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SAM 2 > Gastric Disease > Flashcards

Gastric Disease Flashcards

1
Q

What are the different parts of the stomach from the esophagus to pylorus?

A 
Lower esophageal sphincter
Cardia
Fundus
Body
Antrum
Pylorus
Pyloric sphincter
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2
Q

What two parts of the stomach expand to accommodate food? What part is used for grinding?

A

Expand: Fundus and body
Grinding: Antrum

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3
Q

What are the components in the mucosa of the stomach?

A
  • Superficial epithelium
  • Lamina propria
  • Gastric glands
  • Neuroendocrine cells
  • Muscularis mucosa
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4
Q

What are the gastric glands?

A
  • Mucus neck cells
  • Parietal cells
  • Chief cells
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5
Q

What do the neuroendocrine cells release?

A
  • Enterocromagin (serotonin and histamine release)
  • Somatostatin
  • Gastrin
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6
Q

What is the submucosa comprised of?

A

Dense connective tissue, structural support, blood vessels, lymphatics, and meissner’s plexus

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7
Q

What is Meissner’s plexus?

A

Nervous layer of the submucosa

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8
Q

What is the muscularis layer?

A

Layers of smooth muscle arranged perpendicular to each other

Controlled by Auerbach’s (myenteric) plexus

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9
Q

What is the serosa?

A

Connective tissue layer on the outside of the stomach

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10
Q

What enzymes are involved with protein and fat digestion?

A

Proteins- pepsin

Fat- lipases

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11
Q

What does intrinsic factor do in dogs?

A

Vitamin and mineral absorption

Limited activity in the stomach

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12
Q

What effects gastric motility?

A
  • Migrating motility complex
  • Neural and hormonal stimulus
  • Pressure/distension
  • Nutritional content of food
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13
Q

What does fat do to motility in the stomach?

A

Slows motility

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14
Q

What are some common general pathologies in the stomach?

A
  • Inflammation (gastritis)
  • Ulceration
  • Obstruction
  • Neoplasia
  • Infection
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15
Q

What are some clinical manifestation of gastric pathology?

A

Vomiting, hematemesis, melena, retching, burping, ptylaism, weight loss, distension, pain

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16
Q

What can CBC findings tell us about gastric disease?

A

May have regenerative anemia if bleeding or leukocytosis

Usually nothing of significance

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17
Q

What are some common chemistry findings of gastric disease?

A
  • Hypochloremia, hyponatremia, hypokalemia
  • Azotemia (pre-renal)
  • Elevated BUN if bleeding
  • Metabolic alkalosis with gastric outflow obstruction
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18
Q

What are some findings on UA with gastric disease?

A

Usually nothing

May have paradoxic aciduria with gastric outflow obstruction

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19
Q

What are the pros and cons of gastric endoscopy?

A

Good for inflammation, ulcer, foreign body, and mucosal neoplasia

Bad for disease deeper than mucosa and functional assessment

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20
Q

What are two indications for surgery in the stomach?

A

Biopsy or foreign body

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21
Q

What is acute gastritis?

A
  • Inflammation of the mucosa

- Sudden onset of clinical signs

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22
Q

What things can cause acute gastritis?

A

Drugs, toxins, dietary indiscretion, intolerance, parasites, bacterial, viral, systemic illness

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23
Q

How do we typically manage acute gastritis?

A

Symptomatic and supportive care

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24
Q

How do you definitively diagnose acute gastritis?

A

Biopsy

typically presumptive

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25
Q

What is the diagnosis based on?

A

History, clinical findings, and trial/response to symptomatic care

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26
Q

What treatments can be pursued in cases of acute gastritis?

A
  • Fluids
  • Antacids
  • Antiemetics
  • Pain medications
  • Water and bland diet
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27
Q

T/F: Gastritis doesn’t typically induce significant mucosal changes.

A

False

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28
Q

How do gastric foreign bodies typically present?

A

Obstructive lesions with intermittent or persistent clinical signs

More common in younger animals

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29
Q

What is very important when working up an animal with a suspected FB?

