Stomach Flashcards
Which stomach of Ru is most closely related to the simple-stomached animals in terms of structure & function?
abomasum
(third compartment of new world camelids)
What is the structure of the fundic part of the stomach?
- fundic mucosa is lined by numerous folds & produces HCl acid (parietal cells) & pepsinogen (chief cells)
What is the structure of the pyloric part of the stomach?
- lined by epithelium w/ mucous-secreting glands.
What is the structure of the esophageal part of the stomach in some species?
in Eq, Sw, & Rat, the esophageal part (pars esophagea) is nonglandular & lined by stratified squamous epithelium
What is the dividing line btwn the nonglandular and the glandular epithelium in the horse?
margo plicatus
What are the steps of a postmortem examination of the stomach/abomasum?
- open along the greater curvature & gently scrape away ingesta to examine mucosa, do not wash w/ water
- examine the quality & quantity of the gastric contents & remove them
- examine the gastric mucosa, in particular the colour, thickness, & integrity of the mucosal surfaces
- examine the content for presence of blood (if needed to perform occult blood test)
- always take fundic mucosa for histo, plus obviously pathologic changes
- If Haemonchosis is suspected, first tie off pylorus & cardia to collect content for worm count, & then open the abomasum in a bucket/tray
Who does simple gastric dilation occur in?
- a variety of animals including primates
Explain gastric dilation & volvulus in Dogs?
- in large, deep-chested breeds of dogs, distended stomach w/ food & gas can rotate on mesenteric axis counter clockwise (180, 270, or 360 degrees when the abdomen is viewed from the dorsal aspect), resulting in a gastric volvulus w/ an obstructed esophagus that prevents eructation & thus further contributes to gastric dilation
- the spleen, attached to the stomach by the gastrosplenic ligament, rotates w/ the stomach & is thus folded back upon itself & located in the R cranial abdomen against the diaphragm
- both gastric & splenic vein are compressed, resulting in a congested & edematous gastric wall (venous infarction in later stages) & congested spleen, b/c the arterial blood supply remains patent longer than venous drainage
What are predisposing factors to gastric dilation & volvulus in dogs?
- hereditary predisposition (large breeds)
- obstruction of the cardia that prevents eructation & emesis
- obstruction of the pylorus that prevents passage of gastric contents
- repeated episodes of gastric dilation, overfeeding, &/or postprandial exercise, that contribute to stretching & relaxation of the gastrohepatic ligament
What is the cause of death w/ gastric dilation & volvulus in dogs?
- acid-base imbalance
- increased intragastric pressure interferes w/ venous return from portal circulation
- myocardial depressant factors released from pancreas
- decreased cardiac output & shock
What does gastric dilation & volvulus look like in Sw?
- torsion of the stomach or the small intestine is one of the main causes of sudden death in adult breeding stock
- the twist can involve the stomach, the spleen, part of the liver, &/or the intestine
What does gastric dilation & rupture look like in Eq?
- acute gastric dilation & rupture in equids occurs most frequently as a terminal event in small intestinal obstruction, ileus, & displacement
- it can also be the result of rapid ingestion of fermentable feeds or grains, a situation analogous to grain overload w/ lactic acidosis in cattle
What does gastric dilation & rupture look like in non-human primates?
- in research facilities occasionally develop acute gastric dilation associated w/ food restriction & accidental overfeeding
- this cause is unknown, but two principal factors seem to be the intragastric fermentation associated w/ Clostridium perfringens, & abnormal gastric function
In other animals what is gastric/abomasal dilation usually secondary to?
- ulcers, pyloric stenosis, overeating, gastritis/abomesitis, vagal indigestion, etc.
What are the clinical consequences of gastric dilation?
- severe distention compromises respiration & cardiovascular function & electrolyte balance
- gastric rupture (usually along the major curvature) is often the ultimate cause of death
How do you distinguish btwn ante-mortem & post-mortem gastric rupture?
