areae gastricae. May progress to pan-gastritis associated with multifocal mucosal atrophy, reduced acid secretion, metaplasia and increased risk of adenocarcinoma. May induce MALT, with potential to transform into lymphoma.
  • Atrophic gastritis – Most common chronic gastritis in patients without H.pylori infection. Autoimmune gastrits is most common cause, destroying body/fundal mucosa (spares antrum). Hypergastrinemia. Antibodies to parietal cells and intrinsic factor with destruction -> reduced acid (achlorrhydia) and IF production, B12 deficiency with atrophic glossitis (beefy red tongue), pernicious anaemia (macrocystic), irreversible neuropathic changes. Reduced/absent folds in fundus and body (‘bald fundus’), narrowed tube-shaped stomach (fundus <80mm), small 1-2mm or absent areae gastricae. Islands of residual oxynitic (acid-produing) mucosa may cause appearance of multiple small polyps/nodules. Small surface elevations in areas of intestinal metaplasia (goblet cells). Endocrine cell hyperplasia parallels mucosal atrophy (in response to reduced acid production), may form multiple small low-grade neuroendocrine/carcinoid tumours.
  • Chronic reactive/erosive gastropathy – From alcohol, aspirin, NSAIDS, steroids, chemical injury, bile reflux. Foveolar hyperplasia, glandular regeneration, mucosal oedema. Erosions and aphthous ulcers, thickened nodular folds in antrum, limited antral distensibility, wall stiffness with limited peristalsis.
  • Eosinophilic gastroenteritis – Diffuse eosinophilic infiltration in wall of stomach and SB, involving any or all layers. Associated with peripheral eosinophilia in 60%, allergic reactions (cow’s milk, soy protein, drugs), collagen vascular disaease (scleroderma, polymyositis), parasitic infections, H.pylori. Markedly thickened and nodular walls (esp antrum, pylorus). Chronic -> narrowed antrum with nodular ‘cobblestone’ pattern.
  • Lymphocytic/varioliform gastritis – F>M, idiopathic but 40% associated with celiac disease. Thickened folds covered by small nodules and central aphthous ulceration. Most affect entire stomach.
  • Granulomatous gastritis – Aggregates of epithelioid histiocytes (tissue macrophages). In Crohn disease, sarcoidosis, mycobacteria, fungi, CMV, H.pylori. Narrowing and rigidity of the antrum from transmural granulomatous inflammation.
    • Crohn gastritis/duodenitis – Gastric antrum ± D1/2. Apthous ulcers -> antral narrowing/strictures, wall thickening, fistulas.
  • Ischaemic gastritis – Atherosclerosis of caeliac and SMA.
  • Radiation gastritis

Hypertrophic gastropathies – Giant cerebriform enlargement of rugal folds from epithelial hyperplasia without significant inflammation. Associated with excessive growth factor. DDx lymphoma.

  • Menetrier disease (giant hypertrophic gastritis) – Rare, hyperplasia of foveloar epithelium with excessive mucous production, hypoproteinaemia (protein-losing enteropathy), hypochlorhydria (low acid production). Markedley enlarged >5mm, nodular and tortuous but pliable folds in fundus and body (esp greater curvature, sparing antrum), hypersecretion (diluted barium and impaired mucosal coating). Smooth serosal surface and normal gastric wall thickness between folds.
  • Zollinger-Ellison syndrome – Gastrin-secreting islet cell tumour (gastrinoma) in pancreas (75%), duodenum (15%) or extraintestinal sites (10%, liver, LN, ovary). 75% sporadic, 25% associated with MEN-1. 60% malignant, but slow-growing. Gastrin causes 5x increase in parietal cells, also hyperplasia of mucous neck cells, mucin hyperproduction and proliferation of endocrine cells (rarely carcinoid tumours). Hyperacidity with multiple peptic ulcers in duodenum, stomach, jejunum. Hypersecretion diluting barium and imparing mucosal coating. Thickened oedematous folds in stomach, duodenum and proximal jejunum.

Complications include:

  • Peptic ulcer disease
  • Mucosal atrophy – Loss of parietal cell mass. May lead to intestinal metaplasia with goblet cells; strong association with gastric adenocarcinoma, esp autoimmune gastritis.
  • Dysplasia – Inflammation-related free radical damage.
  • Gastritis cystica – Exuberunt reactive epithelial proliferation with entrapment of epithelial-lined cysts within the submucosa or deeper layers.

