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Small Animal Medicine > Gastro - Diseases of the Stomach > Flashcards

Gastro - Diseases of the Stomach Flashcards

1
Q

What are gastric ulcers?

A

deep disruption of gastric mucosa down to the muscularis

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2
Q

What is a gastric erosion?

A

A superficial disruption of the gastric mucosa

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3
Q

What do the parietal cells of the stomach produce? What do their receptors respond to?

A

Hydrochloric acid

Respond to gastrin, Ach, and histamine

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4
Q

What is H+ role in gastric ulcers/erosions?

A

There is some type of disruption in the gastric mucosal barrier leading to a back-diffusion of H+ which ultimately the accumulation causes damage

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5
Q

What clinical signs are associated with gastric ulcers/erosions?

A

vomiting, hematemesis, abdominal pain (tucked up abdomen), melena, inappetance, anorexia, and ptyalism (over salivation)

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6
Q

What is found on PE in patients with gastric ulcers/erosions?

A

Pain on abdominal palpation, pale mm, melena on rectal exam

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7
Q

What can cause gastric ulcers/erosions?

A

Drugs, mucosal ischemia, CNS disease, renal disease, liver disease, and mucosal inflammation

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8
Q

What drugs can cause gastric ulcers/erosions?

A

NSAIDs and glucocorticoids

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9
Q

What diagnostic tests can be used for gastric ulcers/erosions?

A

Rectal exam for melena, CBC, biochemistry, urinalysis, diagnostic imaging, and GI endoscopy

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10
Q

What CBC abnormalities are associated with gastric ulcers/erosions?

A

anemia +/- regeneration

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11
Q

What will a high BUN on a patient with a suspected gastric ulcer/erosion indicate?

A

it may suggest GI hemorrhage

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12
Q

What are the treatment goals for gastric ulcers/erosion?

A

Correct the disease (GI or extra GI), give fluid/electrolytes, monitor the GI bleeding, decrease gastric secretions, and increase cytoprotection

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13
Q

What drugs are histamine H2 antagonists?

A

Cimetidine, ranitidine, and famotidine

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14
Q

What do histamine H2 antagonists do?

A

inhibit acid secretion on parietal cells

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15
Q

Histamine H2 antagonists have some efficacy against gastric ulcers/erosions, but what drugs are the best?

A

proton pump inhibitors (PPI)

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16
Q

What is the duration of action of famotidine?

A

48 hours

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17
Q

Which histamine H2 antagonist has prokinetic action?

A

ranitidine

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18
Q

What histamine H2 antagonist has the least hepatic inhibition? the greatest?

A

Least inhibition - famotidine

Greatest inhibition - cimetidine

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19
Q

What is sucralfate?

A

a cytoprotective drug

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20
Q

Why is reflux a problem?

A

because there are irritative agents in the reflux

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21
Q

What does sucralfate do?

A

Provides mucosal protection, inactivates pepsins, and promotes PGE

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22
Q

What disease processes is sucralfate effective in?

A

esophagitis, gastritis, and duodenitis

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23
Q

Why would you want to stagger sucralfate doses when using it with concurrent drugs?

A

because it may inhibit absorption

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24
Q

What drugs are proton-pump inhibitors?

A

Omeprazole (PO) and pantoprazole (IV)

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25
Q

What do proton-pump inhibitors do?

A

Inhibit H/K ATPase pump which reduces gastric volume/acidity

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26
Q

What is one major reason that proton-pump inhibitors are superior to H2 blockers?

A

because it is rare for them to have adverse effects

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27
Q

What disease processes should proton-pump inhibitors be your first chioce?

A

esophagitis or gastritis

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28
Q

What do mucosal PGE’s do?

A

Decreases H secretion, increases gastric blood flow, increases HCO3 production, and increases mucus secretion

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29
Q

What is the prostaglandin E1 analogue that is the drug of choice in cases of NSAID induced gastritis?

A

Misoprostil

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30
Q

Generally, how long is therapy for gastric ulcers/erosions?

A

14-21 days

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31
Q

What can cause delayed gastric emptying?

A

pyloric outflow obstruction or gastric hypomotility

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32
Q

What is the primary sign of delayed gastric emptying?

A

post prandial vomiting >8-10 hours after a meal

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33
Q

How is delayed gastric emptying diagnosed?

A

based on history, radiology, and gastroscopy

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34
Q

What will you see on contrast radiographs in a patient with delayed gastric emptying?

A

There will be filling defects

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35
Q

What is gastric dilation-volvulus (GDV)?

A

rotation of the stomach on its mesenteric axis with gastric distension

36
Q

What breeds have a higher incidence of GDV?

A

giant and deep-chested breeds

37
Q

What historical signs are associated with GDV?

A

acute onset of abdominal distention, retching/vomiting and collapse

38
Q

What PE findings are associated with GDV?

A

Lethargy, abdominal distension, shock, +/- gastric intubation, increased abdominal girth, retching, ptyalism, increased respiratory effort, and poor circulation

39
Q

What risk factors lead to GDV?

