 The gastric mucosa contains three different

types of glands that are named based on their

localization
 Cardiac glands are located in the gastric
cardia
 Fundic glands (also called oxyntic glands) in
the fundus and corpus
 Pyloric glands in the pyloric portion of the
stomach
 Cardiac glands consist mainly of mucus
secreting cells
 Presence of mucous neck cells, chief cells,
and parietal cells
Chief cells
 Located at the base of the fundic gland
 Secrete different isoforms of pepsinogen, a
precursor of the proteolytic enzyme pepsin.
 Located in the upper third of the fundic gland
 Secrete hydrochloric acid, R-protein, and in
dogs, a glycoprotein called intrinsic factor
 Scattered between the chief cells and parietal
cells
 Produce gastric lipase
 Contain mainly mucus-secreting cells and
gastrin-producing endocrine cells (G cells)
 Gastrin stimulates gastric acid secretion and
has an important trophic influence on the
gastric mucosa
 Secretion of bicarbonate and mucus by the
epithelial cell
 The apical surface of the epithelial cells
contains a high proportion of hydrophobic
phospholipids that repel gastric acid
 Epithelial cells contain a high concentration
of intracellular bicarbonate
 Gastric mucosa has the ability to self-repair
 Damaged mucosal cells secrete mucus that
forms a protective layer over the gastric
mucosa
 Enhanced expression of epidermal growth
factor (EGF), transforming growth factor-
alpha (TGFalpha),trefoil peptides (TFPs), and
nitric oxide (NO)
 Prostaglandin E2 and prostacyclin
 Maintain the integrity of the gastric mucosal
barrier
 Stimulate mucus and bicarbonate secretion
 Increase gastric mucosal blood flow
 Regeneration of epithelial cells
 The gastric (lesser curvature) and
gastroepiploic (greater curvature) arteries
supply the stomach and are derived from the
celiac artery
Contamination of abdominal cavity
 Placement of stay sutures
 Use of laparotomy sponges
 Postprocedural intraperitoneal irrigation
 Correction of fluid deficits and electrolyte
abnormalities prior to surgery
 Premedication with systemic gastric acid
blocking drugs – to reduce regurgitation and
post operative vomiting
 Atropine, acepromazine and xylazine – lower
esophageal sphincter tone
Predisposing to
 Esophageal reflux
 Silent regurgitation during surgery
 Esophagitis and aspiration pneumonia
 Gastric dilatation with volvulus
 Gastric ulcer
 Gastric foreign body
 Gastric neoplasia
 Pyloric stenosis
 Enlargement of the stomach associated with
rotation on its mesenteric axis
 Rapid accumulation of gas within the
stomach
 Rotation of the stomach
 Failure of eructation and pyloric emptying
 Increased gastric pressure
 Shock
Intrinsic physical factors
 Body size
 Age
 Body weight
 Breed
 Thoracic depth to width ratio
 Abnormal conformation
 Akitas
 Bloodhounds
 Collies
 Great Danes
 lrish Setters
 Irish Wolfhounds
 Newfoundlands
 Rottweilers
 Saint Bernards
 Standard Poodles and Weimaraners
Environmental risk factors
 Diet – Feed type and pattern
 Stress
 Anesthesia
 Conditions promoting aerophagia
 Post meal excercise
Anatomical risk factors
 Gastric ligament laxity
 Gastric volume and position
 Gastrin hormone
Pathological factors
 Gastric rhythm, motility and emptying
disorders
Other risk factors
 Familial predisposition
 After splenectomy
 Dogs with early history of GDV
 Stomach rotates in a clockwise direction
 Rotation may be 90 to 360 degrees but
usually is 220 to 270 degrees
 Duodenum and pylorus move ventrally and to
the left of the midline and become displaced
between the esophagus and stomach
 Spleen usually is displaced to the right ventral
side of the abdomen
 Distended, painful and tympanic abdomen
 Animal appears anxious, looking or biting at
the abdomen
