Stomach Flashcards
(35 cards)
1
Q
Functional anatomy of the stomach
A
- Lower oesophageal sphincter/cardia
allows entry of ingests + prevents reflux - Fundus
volume accommodation during gastric filling + digestion - Body
stores ingest a + digestion - Antrum
grinds food into smaller particles + digestion - Pylorus
limits the size of food + prevents duodenal reflux
2
Q
Typical clinical signs of gastric diseases
A
- vomiting - common, but not always
- hematemesis, melena
- anorexia
- abdominal pain
- distended abdomen
- diarrhea
- weight loss
3
Q
List of gastric diseases (7)
A
- Acute gastritis
- Gastric ulcer
- Chronic gastritis
- Gastric foreign body
- Delayed gastric emptying (pyloric obstruction and gastric motility disorders)
- Gastric dilatation-volvulus syndrome (GDV)
- Gastric neoplasia
4
Q
Acute gastritis. Aetiology
A
- most common gastric disease
- typically caused by infectious diseases or eating abnormal things (spoiled/contaminated food, foreign objects, toxic agents)
5
Q
Acute gastritis. Clinical signs
A
- acute onset of repeated vomiting
- more common in dogs than cats due to eating habits
- loss of appetite
- rarely fever or abdominal pain
6
Q
Acute gastritis. Diagnosis
A
- by exclusion: good anamnesis, physical examination
- usually gastritis is a self-limiting problem, not life-threatening but it’s very important to exclude life-threatening disorders with similar clinical signs (!)
- DD: parvo (!), ethylene-glycol toxicosis (!), foreign body, diabetic ketoacidosis, uraemia, hypoadrenocorticism, hepatic failure, pancreatitis, hypercalcemia
- ## if condition worsens in 1-3 days —> abdominal US, plain and contrast radiography, blood work
7
Q
Acute gastritis. Treatment and prognosis
A
- symptomatic treatment
- withdrawing food for max 24h, GI diet
- short-term application antiemetics
- fluid therapy in severe vomiting and dehydration
- problem is self-limiting problem and excellent prognosis
8
Q
Gastric ulceration. Severity
A
- more severe than acute gastritis, can be life-threatening
9
Q
Gastric ulceration. Physiology of gastric mucosal barrier
A
- thick MUCUS-BICARBONATE LAYER: a lubricant to prevent mechanical damage (physical and chemical protection)
- underlying GLYCOPROTEIN GEL: traps bicarbonate to maintain surface pH above 6
- gastric EPITHELIAL CELLS: low permeability, ability to rapidly repair, migrate over the defect within a few hours
- SUBMUCOSAL CAPILLARIES: supply oxygen, nutrients
- PROSTAGLANDIN E: produced by GI mucosa, regulates mucus and bicarbonate production, mucosal blood flow, promotes epithelial cells growth and inhibits acid secretion
10
Q
Gastric ulceration. Predisposing factors
A
- NSAIDs: most common cause
- Corticosteroids
- Many metabolic diseases
- Altered gastric flow, stress related factors: hypotension, shock, sepsis, surgery, spinal cord disease, GDV
- Increased secretion of gastric acid: pancreatic gastrin-secreting tumour, mast cell tumour, pyloric outflow obstruction, chronic gastric dilation
- Toxic traumatic agents: bile salts, pancreatic enzymes, lead, foreign bodies, alcohol
- Gastric neoplasia
11
Q
NSAIDs as predisposing factor for gastric ulceration
A
- most common cause
- direct mucosal damage, inhibition of PGs synthesis
- aspirin, phenylbutazone, ketoprofen, flunixin, ibuprofen, naproxen, COX-2 inhibitors too
12
Q
Hydrochloric acid production. Physiology
A
13
Q
What metabolic diseases can be predisposing factor to gastric ulceration ?
A
- liver failure: serum bile acids increase -> gastrin secretion increases -> acid production increases
- hypoadrenocorticism: hypotension, loss of vascular tone
- renal failure: uremic toxins, decreased gastrin metabolism
- acute pancreatitis, IBD, neurological disease
14
Q
Corticosteroids as predisposing factor for gastric ulceration
A
- less ulcerative than NSAIDs
- decrease mucosal cell growth, mucus production
- increase gastric acid secretion
- high-dose, long term, associated with other risk factors
- dexamethasone > prednisone
15
Q
Summary of predisposing factors of gastric ulcers
A
- common usage of NSAIDs
- corticosteroids alone are usually NOT ulcerogenic
- metabolic diseases predispose to GEU, especially chronic liver, kidney diseases and hypoadrenocorticism
- all critically ill patients (severe trauma, major surgery, organ failure, sepsis) should be considered for development of ulcers
16
Q
Gastric ulceration. Clinical signs
A
- intermittent vomiting: variable hematemesis or melena
- physical exam: often normal, anemia, abdominal pain, melena
- lab tests: anaemia; renal failure, liver disease, hypoadrenocorticism (if metabolic background)
- X-ray: usually normal, abnormalities can be noticed in case of perforation
- endoscopy: erosions, ulcers, biopsy is needed - key diagnostic step
17
Q
A
Gastric haemorrhage in gastric ulceration. This condition can happen even after 1 pill of human NSAIDs
18
Q
A
Healing gastric ulcers
19
Q
A
Huge ulcer with thick margin and blood clot in the centre. Seems to be a adenocarcinoma. Biopsy needs to be taken BUT NEVER FROM THE CENTRE BECAUSE IT CAN CAUSE PERFORATION
20
Q
Gastric ulceration. Treatment
A
- elimination of predisposing causes
- symptomatic-supportive therapy: diet, fluid, antiemetics, antacids (PPI), protectants, painkillers (opioids)
- blood transfusion: in case if severe anaemia
- surgical treatment: if uncontrolled hemorrhage or perforation is suspected
21
Q
Chronic gastritis. General info
A
- very common
- diagnosis is difficult and treatment is very difficult
- more common in dogs
- many many causes in the background: usually eating something abnormal, idiopathic or specific causes
22
Q
Chronic gastritis. Symptoms
A
- intermittent vomiting
- no response to symptomatic treatment
- change of appetite ( more or less)
- weight loss
- abdominal pain
23
Q
Chronic gastritis. Diagnosis
A
- endoscopy biopsy + HISTOPATHOLOGY
- lab tests are not specific and not sensitive
- x-rays, USG are not specific and not sensitive
24
Q
Chronic gastritis Specific causes.