A

Taking a great history

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30
Q

How do you diagnose a gastric FB?

A

History and radiographs/US/endoscopy

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31
Q

How do you treat gastric FB?

A

Removal with endoscopy or surgery

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32
Q

What is a poor prognostic indicator for GDV?

A

Necrosis

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33
Q

What is the pathology associated with GDV?

A
  • Compression of CVC and hypovolemic shock
  • Gastric wall necrosis
  • Splenic torsion or avulsion
  • Congestion of abdominal viscera
  • Endotoxic shock
  • DIC
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34
Q

What things predispose animals to GDV?

A

Large breeds
Barrel chested breeds
Eats fast and plays right after
Mass in the abdomen (increased weight and torsion)

35
Q

What are some clinical signs of GDV?

A 
Acute, non-productive retching
Ptyalism
Abdominal distension with tympany
Collapse
Tachycardia with poor pulses
Hypothermia, depression, ventricular tachycardia
36
Q

What is the radiographic finding of a dog with GDV?

A

Right lateral boxing glove or popeye arm appearance

37
Q

How is GDV treated?

A
  • Agressive fluid therapy
  • Decompression via orogastric tube or trocharization
  • Address electrolyte disturbances
  • Surgery
38
Q

What is the mortality rate of GDV?

A

15-30%

More if gastric necrosis, resection, or splenectomy

39
Q

What is the long term therapy to prevent GDV?

A

Bloat bowl and rest after eating

40
Q

What is food bloat?

A

Severe distension of the stomach with food directly after eating

41
Q

How does an animal with food bloat typically present?

A

Acute vomiting or retching, abdominal distension and discomfort

Radiographs- profound distension of stomach with food

42
Q

How do you treat food bloat?

A 
Wait (24-36 hours)
Fluids
Withhold food
Frequent walking
Pain management
Consider lavaging and surgery
43
Q

What can gastric erosion and ulceration due to?

A
  • Mucosal barrier injury
  • Disruption of normal gastroprotection
  • Decrease blood flow
  • Hypersecretion of acid
  • Decreased mucous or bicarb
44
Q

What are erosions and ulcerations secondary to?

A 
Neoplasia (gastrinoma and mast cell)
Hypovolemic shock, hypotension
Trauma
Medication (NSAID or steroids)
Uremic gastritis
45
Q

What are some common findings in animals with erosions and ulcerations?

A

Vomiting, hematemesis, melena, anemia, increased BUN

Radiographs may show defects with contrast studies
Ultrasound may show thickened wall, loss of layering, or free fluid
Endoscopy will show visual confirmation

46
Q

How do you treat gastric erosions and ulcerations?

A 
Treat underlying disease
Suralfate
PPI
Pain management
Transfusion if severe anemia
Analgesia
47
Q

What are the characteristic of helicobacter?

A

Spiral gram negative bacteria

May be normal flora- pathogenicity associated with involvement of inflammatory gastric crypts

48
Q

How does helicobacter gastritis typically present?

A

Acute or chronic vomiting

49
Q

How do you definitively diagnose helicobacter gastritis?

A

Gastric biopsy showing mucosa infiltration with bacteria

50
Q

How do you treat helicobacter gastritis?

A

Clarithromycin, amoxi, metronidazole x2weeks

Resistance has been documented

51
Q

What is gastric pythiosis?

A

Infection with an oomycete (P. insidiosum) in the stomach

52
Q

How does gastric pythiosis typically present?

A

Chronic vomiting and a thickened gastric outflow tract

Characterized by pyogranulomatous inflammation

53
Q

What are the round worms that can be found in the stomach and how do you diagnose/treat them?

A

Toxocara canis/cati, physaloptera, ollulanus tricuspi

Visual or fecal diagnosis; biopsy

Fenbendazole or pyrantel

54
Q

How does gastric esophageal reflux present?

A

Chronic vomiting

Lip licking, hard swallowing, ptyalism, halitosis, esophagitis

55
Q

What is gastric esophageal reflux typically secondary to?

A

Primary gastric or small intestinal disease

56
Q

How is esophageal reflux diagnosed?