 Unproductive retching
 Recumbency and rapid breathing
 Hypersalivation
 Varying signs of shock
 Compensatory – tachycardia, tachypnea,
slow CRT, pale mm
 Decompensatory – Bradycardia, Absent
pulse, Hypotension, No CRT, cold extremities
 History
 Clinical signs
 Physical examination findings
 ECG – Ventricular premature contractions
 Marked hemoconcentration
 Hypokalemia
 Azotemia
 Increased ALT levels
 Increased BUN and Creatinine
 Thrombocytopaenia
 Increased lactate
 Affected animals should be decompressed
before radiographs are taken
 Right lateral and dorsoventral radiographic
views are preferred
 The 'Popeye's arm' sign/ Double bubb le
appearance
 To stabilize cardiovascular, respiratory and
renal systems
 Oxygen therapy
 Fluid therapy
 Dopamine/ Dobutamine @ 2.5 μg/kg/min as
CRI to improve splanchanic blood flow
 Broad spectrum antibiotics
 Antiarrhythmic drugs
 Gastric decompression should be performed
while shock therapy is initiated
 Improves CVS and Resp. function
Performed by
 Orogastric intubation
 Percutaneous gastrocentesis
 Temporary gastrotomy
 The tube selected should be measured from
the external nares to the caudal edge of the
last rib
 To inspect the stomach and spleen so as to
identify and remove damaged or necrotic
tissues
 To decompress the stomach and correct any
malpositioning
 To adhere the stomach to the body wall to
prevent subsequent malpositioning
 Exploration and rotational correction
 Gastropexy
 Gastric invagination
 Gastric resection
 Emergency temporary gastrotomy
 Exploration and rotational correction
 Gastropexy
 Gastric invagination
 Gastric resection
 Standing on the patients’ right side, first
reach your right hand across the abdomen
and place it between the left body wall and
dilated stomach
 Slide your right hand along the sublumbar
body wall and grasp the deep (dorsal) aspect
of the stomach
 Next, place the open palm of your left hand
on the exposed surface of the right side of the
dilated stomach
 Using both hands simultaneously, pull the
deep part of the stomach with your right
hand to begin derotation whilst you push the
right surface of the stomach down toward the
patients sublumbar body wall with your left
hand
 Systematic evaluation of the abdomen
should be performed
 Haemoperitoneum
 Active sites of hemorrhage
 Careful inspection of stomach, spleen and
other abdominal organs
 Splenectomy in case of splenic torsion
 Visual evaluation of gastric wall colour
 Digital palpation of splenic and gastric vessels
for arterial pulsation
 Digital evaluation of gastric wall thickness
 Presence or absence of arterial bleeding from
the cut gastric wall
 Mucosal colour should not be used as an
indication for resection
 Invagination of necrotic areas should be
avoided
 Inflammation
 Ongoing release of inflammatory mediators
 Gastric ulceration
 Bleeding
 Sepsis
 To form permanent adhesion between pyloric
antrum and right lateral body wall
 Should not interfere with normal stomach
position and function
 Should not serve as a structure around
which organs may be trapped
 Belt-loop gastropexy
 Incisional gastropexy
 Circumcostal gastropexy
 Incorportaing gastropexy
 Difficult to perform
 Rib fracture
 Pneumothorax
 Not recommended for routine use as it will be
problem for subsequent procedures
 Fluid therapy
 Antibiotics
 Analgesics
 Gastric motility
 Gastric protectants
 Antiarrhythmic drugs
 More frequent feedings to decrease the
volume of stomach
 Vigorous activity after meals should be
avoided
 Taking excess water after meals
 An area of damaged gastric mucosa to the
level of lamina muscularis mucosae or deeper
 More superficial damage is called erosion
 Aggressive forces are more potent than the
protective forces
 Excess of acid and pepsin