- the only reliable indicator of ante-mortem rupture of the stomach is the presence of hemorrhage along the margins & evidence of acute inflammation (ex: fibrin strands)
- if these changes are not present on gross exam, histo exam of the margins is recommended to rule out postmortem distention & rupture of the stomach/abomasum
Who does abomasal displacement and volvulus usually occur in in cows?
- high-producing dairy cattle during the first 6 weeks after parturition
What are the causes of abomasal displacement & volvulus in cattle?
- abomasal atony due to heavy grain feeding (volatile fatty acids decrease motility)
- impaired movement of ingesta & gas formation
- hypocalcemia at the onset of lactation -> decreased strength of muscle contractions
What are the clinical features of a displaced abomasum (right or left sided)?
- anorexia, dehydration, decreased amount of feces, ketouria, characteristic high-pitched ping subsequent to percussion over displaced abomasum
What is important about a left-sided abomasal displacement?
- most common
- generally nonfatal
What is important about a right-sided abomasal displacement?
- occurs only in 10-15%
- it is considered more significant b/c it may progress to abomasal volvulus resulting in an abomasal venous infarction & death
What is important about Clostridium septicum in abomasitis?
- it is a cause of hemorrhagic abomasitis w/ submucosal emphysema of lambs & occasionally calves (a disease known as BRAXY)
- this disease is most common in Europe, but it occasionally also occurs in North America
- generally, the disease follows ingestion of frozen feeds contaminated w/ the causative Clostridium spp.
- the lesions are produced by the exotoxin of the bacteria, & death therefore is due to an exotoxemia (similar to Clostridial myositis)
What is fundic mucosal infarction in pigs?
- in many cases of septicemia in pigs (ex: salmonellosis, swine dysentery, Glasser’s disease, & colibacillosis), venular thromboses occur in the fundic mucosa/submucosa resulting in congestion, hemorrhage, venous infarction, & ulceration
What is gastritis often associated w/ clinically?
vomiting, dehydration, & metabolic acidosis
what are the different types of gastritis?
- acute mild gastritis
- canine hemorrhagic gastroenteritis (acute hemorrhagic diarrhea syndrome)
- chronic gastritis
Who is acute mild gastritis most common in and why?
- dogs rather than cats due to less discriminating eating habits
What are the clinical signs of acute mild gastritis?
vomiting & inappetence w/o systemic signs
What are the causes of acute mild gastritis?
- ingestion of spoiled or contaminated food, foreign objects, toxic plants, chemicals, NSAIDs
What is the prognosis of acute mild gastritis?
- not fatal & transient
- it is successfully diagnosed & treated clinically (feed withdrawal & antiemetics)
Who does canine hemorrhagic gastroenteritis (acute hemorrhagic diarrhea syndrome) most often occur in?
most often occurs in smaller breeds
What is the cause of canine hemorrhagic gastroenteritis (acute hemorrhagic diarrhea syndrome)?
not clear but infection w/ Clostridium perfringens of unknown type is suspected
What are the clinical signs of canine hemorrhagic gastroenteritis (acute hemorrhagic diarrhea syndrome)?
- hematemesis & hematochezia (often w/ hemoconcentration > PCV .60%)
- on presentation, animal may be moribund & may die due to cardiovascular collapse, renal failure, &/or DIC
What would you see on endoscopy/necroscopy for canine hemorrhagic gastroenteritis (acute hemorrhagic diarrhea syndrome)?
- diffuse hemorrhagic necrosis of gastrointestinal superficial mucosa (most severe in colon)(w/ Clostridial bacteria identified by histo)
Parvo vs canine hemorrhagic gastroenteritis (acute hemorrhagic diarrhea syndrome)?
- parvoviral enteritis may have similar gross appearance, but histologically there is cryptal necrosis in the small intestines & it DOES NOT AFFECT THE STOMACH
What are the clinical signs of chronic gastritis?
