GI: gastric disease Flashcards

1
Q

What two enzymes are produced by the stomach to aid in digestion?

A

Pepsin, gastric lipase

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2
Q

A small amount of instrinsic factor is produced by what cells in the dog stomach?

A

Parietal cells and cells at the base of the antral glands

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3
Q

What breeds are predisposed to hypertrophic gastropathy?

A

Shih Tzu, Basenji

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4
Q

What breed is predisposed to atropic gastritis?

A

Lundehund

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5
Q

Prior to measuring serum gastrin, omeprazole/famotidine must be discontinued for how many days?

A

1 week

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6
Q

What non-gastric diseases can cause an increase in gastrin?

A

Renal and hepatic dysfunction

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7
Q

A gastric pH<3 with an increased serum gastrin raises concerns for that disease process?

A

Gastrinoma (Zollinger-Ellison)

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8
Q

Mast cell tumors and hyperhistaminemia can induce gastric acid secretion. What would the serum gastrin level be?

A

Low

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9
Q

In patients with achlorhydria, what would serum gastrin and gastric pH be?

A

pH >3 with increased serum gastrin (in humans, pH <2.5 with gastrin >1000 is diagnostic)

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10
Q

If a gastrinoma is suspected, what IV infusions can be given for further investigation?

A

Secretin or Ca - neither of these lead to release of gastrin in a normal animal, but both lead to gastrin release from a gastrinoma (highest 2 and 5 minutes after secretin, 60 min after Ca)

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11
Q

What are 3 consequences of a gastrinoma?

A

Gastric antral hypertrophy, hyperacidity, and ulceration

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12
Q

Where is the most common location for a gastrinoma?

A

Right limb or body of the pancreas

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13
Q

What percent of gastrinomas have metastasized at the time of diagnosis?

A

85% (LN, mesentery, spleen, liver)

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14
Q

What prostaglandin is gastroprotective?

A

PGE2

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15
Q

Where are NSAID induced ulcers typically located?

A

Antrum

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16
Q

What is the main side effect of omeprazole?

A

Diarrhea

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17
Q

What is octreotide?

A

Long acting somatostatin analog

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18
Q

How does octreotide affect gastrin/gastric acid?

A

Directly decreases the secretion of gastrin and therefore gastric acid production - can be used in gastrinomas

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19
Q

What is misoprostol and what is it used for?

A

PGE2 analog - protects against NSAID induced ulceration without altering gastric acidity

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20
Q

How does sucralfate work?

A

Binds to areas of denuded epithelial mucosa

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21
Q

Does prophylactic administration of misoprostol, cimetidine, and/or omeprazole prevent gastric erosions in dogs on steroids?

A

No, unlike with NSAIDs. Cause of ulceration due to steroid use is unknown

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22
Q

How do mast cell tumors induce vomiting?

A

Histamine causes H1 activation of the chemoreceptor trigger zone; H2 activation of gastric acid secretion

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23
Q

What is the mechanism of action for metoclopramide?

A

Antagonizes D2-dopamingeric and 5HT3-serotonergic receptors, agonist of 5HT4, cholinergic effects on smooth muscle

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24
Q

What is the mechanism of action of ondansetron?

A

Antagonized peripheral 5HT3 receptors

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25
Q

What is the mechanism of action of maropitant?

A

Antagonized NK1 (neurokinin 1) receptors

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26
Q

Maropitant has been associated with bone marrow hypoplasia in what age of dogs and cats?

A

Dogs <8 weeks, Cats <16 weeks

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27
Q

Gram negative or pathogenic bacteria induce the release of what cytokines from epithelial cells?

A

Proinflammatory - IL-8, IL-1 beta

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28
Q

Commensal bacteria induce the release of what cytokines from epithelial cells?

A

Immunomodulatory - TGFbeta, IL-10

29
Q

What are two treatment protocols for Helicobacter in dogs/cats?

A

Metronidazole, amoxicillin and famotidine
Metronidazole, amoxicillin, bismuth +/- famotidine

30
Q

Following treatment for Helicobacter, what percent of dogs had clearance of the bacteria at 6 months post treatment?

A

43% (high relapse rate)

31
Q

Where do Helicobacter species colonize in the dog/cat?

A

Superficial mucus and gastric glands, particularly in the fundus and cardia

32
Q

What histopathologic changes are more common in dogs/cats infected with Helicobacter?

A

Degeneration of the gastric glands, parietal cell necrosis, LP inflammation

33
Q

What clinical conditions have NOT been linked to Helicobacter infection in dogs/cats?

A

Gastric ulceration, neoplasia, changes in serum gastrin, acid secretion

34
Q

H. pylori induces much more severe proinflammatory cytokine and cellular responses in dogs/cats than natural infection with large Helicobacter species. What does this suggest?

A

Suggests large Helicobacter species are likely commensal. Loss of tolerance to commensal organisms, rather than pathogenicity of these organisms, may contribute to any disease condition

35
Q

Hypertrophy of the fundic mucosa is associated with severe enteropathy in what breed?

A

Basenjis

36
Q

Hypertrophy of the pyloric mucosa is found in what dog breeds and is associated with gastric outflow obstructions?