A

Clinical signs and history, can see mucosal erosion on endoscopy

57
Q

How do you treat esophageal reflux?

A

PPI, treatment of primary disease, sucralfate

58
Q

How does inflammatory gastritis present?

A

Chronic vomiting

59
Q

T/F: The inciting cause of inflammatory gastritis is rarely identified.

A

True

60
Q

How do you diagnose inflammatory gastritis?

A

Endoscopy or surgical biopsy

Infiltration of inflammatory cells in mucosa and lamina propria

61
Q

What is the most common infiltrate in inflammatory gastritis?

A

Lymphoplasmacytic

Eosinophilic and mast cells are also found

62
Q

How do you treat inflammatory gastritis?

A

Antacid and gastroprotectants
Diet trial
Empiric deworming
Immune modulation with corticosteroids or cyclosporine

63
Q

How does atrophic gastritis present?

A

Chronic vomiting

Mononuclear cell infiltrat with thinning of gastic mucosa and atrophy of gastric glands

64
Q

How do you treat atrophic gastritis?

A

Same as inflammatory disease

65
Q

What breed is predisposed to atrophic gastritis?

A

Norwegian lundehund

66
Q

How does hypertrophic gastropathy present?

A

Chronic projectile vomiting hours after eating

Diffuse or focal hypertrophy of mucosa and/or muscularis with inflammatory infiltrates

67
Q

What is hypertrophic gastritis associated with?

A

Hypergastrinemic conditions- decrease clearance from renal or liver disease or gastrin secreting tumors

68
Q

Where is hypertrophic gastritis typically most pronounced?

A

Pyloric outflow region

69
Q

What breeds is hypertrophic gastritis most commonly seen in?

A

Older small breed dogs

70
Q

How do you treat hypertrophic gastropathy?

A

Treat the underlying disease with surgical resection of thickened tissues if indicated

71
Q

What is pyloric stenosis?

A

Congenital or acquired muscular thickening of pyloric sphincter delaying gastric emptying

72
Q

What are the clinical signs of pyloric stenosis?

A

Vomiting several hours after a meal

Poor weight gain, aspiration pneumonia, depression, dehydration

73
Q

How do you treat pyloric stenosis?

A

Medical management of systemic effects (dehydration and acid-base)

Surgical correction (pyloromyotomy)

74
Q

What are come acquired causes of pyloric stenosis?

A

Inflammation and neoplasia

75
Q

What is a gastrinoma?

A

A tumor in the pancrease of the APUD cells that stimulates hypersecretion of gastric acid

76
Q

What are the clinical signs of a gastrinoma?

A

Chronic vomiting

Thickened gastric wall, hypertrophy of pylorus, gastric ulceration

77
Q

How do you diagnose a gastrinoma?

A

Assess gastrin levels- low pH of juice with a high gastrin level
Nuclear medicine studies
Biopsy

78
Q

How do you treat a gastrinoma?

A

Surgical removal but has often metastasized at time of diagnosis
PPI
Octreotide (inhibition of gastrin)

Guarded to poor prognosis

79
Q

What are the benign neoplasms found in the stomach?

A

Leiomyoma and adenomatous polyps

80
Q

What are the malignant neoplasms found in the stomach?

A

Adenocarcinoma
Lymphosarcoma
Leiomyosarcoma
Gastrinoma

81
Q

What is delayed gastric emptying motility disorders?

A

Any disorder that causes the stomach to not empty as fast as it should

aka GERD or bilious vomiting syndrome

82
Q

What is GERD typically due to?

A

Inflammation, infection, obstruction, electrolyte disturbances, opioids, or surgery

Diffuse gastritis/gastroenteritis, pancreatitis, NM disease, pylori stenosis, foreign body, idiopathic

83
Q

How long should a normal stomach take to be empty?

A

8 hours

Can take longer if stressed

84
Q

How do you treat GERD?

A

Gastric motility promoters

Cisapride, metoclopramide, erythromycin, ranitidine, lower protein and fat diets

SAM 2 (21 decks)

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