- emesis & if intestines are also affected than diarrhea & occasionally hematochezia
- dehydration
What are the different types of chronic gastritis?
- eosinophilic gastritis as part of gastroenteritis or gastroenterocolitis
- lymphoplasmacytic gastritis
- hyperplastic (also called hypertrophic) gastritis in dogs
- uremic gastritis
Who is eosinophilic gastritis as part of gastroenteritis or gastroenterocolitis seen in?
in dogs & less commonly in cats
What is the etiology of eosinophilic gastritis as part of gastroenteritis or gastroenterocolitis?
etiology is poorly understood: 2 conditions should be considered when the diagnosis of eosinophilic gastroenteritis is made on an endoscopic biopsy of the stomach, duodenum , & colon (REMEMBER TO ALWAYS SAMPLE ALL 3 SITES WHEN DOING ENDOSCOPIC GIT BIOPSY TO INCREASE THE CHANCE OF YOUR DIAGNOSIS!!!):
1. Parasites
2. hypersensitivity reaction to unknown allergen or food intolerance
why should you consider parasites w/ eosinophilic gastritis as part of gastroenteritis or gastroenterocolitis?
- gastrointestinal parasites (ex: Toxocara canis, Physaloptera canis, Ollulanus tricuspis, Trichuris vulpis, Ancylostoma spp - last two can cause blood & protein loss) & their products induce variable degrees of eosinophilic inflammation occasionally w/ mild to moderate hyperplasia
why should you consider a hypersensitivity reaction to an unknown allergen or food intolerance w/ eosinophilic gastritis as part of gastroenteritis or gastroenterocolitis?
- most likely due to feed ingredients or preservatives or medications (allergens)
- sometimes this is accompanied by a peripheral eosinophilia & skin disease
- more severe aspect of this condition can present as hemorrhagic enteritis
What will you see with endoscopy w/ eosinophilic gastritis as part of gastroenteritis or gastroenterocolitis?
- the gross lesions of eosinophilic gastroenteritis are rather nonspecific (mild hyperemia & thickening of the mucosa, increased amounts of mucus)
How do we diagnose eosinophilic gastritis as part of gastroenteritis or gastroenterocolitis?
Histo
What is the cause of lymphoplasmacytic gastritis?
not determined - chronic irritative/antigenic stimulus by gastric bacteria (including Helicobacter spp.) suspected
What is characteristic of hyperplastic (hypertrophic) gastritis in dogs?
thickened rugae secondary to hyperplasia of gastric glands
What are the causes of hyperplastic (hypertrophic) gastritis in dogs?
- chronic retention of gastric fluid & reflux of intestinal bile
- immune-mediated process resulting in hyperplastic lymphoplasmacyctic gastritis
- idiopathic
What is FOCAL hyperplastic (hypertrophic) gastritis in dogs?
Antral (pyloric) hyperplastic (hypertrophic) gastritis:
- in older small breed dogs
- clinical signs of upper GI obstruction (post-prandial vomiting)
- diagnosis by endoscopy & radiography (endoscopic biopsy may not be useful diagnostic test b/c samples are taken only from the superficial mucosa)
- must be differentiated from pyloric obstruction due to pyloric muscular hypertrophy which presents w/ similar clinical signs (may need imaging or laparoscopy to differentiate from pyloric hyperplastic gastritis)
What is DIFFUSE hyperplastic (hypertrophic) gastritis in dogs?
- chronic giant hypertrophic gastropathy is a rare disease in Ca which are affected by weight loss, D+, V+, & hypoproteinemia
- cause is unknown
- ante-mortem diagnosis is made by endoscopy
Who, besides Ca, can also get hyperplastic (hypertrophic) gastritis?
- described also in primates & Eq due to parasitism
What is the cause of uremic gastritis?
chronic renal disease/failure
What would you see on endoscopy/necropsy in uremic gastritis? What about microscopic exam?
