Stomach Flashcards
Functional anatomy of the stomach
- 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
Typical clinical signs of gastric diseases
- vomiting - common, but not always
- hematemesis, melena
- anorexia
- abdominal pain
- distended abdomen
- diarrhea
- weight loss
List of gastric diseases (7)
- 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
Acute gastritis. Aetiology
- most common gastric disease
- typically caused by infectious diseases or eating abnormal things (spoiled/contaminated food, foreign objects, toxic agents)
Acute gastritis. Clinical signs
- acute onset of repeated vomiting
- more common in dogs than cats due to eating habits
- loss of appetite
- rarely fever or abdominal pain
Acute gastritis. Diagnosis
- 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
Acute gastritis. Treatment and prognosis
- 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
Gastric ulceration. Severity
- more severe than acute gastritis, can be life-threatening
Gastric ulceration. Physiology of gastric mucosal barrier
- 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
Gastric ulceration. Predisposing factors
- 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
NSAIDs as predisposing factor for gastric ulceration
- most common cause
- direct mucosal damage, inhibition of PGs synthesis
- aspirin, phenylbutazone, ketoprofen, flunixin, ibuprofen, naproxen, COX-2 inhibitors too
Hydrochloric acid production. Physiology
What metabolic diseases can be predisposing factor to gastric ulceration ?
- 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
Corticosteroids as predisposing factor for gastric ulceration
- 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
Summary of predisposing factors of gastric ulcers
- 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
Gastric ulceration. Clinical signs
- 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
Gastric haemorrhage in gastric ulceration. This condition can happen even after 1 pill of human NSAIDs
Healing gastric ulcers
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
Gastric ulceration. Treatment
- 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
Chronic gastritis. General info
- 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
Chronic gastritis. Symptoms
- intermittent vomiting
- no response to symptomatic treatment
- change of appetite ( more or less)
- weight loss
- abdominal pain
Chronic gastritis. Diagnosis
- endoscopy biopsy + HISTOPATHOLOGY
- lab tests are not specific and not sensitive
- x-rays, USG are not specific and not sensitive
Chronic gastritis Specific causes.
- Helicobacter-associated gastritis
- parasitic gastritis
- dietary antigens
- foreign material (e.g. sand contaminated food)
- fungal origin (Pythiosis, Histoplasmosis)
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
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)
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
Treatment of idiopathic chronic gastritis
after exclusion all other possible causes (elimination diet, anti parasitic treatment, helicobacter elimination therapy)
- immunosuppressive therapy
- antacids, protectants, prokinetics
-
Immunosuppressive therapy
Dog: prednisolone -> azathioprine, cyclosporine
Cat: prednisolone -> chlorambucil
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)
Delayed gastric emptying. Aetiology
- Obstruction in the pylorus (complete <-> partial): USG, endoscopy
- Motility disorders without obstruction: on the basis of the exclusion of obstruction
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
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
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)
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