Ulcers

Full-thickness mucosal defect, extending past lamina propria into submucosa, muscularis propria. 95% of gastric/peptic ulcers are benign, but all should be examined endoscopically or followed-up to check healing. Barium-filled crater on dependent wall; ring shadow (Ba coating on edge of crater) on nondependent wall, double ring shadow if base is broader than neck; crescenteric or semilunar line when on tangent oblique.

Acute/aphthous gastric ulcers – Common, from NAIDS (cyclooxygenase inhibition preventing prostaglandin synthesis and hence reduced bicarbonate, increased acid, reduced mucin, reduced perfusion), severe physiologic stress (stress ulcers from shock, sepsis, severe trauma), Crohn’s. Rounded small <10mm with central cavity filling with contrast, base stained brown/black by acid digestion of extravasated blood, margins not indurated. Anywhere in stomach (cf peptic ulcers), most often multiple. Sharply marginated. No scarring or thickened vessels (cf peptic ulcers). Normal rugal folds. Heal after days-weeks.

Peptic ulcer disease (PUD) – Imbalance of mucosal defenses and damaging forces (sames causes as gastritis). 65% from H.pylori-induced hyperchlorhydic chronic gastritis, 30% NSAIDS, others include chronic gastritis, hyperparathyroidism, radiotherapy, Zollinger-Ellison syndrome, viruses. Duodenal ulcers (4x more common than stomach) – 95% associated with H.pylori, 95% in duodenal bulb, most anterior wall; postbublar more commonly associated with serious haemorrhage. Duodenal ulcers associated with increased acid production, gastric with normal/decreased acid, but HCl must be present for ulceration to occur. May occur in oesophagus with GORD. Round, oval or linear. Solitary in >80%. Most <10mm, giant ulcers are >20mm resembling diverticula or deformed bulb. Mucosa intact to very edge of ulcer crater, margins level with rest of mucosa. Tend to have smooth ulcer mound with tapered edges, sharptly punched-out, oedematous collar with overhanging edge, projects beyond expected lumen, smooth radiating folds extend into crater, depth > width, sharp contours, Hampton line (thin sharp lucent line traversing orifice due to overhaning mucosa), incisura sign (infolding of gastric wall ‘pointing’ towards ulcer). Ulcer craters have no mucosal lining, no mucosal relief pattern, no peristalsis. Cx bleeding (melena, haematemesis, haematochezia), obstruction, perforation (free into peritoneum or adjacent organ). Notoriosly chronic, recurrent. Malignant transformation is very rare.

Malignant ulcers from adenocarcinoma, lymphoma, GIST. Irregular, located within lumen, eccentric within tumour mound, width > depth, nodular/rolled/irregular/shouldered edges, Carmen meniscus sign (large flat-based ulcer with heaped up edges folding inwards, trapping lens-shaped barium convex to lumen).

Neoplasm

Polyps, nodules or massses project above the level of surrounding mucosa. 90% of tumours in duodenal bulb are benign, 50% in 2nd/3rd parts, most are malignant in 4th part.

DDx

  • Ectopic pancreas – Common, intramural usually antrum or proximal D2. Heterotopic pancreatic tissue up to 50mm covered by gastric mucosa. Most nipple or cone shaped with small central orifice/dimple.
  • Bezoar/foreign body – Acumulated ingested material composted of hair (trichobezoar), fruit/vegetable products (phytobezoar) or milk-fed infants (lactobezoar).
  • Extrinsic impression – Pancreatic, splenic, hepatic, GB, adrenals, kidneys, colon, retroperitoneal masses.
  • Varices – Smooth, lobulated esp fundus, usually associated with oesophageal varices (may be isolated with splenic vein occlusion).
  • Flexural pseudotumours (duodenum) – Redundant mucosa causing filling defect with central barium collection, rounded swirled mucosal folds on inner aspect of flexures.
  • Lymphoid hyperplasia – Small 1-3mm polypoid nodules throughout the bowel. Usually benign. Associated with immunodeficiency in adults.
  • Brunner gland hyperplasia – Brunner glands are in submucosa in the duodenum above Sphincter of Oddi, producing mucous rich bicarbonate/alkaline which neutralises stomach acid, produces alkaline environment to activate intestinal enzymes, and lubricates intestinal wall. Hyperplasia causes multiple nodular filling defects, associated with hyperacidity. Brunner gland adenoma causes a solitary filling defect.

Polyps

Gastric much more common than duodenal. On dependent surface appear as filling defect in barium pool, on non-dependent surfaces are covered with thin coat of barium etched in white. Bowler hat sign from acute angle of attachment to mucosa. Mexican hat sign – two concentric rings when seen end-on. Commonly multiple.