 Breakdown of protective forces

 Increased gastrin – Renal failure and
gastrinomas
 Increased histamine – Mast cell tumors
 Alteration of mucosal blood flow – NSAID,
Corticosteroids
 Interruption of gastric blood flow – GDV,
spinal injury
 Disruption of normal mucosal architecture
and alter blood flow – gastric tumors and
inflammatory stomach diseases
 Aberrations in mucosal protective functions-
Liver disease and hypoadrenocorticism
 Acid back diffusion
 Surgical alteration of gastric outflow -
Gastrojejunostomy
 Chronic vomiting with or without
hematemesis
 Melena and pale mucous membranes may
also be observed if bleeding is severe
 Inappetence and anorexia
 Abdominal pain
 Weakness
 Clinical signs
 Lab findings
 Diagnostic imaging
 Non-regenerative anemia
 Electrolyte abnormalities
 Elevated serum gastrin levels – gastrinomas,
decreased hepatic/ renal clearance
 Elevated serum histamine levels - mast cell
tumor or mastocytosis
 Plain radiography is not useful
 Contrast radiography may reveal filling
defects but doesnot allow detailed mucosal
evaluation
Ultrasound
 Detects gastric thickening associated with
ulcers
 Best tool for diagnosing gastric ulcer
 Treating the underlying cause/inciting cause
 Correcting secondary conditions
 Symptomatic-supportive therapy to enhance
mucosal defenses
 The rate of fluid administration depends on
the presence or absence of shock, the degree
of dehydration and the presence of diseases
 Analogues of histamine
 Competitively and reversibly inhibit the
binding of histamine to H2 receptors on the
gastric parietal cell
 Reduce intracellular cAMP concentrations
and thereby the secretion of acid by gastric
parietal cells
 Render the cell less responsive to stimulation
by acetylcholine and gastrin

 Increase the luminal secretion of bicarbonate

and mucus as well as raising mucosal blood
flow
 Ranitidine : 1–2 mg/kg PO, IV q 12 h
 Cimetidine : 5–10 mg/kg PO, IV q 8 h
 Famotidine: 0.5–1 mg/kg PO, IV q 12–24 h
 Nizatidine : 5 mg/kg PO q 24 h

Order of potency
 Famotidine > Ranitidine = Nizatidine >
Cimetidine
 Cimetidine - inhibits the hepatic cytochrome
P-450 system, short half life
 Ranitidine – Inhibitis hepatic enzymes, has
prokinetic activity
 Famotidine – no inhibition on hepatic
cytochrome p-450 system
 Nizatidine – prokinetic activity, does not
inhibit hepatic microsomal enzymes
 H+-K+ ATPase catalyzes the exchange of
cytosolic hydrogen ions for luminal
potassium ions and is referred to as a proton
pump
 Acid secretion is inhibited irreversibly
regardless of the secretagogue
 Omeprazole, lansoprazole, rabeprazole,
pantoprazole, and esomeprazole
 Pantoprazole and lansoprazole - intravenous
formulations
 Enteric-coated capsule – weak base
 20-mg capsule with 10 ml of 8.4% sodium
bicarbonate (NaHCO3) to make a 2-mg/ml
solution
 PPIs are capable of inhibiting H+-K+ ATPase
only when it is present on the apical
membrane of the parietal cell
 In fasting state, only approximately 10% of
proton pumps are actively secreting at the
canalicular surface
 A large reserve of additional proton pumps is
postprandially recruited
 1 hour before a meal - that the peak serum
concentration coincides with the maximal
activity of proton pump secretion
 Omeprazole - 0.7 mg/kg PO q 24 h
 Should be used with caution in patients with
liver disease
 Inhibits hepatic microsomal cytochrome P-
450 enzymes
 Effective in NSAID induced ulcers
 Sucralfate
 Synthetic prostaglandins
 Sucralfate dissociates after oral ingestion to
sucrose octasulfate and aluminum hydroxide