A

Deep chested, increased H:W ratio, increase in swallowed air, and decreased gastric emptying

40
Q

What pathophysiologic changes does GDV cause?

A

Gastric distension, poor perfusion due to reduced CO, gastric mucosal ischemia, DIC due to vascular sludging, genesis of cardiac arrhythmias, and progressive respiratory depression

41
Q

True or False: Passing a stomach tube rules out GDV

A

false

42
Q

How is GDV diagnosed?

A

History, PE, and radiograph (confirms)

43
Q

What will a radiograph show in a patient with GDV?

A

abnormal pyloric location and a double bubble appearance

44
Q

What will CBC/biochemistry show in a patient with GDV?

A

Increased hematocrit (PCV), hypokalemia, and variable acid-base (acidosis usually)

45
Q

What radiographic view should you always take when you suspect GDV?

A

right lateral view

46
Q

How is a simple dilation managed?

A

Decompress the stomach with a stomach tube, +/- a gastric lavage, prokinetics to increase emptying, and observe for progression to GDV

47
Q

What are the three major goals of therapy for GDV?

A

Gastric decompression, correction of metabolic and systemic abnormalities, and anatomic repositioning

48
Q

If the lactate is less than 6, what is the chance of survival?

A

99% chance of survival

49
Q

What is the procedure for anatomic relocation in GDV cases?

A

resection/gastropexy

50
Q

What type of IV line is best for GDV treatment?

A

central IV line

51
Q

Is fluid therapy needed for GDV cases?

A

yes - aggressive fluid therapy

52
Q

When would you use bicarbonate in GDV cases?

A

if the patient is acidotic

53
Q

When would you use antibiotics in GDV cases?

A

If the patient is septic or if there is a GI perforation

54
Q

What would you use to treat for an arrhythmia or tachycardia in GDV cases?

A

Lidocaine and/or sotalol

55
Q

What GDV risk factors are associated with mortality?

A

Delayed diagnosis, gastric necrosis, splenectomy, multiform PVC’s, large resection, and if the lactate is greater than 6mmol

56
Q

With surgery, what is the percentage of mortality?

A

15%

57
Q

There is a higher mortality rate if what happens?

A

gastric necrosis, perforation, or a splenectomy

58
Q

What therapy is important to improve a patients prognosis?

A

nutritional therapy

59
Q

What is the nutritional therapy recommended for GDV patients?

A

Fentanyl for pain management, small frequent feedings but no dry kibble, and prokinetics to empty the stomach

60
Q

What are the three most common causes of intestinal obstruction?

A

foreign bodies, intussusception/volvulus/torsion, and intestinal neoplasia

61
Q

Aside from the most common causes of intestinal obstruction, what else can cause it?

A

bowel incarceration, adhesions or strictures, and intramural lesions

62
Q

What is the most common type of intestinal obstruction?

A

simple obstruction

63
Q

What is occluded in a simple intestinal obstruction?

A

the lumen only

64
Q

What happens to the vasculature in simple intestinal obstructions?

A

it remains intact

65
Q

Where does distension occur in simple intestinal obstructions?

A

proximal to the obstruction

66
Q

A strangulation obstruction is characterized by _________ vasculature.

A

compromised

67
Q

What are the most common causes of strangulation obstructions?

A

volvulus, hernia, torsion, and intussusception

68
Q

Where does intussusception typically occur?

A

Ileocolic and cecocolic junctions

69
Q

Ileocolic and cecocolic intussusception is most common in dogs of what age?

A

dogs less than 3 months old

70
Q

What clinical signs are seen with ileocolic and cecocolic intussussception?

A

tenesmus, fresh blood, and vomiting

71
Q

How will intussusception appear on radiographs?

A

dilated bowl loops

72
Q

How will intussusception appear on ultrasound?

A

There will be classic target lesions

73
Q

How is intussusception treated?

A

resection/reduction +/- gut plication

74
Q

What common clinical signs are associated with obstruction?

A

acute vomiting, anorexia, and depression predominate

75
Q

What other systemic signs may patients with obstruction have?

A

dehydration, diarrhea, pain, and abdominal distension

76
Q

What is the classic cause of proximal obstruction?

A

foreign body

77
Q

When will the onset of clinical signs begin with proximal obstruction and what are they?

A

Acute; intense clinical signs, severe vomiting and dehydration

78
Q

Is distal obstruction acute or chronic?

A

chronic

79
Q

What clinical signs are associated with distal obstruction?

A

vague, intermittent signs

80
Q

What lesions is distal obstruction seen with?

A

intestinal mass lesions

81
Q

How is obstruction diagnosed?

A

abdominal palpation and radiographs

82
Q

What will intussusception feel like on abdominal palpation?

A

a sausage-like structure

83
Q

What will you see on a radiograph as evidence of obstruction?

A

gas or fluid distension - luminal opacity

Plication with linear foreign body

84
Q

If there is a perforation due to obstruction, what procedure would you want to do?

A

abdominocentesis

85
Q

If there is an esophageal or gastric foreign body, what diagnostic procedure would you want to do?

A

GI endoscopy

Small Animal Medicine (100 decks)

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