Disease of the Stomach

Question 1

What are the specialized secretory cells in the stomach called?

Answer 1

1. mucus neck cells: pepsinogen A, gastric lipase
2. Parietal cells: HCl, pepsinogen A, intrinsic factor
3. Chief cells: pepsinogen A

Question 2

Where the secretory cells located?

Answer 2

Fundus: enterochromaffin-like and somatostatin producing cells
Antrum: gastrin and somatostatin producing cells

Question 3

What the 3 layers of gastric wall?

Answer 3

inner: mucosa
middle: muscularis
outer: serosa

Question 4

What stimulates gastrin production?

Answer 4

luminal peptides, digested protein, acetylcholine and gastrin-releasing peptides

Question 5

Where is gastrin release from?

Answer 5

G cells

Question 6

How does histamine effect gastrin release?

Answer 6

Histamine from mast cell (and binding of acetylcholine and gastric to parietal cells) contribute to secretion

Question 7

What’s the role of somatostatin?

Answer 7

It’s released when pH <3
- decreases gastrin, histamine, and acid secretion

Question 8

Where is gastric acid produced?

Answer 8

parietal cells

Question 9

How is gastric mucosa protected from the acid?

Answer 9

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

Question 10

Which nutrients slow down gastric emtpying?

Answer 10

carbohydrates, amino acids, and esp fat, can slow down gastric emptying

Question 11

What’s the role of CCK and how is it sitmulated?

Answer 11

CCK is secreted in response to fatty acids and amino acids –> slows down gastric emptying

Question 12

Which is the major organ for secretion of intrinsic factor?

Answer 12

pancreas
also produced by parietal cells in the stomach

Question 13

Why is intrinsic factor important?

Answer 13

required for cobalamin production

Question 14

What’s the role of motilin on gastric emptying?

Answer 14

in fasted state, motilin will stimulate expulsion of large, undigestible solids by phase III of the migrating motility complex

Question 15

Which bacteria can lead to a false (+) for helicobacter due to their urease production?

Answer 15

Proteus and E coli

Question 16

What’s the treatment principle for acute gastritis?

Answer 16

symptomatic supportive therapy
- fluid therapy
- dietary restriction and modification
- Pepto Bismol (1ml/5kg PO q8h)
- sucralfate (0.5-1g/kg PO q8h)

Question 17

What’s the etiology of gastric ulcer/ erosion?

Answer 17

Due to impaired gastric mucosal barrier –> direct injury, interference with PGE2, mucus or bicarbonate, decreased blood flow, and hypersecretion of gastric acid

Question 18

What are some risk factors for gastric ulcer/ erosion?

Answer 18

• drug induced: NSAID, glucocorticoids
• uremia/ CKD
• hepatic failure
• Addison’s
• hypotension

Question 18

What are the treatment principles for gastric ulcer/ erosion?

Answer 18

1. fluid therapy, may need to supplement with K+
2. reduction of acid production: H2 blocker (famotidine), gastrin blocker (proglumide), acetylcholine blocker (atropine), proton pump inhibitor (omeprazole)
   - somatostatin analogue - octreotide
3. mucosal protection: PGE2 analogue (misoprostol) –> protects against NSAID-induced gastric erosion without decreasing acid production (3-5mcg/kg PO q8h); sucralfate
4. antiemetics: metoclopramide (CRI), maropitant
5. antibiotics: cephalosporines
6. analgesics: buprenorphine

Question 19

Where is NSAID-induced ulcer most likely found?

Answer 19

by the antrum, usually not associated with marked thickening or irregular edges

Question 20

What are the treatment principles for GDV?

Answer 20

1. fluid resuscitation - correct electrolyte abnormalities
2. adjunct therapy for endotoxic shock and reperfusion: prednisone sodium succinate, broad spectrum antibiotics (ex. cephalosporin, fluoroquinolone)
3. cardiac arrhythmia: lidocaine (1-2mg/kg iV bolus, followed by 50-75mcg/g/min)

Question 20

How is chronic gastritis diagnosed?

Answer 20

based on biopsy - the histology will aid in sub classification

Question 21

What’s the cause of chronic gastritis?

Answer 21

• rarely identified
• food/ dietary sensitivity
• loss of tolerance to bacterial/ dietary antigens

Question 22

What kind of immune response does the body have towards gram (-) / pathogenic bacteria vs. commensal or bacteria such as Strep faecium or Lactobacillus spp?