  • Hyperplastic/inflammatory polyps (75%) – Most <15mm, hyperplastic reaction to mucosal injury esp chronic gastritis. Anywhere in stomach. Benign. Most common 50-60yo. May regress after eradication of H.pylori. Those >15mm should be excised due to high risk of dysplasia.
  • Fundic gland polyps – Sporadic or associated with FAP. Glandular hyperplasia from increased gastrin secretion in PPI treatment. F:M 5:1, average 50yo. Most in body and fundus, well-circumscribed, smooth surface. Single or multiple. Composed of cystically dilated irregular glands. Absent/minimal inflammation.
  • Adenomatous polyp (10%, gastric adenoma) – True neoplasms with epithelial dysplasia and malignant potential increasing with size. Gastric or duodenal, pedunculated or sessile. Most solitary in antrum, >20mm. May be multiple in polyposis syndromes. Most occur in a background of chronic gastritis with atrophy and intestinal metaplasia. Any polyp >10mm, lobulated or pedunculated should be biopsied. Lesions >20mm have high risk of adenocarcinoma.
    • Villous adenomas – Multiple frondlike projections (cauliflower or soap-bubble appearances with barium trapped in clefts), 30-90mm, mobile and deform with compression. High malignant potential increasing with size.
  • Hamartomatous polyps – In peutz-Jegher syndrome. Benign.

Gastric Carcinoma

95% adenocarcinomas, remainder are diffuse anaplastic (signet-ring), SCC or rare cell types. Increased risk with smoking, pernicious anaemia, atrophic gastritis with intestinal metaplasia, gastrojejunostomy, H.pylori, certain areas (Japan, Finland, Chile, Iceland), 50-70yo, lower SES, partial gastrectomy. Poor prognosis 10-20% 5yr. Risk of overall gastric cancer has reduced markedly over time (less ingested carcinogens), but increasing risk of tumours at cardia (Barrett oesophagitis). This reduction has occured in intestinal morphology tumours, which now ~ diffuse infiltrative tumorus in incidence. Most near cardia, antrum or lesser curvature. Focal or diffuse (linitus plastica) wall thickening >10mm, mass ± ulceration, invasion of perigastric fat with stranding or ill-defined. Mucinous adenocarcinomas may have stippled calcification. Direct spread to peritoneum (seeding causing carcinomatosis or Krukenberg ovarian tumours). LN include perigastric along lesser curvature, coeliac axis, hepatoduodenal, retropancreatic, mesenteric, paraaortic, Virchow’s node (supraclavicular sentinal node), Sister Mary Joseph nodules (periumbilical subcutaneous nodules). Metastases to liver, adrenals, ovaries; rarely bone and lung.

Growth patterns include:

  • Intestinal morphology (type 1) – Tend to form bulky tumours with glandular structures, more commonly distal. Usually develop from precursor lesions, predominate in high-risk areas, higher risk with atrophic gastritis. M:F 2:1.
    • Polypoid mass (33%) – Most broad-based or papillary. Polyps >10mm.
    • Ulcerative mass (33%) – Malignant ulcers are shallow, irregular ulcers with nodular adjacent mucosa.
  • Diffuse infiltrative (type 2) – Signet-ring tumours (large mucin vaculoues pushing nucleus to periphery), often evoke desmoplastic reaction, stiffening the gastric wall. Poorly cohesive cells which infiltrate. Involves any part of the stomach, esp the cardia. Uniform incidence across countries, no precursor lesions, M:F.
    • Scirrhous (15%) – Diffuse infiltration of wall by poorly/un-differentiated cells, thickened and rigid (stomach doesn’t move, failure to distend), ‘linitis plastica’ or ‘leather water-bottle stomach’.
    • Superficial spreading – Through mucosa and submucosa causing plaque-like or bizarre nodular fold thickening, superficial ulceration, minimal mass effect.

Duodenal Adenocarcinoma

Rare. Patterns include polypoid mass, ulcerative mass, annular constricting lesion with shouldering. LN in 2/3 at presentation.

Lymphoma

50% of primary GI lymphoma. 80% are extra-nodal marginal zone B-cell NHL (MALTomas). GIT most frequent site for EBV induced B-cell lymphomas due to oral immunosupressants, HIV. Increased risk with H.pylori. Tends to be multiple. Remains confined to bowel wall for longer than carcinoma, hence better prognosis. Growth patterns include polypoid mass, ulcerative mass, multiple submucosal nodules (larger than lymphoid hyperplasia, may ulcerate causing ‘bull’s-eye’ appearance) or diffuse infiltration. Marked wall thickening 40-50mm, circumferential without luminal narrowing (rarely linitus plastica with stiff narrowing), homogeneous, extensive adenopathy (esp below renal hila), transpyloric spread to duodenum. Doesn’t tend to invade perigastric fat (cf carcinoma).