A

Brachycephalics, Lhasa Apso

37
Q

What worm is capable of causing parasitic gastritis in cats?

A

Ollulanus tricuspis

38
Q

How is Ollulanus tricuspis transmitted?

A

Cat to cat by eating vomit. Yes, eating vomit. Not found in feces

39
Q

What endoscopic and histologic changes are found with Ollulanus tricuspis infection?

A

Rugal fold hyperplasia, 2-3mm nodules
LP infiltrates, lymphoid follicle hyperplasia, fibrosis

40
Q

How is Ollulanus tricuspis infection diagnosed? Treated?

A
  • Examination of gastric juice, vomit, or histopath. Not found in feces.
  • Treatment = fenbendazole
41
Q

What worm is capable of causing parasitic gastritis in dogs AND cats?

A

Physaloptera spp. 2-6cm long worms

42
Q

What are the intermediate and paratenic hosts of Physaloptera?

A

Cockroaches, beetles
Lizards, hedgehogs

43
Q

Atrophic gastritis characterized by reduction in parietal cells and hyperplasia of neuroendocrine cells has been associated with gastric adenocarcinoma in what dog breed?

A

Lundehunds

44
Q

What is the suspected cause of bilious vomiting syndrome?

A

Motility disorder characterized by duodenogastric reflux

45
Q

What is the mechanism by which erythromycin promotes gastric motility?

A

Releases motilin to act on motilin receptors and mimic phase III of the inter digestive migrating motility complex to empty the stomach of solids

46
Q

What is the most common gastric neoplasm in dogs? In cats?

A

Dogs: Adenocarcinoma (47-72%)
Cats: Lymphoma

47
Q

Where do gastric carcinomas most commonly occur in the dog?

A

Lesser curvature and pylorus

48
Q

In a retrospective analysis of dogs and cats with gastric neoplasia, what percent of neoplasms were identified on ultrasound? On endoscopy?

A

50% on ultrasound, 95% on endoscopy

49
Q

In a retrospective analysis of dogs and cats with gastric neoplasia, what neoplasm was the most commonly missed by ultrasound?

A

Lymphoma

50
Q

In a prospective clinical trial, did laparoscopic assisted gastropexy affect GI transit time in healthy dogs?

A

Nope!

51
Q

Does the cat esophagus enter the abdomen?

A

No - transitions directly into the stomach at the diaphragm level

52
Q

How small must particles be to enter the duodenum?

A

2mm

53
Q

How often do motilin plasma levels increase and what do they trigger?

A

Every 90-120 minutes, trigger migrating motor complexes

54
Q

What cat breed can develop pyloric stenosis at a young age?

A

Siamese

55
Q

Where are 5HT4 receptors located? Activation of these receptors results in what changes?

A

Located on enteric cholinergic neurons that innervate intestinal smooth muscle. Activation results in release of acetylcholine in the synaptic cleft and excitation of the cell membrane to increase motility

56
Q

How does gastroesophageal intussusception differ from a hiatal hernia?

A

The gastroesophageal junction remains in the normal anatomic position with an intussusception

57
Q

What is the average age of dogs with gastroesophageal intussusception?

A

Young - 13 months

58
Q

What was the survival to discharge and MST for dogs with gastroesophageal intussusception?

A

88% survival to discharge, MST 995 days

59
Q

What is common following surgical correction of gastroesophageal intussusception?

A

Persistent regurgitation, although some dogs had prior megaesophagus so ??

60
Q

What two drugs have been shown to increase gastric transit time in healthy cats?

A

Metoclopramide, erythromycin (equally effective)

61
Q

Chronic gastritis with lymphofollicular hyperplasia is associated with what other disease condition?

A

Chronic upper airway obstruction - brachycephalics, inspiratory dyspnea

62
Q

Compared to dogs with chronic gastritis, dogs with gastric carcinoma displayed what changes?

A

Older (10 vs 6.5 yrs), lower BCS (3 vs 4.5), higher CRP (>25), low folate

63
Q

Describe feline gastrointestinal eosinophilic sclerosing fibroplasia

A

Presence of eosinophilic masses confined to the GI tract and local LNs - cause unknown

64
Q

What breed of cat is over-represented in cases of feline gastrointestinal eosinophilic sclerosing fibroplasia?

A

Ragdolls

65
Q

What is a common physical exam finding in cats with feline gastrointestinal eosinophilic sclerosing fibroplasia?

A

Firm, irregular fixed abdominal mass in the cranial or mid-abdomen

66
Q

In cats with feline gastrointestinal eosinophilic sclerosing fibroplasia, what are common clinicopathologic changes?

A

Peripheral eosinophilia (50%), hyperglobulinemia (70%)

67
Q

When IV apomorphine is administered, what percent of dogs successfully vomit up foreign material?

A

76% in one study (495 dogs), 78% in another (61 dogs)

68
Q

What factors were associated with successful emesis of foreign material after apomorphine? With unsuccessful emesis?

A

Success: young dogs, dogs ingesting fabric, leather, or bathroom waste
Unsuccessful: longer time between consumption and administration of apo, dogs that received opioids, sedatives, or antiemetics first