9.5.2: Gastric disease Flashcards

1
Q

Acute gastric disease differentials

A
  • Trauma (e.g. FB)
  • Toxin: dietary indiscretion, drugs
  • Inflammatory = acute gastritis: immune-mediated or infectious
  • Vascular: dilatation (+volvulus)
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2
Q

What are some possible causes of acute gastritis?

A

Acute gastritis may be immune-mediated or infectious.
Immune-mediated
* Dietary indiscretion
* Idiopathic (lymphocytic plamascytic / eosinophilic)

Infectious
* Bacterial e.g. helicobacter
* Viral (as part of gastroenteritis)
* Fungal unlikely
* Parasitic (part of gastroenteritis)
* Protozoal (part of gastroenteritis)

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3
Q

True/false: most cases of acute gastritis are self limiting.

How can you support these cases?

A

True

Treat these patients as follows:
* Time
* Reduce toxin exposure
* IVFT if necessary
* Anti-emetics e.g. maropitant
* Reduce acid damage: highly digestible diet. Specific medications probably not indicated at this stage.

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4
Q

Risk factors and diagnostics for acute gastritis caused by foreign body

A

Risk factors
* Scavenger
* Acute, severe vomiting
* Abdo pain or palpable obstruction

Diagnosis
* Plain/ contrast radiography
* Ultrasonography
* CT
* Endoscopy

Treat by removal!

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5
Q

Differentials for chronic (3+ week) gastric disease

A
  • Inflammatory: immune mediated or infectious
  • Neoplastic: lymphoma, carcinoma, benign e.g. polyp, gastrinoma
  • Metabolic: billous vomiting, gastric ulceration, secondary gastroparesis
  • Degenerative: chronic hypertrophic pyloric gastropathy, pyloric stenosis
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6
Q

Differentials for chronic gastritis

A

Immune mediated:
* Dietary indiscretion
* Idiopathic (lymphocytic plasmacytic / eosinophilic)

Infectious
* Bacterial: Helicobacter

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7
Q

What are the main diagnostics for chronic gastric disease?

A
  • Bloodwork - look for underlying cause - least invasive and expensive
  • Ultrasound
  • Plain/ contrast radiography
  • (CT)
  • Gastroscopy + biopsy - most invasive and expensive
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8
Q

Causes and treatment of gastroparesis

A

Causes
* May be primary and present with any other gastric disease
* May be secondary to hypokalaemia, hyper/hypocalcaemia, significant illness, opioid usage

Treatment
Prokinetics: metoclopramide / cisapride

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9
Q

Causes of mucosal barrier disruption

A
  • Usually a progression of acute to chronic gastritis (immune mediated or bacterial infection)
  • Metabolic diseases e.g. hepatic diseases, uraemia -> portal hypertension which backs up -> increased pressure / damage to gastric vasculature -> less mucus and bicarbonate produced
  • Reduced perfusion and prostaglandin production (e.g. NSAIDs, steroids, post-surgery)
  • Neoplasia: MCT, gastrinoma
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10
Q

When should you consider Helicobacter as a differential? What should you treat it with?

A
  • Consider if non-responsive to standard medications and diet
  • Pathogenicity is unclear in animals - in humans it causes chronic gastritis
  • In humans triple therapy: amoxiclav + metronidazole + proton pump inhibitor
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11
Q

Clinical signs of mucosal barrier disruption

A
  • Chronic vomiting
  • Haematemesis
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12
Q

Diagnostics and treatment for mucosal barrier disruption

A

Diagnostics
* Ultrasound - thickened gastric wall on ultrasound, reduced motility, lymphadenopathy
* Endoscopy - may look similar to gastric neoplasia, biopsy for definitive diagnosis

Treatment
* Symptomatic
* Diet / antibiotics / immunosuppressive

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13
Q

Detailed treatment plan for mucosal barrier disruption

A
  1. Treat underlying cause: hypoallergenic diet, antibiotics for Helicobacter, immunosuppressives for immune-mediated disease
  2. Reduce toxin exposure
  3. IVFT if needed
  4. Anti-emetics e.g. maropitant, (ondansetron, metoclopramide)
  5. Reduce acid secretion: highly digestible diet, proton pump inhibitors / H2 antagonists / antacids / synthetic prostaglandins / sucralfate
  6. Prokinetics e.g. cisapride, metoclopramide
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14
Q

What is the most effective way to stop acid production?

A

Proton pump inhibitors - they block the common pathway

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15
Q

1 and 2

A
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16
Q

3 and 4

A
17
Q

5 and 6

A
18
Q

7 and 8

A
19
Q

9 and 10

A
20
Q

What is the end point of chronic gastritis?

A

Gastric ulceration

21
Q

What conditions could lead to gastric ulceration?

A
  • Metabolic diseases e.g. uraemia, severe hepatic disease, hypoadrenocorticism
  • Reduced gastric perfusion e.g. NSAIDs, steroids, post-surgery
  • Neoplasia e.g. local, MCT, gastrinoma
22
Q

What should you consider if planning to take a biopsy from a case with gastric ulceration?

A

Be careful when you biopsy - could perforate!

23
Q

Clinical findings and diagnostics for gastric ulceration

A
24
Q

Clinical presentation and treatment of bilious vomiting

A
  • Very common, often in small dogs
  • Chronic intermittent bilious vomit
  • Typically occurs in early morning on an empty stomach - extended period of time without food
  • Usually responds to diet alteration: low fat, low fibre, frequent meals (early breakfast and meal before bed)
25
Q

Clinical sigs, diagnosis, treatment and prognosis of carcinoma

A
26
Q

Characteristics of gastrinoma

A
  • Rare neuroendocrine tumour in pancreas
  • Autonomous gastrin secretion
  • Ulceration/ erosion along the GIT
27
Q

Clinical signs, diagnostics, treatment and prognosis of lymphoma

A