Stomach / Abomasum Flashcards
Glandular Regions of Stomach
Cardia
Fundus/body
Pylorus
Cardia region
Region of stomach at cranial end
Secretes mucin
Surface foveolar cells
Fundus/body
Mid region of glandular stomach
Secretes pepsinogen, HCl and mucin
Parietal and chief cells
Pylorus
Caudal region of glandular stomach
Secretes mucin and gastric
G cells
Margo Plicata
Margin between glandular / non glandular epithelium in horse stomach
Common site of ulceration
Components of Mucosal barrier
Mucous “gel” secretions - lubricates and protects from self-digestion
Bicarbonate ions - buffers HCl
Replacement cells - cells cycle every 3-5 d
Blood flow - provides O2 and nutrients (energy) for cell growth
Prostaglandin
Regulates:
- bicarb / mucus secretions
- cell turnover
- micro vascular blood flow (also cell turnover)
Erosion
Superficial mucosal defect limited to mucosa/lamina propria
Ulcer
Deep mucosal defect that extends through the epithelium into the submucosa/wall
Bleeds more than erosions
Acute gastric ulcer
Red to brown mucosal depression
Active bleeding +/- fibrin layer
“Coffee ground” digested blood common
Chronic gastric ulcer
Raised tan “indurated” crater-like
(Tan base from re-epithelialization)
Possible active hemorrhage
Sequelae of gastric ulcers
Bleeding —> anemia —> internal exsanguination
Transmural perforation —> septic peritonitis
Healing/fibrous scar —> dysmotility/obstruction —> impaction
General cause of gastric ulcers
Increased parietal/chief cell secretion
Decreased mucosal barrier
Clinical signs of gastric ulcers
Anorexia
Dog/cat: vomiting, abdominal pain, anemia, melena
Cattle: decreased milk, palpable discomfort, melena
Horses: poor performance, bruxism (teeth grinding)
Swine: peracute death
Factors leading to gastric ulcer
Vascular compromise (drugs, stress, displacements)
Dietary disturbance
Trauma/toxins
Neoplasms
Infectious/inflammatory diseases
Pharmacologic cause of ulcers
NSAIDS (COX 1 and 2) inhibitors
Steroids
Pathogenesis of NSAID ulcers
Cox 1/2 enzyme inhibition —> decrease prostaglandin synthesis —> increase acid by parietal cells, decrease bicarbo/mucus, decrease mucosal circulation, decrease replacement cells
Pathogenesis of stress ulcers
Epi/norepinephrine release —> vasoconstriction / decrease gastric wall perfusion —> focal ischemia —> focal coagulation necrosis —> erosion —> ulcer
Pathogenesis of displacement / dilatation ulcers
Gastric dial action —> volvulus —> passive congestion —> ischemia —> infarct —> ulcer
Secondary complications of gastric dilation / displacement
Cardiovascular collapse (compression of vena cava)
Pulmonary atelectasis
Septic peritonitis (if perforating ulcer)
Examples of gastric displacements / dialations
LDA/RDA (bovine abomasal displacements)
Canine GDV syndrome (—> CV collapse)
Equine acute gastric dilation (—> rupture)
Dietary disturbances leading to gastric ulcers
Canine: dietary indiscretion
Bovine: transition from milk to fiber diet, post-parturient diet
Swine: small feed particle size
Ulcer by direct trauma
Exogenous: obstruction, foreign body, exogenous chemicals / caustic substances
Endogenous: bile reflux, uremic toxins, caustic digestive fluids
Endogenous gastric neoplasms
Canine: adenocarcinoma
Equine: squamous cell carcinoma