Answer 22

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

Question 23

How is helicobacter treated?

Answer 23

Amoxicillin, metronidazole, and famotidine

Question 24

Hypertrophy of the fundic mucosa is frequently associated with severe enteropathy is seen in which breed?

Answer 24

Basenji

Question 25

Which breed can have stomatocytosis, hemolytic anemia, icterus, and polyneuropathy?

Answer 25

Drentse Patrijshonds

Question 26

Which breeds can have hypertrophy of the pyloric mucosa associated outflow obstruction?

Answer 26

small brachycephalic breeds: Lhasa Apso

Question 27

Hyperglobulinemia and hypoalbuminemia can be associated with which cause of chronic gastritis?

Answer 27

- Basenjis with gastropathy or enteropathy - canine gastric pythiosis

Question 28

Panhypoproteinemia is a feature in which chronic gastritis?

Answer 28

- gastroenteropathy in Lundehunds - moderate to severe IBD - GI lymphoma - GI histoplasmosis

Question 29

If the patient is vomiting excessive bile stained fluid, where type of gastritis is it?

Answer 29

duodenogastric reflux-associated gastritis

Question 30

if the patient is vomiting mostly clear fluids, which type of gastritis is it?

Answer 30

hypersecretion of gastric acids

Question 31

How can helicobacter be diagnosed?

Answer 31

Impression smear of biopsy samples

Question 32

How is chronic gastritis treated?

Answer 32

based on underlying etiology - parasitic: can be difficult to identify causative agent (ex. ollulanus tricuspis, Physaloptera spp.) --> can do broad spectrum dewormer like febendazole

Question 33

What are some physical features of gastric phytosis?

Answer 33

- 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

Question 34

When should Helicobacter associated gastritis be treated?

Answer 34

only if symptomatic and have biopsy confirmed Helicobacter spp. infection and gastritis

Question 35

What supportive therapy can be done for chronic gastritis of unknown cause?

Answer 35

- 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)

Question 36

What's the clinical sign seen with delayed gastric emptying and motility disorders?

Answer 36

Vomiting at least 8, often 10-16h post eating

Question 37

What are the main causes of delayed gastric emptying and motility disorders?

Answer 37

- outflow obstruction - defective propulsion

Question 38

What's the treatment for delayed gastric emptying and motility disorders?

Answer 38

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

Question 39

What is the most common gastric neoplasia in the dog?

Answer 39

gastric adenocarcinoma (extremely rare in the cat)

Question 40

What is the most common GI neoplasia in the dog and cat?

Answer 40

lymphoma - small cell lymphoma in cat = more localized to the GI tract

Question 41

Which gastric neoplasia has the best prognosis: adenocarcinoma, lymphoma, or leiomyosarcoma?

Answer 41

Leiomyosarcoma -- can have paraneoplastic hypoglycemia

Question 42

Is feline gastric lymphoma associated with FeLV?

Answer 42

no

Question 43

Where is the most common location for gastric adenocarcinoma in the dog?

Answer 43

lesser curvature and pyloric region - annular or stenosing lesions - frequent metastasis

Question 44

What are the 3 morphological patterns of gastric adenocarcinoma?

Answer 44

1. diffuse, infiltrating nonulcerating lesions --> leather bottle appearance as described in people 2. localized, raised, thickened plaque, with ulcerative centre 3. raised, polypoid, sessile lesion, projecting into the lumen

Question 45

What's the appearance of LSA on gastroscopy?

Answer 45

diffuse, smooth, or cobblestone-like thickening of the rugae

Question 46

What's the appearance of adenocarcinoma on gastroscopy?

Answer 46

focal, dark pink to red masses, may be slightly pedunculated

Question 47

What's the treatment for gastric neoplasia?

Answer 47

surgery, except for LSA (chemo)

Question 48

What's the prognosis for gastric adenocarcinoma?

Answer 48

poor, metastasis = common ~6m

Question 49

What's the prognosis for gastric leiomyosarcoma?

Answer 49

good, slow growing, can still be favorable despite metastasis

Question 50

What's the prognosis for gastric LSA?

Answer 50

dog = poor cat, good if small cell, T cell; large cell = much poorer prognosis