- major gross lesions are nonspecific congestion & edema of the gastric mucosa w/ occasional ulceration
- caused by injury to capillaries w/in the lamina propria associated w/ elevated concentrations of nitrogen-derived metabolic waste products in the systemic circulation from kidney failure
- microscopic exam reveals mineralization of the glands, vessels, & lamina propria of the gastric mucosa
gross lesions of uremia in dogs?
- severe bilateral renal fibrosis (etc.) -> chronic renal failure
- secondary bilateral parathyroid hyperplasia
- bilateral erosive glossitis (+/- stomatitis)
- mineralization of intercostal muscles
- uremic gastritis w/ mid-mucosal mineralization
- uremic pneumonitis
- osteodystrophy fibrosa (osteopenia)
What is an ulcer?
- a mucosal defect in which the entire epithelial thickness w/ the basement membrane is lost
What is a perforating ulcer?
- penetration through the remaining tissue layers to the peritoneal cavity
What is an erosion?
- partial- thickness epithelial loss
How are chronic ulcers different from acute ulcers?
chronic ulcers have an indurated rim caused by fibrosis & epithelial hyperplasia (attempts of epithelial regeneration)
What would you see on endoscopy/ necropsy w/ gastric ulcers?
- sharply demarcated areas of mucosal loss often covered w/ exudate
What are the clinical signs of gastric ulcers?
- vomiting & hematemesis
- anorexia
- abdominal pain
- anemia secondary to gastric bleeding resulting in melena (digested blood in feces)
- decreased production (ex: milk) & performance
- exsanguination -> death
- peritonitis & septicemia due to perforating ulcer -> death
What is the pathogenesis of gastric ulcers?
conditions necessary for ulcer development could be boiled down to an imbalance btwn acid secretion & mucosal protection:
- high gastric acidity
- infection
- local disturbances in blood flow
- NSAIDs
- local disturbances or trauma to the mucosal epithelial barrier
Relationship btwn high gastric acidity and the pathogenesis of gastric ulcers?
- mast cell tumours in dogs & occasionally cats stimulate gastric HCl secretion through histamine release
- gastrinoma: functional tumour of G-cells in duodenum or pancreatic islets that produce gastrin which increases the secretion of HCl & causes gastric ulceration (occurs rarely in Ca; in humans it is called Zollinger-Ellison syndrome)
Relationship btwn infection and the pathogenesis of gastric ulcers?
- in certain primates (including humans), a substantial portion of gastric & duodenal ulcers are the result of infection w/ Helicobacter pylori (this same bacterium has been epidemiologically linked to gastric adenocarcinoma)
- in ferrets, Helicobacter mustelae acts similarly
- in dogs & cats, similar gastric Helicobacter-like organisms (GHLOs) are present in the stomach, but their relationship w/ ulcer formation or neoplasia is not established at this stage (it appears that the stomachs of as many animals w/o ulcers are as heavily colonized by these bacteria as are those animals w/ ulcers)
Relationship btwn local disturbances in blood flow and the pathogenesis of gastric ulcers?
- stress-induced disturbance in blood flow by neurogenic, hypovolemic, or septic shock results in gastric ischemia
Relationship btwn NSAIDs and the pathogenesis of gastric ulcers?
- NSAIDs depress prostaglandin formation resulting in decreased blood perfusion, decreased secretion of bicarbonate (buffering system disrupted), & some of them have direct toxic effects on vascular endothelium (ex: phenylbutazone)
Relationship btwn local disturbances or trauma to the mucosal epithelial barrier and the pathogenesis of gastric ulcers?
- this injury can be due to back flush of bile salts from the duodenum or ingestion of lipid SOLVENTS ex: alcohol
What are gastric ulcers like in horses?
