Gastroenterology - Gastric Diseases Flashcards

1
Q

Which part of the stomach expands for food?

A

fundus and body

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2
Q

What are the components of the mucosa layer of the stomach?

A
  • superficial epithelium
  • lamina propria
  • gastric glands
  • neuroendocrine cells
  • muscularis mucosa
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3
Q

Which cells make up the gastric glands of the stomach?

A

mucous neck cells
parietal cells
chief cells

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4
Q

What is the lamina propria of the stomach made up of?

A

loose connective tissue
immune system cells
nutritional support

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5
Q

What is produced by the gastric neuroendocrine cells?

A
  • enterocromafin (serotonin, histamine)
  • somatostatin
  • gastrin
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6
Q

What is the submucosa of the stomach made up of?

A
  • dense connective tissue: structural support
  • blood vessels
  • lymphatics
  • Meissner’s plexus
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7
Q

What is the muscularis of the stomach made up of?

A
  • layers of perpendicular smooth muscle

- Auerbach’s (myenteric) plexis

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8
Q

Which enzyme is responsible for protein digestion?

Fat digestion?

A

protein - pepsin

fat - gastric lipase

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9
Q

What influences/controls motility of the GIT?

A
  • migrating motility complex
  • neural and hormonal stimulus
  • pressure/distension (mechanoreceptors)
  • nutritional content of food
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10
Q

What is acute gastritis?

A

inflammation of the stomach lining

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11
Q

What is the pathology associated with GDV?

A
  • compression of CVC > impaired venous return > hypovolemic shock
  • gastric wall necrosis
  • splenic torsion or avulsion
  • congestion of viscera
  • endotoxic shock
  • DIC
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12
Q

What are the clinical signs associated with GDV?

A
  • acute, non-productive retching
  • pytalism
  • abdominal distension
  • collapse
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13
Q

What is found on physical exam of a dog with GDV?

A
  • abdominal distension
  • tachycardia, poor pulses
  • hypothermia
  • depression
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14
Q

How is GDV diagnosed?

A

radiographs

  • right lateral view most important
  • “popeye arm”
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15
Q

How is GDV treated?

A
  • aggressive fluid therapy
  • decompression
  • surgery ASAP
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16
Q

What is the treatment for food bloat?

A
  • fluid support
  • withhold food
  • walk frequently
  • pain management
  • +/- lavage or surgery
17
Q

What are the possible causes of mucosal barrier injury?

A
  • disruption of normal gastroprotection
  • decreased blood flow
  • hypersecretion of acid
  • decreased mucous or bicarbonate
18
Q

What conditions can cause secondary gastric ulcers/erosion?

A
  • neoplasia
  • hypovolemic shock/hypotension
  • trauma
  • medication (NSAIDs)
  • uremic gastritis
19
Q

What are the clinical signs associated with gastric ulceration/erosion?

A

vomiting, hematemesis, melena, retching, inappetence

20
Q

How is gastric ulceration/erosion diagnosed?

A
  • radiographs with contrast
  • ultrasound
  • endoscopy for confirmation
  • MDB and fecal
21
Q

How is gastric ulceration/erosion treated?

A
  • treat primary disease
  • mucosal protectants
  • proton pump inhibitors
  • pain management
  • blood transfusion
  • nutrition
22
Q

What type of bacteria is Helicobacter pylori?

A

spiral

gram negative

23
Q

How is Helicobacter gastritis treated?

A

Clorithromycin
Amoxicillin
Metronidazole

24
Q

Which parasites can cause gastric disease?

A
  • Toxocara
  • Physalloptera
  • Ollulanus tricuspi
25
Q

Describe gastric pythiosis

A
  • chronic vomiting
  • thickened gastric outflow tract
  • pyogranulomatous inflammation
  • cause by fungus: P. insidiosum
26
Q

What are the clinical signs associated with gastric esophageal reflux?

A
  • chronic vomiting

- lip licking, hard swallow, pytalism, halitosis, esophagitis

27
Q

What is the usual cause of gastric esophageal reflux?

A

secondary to gastric or small intestinal disease

28
Q

How is gastric esophageal reflux treated?

A
  • proton pump inhibitor
  • treat primary disease
  • sucralfate
29
Q

What is the main clinical signs of inflammatory gastritis?

A

chronic vomiting

30
Q

How is inflammatory gastritis diagnosed?

A

endoscopy or surgical biopsy

- infiltrate of inflammatory cells in mucosa and lamina propria

31
Q

How is lymphoplasmacytic and eosinophilic gastritis treated?

A
  • symptomatic therapy (antacid and antiemetics)
  • empiric deworming (Fenbendazole or Pyrantel pamoate)
  • diet trial
  • immune modulation
32
Q

What pathology is found with atrophic gastritis?

A
  • marked mononuclear cell infiltrate
  • thinning of gastric mucosa
  • atrophy of gastric glands
  • replacement by fibrous tissue
  • impaired ingestion
33
Q

What pathology is found with hypertrophic gastropathy?

A
  • diffuse or focal hypertrophy of mucosa and/or muscularis

- inflammatory infiltrates

34
Q

What is pyloric stenosis?

A
  • muscular thickening of pyloric sphincter

- delayed gastric emptying

35
Q

What pathology and clinical signs are found with gastrinoma?

A
  • thickened gastric wall
  • hypertrophy of pylorus
  • gastric ulceration
  • reflux esophagitis
  • chronic vomiting
  • +/- diarrhea
36
Q

What is gastrinoma?

A
  • tumor in pancreas of the APUD cells

- hypersecretion of gastric acid

37
Q

How is gastrinoma diagnosed?

A
  • gastrin levels
  • low pH of gastric juice with a high gastrin level
  • ultrasound, CT, scintigraphy
  • biopsy
38
Q

How is gastrinoma treated?

A
  • surgical removal
  • proton pump inhibitor
  • Octreotide to inhibit gastrin