Disease of the Stomach Flashcards
What are the specialized secretory cells in the stomach called?
- mucus neck cells: pepsinogen A, gastric lipase
- Parietal cells: HCl, pepsinogen A, intrinsic factor
- Chief cells: pepsinogen A
Where the secretory cells located?
Fundus: enterochromaffin-like and somatostatin producing cells
Antrum: gastrin and somatostatin producing cells
What the 3 layers of gastric wall?
inner: mucosa
middle: muscularis
outer: serosa
What stimulates gastrin production?
luminal peptides, digested protein, acetylcholine and gastrin-releasing peptides
Where is gastrin release from?
G cells
How does histamine effect gastrin release?
Histamine from mast cell (and binding of acetylcholine and gastric to parietal cells) contribute to secretion
What’s the role of somatostatin?
It’s released when pH <3
- decreases gastrin, histamine, and acid secretion
Where is gastric acid produced?
parietal cells
How is gastric mucosa protected from the acid?
gastric mucosal barrier
- layer of bicarbonate rich mucus
- has increased mucosal blood supply –> brings lots of O2, bicarbonate and nutrients
- local production of PGE2 modulate blood flow, bicarbonate secretion, and cell renewal
Which nutrients slow down gastric emtpying?
carbohydrates, amino acids, and esp fat, can slow down gastric emptying
What’s the role of CCK and how is it sitmulated?
CCK is secreted in response to fatty acids and amino acids –> slows down gastric emptying
Which is the major organ for secretion of intrinsic factor?
pancreas
also produced by parietal cells in the stomach
Why is intrinsic factor important?
required for cobalamin production
What’s the role of motilin on gastric emptying?
in fasted state, motilin will stimulate expulsion of large, undigestible solids by phase III of the migrating motility complex
Which bacteria can lead to a false (+) for helicobacter due to their urease production?
Proteus and E coli
What’s the treatment principle for acute gastritis?
symptomatic supportive therapy
- fluid therapy
- dietary restriction and modification
- Pepto Bismol (1ml/5kg PO q8h)
- sucralfate (0.5-1g/kg PO q8h)
What’s the etiology of gastric ulcer/ erosion?
Due to impaired gastric mucosal barrier –> direct injury, interference with PGE2, mucus or bicarbonate, decreased blood flow, and hypersecretion of gastric acid
What are some risk factors for gastric ulcer/ erosion?
- drug induced: NSAID, glucocorticoids
- uremia/ CKD
- hepatic failure
- Addison’s
- hypotension
What are the treatment principles for gastric ulcer/ erosion?
- fluid therapy, may need to supplement with K+
- reduction of acid production: H2 blocker (famotidine), gastrin blocker (proglumide), acetylcholine blocker (atropine), proton pump inhibitor (omeprazole)
- somatostatin analogue - octreotide - mucosal protection: PGE2 analogue (misoprostol) –> protects against NSAID-induced gastric erosion without decreasing acid production (3-5mcg/kg PO q8h); sucralfate
- antiemetics: metoclopramide (CRI), maropitant
- antibiotics: cephalosporines
- analgesics: buprenorphine
Where is NSAID-induced ulcer most likely found?
by the antrum, usually not associated with marked thickening or irregular edges
What are the treatment principles for GDV?
- fluid resuscitation - correct electrolyte abnormalities
- adjunct therapy for endotoxic shock and reperfusion: prednisone sodium succinate, broad spectrum antibiotics (ex. cephalosporin, fluoroquinolone)
- cardiac arrhythmia: lidocaine (1-2mg/kg iV bolus, followed by 50-75mcg/g/min)
How is chronic gastritis diagnosed?
based on biopsy - the histology will aid in sub classification
What’s the cause of chronic gastritis?
- rarely identified
- food/ dietary sensitivity
- loss of tolerance to bacterial/ dietary antigens
What kind of immune response does the body have towards gram (-) / pathogenic bacteria vs. commensal or bacteria such as Strep faecium or Lactobacillus spp?
Gram (-)/ pathogenic bacteria: induce pro-inflammatory cytokines –> IL8, IL-1 beta)
With commensals or Strep faecium or Lactobacillus spp: immunomodulatory cytokines –> TGF-beta, or IL-10
How is helicobacter treated?
