Gastric Disease in Dogs and Cats Flashcards
(57 cards)
1
Q
Name 5 causes of sudden onset vomiting (6)
A
- Diet
- Change
- Scavenging
- Foreign body
- Drug side effects
- Toxins
- Systemic disease
- Infection
2
Q
Why are dogs and cats normally resistant to bacterial gastritis?
A
- Stomach is a tough holding tank which hold onto everything until it has been ground to allow it to pass on. FB can escape this
- Barrier to infection & colonisation of SI
- Sterile environment
3
Q
When do problems arise with bacterial gastritis? (2)
A
- Neonates
- Abnormal gastric environment
- Food related
- Antacids
4
Q
Discuss what you think might be happening here
A
Lumpy stomach – Think it is worrying like a lymphoma
Was just IBD which had quite an eosinophilic
Biopsies are the best to enable good treatment
5
Q
How do we describe the pathology of chronic gastritis? (6)
A
- Cell infiltrates, What is predominate? Is it a mix? – help tell us the underlying cause
- Eosinophilic – weird hypersensitivity or idiopathic
- Lymphocytic
- Plasmacytic
- Granulomatous
- Mixed
- Atrophic/hypertrophic
- Fibrotic
- Oedematous
- Metaplastic
- Ulcerative
6
Q
What cause of chronic gastritis are we most worried about in humans? But think it has no relevance in dogs these days
A
•Helicobacter spp
7
Q
Benign helicobacter is a common finding in dogs and cats. What may it be associted with (3)
A
- Gastric gland degeneration
- Mononuclear cell infiltrates
- Lymphoid hyperplasia
8
Q
What is malignant helicobacter associated with in people? (5)
A
- Chronic inflammation
- Immune response
- Gastric ulceration
- Malignant transformation
- In people has a link to a gastric ulcer
9
Q
Where is a common site of a gastric ulcer?
A
Lesser curvature
10
Q
What can be seen?
A
Ulcer on the lesser curvature of stomach
= common site of ulcers in dogs
Can also be associated with gastric disease
11
Q
Why does stomach acid not normally cause ulceration in the stomach? (4)
A
- Tight intercellular junctions (barrier function)
- Mucus layer
- Bicarbonate rich in a healthy stomach prevents against ulcers
- Local prostaglandins (PG E2) controlling
- Mucosal blood flow
- Bicarbonate production
- Mucus
- Rapid epithelial repair
- Constant repair – susceptible to damage with chemo. High turnover system
12
Q
What would your worry be here?
A
This ulcer is small but has a deep crater.
If you get through this wall – perforation is an accident waiting to happen
13
Q
What are the 3 general causes in a failure of the mucosal barrier?
A
- Acid hypersecretion
- Direct physical injury
- Reduction in PG E2
- Cox inhibitors
- NSAIDs
- Cox inhibitors
14
Q
Define benign
A
Not malignant/neoplastic. Can still be life threatening
15
Q
What is the benign cause of iatrogenic gastric ulcers?
A
- Drugs - NSAIDs
- Drug combos - NSAIDs and steroids
16
Q
What is the worst case scenario of NSAID ulcers?
A
- Severe GI haemorrhage from the ulcer itself eroding through
- = Debilitated patient
- Then get gastric or duodenal perforation
- Leading on to Septic peritonitis
- Almost always means Death
- Leading on to Septic peritonitis
- Then get gastric or duodenal perforation
- = Debilitated patient
17
Q
Name 3 benign metabolic/endocrine causes of gastric ulcers (4)
A
- Hypoadrenocorticism
- Azotaemia
- CKD
- AKI
- Liver disease +/- portal hypertension
- Perfusion related?
- More likely duodenal ulcerations
- (Mast cell tumours anywhere)
- Aggressive anywhere which degranulates which produce histamine and then can cause ulcer
18
Q
Other than metablic, name 3 benign causes of gastric ulcers (4)
A
- Inflammatory bowel disease complication
- Shock, sepsis, hypotension (ie perfusion related)
- Stress
- surgery?
