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Internal Medicine/ Ettinger > Disease of the Stomach > Flashcards

Disease of the Stomach Flashcards

1
Q

What are the specialized secretory cells in the stomach called?

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

Where the secretory cells located?

A

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

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3
Q

What the 3 layers of gastric wall?

A

inner: mucosa
middle: muscularis
outer: serosa

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4
Q

What stimulates gastrin production?

A

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

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5
Q

Where is gastrin release from?

A

G cells

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6
Q

How does histamine effect gastrin release?

A

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

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7
Q

What’s the role of somatostatin?

A

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

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8
Q

Where is gastric acid produced?

A

parietal cells

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9
Q

How is gastric mucosa protected from the acid?

A

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

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10
Q

Which nutrients slow down gastric emtpying?

A

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

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11
Q

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

A

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

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12
Q

Which is the major organ for secretion of intrinsic factor?

A

pancreas
also produced by parietal cells in the stomach

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13
Q

Why is intrinsic factor important?

A

required for cobalamin production

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14
Q

What’s the role of motilin on gastric emptying?

A

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

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15
Q

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

A

Proteus and E coli

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16
Q

What’s the treatment principle for acute gastritis?

A

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

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17
Q

What’s the etiology of gastric ulcer/ erosion?

A

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

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18
Q

What are some risk factors for gastric ulcer/ erosion?

A
  • drug induced: NSAID, glucocorticoids
  • uremia/ CKD
  • hepatic failure
  • Addison’s
  • hypotension
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18
Q

What are the treatment principles for gastric ulcer/ erosion?

A
  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
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19
Q

Where is NSAID-induced ulcer most likely found?

A

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

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20
Q

What are the treatment principles for GDV?

A
  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)
20
Q

How is chronic gastritis diagnosed?

A

based on biopsy - the histology will aid in sub classification

21
Q

What’s the cause of chronic gastritis?

A
  • rarely identified
  • food/ dietary sensitivity
  • loss of tolerance to bacterial/ dietary antigens
22
Q

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

A

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

23
Q

How is helicobacter treated?

A

Amoxicillin, metronidazole, and famotidine

24
Q

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

A

Basenji

25
Q

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

A

Drentse Patrijshonds

26
Q

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

A

small brachycephalic breeds: Lhasa Apso

27
Q

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

A
  • Basenjis with gastropathy or enteropathy
  • canine gastric pythiosis
28
Q

Panhypoproteinemia is a feature in which chronic gastritis?

A
  • gastroenteropathy in Lundehunds
  • moderate to severe IBD
  • GI lymphoma
  • GI histoplasmosis
29
Q

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

A

duodenogastric reflux-associated gastritis

30
Q

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

A

hypersecretion of gastric acids

31
Q

How can helicobacter be diagnosed?

A

Impression smear of biopsy samples

32
Q

How is chronic gastritis treated?

A

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

33
Q

What are some physical features of gastric phytosis?

A
  • 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
34
Q

When should Helicobacter associated gastritis be treated?

A

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

35
Q

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

A
  • 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)
36
Q

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

A

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

37
Q

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

A
  • outflow obstruction
  • defective propulsion
38
Q

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

A

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

39
Q

What is the most common gastric neoplasia in the dog?

A

gastric adenocarcinoma
(extremely rare in the cat)

40
Q

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

A

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

41
Q

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

A

Leiomyosarcoma – can have paraneoplastic hypoglycemia

42
Q

Is feline gastric lymphoma associated with FeLV?

A

no

43
Q

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

A

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

44
Q

What are the 3 morphological patterns of gastric adenocarcinoma?

A
  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
45
Q

What’s the appearance of LSA on gastroscopy?

A

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

46
Q

What’s the appearance of adenocarcinoma on gastroscopy?

A

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

47
Q

What’s the treatment for gastric neoplasia?

A

surgery, except for LSA (chemo)

48
Q

What’s the prognosis for gastric adenocarcinoma?

A

poor, metastasis = common
~6m

49
Q

What’s the prognosis for gastric leiomyosarcoma?

A

good, slow growing, can still be favorable despite metastasis

50
Q

What’s the prognosis for gastric LSA?

A

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

Internal Medicine/ Ettinger (93 decks)

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