- ulceration is affecting almost always only pars esophagea
- many foals are affected asymptomatically
- some w/ severe gastric ulceration may have abdominal pain, bruxism (grinding of the teeth), ptyalism, & gastric reflux
- in 40-90% of competitive & performance horses, ulceration of pars esophagea is present & is most severe in those that are worked the hardest
What are gastric ulcers like in pigs?
- ulceration is also affecting only pars esophagea
- it occurs commonly in penned pigs & is associated w/ multiple factors: finely ground grain, ingredients in diets (large quantities of skimmed milk or whey), & stress of confinement rearing, etc.
- occasionally, it is fatal due to exsanguination
What are gastric ulcers like in cattle?
- significance of abomasal ulceration ranges from subclinical to fatal
- in calves, ulcers are associated w/ dietary changes or mechanical irritation of the abomasum by roughage
- in dairy cattle, ulcers are associated w/ heavy grain feeding (lactic acidosis) at the time of parturition, displacement of the abomasum, BVD, impaction, torsion, & gastric lymphoma
Relevancy of parasitism?
- parasitic diseases are relatively easy to prevent & control by modern anthelmintics
- accordingly, they are not v commonly encountered in clinical practice
- however, resistance to drugs & climate change (more rain in the prairies) appear to be related to higher incidence of parasitic diseases in small Ru
What are the gastric parasites of horses?
- Gasterophilus intestinalis & Gasterophilus nasalis (equine bots) are commonly seen in Eq on inadequate deworming regimens (this may be a hint to check for more important pathogenic parasites ex: Strongylus vulgaris)
- Bot fly (Gasterophilus intestinalis) lays eggs on the hairs of the distal limbs of the horse, & bot fly (Gasterophilus nasalis) lays its eggs around the nose of the horse.
- the larvae hatch after being moistened & warmed by licking , invade oral mucosa, & travel to the pars esophagea (Gasterophilus intestinalis) & glandular stomach & duodenum (Gasterophilus nasalis)
- both spp attach to the mucosa via their hooked mouthparts (maxillae)
- the larvae pass in the feces (next year), pupate, & develop into flies
- bot flies may annoy horses which may injure themselves by trying to get rid of the flies
- larvae cause minimal damage which is usually clinically insignificant, but suggest inadequate deworming protocol
What are important abomasal parasites of Ru?
- haemonchus contortus
- ostertagia ostertagi & Ostertagia circumcincta
Who is Haemonchus contortus?
- known as the barber pole worm
- most common in sheep & goats
What is the lifecycle of Haemonchus contortus?
- hyperinfested pastures containing numerous 3rd-stage larvae are the source of infection which can be acute (sudden death), subacute (hypoproteinemia & anemia), or chronic (weight loss & eventual hypoproteinemia & anemia)
- larvae on grasses are ingested by the host & enter the abomasum, where they may lie dormant w/in the gastric glands (hypobiosis) during periods of climatic adversity (cold or dryness)
- hypobiosis may be terminated in females by stress of parturition during spring, which will follow w/ subsequent contamination of pastures & lamb infection
- after development to adults, they exit from the abomasal glands to the surface, attach via a buccal tooth & suck blood
- eggs pass in the feces, completing the life cycle
what are the clinical signs of Haemonchus contortus?
they are blood feeders (loss of both erythrocytes & protein), therefore they cause:
- severe anemia -> pale mucous mbs
- hypoproteinemia -> generalized edema (bottle jaw)
- weight loss (non-specific sign)
- usually w/o D+ if not complicated by other GIT disorders
How do we diagnose Haemonchus contortus?
- presumptive diagnosis may be made based on observation of a large number of adult worms in abomasum together w/ severe hypoproteinemia (edema) & anemia observed clinically or at post mortem exam
- the definitive diagnosis at necropsy is based on semiquantification of abomasal parasite load together w/ anemia & generalized edema due to hypoproteinemia
Who affects calves w/ similar signs to Haemonchus contortus in sheep?