- high performance athletes?
- Idiopathic
19
Q
What is this?
A
Cat with GI lymphoma
20
Q
Name 2 malignant causes of gastric ulcers (3)
A
- 1ry gastric neoplasia
- Carcinoma/adenocarcinoma
- Lymphoma
- Leiomyoma
- Tends to be a benign tumour
- Gastrinoma
- Gastrin producing tumour in the pancreas
- Mast cell tumours
- Degranulation causes histamine release
- Ulcerogenic
21
Q
What is this?
A
Polypoid mass close to pylorus
22
Q
Name physical causes of gastric ulceration (6)
A
- Foreign body
- +/- Gastritis
- +/- Ulceration
- Obstruction?
- Perforation?
- Less common than in the intestine as the gastric wall Is pretty tough – so rare to do
- Mass lesions causing outflow obstruction
- Neoplastic
- Inflammatory
- Granuloma
- Polyp
- Gastric dilation +/- volvulus
- Hypertrophic gastritis
- outflow tract obstruction
- breed related
- brachycephalics
- Congenital pyloric stenosis
- Possibly “extra gastric” mass lesions
23
Q
With gastric motility disorders, what is stasis often associated with? (4)
A
- Chronic gastritis/IBD
- Gastric ulceration
- Infiltrating neoplasia e.g. lymphoma
- Pancreatitis
24
Q
Name 4 metabolic causes of gastric stasis (5)
A
- Hypokalaemia
- Hyper/ hypocalcaemia
- Acidosis
- Encephalopathy
- Post viral
25
Name 5 functional causes casing delayed gastric emptying (6)
* Post op
* Local inflammation
* Drug related
* opioids
* Pain, anxiety, fear
* Dysautonomia
* High fat diet
26
Name 5 neoplasms of gastric disease (6)
* Carcinoma
* breed & sex predisposition in dogs?
* Lymphoma
* GI lymphoma common in cats
* Leiomyoma
* Leiomyosarcoma
* Fibrosarcoma
* Carcinoid tumours
27
What is the signalment for gastric carcinomas?
Age? Sex? Breed?
Median 10 years
Males
Belgian shpeherd dogs
28
What are the 3 common clinical signs of a gastric carcinoma?
* vomiting
* anorexia
* weight loss
29
What is this?
Gastric lymphoma
30
What is seen in Bilious vomiting syndrome and when?
* chronic intermittent bilious vomit
* typically early morning on an empty stomach
31
Name the clinical signs of gastric disease
* vomiting
* salivation
* burping
* retching
* reflux/gulping
* poor appetite
* melaena
* weight loss
* halitosis
* abdominal pain
* bloating/distension
32
What is this?
Gastric dilation & volvulus
33
Is gastric ulcer more common in dogs or cats?
What are the clinical signs?
Dogs :
## Footnote
* poor appetite
* salivation
* abdominal pain
* haematemesis
* melaena
* weight loss
* anaemia
* underlying primary disease
34
What screening tests can we do for gastric disease?
Blood and urine tests
35
What is this?
Healing gastric ulcer
On the lesser curvature
Biopsy around the EDGE do not want to poke biopsy forceps through
36
What is seen in a pylotic outflor tract obstruction and how can we test?
* Vomiting 6-8 hours after food
* Bloods can be a useful indicator….
* Hypochloraemia
* Hypokalaemia
* Metabolic alkalosis?
* (Metabolic acidosis?)
* Distended food filled stomach on plain abdominal radiographs
37
What diagnostic imaging can we do to investigate gastric disease?
* radiography
* positional radiography
* contrast radiography
* transit times?
* retention of barium?
* filling defects
* ultrasound
* gastric motility?
* wall thickening
* focal?
* diffuse?
* layering?