Amoxicillin, metronidazole, and famotidine
Hypertrophy of the fundic mucosa is frequently associated with severe enteropathy is seen in which breed?
Basenji
Which breed can have stomatocytosis, hemolytic anemia, icterus, and polyneuropathy?
Drentse Patrijshonds
Which breeds can have hypertrophy of the pyloric mucosa associated outflow obstruction?
small brachycephalic breeds: Lhasa Apso
Hyperglobulinemia and hypoalbuminemia can be associated with which cause of chronic gastritis?
- Basenjis with gastropathy or enteropathy
- canine gastric pythiosis
Panhypoproteinemia is a feature in which chronic gastritis?
- gastroenteropathy in Lundehunds
- moderate to severe IBD
- GI lymphoma
- GI histoplasmosis
If the patient is vomiting excessive bile stained fluid, where type of gastritis is it?
duodenogastric reflux-associated gastritis
if the patient is vomiting mostly clear fluids, which type of gastritis is it?
hypersecretion of gastric acids
How can helicobacter be diagnosed?
Impression smear of biopsy samples
How is chronic gastritis treated?
based on underlying etiology
- parasitic: can be difficult to identify causative agent (ex. ollulanus tricuspis, Physaloptera spp.) –> can do broad spectrum dewormer like febendazole
What are some physical features of gastric phytosis?
- transmural thickening of gastric outflow tract
- histo = pyogranulomatous infection
- may need special stain
- Tx = aggressive surgical resection + itraconazole
- Px = poor, <25% will be cured with medical therapy alone
When should Helicobacter associated gastritis be treated?
only if symptomatic and have biopsy confirmed Helicobacter spp. infection and gastritis
What supportive therapy can be done for chronic gastritis of unknown cause?
- diet high in carb, low in fat –> faciliate gastric emptying
- prednisone
- antacid
- if still not working, immunosuppressive agents may be needed (but often not required): chlorambucil (safter alternative than azathioprine)
What’s the clinical sign seen with delayed gastric emptying and motility disorders?
Vomiting at least 8, often 10-16h post eating
What are the main causes of delayed gastric emptying and motility disorders?
- outflow obstruction
- defective propulsion
What’s the treatment for delayed gastric emptying and motility disorders?
pending the underlying cause
- Surgery: pyloric stenosis, polyps, non-gastrin induced hypertrophic gastropathy; neoplasia
- Medical management: gastric ulcers, erosions
- Diet: small semi-liquid, protein and fat restricted
What is the most common gastric neoplasia in the dog?
gastric adenocarcinoma
(extremely rare in the cat)
What is the most common GI neoplasia in the dog and cat?
lymphoma
- small cell lymphoma in cat = more localized to the GI tract
Which gastric neoplasia has the best prognosis: adenocarcinoma, lymphoma, or leiomyosarcoma?
Leiomyosarcoma – can have paraneoplastic hypoglycemia
Is feline gastric lymphoma associated with FeLV?
no
Where is the most common location for gastric adenocarcinoma in the dog?
lesser curvature and pyloric region
- annular or stenosing lesions
- frequent metastasis
What are the 3 morphological patterns of gastric adenocarcinoma?
- diffuse, infiltrating nonulcerating lesions –> leather bottle appearance as described in people
- localized, raised, thickened plaque, with ulcerative centre
- raised, polypoid, sessile lesion, projecting into the lumen
What’s the appearance of LSA on gastroscopy?
diffuse, smooth, or cobblestone-like thickening of the rugae
What’s the appearance of adenocarcinoma on gastroscopy?
focal, dark pink to red masses, may be slightly pedunculated
What’s the treatment for gastric neoplasia?
surgery, except for LSA (chemo)
What’s the prognosis for gastric adenocarcinoma?
poor, metastasis = common
~6m
What’s the prognosis for gastric leiomyosarcoma?
good, slow growing, can still be favorable despite metastasis
What’s the prognosis for gastric LSA?
dog = poor
cat, good if small cell, T cell; large cell = much poorer prognosis