Haemonchus placei
Who are Ostertagia ostertagi & Ostertagia circumcincta
- cause ostertagiosis in cattle & sheep, respectively
What are the lifecycles of ostertagia ostertagi & Ostertagia circumcincta?
- animals ingest L3 larvae which burrow into the abomasum glands & molt into early stage of L4 larvae
- if development into adult stage proceeds immediately ‘Type I’ disease occurs
- if the larvae become dormant (hypobiosis), the disease will be delayed & it happens during synchronous maturation & emergence of hypobiotic larvae from the mucosa usually during winter (this is called Type II disease)
How are abomasal glands significantly damaged by larval development & emergence w/ ostertagia ostertagi & Ostertagia circumcincta?
- parietal & chief cells are replaced by mucus cells (mucous cells from metaplasia & hyperplasia) accompanied by inflammation
- loss of parietal cell results in loss of acidic pH (abomasal achlorhydria)
- intercellular junction btwn poorly differentiated mucus cells are not tight (leaky) resulting in: protein-losing gastropathy -> systemic hypoproteinemia; back-diffusion of pepsinogen into lamina propria & circulation)
What are the clinical signs of ostertagia ostertagi & Ostertagia circumcincta?
inappetence, D+, wasting, generalized edema (due to hypoproteinemia)
What would you see on necropsy w/ ostertagia ostertagi & Ostertagia circumcincta?
- ‘Morocco leather’ or ‘cobblestone’ appearance of the abomasum of heavily infested animals
- generalized edema due to hypoproteinemia (NO anemia)
- diagnosis: above 2 findings are often sufficient for diagnosis (proper worm count w/ digestion of abomasal mucosa may be performed to confirm diagnosis
Who causes mucosal thickening & mucus metaplasia/hyperplasia in the stomach of pigs?
Hyostrongylus rubidis
What does neoplasia of the stomach look like in Eq?
SCC of the pars esophagea is v invasive & metastatic
What does neoplasia of the stomach look like in Bo?
lymphoma is caused by the Bo leukemia virus & has an apparent predilection for the abomasum, R atrium, & uterus
What does neoplasia of the stomach look like in Ca & Fe?
gastric adenocarcinoma is locally invasive & metastatic; lymphomasarcoma can also occur
Fundic gland
Postmortem exam of stomach or abomasum
Postmortem exam of stomach or abomasum
where should you take a sample of the stomach for histo?
gastric dilation in rabbit
Ca
gastric dilation & volvulus
Eq
Gastric dilation & rupture
Eq
gastric dilation & rupture
Eq
gastric dilation & rupture (fibrinous)
What 4 things happen when you obstruct a blood vessel?
- congestion
- edema
- hemorrhage
- necrosis/ischemia
Calf
abomasal volvulus
calf
abomasal volvulus (opened)
calf
mycotic abomasitis
calf
mycotic abomasitis & omasitis
Hemorrhagic & emphysematous abomasitis (do not confuse w/ torsion)
Hemorrhagic & emphysematous abomasitis (do not confuse w/ torsion - can see emphysema inside & not diffuse discolouration)
hemorrhagic & emphysematous abomasitis
ca & fe
gastritis
Ca
hemorrhagic gastritis
Physaloptera rara
antral (pyloric) hyperplastic gastritis
antral (pyloric) hyperplastic gastritis
hyperplastic gastritis
biopsy will reveal mineralization, Fe
uremic gastritis
Eq
pars esophagea ulceration
Ca
gastric ulcer w/ exsanguination
perforating abomasal ulcer
Eq
gasterophiliasis
anemia
Haemonchus contortus
Haemonchus contortus
What is this condition called?
bottle jaw
Ostertagia ostertagi
Ostertagia ostertagi
Who?
Ostertagia ostertagi arrested larva (early L4) in fundic gland
How do you need to change your sampling method for the stomach when you suspect Ostertagia ostertagi?
need to sample further down b/c mucus cells will be extended