* endoscopy
38
What can be seen in these images?
Both have evidence of delayed gastric emptying – fluid filled stomach
Right lateral recumbent – pylorus full
In stomach position – so think air and fluid distended
39
What can be seen?
Pyloric outflow obstruction
## Footnote
Thick hypertrophic gastric wall at the outflow of the stomach
Intricate surgery needed
= a form of gastritis à hypertrophic gastritis
40
How long do we fast a patient for endoscope?
12-24 hours
41
Why do we need to be careful when biopsying an ulcer? (2)
* Perforation
* Non diagnostic samples
42
How might we procide supportive care or gastric disease? (4)
* Self limiting disease
* Dietary management
* Low fat
* Diet trial for food intolerance/allergy?
* Single source protein
* Single source CHO
* Novel protein?
* Hydrolysed protein?
* Anti emetic
43
What fluid therapy considerations do we need to have?
* Based on history & physical examination
* Route of administration
* What to give?
* Usually isotonic crystalloid
* Hartmanns
* 0.9% saline
* What rate?
* Bolus or constant rate
* +/- Potassium
44
When is sucralfate given? How does it work?
Polyaluminium sucrose sulphate
* Given before and after feeding
* 2 hours after other drugs due to interactions
* Binds to tissue to create a barrier effect
* Sucrose released from AlOH – binds exudate
* Stimulates PG production and improves mucosal blood flow
45
When are antacids given? (3)
* Gastric ulceration
* Chronic gastritis
* Reflux oesophagitis
46
How do antacids work? Name examples.
* Proton pump inhibitor
* Omeprazole
* H + /K + atpase inhibitors
* Probably the single most useful antacids – increase pH of the stomach
* H2 blocker – used to use a lot of these. Some are still used but omeprazole is the go to
* Ranitidine
* Also has a role as prokinetic? Increase gastric motility
* Cimetidine
* Famotidine
47
What is aluminium hydroxide useed for and how does it work?
* Uraemic gastritis
* Phosphate binder
* Not always palatable
* High doses required
48
What can diet trials be used for? What is diagnosis based on?
Chronic gastritis/IBD
Based o ruling out other disease and response to diet trial
49
Corticosteroids:
A) What is it used for?
B) When do we use?
C) What must justify the use?
A) Chronic gastritis/IBD
B) No response to Diet or +/- gastroprotectants
C) Severity o clinical signs justifies side effects
50
What 3 concurrent diseases are common in cats?
* GI disease
* Cholangiohepatitis
* Pancreatitis
51
When may surgical intervention be the best option? (4)
* Pyloric outflow obstruction
* Foreign bodies if can’t be retrieved by endoscopy
* Perforated ulcers
* Tumour resection
52
What is this?
Hiatal hernia
53
How do you diagnose a gastrinoma?
* histopath?
* gastrin levels high in face of low gastric fluid pH
54
What is a gastrinoma and what is seen?
* rare neuroendocrine tumour in pancreas
* autonomous gastrin secretion
* HCl hypersecretion
* persistent vomiting
* ulceration/erosion
* duodenum
* stomach
* oesophagus
* antral hypertrophy
* outflow tract obstruction
55
How to COX inhibitors work? What are the effects?
* COX enzyme inhibitors
* prevent production of prostaglandins and thromboxanes from cell membrane phospholipids
* anti inflammatory effect: decrease PG E2 and PGF2α
* reduced platelet aggregation and adhesiveness: decrease thromboxane
* anti pyretic effect: inhibit production of centrally produced PGs
56
What is the major concern for NSAIDs?
PG inhibition adversely affects GI blood flow and reduces HCO3 and mucus production
57
Name 3 prokinetics and the effect?
* Metoclopramide
* Anti emetic
* Anti dopaminergic and cholinergic (upper GIT)
* Erythromycin
* Releases motilin and has some emetic effects
* Ranitidine
* Anticholinesterase effects