Gastrointestinal Stromal Tumour (GIST)

Most common mesenchymal GI tumour, 60-70% from stomach. M slightly > F, peak 60yo (<10% <40yo). Defined by presence of c-Kit (CD117) cell surface marker mutation. Spindle cell or epithelioid cell types. Whorled texture, fleshy pale tumour. In duodenum most common in 2nd/3rd parts. 10-30% are malignant, more common distally. Tends to have long period of silent growth to large size, mostly exophytic extraluminal, occasionally mixed intra/extra-luminal, rarely completely intraluminal. Usually unable to definitively identify connection with stomach. Submucosal nodules/masses, may have overlying ulceration (bull’s-eye appearance, may cause bleeding), common necrosis. Uncommonly dystrophic calcification, cystic change. Metastases -> multiple serosal peritoneal nodules or liver nodules; spread outside abdomen is uncommon. Doesn’t tend to spread to lymph nodes. Differentiation between benign/malignant is difficult to distinguish histologically and is based on size (40-50mm cf >100mm), gross appearance (homogeneous vs heterogeneous with necrosis/haemorrhage/liquefaction and irregular enhancement), and behaviour.

Gastric Carcinoid Tumours

<10% of all GI carcinoids. May be assocociated with endocrine cell hyperplasia, chronic atrophic gastritis, Zollinger-Ellison syndrome. Well-differentiated neuroendocrine carcinoma. Intramural or submucosal masses creating small polypoid lesions. Overyling mucosa may be ulcerated. May have deep involvement into mesentery. Tends to be yellow/tan, firm from intese desmoplastic reaction. Foregut carcinoid tumours (oesophagus, stomach, duodenum proximal to ligament of Treitz) rarey metastasize cf midgut tumours.

Lipomas

Submucosal, benign, well-defined, occasionally ulcerates.

Leiomyoma and Leiomyosarcoma

Many are now classified as GISTSs. True leiomyomas/leiomyosarcomas/leiomyoblastomas are very rare in the stomach.

Metastases

Focal/diffuse wall thickening >10mm, submucosal nodules or masses ± ulceration. Commonly from melanoma, breast (linitus plastica), lung, other GI tumours.

Kaposi Sarcoma

Associated with AIDS. Variable appearances including polypoid mass, thickened folds, multiple submucosal masses, linitus plastica.

Miscellaneous

Congenital

Intraluminal duodenal diverticula from thin incomplete congenital diaphragm, stretched by contents forming ‘windsock’ configuration.

Annular pancreas – Increased risk with Down syndrome. 50% don’t present until adulthood with N&V, pain, occasionally jaundice. Eccentric/concentric narrowing of D2. Associated with postbulbar peptic ulcers.

Gastric Mucosal Prolapse

(Heterotopic gastric mucosa). Prolapse of gastric mucosa through pylorus during peristalsis. Lobulated filling defect at base of duodenal bulb, changes with peristalsis. Common at endoscopy, less common radiographically.

Intramural Haematoma

In duodenum esp D3 from trauma, anticoagulation, bleeding diatheses. Regular thickened folds (‘stack of coins’), partial/complete duodenal obstruction.

Diverticula

Duodenal diverticula in 5%, usually incidental. May be multiple, most commonly inner D2. Mucosal folds enter neck of diverticulum and change appearance with peristalsis (cf ulcers). Rare Cx include perforation, haemorrhage, obstruction of ampulla of Vater.

Gastric Surgery

Reflux and HH surgery:

  • Fundoplication – Gastric fundus wrapped around lower oespophagus, reinforcing the gastro-oesophageal sphincter.

Bariatric surgery:

  • Intra gastric balloon.
  • Laparosocpic gastric band (lap band) – Silicone band around upper stomach, may be adjustable with port.
  • Sleeve gastrectomy – Most of stomach along greater curvature removed leaving a thin tube.
  • Stomach stapling – Hole made in stomach with a verticle staple line to fundus and band to lesser curve, creating a small proximal pouch.
  • Roux-en-Y gastric bypass – Small proximal gastric pouch connected to alimentary/Roux limb (jejunum) end-end (gastrojejunostomy). The larger excluded portion of stomach connects normally to the duodenum (biliary intestinal limb) which is connected to the Roux limb distally either end-end or side-side (jejuno-jejunostomy).