 Sucrose octasulfate reacts in the stomach

with hydrochloric acid to form a paste-like
complex that has greater affinity for
damaged tissue than the normal mucosa
 This adhering complex prevents further
damage of the gastric mucosa by pepsin,
acid, or bile
 Accelerates gastric mucosal healing
 Inactivates pepsin
 Stimulates endogenous prostaglandin
synthesis
 0.5–1 g PO q 8 h
 Orally administered drugs, however, should
be given 2 hours apart as sucralfate can affect
their absorption
 Interactions- Fluoroquinolones, tetracycline,
theophylline, aminophylline, and digoxin
 Synthetic analogue of PGE
 Acid-inhibitory and mucosal-protective
properties
 Increasing bicarbonate secretion, mucus
production, and mucosal blood flow, -
increasing epithelialization
 Decreases intracellular cAMP levels, leading
to decreased activity of the luminal H+-K+
ATPase pump
 Prevention of NSAID-induced ulcers
 Although orally administered, it has to be
absorbed into the circulation to be effective
 Causes abortions and diarrhea
 Avoided in pregnant animals
 2–5 μg/kg PO q 8–12 h
 Given 3-4 times a day
 Weak bases that transiently neutralize gastric
HCl in the gastric lumen
 Stimulating mucosal PG production
 Decrease pepsin activity
 Bind to bile acids in the stomach
 Neutralize hydrogen chloride, forming
magnesium chloride or aluminum chloride
and water
 Inactivating pepsin, binding bile acids, and
inducing local PG synthesis
 Constipation and diarrhea
 Produce carbon dioxide (CO2) and sodium
chloride
 Cause more serious side effects
 CO2 formation results in gastric distention
and belching
 Systemic absorption of sodium can
exacerbate fluid retention in patients with
heart failure, hypertension, and renal
insufficiency
 Dose : 0.5 -1 ml/kg
 Octreotide
 Used to rapidly decrease gastric acid
secretion
 May also help to control gastric bleeding
 Drugs block the action of the H+-K+-ATPase
by competing with K
 Soraprazan and Revaprazan
 Antiemetic therapy
 Antibiotics
 Analgesics
 If medical therapy does not substantially
alleviate clinical signs within 6 to 7 days
 If bleeding is profuse and life threatening
 Suspected for gastric perforation
 Partial gastrectomy
 Anything ingested by an animal that cannot
be digested (e.g., rocks and plastic) or that is
slowly digested (bones)

 Linear foreign bodies usually are pieces of

string, yarn, thread, cloth, or dental floss
 Gastric outflow obstruction
 Gastric perforation
 Systemic illness due to breakdown and
absorption of foreign material
 Dogs are indiscriminate eaters and often
ingest rocks, plastic toys, cooking bags, and
other objects

 Cats more commonly ingest linear material

(e.g., yarn or sewing thread attached to a
needle)

 Young animals more commonly ingest

foreign bodies than do older animals
 Asymptomatic
 Cause vomiting as a result of outflow
obstruction, gastric distention, and/or
mucosal irritation
 Vomiting often is absent if the foreign body
is in the gastric fundus and does not
obstruct the pylorus
 Abdominal pain
 Hematemesis
 Melena
 CNS signs
 Anorexia
 Lethargy
 Respiratory dysfunction
 Clinical signs
 Radiography
 Contrast radiography
 Endoscopy
 Metabolic and acid-base abnormalities
should be identified and corrected
 Gastrotomy
 Fluid therapy
 A bland diet should be fed starting 12 to 24
hours after surgery if the patient is not
vomiting
 Relatively uncommon in cats and dogs
 No anatomical predisposition for any
particular region
 Lesser curvature of the stomach has been a
frequently described location for gastric
tumors
 Adenocarcinoma
 Lymphoma (cats)
 Mast cell tumor
 Leiomyoma
 Leiomyosarcoma
 Fibrosarcoma
 Chow Chow, Staffordshire Bull terrier, and
Rough Collie for gastric carcinoma
 Belgian Shepherd for mucinous
adenocarcinoma
 Aerophagia

Anemia
Hypoproteinemia

Outflow obstruction
 Anorexia
 Hemetemesis
 Hematochezia
 Melena
 Abdominal pain
 Poor nutritional intake
 Weight loss
 Abnormal gastric motility
 Increased frequency of barborygmus
 Excessive fluid or gas in the stomach despite
fasting
 Presence of mass
 Caudal displacement of gastric axis on a
lateral radiography
 Gastric wall thickening
 Distortion of gastric lumen
 Presence of filling defect
 Derangement of rugal folds due to tumor
infiltration
 Ultrasonography
 Biopsy
 Treating secondary effects
 Motility enhancers to cure retention
 Chemotherapy
 Invasion of gastric wall – partial gastrectomy
 Pylorus – pyloric resection and
gastroduodenostomy
 Distal stomach and proximal duodenum -
gastrojejunostomy