A
- Helicobacter-associated gastritis
- parasitic gastritis
- dietary antigens
- foreign material (e.g. sand contaminated food)
- fungal origin (Pythiosis, Histoplasmosis)
25
Histologic classification of chronic gastritis (can be helpful to narrow the list of possible backgrounds)
- **lymphocytic-plasmacystic**: very common, therefore not very informative
Helicobacter-associated gastritis (esp cats), immune response to dietary antigens, idiopathic
DD: lymphoma
- **eosinophilic**
hypersensitivity to food/ immune response to parasites/ foreign materials/ mast cell tumour, idiopathic
- **granulomatous**: rare
chronic infections, immune response
- **atrophic gastritis**: severe form with glandular atrophy and fibrosis, irreversible, leads to life-long to dyspepsia
- **hypertrophic gastritis**: rare, idiopathic or can be due to long term PPI therapy
26
Helicobacter-associated gastritis
- in human: helicobacter pylori: pathogenic bacteria causing gastritis, ulcers, tumours. But not in pets
- DOG and CAT: facultative pathogen, found in healthy animals
- diagnosis: prove gastritis (histopath) -> find helicobacter -> RULE OUT other possible causes -> treatment of helicobacter-associated gastritis
- treatment: AB (amoxicillin + metronidazole) and PPI for 2 weeks and bismuth salts for 6 weeks
- recurrence of infection after treatment is common
- if patient doesn’t feel better after this treatment, we need to consider idiopathic form (immunosuppressive therapy)
27
Parasitic gastritis
- rare but even 1 worm can cause symptoms
- **Physaloptera rara**: dog
- **Ollulanus tricuspis**: cat
- diagnosis: endoscopy (1-4 cm long nematodes in the fundus); fecal flotation is difficult
- treatment will kill them easily: pyrantel in dogs, fenbendazolein cats
28
Treatment of idiopathic chronic gastritis
after exclusion all other possible causes (elimination diet, anti parasitic treatment, helicobacter elimination therapy)
- **immunosuppressive therapy**
- antacids, protectants, prokinetics
-
29
Immunosuppressive therapy
Dog: prednisolone -> azathioprine, cyclosporine
Cat: prednisolone -> chlorambucil
30
Gastric foreign body
- can be both acute (obstruction) and chronic
- **vomiting**
- often diagnosed accidentally (if owner hasn’t seen)
- if we know there is a foreign body -> **endoscopy**
- treatment: endoscopic removal/surgery
- important that it can be both cause and consequence of gastric disorder (for example pica develops due to gastritis that leads to having foreign body)
31
Delayed gastric emptying. Aetiology
1. Obstruction in the pylorus (complete <-> partial): USG, endoscopy
2. Motility disorders without obstruction: on the basis of the exclusion of obstruction
32
Delayed gastric emptying. History and diagnosis
- history: vomiting after more than 8-10h of eating
- visual diagnostics is helpful but not necessary for suspecting delayed gastric emptying (based on anamnesis)
- if during endoscopy of **fasted** animal we can see undigested food in the stomach —> delayed gastric emptying —> checking pylorus for obstruction
33
Pyloric stenosis. Diagnosis
CONGENITAL: small breeds or brachyocephalic
ACQUIRED: hypertrophy of mucosal and/or muscular layer
Diagnosis:
- **projectile vomiting**: 6-8 h after eating
- x-ray: contrast study
- endoscopy!
Treatment: **surgery**
34
Primary (idiopathic) gastric motility disorders
- clin signs: discomfort, bloating, chronic vomiting, signs of GOR
- d: elimination of obstructive and metabolic causes
- treatment: diet (frequent, liquid, low-fat, GI diet) + prokinetics (cisapride, pricalopride, metoclopramide, ranitidine, mirtazapine)
35
Gastric neoplasia
- low incidence in pets
- usually malignant: lymphoma (cats), adenocarcinoma (dogs)
- chronic vomiting, weight loss
- thickened mucous in endoscopy !!
- d: histopath!
- treatment: surgery (adenocarcinoma) + chemotherapy
- prognosis is guarded
